Cardiopulmonary Bypass

Cardiopulmonary Bypass
Third Edition
P bli h d li b C b id i i P
Edited by
Florian Falter
Royal Papworth Hospital, Cambridge
Albert C Perrino
Yale University Medical Center, New Haven, CT
Robert A. Baker
Flinders Medical Centre and Flinders University, Adelaide
The editors are very grateful to Dr Ghosh, who started this project and led the first two editions
from idea to printed book
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DOI: 10.1017/9781009008143
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First published 2009
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Third edition 2022
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Library of Congress Cataloging-in-Publication Data
Names: Falter, Florian, editor. | Perrino, Albert C., Jr. editor. | Baker, Robert A,
1960- editor.
Title: Cardiopulmonary bypass / edited by Florian Falter, Albert C. Perrino,
Robert A. Baker.
Other titles: Cardiopulmonary bypass (Ghosh)
Description: Third edition. | Cambridge, United Kingdom ; New York, NY :
Cambridge University Press, [2022] | Preceded by Cardiopulmonary
bypass / edited by Sunit Ghosh, Florian Falter, Albert C. Perrino, Jr.
Second edition. 2015 | Includes bibliographical references and index.
Identifiers: LCCN 2022010263 (print) | LCCN 2022010264 (ebook) |
ISBN 9781009009621 (paperback) | ISBN 9781009008143 (epub)
Subjects: MESH: Cardiopulmonary Bypass–methods | Cardiac Surgical
Procedures–methods
Classification: LCC RD598 (print) | LCC RD598 (ebook) | NLM WG 168.5 |
DDC 617.4/120592–dc23/eng/20220511
LC record available at https://lccn.loc.gov/2022010263
LC ebook record available at https://lccn.loc.gov/2022010264
ISBN 978-1-009-00962-1 Paperback
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persistence or accuracy of URLs for external or third-party internet websites
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such websites is, or will remain, accurate or appropriate.
..................................................................
Every effort has been made in preparing this book to provide accurate and up-to-
date information that is in accord with accepted standards and practice at the time
of publication. Although case histories are drawn from actual cases, every effort has
been made to disguise the identities of the individuals involved. Nevertheless, the
authors, editors, and publishers can make no warranties that the information
contained herein is totally free from error, not least because clinical standards are
constantly changing through research and regulation. The authors, editors, and
publishers therefore disclaim all liability for direct or consequential damages
resulting from the use of material contained in this book. Readers are strongly
advised to pay careful attention to information provided by the manufacturer of
any drugs or equipment that they plan to use.
Contents
List of Contributors vi
Foreword ix
Alan Merry 11 Myocardial Preservation during
Cardiopulmonary Bypass 102
Gudrun Kunst, Luc Puis and Tom Gilbey
1 Human Factors and Teamwork in 12 Weaning from Cardiopulmonary Bypass 112
Cardiac Surgery 1 Joanne F Irons, Kenneth G Shann
Lindsay Wetzel, David Fitzgerald, Thoralf M and Michael Poullis
Sundt and James H Abernathy III
13 Intraoperative Mechanical Circulatory
2 Equipment for Cardiopulmonary Bypass 9 Support and Other Uses of
Simon Anderson and Amanda Crosby Cardiopulmonary Bypass 123
Mark Buckland and Jessica Underwood
3 Monitoring during
Cardiopulmonary Bypass 25 14 Mechanical Circulatory Support 138
Richard F Newland and Pascal Starinieri Jason M Ali, Ayyaz Ali and Yasir Abu-Omar
4 Cardiopulmonary Bypass Circuit Setup and 15 Cardiopulmonary Bypass for Pediatric
Safety Checks 34 Cardiac Surgery 150
Victoria Molyneux and Shahna Helmick Joseph J Sistino and Timothy J Jones
5 Priming Solutions for Cardiopulmonary 16 Coagulopathy and Hematological Disorders
Bypass Circuits 42 Associated with
Filip De Somer and Robert Young Cardiopulmonary Bypass 156
Bruce D Spiess and Erik Ortmann
6 Anticoagulation for
Cardiopulmonary Bypass 49 17 Inflammation and Organ Damage during
Martin Besser and Linda Shore-Lesserson Cardiopulmonary Bypass 166
R Clive Landis and Sherif Assaad
7 Conduct of Cardiopulmonary Bypass 57
Christiana Burt, Timothy A Dickinson, Narain 18 Neuromonitoring and Cerebral Morbidity
Moorjani and Caitlin Blau Associated with
8 Minimal Invasive Etienne J Couture, Stéphanie Jarry and André
Extracorporeal Circulation 71 Y Denault
Kyriakos Anastasiadis, Polychronis Antonitsis,
Helena Argiriadou and Apostolos 19 Renal Morbidity Associated with
Deliopoulos Cardiopulmonary Bypass 184
Juan Pablo Domecq and Robert C Albright
9 Considerations for Operations Involving Deep
Hypothermic Circulatory Arrest 80 20 Common and Uncommon Disasters during
Pingping Song and Joseph E Arrowsmith Cardiopulmonary Bypass 194
Gregory M Janelle, Jane Ottens and Michael Franklin
10 Metabolic Management during
Jonathan Brand and Edward M Darling
Index 205 v
Contributors
James H. Abernathy III Helena Argiriadou

Associate Professor, Interim Executive Vice Chair, Cardiac Anesthesiologist, Assistant Professor,
ACCM Chief, Division of Cardiac Anesthesiology Aristotle University of Thessaloniki
Core Faculty, Armstrong Institute of Patient Safety,
Department of Anesthesiology & Critical Care Joseph E. Arrowsmith
Medicine, Johns Hopkins University Consultant Anaesthetist, Department of Anaesthesia
& Intensive Care Medicine, Royal Papworth
Yasir Abu-Omar Hospital
Director, Cardiothoracic Transplantation and
Mechanical Circulatory Support, University Hospitals Sherif Assaad
Cleveland Medical Center Associate Professor, Cleveland Clinic Lerner College
of Medicine | Case Western Reserve University, and
Robert C. Albright Jr Staff Anesthesiologist, Department of Cardiothoracic
Consultant, Division of Nephrology and HTN Mayo Anesthesiology | Anesthesiology Institute, Cleveland
Clinic Rochester; Professor of Medicine, Division of Clinic
Nephrology and HTN, Mayo Clinic College of
Medicine, Mayo Clinic, Rochester; Regional Vice Martin Besser
President, Mayo Clinic Health System Southeast; Consultant Haematologist, Royal Papworth
Professor of Medicine; Consultant, Division of Hospital
Nephrology and Hypertension Caitlin Blau
Ayyaz Ali Perfusion Supervisor, Mayo Clinic
Vice Chairman of Cardiac Surgery and Surgical Jonathan Brand
Director of Heart Transplantation and Mechanical
Clinical Director and Consultant in Cardiothoracic
Circulatory Support, Hartford Hospital
Anaesthesia and Critical Care, James Cook University
Jason M. Ali Hospital, Middlesbrough
Locum Consultant in Cardiothoracic and Transplant Mark Buckland
Surgery, Royal Papworth Hospital
Deputy Director, Head of Cardiothoracic
Kyriakos Anastasiadis Anaesthesia, Department of Anaesthesiology &
Professor, Department of Cardiothoracic Surgery, Perioperative Medicine, Alfred Hospital and Monash
Aristotle University of Thessaloniki University
Simon Anderson Christiana Burt

Clinical Perfusion Team Leader, Cambridge Consultant Anaesthetist, Royal Papworth Hospital
Perfusion Services, Royal Papworth Hospital Etienne J. Couture
Polychronis Antonitsis Anesthesiologist & Intensivist, Institut universitaire
Associate Professor, Department of Cardiothoracic de cardiologie et de pneumologie de Québec –
Surgery, Aristotle University of Thessaloniki Université Laval (IUCPQ-UL)
vi
List of Contributors
Amanda Crosby Joanne F. Irons

Staff Perfusionist, University of Tennessee Medical Senior Lecturer, University of Sydney; Staff Specialist
Center Anaesthetist, Royal Prince Alfred Hospital
Edward M. Darling Gregory M. Janelle
Associate Professor, College of Health Professions, Professor of Anesthesiology and Surgery and Associate
Department of Cardiovascular Perfusion, SUNY Chair for Clinical Affairs, Department of Anesthesiology,
Upstate Medical University; Faculty/Clinical University of Florida College of Medicine
Coordinator
Stéphanie Jarry
Filip De Somer PhD candidate, Department of Anesthesiology,
Professor in Perfusion Technology, University Ghent, Montreal Heart Institute, Université de Montréal
Chief Perfusionist, University Hospital Ghent
Timothy J. Jones
Apostolos Deliopoulo Consultant Congenital Cardiac Surgeon, Birmingham
Perfusionist, Cardiothoracic Department, Aristotle Women’s and Children’s Hospital, University
University of Thessaloniki Hospitals Birmingham; Honorary Senior Lecturer,
Institute of Cardiovascular Science, University of
André Y. Denault Birmingham
Professor, and Anesthesiologist & Intensivist,
Montreal Heart Institute, Université de Montréal Gudrun Kunst
Professor of Cardiovascular Anaesthesia, Department
Timothy A. Dickinson of Anaesthetics and Pain Medicine, King’s College
Assistant Professor of Surgery, CCP, Mayo Clinic; Hospital NHS Foundation Trust & School of
Director, Perfusion Services Cardiovascular Medicine and Sciences, King’s College
Juan Pablo Domecq London; Consultant Anaesthetist and Professor of
Cardiovascular Anaesthesia, British Heart
Senior Associate Consultant, Division of Nephrology,
Foundation Centre of Research Excellence
Hypertension and Critical Care Medicine, Mayo Clinic,
Rochester, and Mayo Clinic, Mankato; Assistant R. Clive Landis
Professor of Medicine, Mayo Clinic College of Medicine Professor of Cardiovascular Research, and Pro Vice
David Fitzgerald Chancellor and Principal, The University of the West
Indies, Cave Hill Campus
Assistant Professor, Division Director, CVP Program,
Medical University of South Carolina Victoria Molyneux
Michael Franklin Senior Clinical Perfusionist, Great Ormond Street
Hospital for Children NHS Foundation Trust
Clinical Assistant Professor – Cardiothoracic
Anesthesiology, University of Florida Narain Moorjani
Tom Gilbey Consultant Cardiac Surgeon & Clinical Lead for
Cardiac Surgery, Royal Papworth Hospital; Affiliated
Anaesthetic Registrar and NIHR Academic Clinical
Assistant Professor, University of Cambridge;
Fellow, Department of Anaesthetics and Pain
President, Society for Cardiothoracic Surgery in Great
Medicine, King’s College Hospital NHS Foundation
Britain & Ireland
Trust
Richard F. Newland
Shahna Helmick
Senior Perfusionist & Clinical Lead for Perfusion,
Program Director of Perfusion Education, University
Flinders Medical Centre and Lecturer, Flinders
of Iowa Hospitals and Clinics
University
vii
List of Contributors
Erik Ortmann Center; Medical Director, Cardiothoracic Intensive

Chair, Department of Anaesthesiology, Care Unit
Schüchtermann-Heart-Centre
Bruce D. Spiess
Jane Ottens Professor and Associate Chair (Research), University
Chief Perfusionist, Ashford Hospital of Florida College of Medicine
Michael Poullis Pascal Starinieri

Senior Fellow Cardiothoracic Surgery, Manchester Clinical Perfusionist, JESSA Hospital
Royal Infirmary
Thoralf M. Sundt
Luc Puis Chief, Division of Cardiac Surgery, Director of
Senior Perfusionist, University Hospital Brussels, Cardiac Surgery Clinical Service, and Edward D.
Center for Heart and Vascular Diseases Churchill Professor of Surgery, Harvard
Medical School, Massachusetts General
Kenneth G. Shann Hospital
Director, Perfusion Services, Massachusetts General
Hospital Jessica Underwood
Perfusionist, Alfred Hospital; Director, Victorian
Linda Shore-Lesserson Perfusion Specialists
Professor of Anesthesiology, Zucker School of
Medicine at Hofstra Northwell; Vice Chair Academic Lindsay Wetzel
Affairs; Director, Cardiovascular Anesthesiology Cardiac Anesthesiologist, TriHealth Heart Institute -
Seven Hills Anesthesia
Joseph J. Sistino
Professor Emeritus, Medical University of South Robert Young
Carolina College of Health Professions Specialist Cardiothoracic Anaesthetist, Department of
Anaesthesia, Flinders Medical Centre
Pingping Song
Assistant Professor, Department of Anesthesiology &
Pain Medicine, University of Washington Medical
viii
Foreword
Six years after the publication of the second edition of edition, the editors have achieved a consistency of
Cardiopulmonary Bypass, Florian Falter, Robert style and message with a minimum of repetition.
Baker and Albert C Perrino have produced a substan- Thus, the book feels coherent and has a logical flow
tial revision of this highly regarded text. Success in of ideas. As before, there is effective use of illustra-
cardiac surgery requires each member of the team to tions and tables and a good bibliography of selected
be expert in the theory and capable in the practice of references for each chapter. The book will continue to
their individual discipline, but it also requires them to provide an outstanding introduction to this field of
work together effectively as a team, often for long practice, both for surgeons and anesthetists, who pri-
hours under considerable stress. It is thus very pleas- marily need to understand and contribute to the
ing to see a strong new emphasis on teamwork, com- management of cardiopulmonary bypass or mechan-
munication and human factors added to this already ical circulatory support, and for perfusionists who
excellent book. This emphasis is reflected in the also have to set up and run the equipment. For those
renewed authorship of each chapter, which (in most already expert in this field, it will provide a technically
cases) now includes all three of the disciplines key to up-to-date source for revision of the relevant topics
the management of cardiopulmonary bypass – anes- from a highly contemporary perspective.
thesia, perfusion and surgery. The list of editors and The editors work in leading institutions in their
authors is a “Who’s Who” of this field and reflects not respective countries (England, Australia and the
only deep expertise in the relevant topics but also United States). Each is known for leadership and
established ability to disseminate knowledge through innovation within their discipline. The same can be
lecturing and writing. The result, as one might expect, said for the chapter authors. It is unsurprising that the
is a scientifically sound, clearly written and highly book carries a tone of authority that will leave readers
accessible text. It is a text that will (like the previous confident in the reliability of the information and the
edition) be an excellent source of practical hands-on soundness of the perspectives within it.
advice on how to apply the underpinning principles I offer the editors and the authors my hearty
to the everyday practice of cardiopulmonary bypass congratulations.
within the dynamic context of cardiac surgery.
The number of chapters has increased from 16 to Alan Merry FANZCA, FFPMANZCA, FRSNZ
20, but new material has been incorporated through- Professor of Anaesthesiology, University of
out. The themes of teamwork, communication, Auckland,
checklists and safety (both Safety-I and Safety-II) Specialist in Anaesthesia, Auckland City Hospital,
run through the entire book. As with the previous New Zealand.
ix
Chapter
Human Factors and Teamwork in
1 Cardiac Surgery
Lindsay Wetzel, David Fitzgerald, Thoralf M Sundt and James H Abernathy III
Teams are especially critical for avoiding errors

Today we face many problems. Some are created and for responding to unexpected events that can
essentially by ourselves based on divisions due to result in catastrophic complications if not managed
ideology, religion, race, economic status, or other appropriately. The elite cardiac operating room rep-
factors. Therefore, the time has come for us to think resents a delicate symphony of quick decision-
on a deeper level, on the human level, and from that making, refined technical skill and sound judgment
level we should appreciate and respect the sameness of by each member of a large multidisciplinary team
others as human beings. consisting of perfusionists, surgeons, anesthesiolo-
—Dalai Lama gists, fellows, residents, nurses, surgical technologists
and other highly trained, capable healthcare
In the current healthcare environment, there is an providers.
increasing focus on providing high quality patient A hallmark feature of successful teams is effective
care at ever lower costs while patients rightly expect and open communication. The cardiac operating
excellent outcomes. Cardiac surgery in particular is room is a high stakes environment where small break-
dependent on several disciplines working together downs in communication and teamwork can have
closely and having a good appreciation of the chal- significant consequences on safe patient care and
lenges facing each one. High quality outcomes are outcome. With that in mind, organizations that
dependent upon a wide array of factors, ranging from accredit healthcare providers, such as The Joint
patient specific issues, to provider acumen and tech- Commission in the United States, have pinpointed
nical skills, to ancillary support systems and increas- teamwork as being critical to thriving healthcare
ingly to organizational factors. organizations that provide optimal patient care and
Successful healthcare organizations understand minimize medical error.
the importance of using teams efficiently to accom-
plish difficult and complex tasks. Teams are assem-
bled with a central, unifying objective in mind and
Error
specific roles are assigned to each member in order to Before we understand teams, we must understand the
achieve this goal. This allows members to play to their root cause of error. It is increasingly recognized that
individual skill set and operate within their comfort most medical errors are avoidable. Rather than being
zone. Advanced technology, streamlined techniques, related to a lapse of technical skill, poor medical
and improved science, much of which is outlined in decision-making, inadequate knowledge or subopti-
the chapters of this text, have no doubt improved mal training, they are more commonly the result of a
practitioner skills and enhanced care. Importantly, a breakdown in effective communication, in teamwork
shared mental model gives what would otherwise be a or during transition of care. Addressing system-based
group of skilled individuals working in isolation the issues, breakdowns in cognitive networks and advan-
ability to successfully tackle increasingly complex cing team-based approaches are essential to high
tasks together. Teams generally provide a purpose quality care.
and a broader sense of meaning to each member, The famous human factors engineer, James
creating a sense of mutual support which can bind Reason, described all systems as containing both
individuals together. active and latent failures. Active failures represent
1
h //d i /10 1017/9781009008143 001 P bli h d li b C b id i i P

Table 1.1. Overview of Safety 1 and 2
Safety 1 Safety 2
Definition of That as few things as possible go wrong. That as many things as possible go right.
Safety
Safety Reactive, respond when something happens or Proactive, continuously trying to anticipate
management is categorized as an unacceptable risk. developments and events.
principle
View of the Humans are predominantly seen as a liability or Humans are seen as a resource necessary for
human factor hazard. They are a problem to be fixed. system flexibility and resilience. They provide
in safety flexible solutions to many potential
management problems.
Accident Accidents are caused by failures and Things basically happen in the same way,
investigation malfunctions. The purpose of an investigation regardless of the outcome. The purpose of
is to identify the causes. an investigation is to understand how things
usually go right as a basis for explaining how
things occasionally go wrong.
Risk assessment Accidents are caused by failures and To understand the conditions where
malfunctions. The purpose of an investigation performance variability can become difficult
is to identify causes and contributory factors. or impossible to monitor and control.
Reprinted from, From Safety-I to Safety-II: A White Paper, Hollnagel E et al. Retrieved from www.england.nhs.uk/signuptosafety/wp-content/
uploads/sites/16/2015/10/safety-1-safety-2-whte-papr.pdf. Copyright 2015 by Erik Hollnagel, Robert L Wears, Jeffrey Braithwaite.
errors made by individuals at the service delivery end 2 embraces the variability in the healthcare delivery
(the operating room team); latent failures are organ- system and seeks to understand it. For example: Sally,
izational deficiencies (hospital wide, governmental, a perfusionist, is sought-after for complicated cases.
manufacturers, etc.) that are lurking in the back- She is talented clinically, communicates well, shares
ground contributing to active failures. Latent failures what she is thinking, makes good decisions and is
can be thought of as the holes in the Swiss cheese. steady under pressure. Sally’s resilience serves the
When errors occur, the majority of healthcare team well and, when Sally is there, it performs better.
organizations focus on the active failures, the most Rather than punishing people for making poor deci-
obvious of failures, through investigations like root sions (Safety 1), Safety 2 seeks to understand what
cause analyses or Morbidity & Mortality conferences. Sally does well and how this can be transferred to
Questions typically asked are: “who made mistakes?” other situations.
or “who didn’t follow the rules?.” This type of think- The two different perspectives are best summar-
ing with an emphasis on the negative has been coined ized in Table 1.1.
“Safety 1.” Safety 1 seeks to find the errors, the flaws,
the vulnerabilities. An alternative perspective, how-
ever, has emerged called “Safety 2.” In delivering The Human Factors Perspective
complex, complicated healthcare we do a lot of good Catchpole and McCulloch define human factors as:
and most times, we do it correctly. We manage to do “Enhancing clinical performance through an under-
this despite operating in increasingly complex standing of the effects of teamwork, tasks, equipment,
systems, with ever changing providers and more and workspace, culture and organization on human behav-
more demanding patients. The reason things go right ior and abilities and application of the knowledge in
is not that people behave as they are supposed to but clinical settings.” Or, stated more simply, “The science
because people adapt to the conditions they work in of improving human performance and well-being by
to make outcomes better. Understanding how people examining all the effectors of human performance.”
and the systems they work in adjust in order to Insights into the human factors perspective show
2
provide great care is how “Safety 2” is framed. Safety us that stress and fatigue, shortcomings in human

Chapter 1: Human Factors and Teamwork in Cardiac Surgery
Figure 1.1 Systems Engineering Initiative for Patient Safety (SEIPS) 2.0: A model of work system and patient safety. (Reprinted from Holden RJ,
Carayon P, Gurses AP et al. SEIPS 2.0: A human factors framework for studying and improving the work of healthcare professionals and patients. Ergonomics.
2013;56(11):1669–1686.)
memory, interruptions and distractions, overesti- healthcare performance and outcomes. It celebrates
mation of ability and overreliance on multi-tasking measures which foster quality patient care and pin-
can make even the most seasoned healthcare pro- points interventions which can help healthcare organ-
viders commit medical errors. One of the first frame- izations achieve and maintain surgical excellence. It is
works by which we can understand these complex juxtaposed to individual-centered approaches which
interactions is the Systems Engineering Initiative for contend that human error is due to deficiencies on a
Patient Safety (SEIPS) (see Figure 1.1). personal level and remedies that are focused on discip-
The SEIPS model provides a framework through linary, punitive and litigious means.
which we can identify and addresses modifiable
factors in the interaction of people and their environ-
ments with regard to patient safety events. For Teamwork
instance, the perfusionist (person) operating the car- Salas and coworkers have described teamwork as “a
diopulmonary bypass machine (tool) requires correct distinguishable set of two or more people who inter-
ergonomics, visual and auditory feedback. The com- act dynamically, interdependently, and adaptively
plex machine the person operates should be situated towards a common and valued goal, who have each
in a location that provides short tubing length, is not been assigned specific roles or functions to perform
at risk of being hit by opening OR doors and provides and who have a limited life-span membership.”
the perfusionist with clear lines of sight to the Teams share a common mission and must adapt to
anesthesiologist, the surgeon and the monitor so that the dynamics and demands of various tasks in order
communication is unencumbered (environment). to achieve their end goal. Teams collaborate, they
Outcomes are not only affected by technical skill, synthesize and integrate information and coordinate
but by the intersection of healthcare environment, among members to share responsibilities in a way
team ethos, workload, team member morale, technol- that makes best use of the strengths of each individ-
ogy, effective communication and organizational vari- ual. Successful teamwork is characterized by mutual
ables. The SEIPS model contends that medical error trust, effective communication, realistic goal setting,
can be a natural consequence of system wide break- fair division of tasks, desire to achieve a common goal 3
downs in the vast array of factors which influence and a shared passion for excellence.

Figure 1.2 Mental workload in the cardiac surgery operating room varies across the cardiac surgery procedure for individual providers
depending on task complexity and responsibilities. CRNA indicates certified registered nurse anesthetist; CST, certified surgical technologist;
NASA, National Aeronautics and Space Administration; Postop, postoperative; Prep, surgical preparation; RN, registered nurse; and TLX, Task
Load Index. (Reprinted from The Journal of Thoracic and Cardiovascular Surgery, Volume 139, Issue 2, RK Wadhera et al., Is the “sterile cockpit” concept applicable
to cardiovascular surgery critical intervals or critical events? The impact of protocol-driven communication during cardiopulmonary bypass, Pages 312–319.
Copyright © 2010, with permission from Elsevier.)
The Joint Commission recognizes communication during takeoff and landing or in unusual or stressful
as one of the top three contributing factors to sentinel situations. This principle is equally applicable to pro-
events. Broadly speaking, communication is “the ceedings in the cardiac operating room – going on
exchange of information between a sender and a and coming off bypass, as an example, are treated
receiver.” Effective communication is characterized similar to starting and landing. Some healthcare
by clarity, comprehensiveness and confirming that organizations have implemented the rule that when
the message has been relayed effectively. It contrib- one member of the team spots trouble they call out
utes to a shared mental awareness, clarifies what team “10,000 feet” to get attention and change the mood
members are worried about, identifies any issues that and focus in the room to problem-solving mode.
have arisen previously during similar moments and Closed-loop communication or “call back,” whereby
establishes an understanding of how to successfully the speaker’s message is repeated or paraphrased by
navigate these scenarios. Fostering an environment the receiver, is an effective way to reduce communi-
which cultivates open, truthful, adaptable, succinct cation ambiguity, miscues, and non-verbalized critical
and constructive communication is critical to any actions.
successful team. We must recognize that at no point during a case
Clear communication is vital during times of is the mental workload the same for all providers
stress. Critical situations don’t need bystanders, they (Figure 1.2). While the patient is on bypass the per-
require the key team members to be in the room and fusionist is working hard while the anesthesiologist
rely on them adhering to their assigned roles. The might have less to concentrate on; during the induc-
“sterile cockpit” concept, widely in use in military and tion of anesthesia, the surgeon will usually be doing
commercial aviation, describes the banning of non- something unrelated; during the vitally important
essential communication during critical periods asso- instrument count the scrub and circulating nurses
4 ciated with high-risk and high mental workload. In are ensuring nothing will be left behind while the rest
aviation, chatting is not allowed below 10,000 feet of the room is congratulating themselves on a job well

done. Understanding when different members find hand, overcome challenges in such a way that both
themselves in a period of increased mental workload performance and cohesion are at least sustained, if
helps the entire team to identify the times where we not improved, eventually leading to improved out-
can help our colleagues. comes. The underpinnings of resilience are a shared
Transition of care is an especially high-risk period vision and mission, healthy relationships and invested
for communication breakdown. Handoff of a patient team members. Resilient teams
when OR staff change shift or from operating room to – support each other and encourage recovery after
ICU staff are particularly vulnerable times. In the difficult situations,
absence of standardized clinical practice guidelines, – don’t lay blame on individuals after such
handoffs between providers may be highly variable situations but engage in learning through effective
and unstructured, missing important content items communication and constructive criticism to
during transfer. Poor information transfers also lead facilitate a different outcome in the future.
to incomplete clinical tasks and disruptions in care.
A team which can band together during times of
Standardized handoffs, such as the recently published
duress and lean on one another for support will
AmSECT perfusion handoff tool or the Formula
invariably arise from challenging situations stronger
1 type OR to ICU handoff tool proposed by
and better equipped to deal with future problems.
Catchpole, greatly improve the accuracy of informa-
This is particularly true for the cardiac operating
tion transfer (see Figure 1.3).
room.
Leadership
Leadership style in the cardiac operating room can Practical Solutions
have a significant impact on the function of the entire Breakdown in teamwork is commonly attributed to a
team. Transactional leaders focus more on individual lack of role clarity among team members or ineffect-
tasks, responsibilities and blame. They rarely see the ive communication. Proposals to improve communi-
big picture and engage in unilateral communication cation and to reduce the possibility of error include,
which is not conducive to a team focused environ- but are not limited to, standardized intraoperative
ment. Transformational leaders foster an environ- communication, preoperative briefings, and post-
ment of enthusiasm, learning, cooperation and a operative debriefings.
collective mission. Studies have shown a higher level
of teamwork and information sharing with trans- Standardized Conversations
formational leadership styles. Within a culture of
Standardizing communication practices facilitates
excellence, there must also be a commitment to
stronger team communication and helps all
respect. Professionalism and courtesy are not negoti-
team members “speak the same language.”
able. Effective leaders aim to flatten the hierarchy,
Communicating in a closed-loop, or read-back, fash-
create familiarity and foster an environment where
ion ensures that the entire team is aware of what is
everyone feels safe to speak up and participate. If
occurring and helps in retaining the shared mental
there was an easy button for establishing a culture of
model. Operating rooms can be chaotic places
excellence and effective leadership, we might not have
where background noise makes hearing difficult.
a need for this chapter. Personal and institutional
Acknowledging comments and questions ensures that
willingness to embrace tools such as Just Culture are
communications have been heard and understood.
important to tilt behavior toward personal account-
Repeating back essential information confirms that
ability and adaptability.
the sender’s message has been received. It is import-
ant to foster an environment where closed-loop com-
Repair, Recovery and Resilience munication is encouraged and not looked at as
Resilience alludes to the capacity of individuals and of disengagement (i.e. the individual repeating the mes-
teams to withstand and recover from pressures, stres- sage was not paying attention and hence needs clari-
sors and challenges. Failure to recover from an unex- fication.) Knowing team members by name helps to
pected event is a characteristic of poor performing make communications more direct and removes 5
perioperative programs. Resilient teams, on the other ambiguity as to who is being addressed.

Figure 1.3 AmSECT perfusionist handoff checklist. (Reproduced with kind permission of the AmSECT Safety Committee.)
6

Briefing and Debriefing providing recognized programs to integrate team-

work into clinical practice. Many of these programs
Briefings, both preoperative and postoperative, have
have drawn on decades worth of evidence-based
been implemented to promote information exchange
research pertaining to team building, culture change
and team cohesion. They originated in the aviation
and teamwork in organizations such as the military,
and nuclear power industries to ensure that important
nuclear power and aviation. Their goal is to help
information was communicated to every team
improve teamwork and communication skills. They
member. Preoperative briefings are an opportunity
offer open and accessible training programs in com-
for all operating room personnel to introduce them-
munication, leadership, situation monitoring and
selves with name and role and identify any concerns.
mutual support (see Figure 1.4).
Introduction of team members encourages team
Providing this training to OR teams has been
familiarity which has been linked to improved team-
shown to improve teamwork, communication, reduce
work. The operative plan needs to be discussed and
surgical mortality and morbidity, increase efficiency,
anticipated difficulties are communicated to develop
and improve patient satisfaction. However, sustain-
strategies as to how to deal with them. Any equipment
ability remains a challenge and often comes with the
requirements or lack of certain pieces of kit need to be
need for repeat training.
highlighted. If everybody is on the same page the
team is able to develop a shared mental model of the
work ahead, creating a sense of teamwork and collab- Non-Technical Skill Assessment Tools
oration. Conducting team briefings before every case Several non-technical skill (NTS) taxonomies aimed
is especially important for newer surgical teams or for at rating behavior in the operating department have
teams with new members who may not be aware of been reported in the literature. These instruments are
the unwritten or unspoken traditions. Open commu- designed to measure performance of multidisciplin-
nication before the case establishes a road map for ary team interactions, such as decision-making, situ-
conducting the case and helps minimize disruptions ational awareness, leadership, communication and
during the surgery (i.e. leaving the room to obtain teamwork. Several of the taxonomies have been pre-
equipment and supplies). viously adapted for the cardiac surgical arena and
The briefing, as described here, is distinct and beyond, including NOTSS (Non-Technical Skills
separate from a “time-out.” The “time-out” pause is for Surgeons), Oxford Non-Technical Skills
intended to ensure the right patient, right side, and (NOTECHS), and ANTS (Anaesthetists’ Non-
right operation. Technical Skills). Rating systems assess individual
Postoperative debriefings are equally critical as practitioner’s non-technical skills and team behavior.
they provide an opportunity for the team to under- They should be used as a metric and an incentive for
stand what went well during the case and identify individuals as well as institutions to improve their
areas for improvement in coming procedures. It is performance. While conventional wisdom may sug-
important to make postoperative briefings an arena gest that enhancing NTS performance will confer
for constructive feedback and not for blaming and significant improvements in the safety and the effi-
finger-pointing. When executed effectively, debrief- ciency of patient care, the implementation across
ings improve teamwork, communication and unity. medical education and healthcare institutions is
As teams gain experience together, debriefings will patchy. Unfortunately, there is no silver bullet to
help solve problems encountered during the case, accomplishing perfect team-based performance.
address “near misses” and hopefully prevent these Change often starts small and propagates. Start small,
issues from reoccurring in the future. build a well-functioning unit. Then, through good
outcomes and happy staff, demonstrate what
Creating the Team works for the broader organization. If you live and
Implementing formalized team training in the cardiac work in an organization whose leadership does not
operating room is a vital measure in decreasing value these concepts, press on anyway. Create the
surgical morbidity and mortality. There are numer- culture you want, where you work. Change starts
ous organizations, nationally and internationally, with you. 7

PROFESSIONAL TEAM BEHAVIOUR

• Inclusivity • Humility
• Enthusiasm • Honesty
• Equality • Integrity
• Clear communication • Civility
• Authenticity
Teamwork
& Leadership
Cooperation
COMMUNICATION
Situation Decision
Awareness Making
• Frequent updates • Decisions clearly
• Announces changes of plan communicated
• Clarifying confusion • Responsibility clear
• Input encouraged • Regular reviews
Figure 1.4 A visual model with the basic but critical concepts enabling teams to work together effectively. (Reproduced with kind permission
from Atrainability, https://atrainability.co.uk)
Suggested Further Reading statement from the American

Heart Association. Circulation.
patient outcomes. Am J Surg.
2009;197(5):678–685.
1. Wiegmann DA, Eggman AA, 2013;128:1139–1169.
Elbardissi AW, Parker SH, Sundt 7. Neily J, Mills PD, Young-Xu Y et al.
TM 3rd. Improving cardiac surgical 4. El Bardissi AW, Wiegmann DA, Association between
care: A work systems approach. Dearani JA, Daly RC, Sundt TM implementation of a medical team
Appl Ergon. 2010;41(5):701–712. 3rd. Application of the human training program and surgical
factors analysis and classification mortality. JAMA. 2010;304
2. Wahr JA, Abernathy JH. system methodology to the (15):1693–1700.
Improving patient safety in the cardiovascular surgery operating
cardiac operating room: Doing 8. Jung JJ, Yule S, Boet S, Szasz P,
room. Ann Thorac Surg. 2007;83 Schulthess P, Grantcharov T.
the right thing the right way, every (4):1412–1419.
time. Curr Anesthesiol Nontechnical skills assessment of
Rep. 2014;4:113–123. 5. Wadhera RK, Parker SH, the collective surgical team using
Burkhart HM et al. Is the “sterile the Non-Technical Skills for
3. Wahr JA, Prager RL, Abernathy cockpit” concept applicable to Surgeons (NOTSS) system. Ann
JH 3rd et al. On behalf of the cardiovascular surgery critical Surg. February 21, 2019.
American Heart Association intervals or critical events? The
Council on Cardiovascular 9. Gillespie BM, Harbeck E, Kang E,
impact of protocol-driven Steel C, Fairweather N, Chaboyer
Surgery and Anesthesia, Council communication during
on Cardiovascular and Stroke W. Correlates of non-technical skills
cardiopulmonary bypass. J Thorac in surgery: A prospective study. BMJ
Nursing, and Council on Quality Cardiovasc Surg. 2010;139
of Care and Outcomes Research. Open. 2017;7(1):e014480.
(2):312–319.
Patient safety in the cardiac 10. Flin R, Patey R, Glavin R, Maran N.
8 operating room: Human factors 6. Mazzocco K, Petitti DB, Fong KT Anaesthetists’ non-technical skills.
and teamwork: A scientific et al. Surgical team behaviors and Br J Anaesth. 2010;105(1):38–44.

Chapter
Equipment for Cardiopulmonary Bypass
2 Simon Anderson and Amanda Crosby
Cardiopulmonary bypass (CPB) provides optimum The heart lung machine and circuitry used in
conditions for cardiothoracic surgery by combining procedures today has advanced significantly since
a pump to substitute for the function of the heart and the advent of extracorporeal circulation and the first
a gas exchange device, the “oxygenator,” to act as an attempts at its use. The basic principles, however,
artificial lung. CPB therefore allows the heart and remain the same to this day:
lungs to be temporarily suspended, to facilitate car- Venous blood is drained by gravity or assistance
diac, vascular or thoracic surgery in a safe, still, blood- into a reservoir via a cannula placed in a large
less and controlled environment. vein, most typically the right atrium or vena cava.
Blood is then pumped through the oxygenating
History device and an arterial filter. Transit through the
The first successful open procedures were performed oxygenator reduces the partial pressure of carbon
in 1954 by Dr. Clarence Walton Lillehei using a cross- dioxide in the blood and raises oxygen content.
circulation technique, acting as an extracorporeal cir- Current models have the oxygenator, heat
cuit. This approach worked by circulating the parent’s exchanger and filter incorporated in one
arterial blood into the recipient and controlling the component (Figure 2.1 a and b)
amount of venous blood being returned, giving the It is next returned into the patient’s arterial system
surgeon up to an hour to perform cardiac surgery. through a cannula in a large artery, most typically
The concept of the heart lung machine (HLM) and the aorta.
cardiopulmonary bypass circuit arose from this tech- Older technology and bypass circuits consisted of
nique of “cross-circulation.” large components that required manual cleaning,
The development of the heart lung machine in were reused after sterilization, and were primed with
1953 was preceded by a number of perfusion pumps. up to 14 units of blood. Due to the advances in
The design of the first such pump originated in technology and techniques, CPB circuits today are
1935 by Charles Lindbergh in collaboration with Dr. more reliable, have more safety devices and are
Alex Carrel. The pump was used to keep organs disposable.
functioning outside of the body with a solution
developed by Carrel to perfuse organs, only limited
by the eventual failure of the organ itself or the Tubing
breakdown of the constituents in the perfusate. In The cardiopulmonary bypass circuit is created with
1953 Dr. John Gibbon used the first total CPB system. tubing connected to the various components required
Gibbon operated on four patients with congenital to support the circulatory system and allow close
heart disease with only one survivor, and considered monitoring. Table 2.1 provides an overview of the
this series of work a failure, however his efforts were main components of a HLM. Different types of
an inspiration to researchers around the world. The tubing may be used throughout the circuit depending
emergence of the DeWall-Lillehei helix reservoir with on what function it serves, for example, tubing used
a bubble oxygenator in 1955 was the first disposable, to monitor pressure is different to tubing for the
efficient, and inexpensive bypass circuit, this innov- actual circulatory support. Tubing should be pos-
ation fueled the rapid expansion into open-heart sur- itioned in an orientation that avoids kinks and allows
gery after 1956. for smooth curves to limit areas of high velocity or 9

Simon Anderson and Amanda Crosby
(a) Venous
Femoral Vent return
catheters Sucker catheter catheter
Venous
HCT/SAT Cardioplegia
Venous cannula
cardiotomy reservoir
Venous
BGM Arterial
Cardioplegia cannula
Arterial BGM Arterial Bubble
detector solution
• Bubble trap
• Temperature
• Pressure
To cardioplegia Centrifugal Blood from Heat exchange
pump (or Roller oxygenator
Oxygenator with
roller pump) pump
reservoir and
heat exchange
Dual
Arterial Suction Vent Cardioplegia cooler/heater
Temperature
control and Perfusion system (heart-lung machine)
monitoring
system
Figure 2.1 (a) Typical configuration of a basic cardiopulmonary bypass circuit. BGM = blood gas monitor; SAT = oxygen saturation. (b) Full HLM in use.
10

Chapter 2: Equipment for Cardiopulmonary Bypass
Table 2.1. Components of the CPB machine and the Table 2.2. Commonly used biocompatible tubing coatings
extracorporeal circuit
Manufacturer and Description of Coating
Equipment Function Coating Properties
Oxygenator system, Oxygenate, remove carbon Gore – Carmeda Covalent bonding of heparin
venous reservoir, dioxide and cool/ molecules
oxygenator, heat rewarm blood
exchanger Baxter - Duraflo II Heparin ionically joined with
ammonium and attached to
Gas line and FiO2 blender Delivers fresh gas to the surface
oxygenator in a
controlled mixture Terumo – Xcoating Biopassive polymer creates
hydrophobic and hydrophilic
Arterial pump Pumps blood at a set flow properties without heparin
rate to the patient
Maquet – Bioline Heparin and albumin attached
Cardiotomy suckers and Scavenges blood from the to polypeptides on tubing
vents operative field and vents surface
the heart
LivaNova – P.H.I.S.O. Phosphorylcholine
Arterial line filter Removes microaggregates Coating
and particulate matter
>40 μm Medtronic – Cortiva Endpoint-attached heparin
BioActive Surface coating
Cardioplegia systems Deliver high-dose
potassium solutions to
arrest the heart and
preserve the
myocardium PVC when the tubing is occluded but can release
more particles. Silicone rubber is sometimes utilized
Cannulae Connect the patient to the
extracorporeal circuit in the arterial pump roller head as an alternative to
commonly used PVC tubing.
Tubing used during CPB is subject to repeated
compression in pump roller heads. This intermittent
stagnation. Any junctions or connections between compression can degrade the integrity of the walls of
components have to be secured tightly to prevent the tubing and may cause plastic micro particles to be
leaks or air ingress. Clinicians must consider the released, this is called spallation.
intended use of the tubing when choosing materials Tubing can be made with a biocompatible coating
to create the circuit. (see Table 2.2), which may help reduce the inflamma-
Polyvinylchloride (PVC) is the predominant tory response to foreign material. Sequelae from the
tubing material used today in cardiopulmonary inflammatory response include platelet activation, ini-
bypass, but latex rubber and silicone rubber are other tiation of the coagulation cascade, decreased levels of
options. PVC is made up of polymer chains with circulating coagulation factors, activation of endothe-
polar carbon-chloride (C-Cl) bonds. These bonds lial cells and leukocytes, releasing mediators that may
result in considerable intermolecular attraction between contribute to capillary leakage and tissue edema. This
the polymer chains, making PVC a fairly strong material. is discussed in more detail in Chapter 17.
On its own, PVC is a rigid plastic, but plasticizers are There are a number of surface coatings available
added to the type of tubing used in a circuit, which make on the market today. One type of circuit coating uses
it malleable and easier to manipulate. both hydrophobic and hydrophilic properties to form
Silicone rubber is a semi organic synthetic. Its a new layer on top of the tubing that reduces protein
structure consists of a chain of silicon and oxygen denaturation and platelet adhesion. Since this coating
atoms rather than carbon and hydrogen atoms, as is is made from a non-heparin-based biopassive poly-
the case with other types of rubber. The molecular mer Poly(2-methoxyethylacrylate) (PMEA), this
structure of silicone rubber results in a very flexible tubing can be used on heparin sensitive or intolerant 11
but weak chain. Silicone produces less hemolysis than patients. Another type of biocompatible tubing is

Table 2.3. Tubing sizes commonly used in different parts of the extracorporeal circuit (adults only)
Tubing size Prime Max flow (l/min) Max flow (l/ Function
volume (To keep min)
(cc/ft/ml/ pressure (To keep
30cm) gradient <10 Reynolds
mmH*) number
<1000*)
3/16” (4.5 mm) 5.4 /4.7 0.2 1.8 Cardioplegia section of the blood
cardioplegia delivery system
1/4” (6.0 mm) 9.84/8.5 0.9 2.1 Suction tubing, blood section of the blood
cardioplegia delivery system
3/8” (9.0 mm) 21.6 /19.1 4.0 3.7 Arterial pump line for flow rates <6.7 l/
minute, majority of the arterial tubing in
the extracorporeal circuit
1/2” (12.0 mm) 42/33.9 7.0 5.0 Venous line, larger tubing is required to
gravity drain blood from the patient
*
Source: Hessel EA II, Hill AG in Gravlee GP et al.: Cardiopulmonary Bypass: Principles and Practice. Lippincott Williams & Wilkins, 2000,
Table 5.4
made from phosphorylcholine that mimics the nat- to crystalloid needed, and the type of delivery device.
ural endothelium to reduce platelet activation and cell When choosing tubing for scavenging blood from the
adhesion to the tubing surface. Some tubing contains surgical field and venting of the heart or aorta, the
heparin, which should be noted when providing care decision is usually based on institutional protocol, but
to a heparin intolerant patient. Some institutions will take into account the volume of the tubing length
maintain a small stock of non-coated circuits for these and the displacement per revolution of the pump
patients. Regardless of the type or manufacturer head.
selected, biocompatible tubing can improve platelet
preservation and reduce the inflammatory response
to foreign surfaces. Arterial Cannulae
Selecting the appropriate tubing size is based on The arterial cannula is used to deliver oxygenated,
the application. Larger bore tubing requires less pressurized blood from the HLM directly into the
pump head revolutions needed to displace the same patient’s arterial system. The size of the vessel that is
amount of volume as smaller tubing, meaning less being cannulated and the patient’s required blood
mechanical stress from repeated compression. The flow are considered in selecting the appropriately
internal diameter as well as the length should be sized cannula.
carefully considered as both will affect the priming The ascending aorta is most used as the site of
volume. While a larger internal diameter allows for arterial cannulation for routine cardiovascular sur-
greater flow at lower pressures, it has a higher prime gery allowing antegrade flow to the cerebral and body
volume, increased contact activation, less resistance, circulation. The asceding aorta is large caliber, has a
and a larger pressure gradient. There are many low associated incidence of aortic dissection
factors to consider when selecting the best fit for the (0.01–0.09%), and is easy access when using a median
application required (see Table 2.3). When deciding sternotomy approach. After sternotomy and expos-
upon the size of arterial and venous tubing, the ure, the surgeon can assess the size of the aorta before
patient’s body surface area (BSA) and calculated car- choosing the most appropriate caliber cannula (see
diac index can help guide the appropriate size of Figure 2.2).
tubing. Tubing for cardioplegia administration is Developments in cannula design allow the use of
12 based on the solution being used, the ratio of blood thin wall cannulae. By having a larger effective

DLP® Flexible Arch Cannulae EOPA® Arterial Cannulae

200 200
18 Fr
160 160
Pressure Loss (mm Hg)

22 Fr
20 Fr
120 120 20 Fr
24 Fr
80 80
22 Fr
40 40
24 Fr
0 0
0 1 2 3 4 5 6 0 1 2 3 4 5 6
Flow Rate (L/min of water) Flow Rate (L/min of water)
Select Series® Straight Tip Arterial Cannulae Edwards Soft flow/EZ glide)
200
100
20 Fr 21 Fr. Straight
160
80
Pressure Drop (mm Hg)
140
60 22 Fr
21 Fr. Curved
80 24 Fr. Straight
40 24 Fr
24 Fr. Curved
20 40
0 0
0 1 2 3 4 5 6
0 1 2 3 4 5 6
Flow Rate (L/min of water) Flow Rate (L/min), H2O at Room Temperature
Figure 2.2 Cannula flow profiles.
internal diameter, they achieve lower resistance to

Rings
flow. Subsequently, within the extracorporeal circuit, Straight tip
this leads to a reduction in arterial line pressure and
allows an increase in blood flow. Further develop-
ments come in the form of angled tip arterial cannu-
lae. These manipulate the flow characteristics of blood
leaving the cannula to produce a spray effect, disper-
Bump
sing blood into the aorta. This design not only min-
imizes damage to the vessel wall by directing blood Curved tip
flow toward the aortic arch rather than toward the
vessel wall, but also reduces the pressure drop at the
tip of the cannula. Figure 2.3 shows several designs of
aortic cannulae. Suture
Axillary, subclavian and femoral arteries are
Flange
examples of alternative arterial peripheral cannulation
sites, typically during complex or redo surgery. The
femoral cannulae are longer than conventional ones
and incorporate a spirally wound wire within their Figure 2.3 Commonly used arterial cannulae. (Reproduced with kind 13
wall to prevent “kinking” (see Figure 2.4). X-ray permission from Edwards Lifesciences.)

Figure 2.4 Femoral reinforced cannula. Biomedicus Life SupportTM 21Fr. (Reproduced with ©2020 Medtronic. All rights reserved. Used with the
permission of Medtronic.)
imaging or transesophageal echocardiography (TEE) a bloodless field for the surgeon. Figure 2.5 shows
is used to confirm correct cannula position. Axillary commonly used venous cannulae.
and subclavian cannulation is most commonly Femoral cannulation can be utilized for more
achieved by suturing a dacron graft end-to-side onto complex surgery. In this instance, a long cannula,
the vessel and a 3/8 3/8 inch connector to connect which is in essence an elongated single-stage cannula,
to the HLM arterial line. is typically passed over a guide wire up the femoral
vein into the IVC and RA to achieve venous drainage.
These cannulae are generally placed under TEE
Venous Cannulae guidance. As with arterial cannulation sites, the size
Venous cannulation provides the means to drain and length of the venous cannulae are patient specific
deoxygenated blood from the patient’s venous system and are determined by body surface area (BSA),
into the extracorporeal circuit. It is important to use required full flow and vessel size. In an average height
appropriately sized cannulae in order to obtain max- adult (170 cm, 80 kg), a 25 Fr/55 cm cannula provides
imum venous drainage from the patient so that full sufficient venous drainage from the IVC. However, in
flow can be achieved when CPB is commenced. The smaller patients, a 38cm length cannula may be a
type of venous cannulation used depends on the better option to ensure the cannula is short enough
operation being undertaken. For cardiac surgery not to be positioned in the IVC and not too long to
involving opening chambers of the right heart, for potentially perforate the right atrium or SVC during
example, coronary artery bypass grafts (CABG) or cannulation.
aortic valve replacement (AVR), a two-stage venous
cannula is often used. The tip of this type of cannula Perfusion Pumps
sits in the inferior vena cava (IVC) and drains blood
Perfusion pumps, in the arterial position, propel
from the IVC through holes around the tip; a second
blood forward through the circuit. There are two
series of holes a few centimeters above the tip is sited
main types: positive displacement roller pumps and
in the right atrium to drain venous blood from the
the impeller centrifugal pumps.
superior vena cava (SVC).
During procedures that require the right atrium
(RA) to be opened, bicaval cannulation, where a Roller Pumps
single-stage cannula sits in each of the inferior and A peristaltic pump or “roller pump” is a positive
superior vena cava, is necessary. The two single-stage displacement pump used for moving fluid. Initial
cannulae are connected to the venous line of the CPB HLM technology in the 1950s used a similar peristal-
circuit using a Y-connector. This approach avoids air tic pump, and the technology has not greatly changed
entry into the CPB circuit from the distal series of from its inception. The raceway or the pump header
holes of a two-stage cannula, as they would be sitting accepts a length of tubing, the rotor and roller com-
in the open RA. Air entry would impede venous bination inside the middle of the pump housing
14 drainage – or stop it completely in case of an “air rotate in a clockwise or counterclockwise direction.
lock” – leading to the patient’s calculated full flow Typically, there will be two or more rollers that com-
becoming unachievable in addition to not providing press the tubing and a clutch mechanism to set the

Figure 2.5 Commonly used venous cannulae (a) DLPTM single-stage cannula (b) Bi-caval cannulation technique (c) MC2TM two-stage cannula. 15
(Reproduced with ©2020 Medtronic. All rights reserved. Used with the permission of Medtronic.)

Blood leaves Figure 2.6 Line drawing of a

roller pump.
pump
Blood enters
pump
Rollers force blood

through tubing in
a peristal motion
Omega, or
horseshoe raceway
degree of tubing occlusion, regulating the amount of pressure. As they operate independently of resistance
compression applied to the tubing. Under-occlusive, or pressure, pressures within the circuit must be
or too loose, tubing may result in retrograde flow or monitored. It is essential to limit the pump flow if
inaccurate flow calculations, while over-occlusion, or system pressure becomes excessive. Sudden occlusion
too tight, may increase hemolysis, spallation, and of the inlet of the roller head can create extreme
inaccurate flow calculations. The roller head occlu- negative pressure to the point where the tubing may
sion should be measured before each case to ensure it cavitate and create air bubbles in the circuit.
has the desired setting for the operation. The methods Very similar to the heart, output of a roller pump
to test occlusions are described in detail in Chapter 4. is determined by the internal diameter of the tubing
As the rollers compress and occlude the tubing, the (= stroke volume) and the number of revolutions of
fluid is moved in the corresponding direction(see the pump head (= beats per minute). The larger the
Figure 2.6). The tubing inside the raceway is held in a tubing in the raceway, the less rpms are needed to
fixed position by brackets or a locking mechanism and maintain the same output of smaller tubing. Note that
returns to its natural state once the roller passes over it. reading or recording blood flow directly from the
This intermittent occlusion creates positive and negative arterial roller head does not account for any shunts
pressures on either side of the occlusion point, which is that may be present downstream in the circuit, and
the driving force for the movement of fluid. Positive thus the actual flow reaching the patient may be less.
pressure created by the roller propels fluid and the recoil
of the tubing creates negative pressure refilling the tube.
Roller pumps can be used in any position. They Centrifugal Pumps
can be belt driven or have direct drive systems and are Centrifugal pumps are non-occlusive pumps and utilize
16
not affected by circuit resistance or hydrostatic a magnet and impeller combination to propel blood

(b)
3/8” Blood inlet with two barbs for Durable bearing

gentle flow of blood into pump
Durable, chemical resistant

3/8” Blood outlet with two polycarbonate housing
barbs is compatible with
adult perfusion circuits
Ceramic pivot shaft

for low friction and
low heat generation
Six low-profile impeller fins for Smooth cone for

low turbulence low shear on red blood cells
Internal molded magnet for torque

coupling with external motor Sweeper to prevent blood
stagnation on bottom of pump
Figure 2.7 Centrifugal pump head (a) Medtronic AffinityTM. (b) Schematic cut through of AffinityTM centrifugal pump. (Reproduced with ©2020
Medtronic. All rights reserved. Used with the permission of Medtronic.)
through the CPB circuit. The pump consists of a hard amount of forward flow will decrease, unless the rpms
outer shell which incorporates an impeller design are altered to counter this. For this reason, centrifugal
coupled magnetically with an electric motor and shaft pumps have the potential to allow retrograde flow,
or pin. When the console is turned on and the rpms are however most flow meters will alert the user if this
increased, the cones or fins spin rapidly, creating posi- occurs. Unlike roller pumps whose flow is calculated
tive pressure that propels fluid forward (see Figure 2.7). based on tubing diameter and rpm (stroke volume and
Centrifugal pumps, much like the heart, are after- beats per minute), centrifugal heads require ultrasonic 17
load sensitive. If the post-pump resistance increases, the or electromagnetic meters to accurately determine

blood flow. Unlike rollers, centrifugal pumps do not Table 2.4. Common centrifugal heads, adult sizes
need to be pressure regulated because they will not be Manufacturer Centrifugal Brief Description
able to generate forward flow if the tubing is kinked, Head
clamped, or suddenly occluded. When used for CPB, a
special centrifugal head motor that can be manually LivaNova Revolution Open impeller design,
with impregnated
operated must be available as backup.
nylon magnet and
The perceived benefits of the centrifugal pump are
seal-less low friction
its low prime volume and, because of its non- bearings – 57 ml
occlusive nature, less hemolysis. Despite extensive prime volume
research, there is little clinical evidence to show any
Terumo CAPIOX SP Polycarbonate housing,
benefit of CPB with centrifugal over CPB with roller
impeller design, lip
pumps. Centrifugal pumps may produce less hemoly-
seal – 45 ml prime
sis and platelet activation than roller pumps, but this volume
does not correlate with any difference in clinical out-
come. Centrifugal pumps are less likely to create air Medtronic Affinity CP Low profile fins,
ceramic pivot
embolism situations because as air is introduced to
bearings, no stasis
the cone, the pump will deprime and cease forward
zones – 40 ml prime
flow. Clinicians should remain vigilant, though, as volume
there have been reports of air ingress into circuits
using centrifugal pumps. Centrifugal pumpheads are Abbott - Centrimag Free-floating
Thoratec magnetically
expensive, adding a signficant additional cost to the
levitated rotor, has
CPB circuit. Clinicians favoring centrifugal systems
no bearings or seals
have argued that the ability to create smaller circuits creating minimal
due to remote drive capabilities, allows the circuit to stasis zones – 31 ml
be closer to the surgical field unlike the fixed console prime volume
based roller head position. The new generation roller
Gettinge - Rotaflow RF- Peg-top, one-point
pumps have largely overcome this issue and tubing
Maquet 32 sapphire bearing –
length has decreased significantly in recent years. The 32 ml prime volume
decision to use centrifugal pumps or roller pumps for
CPB is largely determined by institutional factors
rather than clinical indication. Table 2.4 summarizes
commonly used adult centrifugal pump heads. The reservoir acts as a chamber for the venous blood
Centrifugal head technology is not only used in to drain into before it is pumped through the oxygen-
cardiopulmonary bypass cases but also in extracor- ator and permits ready access for the addition of fluids
poreal membrane oxygenation (ECMO) and ven- and drugs. To reduce the risk of perfusion accidents, the
tricular assist devices (VADs). Certain models level of fluid is monitored for the duration of CPB to
possess fins or channels to help avoid areas of stagna- prevent the reservoir from emptying and air entering
tion, while others have magnetically levitated bearing- the circuit. Each manufacturer details the minimum
less motors to reduce heat generation. Each has a set safe fluid level necessary to achieve the rated flow of
rpm needed to generate forward flow, this minimum their device. Low level alarms (see also Chapter 3), often
number will be different with blood viscosity (hemo- coupled to automatic cessation of pump flow when
globin) and patients’ vascular resistance pressure. triggered, add additional safety. Gross air embolism
incidents can still occur if arterial flow exceeds venous
drainage, subsequently emptying the reservoir.
Reservoirs Vacuum-assisted venous drainage may be used to
Cardiotomy reservoirs may be hardshell or softshell optimize venous drainage during CPB. Using vacuum
(collapsible). Hardshell reservoirs usually comprise of assistance can reduce hemodilution and subsequent
a durable polycarbonate housing, a high-efficiency transfusion requirements because improved drainage
18 polyester depth filter and a polyurethane defoamer requires fewer “top-ups” with crystalloids or colloids.
(see Figure 2.8). With the top of the cardiotomy reservoir positioned

which can occur if the suckers are left running at a

high level for prolonged periods. The blood returned
from the intracardiac “vent” suckers is also returned
to the reservoir.
Collapsible reservoirs are used mainly for pediat-
ric or mini bypass cases and are dicussed in more
detail in Chapters 8 and 15.
Oxygenators
The evolution of the oxygenator has been critical to
the success of cardiac surgery and advanced patient
care. Oxygenators are most often described as artifi-
cial lungs as they provide an alveolar capillary system
for gas transfer. The general design goals are efficient
gas exchange, low prime volume, minimized trauma
to blood and efficient cooling and heating capabilities.
Figure 2.8 Fusion reservoir. (Reproduced with ©2020 Medtronic. All
TM
There are two main types of oxygenators com-
rights reserved. Used with the permission of Medtronic.)
monly used in adult cases today, microporous poly-
propylene (PPL) and non-porous polymethylpentene
(PMP). Both are hollow fiber membrane oxygenators,
which are named for the membrane that separates the
at the level of the patient’s atrium, a negative pressure gas and blood phases. The main difference is their
of approximately 60 mmHg is applied when max- duration of use – the PMP type oxygenators typically
imal gravity drainage is reached. The negative pres- maintain gas exchange longer. While PPL oxygen-
sure can be increased by small amounts during CPB, ators are more common, extended use can cause
when the fluid in the reservoir decreases to the safety plasma leaks across the membrane from the blood
limit level. For weaning from bypass, the negative phase into the gas phase, resulting in decreased gas
pressure is gradually decreased to zero, the reservoir exchange efficiency. The non-porous fibers of the
is opened, and the venous line progressively closed. PMP oxygenator make them more durable than
Blood scavenged from the operative field via PPL, and they are typically used for longer term
suckers is also returned to the reservoir. Suction relies applications such as ECMO. The lack of pores does
on the “Venturi” effect, which is the change in pres- not allow exchange of volatile anesthetics, making
sure and fluid velocity through a narrowing in a tube. PMP oxygenators unsuitable for use with CPB.
Suctioning blood from the operative field causes Oxygenators are regulated by federal guidelines,
damage to blood cells and also results in concomitant allowing their use for periods of time usually up to six
entrainment of high volumes of air. The salvaged hours. While using them longer is designated as off
blood may contain tissue and other debris and is label, it is a widespread and acceptable application of
highly activated with inflammatory cells. It is vital the technology to facilitate bridging to recovery or
that this blood is filtered through the reservoir before transplantation when other advanced treatments
being pumped to the patient. Advances in technology have failed.
have seen a more widespread use of reservoirs con- Once entering the device, blood first passes over
taining separate chambers for venous blood and car- the integrated heat exchanger before moving into the
diotomy suction, allowing the suction blood only to oxygenator compartment, where gas exchange takes
be added into the circuit when required. Segregating place (see Figure 2.9). O2 concentration and flow of
suction blood that way has the advantage that it can the sweep gas, which drives gas exchange, are regu-
be passed through a specific filter that absorbs lipid lated with a gas blender and a flow meter integrated
cells, which have been shown to impair oxygenator into the HLM. The sweep is piped into the oxygenator
effectiveness. The reservoir is constantly vented to inlet port, its distribution throughout the membrane’s 19
prevent the entrained air causing a pressure buildup, capillary system varies with the oxygenator used and

the patient’s size. Typically the flow is 2–4 l/min for Cooling the blood, and thus cooling the patient,
adults, depending on blood flow and the desired CO2 results in a lower metabolic demand that helps ensure
removal rate. Volatile anesthetics can be added all tissues are being adequately perfused while on
depending on oxygenator type and HLM in use. bypass. Chapters 9 and 10 discuss temperature man-
Gas scavenging can be attached to the exhaust port. agement and rewarming strategies in more detail.
Gas sampling to determine O2 consumption and end- Intended duration of use, requirement for volatile
tidal CO2 can be attached at this point as well. anesthetics, prime volume, biocompatible coating, gas
Integrating the heat exchanger and arterial line exchange capacity, and the heat exchanger’s efficiency
filter into the oxygenator has decreased circuit size are the main determinants that inform the choice of
and reducted prime volume. The heat exchanger is oxygenator used for a case.
separated from the blood phase by a highly thermal
conductive material and is biologically inert. An Gas Supply System
external heater cooler is connected with thick water
The gas supply is connected to the blender, which
lines, usually made of antimicrobial-coated tubing.
mixes oxygen and air to provide the desired FiO2
Fine control of the water bath temperature allows
and to a flow meter to regulate sweep gas flow (see
precise regulation of the patient temperature.
Figure 2.10). CO2 may be added to the sweep when
pH-stat blood gas management is desired during
hypothermia or cases requiring deep hypothermic
circulatory arrest (DHCA, see Chapter 9). Blending
units and flow meters may be mechanical, but are
now mostly digitally controlled via the HLM.
Continuous inspired O2 analysis is mandatory to
prevent the inadvertent administration of a hypoxic
mixture.
Filters and Bubble Traps

Air entrainment through the venous return line, fluid,
drug and blood administration through the cardiot-
omy reservoir, as well as ingress of air and particulate
matter from cardiotomy suckers and vents, all con-
Figure 2.9 FusionTM oxygenator combined with and a heat tribute to the embolic load patients may be exposed
exchanger in a single unit. (Reproduced with ©2020 Jose Canamares. All
rights reserved. Used with the permission of Jose Canamares.) to. While it is not possible to eliminate the embolic
load in its entirety, the use of arterial filters and
Figure 2.10 LivaNova S5W Electronic Gas Blender,

courtesy of LivaNova PLC. (Reproduced with kind permission
from LivaNova.) Photograph by Jose Canamares used with
permission.
20

Table 2.5. Filtration devices used within the cardiopulmonary Depth filters create a tortuous path between fibers
bypass circuit
and retain particles mechanically. Screen filters are
Filter type Application and specification the most common type and are typically made of a
woven polyester mesh. They are usually pleated to
Gas line Removes 99.999% of bacteria found in
allow for a larger surface area in a confined space
the gas stream minimizing cross-
contamination between the patient
and trap particulates or emboli that are larger than
and the equipment their particular pore size. Filters come in a size range
from 0.2 μm for gas line filters to 40μm for arterial
Pre-CPB 0.2 μm filter is used during the priming
line filters.
and recirculation phase. It is
0.2μm pre-bypass filters are meant to capture any
designed for the removal of
inadvertent particulate debris and particles left from the manufacturing process and are
microbial contaminants and their removed after priming and before initiating bypass.
associated endotoxins Separate arterial line filters are indicated for use in
all CPB procedures where the oxygenator does not
Arterial line Designed to remove microemboli
have an integrated filter. The main goal of an arterial
>20 μm in size from the perfusate
during extracorporeal circulation. filter, whether integrated into the oxygenator or not,
This includes gas emboli, fat emboli is to stop gaseous macro-emboli from entering the
and aggregates composed of circulation, although there is some debate about
platelets, red blood cells and other their effectiveness. Several arterial filters with varying
debris. Pore size depends on characteristics are commercially available (see
manufacturer Table 2.6).
Venous Designed to remove debris and gross The US Food and Drug Administration (FDA)
reservoir air, some models may contain a have outlined key areas of importance pertaining to
defoamer to reduce bubbles from arterial line filters (FDA, 2000). The following list sets
incoming suction or ports forth the risks to health associated with this device
Cardioplegia Blood cardioplegia: >40 μm filter. that were identified in the proposed classification
Crystalloid cardioplegia: >0.2 μm ruling (dated February 26, 1979), as well as additional
filter. Low priming volume filter for adverse event reporting since the classification ruling:
cell-free solutions. Removes Amount of damage to formed blood elements,
inadvertent particulate debris and clotting and hemolysis
microbial contaminants and their Degree of pressure drop resulting in inadequate
associated endotoxins
blood flow, damage to the device or structural
Leukodepletion Reduces the levels of leukocytes, integrity and damage to the arterial line
either from the arterial line or Structural integrity of the product
cardioplegia system, and excludes
Excessive pressure gradients, for example, blood
microemboli >40 μm
damage and inadequate blood flow
Blood Designed to reduce the levels of Filtration efficiency and gas emboli-handling
transfusion leukocytes and microaggregates capacities
from one unit of packed red blood
User error
cells or whole blood, used when
giving blood products to the Blood incompatibility and the requirements of
patient ISO 10993: Biological Evaluation of Medical
Devices
Cell salvage Designed for the filtration of salvaged
blood, to remove potentially
Compatibility of the product when exposed to
harmful microaggregates,
circulating blood and infections
leukocytes and lipid particles Shelf life
These stringent criteria aim to ensure the production
bubble traps can reduce this significantly. Table 2.5 of high-quality arterial line filters that will not
gives an overview of the filters most commonly used have any deleterious effects on the CPB circuit or 21
in CPB circuits. patient.

Table 2.6. Different commercially available arterial line filters, both external and integrated
Manufacturer Filter type Fiber material Filter size (μm)

LivaNova Screen, External Phosphorylcholine-coated polyester net 27, 40, 120
Screen, Integrated Phosphorylcholine-coated polyester net 38
Medtronic Screen, External Cortiva Bioactive surface coating or uncoated 20 or 38
Screen, Integrated Cortiva Bioactive surface coating or uncoated 25
Terumo Screen, External Polyester, X-coating 37
Screen, Integrated Polyester, X-coating 32
Pall Screen, External Heparin-coated polyester 40
Lifeline-Delhi Screen, External Polyester 40, 20
Membrane solutions Screen, External Woven Polyester 40
Suckers and Vents (LV) apex can be associated with particularly serious
consequences including:
The suckers allow spilled blood from the operative
field to be returned to the circuit via the reservoir, but LV wall rupture if inadequately closed
they can also be used to help salvage emergency Damage to the LV wall due to excessive suction
situations. In case of life-threatening, excessive bleed- Embolization through air entrained into the LV
ing before venous cannulation has been established, through the vent site.
the suckers can be used to scavenge blood to the
venous reservoir and subsequently be transfused back Cardioplegia Delivery Systems
into the patient via the arterial line. This is commonly One of the major concerns during cardiac surgery is
known as “sucker bypass” and grants the surgeon protection of the myocardium during procedures.
time to attempt to fix the problem at least Cardioplegia solution is administered to maintain
temporarily. controlled and protected electrical arrest of the myo-
“Vent” suckers are used to drain blood from the cardium during the ischemic period. Chapter 11 is
left ventricular cavity, typically via these sites: dedicated to myocardial protection techniques.
Aortic root Regardless of the type of cardioplegia delivery
Right superior pulmonary vein device, monitoring of temperature, appropriate deliv-
Left atrium or pulmonary artery ery pressure, and time intervals between doses are
Left ventricle critical to the success of the operation.
Left ventricular apex Cardioplegia delivery systems typically include a
line for pressure monitoring, an over-pressure relief
The main reasons for venting the heart during CPB
valve, and a recirculation line for easy priming or de-
are to:
airing. Pressure monitoring is essential when deliver-
prevent distension of the heart ing cardioplegia into small vessels and the coronary
evacuate air from the cardiac chambers during the sinus to prevent damage. An air detection device is
de-airing phase of the procedure often added to the infusion line for additional protec-
improve surgical exposure tion against microemboli. Most cardioplegia delivery
reduce myocardial rewarming systems today have their own dedicated integrated
create a dry surgical field. heat exchanger. This heat exchanger and accompany-
There are complications associated with all sites used ing water lines are separate from the oxygenator since
for venting, most commonly relating to injury to cardioplegia is typically delivered at temperatures
22 much colder than the patient’s core temperature.
tissues at the site. Venting via the left ventricular

Table 2.7. Cardioplegia delivery systems
Manufacturer Integrated Air Delivery System

Heat Trap
Exchanger
LivaNova Yes Yes Dual roller head or
dual shims
adapter for two
sizes of tubing
for different
ratio options
Medtronic Yes Yes Blood
cardioplegia 4:1
ratio via roller
pump (can also
be used with a
syringe driver
for the
potassium
solutions)
Figure 2.11 Cardioplegia delivery system allows mixing of blood
and cardioplegia solution and warming or cooling of solution by Getinge Yes Yes Blood or
MyothermTM. (Reproduced with ©2020 Jose Canamares. All rights reserved. crystalloid
Used with the permission of Jose Canamares.) Photograph by Jose cardioplegia
Canamares used with permission.
ratio via roller
pump
Cardioplegia delivery systems vary from simple to depending on
complex. Administration in early procedures was accom- tubing set
plished by either using a pressure bag at the head of the
Quest Medical Yes Yes Piston pump
surgical field or elevating glass bottles to the operating for microplegia
theater ceiling via a pulley system and a needle inserted or compatible
directly into the cross-clamped aorta. More complex for numerous
microplegia systems require hardware to be added to the ratios including
heart lung machine and deliver specific aliquot measure- all crystalloid
ments of medications to arrest and protect the myocar-
dium. Standard blood cardioplegia delivery systems use
venous side (low pressure port) to provide a driving
roller pumps and specific tubing sizes to deliver a set ratio
force for blood through the membrane.
of blood to clear cardioplegic solutions (see Figure 2.11).
Hemofilters are used to concentrate blood in
Table 2.7 summarizes the characteristics of some
order to maintain or increase hematocrit (HCT) levels
of the most commonly used cardioplegia systems.
in the presence of excess fluid and can to a degree help
While many designs are available, every system
avoid blood transfusion. They may also be used to
should be capable of changing the ratio of blood to
manage electrolyte or acid/base derangements.
crystalloid, control flow to administer through differ-
The rate of filtration is dependent on the trans-
ent routes of the heart, and be temperature controlled
membrane pressure and the surface area of the filter
to allow cold, warm, or tepid doses of cardioplegia.
and is typically 30–50 ml/minute. The Sieving coeffi-
cient denotes whether a substance will be retained or
Hemofilters passed through the membrane to be filtered out.
Ultrafilters or hemoconcentrators contain semi- Sieving coefficients are based on molecular weight
permeable, hollow fiber membranes that permit pas- and the pore size on the filter. Depending on the
sage of water and electrolytes out of the blood. They membrane used, molecules of up to 50,000 Daltons
are normally connected to the CPB circuit at the are removed. It is important to note that molecules 23
arterial side (high pressure port) and returned to the like heparin or sodium bicarbonate are partially

filtered and their level should be monitored when caused by CPB, mainly through minimizing circuit
using a hemoconcentrator. size, introducing biocompatible surfaces where
possible and reducing prime volume to as little
Miniaturized Extracorporeal as 500 ml. As promising as the concept sounds, it
has not yet found its way into mainstream
Circulation (MiECC) clinical practice. MiECC is discussed in detail in
There has been increasing interest in miniaturized Chapter 8.
bypass circuits. Their aim is to decrease the trauma
Suggested Further Reading Circulation. 2000;102: Iv-87–Iv-93

0
8. Dickinson TA, Riley JB, Crowley JC,
Zabetakis PM. In vitro evaluation of
1. Gourlay T. Biomaterial the air separation ability of four
development for cardiopulmonary 5. Black S, Bolman RM III. C.
Walton Lillehei and the birth of cardiovascular manufacturer
bypass. Perfusion. 2001 extracorporeal circuit designs.
September; 16(5): 381–90. open heart surgery. J Card Surg
2006; 21: 205–208. Journal of Extra Corporeal
2. Kim WG, Yoon CJ. Roller pump Technology 2006; 38: 206–213.
induced tubing wear of 6. Johagen D, Appelblad M,
Svenmarker S. Can the oxygenator 9. Durandy Y.Vacuum-assisted
polyvinylchloride and silicone venous drainage, angel or demon:
rubber tubing: Phase contrast and screen filter reduce gaseous
microemboli? The Journal of PRO? Journal of Extra Corporeal
scanning electron microscopic Technology 2013; 45: 122–127.
studies. Artif Organs. 1998 Extra-corporeal Technology 2014;
October; 22(10): 892–897. 46: 60–66. 10. Potger KC, McMillan D, Ambrose
7. Saczkowski R, Maklin M, Mesana M. Microbubble generation and
3. Rodney F Patterson, Silicones. in transmission of Medtronic’s
Handbook of Thermoset Plastics T, Boodhwani M, Ruel M.
Centrifugal pump and roller affinity hardshell venous reservoir
(Second Edition), 1998. and collapsible venous reservoir
pump in adult cardiac surgery:
4. Denton A Cooley and O H A meta-analysis of randomized bag: An in-vitro comparison.
Frazier. The Past 50 Years of controlled trials. Artificial Organs Journal of Extra Corporeal
Cardiovascular Surgery. 2012; 36: 668–676. Technology 2011; 43: 115–122.
24

Chapter
Monitoring during Cardiopulmonary Bypass
3 Richard F Newland and Pascal Starinieri
A fundamental area of responsibility for the perfusio- Heart Lung Machine

nist during cardiopulmonary bypass (CPB) is to
monitor, respond to, and document heart lung The complexity and extreme invasiveness of CPB
machine (HLM) parameters as well as physiological demands that strict attention is paid to all aspects of
variables obtained from the anesthetic monitor and extracorporeal flow, with importance placed on pro-
other physiological monitoring devices. The heart viding a safe environment for both the patient and
lung machine typically provides monitoring of blood personnel. Technological advancements, together
flow and circuit pressures (e.g., arterial, cardioplegia), with an increased understanding of the pathophysio-
temperatures (e.g., arterial, venous, cardioplegia, oxy- logical effects of extracorporeal flow, have made the
genator inflow and outflow), oxygen and air supply conduct of CPB both safe and reliable. An essential
and timers (e.g., CPB time, myocardial ischemia, cir- part of this success has been the development of
culatory arrest). Patient physiological parameters are monitoring devices that measure the combination of
monitored via the anesthetic monitor (e.g., arterial both physiological and mechanical functions that are
and central venous blood pressure, heart rate and unique to CPB.
ECG, core body temperature, oxygen saturation, cap-
nography). Blood gas parameters may be monitored Blood and Gas Flow
using devices that provide continuous measurements The HLM typically measures systemic blood flow
and/or intermittently using point of care or labora- continuously and in real time either via
tory blood gas analyzers. Non-invasive methods the rpm of a roller pump and with knowledge of
may be used for cerebral monitoring, such as the tubing size placed through the raceway or
regional cerebral tissue oxygenation and electroen- an ultrasonic flow probe.
cephalography (EEG) based depth of anesthesia.
Blood flow may also be monitored using continuous
Anticoagulation is monitored using point of care
blood gas monitoring systems (see below).
devices that measure the activated clotting time.
A measurement of blood flow distal to any circuit
These parameters together with procedural events
shunts is important to provide an accurate under-
and CPB interventions should be accurately recorded
standing of actual blood flow to the patient.
to provide documentation of the CPB period. CPB
A continuous supply of oxygen and air is delivered
monitoring recommendations published in the 2019
to the oxygenator during CPB while some specialist
EACTS/EACTA/EBCP guidelines on cardiopulmon-
procedures might require adding CO2 into the gas
ary bypass in adult cardiac surgery are summarized
mix. Modern heart lung machines are equipped with
in Table 3.1. Combined recommendations of the
digital flowmeters rather than the older style rota-
Society of Clinical Perfusion Scientists of Great
meters. Electronic gas blenders are generally con-
Britain and Ireland for Standards of Monitoring
trolled from the HLM work panel, while manual
and Safety during CPB and the American Society
blenders have a ball or cylinder rotameter which is
of ExtraCorporeal Technology Standards and
read against a scale and therefore cannot be continu-
Guidelines for Perfusion Practice are summarized in
ously monitored electronically. Monitoring gas
Table 3.2.
25

Richard F Newland and Pascal Starinieri
Table 3.1. Summary of Class I recommendations CPB Table 3.2. Recommended extracorporeal circuit parameters for
monitoring parameters from the 2019 EACTS/EACTA/ Standards of Monitoring and Safety during CPB by the Society of
EBCP guidelines Clinical Perfusion Scientists of Great Britain and Ireland and the
American Society of ExtraCorporeal Technology Standards and
It is recommended that pressure monitoring devices are Guidelines for Perfusion Practice.
used on the arterial line and cardioplegia delivery
systems during CPB. Oxygen saturation of the blood in the arterial line
A bubble detector is recommended during CPB Oxygen saturation of the blood in the venous return line
procedures on all inflow lines. The flow of the blood to the patient (best measured
It is recommended to use a level sensor during CPB after shunt lines with a separate flow meter)
procedures utilizing a (hard-shell) reservoir. Arterial line pressure (preferably before AND after the
Continuous arterial line pressure monitoring oxygenator)
(preoxygenator and postoxygenator) in the CPB Gas flow and oxygen fraction to the oxygenator
circuit is recommended.
Venous occlusion percentage
Continuous oxygenator arterial outlet temperature
Oxygen concentration in the gas to the oxygenator
monitoring is recommended.
Level sensor during CPB procedures utilizing (hard-shell)
It is recommended to continuously monitor SvO2 and
reservoir
HCT levels during CPB.
Cardioplegia dose, delivery method, line pressure
Monitoring of blood gas analyses through regular
(antegrade), coronary sinus pressure (retrograde), and
intervals or continuous observation is recommended
ischemic intervals
during CPB.
Blood temperature at the arterial outlet and venous inlet
It is recommended to objectively report, adequately
of the oxygenator
record and properly analyse all adverse events related
to CPB practice in an efficient and timely manner. Water temperature in the heater-cooler system
It is recommended that the perfusionist collect data Anticoagulation – Activated Clotting Time (ACT)
concerning the conduct of perfusion via a clinical
Arterial blood gases (regularly or continuously)
registry or database and use such data to actively
containing the following measurements:
participate in institutional and departmental quality
assurance and improvement programmes. pH
It is recommended that the venous line pressure be pCO2
monitored when using assisted venous drainage. pO2
SaO2
HCO3
supply and exchange, together with an oxygen analyzer Base excess
to display the O2 concentration delivered at any point in
Haemoglobin (Hb)
time, is mandatory. Volatile anesthetics may also be used
via the heart lung machine gas delivery system during Haematocrit (HCT)
CPB to maintain anesthesia and/or as an adjunct to Potassium
blood pressure control. A scavenging system for waste
Sodium
anesthetic gases is recommended as being mandatory in
many countries, as volatile anesthetic agent waste is a Glucose (or other point-of-care device)
risk to staff. The end-tidal anesthetic gas concentration Lactate
can be monitored at the oxygenator exhaust port.
Temperature rate and oxygen consumption reduce by 50% for

The purpose of using hypothermia is to provide a every 7°C of temperature drop.
26 degree of organ protection and safety margin during Core temperature monitoring sites include naso-
cardiopulmonary bypass. As a general rule, metabolic pharynx, tympanic membrane, bladder, esophagus,

Chapter 3: Monitoring during Cardiopulmonary Bypass
rectum, pulmonary artery, jugular bulb, arterial Table 3.3. 2015 STS/SCA/AmSect Clinical Practice Guidelines on
temperature monitoring during CPB
inflow, and venous return. Nasopharyngeal, jugular
bulb and arterial inflow temperature give an estimate CLASS I RECOMMENDATIONS
of cerebral temperature. Due to its invasive nature
The oxygenator arterial outlet blood temperature is
and cumbersome placement, jugular bulb probes are recommended to be utilized as a surrogate for
rarely used and the oxygenator arterial outlet blood cerebral temperature measurement during CPB. (Class
temperature is recommended as the surrogate for I, Level C)
cerebral temperature. Oxygenator inlet and outlet
To monitor cerebral perfusate temperature during
temperatures are measured using thermistors.
warming, it should be assumed that the oxygenator
Monitoring the temperature of the arterial blood arterial outlet blood temperature under-estimates
delivered to the body and of venous return blood cerebral perfusate temperature. (Class I, Level C)
helps to protect sensitive organs such as the brain
and to confirm adequacy of cooling and rewarming. Surgical teams should limit arterial outlet blood
temperature to <37°C to avoid cerebral
A temperature gradient of less than 10°C between
hyperthermia. (Class 1, Level C)
arterial outlet and venous inlet is recommended
during cooling to avoid cerebral injury, generation Temperature gradients between the arterial outlet and
of gaseous emboli or outgassing when blood is venous inflow on the oxygenator during CPB cooling
returned to the patient. Maintaining a low gradient should not exceed 10°C to avoid generation of
gaseous emboli. (Class 1, Level C)
between inflow and outflow temperature is equally
important during rewarming from hypothermia as a CLASS IIa RECOMMENDATIONS
fast temperature rise is associated with poor neuro- Pulmonary artery or nasopharyngeal temperature recording
logical outcomes. The perfusate temperature to the is reasonable for weaning and immediate post-bypass
body should not exceed 37°C. temperature measurement. (Class IIa, Level C)
The measurement accuracy of the thermistors is Rewarming when arterial blood outlet temperature 30°C:
affected by their immersion depth. The recommenda- i. To achieve the desired temperature for separation from
tions with regard to temperature monitoring during bypass, it is reasonable to maintain a temperature
CPB published in the 2015 STS/SCA/AMSECT gradient between arterial outlet temperature and the
Clinical Practice Guidelines are summarized in venous inflow of 4°C. (Class IIa, Level B)
Table 3.3. ii. To achieve the desired temperature for separation from
bypass, it is reasonable to maintain a rewarming rate of
0.5°C/min. (Class IIa, Level B)
Pressure Rewarming when arterial blood outlet temperature
Adequate blood pressure is one of the factors neces- <30°C: To achieve the desired temperature for
sary for adequate perfusion of vital organs. It is gen- separation from bypass, it is reasonable to maintain a
erally agreed that in most cases a mean systemic maximal gradient of 10°C between arterial outlet
arterial pressure (MAP) of 50–80 mmHg provides temperature and venous inflow. (Class IIa, Level C)
sufficient end-organ perfusion while cerebral autore-
gulation is preserved.
Circuit pressures are monitored primarily for safety
reasons, in order to avoid over-pressurization and the vasculature, coronary ostia or coronary sinus,
potential for circuit disconnection, cannula dislodge- depending on the route of delivery. The most com-
ment or vascular and tissue injury. Monitoring of cir- monly used mode of giving cardioplegia is antegrade,
cuit line pressure can also provide an indication of directly into the aortic root proximal to the aortic cross-
adequate positioning of cannulae, in particular ensuring clamp or into the coronary ostia at a line pressure of
that the aortic cannula is correctly positioned to avoid 80–150 mmHg. Retrograde cardioplegia is adminis-
dissection. Both pre- and post-oxygenator monitoring tered via a catheter in the coronary sinus, using a flow
is recommended to detect changes in transmembrane of 200–400 ml/min to a coronary sinus pressure of
pressure, as rises may indicate platelet deposition/aggre- between 30 and 80 mmHg.
gation within the oxygenator. Cardioplegia line pres- Servo regulation of pump flow rate coupled to 27
sure monitoring may avoid injury to the coronary pressure limits is an important safety feature of the

(a) Low level detector (b) Bubble detector

Figure 3.1 Detectors for low reservoir blood level (a) and air emboli (b). (Livanova, UK.)
HLM. The higher limit has to be set in a way that Low Level and Air Bubble Detection
stops the pump causing injury at the cannulation site,
Heart lung machines have alarm systems embedded
generally at <250 mmHg. Cardioplegia pressure is
within monitoring on the display panel of the HLM.
typically limited at lower pressures, depending on
Alarms either provide an audible and/or visual indi-
the route of delivery (<150 mmHg antegrade and
cation to the perfusionist or, more critically, can
<80 mmHg retrograde).
adjust or entirely stop pump flow if necessary when
The negative pressure inside the venous reservoir
servo-regulated. Checking alarm levels and function-
is monitored when either vacuum-assisted venous
ality is part of the pre CPB checklist; alarms must be
drainage (VAVD) or kinetic-assisted venous drainage
engaged prior to the initiation of CPB.
(KAVD) is used. The vacuum is typically adjusted in a
The low level alarm is a critical safety feature on
way that the negative pressure does not exceed
the HLM. A sensor on the venous reservoir is placed
30mmHg in order to reduce hemolysis and the risk
at a level below which there is the danger of emptying
of air entrainment into the venous line or across the
the reservoir and entraining air into the arterial cir-
membrane oxygenator. The latter can potentially lead
culation (see Figure 3.1a). If triggered, the servo regu-
to serious harm to the patient through gaseous arter-
lation will stop or significantly reduce the flow rate of
ial micro emboli or massive arterial embolization.
the arterial pump in addition to sounding an acoustic
Negative pressure in the venous line during kinetic-
alarm. The pump will only resume flow once the fluid
assisted venous drainage should not exceed ‒80
level is above the sensor again. Ultrasonic air bubble
mmHg to avoid cavitation and hemolysis. Other cir-
detectors on the arterial side of the HLM operate in
cuit pressures monitored may include antegrade or
the same way to protect against gross air embolism
retrograde cerebral perfusion with servo regulation
(see Figure 3.1b). Both alarm systems received a Class
limits around 150 mmHg for antegrade and
I recommendation in the 2019 EACTS/EACTA/
80 mmHg retrograde.
EBCP guidelines.
Circuit pressures are usually monitored using
Bubble detectors may also be used in the cardio-
reusable electronic transducers, where the fluid is
plegia line, and the venous line in minimized
28 isolated from the transducer by a dedicated disposable
CPB circuits. Although contemporary equipment,
circuit component.

technology, and perfusion techniques have reduced

the potential for massive air embolism, arterial gas-
eous microemboli still remain a concern. Integrated
air bubble detectors can provide quantification of
microbubbles during CPB, yet the values they report
have been found to be less reliable than those gener-
ated by specifically designed microemboli detectors.
This suggests that that microbubble counts from air
bubble detectors integrated in the circuit should not
be reported. However, any events where the low level
and/or air bubble alarms have been triggered should
be included in the perfusion record.
Calibration of Heart Lung Machine

Monitoring Systems Figure 3.2 Terumo CDI550 in-line blood gas analyzer. (Terumo
Cardiovascular Systems Corp., Ann Arbor, MI.)
All monitors and alarms used should be calibrated
and maintained regularly according to the manufac-
turer’s instructions and the recommended service limb and HCO3 and K+ using direct blood contact,
schedule. All equipment must be checked before use while SO2, Hct and Hb are measured using optical
(see Chapter 4 for more detail). reflectance (see Figure 3.2). The cost of the disposable
sensors associated with this technology has led to the
CDI technology not always being routinely adopted.
Gas Exchange In some centers it is used for complex or prolonged
The primary function of the respiratory system is to cases – such as when blood gas management strategy
take in oxygen and eliminate carbon dioxide. Inhaled is changed from α-stat to pH-stat during cooling or
oxygen enters the lungs and reaches the alveoli where rewarming in procedures involving deep hypothermic
it passes through the air-blood barrier and into the circulatory arrest (DHCA).
blood in the capillaries. Similarly, carbon dioxide The System M (Spectrum Medical, Gloucester,
passes from the blood into the alveoli and is then UK) is an example of a diagnostic monitor which
exhaled. Oxygenators on the HLM function using provides continuous non-invasive measurement of
exactly the same principle. blood gases (pCO2, pO2), SO2, flow and bubble/
emboli detection and ventilation parameters (sweep,
In-line Blood Gas Analysis, Venous Saturation oxygenator inlet O2 and outlet CO2) as well as Hb,
however no electrolyte measurements are provided.
and Hematocrit Monitors The reusable sensors are attached to the circuit, neg-
The theoretical advantages of using continuous in- ating the requirement of ongoing disposable costs (see
line blood gas and electrolyte monitoring during Figure 3.3).
CPB are well established; however, the clinical impact The 95% limits of agreement both devices have
remains controversial. The available devices may be with laboratory or point of care blood gas analysis do
divided into those using electrochemical electrodes not allow complete substitution and they should be
and cuvettes, which are placed in the circuit, and considered as trending devices only. The few random-
those that use light absorbance or reflectance, which ized studies that have evaluated the efficacy of these
require sensors placed external to the circuit tubing. devices found that they lead to improved adherence to
The Terumo CDI550 in-line blood gas analyzer institutional perfusion protocols, which did not trans-
(Terumo Cardiovascular Systems Corp., Ann Arbor, late into improved patient outcomes.
MI) is an optical fluorescence and reflectance based More basic forms of in-line monitoring, using
in-line system that continuously monitors 12 key absorbance or reflectance of infrared light signals,
blood gas parameters. Fluorescence sensors measure are commonly used to continuously monitor venous
pH, pCO2, pO2 on both the arterial and the venous and arterial blood oxygen saturations during CPB. 29

Figure 3.3 M4 monitor. (Spectrum Medical, UK.)
Similar to the more advanced devices above, they lack improved neurocognitive function in patients under-
in accuracy but are valuable tools for observing and going NIRS based algorithms to improve oxygen
recording trends. supply/demand ratio, recent randomized trials and a
As a minimum, it is recommended to continu- recently published meta-analysis and systematic
ously monitor SvO2 and Hct and perform full blood review showed no clinical benefit. Cerebral saturation
gas analyses at regular intervals throughout the dur- monitoring is discussed in more detail in Chapter 18
ation of CPB (Class I recommendation, 2019 EACTS/ and its clinical application in Chapter 9.
EACTA/EBCP guidelines).
Oxygen Delivery and Carbon
Cerebral Oxygen Saturation Dioxide Extraction
Adverse cerebral outcomes after cardiac surgery are Oxygen delivery (DO2) is determined by hemoglobin,
associated with increased mortality, prolonged ICU
arterial blood flow, oxygen saturation and PaO2.
and hospital stay and the use of additional healthcare
Many current HLM monitors are able to continuously
resources. Continuous monitoring of cerebral oxygen
calculate and display DO2 during CPB. Alternatively
saturation may provide a tool to detect an imbalance
it can be calculated manually from reference charts.
between cerebral oxygen demand and supply and may
Evidence from a randomized trial and multicenter
decrease the likelihood of intraoperative cerebral injury.
registry data shows that a goal-directed perfusion
Near-infrared spectroscopy (NIRS) can be used to
strategy to maintain oxygen delivery index (DO2i)
monitor cerebral oxygen saturation during cardiac sur- during CPB > 280 mL/min/m2 reduces the incidence
gery. Self-adhesive sensors containing the infrared light of acute kidney injury following cardiac surgery.
source and detectors are placed on one or both sides of the
forehead. Cerebral desaturation is defined as a 20% reduc-
tion from baseline values or an absolute decrease below Anticoagulation Monitoring
50% taking the duration of desaturation into account. Systemic heparinization is required for CPB to avoid
The evidence regarding its clinical benefit is how- coagulation due to contact activation and stasis in the
30
ever contradictory. Although early studies showed reservoir or the operating field. Safe anticoagulation is

ascertained by measuring the activated clotting time need for temporary atrial or ventricular pacing.
(ACT), which is generally done in the operating Pulmonary artery catheter – although not used rou-
theater. The ACT is a highly unspecific whole blood tinely in many parts of the world, the PAC may be
coagulation assay and is influenced by factors such as used to provide assessments of cardiac output and
temperature, hematocrit, fibrinogen level and platelet pulmonary artery pressure, which may help guide
count or function. The majority of centers around the inotropic support during separation from CPB.
world target ACT values between 450 and 550 Transesophageal echocardiography – TEE is
seconds. The ACT is typically measured every 20–30 widely used in cardiac surgery. Recent guidelines by
minutes and recorded in the perfusion record. the American Society of Anesthesiologists and the
The 2018 STS/SCA/AMSECT Clinical Practice Society of Cardiovascular Anesthesiologists recom-
Guidelines recommend as Class 1 evidence that “a mend that, in the absence of contraindications,
functional whole blood test of anticoagulation, in the intraoperative TEE be performed in all cardiac valve
form of a clotting time, should be measured and should and thoracic aortic procedures (Class 1) and is rea-
demonstrate adequate anticoagulation before initi- sonable for CABG operations (Class IIa). The advan-
ation of, and at regular intervals during cardiopul- tages in the use of TEE prior to CPB include
monary bypass. (Level of Evidence C)”
confirming the preoperative diagnosis,
Furthermore, a Class IIa recommendation in the
same publication states “it is reasonable to maintain detecting undiagnosed pathologies,
activated clotting time above 480 seconds during CPB. confirming the success of surgical intervention,
However, this minimum threshold value is an approxi- particularly in valve repairs and replacements,
mation and may vary based upon the bias of the confirming appropriate de-airing after open
instrument being used. For instruments using ‘max- chamber surgery and
imal activation’ of whole blood or microcuvette tech- guiding inotrope management by continuous
nology, values above 400 seconds are frequently assessment of left and right ventricular function.
considered therapeutic. (Level of Evidence C)”
It is important to note that ACT devices from
different manufacturers must not be used inter- Documentation of Intraoperative
changeably. Anticoagulation during cardiopulmonary Monitoring Data: The Cardiopulmonary
bypass is discussed in detail in Chapter 6.
Bypass Record
The CPB or perfusion record is a legal record and
Hemodynamic Monitoring should therefore be accurate and legible. Historically,
Assessment of myocardial function is important both the perfusion record had been handwritten, with the
pre CPB and during separation from CPB. perfusionist documenting physiological parameters
Hemodynamic monitoring includes the electrocar- and heart lung machine values. Typically, this
diogram (ECG), pulmonary artery catheter (PAC) happened every 5–10 minutes, when changes
and transesophageal echocardiography (TEE). occurred or when events or interventions (e.g., drug
Electrocardiogram – ECG monitoring is one of administration) required documentation. A manual
the minimum monitoring requirements during anes- record will always be a snapshot of what occurs
thesia. Although native cardiac function is unneces- during bypass and may be incomplete or inaccurate,
sary during CPB, the ECG can provide important with errors able to be introduced in a number of ways.
clues to These inadequacies include missing data, biased
efficacy of initial cardioplegia delivery by recording, transcription error and subjectivity of
broadening QRS complexes and the appearance of observation. There are a number of systems that are
towering T waves, able to generate an electronic record with the aid of
adequacy of myocardial protection by showing data collection software. They provide automatic data
signs of electrical activity, acquisition and integrate data from the HLM and
early signs of ischemia (ST segment changes or other monitoring systems in the operating room,
ventricular tachyarrhythmias) after cross-clamp most importantly the anesthetic, hemodynamic
removal or before weaning off CPB and
31
monitoring (Figure 3.4). As the number of monitors

(a) Connect Datapad (b) Quantum Workstation

Figure 3.4 Examples of automatic data acquisition and monitoring systems for cardiopulmonary bypass; (a) Connect Datapad (Livanova, UK), (b)
Quantum Workstation. (Spectrum Medical, UK.)
in the operating room increases, the operating team Scientists of Great Britain and Ireland for Standards
needs to observe, record, and respond to more and of Monitoring and Safety during CPB and is a Class
more data. Where this is recorded automatically, the IIa recommendation in the 2019 EACTS/EACTA/
perfusionist and the anesthesiologist are less dis- EBCP guidelines. Comprehensive records also pro-
tracted and more able to concentrate on the patient vide individual departments with the ability to define
rather than on documenting the procedure. The CPB quality metrics based on institutional guidelines.
integrity of the data from automatic data acquisition
removes the bias that is inherent in the manual
record. Application of Electronic Perfusion Data
Apart from creating a record of the patient and Generating an accurate perfusion record is only one
heart lung machine physiological parameters, these component of the value that can be gained from
products provide documentation of CPB equipment, automated electronic perfusion data collection
priming solutions, fluid balance, coagulation and systems. The data provide an enormous resource for
blood gas values, cardioplegia and drug administra- ongoing research activities and quality management.
tion. Electronic perfusion data collection, including The importance and benefits of quality assurance and
32 the ability to produce a printout, is a general recom- quality improvement in healthcare delivery are well
mendation of the Society of Clinical Perfusion recognized. The collected data can be used to monitor

and improve quality of care processes and to report glucose, arterial outlet temperature, and blood gas
practices at an individual or institutional level, or to management during CPB utilizing electronic data.
facilitate multicenter reporting through participation These benchmarks provide a baseline for the imple-
in a CPB registry. mentation of multicenter continuous quality
improvement processes for perfusion practice. By
Registry examining CPB data and related outcomes, registries
have been able to define risk factors associated with
Some examples of CPB registries include the
adverse outcomes.
Northern New England Cardiovascular Disease
One of the problems inherent in determining
Study Group, the Australian and New Zealand
relationships between CPB parameters and the clin-
Collaborative Perfusion Registry (ANZCPR) and the
ical measures of outcomes is the low rate of adverse
PERFORM registry (USA), which is an integral part
events, resulting in the requirement of large cohorts
of the Michigan Society of Thoracic and
to achieve adequate and statistically well powered
Cardiovascular Surgeon Quality Collaborative’s pro-
studies. Amalgamation of collected data provides a
gram. Electronic data collection meets the needs of
means to increase cohort size and therefore reduce
registry endeavors because it provides a method of
the confounding effects of variations in patient risk
transferring de-identified data from multiple sites,
factors and practice changes over time. Registry data
integration of this data into a central database, and a
also play an important role in confirming the gener-
means to generate calculated CPB parameters and
alizability of results of clinical studies and in recom-
perform complex data analysis. The ANZCPR has a
mending them for implementation into clinical
defined process of core metrics and uses these to
practice.
calculate benchmarks for the management of blood
Suggested Further Reading Perfusion Practice: 2013. Baker

RA, Bronson SL, Dickinson TA
during cardiopulmonary bypass.
J Extra Corpor Technol.
1. Puis L, Milojevic M, Boer C et al. et al, on behalf of the International 2018;50:1–14.
2019. 2019 EACTS/EACTA/EBCP Consortium for Evidence-Based
Guidelines on cardiopulmonary 6. Ranucci M, Johnson I, Willcox T
Perfusion for the American et al. Goal-directed perfusion to
bypass in adult cardiac surgery. Society of ExtraCorporeal
Interact Cardiovasc Thorac Surg. reduce acute kidney injury:
Technology. JECT. A randomized trial. J Thorac
February 1, 2020;30(2):161–202. 2013;45:156–166. Cardiovasc Surg. November,
2. Recommendations for Standards 4. Engelman, R, Baker, RA, Likosky 2018;156(5):1918–1927.
of Monitoring during DS et al. The Society of Thoracic
Cardiopulmonary Bypass. The 7. Newland RF, Baker RA,
Surgeons, The Society of Woodman RJ et al. Australian and
Society of Clinical Perfusion Cardiovascular Anesthesiologists,
Scientists of Great Britain and New Zealand Collaborative
and The American Society of Perfusion Registry. Predictive
Ireland, Association of ExtraCorporeal Technology:
Cardiothoracic Anaesthetists, capacity of oxygen delivery during
Clinical practice guidelines for cardiopulmonary bypass on acute
Society for Cardiothoracic cardiopulmonary bypass –
Surgery in Great Britain and kidney injury. Ann Thorac Surg.
Temperature management during June 22, 2019.
Ireland, August 2016. cardiopulmonary bypass. JECT.
3. Report from AmSECT’s 2015;47:145–154. 8. Ottens J, Tuble SC, Sanderson AJ
International Consortium for et al. Improving cardiopulmonary
5. Shore-Lesserson L, Baker RA, bypass: Does continuous blood
Evidence-Based Perfusion: Ferraris V et al. STS/SCA/
American Society of gas monitoring have a role to
AmSECT Clinical practice play? J Extra Corpor Technol.
ExtraCorporeal Technology guidelines: Anticoagulation
Standards and Guidelines for September, 2010;42(3):191–198.
33

Chapter
Cardiopulmonary Bypass Circuit
4 Setup and Safety Checks

Victoria Molyneux and Shahna Helmick
Introduction circuit components should ritualistically follow a rou-

tine dictated by institutional protocols and the process
Assembling the cardiopulmonary bypass (CPB) cir- confirmed by following a recognized, institutionally
cuit and checking the heart lung machine (HLM) for agreed pre-CPB checklist.
faults prior to clinical use is an essential and integral
part of the provision of clinical perfusion. This chap-
ter describes the procedure for setting up the extra- CPB Machine Preparation and Setup
corporeal circuit and the safety checks that should be
undertaken before embarking on a case.
CPB Components
The evolution of CPB has been marked on one Cardiopulmonary bypass circuits are comprised of a
side by sophistication and complexity and on the number of disposable components supported by the
other side by an increased requirement for safety. HLM. We consider four essential elements of the CPB
The death of a pediatric cardiac surgical patient and system that remain the same, despite different manu-
the subsequent Gritten Report of 2007 marked a facturers and different component designs. Principally
turning point for perfusion safety. This led to the these are as follows:
implementation of minimum standards and practice Membrane oxygenator and venous reservoir
recommendations within the United Kingdom. The Cardioplegia system
medical communities in many countries have issued Custom tubing pack
recommendations concerning the training of clinical Arterial line filter (unless integrated in
perfusionists and the use of monitoring and safety oxygenator/reservoir).
devices for CPB. Although studies have not estab-
lished a cause-to-effect relationship, the decrease in
CPB-related mortality may be partly attributed to
CPB Setup
these measures. Vigilance is paramount to the safety These components can be assembled in a myriad of
of CPB. Modern perfusion systems are designed to configurations, depending on institutional and clin-
optimize safety. Technological advances have seen the ician preference and specific patient requirements.
incorporation of automatic, servo-regulated alarms Although there is no universally agreed or commonly
and fail-safe devices; however, the clinical perfusio- used sequence for setting up and priming a standard
nist’s attention to detail, as well as performance of CPB system, the following list provides a general
pre-CPB checklists and protocols, underpins safe routine to ensure a safe setup:
practice. Investigations around the world have repeat- All components are checked for sterility,
edly pointed to medical errors that could have been cleanliness, integrity, and expiration date.
prevented as an important cause of morbidity and The heat exchanger on both the oxygenator and
mortality; human error is a far greater cause of acci- the cardioplegia delivery system (if present) must
dents than mechanical mishap. be leak-tested either upon opening the sterile
Preparing the CPB circuit and HLM, attending to packaging or once the CPB circuit has been set up
the patient’s clinical details and to the surgical but prior to the initiation of priming. In practice
requirements for the procedure all form part of the this is usually done once the CPB circuit has been
process of safe provision of CPB. By necessity, the set up dry. The integrity of the heat exchanger
34 preparation of the HLM and assembly of the CPB may be tested using a pressure occlusion device

Chapter 4: Cardiopulmonary Bypass Circuit Setup and Safety Checks
and ensuring there is no pressure drop once set to for the duration of the procedure. The gas line, the
250 mmHg or by attaching the water lines to the oxygen/air blender, and the exhaust scavenging
heat exchanger and leaving them to run for system (where used) are attached to the
10 minutes prior to priming. This ensures that the appropriate ports on the base of the oxygenator.
barrier between the blood side and the water side Ensuring safe attachment of all connections is
of the devices is intact. essential. Tubing should be pushed over the
Occlusions are set on the main arterial roller connector to at least the second barb. The
pump, the suction pumps, and the cardioplegia sampling port manifold is positioned with taps
pumps. Pump occlusions may be set using one of secured. The arterial line tubing is then put in
two methods: pressure drop or fluid drop. Many place and connected to the venous reservoir outlet
institutional protocols state that pumps should be and oxygenator inlet. Many providers now supply
set to fully occlusive at 240 mmHg. “Fully fully preconnected circuits. When using these it is
occlusive” is defined as a pressure fall of no more essential to visually check that the entire circuit
than 1mmHg per minute. Alternatively, the has been assembled in the correct order. Similarly,
occlusion may be set using the fluid method – if “quick-connect” fittings are used anywhere in
HLM manufacturer Sorin recommends adjusting the circuit, their integrity must be checked.
the occlusion to a one-inch fall per minute in a 30- The cardioplegia circuit is usually positioned
inch column of fluid. Suction occlusion, direction on the HLM. A number of different
and function of pressure relief valves are all configurations are in common use:
checked prior to the initiation of CPB. 1. The cardioplegia pump may accommodate
Speed controls and pump direction are checked to two segments of tubing with varying diameters
be operational and correct. The flow rates and within it so that blood and cardioplegia
tubing size calibrations are set for each individual solution mix in the desired ratio – for example,
case and the rollers on the pumps are checked to a 4:1 blood to high-strength cardioplegia
make sure that they rotate freely. The pump head solution when using Harefield or St. Thomas’
rotation should be smooth and quiet, and servo- solution or 1:4 when using Del Nido
regulated connections should be tested prior to the cardioplegia.
initiation of CPB. 2. The cardioplegia system may comprise of two
Electrical power cord connections are checked to separate mini pumps that may be used to
be secure, and HLM batteries are checked to independently deliver the mix of blood and
ensure that they are fully charged and operational. high strength cardioplegia in the desired ratio.
It is essential that the HLM is connected to an 3. The microplegia technique delivers blood and
uninterrupted power supply (UPS) in the additives for cardioplegia with minimal
operating room. The HLM should be temporarily crystalloid. A number of external devices –
disconnected from the power source, ascertaining such as the Quest MPS2 – offer specific,
the power failure alarm and battery backup unit variable cardioplegia delivery, allowing
are all functional. different ratios (4:1, 8:1, 1:4) or extended arrest
Oxygen and air gas lines are secured to the gas protocols with a single dose strategy.
source and checked for functionality.
A gas scavenging system may be used, either The arteriovenous (AV) loop is connected to the
directly as part of the CPB circuit or as a wider venous reservoir inlet and oxygenator outlet. The
operating room air flow management system. arterial line filter, arterial line pressure transducer
Scavenging is mandatory in the majority of and the arterial line bubble detector are all
countries if a volatile anesthetic vaporizer is part attached to the arterial line tubing. The bubble
of the HLM. The gas exhaust from the oxygenator detector and the pressure transducer are both
has to be unobstructed. coupled to the HLM and are servo-regulated. This
The integrated oxygenator and venous reservoir is ensures that if air is detected in the arterial line, or
placed on its secure holder and oriented in a way the pressure exceeds preset limits, an alarmed
that allows the perfusionist to have it in full view automatic cutout facility is activated. Once 35

handed out onto the operating table, the surgeon Pre-bypass filtration is considered mandatory for
will divide the AV loop prior to aortic cannulation contemporary perfusion practice. Filtration of crys-
and connect the respective ends to the arterial and talloid CPB priming solutions with a pre-bypass filter
venous cannulas. with a pore size of 0.2 micron has been found to
Suction and venting tubing should be color coded effectively reduce the number of microemboli and
to aid communication between the surgeon and endotoxin contamination that may potentially occur
the perfusionist during setting up for the in infusion solutions. The prime volume is added to
procedure. They are fixed into the various roller the venous reservoir. The main arterial pump is
head pump assemblies. To ensure that they are in roughly occluded before turning it on. The perfusio-
the right orientation, suckers and vents should be nist observes the filling of the pump tubing, the oxy-
water tested by the perfusionist and the scrub genator, and any ancillary lines. These must be closed
nurse prior to the initiation of CPB. This water or clamped after priming while fluid is recirculated
test was introduced as a mandatory minimum via the arterial recirculation line back into the venous
standard in the United Kingdom in 2016 to ensure reservoir. The arterial pressure dome – or monitor
that the suction tubing has been placed in the isolator – is primed and secured to the arterial pres-
pump head in the correct orientation and that sure line transducer. The arterial line filter is primed
there is no chance of blowing air into the heart according to the manufacturer’s instructions, and its
instead of sucking air or blood into the venous bypass line is clamped. The main recirculation line
reservoir. Alternatively, checklists to ensure the can then be clamped and priming fluid diverted
safety of suction and venting tubing are used in through the AV loop. Once the loop is filled, the
some jurisdictions to ensure safety. These tests pump can be left recirculating and the tubing
need to be completed prior to the initiation of inspected for air bubbles. Once the main circuit has
CPB. been primed, the cardioplegia circuit is primed. The
The CPB circuit may be flushed with carbon occlusions on the main arterial pump, cardioplegia
dioxide (CO2) prior to priming. CO2 is nearly pumps, and the suction pumps can be set, and tubing
30 times more soluble in blood than nitrogen and direction should also be checked at this point.
flushing the dry circuit is thought to decrease the Institutional protocol will determine whether the
number of gaseous emboli compared to a pump is left to recirculate or whether it is stopped,
conventional circuit once primed. At present, this and the circuit is left pressurized prior to initiation of
is not a universally accepted practice and is subject CPB. Both methods are safe and acceptable practice.
to institutional preference. If a standalone arterial Centrifugal pumps are often used in adult prac-
line filter is being utilized, this filter should now tice. These pumps are non-occlusive and should be
be clamped off and isolated; the arterial line gravity filled to ensure that they are fully de-aired.
should also be clamped if there is a recirculation Centrifugal pump consoles have integrated flow
shunt line distal to the arterial line filter. This step probes and are unidirectional. As they are afterload
is not required if an integrated arterial line filter is sensitive, pump speed must be set to produce forward
being utilized (as is more commonplace flow before initiating CPB. A one-way valve or an
nowadays). electronic, servo-regulated clamp can be placed in
the circuit to prevent retrograde flow.
This is the final stage of setting up the CPB circuit,
Final monitoring checks should be undertaken
after which the perfusionist can move onto the
once circuit setup and priming have been completed.
priming stage.
Arterial and venous circuit temperature probes
should be in place, and pressure transducers should
be calibrated and set to appropriate scales. The fluid-
CPB Priming level sensor of the reservoir has to be set at an appro-
The method for priming varies according to institu- priate level for the case being undertaken. This is
tional protocol. Different centers use different fluids, generally determined by the flow as predicted by the
different volumes, and different drug combinations patient’s cardiac index and the manufacturer’s
based on their institutional preferences (see also instructions for use. The oxygen analyzer should also
36
Chapter 5 for more detail). be calibrated and operational. Backup equipment,

including hand cranks, duplicate components, emer- responded to the Gritten Report by adopting a new
gency lighting, an oxygen cylinder, and ice, should be code of practice and instructing their member organ-
available for the duration of the procedure. Drugs izations to place the highest priority on perfusion
should be drawn up, in conjunction with the Drugs safety. This was to be the biggest shake-up of perfu-
and Fluid Treaty and any Patient Specific Directions, sion minimum standards and recommendations in
and properly labeled. At this point all alarms must be recent years. Perfusion communities throughout the
operational, audible and engaged, and all parameters world have responded by either initiating the devel-
should now be set in preparation for the initiating opment of standards of practice or, as the American
CPB. The final setup checklist should be completed at Society of Extracorporeal Technology (AmSECT) has
this time. done, revising and continuously updating their
Standards and Guidelines to ensure they remain
contemporary.
Human Factors
Healthcare will always involve risks, particularly when
very complex systems and procedures are involved. In The Pre-CPB Checklist
2012, the UK National Patient Safety Agency esti- The World Health Organization (WHO) developed
mated that around 10% of patients admitted to and evaluated a simple checklist in 2007, which has
National Health Service (NHS) hospitals had experi- formed the basis for several iterations specific to
enced a patient safety incident and up to half of those cardiac surgery. Figure 4.1 shows a typical example
incidents could have been prevented, providing a of a cardiac surgical safety checklist. The introduction
similar message to the earlier US Institute of of this extra step has dropped the rate of major
Medicine report “To Err is Human: Building a Safer inpatient complications from 11% to 7% and that of
Health System.” the inpatient death following major operations from
The practice of cardiac surgery demands daily 1.5% to 0.8%.
interface with sophisticated technologies including Specialist checklists are likely to reduce morbidity
the HLM. For many decades the safety checklist con- and mortality more effectively than the available gen-
cept has been an integral part of industries facing eric general surgical checklists. This idea is repre-
high-complexity tasks. Aviation has been at the fore- sented in the cardiac surgical safety checklist with
front of utilization of the safety checklist, and the regard to perfusion. The time-out phase states that
understanding of the importance of human factor “there should be a perfusionist check and briefing to
effects on safety. ensure that the perfusionist is fully aware of the plan
The evolution of CPB over the past half-century for CPB or any special requirements that are needed.”
has mostly been characterized by modifications of Perfusion strategies including patient specific target
component parts. Investigating human factors in car- cooling temperature, cannulation technique and size
diac surgery in general and perfusion in particular has and special equipment are all discussed as part of the
been a relatively recent addition to the quest for safety cardiac surgical safety checklist at the multidisciplin-
(see Chapter 1 for more detail). ary preoperative briefing.
In 2007, in response to the investigation of a fatal The UK Department of Health states that there
pump-related incident in the United Kingdom, the should be a clear requirement to check each compon-
NHS published the Gritten Report. The report pre- ent of the CPB circuit before its operation and that a
sented an independent review of current perfusion standard checklist is signed off by the perfusionist.
practice in the United Kingdom and identified the The format of the checklist may be handwritten or
system-wide failure of perfusion as a profession to part of the electronic patient records. Double
take adequate safety precautions. Gritten highlighted checking of the CPB circuitry by two perfusionists
a series of events that led to the death of a pediatric has in many institutions become minimum standard,
cardiac surgery patient. The report concluded that the as has the availability of a second perfusionist for all
incident was caused by inadvertent human error, CPB cases. Figure 4.2 illustrates the thorough and
perfusion systems failures at national and local levels comprehensive pre-CPB checklist published by
and local system problems. The Society of Clinical American Society of ExtraCorporeal Technology 37
Perfusion Scientists of Great Britain and Ireland (www.amsect.org).

Society for Cardiothoracic Surgery in Great Britain & Ireland
CARDIAC SURGICAL SAFETY CHECKLIST

SIGN IN TIME OUT SIGN OUT
Before Induction of Anaesthesia Before start of Surgery Before patient leaves theatre
IDENTITY CONFIRMED TEAM MEMBERS INTRODUCED (Name & Role)

Has the patient confirmed their identity, site,
INSTRUMENTS, SHARPS & SWAB
procedure and consent. PATIENT AND PROCEDURE CONFIRMED CONFIRMED AS CORRECT
SITE MARKED (or not applicable) Surgeon, Anaesthetist and Registered Practitioner verbally
DEBRIEFING PERFORMED
Surgical Incision/Access agreed. Equipment or procedural problems identified and addressed
CONSENT FORM CORRECT & SIGNED
Implants to be used confirmed THEATRE TEAM BRIEFING COMPLETE OPERATION NOTE DONE
WARD PREPARATION COMPLETE Critical or Unexpected events planned for.
(Fasting, Shower/Hair removal, Glycaemia, Blood) Special equipment requirements ready.
CONCERNS FOR RECOVERY/
INSTRUMENT STERILITY CONFIRMED POST OPERATIVE CARE
MRSA/MSSA STATUS KNOWN
DISCUSSED & RECORDED
Positive? - YES / NO THROMBOPROPHYLAXIS Yes/Not applicable
Pacing Box Mode & Thresholds checked
ANAESTHESIA MACHINE, EQUIPMENT/STAFFING CONCERNS IDENTIFIED

ICU & DRUG CHARTS CHECKED
MONITORING & MEDICATION CHECKS
PERFUSIONIST CHECKS & BRIEFING CORRECT AND FILED
Perfusion regime & prescriptions agreed
COMPLETE Myocardial protection strategy agreed
KNOWN ALLERGIES? YES/NO
Checklist Signed Complete and Correct
SURGICAL SITE INFECTION BUNDLE GIVEN
DIFFICULT AIRWAY/ASPIRATION Surgeon
Prophylactic IV antibiotics within 60 minutes, Idophor
RISK? YES (equipment available)/ NO impregnated drapes, Patient warming, Hair removal,
Glycaemic control
RISK OF EXCESSIVE BLOOD LOSS? IMAGING DISPLAYED AND/OR REVIEWED Anaesthetist
YES / NO If YES preparations and plan agreed
PROCEDURE BRIEFING WITH Patient Label Scrub Nurse

ANAESTHESIA TEAM COMPLETE
SPECIAL EQUIPMENT IDENTIFIED for the SCTS.

Approved by the National Patient Safety Agency DATE
Figure 4.1 Cardiac Surgical Safety Checklist. (Reproduced by kind permission of The Society for Cardiovascular Surgery in Great Britain and Ireland www
.scts.org.)
Checklists have been clearly demonstrated to facili- The patient’s height and weight are essential to
tate multi-step processes to improve team dynamics and calculate:
minimize error. Multiple international organizations ○ Dose of heparin required (usually 300–500 IU/
including the World Health Organization, the Society kg)
of Thoracic Surgery and the National Patient Safety ○ Body Surface Area (BSA) in metres2, which
Agency support their use in surgery. Checklists are is required to determine the calculated
now accepted to be an integral part of surgery as a whole flow rate at normothermia (BSA Cardiac
and, more specifically, in cardiac surgery and CPB. Index) and therefore select appropriate CPB
circuitry as well as arterial and venous
Safety Concerns prior to Commencing CPB cannula and
○ Predicted hematocrit on initiation of CPB.
Before embarking on a case, the perfusionist under-
takes a comprehensive review of the patient’s notes. In Safety issues relating to the pre-operative information
addition to the information required by the checklist the perfusionist needs to know about are summarized
the following details are important: in Table 4.1.
Significant co-morbidities, such as renal dysfunction, Additional checklists may of course be used at
diabetes, genetic conditions affecting CPB. different stages of the operation, for example, perfu-
Metabolic or hematological abnormalities, such as sion handover checklists or prior to weaning from
anemia, sickle cell anemia, thrombocytopenia, CPB. The latter is discussed in further detail in
or hyperkalemia. Chapter 12.
38

Patient Gas Supply

Patient identity confirmed Gas line & filter connections secure
Procedure confirmed Gas exhaust unobstructed
Blood type, antibodies confirmed Source & connections of gas confirmed
Allergies checked Flow metre/gas blender operational
Blood bank number confirmed Hoses leak free
Medical record number confirmed Anaesthetic gas scavenge line operational
Chart reviewed
Components
Sterility and Cleanliness System debubbled
Components checked for package integrity Connections/stopcocks/caps secure
Equipment Clean Appropriate lines clamped/shunts closed
Heat exchanger leak tested Tubing direction traced & correct
Patency of arterial line/cannula confirmed
Pump No tubing kinks noted
Occlusions set One-way valve in correct direction
Speed controls operational Leak-free after pressurisation
Flow meter in correct direction & calibrated
Flow rate indicator correct for patent/tubing size Safety Mechanisms
Rollers rotate freely Alarms operational, audible & engaged
Pump head rotation smooth and quiet Arterial filter/bubble trap debubbled
Holders secure Cardiotomy/hardshell venous reservoir vented
Servo regulated connections tested Vents tested
Venous line occlude calibrated & tested
Electrical Devices securely attached to console
Power cord connections secure
Servo regulated connections secure Assisted Venous Return
Batteries charged and operational Cardiotomy positive-pressure relief valve
present
Negative-pressure relief valve unobstructed
Cardioplegia Vacuum regulator operational
System debubbled and operational
System leak-free after pressurisation Supplies
Solution checked Tubing clamps available
Drugs available & properly labelled
Monitoring Solutions available
Circuit/patient temperature probes placed Blood products available
Pressure transducers calibrated/proper scale Sampling syringes available
Inline sensors calibrated Anaesthetic vaporiser correct
Oxygen analyser calibrated Vaporiser operational & filled
Anticoagulation Backup
Heparin time & dose confirmed Hand cranks available
Anticoagulation tested & reported Duplicate components/hardware available
Emergency lighting/torch available
Temperature Control Backup full oxygen cylinder available
Water source connected & operational Ice available
Temperature range tested & operational
Water lines unobstructed
Signature: Date & Time:
Figure 4.2 Pre-Cardiopulmonary Bypass Checklist. (Reproduced by kind permission of The American Society of ExtraCorporeal Technology.)
AmSECT promotes the use of pre-CPB checklists, or a reasonable equivalent, in clinical perfusion practice. AmSECT encourages perfusionists to
use this checklist as a guide and modify the checklist to accommodate differences in circuit design and variations in institutional clinical
practice. AmSECT can accept no liability whatsoever for the adoption and practice of this suggested checklist.
39

Table 4.1. Pre-CPB Safety Concerns reservoir for air removal, therefore it is essential
Heparin ○ Activated Clotting Time (ACT)
that a safety device is in place to prevent air from
administration >400 seconds or > 3x baseline entering either the centrifugal pump or the venous
(depending on institutional bag. The APS device is activated:
protocol) ○ when air is detected in the venous line,
Arterial ○ Pulsatile swing on an aneroid allowing it to be purged before possible
cannulation pressure gauge connected to a entrainment into the circuit, or
side arm of the arterial line ○ by a level sensor if there is a reduction in the
○ Pump volume transfuses well amount of blood in the bubble trap due to
with no rapid rise in arterial line displacement by entrained air. The level sensor
pressure is servo-regulated and, once activated, the
Venous reservoir ○ Additional fluid available and automatic arterial clamp is closed to
fluid level attached to the circuit temporarily stop flow, allowing the
○ Low-level alarm placed at perfusionist to remove the air.
appropriate level for the case and Bubble sensor post APS system – if the venous
activated bubble trap fails to eliminate sufficient air, the
Oxygen analyzer ○ Functional and alarm activated pump may de-prime. If air passes toward the
pump, the auto clamp is triggered, and the pump
Sweep rate & ○ Appropriate settings for case
FiO2 after review of notes will stop, allowing the air to be displaced into the
soft-shell bag.
Venous cannula ○ De-aired
Electronic Venous Line Occluder (EVO) – can be
CPB shunt lines ○ Clamped used in a manual or automatic mode for clamping
Clamps on ○ Off the venous line.
surgical side MiECC is discussed in detail in Chapter 8.
Alarm overrides ○ Deactivated
Drugs and fluids ○ Available, prepared, labeled
In summary, the many technological developments
Pre-CPB ○ Complete concerning HLM hardware and related components
checklist have made it possible to reduce the incidence of
complications and problems during CPB. The like-
lihood of death or severe injury from CPB-related
incidents has been declining from 1: 1,400–3,200 in
the early 2000s to currently 1: 4,450–4,850 patients,
Minimal Extracorporeal Circulation which is testament to the safety culture in
perfusion.
Safety Features The use of checklists is well established in medi-
Minimally invasive extracorporeal circulation cine, specifically surgery, as well as other industries. It
(MiECC) is the term given to describe a multidisci- has been proven that their use saves lives, time and
plinary strategy focused on the reduction of the adverse money as well as reducing the rate of complications. It
effects of CPB. For MiECC, the safety briefing is con- therefore appears logical to assume that the use of
ducted similar to conventional CPB cases, however the pre-CPB checklists will have similar effects, particu-
team also needs to agree when and how to convert to larly with regard to complications during CPB.
conventional bypass, should MiECC not be adequate. Checklists should be used in an appropriate, diligent,
The safety devices recommended for MiECC are: and professional manner. They need to be adapted to
Pulmonary artery and aortic root vent bubble trap. the specific working environments as well as
Air Protection System (APS) – this is required emerging technologies, and they should be revised
because MiECC does not include an open regularly.
40

Suggested Further Reading cardiopulmonary bypass

machines. Journal of
of patient safety checklists.
European Journal of
1. Department of Health. Guide to Extracorporeal Technology 2009; Cardiothoracic Surgery 2012; 41:
Good Practice in Clinical 41(2):57–63. 993–1004.
Perfusion, London, 2009.
5. Gritten M. The independent root 8. Charriere JM, Pelissie J, Verd C
2. Society of Clinical Perfusion cause analysis report into the et al. Retrospective survey on
Scientists of Great Britain and adverse incident that led to the monitoring/safety devices
Ireland, Association of death of a paediatric cardiac and incidents of cardiopulmonary
Cardiothoracic Anaesthetists and surgery patient at United bypass for cardiac surgery in
Society of Cardiothoracic Bristol Healthcare NHS Trust on France. Journal of
Surgeons in Great Britain and 27th May 2005. NHS Publication ExtraCorporeal Technology 2007;
Ireland. Recommendations for 2007. 39:142–57.
Standards of Monitoring during
Cardiopulmonary Bypass. 2016. 6. NHS England. Decade of 9. Wahba A, Milojevic M, Boer C De
improved outcomes for et al. EACTS/EACTA/EBCP
3. National Patient Safety Agency patients thanks to surgical safety Guidelines on cardiopulmonary
(NPSA). Seven Steps to Patient checklist 2019 www.england.nhs bypass in adult cardiac surgery.
Safety. An Overview Guide for NHS .uk/2019/01/surgical-safety- European Journal of
Staff 2004. www.npsa.nhs.uk/ checklist/ Cardiothoracic Surgery 2019; 00:
sevensteps 1–42. https://doi:10.1093/ejcts/
7. Clark SC, Dunning J, Ottavio RA
4. Weigmann D, Suther T, Neal J et al. EACTS guidelines for the use ezz267
et al. A human factors analysis of
41

Chapter
Priming Solutions for Cardiopulmonary
5 Bypass Circuits
Filip De Somer and Robert Young
The composition of the fluid used to prime cardiopul-

monary bypass (CPB) circuits has been a source of
Blood Flow
great interest and debate ever since the inception of Delivery of oxygen to tissues depends on blood flow
cardiopulmonary bypass in 1953. There has been sig- and oxygen content. Blood flow is inversely related to
nificant progress in our understanding, but the ideal both vascular resistance and viscosity. Hemodilution
priming solution has still to be agreed upon and prac- with crystalloid or colloid prime leads to a reduction
tice continues to vary widely between cardiac units. in overall viscosity, resulting in improved tissue
The volume of contemporary bypass circuits oxygen delivery with reduced risk of organ ischemia
varies enormously from less than 400 ml to over during CPB. The optimal average hematocrit for the
2000 ml for adult circuits and from as little as microcirculation is 30% (Hb 10 g/dL) but this value
120 ml for pediatric CPB. Circuits must be carefully varies from organ to organ. For example, the kidney
de-aired with a compatible priming solution in order needs higher hematocrit values compared to the
to prevent gas emboli from passing into the patient’s heart. As some aspects of cardiac surgery and CPB
circulation at the commencement of CPB. In the early increase blood viscosity (see Table 5.1), prime hemo-
days, circuits were primed with allogeneic whole dilution can be helpful to counterbalance this.
blood. This practice proved to be unsustainable due Under normothermic conditions hematocrit
to issues of availability and cost and the growing values below 24% should be avoided. However,
appreciation of the potential risks, such as infection, oxygen supply to the tissues depends not only on
immunosuppression and various forms of transfusion the carrying capacity of the blood (hemoglobin) but
reactions, associated with its use. The use of a non- also on convective transport. Hemodilution decreases
hemic priming solution was first reported in 1958. hemoglobin concentration and thus oxygen carrying
Crystalloid and colloid priming solutions are capacity. For this reason hemodilution might require
now commonplace. an increase of blood flow to maintain the desired
The partial or total replacement of blood in the oxygen delivery to the organs. To illustrate this, to
prime with other fluids inevitably leads to changes in maintain the same oxygen delivery before and after a
the characteristics of the circulating blood as soon as decrease in hemoglobin concentration from 10 g/dL
CPB is commenced. The impact of these changes can to 8 g/dL, an increase in blood flow by 20% is
be thought of as being both quantitative and qualita- required. During normothermia an oxygen delivery
tive. The quantitative changes depend on the volume of at least 274 mL/min/m² should be maintained to
of the non-blood prime and the effects of hemodilu- preserve renal function.
tion. The qualitative changes depend on the consti- Cardiac surgery carries increased morbidity and
tution of the prime, which may affect electrolyte mortality when the decrease in hemoglobin concen-
concentrations, acid-base balance and osmolarity tration is not compensated by higher blood flow. This
among other things. is not surprising as adequacy of tissue oxygenation
depends on multiple other factors such as tempera-
ture, blood flow, duration of CPB and preoperative
Hemodilution organ function. In a healthy patient under physio-
Hemodilution with commencement of CPB has a logical conditions, a decrease in hemoglobin is com-
number of positive effects but also some less desirable pensated for by an increase in cardiac output. Until
42 effects. recently most centers did not adapt blood flow on

Chapter 5: Priming Solutions for Cardiopulmonary Bypass Circuits
Table 5.1. Factors increasing blood viscosity Table 5.2. Factors affecting hematocrit
prior to the initiation of CPB
Hypothermia A fall of 1°C increases viscosity by 2%
Patient size
Flow rates Low flow rates lead to aggregation
of blood cells (shear rate <10/s) Starting hematocrit
Red cell Turbulent flow and hypothermia Blood loss pre bypass
deformability cause reduced deformability of Intravenous fluids pre CPB
the cell membrane
Urine output pre CPB
Coagulation Activation of clotting cascades leads
to platelet aggregation, and Volume and nature of circuit prime
interaction with plasma proteins Transfusion policy
is primarily achieved by shortening the length of

CPB in the presence of pronounced hemodilution, circuit tubing and removing the venous reservoir,
thus potentially jeopardizing tissue oxygen delivery. which can reduce priming volume to as low as 400
Recent research has shown that individualized goal ml. Over the last decade the quest to reduce circuit
directed tissue perfusion based on calculated oxygen size has led to the evolution of minimal invasive
delivery reduces morbidity post CPB. This is dis- extracorporeal circulation (MiECC) systems,
cussed in more detail in Chapter 10. incorporating circuit and clinical practice
optimization to reduce priming volume. This
Clotting Factors promising approach is not yet in widespread use.
MiECC is discussed in detail in Chapter 8.
A further potential complication of hemodilution is the
Autologous Prime – is done once the patient has
relative reduction in concentrations of clotting factors
been cannulated but prior to establishing CPB and
such as fibrinogen, which can contribute to the coagu-
Blood is passively drained into the circuit,
lopathy associated with CPB (see also Chapter 16).
displacing the prime into a removeable reservoir.
This can take the form of Retrograde Autologous
Drug Bioavailability Prime (RAP), where the patient’s blood is drained
Hemodilution results in a change in the pharmacoki- retrogradely through the aortic cannula, or of
netic behaviour of administered drugs. The plasma Venous Autologous Prime (VAP), where blood is
drug concentration before hemodilution depends on drained antegradely through the venous cannula.
its plasma protein binding, its original distribution The extent of autologous circuit priming is limited
volume and the equilibration between tissue and by the hypotension caused by loss of the patient’s
plasma concentration. Hemodilution, by decreasing intravascular blood volume. This can be
plasma protein concentration, decreases the ratio of ameliorated to some extent by the administration
bound to free drug. With less drug bound, bioavail- of vasopressors. Autologous prime volumes may
ability increases as only unbound compounds can vary from as little as 150 ml to in excess of 1500
diffuse into tissues. Conversely, changes in viscosity ml. The decision to use autologous priming can be
and availability of free drugs may impact their renal based on the predicted hematocrit during CPB
and hepatic clearance. Chapter 10 provides more calculated from the patient’s estimated total blood
detail about drug management during CPB. volume (TBV), intraoperative fluid balance and
starting hematocrit. The total blood volume may
be estimated using the Allen formula (see
Controlling Hemodilution Figure 5.1). Not every patient might be suitable
A number of factors will affect the hematocrit on CPB (see for RAP or VAP and the clinical team needs to
Table 5.2). The perfusionist can influence the hematocrit make a careful decision on a case by case basis.
by modifying the extent of hemodilution in several ways: Adding blood to the prime – this is commonly
Choice of circuit – minimization of prime volume done in pediatric cardiac surgery to achieve a 43
by circuit volume reduction is widely practiced. It target hematocrit where, even with the use of

Filip de Somer and Robert Young
Table 5.3. Typical characteristics of common crystalloid priming solutions
Human 5% glucose 0.9% saline Ringer’s lactate Normosol Plasmalyte

Plasma R 148
[Na+] mmol/l 135–145 154 131 140 140
+
[K ] mmol/l 3.5–5.0 5.4 5 5
2+
[Ca ] mmol/l 2.2–2.6 1.8
2+
[Mg ] mmol/l 0.7–1.0 3 1.5
-
[Cl ] mmol/l 98–106 154 112 98 98
Glucose g/l 4–6 50
Acetate mmol/l 27 27
Lactate mmol/l 0.7–1.8 28
Gluconate mmol/l 23 23
pH 7.4 3.5–6.5 5–7 4–8 6.5–8.0
Osmolarity mOsm/l 275–295 278 308 277 294 295
TBV males = {0.000417 x height (cm)3} + {45.0 x weight (kg)} – 30.

females = {0.000414 x height (cm)3} + {32.8 x weight (kg)} – 30.
TBV x predilution Hct

Hct post dilution =
TBV + PV + CV + intravenous fluids - urine output
PV = priming fluid volume, CV = cardioplegia fluid volume, TBV = total blood volume.
Figure 5.1 The Allen Formula.
minimum volume circuits, the fall in hematocrit Crystalloid Solutions

associated with pure crystalloid/colloid primes
Medically used crystalloids are aqueous solutions of
would be excessive. The use of non-blood primes
various electrolytes with or without glucose. The most
in neonatal and infant surgery is generally not
commonly used crystalloids are summarized in
possible. The specific requirements for pediatric
Table 5.3. These solutions are cheap, widely available
bypass are discussed in more detail in Chapter 15.
and have long shelf lives. When an isosmolar
crystalloid solution is administered intravenously, it
Priming Solutions will distribute throughout the extracellular space.
The ideal priming solution should not cause any Only 25% of the administered volume will remain
physiological disturbance when added to the patient’s in the intravascular space while 75% passes into the
circulation. In reality, however, choice of fluids for interstitium. The hemodilution crystalloids cause
circuit prime will affect oncotic pressure, acid-base leads to a further reduction in the concentration of
balance, glucose homeostasis, osmolarity and individ- the oncotically active components in the blood, pri-
ual electrolyte concentrations. For clinicians there are marily albumin, allowing further movement of fluid
a number of considerations to take into account. into the interstitial space. Excessive volumes of inter-
A first one is the choice of whether to use a crystal- stitial fluid cause tissue edema with the potential for
loid, a colloid or combined crystalloid colloid priming reduced perfusion and organ dysfunction in the post-
44 solution. operative period.

Table 5.4. The properties of colloids currently in clinical use
Albumin Gelofusine Haemaccel HES HES balanced

4%
[Na+] mmol/l 140 150 145 154 137
+
[K ] mmol/l 5 5.1 4
2+
[Ca ] mmol/l 12.5
[Cl-] mmol/l 128 100 145 154 110
Lactate mmol/l 30
Acetate mmol/l 34
Molecular weight (Daltons) 69,000 30,000 35,000 130,000 130,000
Half-life 21 days 8 hours 5 hours 12.1 hours 12.1 hours
pH 6.7–7.3 5.8–7.0 7.3 4–5.5 5.7–6.5
In patients with a large blood volume, the use of including cardioplegia and citrate-containing blood
balanced crystalloid electrolyte solutions for priming products. The extent of these changes is difficult to
is often the first choice as the impact of hemodilution predict. A sensible approach with regard to formu-
will be comparatively small. However, in small lation of the circuit prime is to maintain levels of
patients or in patients where it is anticipated that a key electrolytes such as sodium, potassium, calcium
large volume of crystalloid cardioplegia will be used, a and magnesium at physiologically normal
drastic reduction of colloid oncotic pressure by dilu- concentrations.
tion of plasma proteins can be expected and therefore Independent of the choice of colloid or crystalloid,
colloids or a mixture of colloids with crystalloids a pH balanced solution with an appropriate concen-
might be the better choice. tration of electrolytes is recommended. This will pre-
vent significant biochemical changes when going on
Colloid Solutions bypass.
Colloid solutions are essentially made up of large
organic molecules dispersed in water. Colloids remain Sodium
within the intravascular space to a much larger
Solutions with a high chloride concentration, such as
extent than crystalloids, thereby maintaining oncotic
0.9% saline, will create a hyperchloremic acidosis. The
pressure. The amount of time this oncotic effect
resulting fall in pH will shift the hemoglobin dissoci-
lasts differs between solutions and depends on
ation curve to the right and improve oxygen delivery.
endothelial integrity. Their use in CPB prime has
However, this potential benefit is outweighed by the
been advocated to reduce the sudden fall in oncotic
adverse effects on coagulation, myocardial contract-
pressure associated with crystalloid priming solu-
ility and adrenoceptor function.
tions. Colloids are most commonly used as an add-
Rapid decreases in plasma sodium concentration
ition to a crystalloid prime rather than as the sole
are associated with altered mental status, seizures and
fluid. Available colloids include human albumin solu-
coma, and values of <130 mEq/L are predictive for
tion, gelatins and hydroxyethyl starches and are sum-
stroke. For this reason electrolyte solutions contain-
marized in Table 5.4.
ing low sodium such as Lactate-Ringer (130 mEq/L)
should be replaced by one containing a higher sodium
Electrolyte Management concentration such as Plasma-Lyte (140 mEq/L) in
Electrolyte disturbances are common following car- patients with a low preoperative plasma sodium
diac surgery. Causes include changes in tempera- concentration.
ture, acid-base status, catecholamine levels, diuresis Hyponatremia is one of the most common elec- 45
and the administration of intravenous fluids, trolyte disturbances in cardiac patients, particularly if

they have been on long-term diuretic treatment. citrate in transfused blood or hypomagnesemia.
A modified priming solution needs to be used in cases Hypocalcemia adversely affects coagulation and
where an operation cannot be delayed, and the base- can induce arrhythmias and depress myocardial
line sodium is low enough to suggest that standard function. Calcium is contained in Ringer’s lactate
CPB prime might cause severe harm (generally <125 and in urea-linked gelatin-based colloids. Calcium
mmol/l). The sodium level in the CBP prime can be levels are generally monitored intraoperatively as
adjusted to a level that is similar to that of the part of standard blood gas analyses; supplemental
patient’s serum sodium level by using a mixture of calcium is administered via the bypass circuit as
sodium lactate (Hartmann’s solution) and 5% appropriate.
glucose:
1. Determine the patient’s serum sodium level pre- Magnesium
CPB Hypomagnesemia following cardiac surgery is also
2. Volume (ml) of fluid to remove from 1l common. It can cause arrhythmias, hypertension
Hartmann’s bag and to be replaced with
5% and coronary vasoconstriction. A number of studies
Glucose ¼ 1000 preCPB
131
Na
1000 , i.e. the have identified a link between hypomagnesemia and
fluid volume in the bag remains 1l. post-operative atrial fibrillation. There may also
In addition, autologous priming should be con- be a link with short-term cognitive dysfunction.
sidered to decrease the volume of crystalloids Magnesium is contained in Plasmalyte and
and the use of mannitol should be avoided as it Normosol. Point of care magnesium assays exist but
is hyperosmolar and can worsen cerebral are not in widespread use. Magnesium supplemen-
dehydration. tation is often empirical, and the benefit remains
subject to debate.
Potassium
Potassium levels will inevitably rise after the adminis- Osmolarity and pH
tration of cardioplegia solution. To the contrary, The electrolyte concentration in the prime will define
hypokalemia is most commonly observed in the its osmolarity. Hyperosmolarity, >320 mOsm/L, may
post-operative period due to increased renal excretion cause renal failure and brain damage. Osmolarity (in
as part of the surgical stress response and diuretic use. the absence of mannitol) can be estimated using the
None of the fluids in routine use for circuit priming formula in Figure 5.2.
contain supraphysiological levels of potassium. pH balanced solutions should be used to prevent
Exacerbation of cardioplegia-induced hyperkalemia haemodilution acidosis. These solutions contain
during CPB tends to occur because of hyperglycemia, buffers such as acetate and lactate. Both of these are
acidemia or the administration of large volumes of precursors of bicarbonate (HCO3) and are converted
homologous blood, particularly blood with a longer within 10 min through the citric acid cycle to H2O
storage time. Intraoperative hyperkalemia can be cor- and CO2. In patients with liver disease, acetate is
rected by using an insulin-glucose infusion, increased preferred as its metabolism is less dependant on liver
diuresis or ultrafiltration. function than is that of lactate.
Calcium Glucose
Mild intraoperative hypocalcemia is common. This Maintaining glucose concentration below 180 mg/dL
may occur due to hemodilution, calcium binding to (10 mmol/L) is recommended during CPB and
blood glucose Figure 5.2 Formula for the estimation of Osmolarity.

Osm = (Na x 2) +
( 18 ) + 15
Where Na (mEq/L), blood glucose (mg/dL), Osm = predicted osmolarity
46

postoperatively by the recent STS and EACTS/ diuretic properties are useful for the prevention of
EACTA/EBCP guidelines. Hyperglycemia during excessive fluid accumulation and post-operative inter-
CPB is associated with an increased risk of wound stitial edema. It was thought to have a protective effect
infection, cardiac dysfunction, neurological injury on renal function, possibly by increasing renal blood
and increased overall mortality. The use of glucose flow. More recent studies, however, have indicated
containing priming solutions in both diabetic and that while increasing urine output, mannitol does
non-diabetic patients is not recommended as this not protect renal function and may even have a detri-
can exacerbate the hyperglycemia – caused by surgical mental effect on it. It cannot currently be recom-
stress response, hypothermia, hyperoxia and heparin mended as a prophylactic agent to reduce the
administration – regularly seen during CPB. incidence of acute kidney injury following cardiac
Hyperglycemia increases plasma osmolarity, causing surgery.
movement of water from the intracellular to the
extracellular space and with a subsequent reduction Heparin
in electrolyte concentrations by dilution. A metabolic
Heparin is added to circuit priming solutions either
acidosis may occur due to the dilution of plasma
dosed according to patient weight or as a fixed dose.
bicarbonate. Insulin may be required to obtain a
The rationale behind adding this, in addition to the
satisfactory glucose concentration.
systemic heparin given before aortic cannulation, is to
provide additional safety at initiation of bypass and in
Prime Additives the event of emergency CPB. Doses between 2.500
The fluid prime can be used as a carrier of additional and 5.000 IU of heparin are common as an additive
substances thought to be of clinical benefit. to the prime of an adult CPB circuit.
Commonly used additives include sodium bicarbon-
ate, mannitol and heparin. Corticosteroids are also
used by some centers, however, their use as part of Corticosteroids
CPB prime is subject to much debate. A small number of institutions routinely add cortico-
steroids to the prime. Several studies have examined
the various theoretical benefits of steroids used this
Sodium Bicarbonate (NaHCO3) way. None found any clinical benefit in reducing the
NaHCO3 can be added as a buffer to unbalanced inflammatory response, the rate of post-operative
crystalloid and colloid primes. This will prevent a fall atrial fibrillation or of renal failure. To the contrary,
in bicarbonate levels caused by dilution and amelior- adding steroids to the pump prime has been
ate the metabolic acidosis associated with the use of shown to regularly lead to severe post-operative
unbalanced solutions. In order to prevent this non- hyperglycemia, which can be difficult to manage.
perfusion related acidosis from building up, it is Steroids as additives to CPB prime are currently not
common to add 2.5 mEq NaHCO3 for every 100 mL recommended.
of non-buffered solutions in the circuit. Sodium
bicarbonate should not be given too liberally because
the addition of large volumes can cause hypernatre-
mia. The use of sodium bicarbonate to treat acidosis The constitution of cardiopulmonary bypass prime
caused by transient tissue hypoxia, as may occur with has a significant impact on the perioperative care of
deep hypothermic circulatory arrest, is controversial. patients undergoing cardiac surgery. Minimizing the
volume of prime has become a key goal. Although the
use of crystalloid and colloid fluids is now standard
Mannitol practice, the specific constitution of priming solutions
Mannitol is a hypertonic crystalloid solution that acts varies widely between centers. The challenge remains
as an intravascular volume expander and osmotic to formulate a circuit prime that leads to an optimum
diuretic. It is metabolically inert. Doses of 0.25–0.5 level of hemodilution while minimizing any detri-
g/kg body weight added to the prime are common, mental physical and biochemical changes when mixed
but the evidence of benefit is weak. In theory, its with patients’ blood.
47

Suggested Further Reading 4. Kunst G, Milojevic M, Boer C

et al. 2019 EACTS/EACTA/EBCP
controlled observational study.
Crit Care 2004; 8: 459–466.
1. Miles L, Coulson T, Galhardo C guidelines on cardiopulmonary
et al. Pump priming practices 8. Waskowski J, Pfortmueller A,
bypass in adult cardiac surgery. Br Erdoes G et al. Mannitol for the
and anticoagulation in J Anaesth 2019; 123 (6): 713–757.
cardiac surgery: Results prevention of peri-operative acute
from the Global 5. Najmaii S, Redford D, Larson D. kidney injury: A systematic
Cardiopulmonary Bypass Survey. Hyperglycemia as an effect of review. Eur J Vasc Endovasc Surg
Anesth Analg 2017; 125(6): cardiopulmonary bypass: Intra- 2019; 58(1): 130–140.
1871–1877. operative glucose management. 9. Whitlock R, Devereaux J, Teoh K
J Extra Corpor Technol 2006: 38(2); et al. Methylprednisolone in
2. Ranucci M, Conti D, 168–173.
Castelvecchio S et al. Haematocrit patients undergoing
on cardiopulmonary bypass and 6. Munoz E, Briggs H, Tolpin D cardiopulmonary bypass (SIRS):
outcome after cardiopulmonary et al. Low serum sodium during A randomised, double-blind,
surgery in nontransfused cardiopulmonary bypass predicts placebo-controlled trial. Lancet
patients. Ann Thorac Surg 2010; increased risk of postoperative 2015; 386: 1243–1253.
89: 11–18. stroke after coronary artery 10. Canaday S, Rompala J, Rowles J
bypass graft surgery. J Thorac et al. Chronic severe
3. Ranucci M, Johnson I, Willcox T Cardiovasc Surg 2014; 147:
et al. Goal-directed perfusion to hyponatremia and
1351–1355. cardiopulmonary bypass:
reduce acute kidney injury:
A randomized trial. J Thorac 7. Polderman K, Girbes R. Severe Avoiding osmotic demyelination
Cardiovasc Surg; 2018: 156: electrolyte disorders following syndrome. J Extra Corpor Technol.
1918–1927.e2. cardiac surgery: A prospective 2015;47(4): 228–230.
48

Chapter
Anticoagulation for Cardiopulmonary Bypass
6 Martin Besser and Linda Shore-Lesserson
Anticoagulation is mandatory for any form of extra- introduced impurities, and side effects included fever,
corporeal circulation to prevent activation of the shock and death in laboratory animals. By
coagulation system through contact between blood 1936 Charles and Scott had refined technology and
and artificial surfaces and through blood stasis. The were able to crystallize ‘clean’ heparin as a barium
absence of sufficient anticoagulation is likely to result salt. The first episode of treating venous thromboem-
in clot formation within minutes of aortic cannula- bolism (VTE) is attributed to Lam and McLure in
tion and commencement of CPB, with detrimental 1939 in Detroit. By this time the biosource had
consequences for the patient. Even microvascular changed from canine liver to bovine lung and then
clots can lead to death, in their lesser forms they can porcine mucosa.
lead to organ dysfunction, manifesting mostly either The original US pharmacopeia (USP) from the
as renal or neurological dysfunction. 1950s was based on the action of heparin sodium on
The principles of anticoagulation for cardiopul- sheep plasma. Unexpectedly, between 2007 and 2008,
monary bypass have remained fundamentally thousands of adverse reactions and more than
unchanged in the past 45 years. The majority of 200 deaths occurred when Chinese suppliers contam-
practitioners still give doses of up to 500 IU/kg of inated their product with cartilage-derived oversul-
unfractionated heparin (UFH) prior to CPB. The fated chondroitin sulphate to lower production
effect of heparin is monitored using the Activated costs. As a result, in 2009 the USP standardization
Clotting Time (ACT). The development of improved was changed to match the European units. The stand-
biomaterials is likely to allow reduced intensity of ard now is based on a Factor IIa assay instead of the
anticoagulation. This technology and its application sheep plasma, which has reduced the potency of the
are currently subject to intense research efforts. US stock by about 10% after 2009.
Smaller heparin doses might help to reduce undesir-
able effects such as post-operative bleeding and hep-
arin rebound. Although there are numerous Pharmacology
approaches and protocols in place, there still is no Heparin is a complex mixture of polysaccharides of
universal agreement on how to best treat patients who different chain lengths and a molecular weight
cannot receive heparin but require surgery on CPB. between 3,000 and 30,000 kDa. It has a number of
This chapter briefly outlines the history of heparin unique characteristics that make it particularly suit-
before discussing its pharmacology, intraoperative able for use in CPB.
hemostasis monitoring, the management of heparin It naturally occurs in mast cells and basophils and
resistance and Heparin Induced Thrombocytopenia fulfills a number of physiological functions, such as
(HIT) and the outlook for anticoagulation on CPB. chemotaxis, leukocyte cell diapedesis, upregulation of
overall inflammation, cellular repair, vessel growth
and anti-cancer activity. In addition, heparin activates
Heparin osteoclasts rather than osteoblasts and attenuates pro-
In 1916 at Johns Hopkins University, Jay McLean liferation of vascular smooth muscle cells.
isolated a phosphatide anticoagulant from canine Heparin needs to bind to the enzyme inhibitor
liver which could anticoagulate blood in vitro and in antithrombin III (AT III) which leads to a conforma-
vivo. In 1926 a similar compound was produced by an tional change that inactivates thrombin (Factor II) 49
aquatic extraction. The early production process and other proteases involved in clotting, namely

Martin Besser and Linda Shore-Lesserson
Intrinsic system Extrinsic system

Minor sites
Surface contact Tissue damage
Tissue factor
XII XIIa
XI XIa
IX IXa VIIa VII
VIII VIIIa
x Xa Major site
v Va
Major site
II IIa (Thrombin)
Fibrinogen Fibrin
Figure 6.1 Major and minor sites of heparin action.
Factors IXa, Xa, XIa and XIIa. Thrombin inhibition activity preserved. These kinetics lead to the context-
also blocks activation of Factors V, VIII, XI and of sensitive half-life based on the dose of heparin
platelets. Heparin increases the activity of heparin administered. At a dose of 100 U/kg its half-life is
cofactor II (HC II), which additionally inhibits approximately 60 minutes, increasing to 126 minutes
thrombin. Figure 6.1 gives an overview of the major at a dose of 400 U/kg.
and minor sites of heparin action.
The mode of action of heparin is determined by its
chain length: only a third of molecules have the key Heparin Monitoring
pentasaccharide that interacts with antithrombin, In 1953 Langdell described the Partial Thromboplastin
while short heparin chains of <18 saccharides can Time (PTT) later modified to the activated PTT
only inactivate Factor Xa. In high doses (>1.0 U/ml) (aPTT), which has become the most commonly used
heparin will bind to HC II to interact with clotting laboratory test to monitor heparin outside the
factors independent of antithrombin; at doses >2.0 U/ml operating room. There is a confusing array of different
heparin prevents the generation of factor Xa inde- platforms and technologies to test the adequacy of
pendent of antithrombin via a charge-based inter- anticoagulation for CPB. The two general classes of
action. At these concentrations the activity of heparin monitoring devices are functional assays and
fibrinogen-bound thrombin is also inhibited. quantitative measures of the level of circulating hep-
Heparin activity can be measured by using the plasma arin. If quantitative measures are used to maintain
anti-Xa assay. The target doses for heparin for VTE heparin concentration, a functional test must also be
treatment is 0.3–0.7 anti-Xa IU/ml, whereas during employed to assure adequacy of anticoagulation.
CPB levels of >3 IU/ml are intended. The first clotting time test, described in 1913, was
Heparin is eliminated by two mechanisms, both of the whole blood clotting time (WBCT), or the Lee–
which appear to follow non-linear kinetics: a rapid White WBCT, in which whole blood was placed in a
and saturable mechanism, likely due to internaliza- glass tube and tilted until clotting visibly occurred. In
tion by endothelial cells and macrophages and a the un-activated state this test took more than 30
second, slower mechanism via renal clearance. After minutes, and it was replaced by the activated clotting
administration of smaller doses between 5,000 and time (ACT). The ACT provides the basis on which
10,000 units, heparin is found in urine as an inacti- most functional anticoagulation monitors are mod-
vated and desulphated molecule, while after larger eled. Initially an ACT prolongation of 300 seconds
50 was considered the safe minimum level of
doses it is eliminated intact with its anticoagulant

Chapter 6: Anticoagulation for Cardiopulmonary Bypass
heparinization; later Young et al. described fibrin binding proteins such as vitronectin and Platelet
strand formation during in vivo experiments in Factor 4 (PF4) make the response to an intravenous
monkeys at ACT < 400 seconds. To this day there is bolus of heparin extremely unpredictable.
great institutional variation in heparin dosing and The large interpatient variation in heparin respon-
even more so in ACT values considered safe to go siveness and the potential for heparin resistance make
on CPB. The majority of cardiac centers around the using a functional monitor of heparin anticoagulation
world prefer an ACT between 400 and 550 seconds. (with or without a measure of heparin concentration)
Modern ACT devices are nearly all cartridge critically important in all cardiac surgical patients. In
based, require less than 1 ml of blood to run the assay vitro testing platforms that promote a heparin dose-
and tests can be done in the operating room by non- response calculation are often inconsistent in their
laboratory trained staff. They work on the principle of ability to accurately predict the heparin dose needed
adding blood to an activator, however they differ in for safe CPB initiation. This is because in vitro hep-
the method for clot detection. Clot formation can be arin additives do not always mimic the in vivo
detected using mechanical, optical or amperometric response to a dose of heparin. These dose-response
methods. The time taken to detect clot signals the end curves do, however, provide insight into patients’
of the test and represents the “clotting time.” heparin sensitivity and can identify those who are
Numerous ACT assays are in clinical use and many heparin resistant.
have been studied in clinical trials showing them to be
safe for anticoagulation monitoring during CPB. Maintenance of Heparin Effect
Owing to their different analytical methods, these
Clinicians are able to reassure themselves about main-
devices cannot be used interchangeably and need to
taining a safe level of anticoagulation throughout CPB
be validated before use, particularly when switching
by performing regular ACTs. Although it is a func-
manufacturer. The heterogeneity of the response to
tional test and not a quantitative test, the ACT has
heparin by different ACT devices is so great that
several flaws. Its use has been criticized because of the
minimum therapeutic or safe values remain difficult
extreme variability and the absence of a correlation
to recommend.
with changes in plasma heparin levels. The variation
in ACT values may represent true variability in a
Initiation of CPB patient’s coagulation status or it may be artifactual,
The recommended weight-based dose of unfractio- reflecting altered sensitivity of the ACT to heparin or
nated heparin to achieve safe anticoagulation for other factors influencing anticoagulation during CPB.
aortic cannulation and commencing CPB is 300–500 Many factors commonly encountered during cardiac
U/kg in adult patients. It makes sense to choose an surgery can alter ACT readings. Hemodilution and
initial heparin dose based upon a known institutional relative hypofibrinogenemia caused by the pump
heparin formulation, as heparin preparations vary in prime may increase the ACT; hypothermia increases
potency, different ACT monitoring systems have a the ACT in a “dose-related” fashion; extremes of
certain bias, and patient-specific conditions vary. thrombocytopenia will prolong the ACT; patients
An alternative way to ascertain the dose of heparin treated with platelet inhibitors such as prostacyclin,
needed to safely initiate CPB is to calculate a patient- aspirin or platelet-membrane-receptor antagonists
specific dose-response curve. Such in vitro assays are have a prolonged heparinized ACT. Platelet lysis,
available from different manufacturers. The concept however, significantly shortens the ACT because of
is that a baseline ACT and an ACT with a known the release of platelet membrane components and PF4
amount of heparin are measured. The dose-response which neutralizes heparin. Anesthesia and surgery
relationship generated by connecting these two points shorten the ACT and create a hypercoagulable state,
on a line is then extrapolated to the desired ACT. An possibly by creating a thromboplastic response or
algorithm that incorporates the patient’s baseline through activation of platelets.
ACT, estimated blood volume, and heparin-response Using the plasma anti-Xa activity level as the gold
curve calculates the dose of heparin needed to achieve standard, it has been shown that the ACT does not
adequate anticoagulation. Unfortunately, different correlate well with anti-Xa activity or with whole
concentrations of various endogenous heparin- blood heparin concentration (see Figure 6.2). 51

Figure 6.2 Activated clotting time as measured by i-STAT and Hemochron Signature and heparin activity as measured by anti-Xa at all time
points. ACT, activated clotting time; CPB, cardiopulmonary bypass. (Reproduced from Falter F, MacDonald S, Matthews C et al. Evaluation of Point-of-Care
ACT Coagulometers and Anti-Xa Activity During Cardiopulmonary Bypass. J Cardiothorac Vasc Anesth. November, 2020;34(11):2921–2927.)
Despite this, the ACT remains the most common test increase when CPB is initiated even as the heparin
used to affirm safe initiation and maintenance of concentration decreases. Although measuring
anticoagulation on CPB. The ACT is a functional test heparin concentration on CPB has been shown to
of anticoagulation which is supported as a Class 1 rec- correlate more closely with anti-Xa activity than the
ommendation by the STS/SCA/AmSECT Guidelines ACT, the exclusive use of this test without an ACT is
for Best Practices in Anticoagulation for Cardiac not acceptable for cardiac surgery anticoagulation
Surgery. monitoring. Clinical studies have attempted to
Point of care heparin concentration measurement validate heparin concentration monitoring as a
uses a protamine titration technique. Multiple cham- blood sparing technique, but the variable reproduci-
bers in a cartridge contain tissue thromboplastin and bility of benefits has resulted in a IIb recommenda-
a series of known incremental protamine concentration only.
tions. When heparinized blood is added, the first Clot formation in the bypass circuit and subse-
channel to clot is the channel whose protamine con- quent failure to provide sufficient oxygenation are
centration most accurately neutralizes the heparin inevitable if the safe level of anticoagulation is not
without a heparin or protamine excess. Using maintained throughout CPB. Best practices for
known pharmacokinetics, the device then calculates maintenance of anticoagulation during CPB include
the concentration of heparin in the blood sample. regular interval monitoring – usually every 20–30
Attempting to maintain a stable derived heparin con- minutes – of a functional test of anticoagulation, such
centration will lead to the administration of larger as ACT. Bolus dosing to achieve a pre-specified hep-
doses of heparin than required. The device algorithm arin concentration or routine fixed interval dosing of
does not take into account factors such as hemodilu- heparin during CPB may be used to maintain antic-
tion and hypothermia on CPB, which increase anticoagulation, and both approaches are supported as a
52 oagulation and do not require a stable heparin Class IIb recommendation in the STS/SCA/AmSECT
concentration. In comparison, ACT values typically Best Practices Guidelines.

Table 6.1. Common reasons for heparin resistance

Heparin Resistance
Heparin resistance is defined as an inadequate anti- Antithrombin mediated
coagulant response to heparin despite an adequate Reduced synthesis
plasma concentration. The clinical picture is one of Accelerated clearance
failure to achieve anticoagulation adequate for CPB ○ Nephropathy
with heparin doses of up to 600 IU per kilogram of Accelerated consumption
body weight. In many clinical situations, especially ○ Pre-op heparin use
when heparin desensitization or the presence of a ○ Upregulated hemostatic system
heparin inhibitor is suspected, heparin “resistance”
▪ DIC
can be treated by administering increased doses. If
▪ Endocarditis
the ACT does increase in response to a higher dose,
then a more accurate description of this condition ▪ DVT/PE
would be heparin tachyphylaxis or “altered heparin ○ Mechanical
responsiveness,” which is regularly seen in cardiac ▪ CPB
surgical patients who have been on heparin prior to ▪ VAD
surgery. It is thought that their altered heparin ▪ IABP
responsiveness is due to a reduction of AT3 levels, ▪ ECMO
although numerous other mechanisms have been pro-
Non-Antithrombin mediated
posed (see Table 6.1). The fact that the temporal course
of ACT decrease and AT3 concentration do not mirror Increased heparin binding
each other suggests that AT3 depletion may not be ○ Proteins
solely responsible. Other possible causes of a heparin ▪ Chemokines
resistant state include enhanced factor VIII activity and ▪ Extracellular matrix proteins
platelet effects. AT3 concentrate, available as a heat- ▪ Growth factors
treated human product or in recombinant form, is ▪ Enzymes
indicated as a Class I recommendation for treating ○ Platelets
patients with documented AT3 deficiency. Congenital ▪ Nonspecific binding
AT3 deficiency must be recognized by the inability to
▪ Thrombophilia
increase the ACT even by 50–100% using escalating
▪ Platelet activation
doses of heparin. In these patients, AT3 repletion
should be carefully calculated and administered in close ▪ Nitroglycerin
cooperation with a hematologist. In a patient whose
ACT will not elevate beyond 350–400 seconds, who
aggregate is inactive, has no anticoagulant activity
has been given additional large heparin doses to treat
and is rapidly removed from the circulation.
heparin resistance, to a total dose approaching 600 IU/
Protamine, in the presence of heparin, has intrinsic
kg, an empiric diagnosis of acquired AT3 deficiency is
anticoagulant properties if given at a higher than
usually assumed. In this situation, the STS Blood
necessary dose. Ideally protamine is administered in a
Conservation Guideline recommendation is to admin-
way that leaves neither free drug nor free heparin in
ister AT3. Heparin Induced Thrombocytopenia (HIT,
circulation because non-neutralized heparin results in
see below) should be considered in the differential
clinical bleeding and an excess of protamine may pro-
diagnosis of intraoperative heparin resistance in
duce an undesired coagulopathy. Heparin undergoes
patients receiving preoperative heparin therapy.
metabolism and elimination during the time spent on
CPB and it is difficult to estimate the required dose of
Heparin Neutralization protamine needed to neutralize the remaining heparin
Heparin needs to be neutralized in order to avoid based upon the dose administered and the ACT alone.
unnecessary bleeding after separation from CPB. To Doses of protamine in excess of a 1:1 ratio to the
this day protamine is the only drug licensed for this amount of heparin administered before and during
indication. Protamine, a strong cation, forms a salt CPB are not recommended as they may increase the 53
aggregate with heparin, a strong anion. This salt incidence of protamine-related adverse effects.

Ideally the concentration of heparin in blood is thrombocytopenia. It occurs mostly in response to

measured so that a more accurate dose of protamine UFH and less commonly to low molecular weight
can be given. In recent years there has been renewed heparin (LMWH). The incidence is between 0.2 and
interest in this subject and several approaches to 5% in patients exposed to heparin, with some reports
protamine dosing have been published. suggesting an incidence as high as 15–20% in patients
Pharmacokinetic models have been yielding promis- undergoing cardiac surgery. The increased platelet
ing results in reducing the dose of protamine admin- reactivity causes thrombosis marked by platelet
istered without compromising hemostasis, but they (white) clots. It is often seen 5–14 days after heparin
are so far lacking the confirmatory evidence of ran- exposure and, if unrecognized, it is potentially life-
domized controlled trials. What all these approaches threatening. Treatment requires immediate cessation
have in common is the reduction of the protamine of heparin and the institution of an alternate
dose by 30–50% compared to a 1:1 fixed dose and an anticoagulant.
associated reduction in post-operative blood loss The antibodies associated with HIT often become
from pleural and mediastinal drains. undetectable several weeks after discontinuing hep-
Heparin rebound describes the re-establishment arin and the syndrome does not always reoccur on
of a heparinized state after heparin has been neutral- reexposure. This variability in clinical manifestation
ized. The mechanism behind this phenomenon is not makes the management of patients with a history of
fully understood, but the most common reasons given HIT very complex. The safest option is to avoid
are: further heparin exposure where possible. It is import-
i. a rapid distribution and clearance of protamine, ant to be aware that prothrombin complex concen-
leaving unbound heparin in circulation; trates and other clotting factor concentrates may
ii. residua of low molecular weight heparin contain heparin and may be contraindicated in
fragments; patients known to have HIT.
iii. release of heparin from tissue (endothelium,
connective tissues) after protamine has Alternative Anticoagulants and Other
been cleared.
Sensitive tests are able to detect low levels of residual
Techniques in HIT
heparin for up to six hours after reversal. Clinicians The choices when treating these patients are few but
should always consider heparin rebound if there is there are several options if there is no alternative to
sudden excessive bleeding after a period of stable using heparin:
hemostasis. i. In non-emergency situations surgery has to be
Successful heparin neutralization is usually con- postponed until at least 90 days after the last
firmed by the ACT returning to within 10% of the heparin exposure. This allows the antibody to
baseline. It has to be borne in mind that the ACT is disappear and one short period of heparinization
relatively insensitive to low levels of heparin and is for CPB is generally tolerated
inferior to aPTT, thrombin time, heparin concentra- without complications.
tion monitoring or viscoelastic whole blood assays. In ii. There have been favorable reports of
case of doubt, one or a combination of these more supplementing heparin administration with
sensitive tests should be employed to diagnose the pharmacologic platelet inhibition using
cause for intra- or post-operative bleeding (see prostacyclin, iloprost, aspirin, tirofiban
Chapter 16). or dipyridamole.
iii. Plasmapheresis may be used to reduce antibody
levels and immunoglobulin can be given
Heparin Induced Thrombocytopenia additionally to block platelet activation in the
Heparin induced thrombocytopenia (HIT) is an presence of heparin.
immunologic disorder marked by antibodies that The data to support these interventions indicate that
bind to the heparin–PF4 complex on platelets. they can be used safely, however the lack of random-
Binding of the antibody causes platelet activation, ized controlled trials has rendered them Class IIb
54 hyperaggregability, and moderate degrees of recommendations.

The use of heparin can be avoided altogether Table 6.2. Recommended adaptations for CPB with Bivalirudin
through anticoagulation with direct thrombin inhibi- Heparin Bivalirudin
tors such as argatroban or bivalirudin. These throm- Protocol Protocol
bin inhibitors have become the standard of care in the
management of patients with HIT. Bivalirudin has HLM Setup
been studied in prospective multicenter trials in HIT Prime 5.000–10.000 50 mg Bivalirudin
patients undergoing cardiac surgery on CPB. Its use is IU Heparin
supported in guidelines published by the Society of Pressure Post- Pre-and post-
Thoracic Surgeons/Society of Cardiovascular monitoring membrane membrane
Anesthesiologists/American Society of Extracorporeal on CPB line pressure pressure
Technology, where it receives a Class IIa recommen-
Anticoagulation
dation, and by the American College of Chest
Physicians (ACCP). Bivalirudin has a short half-life Monitoring ACT ACT, aPTTr
of 24 minutes and is auto-digested by thrombin, ACT on CPB >400 sec, >2.5x baseline
especially in static blood. For these reasons, bivaliru- according to
din bolus is accompanied by an infusion during CPB institutional
in order to maintain safe anticoagulation. Because of practice
rapid elimination of the anticoagulant, the blood in aPTTr on CPB >5x baseline
the circuit must always be flowing, and conduits for
Conduct on CPB
parallel flow should be established in the event that
the pump flow must be stopped for a period of time. Avoiding n/a Recirculation
Stasis of blood leads to thrombus formation because stagnation through all
bivalirudin is eliminated. This must be taken into closed shunts
every 10–20
consideration when constructing a CPB circuit for
mins
use with bivalirudin. As there is no direct antidote
to bivalirudin, cessation of its activity occurs by stop- Collection of n/a Every 15–20 mins,
ping the drug infusion. The infusion must be running blood from all blood having
until approximately 15–20 minutes before weaning surgical sat stagnant for
field longer needs to
from CPB, which facilitates continued anticoagula-
be discarded or
tion yet allowing hemostasis after CPB to be achieved
processed with
in a reasonable time frame. See Table 6.2 for the cell salvage
adaptations that need to be made in case a patient is
anticoagulated with bivalirudin. Displacement Standard blood Storage in CPCA-1
of excess storage bag bag
blood
The Future of Anticoagulation for CPB
New anticoagulants that target contact factor activation
such as the monoclonal antibody 3F7 to XIIa or a Table 6.3. Strategies for circuit coating to reduce heparinization
variety of aptamers show promise to either completely
Passivation Phosphrylchlorine
replace or reduce the need for co-treatment with hep-
Albumin
arin. The aptamer 11F7t alone or in combination with
2-methoxyrthylacrylate (PMEA)
R9d-14t, or in its combined form as RNABA4, may be of
particular benefit as heparin replacements. Others that Biomimetics Heparin bonding
target Factor XII (R4c-XII-1t), Kallikrein (Kall1-T4) or Argatroban bonding
N-diazeniumdiolates
factor XI (FELIAP) also allow reduced anticoagulation
RSNO conversions (Cu++)
in combination with conventional heparin or Xa inhibi-
tors. Future CPB tubing is likely to use biomimetics Endothelialization Pre-endothelialization with
such as covalently bonded heparin or direct thrombin patient stem cells
inhibitors like argatroban. Passivation of circuits is cur- 55
rently being attempted using phosphorylcholine,

albumin or poly-2-methoxyethylacrylate (PMEA), An interesting future concept is the pre-endothelia-

which allow the reduction of systemic heparinization lisation of the circuit. This could either be done as pre-
during CPB. Using nitric oxide (NO) releasing mater- endothelialisation with patient stem cells prior to CPB
ials like N-Diazeniumdiolates in combination with a or by in situ capture of patient stem cells. Currently
polymer-linked thrombin inhibitor like argatroban has these concepts are problematic and impractical as they
shown promise. require time to coat a patient circuit (see Table 6.3).
Suggested Further Reading time systems vary in precision and

bias and are not interchangeable
Cardiopulmonary Bypass. Anesth
Analg. 2018.
1. Wardrop D, Keeling D. The story when following heparin
of the discovery of heparin and 7. Miles LF, Coulson TG, Galhardo
management protocols during C et al. Pump priming practices
warfarin. Br J Haematol. 2008;141 cardiopulmonary bypass. J Clin
(6):757–763. and anticoagulation in cardiac
Monit Comput. 2002;17 curgery: Results from the Global
2. Garcia DA, Baglin TP, Weitz JI et al. (5):287–292. Cardiopulmonary Bypass Survey.
Parenteral anticoagulants: 5. Pappalardo F, Franco A, Anesth Analg. December, 2017;
Antithrombotic therapy and Crescenzi G et al. Anticoagulation 125(6):1871–1877.
prevention of thrombosis, 9th ed: management in patients
American College of Chest 8. Lemmer JH Jr., Despotis GJ.
undergoing open heart surgery by Antithrombin III concentrate to
Physicians Evidence-Based Clinical activated clotting time and whole
Practice Guidelines. Chest. 2012;141 treat heparin resistance in patients
blood heparin concentration. undergoing cardiac surgery.
(2 Suppl):e24S–e43S. Perfusion. 2006;21(5):285–290. J Thorac Cardiovasc Surg.
3. Bull BS, Korpman RA, Huse WM 6. Shore-Lesserson L, Baker RA, 2002;123(2):213–217.
et al. Heparin therapy during Ferraris VA et al. The Society of
extracorporeal circulation. 9. Chabata CV, Frederiksen JW,
Thoracic Surgeons, The Society of Sullenger BA et al. Emerging
I. Problems inherent in existing Cardiovascular Anesthesiologists,
heparin protocols. J Thorac applications of aptamers for
and The American Society of anticoagulation and hemostasis.
Cardiovasc Surg. 1975;69 ExtraCorporeal Technology:
(5):674–684. Curr Opin Hematol. 2018;25
Clinical Practice Guidelines – (5):382–388.
4. Welsby IJ, McDonnell E, El- Anticoagulation during
Moalem H et al. Activated clotting
56

Chapter
Conduct of Cardiopulmonary Bypass
7 Christiana Burt, Timothy A Dickinson, Narain Moorjani and Caitlin Blau
The safe conduct of cardiopulmonary bypass (CPB) should be avoided. Cannula selection can be guided
requires excellent teamwork, clear communication using pressure to flow charts, which are provided by
and collaboration between surgical, anesthetic, perfu- the manufacturers. It should be noted that these chart
sion and nursing teams. A comprehensive under- values are usually derived with water as the test fluid.
standing of both the mechanics and physiology of Many different types of cannulae are available and are
CPB is essential to achieve optimum benefit and discussed further in Chapter 2.
reduce the risks. “Straight” arterial cannulae are the most com-
The goals of CPB are to provide a still and blood- monly used type, with some having a flange to allow
less field for the surgeon to operate while not dam- secure fixation to the aorta with minimal tip within
aging the heart muscle. This chapter reviews the the vessel. The straight design allows non-turbulent
conduct of CPB starting with cannulation (arterial blood flow through the cannula, but results in a single
and venous), general management of both the mech- jet of blood, which can cause damage to the aortic
anical and physiological aspects of CPB and finishes wall. The straight nature of the cannula means that
with a section regarding important aspects of CPB the flow direction is reliant on the surgical placement
relating to minimally invasive cardiac surgery (see Figure 7.1).
(MICS). It is important that each institution has Right-angled cannulae have been designed to
detailed protocols and procedures for CPB, and many allow the jet to be directed around the aortic arch,
of the points discussed in this chapter will be per- assuming correct placement. Right-angled “diffusion”
formed within the construct of these protocols. cannulae, with side holes and a sealed end, may
attenuate the damaging jet effect by changing the flow
characteristics inside the aorta. However, concern has
Arterial Cannulation been expressed regarding an increased risk of hem-
The arterial cannula is usually the narrowest part of olysis due to the more turbulent flow through the
the CPB circuit. The resultant high resistance and cannula. These cannulae are not suitable for place-
pressure gradients produce high velocity jets and tur- ment at any site other than the ascending aorta. In
bulence. The effect of the jets on the interior wall of certain situations cannulation of the ascending aorta
the aorta can lead to arterial dissection, embolization or aortic arch can be performed with a guidewire
and flow disturbances in the head and neck vessels. using a Seldinger technique, either to minimize
The hemodynamic properties of an arterial can- trauma to the aorta, or in the presence of acute aortic
nula can be assessed by their “performance index,” dissection, to ensure placement of the cannula into
which is defined as the ratio of pressure gradient to the true lumen in conjunction with transesophageal
cannula outer diameter at any given flow rate. Ideally echocardiographic guidance.
for every case the cannulae are chosen to minimize In addition to direct placement of the arterial
this value. To optimize hemodynamic performance cannula in the aorta, arterial return can also be
the narrowest portion of the catheter that enters the achieved by peripheral arterial cannulation, such as
aorta should be as short as safely possible and the via the femoral, axillary or innominate artery, cannu-
diameter should then gradually increase in size to lation of the side arm of a prosthetic graft or in rare
minimize the gradient. Pressure gradients greater circumstances via the left ventricular apex, and they
than 100 mmHg can cause excessive hemolysis and are discussed in the following section. 57

Christiana Burt, Timothy A Dickinson, Narain Moorjani and Caitlin Blau
Figure 7.1 Aortic cannula options. Dispersion cannulae on top row (A–G). Non-dispersion cannulae on the bottom row (H–S). (Reproduced
from: McDonald et al. “Hydrodynamic evaluation of aortic cardiopulmonary bypass cannulae using particle image velocimetry.” Perfusion 2016; 31(1): 78–86.)
Connecting the Patient cross-clamping unsafe because of the risk of stroke

due to dislodgement and embolization of atheroscler-
The usual cannulation site is the ascending aorta,
otic material, alternative cannulation sites should be
which offers the following advantages:
considered. Retrograde perfusion via femoral arterial
ease cannulation is not without risk of embolization of
safety atheroma either and subclavian or innominate arter-
single incision ial cannulation may be preferable. In the event of a
ability to deliver antegrade flow totally calcified “porcelain aorta,” alternative strat-
size not usually limited by mismatch between egies that minimize aortic handling, such as off pump
vessel and cannula outer diameter (typical sizes coronary artery bypass grafting (OPCAB), the use of
range from 18 Fr to 24 Fr) deep hypothermic circulatory arrest (DHCA) or alter-
no risk of limb ischemia. native catheter based techniques may be appropriate.
Although the site for cannulation in the ascending If the ascending aorta has ruptured in a patient with
aorta is traditionally determined by intraoperative acute aortic syndrome, the arterial cannula can be
digital palpation for calcific atherosclerotic plaques, placed directly in the true lumen following transec-
newer techniques such as epiaortic ultrasound scan- tion of the ascending aorta.
ning have been shown to be more sensitive at deter- After ensuring that the patient is sufficiently antic-
mining plaque-free areas for cannulation (see oagulated (see Chapter 6) prior to insertion of the
Figure 7.2). If the extent of the atherosclerosis is aortic cannula, the chosen site is prepared with place-
58 ment of opposing purse-string sutures and clearance
significant enough to make aortic cannulation and

Chapter 7: Conduct of Cardiopulmonary Bypass
Figure 7.2 Epiaortic ultrasonographic short-axis image of mid ascending (Asc) aorta (Ao) with significant atheroma (arrow) obtained with
linear-array transducer. SO, Saline standoff to enhance acoustic transmission. (Reproduced from Glas KE, Swaminathan M, Reeves ST et al.; Council for
Intraoperative Echocardiography of the American Society of Echocardiography; Society of Cardiovascular Anesthesiologists; Society of Thoracic Surgeons.
Guidelines for the performance of a comprehensive intraoperative epiaortic ultrasonographic examination: Recommendations of the American Society of
Echocardiography and the Society of Cardiovascular Anesthesiologists; endorsed by the Society of Thoracic Surgeons. Anesth Analg. 2008 May;106(5):1376–1384.)
of the adventitial tissue within the boundaries of these the circuit by pumping fluid into the field and ii) from
sutures. With the mean arterial pressure between the cannula by bleeding back prior to reconnection. If
60 and 70 mmHg to avoid excessive bleeding or gross air embolism is noted in the aortic line during
trauma, a full-thickness incision is made in the aortic established CPB, it may be possible for the perfusio-
wall through which the aortic cannula is passed. Only nist to remove the air via recirculation lines within the
1–2 cm of the cannula tip is advanced and directed circuit with only a brief interruption to pump flow. If
toward the arch to avoid inadvertent cannulation of the gross systemic air embolism occurs, de-airing of the
head and neck vessels or trauma to the posterior wall. cerebral circulation has priority. The first step is to
The aortic cannula is immediately de-aired by allowing terminate CPB, followed by removal of the arterial
blood to fill the tubing, which is then clamped and cannula leaving the purse-string sutures loose.
secured with the purse-string sutures. Once securely in Simultaneously, the anesthesiologist places the patient
place, the aortic cannula is connected to the arterial in Trendelenburg position and performs bilateral
inflow tubing of the bypass circuit, also ensuring that carotid compression. The source of air should be
no air is present at the connection site. Once con- identified and remedied followed by de-airing of the
nected, the perfusionist will inform the surgeon of CPB circuit. The arterial line cannula is then inserted
the presence of pulsatility and corresponding mean into the superior vena cava (SVC) or, if present in
arterial line pressure within the system to confirm bicaval cannulation, is connected to an existing SVC
correct intraluminal placement of the cannula – seen cannula. Retrograde cerebral perfusion (RCP) via the
as a “good swing” on analog manometers. SVC using low flow rates of 1–2 liters per minute, at a
blood temperature of 20°C, will enable de-airing of
Complications of Aortic Root Cannulation the cerebral circulation back to the aorta. This should
be performed for 2–3 minutes or until no more air
If air is introduced into the arterial limb of the CPB
can be seen coming out of the aortotomy site. The
circuit during cannulation, it must be disconnected 59
aorta can be re-cannulated upon completion of RCP,
from the aortic cannula and the air removed from i)

Table 7.1. Complications of ascending aortic cannulation Table 7.2. Complications of peripheral cannulation
Inability to introduce Adventitia occluding the Trauma to the vessel

the cannula incision site
Retrograde arterial dissection with retroperitoneal
Inadequate incision size
hemorrhage or extension of dissection to the aortic
Atheromatous plaque
root
within the aortic wall
Thrombosis or embolism
Intramural placement
Hemorrhage
Embolization of atheromatous plaque
Limb ischemia (which can be reduced by using an end
Air embolization on connection to the circuit
to side polytetrafluoroethane (PTFE) or Dacron™ graft
Persistent bleeding around cannula or peri-aortic sutured to the vessel)
hematoma
Malperfusion of cerebral and systemic circulation as a
Malposition of tip toward the aortic valve or into the result of cannulation of the false lumen of an aortic
arch vessels dissection
Dissection of the aorta Lymph fistula or lymphocele
Inadequate size leading to high pressure and low flow Infection
generation
Damage to neighboring neurovascular structures, such
Aneurysm formation at the site of cannulation at a later as femoral vein or brachial plexus
stage
Late vascular stenosis
Femoral cannulation necessitates the of use smaller

and upon recommencing CPB should be run in hypo- 15–21 Fr. cannulae due to the size of the femoral
thermia for 30–45 minutes. The use of relative hypo- vessels, with consequent higher pressure gradients,
thermia increases the solubility of gaseous emboli and jet effects and possibly lower flow rates. This may be
may reduce the extent of cerebral injury. Once surgery improved by cannulation of iliac arteries. The femoral
is completed and the patient has been stabilized, CPB arterial cannula is inserted over a guidewire, either
should be discontinued at a core temperature of 35°C. percutaneously or via a cut-down, and advanced into
Further potential complications of aortic root can- the aorta. Transesophageal echocardiography (TEE)
nulation are summarized in Table 7.1. is used to visualize the guidewire and arterial cannula
in order to achieve optimal placement and minimize
Peripheral Arterial Cannulation vascular injury.
The axillary artery is less likely than the femoral
Peripheral arterial cannulation, most commonly via
artery to have atherosclerotic disease or dissection
the femoral or axillary route, is used in the following
and also has good collateral flow, with less risk of
instances:
limb ischemia. In addition to these benefits, it pro-
1. Establishment of CPB prior to sternotomy or vides antegrade flow, with reduced risk of cerebral
anesthetic induction due to hemodynamic instability embolization. Direct arterial cannulation is uncom-
2. Selected redo-sternotomy procedures to allow for mon. End to side placement of a polytetrafluor-
controlled conditions during sternotomy and oethane (PTFE) or Dacron™ graft is preferable to
exposure of the heart direct cannulation, as it allows for improved limb
3. Aortic aneurysm surgery perfusion distal to the cannulation site. In lieu of
4. Aorta not suitable for cannulation due to using an arterial cannula, a 3/8 inch tubing connector
calcification, such as a “porcelain aorta” is tied onto the end of the graft and attached to the
5. Thoracic surgery arterial line of the CPB circuit.
6. Minimally invasive cardiac surgery (MICS) The potential complications of peripheral cannu-
60 7. Extracorporeal membrane oxygenation (ECMO) lation are summarized in Table 7.2.

Venous Cannulation cavo-atrial and bicaval. In urgent situations, a single

cannula can be placed through the RA appendage.
Venous drainage is vitally important as it not only
influences perfusion pressure in vital organs but also Cavo-atrial – This uses a “two-stage” cannula,
because it is essential for providing the blood source which has a wider proximal portion with side
necessary for pump flow. Blood flow into the CPB holes that lie in the RA, and a narrow extension,
circuit is usually achieved by gravity drainage, using with end and side holes, that extends into the IVC.
the “siphon” effect. Gravity siphoning as the means of This cannula is typically inserted through the right
obtaining adequate drainage relies on: atrial appendage and cannot be used if the right
heart is to be opened as it will invariably
1. no air being present in the tubing between the
entrain air.
patient and the pump, otherwise an “air lock” can
Bicaval – Purse-string sutures are placed on the
develop and stop drainage,
posterior-inferior RA wall and the RA appendage
2. the venous reservoir being kept below the level of
to enable direct cannulation of the IVC and SVC
the patient’s thorax and
respectively. Tapes or snares are passed around
3. the absence of venous line obstructions (e.g. kinks the venae cavae, with the cannulae in place to
or clamps). ensure that the patient’s entire venous return
The degree of venous drainage is determined by flows into the CPB circuit and to prevent air from
the patient’s central venous pressure (CVP) entering the venous lines when opening the RA, or
the difference in height between the patient and blood leaking past the cannulae into the RA. This
the top of the blood level in the venous reservoir is referred to as caval occlusion or total CPB and is
the resistance exerted by the circuit (cannulae, the technique of choice if the right heart is to
lines and connectors). be opened.
The creation of excessive negative pressure in the Most coronary (CABG) and aortic valve (AVR) sur-
venous line may cause the veins to collapse around gery is performed with venous drainage via cavo-
the cannula with intermittent reduction in venous atrial cannulation, while mitral and tricuspid valve
drainage (e.g. venous line chatter) and the potential procedures require bicaval cannulation. While this
for generation of gaseous microemboli (GME) in the approach usually provides adequate drainage, it is
circuit, a phenomenon referred to as “cavitation.” essential to constantly monitor right heart decom-
GME are a known risk of CPB and a specific concern pression and for the perfusionist to communicate
for postoperative neurocognitive dysfunction. Efforts any interruptions in venous return as cannula adjust-
to ameliorate cavitation include partial occluding of ments can be necessary during the operation to
the venous line, reducing vacuum assist venous drain- accommodate changes in heart position or cannula
age (VAVD) pressure and decreasing venous migration. Rarely, the right heart may need to be
cannula size. vented via the pulmonary artery to prevent right
The various available types and sizes of venous ventricular (RV) distension due to return of blood
cannulae are discussed in Chapter 2. The cannula tip into the RA via the coronary sinus. Occasionally, high
is the narrowest component in the venous circuit and SVC or even innominate vein cannulation may be
therefore the limiting factor for venous drainage. The required to facilitate resection of an RA tumor or
appropriate size is selected based on the flow charac- during an operation requiring access to the SVC, such
teristics of the cannula (detailed in the manufacturer’s as some heart transplant or heart-lung transplant
guidelines) and the required cardiac index for the procedures (Domino heart).
patient. One-third of total flow is derived from super- Air entry into the venous side of the circuit may
ior vena cava (SVC) drainage and two-thirds from lead to an “air lock,” causing obstruction of venous
inferior vena cava (IVC) drainage. drainage, or to systemic GME. The most common
reason for air entry is failure to seal the site around
the cannulae adequately or excessive negative venous
Connection to the Patient line pressure. Care must be taken to ensure that
This is usually achieved via right atrial (RA) cannula- purse-string sutures are airtight, and negative venous
tion. The two most common approaches include line pressure is not causing cavitation. If cavitation 61

Figure 7.3 Schematic of multistage cannula position across inferior vena cava (IVC), right atrium (RA) and superior vena cava (SVC).
persists, the surgeon should check that the cannula- utilized in this approach. The SVC cannula is gener-
tion purse-strings are secure and the perfusionist can ally placed percutaneously and under TEE guidance.
either reduce VAVD or partially occlude the venous Venous drainage and subsequent systemic blood
line. The perfusionist should notify the surgeon any- flow can be dramatically augmented utilizing VAVD.
time venous air entrainment is visualized. There are potential hazards associated with VAVD,
In semi-emergency situations, a single stage can- including cavitation and air embolism. Using an
nula – often referred to as a Ross Atrial Basket – can approved vacuum regulator that restricts maximum
be introduced into the RA and, with the arterial vacuum to 80 mmHg and positive and negative
cannula in place, CPB can be rapidly initiated. pressure relief valves on the venous reservoir help
mitigate against these complications.
Peripheral Venous Cannulation Further possible complications associated with
venous cannulation are listed in Table 7.3.
This is usually performed via the femoral or iliac
veins. Indications for peripheral venous cannulation
are the same as for peripheral arterial cannulation, General Sequence of Events for the
with the exception of a calcified aorta. Conduct of CPB
Drainage through peripheral cannulation is Before commencing CPB the perfusionists must have
achieved by using an appropriately sized cannula completed a series of “checks” as detailed in
and passing it so the tip is located in the caval/RA Chapter 4.
junction often using TEE guidance. A multistage can-
nula can be placed via the femoral vein with drainage
holes in the IVC, RA and SVC (see Figure 7.3). Connecting the Patient to the CPB Circuit
Selecting femoral venous cannulae that have numer- The surgeon will ask for permission to divide the
ous side holes permits greater venous drainage and CPB lines
subsequent better arterial blood flow. The pump flow is slowly reduced, and the venous
An additional cannula can be placed in the SVC line clamped, followed by the arterial line and all
62 via the right internal jugular vein to optimize venous recirculation lines
drainage. Typically, a 15–18 Fr peripheral cannula is The ACT is confirmed to be adequate for bypass

Table 7.3. Complications of venous cannulation

Initiating CPB
Low cardiac output due to compression of the heart If the gases have not yet been switched on, they are
during IVC purse-string placement now correctly set according to the patient’s
Damage to SVC/IVC/right pulmonary artery while anticipated full flow
passing tapes around cavae The perfusionist clearly informs the rest of the
Reduction in cardiac output prior to commencement of team that the patient is “going onto bypass”
CPB when cannulae are in place The clamp, or electronic occluder, on the arterial
line is opened and the pump is turned on slowly,
Atrial dysrhythmia
gradually increasing the rpm
Malpositioning of SVC cannula into the azygos vein When going onto bypass with a centrifugal pump,
the cannula tip IVC cannula into the hepatic vein forward pressure must be generated before the
RA cannula into LA in the
line clamp is removed. The drive motor is
presence of an atrial secundum
defect
therefore turned on while the aortic line is still
clamped, in order to generate sufficient forward
RA trauma and bleeding from cannulation sites pressure, to exceed the patient’s arterial pressure;
SVC or IVC laceration on manipulation of cannulated RA above 1500–2000 rpm is usual
Narrowing of cavae after decannulation and closure of The perfusionist must monitor the line pressure
purse-string sutures during this stage, looking for any sign of
obstruction, at the same time as monitoring the
venous and arterial pressures and the blood level in
the venous reservoir, as the pump speed is increased
Having raised the pressure on the venous side, the
The surgeon will cannulate the aorta or peripheral venous clamp, or the electronic venous occluder,
arterial vessel
is slowly opened, and the perfusionist should
As required, the arterial pump is turned to assist control the venous pressure by adjusting venous
in an air free connection clamping until they have achieved full flow for the
When the line is free of air the surgeon will patient. In situations where air is left in the venous
connect the arterial line line prior to initiation of bypass, the venous
The clamp is removed from the arterial line clamps may need to be opened more rapidly to
The perfusionist confirms that the arterial line is avoid air locks, until this air has been removed
reading correctly and is consistent with patient The team is informed when full flow has been
pressures. If using a manometer this is confirmed achieved, the anesthesiologist may discontinue
by an appropriate pulse pressure (“good swing”) ventilation at this point
The patency of the arterial cannula should be Any difficulty in achieving a full venous return is
tested by administering a test dose of pump prime reported immediately to the surgeons, so that they
to the patient while watching for a spike in the can make any adjustment to the venous
arterial line pressure. The perfusionist states if the cannulation that may be necessary; persistent
test was successful venous air should also be reported to the surgeons
If the perfusionist has any doubts about the Once a steady state of perfusion (e.g. target arterial
cannulation, they must inform the surgeon blood flow and blood pressure) has been attained,
immediately and continue to voice their the aorta has been clamped, and cardioplegia has
misgivings until they are confident that the been administered, laboratory tests should be sent
cannula is satisfactorily placed (see also Chapter 10)
The surgeon will cannulate the venous circulation
as required
The pump suckers are ready for salvaging any The Rewarming Phase
blood loss and the shed blood can be retransfused The majority of cases done on CPB are conducted at
through the arterial line (“give what you are temperatures in the range of 30–34°C with the patient 63
getting”) allowed to passively drift to target temperature,

Table 7.4. Temperature management Table 7.5. Adequacy of perfusion
Arterial Blood Temp 13–37ºC Parameter Target

Core Temp 16–37ºC Mean Arterial 60–80 mmHg
Target Core Temp for 35ºC Pressure
separation from CPB Cardiac Index >2.4 L/min/m²
Warming Gradients (Arterial Core temp below DO2 Index >280 mLO2/min/m²
to Venous) 30ºC: 10ºC
Hemoglobin 70–80 g/L
Core temp above
30ºC: 4ºC SvO2 >65%
Rewarming Rate (Core 0.5ºC/min Cerebral Oximetry >50% and/or <20% drop from
Temp) baseline
although some surgeons prefer to stay normothermic. Monitoring during CPB

More complex operations are often conducted at mod- Following commencement of CPB and after the
erate or deep hypothermia (between 28° and 18°C). patient is on full flow with adequate decompression
Rewarming begins after consultation with the sur- of the heart, ventilation can be switched off or
geon. Once commenced, appropriate adjustments to adjusted, based on the lung protection strategy.
gas flows and to blood flows must be made as a rapid Various patient parameters should be continuously
drop in SVO2 may be experienced. An arterial blood monitored to ensure adequate perfusion. Table 7.5
gas sample should be taken during the mid-warming outlines these parameters and their respective targets,
phase, in order to give sufficient time for any correct- which should be adjusted for each patient’s need (see
ive action to be taken before coming off bypass. Final Chapter 3 for detailed review of monitoring).
blood samples may be taken once a core temperature
of >35°C has been attained. Pressure Management
The arterial blood temperature and patient core Mean arterial blood pressure (MAP) – is determined
temperature are used to guide rate and extent of by flow rate and arteriolar resistance. An acceptable
rewarming MAP on CPB is one which provides adequate tissue
A gradient of 10°C between arterial outlet and perfusion. Adequate tissue perfusion is not only influ-
venous inflow on the oxygenator should not be enced by the MAP, but also by pump flow, core body
exceeded temperature, and patient comorbidities. In general, it
The target arterial outlet blood temperature is recommended to maintain higher pressures in the
should not exceed 37.0°C presence of known cerebrovascular disease, in par-
The duration of rewarming has to allow time for ticular carotid stenosis, renal dysfunction or left
distribution of heat between core and peripheral ventricular hypertrophy.
tissues, using vasodilators, if needed, to enhance There mostly is a transient drop in systemic pres-
peripheral blood flow and thus heat distribution sure on commencement of CPB. This is the result of:
It is reasonable to limit the rate of rewarming, 1. vasodilatation associated with the sudden decrease
when the arterial blood temperature is greater in blood viscosity resulting from hemodilution
than 30°C, to 0.5°C per minute through the CPB prime and
Post-CPB an “after drop” in core temperature 2. the systemic inflammatory response associated
occurs as heat is redistributed from core to with CPB.
peripheral tissues; this after drop can be lessened if As CPB continues, vascular resistance gradually
adequate time is allowed for thorough rewarming increases as a result of equilibration of fluid between
The general principles of temperature management the vascular and tissue “compartments,” hemocon-
64 are summarized in Table 7.4 and this is discussed in centration from diuresis, the increase in blood viscos-
more detail in Chapter 9. ity seen with hypothermia and the progressive

increase in circulating levels of catecholamines and Adding VAVD should be considered if correcting the
renin as part of the stress response to CPB. However, above does not improve the situation.
intermittent boluses of vasopressor are commonly Electrocardiogram (ECG) – the ECG must be
required to maintain an acceptable MAP during CPB. observed throughout CPB to ensure that it remains
It is important to emphasize that manipulation of isoelectric during cardioplegic arrest. Persistent ST
MAP alone is not sufficient to guarantee adequate segment changes following removal of the aortic
organ perfusion. Neither a low MAP with a high flow clamp and resumption of myocardial activity may
nor a high MAP with a low flow are sufficient in indicate ischemia from inadequate re-vascularization,
themselves. We advise that whole body oxygen deliv- coronary ostial obstruction, such as by an incorrectly
ery (DO2) be optimized, and vascular resistance seated aortic valve prosthesis, or air/particulate embo-
adjusted with vasopressors or dilators to bring the lization into the coronary arteries.
MAP into the autoregulatory range for critical organ Temperature – the principal reason for hypother-
beds. mic CPB is to protect the heart and other organs by
Pulmonary artery (PA) and left atrial (LA) reducing metabolic rate and thus oxygen require-
pressure – the PA and LA pressures should be close ments. Temperature can be measured in the following
to zero on CPB. LA pressure monitoring can be useful locations: nasopharynx, tympanic membrane, pul-
during CPB to assess left ventricular distension, in monary artery, bladder or rectum, arterial inflow,
particular in cases where an increase in blood flow water entering heat exchanger and venous return.
back to the left heart is expected (cyanotic heart Nasopharyngeal temperature probes underestimate,
disease, large bronchial flow in chronic lung disease but approximate to brain temperature, while the
or aortic regurgitation). It is therefore most com- mixed venous temperature on the CPB circuit is an
monly used during bypass in complex pediatric and approximation of average body temperature.
adult congenital surgery. LA pressure is usually meas- For more detail see Chapters 9 and 11.
ured using a transduced catheter or needle directly Urine output – urine output on CPB is monitored
placed into the left atrium or placed into the left as an indicator of renal perfusion. Indications for diur-
atrium via the right superior pulmonary vein. In cases etic use during CPB include hyperkalemia, hemoglobi-
where a pulmonary artery catheter has been inserted, nuria and hemodilution. Mannitol is an osmotic
the pressure reading at the tip of the catheter can be diuretic which is commonly added to the priming fluid
taken as a surrogate of LA pressure but may not of the bypass circuit in order to stimulate urine produc-
always be accurate, particularly if pulmonary vascular tion during bypass. The aim is to help reduce hypervo-
pathology is present. Care must be taken with PA lemia and may enable hemoglobinuria to be more
catheters to ensure that the catheter tip does not effectively cleared, however there is little clear evidence
migrate proximally, leading to “wedging” and subse- for or against its routine use. Urine output would be
quent PA rupture or lung infarction. Interrogation of expected to be >1 ml/kg/hr (and is often much higher
the PA catheter position with TEE and frequent that this) but it is important to note that acute kidney
observation of the PA waveform are best practice to injury can occur via many different mechanisms and
avoid this complication. may still develop despite adequate urine production.
Central venous pressure (CVP) – on CPB, the CVP Laboratory investigations – are discussed in detail
is expected to be close to zero and no more than in in Chapter 10. At a minimum, monitoring during
single digits. If a potential issue with the central CPB requires measurement of PO2, PCO2, base excess
venous catheter has been excluded, an increase in (BE), hemoglobin, HCT, pH, potassium, glucose, lac-
CVP generally indicates impaired venous drainage. tate, and coagulation status using ACT or heparin
A high CVP during bypass reduces effective perfusion concentration.
of critical organs. A bulging right heart and/or Transesophageal echocardiography (TEE) – TEE
engorgement of the patient’s head and eyes should is applied increasingly as a routine part of cardiac
prompt immediate corrective action. Common causes surgery. It is a useful tool to assess adequacy of de-
are inadequate cannula size, obstruction to the can- airing of the heart, intracardiac structures (valves,
nula tip and insufficient height difference between the sub-valvular apparatus, prostheses, septal walls, left
patient and the reservoir to enable gravity drainage. and right ventricular outflow tracts) and global and 65

regional wall motion. The opportunity to obtain rou- artery is not visible. The tip is seen as being a
tine images of cardiac and valvular function usually mobile echogenic structure which moves around
ends once the patient is transitioned onto cardiopul- inside the blood vessel when the balloon pump is
monary bypass, due to the fact that blood is diverted switched on (see Figure 7.5). Visualization of the
away from the heart, and the chambers will no longer descending aorta or arch can also be used to
be full. There are a few circumstances however in interrogate for the presence of an aortic dissection
which TEE can still be of use: in circumstances where there is a rise in
Sudden loss of venous drainage is often the result pressure in the arterial limb of the bypass circuit
of a two-stage or IVC cannula tip migrating into a or there are difficulties achieving adequate
hepatic vein. This can often be visualized on TEE perfusion.
prior to the surgeon withdrawing the cannula by
the appropriate amount.
In circumstances where the LV cannot be Maintaining a Bloodless Surgical Field
adequately assessed visually (e.g. during
The main aim of CPB is to create a motionless and
minimally invasive surgery or due to extensive
bloodless surgical field. Several different techniques
scar tissue in redo surgery), TEE can be used to see
are used to work in concert to achieve that:
whether aortic regurgitation is resulting in filling
and dilation of the LV during administration of
aortic root cardioplegia. It is extremely important Cardiotomy Suction
to avoid LV dilation as the increase in wall tension After systemic heparinization and confirmation of an
leads to a reduction in subendocardial perfusion adequate ACT, designated cardiotomy suckers are
and possible ischemic complications. If the LV is used to collect shed blood in the reservoir for recircu-
seen to be dilating on TEE, cardioplegia must be lation within the CPB circuit. Cardiotomy suction is
stopped and the LV vent started to empty out the most commonly generated by use of a roller pump. If
chamber before restarting cardioplegia. The the pump rate is too high the negative pressure at the
degree and speed of LV dilation and the ability to sucker tip may lead to hemolysis and occlusion of the
achieve asystole on the ECG will determine sucker. Regular adjusting of the pump rate by
whether this cardioplegia strategy is the perfusionist and of the sucker position by the
persisted with. surgeon helps avoid that problem.
Positioning of coronary sinus cannula: Correct It is essential that the direction of the cardiotomy
position inside the coronary sinus can usually be suckers is confirmed prior to use. The perfusionist
visualized (see Figure 7.4). It is important to and the surgical team need to ensure that they are
monitor the pressure in the cannula during indeed sucking and not blowing air toward the
administration of retrograde cardioplegia to avoid patient. They are generally tested by submerging the
over-pressurizing as pressures greater than tips in clear fluid and observing that the fluid is being
30mmHg may risk rupturing the vein which can sucked away from the field and air is not exiting the
be extremely difficult to repair and can be a sucker creating bubbles. Assessments such as this
catastrophic complication. Sometimes the cannula must be included in pre-bypass checklists.
can slip back into the right atrium despite correct In extreme cases of hemorrhage, such as injury of
initial positioning and will most commonly be the right ventricle during chest entry in a redo oper-
picked up via the lack of rise in pressure on ation, after heparinization and with the arterial can-
administration of cardioplegia. nula in situ, the patient can be placed on “sucker
The descending aorta can still be adequately bypass,” where the shed blood in the operative field
visualized on bypass and this can aid with the provides venous return to the CPB circuit until
positioning of an intra-aortic balloon pump. TEE formal venous cannulation can be secured.
examination can confirm the presence of the wire
in the aorta and can guide placing the balloon tip Adverse Effects of Cardiotomy Suction
just distal to the left subclavian artery origin or Blood suctioned from the surgical field is highly
66 distal to the arch if the origin of the left subclavian “activated.” Hemolysis, coagulation products,

Figure 7.4 Right atrium (RA) with coronary sinus (CS) shown before (a) and after (b) insertion of retrograde cannula into coronary sinus.
microparticles, fat, cellular debris and aggregates of injury caused by cardiotomy suction is the amount
cause a surge in inflammatory mediators (tumor of room air co-aspirated with blood.
necrosis factor alpha (TNF-α), interleukin-6 (IL-6), Commonly used strategies to reduce the side 67
C3a) and endotoxins. Another potential determinant effects of cardiotomy suction are shown in Table 7.6.

Figure 7.5 TEE image of IAPB tip placed in the proximal descending aorta.
Table 7.6. Strategies to reduce the side effects of myocardial oxygen demand, impairs subendocardial
cardiotomy suction perfusion and may result in myofibrillar disruption.
Hemostasis throughout operation to minimize shed On occasions, blood can return from abnormal
blood sources. These include:
Minimize aspiration of air Avoidance of high left-sided SVC
through the cardiotomy negative pressures patent ductus arteriosus (PDA)
suction by Slow rates of suction atrial septal defect/ventricular septal defect
Not sucking the anomalous venous drainage
surgical field dry aortic regurgitation
Keeping the suction tip
under level of blood
systemic to pulmonary shunt.
Filtration of cardiotomy suction blood (leukocyte

depletion)
Detection of LV Distension
The left ventricle needs to be vented if it is filling from
Cell salvage blood instead of cardiotomy suction
any source but not ejecting. It will fill primarily
MiECC because of aortic insufficiency, or during cardioplegia
administration. Surgical inspection and palpation of
the LV to monitor the degree of distension is crucial
Keeping the Heart Relaxed on commencing CPB, during aortic cross-clamping
While on CPB, the left side of the heart receives blood and during initial administration of cardioplegia.
from bronchial arteries and Thebesian veins and the Although LA and PA pressure monitoring can help
right heart receives blood from the coronary sinus detect moderate LV distension, TEE is probably best
and “leakage” around the venous cannulae. As the placed to assess this. If the heart is well decompressed
ventricles are unable to eject during the period of and empty, it will not be possible to obtain recogniz-
arrest, they may be vented to protect the heart from able images. However if there is blood present in the
68 distension. Ventricular distension is undesirable heart then TEE views will be obtainable and can be
because excessive myocardial stretching increases used to assess for active chamber enlargement.

“leakage” past the cannula, which can be minimized

by using bicaval cannulation and caval snares. When
antegrade cardioplegia is administered, releasing the
caval snares will permit venting of cardioplegia solu-
tion returning via the coronary sinus to the right heart.
Placement of a pulmonary arterial vent will keep
the right ventricle empty of fluid. The presence of a
persistent left SVC requires additional drainage of the
coronary sinus or RA in most cases.
The most common vent sites, as illustrated in
Figure 7.6, are:
ascending aorta via aortic root cardioplegia
cannula with vent line – this method does not
allow venting during cardioplegia administration
right superior pulmonary vein – a vent is passed
into the left atrium and through the mitral valve
into the LV
aortic root, using a cardiotomy sucker placed
through the aortic valve into the LV (in patients
undergoing an aortic valve replacement)
left ventricular apex
Figure 7.6 Sites to use to vent the heart during cardiopulmonary pulmonary artery – this may not be effective at
bypass A) aortic root, B) right superior pulmonary vein, C) left
ventricular apex, and D) pulmonary artery. LA = left atrium; MV = venting the LV when there is aortic regurgitation
mitral valve; RV = right ventricle; AO = aorta; PA = pulmonary artery; with a competent mitral valve.
LV = left ventricle. (Reprinted from: Hessel EA II. Circuitry and cannulation
techniques. In Gravlee GP et al. Cardiopulmonary bypass. Philadelphia, PA: It must be remembered that venting the heart is not
Lippincott Williams & Wilkins; 2008:90.) without complications. These can be immediate or
delayed:
“Steal” of systemic perfusion may occur if the
Venting the Heart heart is vented excessively in the presence of aortic
Vent suction is most commonly achieved using a regurgitation
roller pump. The principle is similar to that governing If the vents are not removed with great care, the
cardiotomy suction and therefore the direction of the process can be the source of systemic air
pump must also be confirmed via a “sucker (fluid) embolism. Pressures and filling state should be
test.” The potential for fatal air embolism exists if a modified during vent placement and removal to
sucker attached to an aortic root vent was to pump air mitigate this risk
into the patient instead of removing blood. A one-way Bleeding can occur from the vent site, particularly
valve must also be included to further reduce the risk if an LV apical vent is used
of air being inadvertently introduced via the vent site. Later complications include stenosis of the
The venous cannula effectively vents the right side pulmonary vein or pulmonary artery, or aneurysm
of the heart, keeping it empty of blood except for any of the LV apex, depending on the vent site used.
Suggested Further Reading September 18, 2019, from www

.uptodate.com/contents/
Committee Reviewers. 2019
EACTS/EACTA/EBCP Guidelines
1. Cheung AT, Stafford-Smith M, cardiopulmonary-bypass- on cardiopulmonary bypass in
Heath M (2019). management#H3676286842 adult cardiac surgery. Eur
Cardiopulmonary bypass: J Cardiothorac Surg. October 2, 69
Management. In NA Nussmeier 2. Wahba A, Milojevic M, Boer C
et al. EACTS/EACTA/EBCP 2019
(Ed.), UpToDate. Retrieved

3. Hessel EA 2nd. What’s new in 4. Ramchandani M, Al Jabbari O, surgery. Methodist Debakey

cardiopulmonary bypass. Abu Saleh WK et al. Cannulation Cardiovasc J. January–March,
J Cardiothorac Vasc Anesth. strategies and pitfalls in 2016;12(1):10–3.
August, 2019;33(8):2296–2326. minimally invasive cardiac
70

Chapter
Minimal Invasive Extracorporeal Circulation
8 Kyriakos Anastasiadis, Polychronis Antonitsis, Helena Argiriadou and

Apostolos Deliopoulos
Minimal invasive extracorporeal circulation (MiECC) to reduce injury to blood cells and to minimize
is a recent development in perfusion science. expression of inflammatory mediators, all lines and
MiECC’s unique characteristics include advances oxygenator were coated with heparin, while priming
such as closed circuits with elimination of blood-air volume was reduced to a minimum. Shed blood from
interaction, reduced hemodilution, biocompatible the surgical field was collected, washed and transfused
surfaces, and lack of scavenging and reinfusion of with a cell salvage device, avoiding the adverse effects
unprocessed shed blood. Contemporary hybrid of recirculating unprocessed shed blood from the
(modular) systems allow perfusionists to safely operating field into the CPB circuit.
employ MiECC in the full spectrum of cardiac sur- The last two decades have witnessed numerous
gery. MiECC provides the base for developing a mul- additional advancements in MiECC technology along
tidisciplinary intraoperative strategy which with encouraging clinical results. This evolution led to
encompasses a surgeon’s particular technique and the foundation of the multidisciplinary Minimal
goal-directed perfusion, as well as modified heparin/ Invasive Extracorporeal Technologies International
protamine management. Proponents of MiECC are Society (MiECTiS) in order to promote research,
convinced that it will ultimately replace conventional clinical use and standards to further develop minim-
CPB and become standard practice in cardiac surgery ally invasive perfusion. MiECTiS advocates a multi-
once the potential clinical benefits have been widely disciplinary strategy involving surgery, anesthesiology
accepted. As with traditional extracorporeal circula- and perfusion to promote maximum benefit from this
ton (ECC) techniques, MiECC requires close collab- technology.
oration of surgical, anesthesiology and perfusion The term MiECC has replaced all other descriptive
colleagues for optimal outcome. terminology previously used for minimal extracor-
poreal circulation circuits, such as: miniaturized
The Evolution of Minimal Invasive extracorporeal circulation (MECC), mini extracor-
poreal circulation (mECC), minimized extracorporeal
Extracorporeal Circulation circulation or mini cardiopulmonary bypass (mCPB,
MiECC has its roots in Extracorporeal Life Support mini-CPB).
(ECLS), where a single circuit with low systemic Table 8.1 summarizes the mandatory and add-
inflammation, low hemodilution, and enhanced bio- itional components of a contemporary MiECC
compatibility to reduce anticoagulation is required. circuit.
The successful use of such systems opened a new era
in short-term mechanical circulatory support.
Subsequently, during the mid-90s multidisciplinary Classification of MiECC systems
teams developed minimally invasive CPB systems MiECTiS has adopted a classification of MiECC
for coronary surgery. These first systems comprised systems that reflects how they have evolved over the
of short arterio-venous lines without cardiotomy res- last decade. Figure 8.1 illustrates a Type III / IV
ervoir in order to reduce hemodilution and transfu- circuit, which is the type most commonly used today.
sion requirements. Kinetic venous drainage with Type I systems are derived from ECLS circuits
integration of a centrifugal pump allowed for a com- with the addition of a line to administer
pact closed circuit that could be installed close to the cardioplegia. These systems are suitable for 71
patient’s chest. In order to improve biocompatibility, performing closed-heart surgeries. Soon after

Kyriakos Anastasiadis, Polychronis Antonitsis, Helena Argiriadou and Apostolos Deliopoulos
Table 8.1. Components of MiECC their introduction significant safety concerns

Mandatory Closed CPB circuit
emerged: there was a risk of air entrainment and
Components Biocompatible surfaces air lock, requiring stopping the pump and
Reduced priming volume manually de-airing the circuit.
Centrifugal pump Type II circuits addressed the air entrainment
Membrane oxygenator issue seen with Type I systems by integrating a
Heat exchanger venous bubble trap or air removal system.
Cardioplegia system Type III systems were driven by the desire to use
Venous bubble trap/venous air MiECC technology for open-chamber heart
removing device
surgery, such as valve replacement. The addition
Shed blood management system
of a soft-bag or soft-shell reservoir allows for the
Additional Vents management of the circulatory volume during
Components CPB, which is particularly important in patients
Aortic root
Pulmonary artery / vein with preoperative volume overload, such as in
aortic or mitral insufficiency.
Reservoir
Type IV are modular, hybrid systems which
Soft bag / soft-shell integrate a heparinized venous reservoir as a
Hard-shell (modular standby component, readily available for
systems) conversion to an open, conventional CPB system.
Regulated smart suction This configuration allows the use of MiECC in the
Arterial line filter full spectrum of cardiac surgery including
Soft bag
reservoir
Vent
Oxygenator heat Centrifugal

pump Bubble Cardioplegia
trap
Roller
pumps
Hard shell
reservoir
Figure 8.1 Typical Type III circuit, which can easily be converted into Type IV by removing the clamps from the afferent and efferent tubing
72 from the hardshell reservoir. Any cell salvage, if used, needs to be reinfused into the hardshell reservoir.

Chapter 8: Minimal Invasive Extracorporeal Circulation
complex patients and procedures, as any the patient’s venous compartment the reservoir. This
unexpected perfusion scenarios, such as massive means that fluids have to be used judiciously, i.e.
air entry to the venous side of the circuit or filling up the venous compartment sufficiently with-
accidental excessive blood loss to the out losing the benefit of minimal hemodilution with
mediastinum, can be managed by an easy switch low prime volume. Appropriate use of vasocon-
to standard CPB. strictor or inotropic support before initiating CPB
can help maintain hemodynamic goals.
The Team Approach to MiECC Standard perioperative hemodynamic monitoring
with invasive, continuous mean arterial pressure
It is of utmost importance that all members of the
(MAP), central venous pressure (CVP) and transeso-
team not only comprehend perfusion technology, but
phageal echocardiography (TEE) is often expanded by
that they understand the unique characteristics of
using pulmonary artery catheters (PAC) and continu-
MiECC, particularly what it can and what it cannot
ous cardiac output (CCO). Some centers opt to use
deliver. Continuous excellent communication with
near infrared spectroscopy (NIRS) monitoring of
the perfusionist is of utmost importance, particularly
cerebral oxygenation as an index of global perfusion.
during critical moments, such as during retrograde
Some advocates of MiECC use its unique charac-
priming of the circuit with patient blood via the aortic
teristics – minimal hemodilution, biocompatible sur-
cannula (retrograde autologous prime [RAP]), when
faces, elimination of blood-air interaction and
securing the vent for the cardioplegia line or when
elimination of unprocessed shed blood reinfusion –
removing a vent, in order to avoid accidental air
to use less anticoagulation, aiming for an ACT value
entrainment into the system.
>300 seconds for coronary surgery and >400 seconds
for valve and more complex procedures.
Surgeon’s perspective
Firstly, the surgeon must appreciate that when oper- Perfusionist’s perspective
ating on MiECC shed blood does not recirculate into
MiECC integrates all advancements in perfusion tech-
the bypass circuit and is not available for the circulat-
nology in a single circuit, but also provides a chal-
ing volume. Meticulous operative technique is man-
lenge for the perfusionist.
datory and special attention must be paid to avoiding
Centrifugal pump flow is largely dependent on a
blood loss, not dissimilar to requirements of beating-
balance between the filling status of the patient and
heart surgery.
the systemic vascular resistance and therefore needs
Secondly, all cannulation sites must be secured in
regular adjusting. All commercially available centrifu-
a way that provides an airtight seal. The venous can-
gal pumps are fitted with bubble detectors, which
nula is commonly secured with two purse-string
cause the pump to stop when air reaches the sensor.
sutures and two silk ties; some surgeons arm the
In that case the perfusionist has to immediately de-air
purse strings with Teflon pledgets, particularly when
the bubble trap by applying suction to it, while at the
the right atrial appendage is of poor quality tissue.
same time adding volume to the circuit. Devices that
Some advocate double-snaring the inferior and super-
can purge air automatically can be integrated into the
ior vena cava cannulae during mitral valve surgery to
circuit, removing the need for the perfusionist
mitigate against air entrainment. Any manipulations
to intervene.
of the heart must be done very carefully in order not
The perfusionist has to appreciate the principles of
to displace the venous cannula(e). Lines are connected
a closed circuit, where the patient’s venous compart-
with due diligence to avoid introducing air. Accurate
ment acts as the reservoir. The patient’s volume status
positioning of the venous cannula is essential to
is monitored via several surrogate measures: negative
achieve optimum drainage, which can be assisted by
venous drainage pressure, arterial pressure, cardiople-
placing a pulmonary artery vent.
gia pressure and the amount of blood drained from
the aortic root vent. Pump flow is another sensitive
Anesthesiologist’s perspective parameter, as it decreases with hypovolemia. Moving
MiECC systems are closed and, without the option of the operating table into Trendelenburg position and
73
easily adding fluids as necessary, they effectively make volume replacement and/or administration of

vasoconstrictors are measures to increase the preload. Advantages of a Modular Design

On the other hand, hypervolemia can cause difficul-
Modular MiECC systems (i.e. Type IV) represent the
ties in off-loading the heart and in obtaining a blood-
latest evolution in the field of extracorporeal circula-
less surgical field. In this case, surplus blood volume
tion. They integrate contemporary advancements in
can be decanted into the soft-shell reservoir or the
perfusion technology and address safety concerns. As
table can be moved into the reverse-Trendelenburg
previously described, they are Type III circuits with a
position.
standby hard-shell reservoir connected in parallel to
Understanding the principles of kinetic-assisted
the venous line to allow immediate conversion into a
venous drainage produced by the centrifugal pump is
conventional circuit if required. The circuit configur-
of paramount importance as the negative pressure at
ation of the AHEPA University Hospital Thessaloniki
the venous line provides important information on the
prototype Type IV MiECC circuit is shown in
filling status of the patient. Exceeding 70 mmHg can
Figure 8.2.
result in cavitation with the creation of gaseous micro-
Two recently published series show that modular
emboli and can lead to high blood velocity thereby
configuration ensured 100% technical feasibility for
increasing shear stress and hemolysis at the level of
performing every type of cardiac surgery including
the entrance holes of the cannula and at the wall of the
aortic arch replacements. They reported conversion
cannula. Increasing the assisted venous, and thus the
rates to conventional CPB of 0.8 and 6%. Modular
negative pressure, is not a solution for correcting
configuration is advocated for all cardiac surgical
improper cannula position or hypovolemia.
procedures, including isolated coronary artery bypass
Major determinants of negative pressure are the
grafting, in order to promote more widespread adop-
type, the size and the position of the venous cannula.
tion of MiECC technology in modern cardiac surgical
When increasing the negative pressure, drainage ini-
practice.
tially increases linearly with pressure until any further
increase collapses the surrounding venous wall and no
further advantage in flow will be seen. The ratio Training
between the diameter of the cannula and the vein A MiECC training program can be divided into five
should be around 0.6 in order to avoid collapse of stages (see Figure 8.3). After appropriate proctorship,
the vein around the side holes of the cannula. Re- a dedicated team of surgeon, anesthesiologist and
positioning of the venous cannula may be required to perfusionist can start operating on coronary cases,
provide appropriate flow. In case of bicaval cannula- using at least a Type II MiECC system. Experience
tion, the perfusionist should prompt the surgeon to shows that tangible results, particularly in reducing
check flow in every cannula separately. transfusion requirements, materialize after about
In case of a temporary excess in negative pressure 50 cases.
due to venous cannula displacement while lifting the After having completed 50 cases, it is feasible to
heart, the perfusionist might need to add volume to progress to uncomplicated open-chamber heart sur-
compensate and ensure adequate flow. gery, such as aortic valve replacement. Although these
During surgery with MiECC it is imperative to use operations are doable with a Type II circuit, the
blood mini-cardioplegia (i.e. Calafiore regime) in integration of a soft-shell reservoir (Type III circuit)
order to avoid excessive volume. The cardioplegic is highly recommended for volume management.
solution is delivered with a roller pump in combin- After gaining experience in aortic valve cases,
ation with a high-speed syringe driver. Hyperkalemia more complex mitral and tricuspid valve procedures
during cardioplegia delivery can cause transient vaso- can be pursued with a Type III circuit, although a
dilation but rarely warrants an intervention. modular design is advocated as a “safety net.” With a
Since there is no cardiotomy reservoir in the high level of expertise and confidence in using Type
MiECC circuit, shed blood is collected into a cell IV circuits, any cardiac procedure, even emergency
saver. The collected blood is processed and adminis- aortic dissection repair or demanding redo cases, can
tered as required after weaning off CPB. In case of be performed using MiECC technology.
excessive bleeding, the collected blood can be given Type IV circuits can obviously be used even from
74 back into the circuit directly. Type IV circuits are best the first coronary cases, obviating the need for a
equipped to deal with sudden massive blood loss. staged approach, as part of the learning strategy.

Figure 8.2 The prototype modular type IV AHEPA MiECC circuit (left). Schematic configuration (right). PA: pulmonary artery, VARD: venous air
removal device.
75
Figure 8.3 Proposed MiECC training pathway. Ao arch: aortic arch, AVR: aortic valve replacement, CABG: coronary artery bypass grafting, MVR:
mitral valve replacement, TVR: tricuspid valve replacement.

Figure 8.4 Schematic diagram of perioperative strategy to optimize the use of MiECC. CCO: continuous cardiac output; CO: cardiac output/
circulatory flow; CPB: cardiopulmonary bypass; Ht: hematocrit, Lac: lactate levels; POC: point-of-care; rSO2: cerebral oxygen saturation; TEE:
transesophageal echocardiography.
The Quest for “Physiologic” Perfusion aiming to reduce transfusion, hemoglobin level
should be kept >8 g/dl.
Development of MiECC has initiated a multidisci-
plinary strategy toward “physiologic” perfusion in
cardiac surgery. Despite all advances in surgical tech- Evidenced-Based Clinical Advantages
niques and cardiac anesthesia, this concept could of MiECC
never have been introduced in clinical practice with- As the amount of evidence increases, the use of
out the concomitant advancement in CPB technology. MiECC is gaining traction in various guidelines. The
Figure 8.4 proposes a monitoring algorithm through- 2019 joint guidelines on adult cardiopulmonary
out the perioperative period. Hemodynamic bypass in cardiac surgery by the European Societies
management during the pre-CPB and post-CPB of Cardiac and Thoracic Surgery, Cardiac Anaesthesia
period – either with the help of inotropes or vasocon- and the European Board of Cardiac Perfusion
strictors, with optimizing volume status or by increas- (EACTS, EACTA and EBCP) state that:
ing pump flow – aims to keep cardiac output (CO) >
MiECC should be considered over standard
2.4 L/min/m2 and mixed venous oxygen saturation
conventional CPB systems to increase the
(SvO2) > 70%. During CPB the perfusionist adjusts
biocompatibility of ECC. (Class of
their strategy to goal-directed perfusion, maintaining
recommendation: IIA, Level of evidence: B.)
oxygen delivery (DO2i) > 272 ml/min/m2 and an
oxygen delivery to carbon dioxide production ratio MiECC should be considered over standard
conventional CPB systems to reduce blood loss
(DO2i/VCO2i) > 5, while the oxygen extraction
and the need for transfusion. (Class of
ratio (O2ER) should be kept at <30. Cerebral
recommendation: IIA, Level of evidence: B.)
oximetry monitoring serves as a ‘level alarm’ on-
76 A combination of MiECC features – such as
and off-CPB and a drop of >20% from the baseline
needs to prompt immediate intervention. While coating, the centrifugal pump, the separation of

Table 8.2. MiECC Practice Recommendations
Level of
Evidence
Class I
MiECC systems reduce hemodilution and better preserve hematocrit as well as reduce postoperative A
bleeding and the need for RBC transfusion.
MiECC systems reduce the incidence of postoperative atrial fibrillation. A
MiECC systems preserve renal function. A
MiECC is associated with improved myocardial protection. A
Class IIA
Inflammatory response assessed by specific inflammatory markers is attenuated with use of MiECC. B
MiECC systems can reduce cerebral gaseous microembolism and preserve neurocognitive function. B
MiECC exerts a subclinical protective effect on end-organ function (lung, liver, intestine) which is B
related to enhanced recovery of microvascular organ perfusion.
Class IIB
Within a MiECC strategy, less thrombin generation may permit reduced heparin dose targeted to B
shorter ACT times. When such a strategy is followed, individual heparin dose should be determined
using heparin dose-response monitoring systems.
MiECC appears to offer survival benefit in terms of lower 30-day mortality after CABG procedures. B
Use of short-acting opioids in combination with propofol or volatile anesthetics, and hypnotic effect C
monitoring by processed EEG, is recommended for induction and maintenance of anesthesia for
MiECC-based surgery. TEE findings pertinent to institutional management of MiECC should be
communicated during the preoperative surgical safety time out.
ACT: Activated Clotting Time; CABG: Coronary Artery Bypass Grafting; EEG: Electroencephalogram; MiECC: Minimal Invasive Extracorporeal
Circulation; RBC: Red Blood Cells
cardiotomy suction blood and the use of closed There was no difference in the odds for developing a
systems – should be considered to improve postoperative myocardial infarction. The authors
conventional CPB. (Class of recommendation: conclude that MiECC may represent an attractive
IIA, Level of evidence: C.) compromise between OPCAB and conventional CPB.
The 2017 EACTS/EACTA guidelines on patient blood
management for adult cardiac surgery recommend
considering MiECC to reduce perioperative blood Incorporating the Lessons Learned from
transfusion. A position paper produced by MiECTiS
in 2016 provides a detailed overview of practice rec- MiECC into Practice
ommendations, which are summarized in Table 8.2 Cardiac surgery is by definition a “non-physiologic”
A meta-analysis including 2,700 patients from intervention. MiECC attempts to apply physiology to
24 randomized controlled trials showed that MiECC perfusion. On a cellular level it shows less impairment
is associated with reduced postoperative morbidity of microcirculation and a faster recovery of physiolo-
and lower mortality (0.5% versus 1.7%; p = 0.02) in gic flow compared with conventional flow. At least in
coronary surgery when compared to conventional low-risk coronary surgery, this seems to translate into
CPB. A large network analysis including 22,778 improved organ protection and clinical outcomes
patients showed that MiECC and OPCABG reduce appear to be better than those of patients operated
the odds of 30-day all-cause-mortality, and particu- on using conventional CPB (see Figure 8.5). 77
larly stroke, new onset atrial fibrillation and renal Some teams have introduced the term “optimized
dysfunction, over CABG done on conventional CPB. ECC” (opECC), representing a shift from conventional

Figure 8.5 Schematic representation of the pathophysiologic pathway that leads from preserved microcirculation to improved clinical
outcome with MiECC use.
CPB to advanced perfusion circuits. This trend high-

lights the change in mindset that MiECC has offered to The success of MiECC depends on the engagement of
perfusion, leading perfusionists to improve CPB tech- all three stakeholders of the cardiac surgical team in
nology. An opECC circuit often follows a custom-made order to obtain the maximum benefit. Combining a
design, incorporating relatively easy-to-make changes, multidisciplinary strategy with technological advances
such as using short tubing with biocompatible surfaces, has the potential to make MiECC a “therapy” for
centrifugal pumps, low prime oxygenators and assisted cardiac surgery. The evidence is not strong enough
venous drainage. They might not reach the efficacy of a at present, but it could at some point in the future
MiECC system but are a step toward more physiological replace conventional CPB and become standard prac-
perfusion becoming global practice. tice in cardiac surgery.
Suggested Further Reading 3. Anastasiadis K, Murkin J,

Antonitsis P et al. Use of
minimally invasive extracorporeal
circulation systems; can they
1. D’ Agostino RS, Jacobs JP, minimal invasive extracorporeal become the standard practice
Badhwar V et al. The Society circulation in cardiac surgery: for performing cardiac
of Thoracic Surgeons adult principles, definitions and surgery? Perfusion
cardiac surgery database: potential benefits. A position 2015;30:195–200.
2019 update on outcomes and paper from the Minimal
quality. Ann Thorac Surg 5. Anastasiadis K, Antonitsis P,
Invasive Extra-Corporeal Asteriou C et al. Quantification of
2019;107:24–32. Technologies International operational learning in minimal
2. Benedetto U, Puskas J, Kappetein Society (MiECTiS). Interact invasive extracorporeal
AP et al. Off-Pump versus on- Cardiovasc Thorac Surg circulation. Artif Organs
pump bypass surgery for left 2016;22:647–662. 2017;41:628–636.
main coronary artery disease. 4. Anastasiadis K, Antonitsis P,
J Am Coll Cardiol 6. Alexander Wahba, Milan
78 Argiriadou H et al. Modular Milojevic, Christa Boer et al.
2019;74:729–740.

EACTS/EACTA/EBCP 8. Benedetto U, Angeloni E, Refice S comprehensive Bayesian-

Committee Reviewers, 2019 et al. Is minimized extracorporeal framework network meta-analysis
EACTS/EACTA/EBCP circulation effective to reduce the of 134 randomized controlled
guidelines on cardiopulmonary need for red blood cell transfusion trials involving 22 778 patients.
bypass in adult cardiac surgery, in coronary artery bypass Eur J Cardiothorac Surg
European Journal of Cardio- grafting? Meta-analysis of 2016;49:1428–1440.
Thoracic Surgery, 2020;57(2): randomized controlled trials. 10. Donndorf P, Kuhn F, Vollmar B
210–251. J Thorac Cardiovasc Surg et al. Comparing microvascular
7. Anastasiadis K, Antonitsis P, 2009;38:1450–1453. alterations during minimal
Haidich AB et al. Use of minimal 9. Kowalewski M, Pawliszak W, extracorporeal circulation and
extracorporeal circulation Raffa GM et al. Safety and efficacy conventional cardiopulmonary
improves outcome after heart of miniaturized extracorporeal bypass in coronary artery bypass
surgery; a systematic review and circulation when compared with graft surgery: a prospective,
meta-analysis of randomized off-pump and conventional randomized study. J Thorac
controlled trials. Int J Cardiol coronary artery bypass grafting: Cardiovasc Surg
2013;164:158–169. evidence synthesis from a 2012;144:677–683.
79

Chapter
Considerations for Operations Involving
9 Deep Hypothermic Circulatory Arrest

Pingping Song and Joseph E Arrowsmith
The technique of core cooling (<28°C) and complete autonomic, endocrine, extrapyramidal and adaptive
cessation of blood flow is termed “deep hypothermic behavioral mechanisms to maintain core body tem-
circulatory arrest” (DHCA). This concept arose from perature. Hypothermia – defined as a core tempera-
two overlapping eras in the evolution of modern ture <35°C – occurs when heat losses overwhelm
cardiac surgery: a brief period in the early 1950s when thermoregulatory mechanisms (e.g. cold immersion)
“cold immersion” hypothermia, introduced by or when thermoregulation is impaired by disease or
William Bigelow, was used as the sole method for drugs. Thanks to experiences gained in the manage-
organ protection, and the current epoch of CPB ment of accidents, the physiological effects of hypo-
heralded by John Gibbon and colleagues in 1953. thermia are well understood (see Table 9.2).
Although CPB-induced hypothermia and DHCA for
the management of aortic arch pathology was Preoperative Considerations
described in the 1960s, it was not until the mid-
1970s that DHCA became established as a safe and Preoperative Assessment
relatively simple technique for aortic arch surgery. DHCA is often used in the context of emergency
Nowadays DHCA, either alone or in combination surgery (e.g. acute type A aortic dissection) and it
with other perfusion strategies, has become the main- may not be possible to undertake the usual battery
stay of vital organ protection for a variety of patholo- of “routine” preoperative investigations. Significant
gies and surgical procedures that necessitate the comorbidities, such as coronary artery and cerebro-
complete cessation of blood flow. vascular disease, diabetes mellitus and renal insuffi-
DHCA provides a near bloodless operating field, ciency, should be anticipated on the basis of the
albeit of limited duration, while ameliorating the clinical history, if available. With aortopathy (aortic
major adverse consequences of vital organ ischemia. dissection or aneurysm), special attention needs to be
Cooling of the brain – the organ at greatest ischemic paid to the presence of aortic valve pathology, medi-
risk – reduces cerebral metabolic rate, extending the astinal mass effect, cardiac tamponade and signs of
period of “safe” ischemia from 3 to 4 minutes at end-organ malperfusion.
normothermia to >20 minutes.
Monitoring Considerations
Indications Standard arterial, central venous and peripheral
In addition to being used to facilitate cardiac and venous access is required in all cases. The choice of
thoracic aortic surgery, DHCA is used in a number site(s) for arterial pressure monitoring should be
of pulmonary vascular, urological and neurologic tailored to both the pathology and the surgical can-
procedures (see Table 9.1). nulation strategy. Catheterization of the right radial
artery and either a femoral artery or the left radial
Pathophysiology artery permits arterial pressure monitoring proximal
In homeotherms, body temperature is maintained and distal to the aortic arch.
within a tight range as a result of the dynamic balance The right radial arterial catheter permits monitor-
between heat production and heat loss. Stimulation of ing of cerebral perfusion pressure if antegrade cere-
peripheral cold receptors and temperature sensitive bral perfusion (ACP) via the right axillary or
80 innominate artery cannulation is used. In this case
hypothalamic neurons activates sympathetic

Chapter 9: Considerations for Operations Involving Deep Hypothermic Circulatory Arrest
Table 9.1. Clinical applications of deep hypothermic (TEE). In situations where sternotomy or ascending
circulatory arrest
aortic cannulation pose a high risk of injury to the
Cardiothoracic Aortic arch surgery major vessels or cardiac chambers (such as type
surgery Descending thoracic aortic aneurysm A aortic dissection or re-entry sternotomy), femoral
(DTAA) and thoracoabdominal or right axillary arterial cannulation may initially be
aortic aneurysm (TAAA) repair necessary in combination with femoral venous can-
Pulmonary thromboendarterectomy nulation. Femoro-femoral or axillo-femoral CPB per-
(PTE) mits systemic cooling prior to sternotomy and affords
Complex congenital cardiac a degree of organ protection should chest opening be
reconstructions
accompanied by exsanguination secondary to inad-
Re-entry sternotomy with high risk of
cardiovascular injury
vertent injury to the aorta or the heart. After comple-
tion of the distal aortic repair, placement of the
Neurosurgery Cerebral tumor resection arterial cannula directly into the prosthetic graft or
Basilar artery aneurysm surgery into a sidearm permits restoration of anterograde
Intracranial arteriovenous
flow (Figure 9.1). Femoral arterial cannulation should
malformation resection
be avoided in patients with significant thoracic aortic
Other Resection of mass or tumor with disease to reduce the risk of atheroembolism associ-
atriocaval extension (e.g. renal cell ated with retrograde blood flow.
carcinoma) If ACP is planned, cerebral perfusion can be initi-
Head and neck vessel surgery
ated easily by inserting balloon catheters into the
brachiocephalic and left common carotid arteries
(Figure 9.2).
additional left radial or femoral arterial monitoring is
required because the arterial pressure is interrupted Venous Cannulation
during axillary artery cannulation. Also, the pressure The choice of venous drainage site and cannula type is
measured from the right radial artery is likely to largely dictated by surgical preference and the degree
overestimate systemic perfusion pressure in this set- of access required. Venous cannulae can be placed in
ting. Peripheral venous access should be sited in the the right atrium (RA), a femoral vein or both venae
right arm if division of the left innominate vein (to cavae. In situations where sternotomy carries high
improve surgical access to aortic arch and epiaortic risk of injury to the major vessels or heart, femoral
vessels) is anticipated. venous cannulation is preferable. Bicaval cannulation
Temperature monitoring at two or more sites is is chosen if retrograde cerebral perfusion (RCP) is to
recommended. In most cases, nasopharyngeal or tym- be used with reversal of blood flow in the superior
panic membrane monitoring provides an indication vena cava (SVC). If selective anterograde cerebral
of brain temperature while bladder or rectal monitor- perfusion (SACP) is to be used with cannulation of
ing provides an indication of core temperature. the carotid arteries, adequate cerebral venous drain-
age must be ensured. Again, bicaval cannulation is
preferred to optimize cerebral perfusion pressure and
Surgical Considerations prevent cerebral edema. Removal of a renal or adrenal
Arterial Cannulation tumor extending to the inferior vena cava (IVC) and
RA requires the use of a Ross atrial basket in prefer-
In the context of CPB with DHCA, the three most
ence to bicaval or standard two-stage cannulation to
common sites for arterial cannulation are: ascending
permit full visualization of the cava and to prevent
aorta, right axillary artery and femoral artery. The
tumor embolization into the lungs.
optimal cannulation site is dictated by both the dis-
ease and the goals of surgical reconstruction. In cases
of aortic dissection where cannulation of the Descending Thoracic Aortic Surgery
ascending aorta or a femoral artery is used, perfusion With the development of percutaneously delivered
of the true lumen must be confirmed with epiaortic endovascular stent-grafts, open operations on the des-
81
ultrasound or transesophageal echocardiography cending thoracic aorta have become rare. When

Table 9.2. Physiological effects of hypothermia
Mild (33–35°C) Severe (<28°C)

Neurologic Confusion Depressed consciousness
Amnesia Pupillary dilatation
Apathy – delayed anesthetic recovery Coma
Impaired cognitive function Loss of autoregulation
Neuromuscular Shivering Muscle & joint stiffening
Ataxia Muscle rigor
Dysarthria
Cardiovascular Tachycardia Severe bradycardia
Vasoconstriction Increased SVR, reduced CO
Increased BP, CO ECG changes: J (Osborn) waves, widening of QRS
complex, prolongation of QT interval,
ST changes, T wave inversion,
A-V block.
VF ! Asystole
Respiratory Tachypnea Bradypnea
Left shift Hb-O2 dissociation curve Bronchospasm
Further left shift HbO2 curve
Renal ADH resistance Reduced GFR
Metabolic Cold-induced diuresis Reduced H+ & glucose reabsorption
Reduced drug metabolism Metabolic (lactic) acidosis
Gastrointestinal Ileus
Gastric ulcers
Hepatic dysfunction
Hematology Increased blood viscosity & hemoconcentration Coagulopathy – inhibition of intrinsic/extrinsic
Immunological (2% increase in hematocrit per Celsius drop in pathway enzymes, platelet activation,
temperature) thrombocytopenia (splenic sequestration)
Increased infection risk Leukocyte depletion, impaired neutrophil
function & bacterial phagocytosis
necessary, though, they can be challenging for the entire of ischemic complications. Partial left heart bypass
team. During surgery for descending thoracic aortic (LHB) provides distal aortic perfusion and unloads
aneurysm (DTAA) and thoracoabdominal aortic the left ventricle during aortic occlusion. Evidence
aneurysm (TAAA), when the aneurysmal anatomy pre- suggests that LHB reduces mortality, neurologic
cludes safe cross clamping of the proximal aorta, DHCA injury and the need for postoperative renal replace-
with CPB is necessary for surgical repair and organ ment therapy. LHB is achieved by establishing bypass
protection. The standard surgical approach is via left from left atrium or left inferior pulmonary vein to a
thoracotomy, although this limits access to the heart femoral artery or the descending aorta distal to the
and great vessels. CPB is usually established via femoral aortic cross clamp via an in-line centrifugal pump (see
arterial cannula and a long, fenestrated femoral venous Chapter 13 for more detail).
cannula advanced into the RA during TEE guidance.
The proximal aortic anastomosis is carried out during
DHCA with the aorta open. Perfusion Considerations
When the proximal aorta can be safely clamped,
disruption of distal organ perfusion (spinal cord and Extracorporeal Circulation
82 abdominal viscera) during the proximal aortic anas- DHCA may require modifications to the standard
tomosis contributes significantly to the development CPB setup:

Figure 9.1 Branched arch graft for total arch replacement. After
completion of the distal aortic repair, placement of the arterial
cannula into a sidearm of the graft permits restoration of
anterograde flow. See also the cannulated and snared head and
neck vessels for antegrade cerebral perfusion. (From Brown CR, Bavaria
JE, Desai ND. Ascending and Arch Aortic Aneurysms. In Cohn LH, Adams DH
(Eds.) Cardiac Surgery in the Adult (5th ed.) 2016. New York: McGraw-Hill.
Reproduced with kind permission from McGraw-Hill.)
Figure 9.2 Fully implanted “Frozen Elephant Trunk” aortic arch

Incorporation of a hemofilter to permit graft. Note the cut and oversewn sidearm used for central
hemoconcentration or ultrafiltration aortic perfusion. (Reproduced with kind permission from Terumo.)
during rewarming.
Arteriovenous bypass and accessory arterial lines
to permit adjunct cerebral or cardiac perfusion
strategies (see below). Hemodilution
Standard blood collection bags (citrate phosphate Vasoconstriction, increased plasma viscosity and
dextrose adenine, CPDA-1) to facilitate
reduced erythrocyte plasticity secondary to hypother-
normovolemic hemodilution (see below).
mia lead to impairment of the microcirculation and
Selection of a cardiotomy reservoir of sufficient to tissue ischemia. Acute normovolemic hemodilu-
capacity to accommodate the circulating volume tion (ANH) theoretically mitigates against these
during exsanguination immediately before adverse effects while ensuring adequate tissue oxygen
DHCA. A second reservoir may be required for delivery during hypothermia. Hypothermia reduces
patients with large circulating blood volume. oxygen consumption, permitting perfusion with a
Some centers: hematocrit (Hct) of 0.18–0.22 at 26–28°C. As yet,
○ advocate the use of a centrifugal pump – in there is insufficient evidence to support an “optimal”
preference to a roller pump – to reduce Hct during hypothermic CPB and DHCA.
damage to blood cells and reduce hemolysis. The patient is placed “head down” while 1–4
○ incorporate leukocyte depleting arterial line “units” of venous blood are drained into standard
filters to reduce the inflammatory response to CPDA-1 blood collection bags. Not infrequently, a
vasoconstrictor is required to maintain systemic
83
CPB, reperfusion injury and postoperative
infective complications. blood pressure during this period. The timing of

Table 9.3. Summary of STS/SCA/AmSECT temperature temperature during the period of DHCA. Vasoactive
management guidelines
drugs are used as required to maintain a mean arterial
Oxygenator arterial outlet blood temperature is pressure (MAP) of 50–60 mmHg. The onset of
recommended as a surrogate for cerebral temperature hypothermia-induced ventricular fibrillation (VF)
It should be assumed that the oxygenator arterial outlet
signals the need for either application of an aortic
blood temperature underestimates cerebral perfusate cross clamp (AXC) and administration of cardiople-
temperature during rewarming gia, or more commonly, insertion of a vent to prevent
left ventricular distension. As much of the planned
Arterial outlet blood temperature should be limited to
surgical procedure as possible (e.g. surgical dissection
<37°C to avoid cerebral hyperthermia
and preparation of any prosthetic grafts) should be
The temperature gradient between arterial outlet and carried out during cooling to minimize the duration
venous inflow on the oxygenator during CPB cooling of DHCA.
should not exceed 10°C to avoid generation of The neurophysiologic endpoint of cerebral
gaseous emboli
cooling is electrocortical silence on the electroenceph-
The temperature gradient between arterial outlet and alogram (EEG). Other generally accepted endpoints
venous inflow on the oxygenator during CPB that ensure sufficient cerebral metabolic protection
rewarming should not exceed 10°C to avoid include a nasopharyngeal temperature of 18–25°C,
outgassing when blood is returned to the patient equilibration of brain and core temperatures at the
Pulmonary artery or nasopharyngeal temperature target temperature for 10–15 minutes and jugular
monitoring may be used during weaning from CPB venous oxygen saturation (SJVO2) >95%. Cutaneous
and in the early postoperative period Near Infrared Spectroscopy (NIRS) sensors applied to
It is reasonable to maintain an outflow-inflow gradient the patient’s forehead are used to measure oxygen
4°C and a rewarming rate 0.5°C/min when the saturation in the frontal lobes. Although NIRS pene-
oxygenator arterial outlet temperature is 30°C tration depth is limited and the area measured is
during rewarming necessarily small, it provides a guide to cerebral
It is reasonable to maintain an outflow-inflow gradient oxygen delivery. Most centers aim to maintain NIRS
10°C when the oxygenator arterial outlet within 20% of baseline after induction of anesthesia
temperature is 30°C during rewarming or 50%. Sustained low cerebral oxygen saturation
There is insufficient evidence to determine the optimal
should prompt swift intervention, such as antegrade
temperature for weaning from CPB or retrograde cerebral perfusion. It is important to
note that relying solely on any one of these individual
measures may not be sufficient to ensure adequate
cerebral metabolic suppression. In one published
ANH varies from center to center: in some, blood is
report it was noted that electrocortical silence at a
removed after induction of anesthesia and before
nasopharyngeal temperature of 18°C was not
heparinization, whereas in others, heparinized blood
achieved in around half of the patients studied. This
is removed immediately before the onset of CPB.
emphasizes the need to evaluate all available monitor-
ing parameters, including core and brain tempera-
Temperature Management tures, EEG, evoked potentials, NIRS and SJVO2
The most recent guidelines on temperature manage- before initiating DHCA. (See Chapter 18 for more
ment during CPB were developed jointly by the detail.)
Society of Thoracic Surgeons (STS), the Society of Circulatory arrest: The operating table is placed
Cardiovascular Anesthesiologists (SCA) and the in a slightly head-down position, CPB is stopped and
American Society of Extracorporeal Technology the patient is exsanguinated into the venous reservoir.
(AmSECT). They are summarized in Table 9.3. Once isolated from the patient, blood within the
Cooling: CPB is typically instituted with a con- extracorporeal circuit is recirculated via a shunt
stant flow rate of 2.2–2.4 l/min/m2 and active cooling between the arterial and venous lines in order to
immediately commenced. The application of external prevent stagnation and clotting. The surgical repair
84 ice packs or a cooling cap to the head may augment proceeds with heed to the duration of circulatory
cerebral cooling and help avoid a rise in intracranial arrest. As the intravenous administration of drugs

during DHCA is at best pointless and at worst poten- During the period of rewarming attention should
tially dangerous, all infusions should be discontinued be given to the correction of metabolic abnormalities,
when the CPB pump is switched off. particularly the metabolic (lactic) acidosis that inevit-
Removal of the aortic cross clamp and opening the ably accompanies reperfusion following circulatory
aorta to the atmosphere exposes both the coronary and arrest. Blood lactate concentration increases gradually
cerebral arteries to the risk of air embolism. At the end after the onset of reperfusion and peaks approxi-
of DHCA therefore, adequate de-airing and measures mately six hours after DHCA. A higher hematocrit
such as head-down tilt or flooding the surgical field is desirable during rewarming due to the increased
with crystalloid at 4°C should be undertaken. oxygen carrying capacity and free radical scavenging
Rewarming: This is a critical phase of CPB, effect. Autologous blood, removed prior to CPB, is
during which cerebral injury may be caused or gradually returned to the cardiotomy reservoir during
exacerbated. Infusions of anesthetic drugs should be rewarming to meet the demands of the rising meta-
restarted as soon as the circulation is restored to avoid bolic rate.
inadvertent awareness during rewarming. Following
the reinstitution of CPB, rewarming is typically Acid–Base Management
delayed for approximately 10 minutes. This practice,
There are two strategies to manage blood gases during
known as “cold reperfusion,” has been shown to
DHCA – pH-stat and α-stat. The concept is explained
reduce reperfusion injury in both animal and human
in detail in Chapter 10. In neonates undergoing
studies. The rewarming process is then initiated while
DHCA for repair of congenital heart defects, pH-stat
maintaining the temperature gradient between the
management prior to DHCA appears to be associated
venous inlet and arterial outlet 10°C. Above 30°C,
with fewer complications than α-stat management
this gradient should be 4°C. Rewarming should
and better developmental outcome. Most institutions
proceed slowly, with the rate of temperature rise
use α-stat during DHCA in adult patients. On theor-
limited to no more than 0.5°C/min to avoid exacer-
etical grounds, using pH-stat during cooling and α-
bating any adverse neurological outcome. Excessively
stat during rewarming (the so-called crossover man-
rapid rewarming tends to produce a large core-
agement) has some appeal and is used in some
peripheral temperature gradient, which risks signifi-
centers.
cant “after-drop” following separation from CPB. The
arterial outflow temperature should not exceed 37°C
at any time to avoid cerebral hyperthermia. Glucose Management
Sites typically used for temperature monitoring Insulin resistance and hyperglycemia are common
include the bladder, nasopharynx, tympanic mem- during hypothermic CPB and DHCA. The STS rec-
brane (ear canal) and blood (via the thermistor in ommends that the blood glucose concentration
the PA catheter), as well as the arterial outlet and should be maintained at <10 mmol/l (180 mg/dl) to
venous inlet. Cranial temperature monitoring, using reduce mortality and infectious complications. Tight
a jugular bulb catheter, should be considered a glycemic control during cardiac surgery with or with-
research modality not used in routine clinical care. out DHCA has yet to be proven to offer any neuro-
Although accurate at “steady-state,” studies have protective effect. Where an infusion of insulin is used,
demonstrated that temperature monitoring at extra- the blood glucose concentration should not be
cranial sites tends to lag behind and underestimate allowed to fall below 4.5–6.0 mmol/l (80–110 mg/dl).
jugular bulb blood temperature during rewarming.
Urinary bladder or rectal temperature is considered
to be “core” temperature and used to monitor the Blood Conservation
equilibrium between the blood and peripheral Prolonged CPB and hypothermia produce a coagulo-
tissue temperature. Although there is no agreement pathy secondary to inhibition of intrinsic and extrin-
on the optimal temperature for separation from CPB, sic pathway enzymes, platelet activation and splenic
the typical core body (bladder or rectal) temperature platelet sequestration. Blood conservation is facili-
range is 35.5–36.5°C; the gradient between core tated by meticulous surgery, the use of autologous
and peripheral temperatures should be <5°C at that blood and the administration of allogenic blood com-
ponents guided by the results of point-of-care and
85
point.

laboratory tests of coagulation. In the 2011 update to of the circulatory arrest period that is considered to be
the STS and SCA Blood Conservation Clinical safe. Clinical studies in adults undergoing DHCA
Practice Guidelines, antifibrinolytic agents (e.g., tra- suggest that a safe period of arrest is roughly 20 min-
nexamic acid and ε-aminocaproic acid) are strongly utes at 20°C and 45 minutes at 10°C. Neurologic
recommended (Class IA evidence) for blood conser- complications increase when the duration of DHCA
vation during cardiac surgery. alone without any adjunct cerebral perfusion exceeds
Following publication of the BART study in 2008, 40 minutes. Combining the findings of several studies
the routine use of aprotinin in cardiac surgery effect- of neurologic deficit after DHCA, an arrest time of
ively ceased. In recent years – in territories outside 20 minutes should be considered the maximum toler-
North America – there has been a resurgence of able period of brain ischemia if using DHCA alone
interest in the use of aprotinin in cardiac surgery. (i.e., bladder temperature 18°C or nasopharyngeal
Results following the reintroduction of the drug are temperature 15°C). Certain patient risk factors (e.g.,
eagerly awaited. advanced age, history of stroke, severe atherosclerotic
disease) confer a lower margin of safety. The applica-
Neuroprotection during DHCA tion of external ice packs or a cooling cap to the head
delays brain rewarming during DHCA.
Hypothermia is the principle neuroprotectant during
circulatory arrest. Surgical maneuvers, such as inter-
mittent cerebral perfusion, selective ACP and RCP, Pharmacological Neuroprotection
may also be used to protect the brain and extend the At present no drug is specifically licensed for neuro-
operating time available to the surgeon. protection during cardiac surgery. Over the last four
decades a wide variety of compounds, many with very
Hypothermia Alone promising pre-clinical pharmacological profiles, have
been evaluated for cardiac surgery. These include
Cerebral metabolism decreases by 6–7% for every 1°C
anesthetic agents (barbiturates, propofol, volatile
fall in temperature below 37°C, with consciousness
agents), calcium channel blockers, immunomulators
and autoregulation being lost at 30°C and 25°C
(corticosteroids, cyclosporin), amino acid receptor
respectively. At 18°C, the cerebral metabolic rate for
antagonists (magnesium, remacemide), glutamate-
oxygen (CMRO2) is about 17–30% of that at nor-
release inhibitors (lidocaine, fosphenytoin), antipro-
mothermia and the ischemic tolerance is around
teases (aprotinin, nafamostat) and free radical scaven-
10 times that at normothermia (see Table 9.4).
gers (mannitol, desferrioxamine, allopurinol).
Hypothermia alone provides the simplest form of
Unfortunately none of these agents has demonstrated
neuroprotection. The main concern is the duration
clinical efficacy (see Chapter 18 for more detail). The
observation that thiopental reduces CMRO2 was long
Table 9.4. Calculated maximum duration of hypothermic used as the rationale for its administration during
circulatory arrest cardiac surgery or immediately before the onset of
Temperature Cerebral Maximum DHCA. Although a handful of small studies have
(°C) Metabolic Duration of HCA suggested reduced operative mortality, any beneficial
Rate (minutes) impact on neurologic outcome has not been demon-
(% of strated. Thiopental is no longer available in the USA
baseline) as production ceased in 2011.
37 100 5
30 56 (52–60) 9 (8–10) Cerebral Perfusion Strategies
25 37 (33–42) 14 (12–15) Intermittent Cerebral Perfusion
20 24 (21–29) 21 (17–24) Intermittent systemic perfusion punctuated by periods
15 16 (13–20) 31 (25–38) of DHCA lasting 20 minutes has been used as an
alternative strategy to prolong the total cumulative dur-
10 11 (8–14) 45 (36–62)
86 ation of DHCA. A common application of this tech-
nique is during pulmonary thromboendarterectomy

(PTE). It is suggested that 10 minute periods of inter-

mittent reperfusion preserve neurologic function by
replenishing cerebral high-energy phosphates and
removing accumulated waste products. NIRS can be
used to guide the durations of DHCA and reperfusion
(see neurologic monitoring below).
Selective Antegrade Cerebral

Perfusion (SACP)
This technique involves direct cannulation of the
innominate, axillary or carotid arteries. SACP can be
carried out in either a bilateral or unilateral approach.
Bilateral SACP involves direct cannulation of both
common carotid arteries or insertion of perfusion
cannulae into the ostia of the innominate and left
carotid arteries via the open arch at time of DHCA
(see Figure 9.1). Unilateral SACP is achieved using
right axillary artery cannulation and occlusion of the
innominate and left carotid arteries and relies on an
intact circle of Willis. Oxygenated blood is pumped
via a separate arterial line at 8–12 ml/kg/min to main-
tain a perfusion pressure of 50–70 mmHg – measured
in the ipsilateral radial artery or in a pressure trans-
ducer at the end of the cannula. Although SACP Figure 9.3 Retrograde cerebral perfusion (RCP) established via
permits surgery to be conducted at lesser degrees of cannula in the superior vena cava (SVC) which is looped into the CPB
circuit via a Y-connector. IVC, inferior vena cava
systemic hypothermia (e.g., 22–25°C), it often
requires greater mobilization of the epiaortic vessels
and division of the innominate vein. In addition to substrate delivery provided by RCP are poorly
increasing complexity and crowding the surgical field defined but are unlikely to fulfill the metabolic
with cannulae, SACP is accompanied by the risk of demands of the brain even under deep hypothermia.
cerebral embolization from manipulation of the Suggested blood flow rates for RCP are 200–300 ml/
epiaortic vessels. min with SVC pressure <25 mmHg to prevent cere-
bral edema. SVC pressure is typically monitored via
the side-port of the introducer sheath in the internal
Retrograde Cerebral Perfusion (RCP) jugular vein.
This technique relies on the fact that cerebral veins Theoretical advantages of RCP include:
have no valves and involves the continuous admin-
istration of cold (10–15°C) oxygenated blood via an more homogenous brain cooling
SVC cannula (see Figure 9.3). Blood flow to the washout of embolic material (gaseous and
brain is most likely to occur via the azygos veins particulate) and metabolic waste products
because the internal jugular veins possess valves. prevention of cerebral blood cell microaggregates
The azygos vein has connections to the vertebral fewer thromboembolic events by avoidance of
venous system and the venous plexus of the foramen epiaortic vessel manipulation.
magnum and intracranial sinuses. Massive shunting The prolongation of safe DHCA that can be achieved
via the superficial and deep venous systems, includ- with RCP is less than that with SACP. RCP for >60
ing the internal and external jugular veins, may minutes is a significant predictor of permanent
result in only a small fraction of the blood entering neurologic dysfunction.
the SVC actually reaching the cerebral arteries. For There is currently no expert consensus on which 87
these reasons the exact levels of CBF and metabolic cerebral protection strategy (DHCA alone, DHCA

with SACP, DHCA with RCP) is superior. There have significant cost and lack of level 1A evidence of effi-
been few prospective, randomized trials and the cacy, neurologic monitoring has yet to be universally
majority of published studies comparing these adopted as “standard of care.”
approaches have been retrospective. The conclusions Near infrared spectroscopy (NIRS) allows non-
from the available literature are that: invasive measurement of regional cerebral oxygen
an adjunct form of cerebral protection (SACP or saturation (rSO2). An abrupt bilateral decrease in
RCP) is superior to DHCA alone rSO2 (>20% below the baseline value) may indicate
the method of cerebral perfusion – SACP vs global cerebral ischemia; a significant unilateral
RCP – has no impact on the incidence of decrease of rSO2 may suggest regional compromise
postoperative stroke or permanent neurologic of cerebral perfusion or an embolic event. Both situ-
dysfunction ations must be communicated to the surgeon and
SACP reduces the incidence of temporary perfusionist immediately, prompting interventions
neurologic dysfunction (delirium, confusion, to improve cerebral oxygen delivery. A decrease of
prolonged obtundation without focal deficits or rSO2 >20% from baseline or an absolute rSO2 <50%
radiographic signs of structural brain have been reported to be clinically significant.
abnormalities) compared to RCP. Simplicity and relatively low cost mean that cerebral
NIRS is the most widely used adjunct to routine
A randomized study of DHCA alone versus clinical monitoring.
DHCA with SACP in patients undergoing PTE Measuring venous oxygen saturation at the jugu-
found no difference in postoperative cognitive lar bulb (SJVO2) using a fiberoptic catheter provides a
dysfunction. continuous measure of the global balance between
cerebral oxygen supply and demand. Catheters need
Neurologic Monitoring placing under fluoroscopy and only very few centers
Neurologic monitoring can be considered in three use this modality routinely. Low SJVO2 prior to the
categories: routine clinical observation, monitors of onset of DHCA is associated with adverse neurologic
cerebral substrate delivery and monitors of cerebral outcome. SJVO2 monitoring may also be used to
activity (see Table 9.5). For a monitor to be useful it monitor the adequacy of SACP.
must prompt a corrective intervention before the Transcranial Doppler (TCD) sonography of the
onset of irreversible neurologic injury. Due to their middle cerebral arteries is largely an investigational
technique used to measure CBF velocity (a surrogate
Table 9.5. Neurologic monitoring measure of CBF) and as a means for detecting and
quantifying cerebral microemboli (gaseous and par-
Clinical Arterial pressure
ticulate). Finding acoustic windows in the temporal
Central venous pressure
region of the skull and maintaining probe position are
CPB pump flow rate
Arterial oxygen saturation notoriously difficult. TCD is of limited use during
Hemoglobin concentration DHCA, although it has been used to assess CBF
Arterial PCO 2 during SACP and RCP.
Temperature Chapter 18 provides more in depth discussion of
Pupil size neurologic monitoring.
Substrate delivery Transcranial Doppler sonography
Near infrared spectroscopy
Jugular venous oxygen
Spinal Cord Protection
saturation Surgery involving the descending thoracic aorta may
interrupt blood flow to the spinal cord via the anterior
Cerebral activity Electroencephalography
spinal artery (of Adamkiewicz) and cause paraplegia –
Somatosensory evoked
potentials a devastating complication that occurs in as many as
Auditory evoked potentials one in six cases. Risk factors include the extent and
Motor evoked potentials severity of aortic atheroma, longer duration of AXC
88 application, emergency surgery, previous surgery to
the distal aorta, perioperative hypotension, advanced

age and diabetes mellitus. Besides hypothermia,

the interventions thought to reduce the risk of spinal
cord injury include sequential clamping of the aorta
with re-implantation of intercostal and lumbar seg-
mental vessels, LHB to provide distal perfusion, cere-
brospinal fluid (CSF) drainage and neurophysiologic
monitoring.
Cerebrospinal Fluid Drainage

The production of cerebrospinal fluid (CSF) increases
during ischemia, leading to increased intrathecal pres-
sure soon after the aortic cross clamp is applied.
Spinal cord perfusion pressure (SCPP) is the differ-
ence between MAP and intrathecal pressure (ITP).
Typically, during thoracoabdominal aortic surgery
the SCPP is maintained at 70 mmHg (i.e., MAP
>80 mmHg and ITP <10 mmHg). Maintaining
MAP at a level higher than is usual during conven-
tional cardiac surgery may require a vasopressor infu-
sion, and intermittent CSF drainage may be required
to maintain ITP <10 mmHg.
Both randomized trials and meta-analyses have
demonstrated that CSF drainage reduces the incidence
of paraplegia after open thoracic aortic surgery. It is Figure 9.4 Lumbar cerebrospinal fluid drainage system with CSF
recommended in all patients at high risk for spinal collection bag. Pressure can either be transduced onto the
anesthetic monitoring system or can be read on an analog scale. The
cord ischemia (Class IIa recommendation, level pressure transducer is zeroed at the level of the foramen magnum.
B evidence). In many centers a drainage catheter is
inserted into the intrathecal space at either the L3/4 or
The collection system should be mounted on a dedi-
L4/5 interspace. The catheter is connected to a closed
cated IV pole and the CSF drainage stopcock should
collection system which enables both ITP monitoring
be closed to the patient at all times except for the time
and removal of CSF when clinically indicated
of actively draining the CSF. The transducer should
(Figure 9.4). The risk of direct spinal cord or nerve
be “zeroed” at the level of foramen magnum or the
root damage at this level is small. The timing of cath-
catheter insertion site. During and immediately after
eter insertion is largely driven by institutional practice
surgery, CSF is allowed to drain passively from the
and concerns about bleeding during insertion (which
catheter to maintain an ITP of 8–10 mmHg. Once the
could progress to epidural hematoma with hepariniza-
patient is awake and neurologic signs of ischemia can
tion during the surgery) sufficient to warrant post-
be monitored, the ITP can be allowed to rise to 15–20
ponement or cancellation of surgery. Practice ranges
mmHg. CSF drainage should be limited to 20 ml/hr.
from insertion on the day before surgery to insertion
Rapid drainage of a large volume of CSF should be
immediately before induction of anesthesia. In some
avoided as an abrupt fall in intracranial pressure may
centers, however, a CSF catheter is placed after induc-
cause tearing of the subdural vessels and subarach-
tion of general anesthesia but before placement of all
noid hemorrhage.
invasive lines, which in most cases still allows for a
safety margin of at least one hour before systemic
heparinization. A CSF drainage catheter may also be Neurophysiologic Monitoring
inserted after surgery in lower risk patients who Motor evoked potential (MEP) monitoring is increas-
develop signs of spinal cord ischemia. ingly used to assess descending anterior spinal path-
The management of CSF drains varies between ways, thus providing a measure of the adequacy of
institutions. The following general principles apply: spinal cord perfusion and guiding the need for 89

selective re-implantation of key intercostal arteries. two 20-minute periods of DHCA. Cerebral perfusion
Profound neuromuscular blockade should be avoided adjuncts are not usually needed. RCP is not helpful
when attempting to use MEP monitoring. in PTE because it precludes a bloodless surgical field.
Somatosensory evoked potential (SSEP) monitor- In most cases, DHCA with intermittent systemic
ing provides a means of assessing the integrity and reperfusion is used in preference to SACP, with
function of ascending posterior sensory pathways. NIRS to guide the duration of circulatory arrest.
A fall in SSEP amplitude >50% from baseline A rSO2 of <40% is widely used as the acceptable
should prompt re-implantation of intercostal arteries minimum.
into the graft, along with measures to improve Complications of PTE include pulmonary artery
spinal cord perfusion, mainly increasing mean arterial rupture, reperfusion injury (reperfusion pulmonary
pressure and, where possible, SCPP. It should be edema) and right ventricular failure. The discovery
borne in mind, however, that hypothermia of frank blood in the endotracheal tube following
produces a progressive fall in SSEP signal amplitude separation from CPB typically indicates pulmonary
such that some components disappear between 24°C artery rupture. CPB should be reinstituted immedi-
and 17°C. ately to reduce pulmonary blood flow. Further
attempts to wean from CPB tend to be futile
whereas the institution of central veno-arterial extra-
corporeal membrane oxygenation (ECMO) is associ-
Pulmonary (Thrombo) ated with >50% survival to hospital discharge. By
endarterectomy (PTE) contrast, refractory hypoxia secondary to severe
The incidence of chronic thromboembolic pulmonary reperfusion injury is managed with veno-venous
hypertension (CTEPH) in patients surviving ECMO.
acute pulmonary embolism is up to 4%. Medical
therapy for CTEPH is limited and ultimately only
palliative. When the disease lies proximal enough to DHCA is an established and widely employed tech-
allow surgical excision, PTE offers both symptomatic nique for providing optimal operating conditions
and prognostic benefit as well as the potential to while preserving organ function. Most patients will
restore normal life expectancy. PTE has been shown tolerate 20 minutes of circulatory arrest at 20°C with-
to offer superior outcomes to lung transplantation out significant neurologic impairment. While hypo-
in the CTEPH population (95% one-year survival thermia is the main method of cerebral protection,
versus 85% in lung transplant). As the morbidity other neuroprotective strategies include pharmaco-
and mortality (~4%) associated with PTE have logical methods, tight glycemic control, hemodilu-
fallen, the indications for the procedure have tion, acid–base management, CSF drainage and
widened to include the elderly and younger neurologic monitoring.
patients with mild yet symptomatic pulmonary Surgical techniques such as SACP and intermit-
hypertension. tent reperfusion may be used to prolong the safe
The surgical setup involves bicaval and ascending duration of DHCA. The development of novel
aortic cannulation, and the use of a continuous flow branched vascular grafts allows surgeons to undertake
“cold jacket” placed behind the heart to augment repair of the aortic arch in stages, providing the
myocardial protection. To achieve maximal hemody- means to restore antegrade blood flow to the distal
namic improvement and optimal outcome, a com- aorta and cerebral circulation earlier in the surgical
plete endarterectomy to the distal tail ends of each procedure, and the opportunity to shorten the dur-
pulmonary arterial branch is essential. Due to the ation of CPB with safe, early rewarming.
large amount of bronchial circulation usually present Nevertheless, DHCA inevitably exposes patients to
in these patients, circulatory arrest is necessary to significantly prolonged CPB with all its associated
ensure a bloodless field to perform a thorough risks and adverse effects. Fastidious attention to tem-
endarterectomy. In experienced centers, bilateral perature management during both cooling and
endarterectomy on each side can be performed using rewarming is essential.
90

Suggested Further Reading of electrocerebral inactivity with

deep hypothermia. J Thorac
Anesth Analg 2019; 128(2):
265–277.
1. Arrowsmith JE, Ganugapenta MSSR. Cardiovasc Surg 2014; 147(3):
Intraoperative brain monitoring in 8. Steppan J, Hogue CW Jr. Cerebral
1002–1007. and tissue oximetry. Best Pract Res
cardiac surgery. In Bonser R, Pagano
D, Haverich A (Eds.). Brain 5. Krüger T, Hoffmann I, Blettner M Clin Anaesthesiol 2014; 28(4):
Protection in Cardiac Surgery. et al. Intraoperative 429–439.
London: Springer-Verlag. 2011. neuroprotective drugs without 9. Vuylsteke A, Sharples L, Charman
pp.83–111. beneficial effects? Results of the G et al. Circulatory arrest versus
German Registry for Acute Aortic cerebral perfusion during
2. Chan MJ, Chung T, Glassford NJ Dissection Type A (GERAADA).
et al. Near-Infrared spectroscopy pulmonary endarterectomy
Eur J Cardiothorac Surg 2013; 44 surgery (PEACOG): a randomized
in adult cardiac surgery patients: a (5): 939–946.
systematic review and meta- controlled trial. Lancet 2011; 378
analysis. J Cardiothorac Vasc 6. Misfeld M, Leontyev S, Borger (9800): 1379–1387.
Anesth. 2017; 31(4): 1155–1165. MA et al. What is the best strategy 10. Etz CD, Weigang E, Hartert M
for brain protection in patients et al.Contemporary spinal cord
3. Ghadimi K, Gutsche JT, Setegne SL undergoing aortic arch surgery?
et al. Severity and duration of protection during thoracic and
A single center experience of 636 thoracoabdominal aortic surgery
metabolic acidosis after deep patients. Ann Thorac Surg 2012;
hypothermic circulatory arrest for and endovascular aortic repair: a
93(5): 1502–1508. position paper of the vascular
thoracic aortic surgery.
J Cardiothorac Vasc Anesth 2015; 29 7. Scheeren TWL, Kuizenga MH, domain of the European
(6): 1432–1440. Maurer H et al. Association for Cardio-Thoracic
Electroencephalography and Surgery, European Journal of
4. James ML, Anderson MD, brain oxygenation monitoring in Cardio-Thoracic Surgery, 2015, 47
Swaminathan M et al. Predictors the perioperative period. (6): 943–957.
91

Chapter
Metabolic Management during
10 Cardiopulmonary Bypass
The metabolic management of patients on cardiopul- (venous drainage) while at the same time providing
monary bypass (CPB) is a complex process, involving adequate arterial pump blood flow with good oxygen-
several key biochemical and physiological parameters ator function. The perfusionist should be able to
essential to maintaining homeostasis and reducing achieve the necessary pump flow without constantly
morbidity and mortality associated with CPB and having to add fluid to the circuit or empty the venous
cardiac surgery. There is movement toward goal- reservoir. Sufficient venous drainage (assessed hemo-
directed perfusion (GDP), using indexed parameters dynamically by low central venous or pulmonary
such as carbon dioxide production, oxygen delivery pressure with a non pulsatile arterial pressure trace
and oxygen consumption to individualize perfusion and visually by the heart being relaxed and collapsed)
strategies. This chapter provides an overview over the is the essential starting point to optimizing metabolic
fundamental principles surrounding the metabolic management.
management of the patient on CPB.
Metabolic Markers during CPB
Cardiopulmonary Bypass and the Classic markers of adequate perfusion include achiev-
Challenges of Metabolic Management ing the calculated flow, target arterial pressure, satis-
factory blood gases and a normal mixed venous
The primary challenge for safe and effective extracor-
oxygen saturation (SvO2) as shown in Table 10.1.
poreal circulation is to maintain optimal metabolic
conditions for physiological homeostasis. CPB man-
agement must maintain systemic perfusion and CPB Blood Flow
physiological metabolic processes and must adapt to The desired pump flow rate during CPB is tradition-
the particular demands of each patient. CPB-induced ally determined according to body surface area (BSA)
challenges that must be accounted for to ensure opti- and temperature. At normothermia, an indexed flow
mal metabolic management and prevention of end- rate of 2.2–2.8 l/min/m2 is targeted by most clinical
organ dysfunction include: teams. For the obese patient (BMI > 30 kg/m2), the
– Non pulsatile flow and its distribution traditional target flow calculations may overestimate
– Hemodilution flow requirements and can be modified to more
– Altered hemodynamics and vascular tone closely represent the metabolic need based on lean
– Electrolyte shifts body mass. By setting a BMI of 28 kg/m2 and using
the patient height (m) to calculate mass (kg), a new
– Temperature changes and blood gas strategies
BSA can be derived, and a “lean” target flow calcu-
Any attempt at successful metabolic management lated (see sample calculation in Figure 10.1).
during CPB must address these challenges. Measuring oxygen delivery (DO2) as part of a
GDP strategy, in addition to standard metabolic and
oxygenation parameters, has been suggested as the
Effective Bypass and Circuit Design most accurate means of assessing the adequacy of
Optimizing metabolic management during CPB pump flow.
begins with the ability to achieve technically “good The majority of CPB is undertaken using a con-
bypass.” Good bypass is predicated upon the ability to tinuous flow. It is possible to use pulsatile flow by
92
decompress the venous system and empty the heart using specifically designed pumps or modifying

Chapter 10: Metabolic Management during Cardiopulmonary Bypass
standard pumps. A heterogeneity of literature exists either shown there to be no difference between con-
around this topic with some papers indicating that tinuous and pulsatile flow or the latter to be causing
pulsatile perfusion may reduce renal complications in hemolysis. Pulsatile flow is not a widely accepted
high-risk patients. More recent publications have practice.
Table 10.1. Standard adult CPB metabolic

Mean Arterial Pressure (MAP) during CPB
management parameters In analogy to the physiological circulation the pri-
mary determinants of MAP during CPB are:
Target Monitoring
pump flow and
Blood Flow 2.2–2.8 Centrifugal pump:
systemic vascular resistance.
Rate ultrasonic flow probe
C.I. (l/min/m2) distal to any shunts Ensuring an acceptable MAP during CPB is an
Roller pump: calculated important determinant in maintaining appropriate
from RPM/ultrasonic flow perfusion of vital end-organs, particularly the brain
probe distal to any shunts and kidneys, both of which rely on MAP across a
Mean Arterial 60–80 Arterial pressure transducer range of 35–100 mmHg during physiological flow to
Pressure maintain intrinsic autoregulation. Despite published
(mmHg) standards and prevailing clinical practice having
Arterial and “normal” *
Intermittent sampling from
established a MAP between 50 and 80 mmHg during
Venous circuit ports CPB as an acceptable range, the optimal MAP for
Blood Gases and/or real time in-line each individual patient is still subject to debate. It
sensors has been suggested that MAP during CPB should be
determined by the individual patient’s cerebral auto-
Hematocrit/ >24% Optical cell in venous line
Hemoglobin >8.0 g/dl of CPB circuit
regulation range (based on the preoperative MAP)
rather than universally set ranges. More recent studies
SvO2 (%) >75% Optical cell in venous line suggest a reduced incidence of stroke with higher
of CPB circuit (>70 mmHg) when compared to lower MAPs.
Urine Output >4 ml/ Catheter bag There are many reasons why blood pressure will
kg/ vary during CPB. Higher MAPs may result from
hour inadequate anesthesia/analgesia, systemic vasocon-
Blood Lactate <2.0 Intermittent sampling striction or catecholamine release and may require
mmol/l deepening of anesthesia or the addition of vasodila-
*
See Table 10.2. tors to correct. Conversely, and more commonly,
Traditional Calculation Lean Flow Calculation

Height = 173 cm Height = 173 cm
Weight = 125 kg Adjusted Weight = 28 kg/m2 x (1.73m)2 = 83.8 Kg
BMI = 41.8 Adjusted BMI = 28
BSA = 2.45 Adjusted BSA = 2.01
Target Flow (2.4 C.I) = 5.9 L/min Target “Lean” Flow (2.4 C.I) = 4.8 L/min
BMI = weight/height2
ℎ ℎ ℎ
BSA = 3600
Figure 10.1 Obese patient lean flow sample calculation.

93

Table 10.2. Typical blood gas parameters during CPB to see the success of an intervention in a timely
Circuit Arterial Circuit Venous
manner, which is a clear advantage of over intermit-
Blood Gas Blood Gas tent sampling.
pH 7.35–7.45 7.33–7.44
Acid-Base Balance
PaCO2 4.6–6.0 kPa 5.0–6.4 kPa
Acid-base balance during bypass is integral to the
35–45 mmHg 37.5–48 mmHg
maintenance of physiological homeostasis. Metabolic
PaO2 13–33 kPa >5.2 kPa derangement, particularly acidosis, often results from
100–250 mmHg >39 mmHg DO2/VO2 mismatch which can be corrected by
Oxygen >95% >75% methods described later in this chapter. The bicarbon-
saturations ate (HCO3) buffer system plays a vital role in main-
(SaO2) taining physiological pH. At times of significant
Bicarbonate 22–26 mEq/L 22–26 mEq/L metabolic acidosis during CPB, it becomes necessary
(HCO3-) (mmol/l) (mmol/l) to add HCO3 to correct a persistently low pH (< 7.2)
or a base excess lower than 5. The following simple
Base excess ‒2 to +2 ‒2 to +2
formula can be used to guide HCO3 administration
during CPB: [body weight (kg) 0.15] base defi-
cient = mmol NaHCO3. Care must be taken to avoid
the inherent consequences of the high sodium load
MAP may reduce during CPB. Common causes that comes with buffering. The use of hemofiltration
include increased anesthetic depth with hypothermia, may also correct an ongoing acidosis. It is important to
hemodilution, inflammatory response, ongoing sepsis consider the potential causes of ongoing metabolic
(e.g. endocarditis), perioperative antihypertensive acidosis rather than just correcting its sequela.
medication (particularly ACE inhibitors) and vaso-
plegic syndrome. Current literature supports the use
of alpha agonists, such as phenylephrine, as primary Hematocrit on CPB
vasopressors when treating low MAP on bypass (in Hematocrit (Hct) is an important determinant of
addition to addressing potential underlying causes). DO2. Hemodilution (and hence reduced Hct) is not
uncommon during CPB, particularly when using
Blood Gas Parameters asanguinous circuit prime. Importantly, Hct values
below the accepted range of 22–24% have been asso-
Blood gas management during CPB typically aims for
ciated with poor outcomes and increased morbidity
the ranges shown in Table 10.2. The air/oxygen
and mortality; conversely, excessive increases in the
blender allows titration of both the inspiratory oxygen
Hct with blood transfusion are also associated with
concentration (FiO2) and gas flow (sweep) through
increased morbidity and mortality. It is prudent to
the oxygenator gas phase, providing excellent control
consider strategies such as retrograde autologous
of arterial O2 and CO2. Sampling arterial blood gases
prime, ultrafiltration and minimizing prime volume
from the circuit every 30 minutes and continuous
to optimize Hct to reduce the use of bank blood.
SvO2 in-line monitoring are recommended standards.
Continuous In-line Blood Gas Monitoring Mixed Venous Oxygen Saturation (SVO2)
Sensors placed in the arterial and venous lines of the Historically, an SVO2 > 75% during CPB has been
CPB circuit can provide near real time changes in a considered the primary indicator for an even balance
variety of key parameters including arterial oxygen between DO2 and VO2. The SVO2 should be con-
saturation (SaO2), pH, pCO2, pO2, hematocrit, bicar- sidered in the context of patient temperature. While
bonate, base excess and potassium. When combined organ metabolic demand decreases with hypothermia,
with pump flow rate, these monitors provide continu- the solubility and hemoglobin affinity of oxygen
ous measures of DO2 and oxygen consumption increases at the same time. The SVO2 should therefore
94 (VO2). Continuous monitoring allows necessary increase with decreasing temperature provided perfu-
changes to be made immediately while also being able sion is adequate. Venous saturations of 65–75% at

35–37°C, 76–85% at 32–34°C and 85–100% at 20–32°C generally aim to correct the presumed cause and
are typical. include increasing the pump flow, rewarming to nor-
It is a standard of perfusion practice to monitor mothermia, and checking that the venous pipe does
SVO2 continuously with an in-line optical sensor. not impede venous drainage from the liver. Although
A declining SVO2 suggests an imbalance of DO2 rela- generally done with every blood gas analysis, the
tive to VO2 and the perfusionist will respond by intermittent sampling of blood lactate has the risk of
increasing pump flow and ensuring optimal Hct or delaying timely intervention.
hemoglobin. Although a low SVO2 indicates a prob-
lem with systemic DO2 and is associated with poor Goal-Directed Perfusion Parameters in
postoperative outcomes, a normal SVO2, does not
necessarily guarantee that CPB pump flow is meeting Metabolic Monitoring during CPB
regional and/or organ specific VO2. Goal-directed perfusion is a strategy that algorithmic-
ally monitors both oxygen delivery and carbon diox-
Urine Output ide production during CPB. It uses this information,
combined with the classic metabolic and hemody-
Acute kidney injury (AKI) is common following car-
namic parameters (of stroke volume, end diastolic
diac surgery. The kidneys are particularly sensitive to
volume index, MAP and cardiac index), to provide
hypoperfusion, and urine output (UO) is traditionally
tailored and optimal perfusion for each individual
used as an organic marker of adequate perfusion. UO patient by avoiding a mismatch between oxygen
<2 ml/kg/h can be associated with higher rates of
delivery and consumption. Various studies have dem-
AKI. Limitations of this parameter are that UO
onstrated a reduction in postoperative morbidity
changes can be a late indicator of renal injury, and
associated with the use of GDP. Important constitu-
that it is affected by multiple other factors unrelated
ents of this approach are described below and illus-
to the adequacy of metabolic support. Chapter 19
trated in Table 10.3. GDP parameters tend to be
discusses the impact of CPB on renal function and
indexed to the patient’s BSA.
AKI in more detail.
Blood Lactate Oxygen Delivery

Oxygen delivery is influenced by both pump flow and
Lactate is the predominant metabolic component of
hematocrit and is one of the most significant deter-
glucose metabolism and under normal conditions
minants of “optimal” perfusion. Cardiac surgery is
feeds into the aerobic pathway of glucose utilization.
associated with a 22–40% incidence of AKI and inad-
Despite lactate disturbances commonly occurring equate DO2 is a likely contributor. It has been dem-
during periods of low flow or hypothermic CPB, it
onstrated that maintaining an indexed DO2 (DO2i) >
is recognized that increased lactate levels may be 270–300 mlO2/min/m2 may reduce the incidence of
indicative of inadequate perfusion, in particular of a AKI. Monitoring and maintaining DO2i levels by
mismatch between DO2 and VO2, leading to adjusting pump flow and/or Hct is an important
increased anaerobic metabolism. Numerous studies
aspect of optimizing metabolic management. In add-
have demonstrated that hyperlactatemia (>2.0
ition to maintaining DO2, monitoring the indexed
mmol/l) is associated with significantly worse out-
VO2 (VO2i) can be informative. In an anesthetized
comes. Recently there has been a shift toward atten- patient on CPB, VO2i will normally be in the range of
tion to lactate as a dynamic parameter with an 40–50 mlO2/min/m2.
increase of lactate by more than 200% from baseline
(and irrespective of the baseline level) being associ-
ated with significantly higher mortality. Increased CO2-derived Parameters
lactate levels are not always the result of inadequate Monitoring CO2 production (VCO2i) may allow early
perfusion and alternative reasons must be borne in real time detection of inadequate perfusion. Increases
mind: hypothermia, inadequate hepatic metabolism in VCO2i are often the result of carbon dioxide pro-
(resulting from reduced function or perfusion), oral duction under anerobic conditions. They can be indi-
hypoglycemic agents, altered glycolytic flux or inhib- cative of buffering of hyperlactatemia by the 95
ition of pyruvate dehydrogenase. Treatment strategies bicarbonate system. Therefore, in the presence of

Table 10.3. Goal-Directed perfusion parameters and ratios
All targets are based upon normothermic temperatures during CPB.
Parameter Measurement Targets Considerations & Management

Calculation
Oxygen DO2i = CI x CaO2 x Maintain > 270 mL/min/ If below target, increasing pump flow rate
Delivery Indexed 10 m2 and/or increasing the Hb should be
(DO2i) considered
Oxygen VO2i = CI x (CaO2- Normally 40-50 ml O2/ Higher than expected VO2i
Consumption CvO2) min/m2 under ! consider the depth of anesthesia and
Indexed (VO2i) anesthesia temperature
Carbon Dioxide VCO2i = (VE x <60 mL/min/m2 >60 mL/min/m2, rule out CO2 field flooding
Production ePCO2* x 1.315)
Indexed (VCO2i) /BSA
GDP ratio DO2i/VCO2i Target ratio > 5.0 Increase DO2i if outside target
Oxygen VO2i/ DO2i <40 >40 may suggest trigger for RBC transfusion
Extraction Ratio
(O2ER)
Respiratory VCO2 / VO2i Normal = 0.8–1.0 >1 corresponds to increase in lactate
Quotient production
ePCO2 = exhaled CO2
inadequate DO2i, VCO2i is considered to be a rapid, Respiratory Quotient – The respiratory quotient
indirect marker of lactate generation. The CO2 pro- (RQ) is the ratio of CO2 produced (VCO2) to O2
duction is measured at the gas outlet site of the consumed (VO2). During CPB, anaerobic
oxygenator. metabolism and lactate production have been
shown to positively correlate with RQ > 0.9.
O2 and CO2 Ratios in Metabolic Monitoring These three quotients provide the foundation of
during CPB emerging GDP practice and metabolic management.
Although it might be tempting, practitioners should
GDP Ratio – Pairing DO2i and VCO2i in a ratio is a
not fall into the trap of seeing them in isolation but
key component in the GDP concept. A study by
need to evaluate them in the context of other param-
deSomer et al. found that a DO2i/VCO2i less than
eters such as blood chemistry and temperature.
5.3 was a predictor of postoperative AKI. This
cutoff value has not yet reliably been reproduced in
Electrolytes
other studies, the goal of the GDP ratio is rapid
detection and prevention of anaerobic metabolism Electrolytes play fundamental roles in metabolism
by maintaining a DO2i above 270 mL/min/m2, and cellular energy production alongside generation
VCO2i <60 mL/min/m2 and the DO2i/VCO2i > 5. of resting membrane potentials in both nerve and
O2 Extraction Ratio – The oxygen extraction ratio muscle cells. It is essential to prevent electrolyte dis-
(O2ER) is the ratio of VO2 to DO2. There is some turbances during CPB. The effects of any imbalances
evidence that O2ER is better than a hemoglobin can be cumulative when more than one deficiency
value for guiding transfusion decisions on CPB. exists.
Some studies have demonstrated using O2ER as a
measure of tissue hypoxia and aiming for a value Potassium
of over 40 was associated with a reduction in Potassium is the predominant intracellular cation and
96
single organ failure and length of hospital stay. abnormalities during bypass are common.

Hyperkalemia often results from cardioplegia admin- level of <0.7 mmol/l) is associated with the presence
istration and is mostly self-limiting, rarely needing of arrhythmias (in particular atrial fibrillation but
active treatment. Potassium has many cellular re- also supra- and ventricular arrhythmias), seizures
uptake pathways, promoting the restoration of elec- and worsening of clinical outcomes.
trochemical balance, particularly in response to fluid Intravenous magnesium supplementation with up
shifts and urine production. The tolerance for hyper- to 2g is common during cardiac surgery as there is
kalemia varies between patients and some with suggestion that this can help prevent arrhythmias.
chronic kidney disease tolerate high levels of Magnesium may also be given in an analgesic dose
6mmol/l or above. The presence of ECG abnormal- (50 mg/kg) as part of enhanced recovery protocols
ities and plasma levels above 6.5 mmol/l are often after cardiac surgery. Ideally any magnesium supple-
triggers for instituting treatment. Commonly used mentation should be titrated against plasma levels to
treatments include IV bolus doses of calcium, avoid hypermagnesemia.
dextrose-insulin infusion or forced diuresis with a
loop diuretic. Zero-balance ultrafiltration with a Calcium
potassium free solution (usually sodium chloride) is
Hypocalcemia (defined as a plasma level <2.1 mmol/l)
another option to lower high potassium levels when
is another common electrolyte abnormality, often
removal of excess plasma water is required at the
resulting from hemodilution, hemofiltration and che-
same time, although care must be taken to avoid
lation with citrate in processed blood. Correction of
hypernatremia or hyperchloremia. When hyperkale-
hypocalcemia is required due to the ubiquitous role of
mia exists in the presence of an acidosis, the use of
calcium in cardiovascular and coagulation physiology.
sodium bicarbonate may help to promote the intra-
This is typically achieved by the administration of
cellular movement of potassium. The clinical team
either calcium chloride or calcium gluconate as a bolus
should keep in mind that there might be other reasons
dose. Hypocalcemia should only be corrected after a
than cardioplegia for hyperkalemia. They include red
period of normothermic myocardial reperfusion,
cell transfusion, hyperglycemia, renal failure, ongoing
following cross clamp removal, because of the role it
ischemia from reduced bypass flow or malignant
plays in the cellular signaling of apoptosis and the
hyperthermia and rhabdomyolysis.
possibility of worsening reperfusion injury if given
Hypokalemia is a common preoperative finding,
too early.
often resulting from hemodilution, concomitant diur-
etic use or secondary hyperaldosteronism in congest-
ive cardiac failure. Untreated hypokalemia can Phosphate
precipitate significant arrhythmias and poor ventricu- Phosphate plays a role in many intracellular enzym-
lar function, which can pose serious problems when atic and energy producing pathways and in maintain-
weaning from bypass. Initial treatment of hypokale- ing cellular resting membrane potential. Despite
mia is usually by replacement of potassium at a dose many patients having postoperative hypophosphate-
of 10–20 mmol, which can be given straight into the mia, presumably as a result of intracellular shifting
reservoir. resulting from alterations in acid-base status, intrao-
perative supplementation is not a routine practice in
the majority of institutions. Failure to correct phos-
Magnesium phate levels can lead to undesirable clinical effects
Magnesium is another intracellular cation involved in such as respiratory failure, muscle weakness, or
energy production and utilization. It also plays an impaired cardiac function with reduced cardiac
important role in the stabilization of electrically excit- output. Correcting phosphate levels should be part
able cells and in the regulation of vascular tone. of the postoperative treatment.
Depletion of magnesium during cardiac surgery is
common, often resulting from the concomitant use
of preoperative loop diuretics, hemodilution by the Chloride
pump prime, low magnesium in cardioplegic solu- Chloride is a key component of both normal saline
tions, or ultrafiltration. In both adult and pediatric and unbalanced colloid solutions. Excessive use of
normal saline or unbalanced fluid solutions as either
97
populations, hypomagnesemia (defined as a plasma

infusion fluid, priming volume or as part of intrao- Table 10.4 summarizes the effects on the most
perative cell salvage can lead to a hyperchloremia, in important anesthetic drugs. There are four principal
turn leading to a metabolic acidosis. Despite an mechanisms that are responsible for altered drug
absence of literature detailing the effects on outcome, behavior during CPB:
normal physiological levels should be targeted, and The dilutional effects of priming volume
consideration given to the role of chloride in contrib- changes drug and plasma protein concentrations.
uting to any metabolic acidosis. Altered plasma protein concentrations may
alter the ratio of bound versus free drug leading to
Glucose differing pharmacological activity depending
Hyperglycemia is common during CPB and often on whether a drug is active in its free or
requires an insulin infusion to control blood sugar bound state.
levels. The main causes are: The materials, which various components of the
i. the physiological stress response evoked by bypass circuit are made of, may affect drug
surgical insult leading to decreased insulin binding while some drugs like vancomycin are
sensitivity, sequestered by certain oxygenators.
ii. many cardiac surgical patients are diabetic, and Drug metabolism and clearance behave
quality of sugar control varies widely, proportional to decrease in microcirculatory flow
and hypothermia, both of which lead to reduced
iii. sicker hearts are unable to utilize glucose as an
elimination and the potential for prolonged
energy substrate, predisposing these patients to
pharmacological activity. The effect of some
hyperglycemia,
neuromuscular blocking agents is increased by
iv. the use of some inotropic agents, namely
decreasing systemic temperature.
epinephrine, induce a rise in plasma glucose,
Pulmonary drug sequestration, resulting from
v. addition of steroids to the circuit prime,
lung isolation during aortic cross clamping, may
vi. glucose containing cardioplegia solutions.
lead to increased plasma levels of drugs such as
Hyperglycemia leads to poor outcomes. Morbid con- fentanyl on full reperfusion at the time of
ditions associated with poor perioperative blood sugar separation from bypass.
control include neurological dysfunction, mediastinitis
Volatile anesthetic agents are widely used in cardiac
and increased risk of infection and sepsis. Tight intrao-
anesthesia and can be given throughout the operation,
perative blood glucose control using a titrated insulin
i.e. both on and off bypass, to maintain general anes-
infusion has been associated with improved patient
thesia. The blood:gas partition coefficient of an agent
outcomes and reduced mortality in a number of stud-
determines the rate of physiological response, with
ies. However, there is some debate about the actual
higher coefficients representing slower response rates
blood sugar target required. Tight control to normal
and vice versa. This coefficient is altered as soon as a
glucose levels (4.0–5.5 mmol/l; 70–100 mg/dl) is diffi-
patient is put on CPB – hemodilution reduces it,
cult to achieve, can lead to rebound hypoglycemia and
increasing the response rate; hypothermia increases
is not recommended. This has led to a more recent
it, slowing the response down. Perfusionists must be
“liberal” approach being favored, particularly in dia-
mindful of the effect that both temperature and
betic patients. This approach allows blood glucose to
hemodilution have on the activity and concentrations
rise to 10 mmol/l (180 mg/dl) in diabetics, with non
of volatile anesthetic agents. It is recommended that
diabetic patients only being treated at levels above
anesthetic agent monitoring is attached to the exhaust
7.8 mmol/l (140 mg/dl). The goal in glucose manage-
line of the oxygenator. Anesthetic agents (intravenous
ment is to maintain near to normal blood glucose
and volatile) may contribute to systemic vasodilation,
levels for every patient while not forgetting the dangers
potentially reducing MAP.
of too tight glycemic control.
Nitrous oxide should not be used before or after
bypass due to its insolubility in blood. It can enlarge
Drug Metabolism systemic air bubbles, thereby worsening the conse-
CPB will often cause significant changes in both the quences of any residual systemic air. In addition, it
98 pharmacokinetic and dynamic properties of drugs. can depress myocardial function.

Table 10.4. Summary of the effects of CPB on key anesthetic drugs
Drug Effects of bypass

Volatile Uptake and elimination are inversely proportional to blood:gas solubility coefficient – the
anesthetics higher the coefficient, the more soluble the agent and the slower the onset of action.
Increases in sweep gas flow increases uptake, changes in pump flow do not.
Hemodilution reduces protein binding, increasing the response rate.
Hypothermia increases the blood:gas solubility coefficient, reducing the speed of onset of
volatile anesthetics.
Rewarming reduces the volatile anesthetic blood:gas solubility coefficient and can increase
depth of anesthesia.
Volatile anesthetic agent transfer across the oxygenator membrane can differ between models,
making agent monitoring essential.
Propofol Free drug concentration increases with hemodilution and reduced plasma protein
concentration, leading to increased efficacy of propofol on CPB.
Opioids Free drug concentration increases with hemodilution and reduced plasma
protein concentration.
Hypothermic CPB increases the elimination half-life due to reduced hepatic clearance.
Remifentanil elimination is temperature-dependent, a reduction of infusion rates should be
considered during hypothermic CPB.
Muscle relaxants Free drug concentration decreases with hemodilution.
Requirements fall during CPB.
Benzodiazepines Free drug concentration decreases with hemodilution
Plasma levels can be increased after CPB due to prolonged elimination.
Temperature Management becoming increasingly popular. Moderate (28–32°C),

severe (27–25°C) or deep (<25°C) hypothermia can
Temperature is an important determinant in the
be used depending on the complexity and duration of
metabolic management on CPB. Traditional perfu-
a surgical procedure, the degree of organ preservation
sion strategies have involved the use of controlled
required and often surgical preference. Deep
hypothermia as a protective strategy to reduce sys-
hypothermic circulatory arrest (DHCA) is a tech-
temic metabolic demand and to protect organ func-
nique that can be used to protect brain and organ
tion. Cerebral oxygen consumption (CMRO2)
function in both adult and pediatric surgical proced-
decreases by 7% for every degree Celsius reduction
ures where aortic cross clamp placement is not pos-
in temperature. Together with the subsequent reduc-
sible or total absence of blood flow is required. The
tion in CO2 production, hypothermia is protective
specific considerations for DHCA are discussed in
against cerebral, and by inference, systemic ischemic
depth in Chapter 9. Hypothermic bypass has numer-
injury. This is supported by work using the tempera-
ous benefits including inhibition of catabolic and
ture coefficient Q10, described as the CMRO2 at a
destructive enzyme and neurotransmitter activity,
temperature T divided by the CMRO2 at 10°C lower.
suppression of free radical production and reduction
The higher the Q10, the more cerebral (and other vital
of the metabolic requirements in peripheral tissues.
organ) metabolic activity is suppressed. The less desir-
Additionally, systemic oxygen delivery can be titrated
able physiological consequence of hypothermia is the
to oxygen consumption by reducing pump flow or
leftward shift of the oxygen dissociation curve,
allowing for further reductions in hematocrit.
increasing the affinity of hemoglobin for oxygen, thus
Hypothermia can be achieved passively by letting
reducing tissue oxygen delivery.
the patient cool down or actively using the heater/
CPB is mostly conducted in mild (32–35°C) hypo- 99
cooler unit on CPB. Current recommendations
thermia, although normothermia (36–37°C) is

Table 10.5. Summary of the adverse effects of blood gas values have reduced PaO2 and PaCO2
hypothermic bypass
values and increased pH values, although content
System Consequences remains largely unchanged. There are two strategies
to manage this in clinical practice:
Cardiovascular Vasoconstriction and reduced
microcirculatory flow Alpha stat management - does not correct for
Hypokalemia and arrhythmias hypothermia, measuring samples at 37°C and
Reduced delivery of oxygen allowing alkalosis to occur without intervention
(leftward shift of oxygen during cooling. It is based on the fact that the
dissociation curve) dissociation constant (pK) of the imidazole group
Hematological Increased plasma viscosity of histidine changes with temperature, providing
Impairment of coagulation consistency of its ionization state (alpha) in order
Impairment of platelet function to maintain a constant intracellular pH. The aim is
to allow continued cellular, protein and enzyme
Cerebral Reduction in cerebral
blood flow
activity in a normal environment. Clinical studies
Ischemic injury during demonstrate better preservation of cerebral
rewarming phase autoregulation, flow and neurovascular coupling,
although this comes at the expense of less
Metabolism Metabolic acidosis
homogenous brain cooling and limited reduction
Hyperglycemia due to
impairment of glucose
in oxygen consumption of the brain. The
metabolism disadvantages of this method include increasing
Altered drug metabolism and the “steal” phenomenon from cerebral to
excretion pulmonary circulation in congenital
Altered ABG management cardiac surgery.
Renal Reduced GFR pH stat management – blood gas analysis is
Impairment of renal blood flow corrected to the actual core body temperature and
and increased AKI risk the pH is maintained at 7.4 throughout the period
of hypothermia with the addition of CO2 to the
Infection Increased infection risk
oxygenator gas flow. The higher CO2 content
Altered antibiotic handling
leads to the loss of cerebral autoregulation and to
cerebral vasodilation, increased cerebral oxygen
suggest that the temperature gradient between venous delivery and more homogenous cooling of deeper
inlet and arterial outlet on the oxygenator should not brain structures, albeit with the increased risk of
exceed 10°C to reduce the risk of micro-emboli forming. cerebral edema and a potentially higher micro-
Much debate exists on the optimal site of systemic tem- embolic load. In pediatric practice, where
perature measurement as a reflection of cerebral tem- intraoperative brain injury is the likely result of
perature. Commonly used sites include pulmonary artery global ischemia, this approach has been shown to
catheter tip, nasopharynx, esophagus, ear, bladder and reduce shunt flow and it potentially improves
rectum. Recently the oxygenator arterial outlet tempera- neurobehavioral development.
ture has gained support as the most appropriate surro- Both management strategies work well, however, evi-
gate for cerebral temperature. Practically, many centers dence would suggest alpha stat is preferable in adults,
monitor temperature at more than one site. while pH stat is preferable in pediatric practice, par-
Despite the benefits of hypothermic bypass, it has ticularly with DHCA.
a number of adverse unfavorable consequences,
which are summarized in Table 10.5.
Rewarming from Hypothermic Bypass
Hypothermic Bypass ABG Management: Cautious rewarming following hypothermia is recom-
mended to avoid the risk of cerebral hyperthermia,
Alpha versus pH Stat which is associated with cerebral injury, poor post-
100 Gas solubility increases as temperature decreases. As a operative neurological outcomes, increased infection
result, during hypothermia temperature corrected risk and renal injury. The CMRO2 is uncoupled from

cerebral blood flow in the hyperthermic brain, with guided by a temperature gradient of less than 5°C
subsequent supply and demand mismatch and the between patient core and periphery. The oxygenator
potential for cellular and neuronal injury. Current arterial outlet temperature should be limited to less
recommendations suggest that the temperature gradi- than 37°C to avoid the risk of underestimating true
ent between oxygenator venous inflow and arterial cerebral temperature and causing inadvertent cerebral
outlet does not exceed 10°C and ideally remains less hyperthermia. Rewarming from therapeutic hypo-
than 4°C. The rate of rewarming should be slow and thermia is discussed in more detail in Chapter 9.
Suggested Further Reading 5. Svenmarker S, Hannuksela M,

Haney M. A retrospective analysis
J Cardiothorac Vasc Anesth. 2020
Apr;34(4): 877–884.
1. Murphy GS. Hessel EA 2nd, Groom of the mixed venous oxygen
RC. Optimal perfusion during CPB: 8. Ranucci M, Carboni G, Cotza M
saturation as the target for et al. Carbon dioxide
an evidence-based approach. Anesth systemic blood flow control
Analg 2009; 108:1394. production during CPB:
during CPB. Perfusion 2018; 33: pathophysiology, measure and
2. Baker RA, Nikolic A, Onorati F 453–462. clinical relevance. Perfusion 2017;
et al. 2019 EACTS/EACTA/EBCP 6. Engelman R. Baker RA, Likosky 32: 4–12.
guidelines on CPB in adult cardiac DS et al. The Society of Thoracic
surgery: a tool to better clinical 9. Society of Thoracic Surgeons
Surgeons, the Society of Blood Conservation Guideline
practice. Eur J Cardiothorac Surg Cardiovascular Anesthesiologists,
2020; 57: 207– 209. Task Force. Ferraris VA, Brown
and the American Society of JR, Despotis GJ et al. Update to
3. Reves JG. Toward understanding ExtraCorporeal Technology: the Society of Thoracic Surgeons
cerebral blood flow during CPB: Clinical practice guidelines and the Society of Cardiovascular
implications for the central for CPB temperature Anesthesiologists blood
nervous system. Anesthesiology management during CPB. conservation clinical practice
2019; 130: 609–613. J Cardiothorac Vasc Anesth 2015; guidelines. Ann Thorac Surg 2011;
4. American Society of 29: 1104–1111 91: 944–982.
ExtraCorporeal Technology 7. Govender P, Tosh W, Burt C et al. 10. Kunst G, Milojevic M, Boer C
Standards and Guidelines For Evaluation of increase in et al. 2019 EACTS/EACTA/EBCP
Perfusion Practice. 2017. intraoperative lactate level as a guidelines on CPB in adult
Available from www.amsect.org/ predictor of outcome in adults cardiac surgery. BJA 2019; 123:
d/do/1370 after cardiac surgery. 713–757.
101

Chapter
Myocardial Preservation during
Avoiding unnecessary myocardial damage has been at The term “cardioplegia” was first described by
the forefront of cardiac surgery since its early days. Melrose in 1955. Melrose also induced the first elect-
The ability to arrest and immobilize the heart and ive cardiac arrest using potassium. Potassium concen-
revive it again without loss of function has facilitated trations of 35 to even 50 mmol/l were common.
more and more complex surgeries. Effective myocar- During the 1960s the negative effects of these high
dial protection, particularly for the duration of aortic dose strategies, namely myocardial necrosis and irre-
cross clamping, involves multimodal strategies, con- versible, ischemic myocardial contracture (stone
sisting of temperature management, cardioplegic heart), became increasingly apparent. This led to the
solutions delivered by various routes as well as non- development of solutions with lower concentrations.
cardioplegic techniques like ischemic preconditioning Today solutions typically have concentrations of
through intermittent cross clamping or pharmaco- 12–25 mmol/l.
logical protection. Building on this, in the 1970s Buckberg’s group
As in many other aspects of cardiac surgery, myo- led the effort of developing blood cardioplegia and
cardial protection depends on good communication other techniques like warm, substrate-enriched cardi-
and teamwork. oplegia and reperfusion modalities, such as warm
hyperkalemic reperfusion immediately prior to
History of Myocardial Protection removal of the aortic cross clamp (terminal hot shot),
not only to protect the heart from ischemia but to aid
The basic principle of myocardial protection consists
recovery from damage. The concept of retrograde
of minimizing the myocardium’s oxygen demand
cardioplegia delivered continuously via the coronary
during times of low supply, mainly during the period
sinus was explored at the same time.
when the surgeon requires a bloodless and still oper-
The 1980s saw an increasing interest in combined,
ating field and the aortic cross clamp is on.
intermittent, ante- and retrograde administration of
The most important discoveries occurred:
cardioplegia to provide better protection for the
i. at the end of the nineteenth century, when Ringer right heart.
showed the effect of electrolytes on the regulation The concept of ischemic preconditioning – where
of the heartbeat. short episodes of ischemia prior to a prolonged ische-
ii. in 1935, when Zwikster and Boyd showed that mic event are thought to confer protection from
potassium could reversibly arrest the heart. myocardial reperfusion injury, even if the ischemia
Systemic and topical hypothermia was advocated is administered at a remote region of the body –
early in the use of extracorporeal circulation to pro- caused much excitement after its first description by
vide an extra margin of organ protection as it was Murry in 1986. Subsequent clinical trials were not
feared that the then available technology could not able to reproduce the initial results and this technique
provide sufficiently high blood flows and gas is hardly used today.
exchange to satisfy oxygen demand. The concept of Despite much research there is still a lack of
lowering the metabolism through hypothermia was agreement on numerous aspects of cardioplegia. The
quickly adopted into the science of myocardial debates on crystalloid versus cold blood cardioplegia
protection. or on whole blood microplegia versus diluted blood
102

Chapter 11: Myocardial Preservation during Cardiopulmonary Bypass
cardioplegia – to name but two – are still ongoing. iii. Reperfusion arrhythmias, which are
Several metanalyses have not been able to demon- usually treatable.
strate superiority of any of the currently available iv. Lethal reperfusion injury, mostly driven by the
techniques. presence of reactive oxygen species (ROS),
intracellular calcium overload and inflammation.
Ischemia/Reperfusion Injury and Key Mitochondrial Based Protection

Intracellular Modulators of Cell Survival Mitochondrial based protection has been focused on
Many cardiac surgical procedures require the myo- inhibiting the opening of the mPTP and on opening
cardium to be immobile and bloodless while the of the mitochondrial ATP-dependent potassium
heart-lung machine maintains circulation. The asso- (KATP) channel. Two protective pathways are acti-
ciated insult to the myocardium is twofold: vated by myocardial ischemia, via the G-protein-
coupled cell surface receptors (reperfusion injury
i. Cross clamping of the aorta leads to myocardial
salvage kinase [RISK] – pathway) and via the tumor
ischemia, despite the cardioplegic arrest.
necrosis factor (TNF)-alpha receptors (survivor acti-
ii. Reperfusion after release of the aortic cross clamp
vating factor enhancement [SAFE] pathway).
causes ischemia-reperfusion injury.
Myocardial Ischemia Cardioplegia Techniques

As tissue hypoxia develops after aortic cross Delivering a cardioplegic solution to the myocardium
clamping, acidosis ensues and lactate accumulates in in order to induce diastolic arrest, topping it up
minutes as ATP is consumed much faster than it can intermittently to keep the heart protected during the
be produced in the mitochondria. The intracellular arrest, and re-perfusing the myocardium after surgi-
proton accumulation activates the Na+/H+ ion cal repair is a well-trodden path, repeated the world
exchanger and subsequently the Na+/Ca2+ exchanger, over millions of times each year.
resulting in intracellular Ca2+ accumulation. The principle behind cardioplegia and hypother-
Prolonged, untreated ischemia leads to disruption of mia is to continually match myocardial oxygen supply
the cell membrane, resulting in the leakage of and demand to limit any damage. This means that the
intracellular components into the extracellular main determinants of myocardial energy consump-
compartment. tion – electromechanical activity and left ventricular
Mitochondria supply ATP to cardiomyocytes, but end-diastolic wall tension (LVEDP) – need to be
they have also been identified as activators of cell controlled. Rapid onset of diastolic arrest without
death pathways, modulating the balance between distending the left ventricle immediately after aortic
pro-survival and death. The mitochondrial permea- cross clamping is important. Protection can be fur-
bility transition pore (mPTP) is a nonselective chan- ther enhanced by decreasing the metabolic rate and
nel of the inner mitochondrial membrane. The suppressing electrical activity through cooling (see
acidosis during ischemia causes the mPTP to remain Figure 11.1).
closed. This provides a degree of protection as mPTP
opening causes depolarization and uncoupling of oxi- Physiology of Cardioplegia
dative phosphorylation, resulting in intracellular ATP There is an electrical potential between the intra- and
depletion and cell death. extracellular space. This electrical gradient is main-
tained by ions on either side of the cell membrane.
Ischemia/Reperfusion Cardioplegia solutions are able to rapidly induce car-
diac arrest by altering the electrical gradient across the
Myocardial reperfusion results in different types of
cell membrane of myocytes and by doing so eliminate
cardiac dysfunction:
electrical activity and subsequent mechanical
i. Stunning – reversible, mechanical dysfunction. contraction.
ii. No-reflow phenomenon – the inability to A cell’s resting membrane potential is determined
reperfuse an ischemic region. 103
by the selective permeability of its membrane to ions.

12
Beating nonworking Beating working
8
Fibrillating 10 Arrest
Arrest
6
8
ml/100g/min
ml/100g/min
4 6
4
2
2
0
0
37°C 32°C 28°C 22°C
37°C 22°C 10°C
Figure 11.1 Myocardial O2 demand at various working modes and temperatures.
Figure 11.2 Simplified Nernst equation for K+.
At equilibrium, the ionic flows into and out of the cell potential is reached, the fast Na+ channels open.
are equal in magnitude and there is no net current. This allows Na+ to rush into the myocyte which very
The myocyte membrane is most permeable to K+ and rapidly raises the membrane potential further and
relatively impermeable to other ions; its resting mem- depolarizes the cell. Continued Na+ entry creates a
brane potential is therefore dominated by the K+ +20 mV potential (Phase 0). The positive membrane
equilibrium and is relatively negative at ‒90 mV. potential closes the voltage controlled Na+ channels
Movement of other ions across the membrane is and opens the voltage gated K+ channels, allowing K+
mainly determined by voltage gated channels, which to leave the cell, thereby reducing the membrane
open or close at specific membrane potentials. The potential to +5 mV (Phase 1). At this point the voltage
equilibrium potential for any ion may be calculated gated Ca2+ channels open and Ca2+ enters the myo-
using the Nernst equation (see Figure 11.2). cyte (Phase 2). Calcium influx into the cell results in
The normal value of Co/Ci for K+ is 4/140, i.e. the contraction and this coincides with ventricular sys-
+
K equilibrium potential is calculated as 94 mV. If tole. These Ca2+ channels only remain open transi-
the extracellular K+ concentration rises to 20 mmol/L, ently and, as soon as they close, the membrane
the value for Co/Ci changes to 20/140, and the equi- potential returns to approximately 90 mV, as K+ is
librium potential is 52 mV. Using this simple tool still able to leave the cell via the voltage gated K+
helps appreciate how manipulating the extracellular channels, and the cell membrane repolarizes. The
environment changes the equilibrium potential of the intracellular calcium is reduced, and the cell
cardiac myocyte. relaxes again.
Figure 11.3 shows the normal electrical cycle of a Displacing blood using extracellular cardioplegia
cardiac myocyte. Phase 4 represents the resting mem- with a high K+ concentration makes the cell mem-
brane potential of the cell and coincides with ven- brane potential less negative thus allowing it to
tricular diastole. Normally, as an action potential depolarize more readily. The depolarization causes
propagates through the heart’s conduction system, the voltage gated Ca2+ channels to open and the
104 the myocyte membrane becomes less negative, to transient calcium influx results in contraction (sys-
approximately 70 mV, and once this threshold tole); once the calcium is locked away in the

PHASE 1
Early Repolarization
K+ efflux
Cl- efflux
+20 PHASE 2
Plateau
Ca++ efflux
K+ efflux
0
mV
PHASE 3
Repolarization
K+ efflux
K+ 20 mmol/L –46 PHASE 0 Na+/K+ and Na+/Ca++ exchange
Depolarization
Na+ channel opening
Na+ influx
K+ 10 mmol/L –60
Treshold Potential –65
Resting Potential –85 PHASE 4

Resting State
K+ outward leak Time
Na+ and Ca++ channels closed
Figure 11.3 Cardiac myocyte action potential. The resting membrane potential is 85 mV and the threshold potential for depolarization is
65 mV. Increasing the extracellular potassium leaves the myocytes above the threshold potential and in an arrested state.
sarcoplasmic reticulum again the cell relaxes (dia- were also profoundly depolarizing and caused
stole). Rather than this cycle continuing, the high myocardial damage due to excessive intracellular
extracellular potassium concentration now prevents calcium accumulation. Subsequent work focused
repolarization and the cell stays depolarized. When on reducing the potassium content. The
the resting potential approaches 50 mV, Na+ chan- prototypical extracellular-like crystalloid solutions
nels are deactivated resulting in diastolic arrest. are referred to as St Thomas’ solution.
Potassium is not the only ion which could be used Intracellular-like solutions – Bretschneider and
to manipulate the myocyte electrical membrane coworkers pursued a different strategy in the
potential. Hyponatremia, hypocalcemia and hyper- 1970s. They developed a calcium free, low sodium
magnesemia will all ultimately cause diastolic cardiac cardioplegia solution, which works by reducing
arrest. Hypercalcemia, if profound enough, may cause the trans-membrane Na+ gradient sufficiently to
systolic cardiac arrest. stop enough Na+ entering the myocyte during
phase 0 to cause depolarization. The membrane
Cardioplegia Solutions remains hyperpolarized and arrested in diastole.
Cardioplegia solutions can be divided into crystalloid This solution is known as histidine-tryptophan-
and blood-based solutions, with crystalloids further ketoglutarate (HTK), Bretschneider’s or Custodiol
subdivided into either intracellular or extracellular solution. It is classified as an intracellular
solutions. The key features of cardioplegia solutions cardioplegia solution as its composition is closer
are summarized in Table 11.1. to that of the intracellular environment, in
contrast to the K+ based extracellular
Extracellular-like solutions – The earliest environment-like solutions. It has a large
cardioplegia solutions consisted of crystalloids
buffering capacity and is often given as a single
with a very high potassium content. While these 105
shot designed to protect for up to two hours
were rapidly able to achieve cardiac arrest they

Table 11.1. Different cardioplegic solutions and their components
Extracellular Intracellular Blood

Components St. Thomas St. Thomas Custodiol Del Microplegia Buckberg
Hospital 1 Hospital 2 (HTK, Nido (Miniplegia)
(STH) (STH2, Bretschneider’s)
Plegisol)
NaCl (mMol) 144 110 15
KCl (mEq) 20 16 9 26 ≈28 ≈28
NaHCO3 (mEq) * added 10 13
prior to
use
MgCl2 (mmol/L) 16 16 4 6.6 ≈2–4
CaCl2 (mmol/L) 2.2 1.2 0.015 0.4
Mannitol (g/L) 30 0.4
Histidine 180
(mmol/L)
Histidine-HCl 18
(mmol/L)
Tryptophane 2
(mmol/L)
KH2- 1
ketoglutarate
(mmol/L)
THAM ≈50
(mmol/L)
CPD (mmol/L) ≈20
Other additives procaine lidocaine lidocaine citrate; glutamate/
(adenosine) aspartate on
reperfusion
without interruption. However, hemodilution and example high potassium for rapid arrest (20 mmol/
hyponatremia can be problematic side effects, L) followed by moderate potassium for
particularly in pediatric cases. Mannitol is added maintenance (10 mmol/L). These techniques have
to correct the osmolarity of the solution and evolved into cold, tepid, warm and combined
minimize fluid shifts. strategies, with centers adapting to either a single-
Blood cardioplegia – Buckberg and colleagues shot approach or to recurrent, intermittent doses
developed the concept of blood cardioplegia, which (every 15–20 minutes). Blood and cardioplegia
promised many theoretical advantages including solution are generally mixed in a 4:1 ratio, but
high buffering capacity, oxygen and carbon dioxide variations are common.
transport, free radical scavenging and minimal Perhaps the logical evolution of blood cardioplegia
hemodilution. They also advanced the idea of a is the so-called miniplegia, where oxygenated blood
myocardial protection strategy with different coming from the CPB is minimally diluted by
ingredients and concentrations administered at adding concentrated potassium, magnesium and
106 various stages of the surgical procedure, for other additives via a syringe driver rather than

mixed from a crystalloid solution. This technique Mannitol is added to augment the osmotic
provides maximal control of cardioplegia delivery pressure and prevent myocardial edema.
and least hemodilution.
Del Nido Cardioplegia – Many clinicians feel
that blood is the optimum basis for cardioplegic Delivery of Cardioplegia
solutions and Del Nido popularized the use of a Cardioplegia needs to be delivered directly to the
single shot mixed blood/crystalloid cardioplegia myocyte membrane to induce and then maintain
(1:4) in pediatric cases in the 1990s. This diastolic arrest. Depending on the patient’s pathology,
concept is now gaining traction in adult surgery. the operation and on surgical preference, delivery can
Del Nido Cardioplegia (DNC) is given as a be either antegrade via the coronary arteries and/or
single shot and consists of 26 mEq of potassium retrograde through the coronary sinus into the heart’s
chloride, 13 mL of 1% lidocaine, 3.2 g/L of venous system (see Figure 11.4).
mannitol, 2 g magnesium sulfate, 13 mEq of Cardioplegia delivery is mostly controlled by the
sodium bicarbonate, all in 1000 mL of Plasma- perfusionist. A system consisting of one or two elec-
Lyte A. The advantages are an uninterrupted tronically linked pumps provides the mix of blood
procedure with potentially shorter clamp and and crystalloid cardioplegia, via a separate heat
pump times and less hemodilution. Any clinical exchanger, to the surgeon, who connects it to the
outcome advantages, however, have yet to be desired delivery site. Adequate de-airing and close
determined. temperature and pressure monitoring need to be pro-
vided. The heart has to be completely emptied and
Additives relaxed before the aorta is occluded and cardioplegia
Many constituents have been proposed both as pri- is given.
mary arrest-inducing agents and as additives to
improve myocardial protection. In the former
category high-dose magnesium and the short acting
beta-blocker esmolol are promising, whereas in the
latter category amino acids, sodium channel blockers,
buffers and low-dose magnesium are all added
according to institutional and surgeon preference
and case-specific factors.
Magnesium offers additional arresting potential
by limiting the calcium influx into cells. It
provides a veno-dilating effect, making it useful
when administering cardioplegia through vein
grafts during CABG procedures.
Citrate-Phosphate-Dextrose (CPD) has calcium-
chelating properties, making it useful as an
additive to prevent calcium overload, although the
supporting evidence is poor.
Tris (hydroxymethyl) Aminomethane (THAM) is
sometimes used as a buffer to prevent acidosis, but
its usefulness is contested when using
blood cardioplegia.
Sodium bicarbonate (NaHCO3) is also used as a
buffer but is even more controversial.
Aspartate and glutamate are amino acids and have Figure 11.4 Antegrade and retrograde cardioplegia
delivery circuit. a = aortic cannula, b = coronary sinus cannula, c = 3-
been advocated due to a theoretical ability to way tap to connect cardioplegia line from HLM and easily switch
provide ATP in an anaerobic milieu. The evidence between delivery mode. 107
of their use is poor.

Figure 11.5 (a) DLPTM Double-lumen aortic root cannula, which can be used to deliver cardioplegia and as an aortic root vent. (b) Schematic
drawing of antegrade cardioplegia delivery. (Reproduced with ©2020 Medtronic. All rights reserved. Used with the permission of Medtronic.)
Excellent communication between the perfusio- occlusion forces the aortic valve to close and the
nist, the surgeon and the anesthesiologist is crucial cardioplegia solution into the left and right coronary
during cardioplegia delivery. ostia. The perfusionist controls the flow while the
pressure is servo regulated to avoid excessive values,
Antegrade Delivery which are associated with myocardial edema.
Successful delivery through the aortic root requires
Antegrade cardioplegia is most commonly delivered
a competent aortic valve. Even a small degree of aortic
through a cannula placed in the aortic root, proximal
insufficiency can lead to cardioplegia leakage into the
108 to the aortic clamp, utilizing the native coronary
left ventricle. Not only does this lead to insufficient
circulation (Figure 11.5a and b). Flows of 250–350
perfusion of the myocardium and delayed arrest, but it
ml/min with a pressure of 80–120 mmHg after aortic

Figure 11.6 DLP™ Retrograde cardioplegia

delivery cannula. (Reproduced with ©2020
Medtronic. All rights reserved. Used with the
permission of Medtronic.)
can cause left ventricular distension, further impairing (see Figure 11.6). Retrograde delivery should always
delivery of cardioplegia to the sub-endocardial tissues. be done with continuous sinus pressure monitoring,
There are several options available if the aortic preferably using a servo regulated pump. The pres-
valve is found to be regurgitant: sure should be kept below 40 mmHg to avoid endo-
Direct ostial cardioplegia – the aorta is opened thelial damage or even rupture of the coronary sinus.
after cross clamping and the cardioplegia is Proponents of this technique emphasize that it
delivered directly into the coronary ostia using offers continuous delivery without interruption of the
either a basket-tipped or a gel-tipped special procedure, is not dependent on a competent aortic valve
cannula. The left coronary artery is generally and supplies all of the subendocardial tissue, regardless
perfused first as the left ventricle is more of coronary artery stenoses. Despite these advantages it
susceptible to ischemia. Once cardiac arrest has is regarded as inferior to antegrade methods because:
been achieved the right ostium is perfused before Right-sided protection can be impaired, especially
topping up the left side again. Flows and pressures if the catheter is placed too deep into the sinus,
are generally lower with this technique in order past the posterior interventricular vein
not to cause endothelial damage or dissect the Placement of the catheter is sometimes time-
coronaries. If an intermittent cardioplegia consuming, not always accurate and risks damage
technique is used, the operation needs to be to the sinus
interrupted every 15–20 minutes. Catheters can also slip out of the sinus unnoticed
Retrograde cardioplegia (see below). during manipulation of the heart
Achieving timely arrest is a concern particularly in Induction of cardiac arrest requires more time
patients with severe proximal left main and/or right- than with antegrade delivery.
sided stenoses. The addition of retrograde delivery is Both techniques are often combined, commonly
often chosen in these cases to decrease the risk and giving an induction dose antegrade, followed by
extent of myocardial injury. retrograde maintenance.
Retrograde Delivery Delivery through Vein Grafts

Retrograde cardioplegia should be considered when- Cardioplegia can be delivered through vein grafts
ever antegrade delivery is deemed to be technically once the distal anastomosis is completed. When this
difficult to achieve or to provide insufficient myocar- is done through a pump using a set pressure, this
dial protection (e.g. redo CABG with partially patent technique can give the surgeon the confidence about
grafts, severe mainstem stenosis, ongoing myocardial graft patency and quality of the anastomosis. Flows of
infarction). It can be achieved by placing a cannula in 80–100 ml at a pressure of 100 mmHg are desirable.
the coronary sinus, which is the final drainage zone of
the venous coronary circulation. The cannula is most
commonly placed by palpation and transesophageal Cardioplegia Techniques for Minimal
echocardiography (TEE) offers some guidance.
A circumferential, inflatable balloon near the distal Access Surgery
end of the catheter provides a seal between catheter As minimal access surgery increased in popularity, new 109
and the sinus wall, allowing delivery of cardioplegia methods of achieving myocardial protection were needed.

Longer aortic cannulas and the extended the focus of academic efforts is the avoidance of
Chitwood cross clamp enable standard antegrade car- ischemia/reperfusion injury. Although many con-
dioplegia delivery. A different approach is the use of cepts have shown promise in preclinical and small-
an endoballoon catheter, which is advanced from the scale clinical trials, none have so far found their way
femoral artery and placed into the ascending aorta into mainstream cardiac surgery.
under TEE guidance. Once safely in situ, the balloon
is inflated to occlude the aorta and cardioplegia is Intermittent Cross Clamping/Fibrillation
delivered in standard antegrade manner proximally
The technique of intermittent cross clamping/fibrilla-
to the balloon through one lumen of the catheter. The
tion (ICC) is used in several centers, especially in
catheter provides two transducers, one to measure the
coronary artery bypass graft surgery. It never was
aortic root pressure during cardioplegia delivery and
accepted widely, as operating on a fibrillating heart
the second one to monitor the balloon inflation pres-
is technically more challenging than on a still, flaccid
sure. Specific catheters that are inserted through the
and bloodless field. There is no consensus as to how
jugular vein and can be positioned in the coronary
many consecutive episodes of cross clamp/fibrillation
sinus have been developed for retrograde delivery.
can be considered safe, how long each one should
Intracellular cardioplegia solutions, allowing longer
maximally last and how much time is needed to
clamp times and longer intervals between doses, are
reperfuse between them. There is also an increased
often used during minimal access surgery.
risk of embolic complications associated with
Extremely good communication and coordination
repeated application of the aortic cross clamp.
between perfusionist, surgeon and anesthesiologist
During ICC, the patient is on CPB and cooled to
are crucial during these operations.
28–32 C. While cross clamped, the heart is com-
pletely emptied and a fibrillatory electrode is placed
Temperature Management behind it to induce ventricular fibrillation to reduce
and Cardioplegia myocardial oxygen consumption and also ventricular
Myocardial oxygen demand decreases with decreasing motion. ICC is the archetypical form of ischemic
temperature, as Figure 11.1 illustrates. Before the preconditioning.
introduction of myocardial cardioplegia, systemic Despite the skepticism toward it, ICC has been
hypothermia was the mainstay of myocardial protec- shown to be safe in coronary surgery with clinical results
tion; it remains an adjunct to cardioplegia today. similar to those with cardioplegic arrest. The fibrillator
Crystalloid cardioplegia appears to be most effective provides a useful rescue technique to immobilize the
when administered cold, with delivery temperatures myocardium and reduce oxygen consumption when
as cold as 4 C seen commonly. Cold cardioplegia is cardioplegia administration unexpectedly fails and other
often supplemented with “bathing” the heart in ice- means of myocardial perfusion are unavailable.
cold water during the period of delivery. Oxygenated
blood cardioplegia is more likely to transfer oxygen to Off Pump Surgery (OPCABG)
the myocardium if administered warm, as this min- Avoiding CPB, aortic cross clamping and cardioplegia
imizes the shift of the oxygen dissociation curve to the is seen by some as the ultimate form of myocardial
left. Warm blood cardioplegia (i.e. 37 C) has been protection. For obvious reasons this is only possible
shown to maintain myocardial ATP levels more effi- for coronary artery surgery. However, recent large
ciently. This explains why many surgeons opt to analyses have not shown better long-term outcomes
induce arrest with cold blood cardioplegia and give associated with this technique.
top up doses warm.
Ischemic Preconditioning
Non-Cardioplegic Methods of After commencing CPB, the aorta or the left anterior
Myocardial Protection descending coronary artery is occluded several times
Numerous techniques have been investigated over the followed by short periods of reperfusion before apply-
years as adjuncts or alternatives to cardioplegia. The ing the aortic cross clamp and giving cardioplegia.
110 second aspect of myocardial protection that has been This technique showed initial promising results in

small clinical trials, but overall clinical results were Cyclosporine

inconclusive.
Cyclosporine as an additive to cardioplegia solutions
may be beneficial in protecting the myocardium from
Remote Ischemic Preconditioning ischemia reperfusion injury, by inhibition of mPTP.
This technique is based on the concept that the ische- This potential protective effect has not been demon-
mic conditioning stimulus can confer protective strated convincingly in clinical studies and the
effects on the heart if applied to distal tissues such immunosuppressive effect of the drug can potentially
as arms or legs. It involves up to four episodes of 5- be harmful.
minute inflation/deflation of a standard blood pres-
sure cuff on the patient’s arm after induction of Volatile Anesthetic Agents
anesthesia. After initially promising results two major
Experimental studies suggested that volatile anesthet-
multicenter studies did not show improved patient
ics may protect the myocardium from ischemia/
outcome with this technique.
reperfusion injury. So far clinical studies have yielded
inconclusive results and further trials, particularly
Sodium Hydrogen Exchanger Isoform-1 involving the delivery of volatile agents through the
(NHE-1) HLM while the lungs are not ventilated, are ongoing.
The pharmacological inhibition of the sodium hydrogen Their long-term utility is questionable, though, due to
exchanger isoform-1 (NHE-1) reduces intracellular cal- the significant environmental impact of volatile
cium overload and resulted in myocardial protection in anesthetics.
experimental studies. Whereas subsequent clinical trials
in cardiac surgical patients confirmed the beneficial
effect on the myocardium by a significant reduction in Cardioplegia and hypothermia remain the pillars of
myocardial infarction, overall mortality was increased in myocardial protection during cardiac surgery. Several
patients treated with sodium hydrogen exchanger initially promising new strategies did not show any
inhibitors, due to an increase in cerebrovascular events. benefits in clinical trials.
Suggested Further Reading 4. Kunst G, Klein AA. Peri-operative

anaesthetic myocardial
in all adults undergoing cardiac
surgery: con. J Cardiothor Vasc
1. Yellon DM, Hausenloy DJ. preconditioning and protection – Anesth. 2019; 33: 1791–1794
Myocardial reperfusion injury. cellular mechanisms and clinical
N Engl J Med. 2007; 357: 8. Salerno TA, Ricci M, eds.
relevance in cardiac anaesthesia. Myocardial Protection. First
1121–1135 Anaesthesia. 2015; 70: 467–482 edition. Oxford: Blackwell
2. Xia Z, Li H, Irwin MG. 5. Buckberg GD. Update of current Publishing Ltd. 2004
Myocardial ischaemia reperfusion techniques of myocardial
injury: the challenge of translating 9. Ali JM, Miles LF, Abu-Omar Y
protection. Ann Thorac Surg 1995; et al. Global cardioplegia
ischaemic and anaesthetic 60: 805–814
protection from animal models to practices: results from the Global
humans. Br J Anaesth. 2016; 117: 6. Spellman J. Pro: in favor of more Cardiopulmonary Bypass Survey.
ii44–ii62 generalized use of del Nido J Extra Corpor Technol. 2018; 50:
cardioplegia in adult patients 83–93
3. Davidson SM, Andreadou I, undergoing cardiac surgery.
Garcia-Dorado D et al. Shining 10. Murry CE, Jennings RB, Reimer
J Cardiothor Vasc Anesth 2019; 33: KA. Preconditioning with
the spotlight on cardioprotection: 1785–1790
beyond the cardiomyocyte. ischemia: a delay of lethal cell
Cardiovasc Res. 2019; 115: 7. Gorgy A, Shore-Lesserson L. Del injury in ischemic myocardium.
1115–1116 Nido cardioplegia should be ssed Circulation. 1986; 74: 1124–1136
111

Chapter
Weaning from Cardiopulmonary Bypass
12 Joanne F Irons, Kenneth G Shann and Michael Poullis
The transition from cardiopulmonary bypass (CPB) Several authors have proposed weaning checklists,
to normal circulation requires numerous mechanical, which follow the general themes outlined in Table 12.1.
physiological and pharmacological factors to be Mnemonics help practitioners remember important
coordinated efficiently within a short period of time. points in the checklists, both in routine and in high
Weaning from CPB is often a routine process, how- stress cases. Two common mnemonics used as a check-
ever preexisting poor cardiac function or difficulties list prior to weaning are “CVP” and “TRAVEL” (see
during the operation may make it complex and chal- Table 12.2) and are discussed below. It should be recog-
lenging. Complications encountered during the nized that a number of these steps occur concurrently.
weaning phase may contribute to significant add-
itional perioperative morbidity. Temperature
Patients must be rewarmed prior to separation from
Communication and Teamwork CPB. There is currently insufficient evidence on the
There is a strong correlation between adverse events optimal temperature for weaning. It should be based
and poor communication and coordination during on a balance between avoidance of cerebral hyperther-
this vital time. Communication between team mia with excessive rewarming and minimization of coa-
members and in particular the perfusionist, surgeon gulopathy and transfusion with inadequate rewarming.
and anesthesiologist are key to successful weaning Rewarming targets of nasopharyngeal (NP) or
from CPB. Important information, including surgical esophageal temperatures of 36.5°C and bladder or
interventions, diagnostic data, such as filling status rectal temperatures of 35°C are commonly employed.
and transesophageal echocardiography (TEE) find- Chapters 7 and 9 provide in more depth discus-
ings, and therapeutic decisions surrounding pharma- sion of temperature management during bypass and
cological support and an accurate assessment of the on rewarming from hypothermia.
CPB prior to weaning, need to be conveyed intelli-
gibly and in a timely manner to prevent morbidity. De-airing
Simulation training of standard separation and crisis
Cardiac surgical procedures that require opening of
management should be considered to improve non-
cardiac chambers will inevitably allow introduction of
technical skills and team performance in real-life
air. Air in the right-sided chambers is usually rela-
situations.
tively innocuous if its volume is not substantial
enough to prevent forward flow and there are no
Weaning Checklist intracardiac shunts. Air in the left side is dangerous
Separation from CPB requires the heart to resume its and presents two major risks:
inherent pump function. In order to achieve a smooth 1. cerebral air embolus with postoperative
transition, cardiac function must be optimized prior morbidity, ranging from transient confusion to
to weaning. Delays in either recognizing or treating widespread neurological damage; and
abnormal physiological parameters may lead to poor 2. coronary air embolus, which may cause transient
cardiac performance or failure to separate from CPB and possibly widespread regional ventricular
necessitating a return to extracorporeal circulatory dysfunction and, in the extreme, irreversible
support. myocardial damage.
112

Chapter 12: Weaning from Cardiopulmonary Bypass
Table 12.1. Preparation for weaning from CPB table can be manipulated in a way that it sits at the
Warm patient to target temperature
highest point. TEE can assist with de-airing by iden-
tifying air “pockets” and tracking the success of de-
Correct electrolytes and acid-base status airing until the amount of residual intracardiac air is
Have blood and blood products available considered acceptable (see Figure 12.1).
Ensure sufficient volume in pump reservoir
Achieve target hemoglobin Reperfusion
Restart ventilation Following removal of the aortic cross clamp and prior
to attempting to wean from CPB, adequate reperfu-
Assess heart rate, rhythm and conduction
sion of the myocardium is important to allow myo-
Control arrhythmias cytes time to replenish metabolic substrates,
Ensure pacing wires work and start pacing if required specifically high-energy phosphates (ATP), and “wash
out” the products of anaerobic metabolism and
Consider mechanical support if difficulties are
anticipated
residual cardioplegia.
Initial reperfusion can often be complicated by
tachyarrhythmias or heart block. Some centers prefer
to reduce the risk of reperfusion arrhythmias by
Table 12.2. Checklist mnemonics to aid weaning giving prophylactic anti-arrhythmic agents, such as
“CVP” lidocaine, prior to cross clamp release. There are
many parameters that influence myocardial and
C V P end-organ recovery and there is significant variation
Cold Ventilation Predictors in routine practice across institutions. Clear and prac-
Conduction Vaporizer Protamine
tical advice on blood pressure during or the time
needed for reperfusion is not available in the litera-
Calcium Volume Pressure ture, although it is generally accepted that an
Cardiac Output Visualization Potassium increased reperfusion time is associated with a more
Coagulation Vasopressors Pacer
complete restoration of myocardial function. Full
recovery usually takes at least 20 minutes and during
“TRAVEL” this time there is an increase in myocardial metabolic
T Temperature demand. Surgical sequence may accommodate time
for myocardial reperfusion – for example, the aortic
R Reperfusion Rate Rhythm
anastomoses of coronary grafts may be performed
A Air during the reperfusion period.
V Ventilation
E Electrolytes (including Hemoglobin, Acid-base) Rate/Rhythm/Contractility
L Level Cardiac function should be assessed prior to weaning
from CPB, focusing primarily on heart rate, rhythm
and contractility – visual (right ventricle) and echo-
cardiographic guided (left ventricle). Communication
It is therefore vital that meticulous attention to de- between the surgeon and anesthetist is important as
airing is applied. Direct cardiac agitation, syringing of agreement is needed to formulate a weaning plan in
air from left-sided chambers and venting of the aorta cases where contractility is decreased.
or left-sided chambers is started prior to aortic Ventricular and supraventricular tachycardia at
unclamping and continued until the air has disap- this time should be treated with electrical cardiover-
peared. Hand-bagging the lungs vigorously during sion or defibrillation and anti-arrhythmic therapy
the de-airing process displaces air that accumulates should be considered to increase success and
in the pulmonary veins. The aortic root vent generally reduce recurrence. Adding 150–300 mg amiodarone
113
runs at a rate of 500–1000 ml/min and the operating into the pump as well as keeping the potassium

Joanne F Irons, Kenneth G Shann and Michael Poullis
Figure 12.1 Transesophageal echocardiogram (mid-esophageal left ventricular outflow tract view) showing the heart during de-airing
following aortic valve surgery. Air is seen as white speckles throughout the left heart with an accumulation in the left ventricular outflow tract
(LVOT).
level >5 mmol/l are frequently used when dysrhyth- fibrillation). In cases where AV synchronization is
mias recur and persist during reperfusion. likely to be helpful and effective sinus rhythm is
Following CPB, the ventricles are generally less not yet established, atrial and ventricular epicardial
compliant and will not have their normal capacity to leads should be placed to facilitate sequential AV
respond to changes in preload. The heart rate is pacing.
therefore usually maintained at 80–100 beats per Prophylactic pacing should be considered in
minute to help compensate for this. This “stiff” ven- patients with:
tricle phenomenon increases the relative importance 1. left ventricular hypertrophy, especially those
of the contribution of synchronous atrial contraction undergoing aortic surgery, as they require their
to stroke volume and cardiac output. Thus sinus left atrial “kick” to maintain LV filling,
rhythm is always preferable. Epicardial pacing leads 2. a high risk of conduction defects due to the nature
and an external pacemaker, ideally with dual of the surgical procedure – aortic or mitral valve
chamber function to allow sequential atrio- surgery (AVR or MVR), MVR especially via
ventricular (AV) pacing if required, have to be imme- transeptal approaches and atrial or ventricular
diately available. septum defect (ASD or VSD) repair,
3. atrial fibrillation (AF) and those requiring support
Pacing with an intra-aortic balloon pump (IABP) as
Evaluating the ECG on the anesthesia monitor for regular heart rate improves IABP efficiency,
bradycardia or AV block may identify the need for 4. hypertrophic cardiomyopathy (HCM), especially
epicardial pacing leads. When possible, atrial pacing when undergoing AVR.
is preferable to AV or ventricular pacing. Atrial Commonly, pacing is set at around 80–100 bpm
pacing may be used alone to increase heart rate in immediately post-CPB. The pacing rate should be
patients in sinus rhythm or in a junctional rhythm determined by patient requirement and not by proto-
where AV conduction is intact. Ventricular col. Atrial pacing leads exteriorized on the patient’s
pacing may be employed in isolation when there is right side and ventricular leads on the left help to
114 no effective atrial contraction (e.g. chronic atrial avoid labeling issues and pacing errors.

Inotropes to clear respiratory secretions before ventilation

is resumed.
While the chest is open, direct inspection of the right
Effective mechanical ventilation of the lungs must
ventricle (RV) allows assessment of contractility while
be established prior to ventricular ejection when sig-
the left ventricle (LV) can be difficult to see and is
nificant pulmonary blood flow is reestablished. The
better assessed via TEE.
perfusionist must confirm with the anesthesiologist if
Vasopressors, inotropes and vasodilators must be
they are satisfied with ventilation before significantly
immediately available. The choice of drugs should be
reducing pump flow or weaning from CPB.
based on the patient’s myocardial function, vascular
tone and complexity of surgery as well as individual
and institutional experience and preference. Electrolytes and Acid-Base
Electrolyte abnormalities should be corrected before
Anesthesia separation from CPB in order to optimize myocyte
function.
Patients’ anesthetic demand increases with rewarming
and there is a risk of awareness if this is not managed Potassium (4.0–5.5 mmol/l) – increased
correctly. Anesthesia, analgesia and neuromuscular potassium levels are commonly associated with
blockade must be assessed and supplemented as CPB as a result of giving cardioplegia. In many
required. Weaning from CPB may require either a centers, potassium is maintained at the higher end
change in anesthetic agent (e.g. intravenous to vola- of the normal range in order to suppress
tile) or an adjustment to continuing dose delivery. It arrhythmias. Hyperkalemia, however, can cause
is vital that anesthesia is maintained continuously on conduction abnormalities and impair
and off CPB and this should be confirmed by team contractility. Values above 6.0 mmol/l should
members. The use of processed electroencephalogram serve as an alert and levels above 6.5 mmol/l need
(EEG) or bispectral index (BIS) can be helpful. to be treated in the majority of patients before
weaning. Treatment includes the use of zero-
balance ultrafiltration with a low potassium
Alarms solution, forced diuresis with a loop diuretic such
Alarm settings for many parameters displayed on as furosemide, or an insulin/dextrose infusion
anesthetic monitors and ventilators are adjusted or (e.g. 10 U insulin with 25 g dextrose given over 15
even disabled during CPB. It is vital that physiological minutes). Hypokalemia can cause arrhythmias
monitoring with appropriate alarm settings is re- and should be treated with 10–20 mmol of K+
enabled prior to weaning from CPB. Similarly, alarms either slow iv or given directly into the reservoir of
and safety devices of the CPB machine should not be the CPB circuit if below 4 mmol/l.
disabled during the weaning process Calcium (1.09–1.30 mmol/l) – the concentration
of calcium in plasma may be reduced by
Ventilation hemodilution or transfusion of citrated blood
During CPB the lungs are allowed to deflate fully or (citrate forms a chelate complex with calcium)
remain slightly inflated at low levels of continuous leading to impaired contractility, vasodilatation
positive airway pressure. Prior to weaning from CPB, and coagulopathy. Ionized calcium should be
full and effective reinflation of the lungs has to be maintained above 1.1 mmol/l. Ca++ is typically
ensured with controlled manual alveolar recruitment. administered as an iv bolus of 1–2 g calcium,
If one or both pleural cavities are open, direct visual- either in the form of chloride or gluconate.
ization of the lung is possible and the pleural cavities Practitioners need to be aware of the formulation
should be drained of any accumulated fluid. they are using as a 10% chloride solution contains
Inspection of lung re-expansion should occur if an three times the amount of elemental calcium than
internal mammary artery is used for coronary bypass 10% gluconate solution does.
grafting as the lung is often “squashed” during vessel Magnesium (0.80–1.40 mmol/l) – low magnesium
harvest. If the pleurae are closed, always exclude a is associated with dysrhythmias and should be
pneumothorax by inspecting for bulging pleura. It corrected if below 0.8 mmol/l. Prophylactic
magnesium use regardless of the level may also be
115
may be prudent to apply tracheo-bronchial suction

indicated to reduce the incidence of prior to weaning, although there is wide variation
supraventricular tachyarrhythmia, AF and in clinical practice with regard to the level of
ventricular arrhythmias on removal of the cross acidosis to treat. Acidosis is generally treated with
clamp, although evidence is limited. Treatment sodium bicarbonate (see Chapter 10 for more
consists of 1–2 g of magnesium sulfate either detail). Although cardiac myocytes have effective
given slowly iv or added to the reservoir of the intracellular buffering mechanisms, the
CPB circuit. administration of a large volume in a short period
Glucose (4.0–7.8 mmol/l) – glucose control in the may generate paradoxical intracellular acidosis.
perioperative period has been shown to improve Clearance of this excess generated carbon dioxide
outcome after cardiac surgery. The Society of via the oxygenator may take 5–10 minutes. In
Thoracic Surgeons (STS) Clinical Practice patients with poor cardiac function, weaning from
Guidelines recommend maintaining perioperative CPB should not be attempted until the risk of
glucose levels < 10 mmol/l (180 mg/dL). significant paradoxical intracellular acidosis has
Hyperglycemia above that level should be treated passed and the excess carbon dioxide has been
with intravenous insulin in both diabetic and non- cleared.
diabetic patients. Tight glycemic control within Hemoglobin – for most patients, the hemoglobin
narrow margins such as 3.5–5 mmol (60–90 mg/dl) concentration should be above 7.5 g/dl prior to
has been shown to increase the incidence of termination of CPB but decisions to transfuse
hypoglycemic events and the risk outweighs should be based on the clinical situation. Higher
any benefits. In the absence of treatment Hb levels might be indicated if oxygen delivery is
with insulin, hypoglycemia in association expected to be impaired by a post-CPB low
with CPB is extremely rare and, if encountered, cardiac output state or if bleeding is expected to be
should be judiciously treated and its cause an ongoing problem.
investigated.
Lactate (0.7–2.5 mmol/l) – elevated serum lactate Levels
levels are encountered frequently during
Reservoir volume – there needs to be sufficient
prolonged episodes of CPB, particularly if there volume in the CPB circuit to fill the heart in order
have been periods of low flow or deep to wean it from CPB. Usually at least 300–500 mls
hypothermic circulatory arrest. Treatment of are required to fill the heart. If the reservoir
lactic acidosis per se is not usually instituted but volume is close to the low level sensor it is
increasing values must be seen as a potential essential to add additional volume. To minimize
indicator of inadequate organ perfusion (see also crystalloid requirements the surgeon should check
Chapter 10). the chest and pleural spaces for shed blood and
Acid-base balance – a large proportion of patients consider using the cardiotomy sucker to retrieve.
develop some degree of acidosis during CPB. However, the benefits of direct reinfusion of shed
Acidosis causes myocardial depression, increased mediastinal blood must be weighed against the
pulmonary vascular resistance, reduces the risks of adding blood that is likely to be diluted or
efficacy of inotropic drugs and increases highly activated with inflammatory mediators.
coagulopathy and should be corrected prior Alternatively shed blood is collected to an
to weaning. autotransfusion device where it is washed and the
Increasing or decreasing the sweep gas flow to red blood cells concentrated before
the oxygenator can readily and rapidly treat administration.
respiratory acid-base disorders by altering CO2 Bed position and transducer levels – it is common
levels as appropriate. Metabolic acidosis during surgery, and in particular during
commonly results from iatrogenic sodium cross clamp release, for the operating table
chloride administration, tissue hypoxia, position to be moved. Prior to weaning, the table
catecholamine administration and electrolyte should be returned to a neutral position and
imbalance. It often resolves with the increase in pressure transducers should be leveled and re-
116 flow rate on rewarming but may require treatment zeroed.

Predicting Difficulty incrementally occluding the venous return to the

CPB circuit, thus allowing the heart to fill with
Occasionally weaning from CPB is difficult and iden-
and eject blood, and
tification of patients who will present a particular
challenge allows additional preparations to be made gradually reducing the arterial pump flow to 0.
in advance. The order and speed of these actions will depend on
Commonly encountered risk factors for difficulty the volume in the reservoir, the patient’s ventricular
or failure to wean from CPB include: function and systemic vascular resistance, the surgery
1. poor preoperative ventricular function and any risk factors for failure to wean from CPB.
2. urgent and emergency surgery Preload, contractility and afterload are assessed as the
flow is reduced.
3. prolonged aortic cross clamp time
Weaning from CPB may take just a few seconds in
4. inadequate myocardial protection
a patient with vigorous cardiac activity and typically
5. incomplete surgical repair or revascularization. be taken to “half-flow” and then off CPB. In patients
Several strategies may be considered if weaning from with less promising cardiac function, the weaning
CPB is likely to be difficult: process may need to be protracted. This can take up
Inotropes and vasopressors can be commenced at to 30 or more minutes and may include reducing
rewarming, ensuring they have cleared the dead- pump flow by as little as 0.5 l every 5–10 minutes.
space of administration lines. Some inotropes After each new transition TEE evaluation, titration of
require a loading dose (e.g. enoximone, milrinone, ventricular volume loading by visual inspection of the
levosimendan) which should be given after aortic RV and/or assessment of direct left atrial pressure or
unclamping. pulmonary artery/pulmonary capillary wedge pres-
If sinus rhythm is not established and sure measurements, optimization of inotropes and
supraventricular arrhythmias or ventricular vasoconstrictors and assessment of cardiac rhythm
irritability are present despite correction of should be undertaken. At each stage volume can be
metabolic parameters, anti-arrhythmic treatments added by further occlusion of the venous clamp
should be considered and given in advance of any during “partial bypass” or transient increase in
attempts at weaning from CPB. Direct current arterial flow; volume can be removed by releasing
cardioversion (DCCV) using paddles directly the venous clamp or decreasing arterial
applied to the heart and low energy at 10–20 J is flow. Alternatively, some centers or teams prefer to
often successful. come off bypass and, if the heart does not
An IABP may be inserted before the start of surgery sustain adequate cardiac output, go back on
in patients with poor ventricular function. Or if an bypass and reperfuse the myocardium for a period
IABP is anticipated, but not inserted, a femoral of time.
arterial line may be placed on anesthetic induction The introduction of electronic venous occluders
to allow rapid insertion of a balloon catheter over a has been beneficial to fine tuning venous occlusion
wire in an emergency. during weaning. The vent and cardiotomy suction
may still be working during separation from CPB
and the patient will slowly exsanguinate if this blood
Mechanics of Separation from CPB is not returned. The perfusionist will return the
As soon as cardiovascular, respiratory and metabolic amount gained from vent and suckers to the patient
parameters are within acceptable limits and the 1:1 unless agreed otherwise.
patient is adequately rewarmed and ventilated, the As cardiac stroke volume progressively increases
perfusionist commences weaning in coordination to a level compatible with physiological circulation,
with the anesthesiologist and surgeon. the venous return line is completely occluded, the
Weaning begins with: arterial flow reduced to “off” or “matching vents or
suction” and the transition from CPB to “normal”
confirming with the anesthesiologist that the patient
circulation is complete.
is adequately ventilated – “happy with ventilation?”
117

Table 12.3. Key benefits of TEE during weaning from CPB

Assessment of Cardiac Function and
Inotropic Support Ensure adequate de-airing
Assessment of ventricular contractility and valvular Guide ventricular filling

function is vital during weaning. Myocardial con- Identify global ventricular dysfunction
tractility can be estimated from observing the heart
Guide inotropic support
both directly and with TEE, looking for coordinated
muscle contraction generating an acceptable aortic Ensure adequate surgical success (e.g. valve size,
pressure pulsation and arterial blood pressure. position and function, paravalvular leaks, residual
intracardiac shunts)
Commonly employed quantitative measures of LV
function include assessment of cardiac output with Identify regional wall motion abnormalities
thermodilution and stroke volume and ejection frac- Identify pleural and pericardial effusions
tion assessments by TEE. Any valvular pathology,
Guide insertion and positioning of mechanical support
particularly after repair, needs to be considered at this
devices
stage as well.
The pharmacological and mechanical strategies to Diagnose aortic dissection after decannulation
support the heart during and after weaning from CPB
are considered below and are generally guided by
institutional practice or individual preference.
Inotropic support should ideally be optimized prior selective. Echocardiography during the final stages
to weaning from CPB or during “partial bypass” to of CPB can inform on surgical success after valve
enable successful transition from CPB to repair or replacement, new or unresolved wall motion
physiological circulation. abnormalities, intracardiac shunts and other patholo-
It is worth noting that on initial separation from gies that might make the weaning process difficult. It
CPB, cardiac output and/or vascular tone can be low, is an excellent guide to de-airing after open chamber
and thus arterial blood pressure is frequently low. surgery (see Figure 12.1). Table 12.3 summarizes the
After optimization of preload and rhythm, hypoten- key benefits of using TEE during weaning from CPB.
sion is frequently managed with the use of short In the event of failed weaning from CPB, TEE is a
acting vasoconstrictors. This temporarily increases useful real-time modality for guiding the placement
systemic vascular resistance (SVR), increasing dia- of mechanical support devices such as intra-aortic
stolic blood pressure, which increases coronary artery balloon pumps, ECMO cannulae and ventricular
blood flow, and aids myocardial contraction. assist devices.
Assessment of Afterload
Commonly SVR is low following CPB because of the
Reversal of Anticoagulation
systemic inflammatory response and hemodilution. Protamine is used to reverse heparin anticoagulation
Short acting vasoconstrictors (e.g. metaraminol, phe- after successful transition from CPB to physiological
nylephrine) are administered during CPB and in the circulation. Heparin reversal practices vary among
weaning phase; along with the above agents, infusions centers and are discussed in detail in Chapter 16.
of norepinephrine or vasopressin may be used to Vents and suction must be stopped prior to protam-
maintain SVR in the weaning and post-CPB periods. ine administration.
The amount of vasopressor used by the perfusionist
to maintain blood pressure during CPB may serve as
a guide as to whether infusions will be necessary at the
Residual Blood Management
weaning stage and beyond. It is important to have a blood conservation strategy
in cardiac surgery and transfusion of the residual
volume in the CPB circuit is part of this. Practice
TEE in Weaning from CPB varies among centers and blood can be retransfused
There is a wide variation in the use of TEE in adult directly or processed by cell salvage or ultrafiltration
118
cardiac surgery, ranging from routine to highly in order to minimize allogenic blood transfusion.

Failure to Wean from CPB Pharmacological Choices in Weaning

Inadequate hemodynamic performance, when from CPB
attempting to wean a patient from CPB despite pro-
Administration of inotropes and/or vasopressor infu-
viding optimal conditions, should prompt the team to
sions may be indicated for successful weaning from
consider returning to full CPB, particularly if a deteri-
CPB. Drugs should be titrated to effect, optimizing
oration is catastrophic or unexpected.
blood pressure and heart rate, with patients moni-
Common conditions leading to failure to wean
tored using an appropriate combination of arterial
are:
blood pressure, pulmonary artery catheter, TEE,
surgical complications blood gas analysis and assessments of end-organ per-
arrhythmias fusion such as urine output. The particular thera-
vasodilation/hypotension peutic regimen will be dictated by the hemodynamic
ventricular failure abnormality at hand (e.g. vasodilation versus
hypoxia impaired contractility) along with institutional pref-
bleeding erences. Drugs to be considered for acute hemody-
residual air escaping from left ventricle into namic support during weaning from CPB are:
coronary circulation. Epinephrine – has both alpha and beta-
Table 12.4 summarizes common and procedure spe- adrenoceptor activity. Epinephrine increases
cific problems with weaning from CPB and potential cardiac output by increasing contractility and
management plans. heart rate and is frequently employed where
Reinstituting CPB should not necessarily be moderate to severely impaired cardiac
viewed as an adverse event or failure. It will result in contractility is present. At high dose continuous
a prolongation of the total CPB time, but it allows: infusion, it may cause considerable
vasoconstriction and tachycardia, impair
time for the heart to recover
diastolic function and raise serum lactate
escalation of monitoring concentrations.
reassessing and possibly optimizing of
Dopamine – binds to dopaminergic receptors and
pharmacological support
to alpha and beta-adrenergic receptors. It
(re)adjustment of hematocrit, acid-base, and increases cardiac output by increasing heart rate
electrolytes and contractility; however, at higher doses blood
examination of graft and valvular integrity (e.g. pressure may be increased by raising systemic
kinked coronary bypass grafts, vascular resistance with no increase in cardiac
paraprosthetic leaks) output and may cause dysrhythmias. Dopamine is
implementation of mechanical support generally used with more mild impairment of
hemodynamic performance.
Reinstitution of CPB Dobutamine – is a synthetic catecholamine with a
Whatever the degree of urgency, and even in situ- strong affinity for beta-adrenoceptors and little
ations of cardiac massage, adequate anticoagulation alpha activity. Contractility and heart rate are
needs to be achieved before going back onto CPB and increased along with a reduction in systemic
if time permits an ACT should be obtained prior vascular resistance, leading to a rise in cardiac
to reinstitution. output. At higher doses the effects on heart rate
To assure preparedness it is common to leave the and increased oxygen consumption and demand
CPB lines on the table and to keep the circuit primed tend to dominate and may limit its usefulness in
until at least sternal closure. To facilitate this, the moderate to severe cardiac failure.
circuit is filled with crystalloid fluid via the venous Milrinone and Enoximone – are often referred to
line while being drained of blood. This still allows as “inodilators.” They are bipyridine
retransfusion of the residual blood while keeping the phosphodiesterase-III (PDE III) inhibitors, which
circuit immediately available. block the breakdown of intracellular cyclic AMP
119

Table 12.4. Common problems encountered with weaning from CPB in specific operations and suggested management plan
PROCEDURE ISSUE PLAN

CABG Graft issues Surgical correction
Myocardial protection Rest on CPB, inotropes, mechanical
support
Unrecognized valve issue Surgical correction
Conduction issues Pacing
AVR Myocardial protection Rest on CPB, inotropes, mechanical
support
Air embolus Rest on CPB with increased perfusion
pressure
Valve issue – stuck leaflet, paravalular leak, valve upside down Surgical correction
Coronary occlusion right or left coronary ostial occlusion Surgical correction
MVR Myocardial protection Rest on CPB, inotropes, mechanical
support
pressure
Valve issue - stuck leaflet paravalular leak valve upside down Surgical correction
stitch around a strut if a tissue valve circumflex artery injury
Conduction issues LVOT obstruction (in repair) Pacing
Filling, stop inotropes, slow heart rate,
vasoconstriction, surgical
intervention
ASD Myocardial protection Rest on CPB, inotropes, mechanical
support
pressure
Pulmonary hypertension Pulmonary vasodilators e.g.
phosphodiesterase inhibitors
Anatomical - Residual shunt Coronary sinus impingement Surgical correction
mitral valve issues unrecognized anomalous pulmonary
venous drainage
VSD Myocardial protection Poor RV and/or LV Rest on CPB, inotropes, mechanical
support
pressure
Residual shunt Surgical correction
120

and increase stores of ATP. PDE III inhibitors and may stabilize hemodynamics or improve
improve contractility and because they cause them in the short term.
pulmonary vasodilatation (in addition to systemic Glyceryl trinitrate – is an organic nitrate that is
vasodilation) they are commonly used when right converted to nitric oxide and promotes both
heart dysfunction is present. They are associated venous and arterial dilation. It may be used post-
with a lower incidence of tachycardia and CPB to control hypertension, decreasing
arrhythmia than beta agonists, but they may need myocardial wall tension and oxygen consumption,
to be administered concurrently with a and protecting the integrity of vascular suture lines.
vasoconstrictor to maintain adequate arterial Inhaled pulmonary vasodilators – nitric oxide
pressure. Cardiac output increases without a (NO) is an endogenous smooth muscle relaxant
significant increase in myocardial oxygen and vasodilator produced by nitric oxide synthase.
consumption and demand. Inhaled nitric oxide acts as a selective pulmonary
Norepinephrine – has predominantly alpha- vasodilator and is often used in pulmonary
adrenergic effects and lesser beta-receptor activity. hypertension in order to preserve right heart
It causes smooth muscle contraction and function. Nitric oxide is aerosolized into the
vasoconstriction. Norepinephrine may be useful inspiratory limb of the breathing circuit and the
when the SVR is low, to counter the vasodilator dose titrated up to a maximum of 40 ppm. The
effects of phosphodiesterase-III inhibitors, and to drug is delivered directly to the pulmonary
manage acute right heart dysfunction. A concern vasculature and has an extremely short half-life,
with norepinephrine in high doses is reduced limiting any systemic hypotension. Prolonged
perfusion of the kidneys, gut and extremities, exposure to high concentrations of nitric oxide
resulting in hypoperfusion or overt ischemia. may result in methemoglobinemia and pulmonary
Vasopressin – is also known as anti-diuretic edema. The use of alternative inhaled pulmonary
hormone (ADH) or argipressin. It acts on a family vasodilators, such as epoprostenol, iloprost or
of vasopressin receptors in the smooth muscle of inhaled milrinone, has gained popularity as first
vasculature, resulting in vasoconstriction. line therapy.
However, stimulation of the V1 receptors in the
coronary and pulmonary vasculature causes Pharmacological Side Effects
release of nitric oxide and vasodilation. The action
The more potent a pharmacological agent is, the more
of vasopressin is independent of adrenoreceptors,
serious are the potential side effects. Potent vasocon-
and it may be useful in conjunction with
strictors such as norepinephrine and vasopressin can
norepinephrine for low SVR states.
cause splanchnic vasoconstriction, which can be asso-
Levosimendan – has inodilator properties,
ciated with postoperative gastrointestinal ischemia.
mediated by calcium sensitization of troponin
Potent inotropes, like epinephrine, increase myocar-
C and the opening of potassium channels on the
dial oxygen consumption, and can be associated with
sarcolemma of vascular smooth muscle cells.
a difficult-to-treat acidosis. Phosphodiesterase inhibi-
Levosimendan is also thought to confer
tors, such as enoximone, are potentially arrhythmo-
cardioprotection via its action on mitochondrial
genic. Potent chronotropes include dopamine and
potassium channels in the cardiomyocytes.
dobutamine, which can cause reflex tachycardias and
Hemodynamics are improved without a
arrhythmias.
significant increase in myocardial oxygen
consumption. The evidence for improved
outcomes is equivocal at best, however, and due to Mechanical Support in Weaning from CPB
its very high cost levosimendan is generally only After failure to separate from and returning to CPB,
be used in selected difficult-to-wean patients. attention is directed to identifying and treating revers-
Calcium – may be given as a bolus dose in the ible causes, such as inadequacy of surgery, and to
event of ventricular dilation and poor function optimizing hemodynamics while allowing myocardial
immediately on separating from CPB. Calcium recovery. In a small number of cases the ventricular
has both positive inotropic and vasopressor effects function remains insufficient to maintain adequate 121

organ perfusion, despite appropriate measures. If Veno-arterial extracorporeal membrane oxygen-

necessary mechanical therapies are warranted to ation (VA ECMO) – is a means of mechanically
facilitate separation from CPB. Strategies are dis- supporting the heart (and lungs) using a modified
cussed briefly here and mechanical support is CPB circuit, often making use of the existing bypass
described in greater detail in Chapter 14. cannulation. ECMO may continue for a period of
Intra-aortic balloon pump (IABP) – the most days to weeks until myocardial recovery has been
commonly used method of mechanical therapy, achieved or as a bridge to VAD or transplant.
intra-aortic balloon counterpulsation is achieved Ventricular assist device (VAD) – may be applied
using a balloon-tipped catheter that is positioned to either one or both ventricles to support a failing
within the descending aorta, with the tip just distal heart and preserve organ perfusion. Few data exist to
to the origin of the left subclavian artery. Inflation of support the use of VAD over ECMO when a patient
the balloon coincides with diastole, timed with the fails to separate from CPB. The decision to implement
dichrotic notch on the arterial waveform or the either technique should be based on center-specific
T wave on the ECG. The benefits of arterial counter- expertise and experience and specific patient condi-
pulsation lie with the augmented coronary flow and tion. The benefits of VA ECMO over VAD are that
improved myocardial oxygen delivery that occur the single VA ECMO circuit supports both ventricles
through increases in diastolic blood pressure from and also the lungs and can be more rapidly initiated
balloon inflation and the decrease in LV afterload that since cannulae are already in situ and only a change of
occurs during balloon deflation, thus reducing myo- circuit is required.
cardial oxygen demand while increasing delivery.
Suggested Further Reading cardiac surgery.” Annals of Cardiac

Anaesthesia 15.3 (2012): 206.
dysfunction is predictive of
difficult weaning from
1. Cui Wilson W, Ramsay James G. cardiopulmonary bypass,
“Pharmacologic approaches to 4. Murkin J M, Arango Murkin M.
Near-infrared spectroscopy as an Anesthesia & Analgesia: February
weaning from cardiopulmonary 2001,92(2): 291–298
bypass and extracorporeal index of brain and tissue
membrane oxygenation.” Best oxygenation. British Journal of 7. Vakamudi M. Weaning from
Practice & Research Clinical Anaesthesia. 103,suppl1,2009, cardiopulmonary bypass:
Anaesthesiology 29.2 (2015): i3–i13. problems and remedies. Ann Card
257–270. 5. Totaro R J, Raper R F. Anaesth. July 2004;7(2): 178–185.
2. Kim Heezoo. “Weaning from Epinephrine-induced lactic 8. Cui WW, Ramsay JG.
cardiopulmonary bypass.” Korean acidosis following Pharmacologic approaches to
Journal of Anesthesiology 64.6 cardiopulmonary bypass. Crit weaning from cardiopulmonary
(2013): 487. Care Med. October 1997;25(10): bypass and extracorporeal
1693–1699. membrane oxygenation. Best
3. Licker Marc et al. “Clinical review: Pract Res Clin Anaesthesiol. June
management of weaning from 6. Bernard Francis, Denault André,
Babin Denis et al. Diastolic 2015;29(2): 257–270.
cardiopulmonary bypass after
122

Chapter
Intraoperative Mechanical Circulatory
13 Support and Other Uses of

Both cardiopulmonary bypass (CPB) and its “off- hours. Following this, ECMO was successfully used
spring,” extracorporeal membrane oxygenation to support neonates by Bartlett and others in 1975.
(ECMO), are forms of mechanical circulatory support These successes led to the enthusiastic application
(MCS) utilized for short or long-term supplementa- of MCS to provide cardiorespiratory support for a
tion of native cardiac and/or respiratory function. As range of indications, but overall results were poor.
institutions tackle more complex pathologies, the The therapy became confined to a few expert centers
indications for these specialist techniques are becom- that persisted and developed the techniques, including
ing increasingly broad. This chapter addresses thor- veno-venous (VV ECMO) and veno-arterial ECMO
acic surgical requirements for MCS including (VA ECMO). In 2009, the CESAR trial demonstrated
mediastinal mass and tumor excision, complex MCS clinical efficacy and cost effectiveness of ECMO in the
techniques employed during thoracic aortic surgery treatment of adult acute respiratory distress syn-
and specialist techniques utilized during donor organ drome (ARDS), compared with advanced conven-
procurement and heart, lung and liver transplant- tional therapy in designated expert centers. Shortly
ation. Emergent uses of MCS both inside and outside after this, the publication of good results of the use of
the operating room are also discussed, including ECMO in supporting patients effected by the H1N1
endobronchial hemorrhage, extracorporeal cardio- influenza pandemic in Australia and New Zealand
pulmonary resuscitation (ECPR) and MCS for treat- established MCS as an acceptable and feasible therapy
ment of hypothermic circulatory arrest and trauma to support patients with severe acute pulmonary fail-
patients. MCS is also highlighted as a crucial preemp- ure. The advances in equipment, technique and
tive tool to support patients during induction of anes- expertise that led to acceptance of MCS for successful
thesia, whether it be due to difficult airways or risk of long-term respiratory support have made its use in
pulmonary hypertensive circulatory collapse. acute and longer term circulatory support accepted as
Historically, conventional CPB has been the a standard of care both in and outside the operating
mechanical circulatory support system of choice, but room in institutions with appropriate expertise and
with evolution of equipment, technique and experi- experience.
ence, ECMO has become an almost exclusive “player”
in the support realm and is being used more and
more in the surgical arena. MCS Equipment Selection
With ever increasing clinical applications of MCS and
a multitude of hardware and consumable options,
Historical Perspective of MCS in Cardiac early communication of the surgical plan is vital,
and Respiratory Failure especially in complex procedures, like those on the
Although CPB has been utilized for cardiac surgery thoracic aorta, as perfusion equipment needs to be
since the 1950s, the first successful report of its use as tailored to the style of MCS required (see Table 13.1).
a form of cardiorespiratory support was in 1972 when It is worth noting that there may be a number
Hill and colleagues used a heart-lung machine to MCS options to achieve the support goals for a given
support a young man, who had developed acute procedure; each of these will have a number of clinical
respiratory distress syndrome (ARDS) after repair of advantages and disadvantages that need to be con-
a traumatic aortic disruption, for a period of 75 sidered (see Table 13.2). 123

Table 13.1. Mechanical circulatory support style and perfusion equipment suitability
Centrifugal pump ECMO Open Open bypass circuit +

and heat exchanger circuit bypass specialized add-on
circuit circuitry
Left Heart Bypass Y Y Y Y
Partial Cardiopulmonary Bypass N Y Y Y
Complete Cardiopulmonary Bypass N Y Y Y
Complete Cardiopulmonary Bypass N N Y Y
with Hypothermic Circulatory
Arrest
Selective Spinal/ Reno-Visceral N N N Y
Hypothermic Perfusion
Table 13.2. Advantages and disadvantages of various perfusion equipment options
Perfusion Equipment Advantages Disadvantages

Centrifugal pump with Technically simple Custom tubing pack may be required
heat exchanger Economical Unable to salvage whole blood from
Full heparinization not required the surgical field directly into the
Low prime volume circuit, leading to heavy cell saver use
Temperature control and greater likelihood of transfusion
Completely reliant on lungs for
oxygenation
Anesthetist is required to give volume
and maintain adequate filling
Anesthetist is required to manage
blood pressure and administer
any drugs
Risk of air embolism in the setting of
access cannula dislodgement
ECMO circuit (centrifugal Circuit and hardware readily available Unable to salvage whole blood from
pump, heat exchanger in most institutions the surgical field directly into the
and oxygenator) Full heparinization not required circuit, leading to heavy cell saver use
Low prime volume and greater likelihood of transfusion
Temperature control Anesthetist is required to give volume
Oxygenator support and maintain adequate filling
Anesthetist is required to manage
blood pressure and administer
any drugs
Risk of air embolism in the setting of
access cannula dislodgement
124

Chapter 13: Intraoperative Mechanical Circulatory Support and Other Uses of Cardiopulmonary Bypass
Table 13.2. (cont.)
Perfusion Equipment Advantages Disadvantages

Complete heart-lung Circuit and hardware readily available Full heparinization required
machine with open in most institutions Larger priming volume
cardiopulmonary Temperature control Greater technical complexity,
bypass circuit Oxygenator support particularly if selective organ
Cardiotomy and several other pumps perfusion or hypothermic circulatory
available as sump suckers to salvage arrest is used
whole blood from the surgical field
Reduced requirement for cell saver
processing
Complete control of filling
Complete control of blood pressure
Readily able to administer fluids, blood
products or pharmacological agents as
required
Ability to add additional pumps or
circuitry as required
Inclusion of an open reservoir, reduces
risk of air embolism in the setting of
access cannula dislodgment, assuming
level and bubble safety sensors and
arterial pump servo-regulation are
utilized
Thoracic Surgeries then it should be done preemptively rather than as

There are a large number of case reports/series standby with rescue, as it takes at least 5–10 minutes
describing a wide range of both diagnostic and thera- to initiate support, even with experienced hands in
peutic procedures on non-cardiac thoracic structures the room.
that have made use of MCS. The approach to the difficult airway promulgated
by the learned anesthesia societies and colleges world-
Anterior Mediastinal Masses and wide rely on four fundamental techniques – bag-mask
ventilation (BMV), supraglottic airways (SGA), trach-
Difficult Airways eal intubation (ETT) and front-of-neck airway. If the
Anterior mediastinal masses, causing airway or car- obstruction occurs at or lower than the glottis, the
diovascular compromise by compression, have always above may not be enough to maintain oxygenation.
provided a challenge during induction of anesthesia Some have suggested elective use of MCS to maintain
and positioning for surgery. The traditional approach gas exchange as the potential fifth option in the non-
of maintaining spontaneous ventilation and use of urgent situation. Several groups have described use of
fiberoptic intubation is wise but may not guarantee CPB and ECMO (both VA and VV) in the manage-
protection from airway compression or circulatory ment of lesions causing subtotal obstruction of the
collapse. Several groups have described the use of airway at or below the glottis. These include creation
awake CPB or ECMO in a range of patients with of end-tracheostomy and resection of invasive thyroid
awake peripheral cannulation and initiating circula- cancer using awake peripheral VA ECMO; bronchos-
tory support prior to induction of anesthesia and copy, stenting and tracheostomy for “benign”
intubation; the pathologies dealt with included mas- obstructing tracheal lesions on CPB; use of VV
sive intrathoracic goiter, thymoma and teratoma. ECMO and high flow nasal oxygen for debridement
Most authors make the point that if there is enough of distal airway melanoma metastases; and broncho-
concern to consider use of bypass or ECMO support,
125
scopic laser resection of tracheal papillomatosis, with

awake VV ECMO established prior to induction. Both Over time several adjunct therapies have been
CPB and ECMO have also been used to support adopted to address the major challenges associated with
pediatric tracheal reconstruction for congenital trach- open surgical repair – hemodynamic instability and
eal stenosis. Both support techniques have pros and protection from spinal cord and reno-visceral malper-
cons, but overall results and outcomes are fusion. Arguably one of the greatest protectors against
comparable. hypoperfusion and hemodynamic instability through-
out the procedure is assistance provided by MCS.
Thoracic and Abdominal Tumor Surgery In its simplest form, distal aortic perfusion pre-
serves blood flow to the lower extremities and vital
A number of groups have reported case series using
organs during fashioning of the proximal anasto-
CPB for surgical resection of locally advanced thoracic
mosis. In particular, the inherently vulnerable spinal
malignancies, particularly where the tumor involves
cord and kidneys can be protected from ischemic
chambers of the heart or great vessels. These show that
injury by maintaining blood flow to the renal and
the use of CPB is associated with reasonable early
intercostal arteries, as well as perfusion via collateral
morbidity and mortality. The importance of patient
circulations. A 2012 Cochrane Review found evidence
selection is key with better long-term results dependent
from observational studies suggesting that distal
on shorter bypass times, the nature of the tumor and
aortic perfusion during open thoracoabdominal
the extent of lung resection.
aortic aneurysm repair reduces the incidence of
Renal cell carcinomas with tumor thrombi invad-
neurological deficits, with the greatest benefits seen
ing the inferior vena cava (IVC) have a poor progno-
in Crawford extent II aneurysms. The review however
sis; however, if the tumor can be resected in its
did note a, likely ethically-driven, lack of randomized
entirety via radical nephrectomy and IVC thrombect-
controlled trials comparing open surgical repair with
omy, overall survival is reasonable. In situations
or without distal perfusion, as the use of MCS has
where the tumor thrombus extends into the retro-
become an accepted prophylactic strategy used to
hepatic or supra-diaphragmatic IVC or into the right
combat ischemic complications.
atrium (RA), CPB can be used with standard arterial
MCS may be utilized in a variety of forms during
cannulation and venous drainage via the superior
open surgical repair including, but not limited to,
vena cava (SVC) and the IVC below the tumor
intermittent or continuous, selective hypothermic per-
thrombus, enabling en-bloc tumor removal. In cir-
fusion, distal aortic perfusion via left heart bypass or
cumstances where the thrombus extends beyond the
partial cardiopulmonary bypass and complete cardio-
RA into the pulmonary artery (PA) it is possible to
pulmonary bypass, often including deep or profound
cool the patient to 18–20°C and remove it under deep
hypothermic circulatory arrest (Table 13.1). The tech-
hypothermic circulatory arrest (DHCA).
niques employed in a given case depend on the extent
of disease, operative plan and surgical preference.
Thoracic Aortic Surgery
In recent years, treatment for aneurysms of the descend- Left Heart Bypass
ing thoracic aorta (segments distal to the left subclavian Left heart bypass can be achieved via pulmonary vein
artery to the diaphragm) and thoracoabdominal aorta or left atrial access cannulation and femoral arterial or
(segments distal to the left subclavian artery to the iliac distal aortic return cannulation (see Figure 13.1). Some
arteries) has focused on endovascular stent-graft repairs. left atrial filling is maintained throughout the system-
Endovascular treatment has the obvious appeal of a atic clamping of the thoracic descending and thora-
minimal access approach and a reduced average mortal- coabdominal aorta to allow proximal perfusion via left
ity rate (5.8%) compared to open surgery (13.9%). ventricular ejection, while distal perfusion is provided
However, it is not without its limitations, including by the femoral arterial or distal aortic return cannula.
reduced suitability with increased complexity and extent The perfusion and anesthetic teams work to ensure
of disease, anatomic confounders such as aortic angula- that proximal and distal perfusion pressures, measured
tion and tortuosity, landing zone inadequacy and risk of by way of radial and femoral arterial lines, are main-
endoleak leading to reintervention. Open surgical repair tained in equilibrium throughout the procedure and to
126 remains an indispensable treatment modality, particu- prevent accidental emptying of the left atrium during
larly in the setting of complex pathologies. the procedure. Proximal perfusion is being provided by

PROXIMAL
CLAMP
INFLOW
CANNULA
LEFT
ATRIUM
DISTAL
CLAMP
LINES FOR SELECTIVE PERFUSION

OF SPLANCNIC VESSELS
CENTRIFUGAL
PUMP
PRESSURE FLOW
OUTFLOW MONITOR METER
CANNULA
FEMORAL
ARTERY
Figure 13.1 Left heart bypass: inflow cannula in left pulmonary vein or in left atrium and return to femoral artery or distal aorta (it is possible
to incorporate an oxygenator in this circuit for additional support). (De Simone F, De Luca M. Left Heart Bypass (Ch24) in Thoraco-Abdominal Aorta:
Surgical and Anesthetic Management. R. Chiesa et al. (eds.) © Springer-Verlag Italia 2011.)
the heart and it is therefore important to avoid to turn off ventilation to one or both lungs and rely
moderate–deep hypothermia in order to prevent tem- on the extracorporeal oxygenator, as well as selective
perature related arrhythmias. In the instance where spinal and reno-visceral perfusion. These perfusion
aortic cross clamping at the distal aortic arch is not techniques provide superior surgical access, visibility
possible due to atherosclerotic plaque or further aneur- and flexibility with the operative plan, as well as the
ysmal tissue, complete cardiopulmonary bypass is ability to perform the procedure with reduced time
likely to be the chosen modality of mechanical circula- pressure, which is evoked by the known risks associ-
tory support to allow for DHCA during open proximal ated with prolonged ischemic clamp time in the
anastomosis, with the option to continue perfusing absence of hypothermia or selective perfusion.
tissues distal to the aortic cross clamp.
Selective Spinal and Reno-visceral Perfusion
Partial or Complete Cardiopulmonary Bypass Matalanis et al are pioneering the “branch first” sur-
Partial or complete cardiopulmonary bypass is often gical approach in tackling Crawford extent II thora-
achieved via femoral venous access cannulation and coabdominal aneurysms in an attempt to maximize
femoral arterial or distal aortic return cannulation. the benefits provided by MCS and to provide near
This setup affords the surgical team the ability to continuous reno-vascular perfusion (see Figure 13.2a
utilize the full possibility of perfusion techniques, and b). In this approach, partial bypass is instituted 127
including hypothermia, circulatory arrest, the ability via femoral-femoral cannulation, using an open

(a)
sling around
superior mesenteric
artery
sling around
celiac artery
left renal artery
(b)
large intercostal
artery
right renal artery
128 Figure 13.2 Branch first approach to thoraco-abdominal aneurysm repair. (a) Sequential debranching and perfusion of reno-visceral vessels
using a trifurcated graft with perfusion limb. (b) Clutter-free access to the abdominal aorta, with left renal, SMA, coeliac trunk being perfused by
the graft and smaller lumbar arteries already ligated, allowing access to aortic pathology. (Reproduced with kind permissions from Matalanis and
Ch’ng, Semin Thorac Cardiovasc Surg 2020; 31.4:627–872.)

bypass circuit with specialized add-on circuitry pre- Normothermic Regional Perfusion (NRP) – also
pared for selective reno-visceral perfusion using an involves prompt sternotomy after declaration of death
additional roller pump, and intercostal artery perfu- followed by heparinizing via the right atrium and
sion using the cardioplegia pump. This technique pulmonary artery and clamping of the innominate,
provides complete mechanical circulatory support left carotid and left subclavian arteries to ensure that
flexibility including systemic and selective tempera- cerebral circulation cannot be restored. MCS is insti-
ture control, partial or complete cardiopulmonary tuted via right atrial access and an aortic return can-
bypass, selective perfusion and the option of nula. Following restoration of mechanical ventilation,
hypothermic circulatory arrest if required. cardiac reanimation and a period of reperfusion,
MCS is weaned. Suitability of the reanimated heart
for transplantation is assessed functionally via transe-
Circulatory Support during Donor sophageal echocardiogram and thermodilution car-
Organ Procurement diac output measurements. If found suitable the
donor heart is prepared for transport to the recipient
Organ Donation for Heart Transplantation hospital. These hearts are then given cold cardiople-
Heart procurement after the cessation of cardiac gia, procured and transported using either the OCS
activity was utilized for the first and other early car- system or conventional cold storage.
diac transplants, as brain death criteria and legisla-
tion were not widely established until the early to
mid-eighties. With revised legislation and commer- Organ Donation for Lung Transplantation
cial availability of specialized MCS devices some The lung transplant community were much earlier
groups have revived the donation after cardiac death adopters of the DCD pathway, largely due to fewer
(DCD) heart transplant pathway. The first report of ethical hurdles and the decreased vulnerability of the
three successful cases of orthotopic cardiac trans- lungs to warm ischemia, allowing a simple retrieval
plantation using hearts from DCD was published in and transportation strategy utilizing pneumoplegic
2014. Promising outcomes have helped spread this cold storage. The International Society for Heart
technique and globally its uptake is increasing and Lung Transplantation (ISHLT) DCD Registry
rapidly. has reported comparable 5-year survival rates, of
DCD donation involves either direct procurement 63% and 61%, between DCD and donation after
and perfusion, direct procurement and cold storage brainstem death (DBD) lung donor recipients,
or normothermic regional perfusion (NRP) (see respectively. With a large number of lung
Figure 13.3). donor offers available, efforts have been focusing on
Direct procurement and perfusion (DPP) – increasing the percentage of organs that can be
involves prompt transfer of the donor to the operat- accepted as suitable for transplantation by using pre-
ing room after death has been declared, with exped- transplant, normothermic, ex vivo lung perfusion
itious sternotomy, administration of cold cardioplegia (EVLP).
and removal of the heart following standard surgical EVLP allows explanted donor lungs to be perfused
technique. The organ is then connected to the and ventilated in order to thoroughly assess their
Transmedics Organ Care System (OCS™) (see suitability for transplantation prior to implant. This
Figure 13.4) and perfused at normothermia with a is particularly useful in marginal organs which sit
mixture of a priming solution and 1.5 liters of hepar- outside an institution’s standard donor organ accept-
inized donor blood. The flow rate is initially set at ance criteria. Not only can marginal organs be
1 l/min and adjusted to maintain a mean aortic assessed during EVLP, but they can potentially be
pressure of 65–90 mmHg, coronary blood flow of reconditioned using various resuscitative maneuvers,
650–900 ml/min and a heart rate of 65–100 beats/min. rescuing and restoring donor organs that would have
The suitability of the reanimated heart for transplant- otherwise been discarded.
ation is assessed functionally, via macroscopic assess- The XVIVO system (Figure 13.5) is usually
ment, and biochemically with serial lactate located at the recipient hospital for reanimation and
measurements. The design of the device also allows assessment of distantly retrieved, marginal donor
129
epicardial echocardiography in an aseptic manner. lungs prior to implant. The explanted lungs, which

WLST
Circulatory arrest.
Hands – off asystolic observation period

(2 – 5 minutes depending on local guidelines).
Declaration of circulatory death.
Donor immediately transferred to the OR where

they are prepped and draped for procurement.
Simultaneous tracheal re-intubation and

median sternotomy performed.
DPP Pathway NRP Pathway
Supplemented cold crystalloid cardioplegia Donor placed on cardiopulmonary bypass,

administered via the aortic root. with the exclusion of cerebral perfusion.
Excised donor heart placed on OCS.

In vivo functional assessment, via
transoesophageal echocardiogram and
pulmonary artery catheter thermodilution
Ex vivo metabolic assessment via cardiac output measurement, following
measurement of myocardial lactate reanimation and weaning from
extraction on OCS. cardiopulmonary bypass.
Beating heart transported to recipient

Transported to recipient hospital under
hospital under normothermic, continuous
cardioplegic arrest and cold storage.
ex vivo perfusion on OCS.
Beating heart on OCS arrested with 1L of

cold St Thomas’ cardioplegia at recipient
hospital.
Donor heart implantation.
Figure 13.3 Donation after circulatory death organ procurement pathway for heart transplantation.
130

Figure 13.4 TransMedics Organ Care System

with heart in situ on rig.
have been flushed with cold Perfadex solution, sit subsequently passes through a leukocyte depleting
inside a sterile dome, connected to a mechanical ven- filter to the pulmonary artery return cannula for
tilator and a perfusion circuit, which are incorporated reoxygenation in the donor lungs. Lungs usually
into the device. The perfusion circuit priming solu- remain on the EVLP system for 4–6 hours, with
tion is two liters of acellular, manufacturer-supplied hourly recruitment maneuvers and partial exchange
Steen solution, supplemented with heparin, methyl- of the perfusate solution to ensure provision of
prednisolone and imipenem antibacterial agent. adequate metabolites. If the lungs are deemed viable
During operation, perfusate, oxygenated by the mech- for transplantation following functional assessment,
anically ventilated lungs, drains from a left atrial they are cooled, flushed with cold Perfadex solution
pulmonary vein cuff cannula into a hard-shell reser- and are kept under cold storage until implant.
voir. The perfusate is then pumped via a centrifugal To date EVLP is yielding promising results. A recent
pump from the reservoir through a gas exchange multicenter US study (the NOVEL trial) comparing
membrane, which is supplied with a specialized sweep transplants utilizing organs that met standard procure-
gas, containing 6% oxygen, 8% carbon dioxide and ment criteria, with those utilizing marginal donor lungs
86% nitrogen, so that deoxygenation of the perfusate that underwent pre-transplantation EVLP, found com-
occurs due to the low oxygen concentration. The gas parable early survival.
exchange membrane also contains a heat exchanger to A portable lung Transmedics OCS was introduced
enable temperature control of the perfusate. From the relatively recently; clinical reviews have commenced 131
gas exchange membrane, the deoxygenated perfusate but are still in their infancy.

Figure 13.5 XVIVO lung perfusion system.
Circulatory Support during pulmonary arterial hypertension (PAH) undergoing

heart-lung transplantation. During initiation of awake
Organ Implant bypass, the surgical team is scrubbed, patient prepped
and draped, peripheral cannulae inserted with local
Heart and Heart-Lung Transplantation anesthetic, and bypass slowly commenced. Following
That standard cardiopulmonary bypass needs to be induction of anesthesia, the venous cannula position
used for both heart and en bloc heart-lung transplants is optimized using transesophageal echocardiographic
is obvious. The variations of the standard central bi- guidance, to optimize flows.
caval and aortic cannulation will be dependent on the The subsequent surgery and bypass manage-
indications for transplant, whether there have been ment follow the principles discussed in the rest of this
any previous surgeries including ventricular assist book.
device (VAD) insertion (see also Chapter 14) and
whether the recipient is on ECMO at the time of
transplant. These may include putting a “Y” in the Lung Transplantation
venous line to allow for SVC cannulation, as well as Single or bilateral lung transplantation can be per-
femoral venous and arterial cannulation. Peripheral formed using sequential one lung ventilation (OLV)
cannulation may occur with or without commence- or with extracorporeal circulatory support. Practice
132 ment of bypass prior to sternotomy or awake com- varies widely across the world with some high volume
mencement of bypass prior to induction of units utilizing MCS in only 20% of cases, others for
anesthesia, particularly in patients with severe almost all. There seems to be a consensus among

transplant centers that the sickest patients should be cannulation of the portal vein in cases of persistent
put on MCS electively. These include: portal hypertension, with return via the percuta-
– all cases of primary PAH, neously cannulated internal jugular or axillary vein.
– other types of pulmonary hypertension when the Although a simple centrifugal pump could be utilized,
pulmonary artery pressures approach or exceed most units use a complete ECMO style MCS circuit
systemic blood pressure, with integrated heat exchanger and oxygenator. This
– severely compromised right ventricular function, has the advantages of
– if there is need to correct a coexistent cardiac – allowing maintenance of body temperature,
problem (such as valve or coronary lesions) and – potential to assist oxygenation and
– when the patient is on preexisting MCS. – “tip to tip” heparin bonding of all circuit
components, avoiding heparinization in what
Both CPB and VA ECMO are used; both are able to
historically has been a notoriously “bloody”
replace or support the functions of the heart and lungs.
procedure.
The primary difference between the two is the absence
of a venous reservoir and the inability to suction spilled
blood from the operative area in ECMO systems and
the potential to run at much lower levels of anticoagu- Emergent or Bail-out Applications
lation, particularly if heparin bonded circuit compon-
ents are used in ECMO (see also Table 13.2).
of MCS
Two meta-analyses using almost the same pool of
papers came to the conclusions that there may be
Perioperative
some advantage in using ECMO compared with Cardiac teams have cause to heed and invoke the late
CPB, but there was no significant difference in long- Norman Shumway’s second law – “the pump is your
term outcomes and that further randomized trials friend” – to take advantage of the hemodynamic
were needed. stability and optimized gas exchange that CPB can
provide when intraoperative problems occur. In all of
Liver Transplantation the operations discussed above, case reports and
series exist where MCS was not used initially but
MCS may be utilized during liver transplantation,
was employed to bail out of a deteriorating situation.
either as a standby hemodynamic rescue option or
As Table 13.2 shows, CPB requires full anticoagula-
electively employed to provide hepatoportal circula-
tion; VA ECMO on the other hand enables the same
tory decompression and hemodynamic stability. MCS
level of hemodynamic and gas exchange support
largely achieves these goals by ensuring adequate sys-
with little or no anticoagulation, at least in the
temic venous return, which may be compromised
short term. One of the best demonstrations is VA
secondary to surgically-induced IVC obstruction.
ECMO support in case of massive endobronchial
Assisted return of blood distal to the hepatic vessels
hemorrhage after pulmonary endarterectomy for
enables maintenance of right atrial filling pressures,
chronic thromboembolic pulmonary hypertension.
allowing the heart and lungs to provide adequate
Short-term VA ECMO after weaning from CPB
cardiorespiratory function.
and heparin reversal enables effective resolution
Classic liver transplantation involved complete
of this feared complication with 87% long-term
cross clamping and replacement of the retrohepatic
survival.
IVC, thus the use of MCS was far more common. In
modern “piggy-back” hepatic transplant, the retrohe-
patic IVC is preserved and only partially cross Outside the Operating Room
clamped, reducing the need for MCS. Cardiogenic shock is probably the biggest indication
Today, in most high volume units, MCS is for using MCS outside the operating room, with acute
reserved for patients with a high Model of End-stage myocardial infarction by far the commonest cause.
Liver Disease (MELD) score, as this is where it may Other common indications include acute myocarditis
have the greatest benefits in reducing adverse renal, and acute decompensation of chronic heart failure.
respiratory and hemodynamic outcomes. MCS in the form of VA ECMO can provide complete
support, enabling stabilization of the clinical situation
133
Cannulation is usually percutaneous via a short
femoral venous cannula, with or without direct and a bridge to decision making.

Three indications for emergent MCS warrant Table 13.3. Staging guide of accidental hypothermia
special mention: Stages Clinical findings Core
ECPR – describes the use of extracorporeal temperature
technology in patients who suffered a cardiac (oC)
arrest and who are proving refractory to standard
Hypothermia Conscious, shivering 35–32oC
advanced cardiac life support (ACLS) measures. I [mild] HTI
The CHEER trial from 2015 demonstrated
feasibility and reasonable outcomes in patients Hypothermia Impaired <32–28oC
II consciousness,
who suffered >30 minutes refractory cardiac
[moderate] may or may not
arrest, in or out of hospital, that were managed by
HTII be shivering
a combination of mechanical CPR and VA
ECMO. Twenty-four of 26 eligible patients were Hypothermia Unconscious, vital <28oC
established on ECMO within a median time of III [severe] signs present
HTIII
56 minutes from collapse. Survival to hospital
discharge with good neurological recovery Hypothermia Apparent death, vital Variable
occurred in 14/26 (54%) of patients. Factors IV [severe] signs absent
associated with poor outcome included age >65, HT IV
unwitnessed arrest, asystole, terminal illness,
known preexisting severe neurological injury, no before initiation of MCS at the earliest
flow, i.e. no effective extracorporeal circulation opportunity. This most commonly involves VA
(ECC) > 10 minutes, and lactate > 18 mmol/l on ECMO via femoral arterial and venous
ECC initiation. Other case series using a similar cannulation, providing immediate restoration of
approach have achieved much more modest circulation and gas exchange as well as enabling
outcomes, fanning the discussion who should be rapid rewarming. Most groups recommended
offered this costly and resource-intensive therapy. increasing flows gradually with the initial circuit
Accidental hypothermic cardiac arrest (HCA) – temperature about the same as that of the patient.
the cardiovascular effects of hypothermia are well Rewarming should occur at a rate of between
known to anyone involved in management of 1–4oC per hour to a target temperature >
cardiac surgery and CPB. As the core temperature 32oC and continue until a stable cardiac rhythm
falls below 30oC cardiac activity and rhythm are with adequate perfusion and gas exchange is
affected, at <28oC ventricular fibrillation is established and supported with modern post
common, vasoconstrictive failure and then cardiac arrest management. Withdrawal of MCS
asystole occur at around 20oC. Accidental should be considered if there is no return of
hypothermia – i.e. core temperature <35oC – is spontaneous circulation (ROSC) at 32–35oC.
thought to cause approximately 1500 deaths per Most management guides, such as ICAR
annum in North America alone. It is normally MEDCOM or the Bernese Hypothermia
associated with colder climates involving snow Algorithm (see Figure 13.6), endorse this
and icy bodies of water, but can also occur in approach unless there are obvious signs of
more moderate climates, where exposure, irreversible death.
intoxication and other cofactors play a role.
A recent individual patient data meta-analysis of over
A clinical staging guide – the Swiss Staging
650 MCS treated cases of HCA showed a mean overall
System – is used in the field to plan and prioritize
survival rate of 46%, with 40.3% having good
management (see Table 13.3). In patients with HT
neurological outcomes. This compares very favorably
IV (hypothermic cardiac arrest) and no overt
with a survival rate of 10–37% in non MCS treated
signs of life, the dilemma is differentiating
HCA victims. Attempts to develop a more reliable
between actual death and potential viability.
outcome prediction scoring system led to the HOPE
The results of several clinical series have led to
score (Hypothermia Outcome Prediction after ECLS)
the notion that “no one is dead until warm and
based on gender, asphyxia related mechanism of
134 dead” and thus most victims are rescued with
arrest, age, potassium level, duration of CPR and
basic and advanced cardiac life support treatment
temperature. The score has subsequently been

Patient’s appropriate history

or core temperature <35°C
Vital signs present

Yes No
Impaired consciousness - Obvious signs of irreversible death(*) Yes

No Yes - Valid DNR order to any Consider withholding or
- Conditions unsafe for rescuer termination of CPR
- Avalanche burial >6 min, airway
Prehospital cardiac instability packed with snow and asystole
Transport to nearest hospital if
injured; consider onsite or hospital - SBP <90 mmHg(†)
treatment if uninjured - Ventricular arrhythmias No to all
- Core temperature <28°C
- Start CPR, do not delay transport
No to all Yes to any - Prevent further heat loss
HT I(;) - Airway management and up to 3 doses
- Warm environment and dry clothing of ALS medication/defibrillation
Transport to nearest Transport to hospital
- Warm sweet drinks
appropriate hospital with ECMO/CPB(S)
- Active movement
Cardiac arrest from alternatative cause
prior to cooling Yes
to any Transport to nearest appropriate
HT II or III(‡) - Major trauma or drowning hospital or manage as per
- Minimal and cautions movements to avoid arrhythmias - Witnessed arrest supervising MD
- Prevent further heat loss - Avalanche burial <60 min
- Active external and minimally invasive rewarming
techniques(I I) No to all
- Airway management as required Consider tests to confirm need
for ECMO/CPB(¶) No to any
- Core temperature <30°C
-1
- Serum potassium <12 mmol L
Yes to all
Transport to hospital with ECMO/CPB($);

do NOT terminate CPR
Cardiac HT IV(‡)
- Prepare for multi-organ failure and need for instability - Rewarm with ECMO/CPB No
ECMO respiratory support resolved - If ECMO/CPB not available, CPR with ROSC Consider termination of
- Post arrest management active external and alternative internal CPR
rewarming(**)
- Consider targeted temperature 32-34°Cx24 hr
- Rewarm to >32°C core temperature
Figure 13.6 Management in Accidental Hypothermia. (*) Decapitation; truncal transection; whole body decomposed or whole body frozen
solid (chest wall not compressible). (†) SBP <90 mmHg is a reasonable prehospital estimate of cardiac instability but for in-hospital decisions,
the minimum sufficient circulation for a deeply hypothermic patient (e.g. <28°C) has not been defined. (‡) Swiss staging of accidental
hypothermia. In remote areas, transport decisions should balance the risk of increased transport time with the potential benefit of treatment in
an ECLS center. (||) Warm environment, chemical, electrical, or forced air heating packs or blankets, and warm IV fluids (38–42°C). In case of
cardiac instability refractory to medical management, consider rewarming with ECLS. If the decision is made to stop at an intermediate hospital
to measure serum potassium, a hospital en route toward the ECLS center should be chosen. CPR denotes cardiopulmonary resuscitation, DNR
do-not-resuscitate, ECLS extracorporeal life support, HT hypothermia, MD medical doctor, ROSC return of spontaneous circulation, SBP systolic
blood pressure.
validated as a predictive tool and may be helpful in including a national trauma database, a systematic
the triage of whether or not to use MCS rewarming in review of published series of MCS in trauma
the HCA patient and is available online (www victims and a review of trauma patients in the
.hypothermiascore.org). ELSO registry, showed an overall survival to
ECLS in trauma patients – The use of VA ECMO discharge of between 50 and 79%.
to provide circulatory support to patients with A review of ECMO support in traumatic injury from
acute traumatic cardiac arrest or cardiogenic five ECMO centers in the United Kingdom identified
shock presenting to hospital has been reported in 52 patients with an overall mortality of 15%. Forty of the
several case series, but survival rates of 14–20% patients had surgical procedures prior to ECMO. The
have been unimpressive. authors found an overall incidence of bleeding compli-
Outside of the above circumstances there is cations of 50% but no difference in incidence between
evidence that MCS for respiratory or circulatory those receiving and not receiving anticoagulation, and
failure developing in trauma patients, during or only four patients requiring return to the OR. They
135
after stabilization in hospital, is an effective concluded that ECMO does not appear to worsen trau-
option. A number of retrospective reviews, matic injury despite use of anticoagulation.

Table 13.4. Methods of combining continuous renal replacement therapy with extracorporeal life support
Combination Type Advantages Disadvantages/risks

CRRT & ECLS
Integrated In-line haemofilter Easy setup Less precise ultrafiltration &
approach Low cost limited solute clearance
Flow turbulence and risk of
hemolysis
Integration of CRRT Both ultrafiltration and solute clearance Potential exposure of CRRT
device in ECMO Mode of solute clearance not restricted device to excessive
circuit Control of ultrafiltration pressure
No need for separate vascular access or Risk of air entrapment
anticoagulation Turbulent flow and
hemolysis
Shunt within ECLS circuit
Thrombosis risk on extra
circuit connectors
Connection of CRRT Control of ultrafiltration Potential of interfering with
device to Pressure in safe range of CRRT device oxygenator
oxygenator
Parallel Separate CRRT and Provision of solute and ultrafiltration clearance Need for separate vascular
systems ECLS circuits Mode of solute clearance not restricted access
Precise control over fluid removal Two extracorporeal circuits
A degree of “independence” from ECLS in terms of to be managed
coagulation management and circuit changes Higher extracorporeal blood
volume
Organ Support during ECLS A parallel system requires separate cannulation and
managing two extracorporeal circuits. The integrated
Patients receiving ECLS are still at risk of running
approach with in-line hemofilter, while easier and less
into problems with other organ systems. This can be
expensive, offers less precise filtration and an increased
due to the primary disease process, or because of
risk of hemolysis. The CRRT device can be “plumbed”
exposure to ECLS and its circuit. The most vulnerable
into the ECLS circuit in a number of places each with
organs, with greatest impact of their failure, are the
pros and cons. These devices offer the most flexibility
kidneys. The incidence of acute kidney injury (AKI)
in control of the filtration process but are characteris-
can be as high as 85% in patients on ECLS, is most
tically “low pressure” systems and need modification to
often multifactorial in nature and has significant
be incorporated in the relatively increased pressures of
effect on fluid management and outcome. Renal
an ECLS circuit. A number of approaches used include
replacement therapy (RRT) should be considered
incorporating some type of “reduction” device on the
even though it represents a significant increase in
inflow or simply adjusting the pressure alarm limits in
the complexity of care. In most circumstances, this
suitable CRRT systems. It is worth noting that any
is done continuously (CRRT).
integrated CRRT system will lead to a shunt within
Broadly speaking there are two ways to do this; a
the ECLS circuit but this is usually less than 5%. Some
parallel system with separate CRRT and ECLS circuits
centers routinely have the CRRT drainage and return
or an integrated approach with either a hemofilter in-
between the pump and oxygenator of the circuit with
line or a CRRT device “plumbed” into the ECMO
pressure alarms on the CRRT system adjusted appro-
circuit. Each of these approaches have a number of
priately; other centers vary, with perhaps the major
advantages/disadvantages as described in Table 13.4
determinant being local expertise of staff and availabil-
136 and, while a detailed discussion is beyond the scope of
ity of the various systems.
this chapter, a number of points need be made.

Suggested Further Reading Cardiovasc Surg 2020; 31.4:

627–872.
10. Stub D, Bernard S, Pellegrino V
et al. Refractory cardiac arrest
1. Surman TL, Worthington MG, treated with mechanical CPR,
Nadal JM. Cardiopulmonary 6. Page A, Messer S. Large SR heart
transplantation from donation hypothermia, ECMO and early
bypass in non-cardiac surgery. reperfusion (the CHEER trial).
Heart Lung Circ 2019; 28: after circulatory determined
death. Ann Cardiothorac Surg. Resuscitation 86; 2015: 88–94.
959–969.
2018;7(1): 75–81. 11. Paal P, Gordon L, Strapazzon G
2. Slinger P, Karsli C. Management et al. International Commission
of the patient with a large anterior 7. Van Raemdonck D, Keshavjee S,
Levvey B et al. Donation after for Mountain Emergency
mediastinal mass: recurring medicine (ICAR MEDCOM):
myths. Curr Opin Anaesthesiol circulatory death in lung
transplantation – Five-year accidental hypothermia – an
2007; 20: 1–3. update. Scan J of Trauma Resus
follow-up from ISHLT registry.
3. Arif R, Eichorn F, Kallenbach K J Heart Lung Transplant 2019; 38: Emerg Med 2016; 24: 111.
et al. Resection of thoracic 1235–1245. 12. Kruitt N, Prusak M, Miller M
malignancies infiltrating cardiac et al. Assessment of safety and
structures with use of 8. Kiziltug H, Falter F. Circulatory
support during lung bleeding risk in the use of
cardiopulmonary bypass. extracorporeal membrane
J Cardiothor Surg 2015; 10: 87–94. transplantation. Curr
Opin Anaesthesiol 2020; 33: oxygenation for multitrauma
4. Hsu C, Kwan G, Van Driel M 37–42. patients: a multicenter review.
et al. Distal aortic perfusion J Trauma Acute Care Surg 2019;
during thoracoabdominal 9. Czigany Z, Scherer M, Pratschke J 86: 967–973.
aneurysm repair for prevention of et al. Technical aspects of
orthotopic liver transplantation – 13. Ostermann M, Connor M,
paraplegia. Cochrane Database Kashani K. Continuous renal
Syst Rev 2012; 3: CD008197. A survey-based study within the
Eurotransplant, Swisstransplant, replacement therapy during
5. Matalanis G, Ch’ng S. Scandiatransplant and British extracorporeal membrane
Thoracoabdominal aortic transplantation society networks. oxygenation: why, when and how?
aneurysm – The branch first J Gastrointest Surg 2019; 23: Curr Opin Crit Care 2018, 24:
technique. Semin Thorac 529–537. 493–503.
137

Mechanical Circulatory Support
Chapter
14 Jason M Ali, Ayyaz Ali and Yasir Abu-Omar
Over the last decade there has been a significant ventricular performance (Table 14.2). The IABP com-
increase in the utilization of mechanical circulatory prises a drive console with a pump and a double-
support (MCS) devices. Traditionally, MCS was lumen balloon catheter that is typically introduced
reserved as a “bridge to transplantation” primarily percutaneously into the femoral artery. The tip of
for patients with end-stage heart failure who were the balloon is ideally positioned just distal to the left
deemed candidates for transplantation. Nowadays, subclavian artery to reduce the risk of occluding
advanced MCS devices are commonplace in the car- the cerebral arteries proximally and abdominal vis-
diothoracic intensive care. The indications for their ceral arteries distally (see Figure 14.1). One lumen
use have broadened to include the prophylactic is used for pressure monitoring, helium is delivered
use in high-risk percutaneous coronary interventions into and removed from the balloon through the
or surgery, as an adjunct to cardiopulmonary other one. Helium is used due to its low viscosity
resuscitation (ECPR, see also Chapter 13) and as part (permitting rapid transfer) and high blood solubility
of the routine management of intractable cardiogenic (reducing the impact of gas embolism should the
shock. balloon rupture). If there is no contraindication
There are several forms of MCS that are typically patients should receive therapeutic anticoagulation
classified as either temporary or durable and will be to reduce the risk of thromboembolic events. Distal
discussed in this chapter. Temporary MCS devices limb perfusion must be examined regularly, and
(Table 14.1) include the intra-aortic balloon pump distal pulses checked either by palpation or with a
(IABP), the Impella (Abiomed), the TandemHeart handheld Doppler probe. The leg should be checked
system (CardiacAssist), veno-arterial extracorporeal regularly for the development of compartment
membrane oxygenation (VA-ECMO) and temporary syndrome.
ventricular assist devices (VAD). These devices are The hemodynamic effects of the IABP (see
typically used in the context of acute, intractable Table 14.3) depend upon the counterpulsation that
cardiogenic shock from a range of etiologies results from balloon inflation and deflation at precise
including myocardial infarction, post-cardiotomy points in the cardiac cycle which are controlled by the
failure, myocarditis and acute deterioration in drive console, using either pressure or electrocardio-
patients with end-stage cardiac failure. Durable MCS gram triggers. Figure 14.2 shows how the balloon
devices are the implantable left and right VADs. inflation is timed to occur immediately after aortic
These devices are most commonly used as valve closure resulting in augmentation of the dia-
either a bridge to transplantation/candidacy or as stolic pressure (“diastolic augmentation”). This
destination therapy, in patients with end-stage cardiac results in increased coronary artery perfusion and
failure. therefore improved myocardial oxygen delivery.
Balloon deflation is timed to occur immediately prior
to the opening of the aortic valve, creating a vacuum
Intra-aortic Balloon Pump effect leading to reduced afterload which leads to
The IABP is the commonest form of mechanical reduced myocardial stroke work and oxygen demand.
support utilized in cardiac practice. Its first use was The reduced afterload can additionally increase car-
in the 1960s following the work of Kantrowitz who diac output, although this increase is believed to be
138 identified that “diastolic augmentation” could be util- small (0.5–1 liter/minute at most), and of course is
ized to improve myocardial oxygenation and thus dependent upon the ventricular function.

Chapter 14: Mechanical Circulatory Support
Table 14.1. Comparison of temporary mechanical circulatory support devices
Intra-aortic Impella TandemHeart Veno-arterial ECMO Central

balloon ventricular
pump assist device
Pump Pneumatic Axial Axial Centrifugal Centrifugal
mechanism
Insertion Descending Into left ventricle Cannula into left Peripheral (e.g. femoral Central
technique aorta via retrogradely atrium. Inserted artery and vein cannulation
femoral via femoral through femoral cannulation) or (left atrial
artery artery and vein with trans- central (right atrial and
through septal puncture and ascending aorta ascending
aortic valve cannulation) aorta)
Risk of limb + ++ ++ +++ (if peripheral) -
ischemia
Anticoagulation + ++ ++ +++ +++
Hemolysis + ++ ++ ++ ++
Hemodynamic 0.5–1 L/min 2.5 or 5.5 L/min 4 L/min >4.5 L/min >4.5 L/min
support Reduced Unchanged Increased Increased Increased
– Cardiac Slightly Slightly Reduced Reduced Reduced
output reduced reduced Reduced Reduced Reduced
increase Slight Reduced Unknown Unknown Unknown
– Afterload increase Unknown Improved Improved Improved
– LV preload Slight Improved
increase
– LV stroke Little
volume change
– Coronary
perfusion
– Systemic
perfusion
Management of the Patient with IABP The effectiveness of IABP augmentation is dimin-
ished when there is excessive tachycardia (>120 bpm)
The frequency and magnitude of balloon augmenta-
or when the cardiac rhythm is irregular e.g. atrial
tion can be controlled via the balloon pump console.
fibrillation. If the cardiac index is maintained above
The inflation ratio refers to the number of balloon
2.2 l/min/m2 with acceptable preload (pulmonary
inflations to the number of QRS complexes and can
capillary wedge pressure <15 mmHg), attempts can
be set at 1:1, 1:2 or 1:3. The magnitude of augmenta-
be made to wean the IABP. Firstly, augmentation is
tion can range from 10% to 100%. During normal use,
reduced to 50% for 2–4 hours. The inflation ratio is
maximal IABP support is provided with a 1:1 infla-
then reduced from 1:1 to 1:2 for another 2–4 hours
tion ratio at 100% augmentation. The timing of the
and then to 1:3 before the balloon catheter is
inflation/deflation triggers should be checked regu-
removed. The IABP must be switched off and the
larly and adjusted when required to optimize the
catheter completely deflated just prior to removal.
support provided. Current consoles have an “auto-
Heparin infusion should be discontinued at the start
pilot” mode which uses an algorithm to automatically
of the weaning process so that coagulation is normal-
select the best ECG lead and trigger source to opti-
ized by the time the catheter is ready for removal. 139
mize the inflation and deflation timing.

Jason M Ali, Ayyaz Ali and Yasir Abu-Omar
Complications of IABP Use cerebrovascular accident, thrombocytopenia from

platelet deposition on the balloon and mechanical
The incidence of complications in patients with an
disruption, hemolysis, infection and complications
IABP is 7%, with major complications occurring in
of immobility in cases of prolonged therapy due to
2.6%. IABP-related mortality is estimated to be 0.5%.
the requirement to be bedbound. Balloon rupture is a
The commonest complications are vascular and
rare but serious complication that can result in gas
include limb ischemia and vascular trauma (dissec-
embolism.
tion or laceration) leading to false aneurysm, hema-
toma or hemorrhage. Incorrectly sized IABP catheters
can lead to compromised abdominal visceral perfu- Extracorporeal Membrane
sion. Non-vascular complications include Oxygenation (ECMO)
ECMO is an advanced form of temporary life support
Table 14.2. Indications for intra-aortic balloon pump that can be utilized to aid respiratory and/or cardiac
function. It evolved from CPB technology and has
Ischemic myocardium ○ Unstable angina despite
been in use since the 1970s. When support of respira-
maximal medical
therapy
tory function alone is required, the oxygenated blood
is returned to the venous circulation (veno-venous
○ Ischemia-induced
ventricular arrhythmia
ECMO or VV-ECMO), relying on intrinsic cardiac
function. When circulatory support is required in
○ Elective support in high-
addition to gas exchange, the oxygenated blood is
risk percutaneous
coronary interventions reinfused into the systemic arterial circulation
(veno-arterial ECMO or VA-ECMO).
Structural complications ○ Ventricular septal defect
of acute myocardial ○ Acute mitral valve
infarction regurgitation
Circuit Design
Many circuit configurations can be constructed for
Cardiogenic shock ○ Post myocardial
VA-ECMO. The common components include a
infarction
venous cannula which drains deoxygenated blood
○ Acute myocarditis
through heparin-bonded tubing to a membrane oxy-
○ Acute deterioration of genator and then via a non-pulsatile centrifugal pump
chronic heart failure to an arterial cannula. Cannulation for VA-ECMO
○ Post-cardiotomy can be peripheral, typically with femoral venous
○ Primary graft failure of drainage and femoral arterial return (see
the donor heart Figure 14.3); or central with right atrial venous drain-
following heart age and ascending aorta return (see Figure 14.4). The
transplant
Radio-opaque
Balloon
marker
Pressure
monitoring
line
140 Helium inflation/deflation line
Figure 14.1 Intra-aortic balloon pump catheter and optimal position in the aorta. (Reprinted with the permission of Maquet.)

Table 14.3. Physiological effects of the intra-aortic patient must be therapeutically anticoagulated to
balloon pump
minimize the risk of thrombosis/thromboembolism.
Balloon deflation ○ Reduces left ventricular
during ventricular afterload Indications
systole ○ Reduces peak LV wall stress The use of VA-ECMO and other advanced mechan-
and LV stroke work ical circulatory support devices is generally indicated
○ Decreases myocardial in patients with refractory cardiogenic shock
oxygen demand despite maximal inotropic support and use of an
○ Reduces mitral valve IABP. The goal is to prevent development of end-
regurgitation organ injury, facilitating myocardial recovery or
○ Increases LV ejection evaluation of further therapeutic decisions (see also
fraction Chapter 13). The common indications are summar-
Balloon inflation ○ Increases coronary perfusion ized in Table 14.4.
during ventricular pressure
diastole ○ Augments coronary Contraindications
blood flow
Commencing VA-ECMO is a major decision and
○ Improves myocardial ideally it should be made with multidisciplinary
oxygen delivery
involvement of cardiologists, cardiothoracic surgeons
○ Improves end-organ and specialist anesthesiologists or intensivists. VA-
perfusion e.g. kidneys,
ECMO should only be used in patients in whom there
liver, etc.
is anticipated early recovery or when it is being used
Overall effects ○ Augments cardiac output as a bridge to more definitive management, for
○ Reduces pulmonary example transplantation or long-term VAD support
capillary wedge pressure (“bridge to decision”). Therefore, ECMO is contra-
○ Relieves pulmonary indicated in patients with non-recoverable cardiac
congestion and tendency failure who are not candidates for transplantation
for edema or VAD implantation due to other significant
Augmented Non-Augmented
beat beat
110
70
30
IABP
inflation interval Dichrotic
notch 141
Figure 14.2 Aortic pressure trace with IABP inflation set to 1:2. The IABP inflation interval has been highlighted to show balloon inflation at
the dichrotic notch and deflation just before cardiac systole. (Reproduced from Core Topics in Cardiothoracic Critical Care.)

Ascending aorta
Left atrium
Pump
Right atrium
Right ventricle
Left ventricle
Oxygenator
Descending aorta
Inferior vena cava
Femoral artery
Femoral vein
Drainage cannula
Reperfusion line
Return cannula
Figure 14.3 Peripheral ECMO. The blood is drained from a large vein, typically IVC, using femoral access. It is then pumped through an
oxygenator and returned to the patient into the femoral artery in a retrograde fashion. Reperfusion line from inflow cannula is inserted into the
distal femoral artery to provide distal limb perfusion. (Reproduced from Core Topics in Cardiothoracic Critical Care.)
Ascending aorta
Drainage cannula
Left atrium
Return cannula
Pump
Right atrium
Right ventricle
Left ventricle
Oxygenator
Descending aorta
Inferior vena cava
Figure 14.4 Central ECMO diagram: Using open chest the blood is drained via a cannula from a central vein (IVC or SVC) or right atrium. It is
pumped through an oxygenator and returned through an arterial cannula into the ascending aorta. The chest can be left open for a short
while, or the cannulae can be tunneled under the skin and chest closed. (Reproduced from Core Topics in Cardiothoracic Critical Care.)
142

Table 14.4. Indications for cardiac VA-ECMO Table 14.5. Complication rates of cardiac VA-ECMO
Acute myocardial infarction with cardiogenic shock/ Complication Incidence

arrest (%)
Fulminant myocarditis Acute kidney injury 55.6
Acute exacerbations of chronic heart failure Renal replacement therapy 46.0
Cardiac failure due to intractable arrhythmias Re-thoracotomy for bleeding or 41.9
Post-cardiotomy cardiac failure tamponade in post-cardiotomy
patients
Primary graft failure following cardiac transplantation
Major or significant bleeding 40.8
Acute heart failure secondary to drug toxicity
Significant infection 30.4
Post cardiac arrest (as part of Advanced Life Support)
Lower extremity ischemia 16.9
Neurological complications 13.9
Fasciotomy or compartment syndrome 10.3
comorbidities. Relative contraindications to VA-
ECMO include the presence of severe aortic regurgi- Stroke 5.9
tation, aortic dissection, contraindications to thera- Lower extremity amputation 4.7
peutic anticoagulation (such as active bleeding, a
hemorrhagic intracranial event), pre-existing multi-
organ failure and patients who have been mechanic-
the native cardiac output, leading to local hypoxemia
ally ventilated for >10–14 days.
mainly in the coronary and cerebral circulation.
Monitoring of cerebral saturations and right radial
Complications artery blood gases can be indicative of this
ECMO comes with significant associated morbidity. differential cyanosis.
The major complications are thrombotic and hemor- A recent meta-analysis has summarized the com-
rhagic in nature and highlight the difficult balancing plications of VA-ECMO (see Table 14.5).
act between ensuring adequate anticoagulation and
causing excess bleeding on the one hand and unwanted Clinical Outcomes
thrombotic risk on the other. Patients on ECMO
Survival of patients supported with VA-ECMO is
mostly have very restricted mobility, similar to those
dependent on a range of factors including the under-
with IABP and are likely to suffer similar complica-
lying diagnosis and the presence of end-organ injury
tions. Tunneling lines through the chest wall, allowing
prior to commencement. The Extracorporeal Life
formal chest closure, gives patients on central VA-
Support Organization (ELSO) registry reports that
ECMO the benefit of increased mobility, reducing the
62% of adult patients treated for all indications with
number of thromboembolic complications and min-
VA-ECMO survive extracorporeal life support, with
imizing deconditioning while on support.
45% surviving to hospital discharge or transfer.
The Harlequin syndrome describes a differential
cyanosis associated with peripheral VA-ECMO.
Oxygenated blood is pumped retrograde through the Managing Patients on VA-ECMO
descending aorta into the ascending aorta to perfuse Patients supported with VA-ECMO will be managed
the coronary arteries and cerebral vessels; native ven- in an intensive care unit by multidisciplinary special-
tilation can often be inadequate and the blood exiting ists. ECMO support should be titrated to clinical
the left ventricle will be relatively deoxygenated. If targets, which may include:
there is native left ventricular output there will be a – arterial oxygen saturations >90%
“mixing zone” where ejected native, poorly oxygen- – venous oxygen saturations >70%
ated anterograde and highly oxygenated retrograde – adequate tissue perfusion – as judged by end-
blood meet. Any vascular bed proximal to the mixing organ function (urinary output, gut function, 143
zone receives blood with poor oxygen content from cerebral function) and lactate levels.

Pumping blood into the arterial system during VA-

ECMO alters loading conditions and can worsen LV
Ventricular Assist Devices
A number of different devices are available. They
function. It is imperative that any remaining native
differ by the intended duration of support (temporary
cardiac stroke volume is assessed and maintained to
versus long-term) and by the method of implantation
avoid complications of left ventricular stasis and dis-
(percutaneous, central and implantable).
tension, pulmonary hypertension or intracardiac
thrombus formation. Echocardiography is a useful
tool to inform on the cardiac volume status, to guide Indications for VAD
concomitant inotrope and IABP use and to inform
VADs have a broad range of applications, the
about recovery of cardiac function. Persistent ven-
common indications include:
tricular distension and pulmonary hypertension will
Bridge to Recovery: In some cases of post-
need to be managed with LV venting via the left
cardiotomy shock and fulminant myocarditis, VAD
ventricular apex, or trans-septally via the atrium.
therapy can provide a period of circulatory support
Anticoagulation must be monitored to prevent
until cardiac function recovers after which the VAD
circuit thrombosis and embolism, which could be
can be weaned and removed, a process known as
fatal. For patients receiving unfractionated heparin
“bridge to recovery.”
an activated clotting time (ACT) of 180–210 seconds
Bridge to Transplant: Occasionally, a VAD is
or an APR (normalized aPTT) of 1.8–2.2 are
utilized for patients with deteriorating cardiac func-
recommended.
tion or end-organ function while waiting for a heart
Mechanical ventilation is usually conducted with
transplant. Here the VAD is used to buy time for the
lung protection in mind. Reduction in the ventilator
patient until a suitable donor heart can be found, a
support is often accompanied by increased venous
process called “bridge to transplant” or BTT.
return and cardiac output. When cardiac recovery
Bridge to Candidacy: This third indication
occurs and increasing amounts of blood are ejected
involves patients who would otherwise be transplant
from the right ventricle, increased ventilation may be
candidates except for one or more serious, but poten-
necessary to prevent deoxygenated blood from reach-
tially reversible, complications of advanced heart fail-
ing the left atrium.
ure, such as pulmonary hypertension or renal
dysfunction. Unless reversed, such complication(s)
Weaning VA-ECMO prevent transplantation and these patients will invari-
ably die from their heart failure. Pulmonary vascular
It is important to develop an individualized weaning
resistance elevated due to left ventricular failure and
strategy for each patient. VA-ECMO support will
pulmonary venous congestion often revert to normal
only be possible for 1–2 weeks and can therefore ever
levels with mechanical unloading of the left ventricle;
only be a temporary measure to support the recovery
renal or hepatic dysfunction due to chronic low car-
of heart function or a bridge to another treatment.
diac output can often be reversed with improved
Some patients cannot be weaned off support and may
systemic perfusion. An implantable VAD can often
be candidates for urgent cardiac transplantation or, if
achieve both over time.
no donor organ becomes available in a timely enough
Destination Therapy: An implantable VAD can
manner, a planned VAD implant.
be offered as permanent support for selected patients
Once adequate recovery is thought to have
with advanced heart failure who are not transplant
occurred, an attempt to wean off ECMO can be made.
candidates and are unlikely ever to become candi-
This is usually accomplished by daily incremental
dates. The boundary between “bridge to candidacy”
reduction in flow by approximately 0.5 L, until the
and “destination therapy” is often blurred.
ECMO support is only 1.5–2.0 l/min. During this
time, careful assessment of end-organ function is
vital. Most patients will require additional inotropic The VAD Decision-Making Process
support. Final decannulation usually occurs in the
The key decisions include:
operating room as formal vessel repair for peripheral
cannulation, and chest closure for central cannulation which patient to support with a VAD
144 when to insert a VAD
will be necessary.

whether the patient requires a left ventricular Table 14.6. INTERMACS Level of limitation at time of implant
VAD (LVAD) alone or biventricular VAD INTERMACS Description Time Frame for Definitive
devices (BiVAD) Profile Intervention
which VAD system to use.
Profile 1 Critical Emergency intervention
These are often difficult to make and are influenced cardiogenic within hours
by a number of factors including the acuity of onset, shock
the severity of heart failure, patient comorbidities, Profile 2 Progressive Urgent intervention
expected transplant waiting times, device and decline within days
resource availability and institutional experience.
Up until a few years ago, patients with heart Profile 3 Stable but Elective intervention
inotrope within days/weeks
failure were mostly stratified according to the New
dependent
York Heart Association (NYHA) classification.
Although this provides an assessment of patients’ Profile 4 Resting Elective intervention
functional status, Class IV heart failure symptoms symptoms within months
include a very broad spectrum ranging from those Profile 5 Exertion Variable urgency,
who are stable on oral therapy to those who may be intolerant maintain nutrition and
pre-terminal on maximal inotropic support. As the organ function
treatment strategy varies with the severity of heart Profile 6 Exertion Variable urgency,
failure a further sub-classification of patients with limited maintain nutrition and
advanced heart failure became necessary. organ function
The Interagency Registry of Mechanically Assisted Profile 7 Advanced Transplant or MCSD may
Circulatory Support (INTERMACS) was established NYHA III not be currently
as a mandatory registry for all patients receiving an indicated
implantable mechanical circulatory support device
(MCSD) in the USA. Based on patient characteristics
at the time of device implantation and outcome analy-
sis, seven profiles have been defined to further stratify generation.” Continuous flow devices are generally
patients in advanced heart failure, with Profile 1 being more compact, silent in operation and more durable.
the most severely ill. NHYA Class IV patients are now Dimensions and weight have decreased significantly,
sub-divided into Profiles 1–6 while those in NYHA all modern devices are fully implantable and obvi-
Class IIIb are described as Profile 7 (see Table 14.6). ously require normal lung function.
Types of Ventricular Assist Devices Percutaneous Temporary Ventricular

Technical developments in mechanical circulatory Assist Devices
support have progressed rapidly over the last 20 years. TandemHeart – The TandemHeart system
There is now a large range of systems available for (CardiacAssist) is an extracorporeal axial flow pump.
clinical use. These can be classified into temporary The TandemHeart works by contributing blood flow
systems and long-term systems. The earliest “first to the aorta, working in parallel – or “tandem” – to
generation” devices were based on a volume displace- the LV. The venous inflow cannula is inserted percu-
ment mechanism and generated pulsatile blood flow. taneously into the femoral vein, advanced into the
These devices were bulky in design, noisy in oper- right atrium and finally placed transeptally into the
ation, often were extracorporeal and had limited dur- left atrium. It is connected to a centrifugal pump
ability. Most of the newer devices have moved to which provides up to 4 l/minute flow to an arterial
rotary blood pump technology with a single moving outflow cannula in the femoral artery, effectively
part. They can either be of an axial flow design or bypassing the LV. Offloading blood from the left
have a centrifugal configuration. Implantable LVADs atrium reduces LV preload, wall stress and therefore
with mechanical bearings are referred to as “second oxygen demand. This facilitates increased cardiac
generation,” while those with magnetic levitation or output and systemic perfusion pressures. 145
hydrodynamic bearings are referred to as “third A continuous infusion of heparinized saline flows

Table 14.7. Summary of complication rates of temporary

percutaneous mechanical circulatory support devices
Complication Impella TandemHeart

(%) (%)
Major bleeding 0.05–54 53–59
Access site bleeding 2–40 8–53
Hemolysis 10–46 5.3
Cerebrovascular 2.4–6.3 –
accident
Limb ischemia 0.07–10 3.4–11
Vascular injury requiring 1.3–2 0.85–13
surgery
Access site infection 1.1 16
Sepsis 0.16–19 29.9
Device migration 0.05–23 8
Device malfunction 0.16–17 –
Figure 14.5 Diagram showing an Impella device advanced
retrogradely into the left ventricle via the aorta. (Reproduced from Core
Topics in Cardiothoracic Critical Care.)
into the lower chamber of the pump, providing lubri-
cation and cooling and prevents thrombus formation.
The most common indications include the treat-
LV is sucked into the inlet area near the tip of the
ment of acute myocardial infarction complicated by
device and is delivered into the aortic root through
cardiogenic shock and to facilitate high-risk PCI.
With increasing experience, the indications the outlet, thus offloading the left ventricle. The
broadened to include acute decompensation of end- device comes in various sizes and can provide flow
stage heart failure, post-cardiotomy cardiogenic of up to 5 l/min.
The physiological effects, indications and contra-
shock, and to facilitate off-pump coronary bypass
indications are essentially the same as for the
surgery in high-risk patients. The requirement for
TandemHeart. The absence of the requirement for a
and the technical challenge of a trans-septal puncture
trans-septal puncture has led to the Impella becoming
has limited its widespread uptake.
the preferred device in many centers. The recently
Impaired right ventricular function and severe
aortic regurgitation are specific contraindications to approved Impella RP has been designed to provide
the use of the TandemHeart. Additionally, severe right ventricular support.
peripheral vascular disease may preclude percutan- Similar to the TandemHeart, the Impella’s ability
to increase cardiac output is superior to that of the
eous cannula placement. Patients must be anticoagu-
IABP. The main complications for both devices are
lated to reduce the risk of thromboembolism.
summarized in Table 14.7.
Complications associated with trans-septal puncture
are an important limitation of this device. If the
inflow catheter is dislodged into the right atrium, a Central Ventricular Assist Devices
large right to left shunt can develop (see Table 14.7). For patients with refractory cardiogenic shock despite
Impella – The Impella (Abiomed) is a non- IABP therapy, an alternative to VA-ECMO is the use
pulsatile axial flow Archimedes screw pump designed of a temporary central VAD. In general, it is prefer-
to propel blood into the ascending aorta in series with able to cannulate the ventricle directly as VAD inflow
the LV (see Figure 14.5). The device is introduced to because this configuration provides superior ven-
146 the left ventricle retrogradely through the femoral tricular decompression, avoids ventricular stasis and
artery or through the axillary artery. Blood from the affords higher flow rates. Biatrial cannulation is

Figure 14.6 Diagram of the HeartMate 3 left

ventricular assist device. (Reproduced with
permission of Abbott, © 2020. All rights reserved.)
Outflow graft Pump
Percutaneous cable
Battery
Modular driveline
Controller
preferred when recovery is expected and there is The most frequently implanted third generation
residual ventricular function. LVADs include the HeartWare HVAD (Medtronic,
The output of an LVAD is dependent on adequate Minneapolis, MN, USA) and the HeartMate 3
right ventricular function. Likewise, an RVAD can (Abbott, St Paul, MN, USA [see Figure 14.6]). The
only provide benefit if the native left ventricle can HeartWare is a centrifugal pump and the HeartMate
generate enough stroke work to cope with the pul- 3 has a fully magnetically levitated, self-centering
monary blood flow produced by the RVAD. If both rotor. Both are designed for full intrapericardial
native ventricles are failing, two VADs are required in implantation obviating the need for creation of a
order to provide biventricular assistance to support “pump pocket.” Although implantation often involves
the circulation (BiVAD). a full sternotomy and cardiopulmonary bypass, min-
One commonly used system is the Levitronix imally invasive and off-pump techniques have been
CentriMag. The CentriMag is a continuous flow successfully utilized.
extracorporeal system comprising of a single-use These devices are used for LV support, bypassing
polycarbonate centrifugal pump with a magnetically and offloading it while allowing it to contract with
levitated impeller, a motor and a primary drive con- significantly reduced work. The cannulation strategy
sole, similar to VA-ECMO (see Figure 14.4). It is can protect against LV distension which can occur
intended for short-term left, right or biventricular with VA-ECMO if the LV is not vented. Offloading
support of up to 30 days duration. The pump is the LV will result in a reduction in the RV afterload
designed to minimize friction and heat generation, and usually improves RV function.
and to reduce shear forces on blood cells thus pre- RV failure has been reported in 5–44% in patients
venting hemolysis. It achieves rotation without fric- after LVAD implantation. It can be very difficult to
tion or wear at speeds of 1500–5500 rpm, providing predict preoperatively and may be severe enough to
flow rates of 5.0–6.0 l/minute. require additional, usually temporary, right ventricu-
The inflow and outflow cannulae can be rapidly lar mechanical support. RV failure can be precipitated
inserted into the beating heart and great vessels with by previously undetected or underestimated elevated
or without cardiopulmonary bypass. Other clinical pulmonary vascular resistance (PVR) and/or exces-
equipment such as a membrane oxygenator or sive LVAD flow rate. It is prudent to limit the
hemofilter can be spliced into the system. Although LVAD flow rate in the first few days in order to avoid
patients supported with the CentriMag are kept on overwhelming the RV or shifting the ventricular
the intensive care unit, they can be carefully mobilized septum to the left and distorting RV dynamics.
and can undergo physiotherapy. Because of its The indications for LVAD therapy are well-
simplicity and versatility, the CentriMag has become defined and are very similar to those for VA-ECMO.
one of the most widely adopted temporary MCS In some countries durable, implantable LVADs are
device. increasingly being utilized as a destination therapy for
147

selected patients and this is likely to become the Table 14.8. Perioperative LVAD patient management
commonest indication in the future. A total artificial Broad-spectrum prophylactic antibiotics and antifungal
heart can be used as an alternative to two implantable agents
VADs in patients with severe biventricular failure in
need of mechanical support and in some specialist Transesophageal echocardiography
○ Confirm aortic valve competence
centers as a bridge to transplantation in these cases.
○ Exclude patent foramen ovale and ASD
○ Confirm deairing
VAD Patient Management ○ Check LVAD cannula position
Patients requiring a VAD implant are probably
○ Confirm decompression of LA and LV during LVAD
among the highest risk patients to undergo cardiac
support
surgery. They have severe heart failure and are either
○ Monitor right ventricular and tricuspid valve function
in impending or established end-organ failure. A low
when weaning from CPB
cardiac output state coupled with systemic venous
○ Assess the inter atrial septum and adjust flows to
congestion result in compromised organ perfusion.
maintain central position
The kidneys become refractory to diuretic therapy
and hepatic dysfunction manifests as coagulation If using cardiopulmonary bypass:
abnormalities. The lungs are stiff from pulmonary ○ Normothermic CPB
congestion increasing the work of breathing and ○ Continuous ventilation of the lungs with nitric oxide
many patients are grossly fluid overloaded. They are at 10 ppm
often on multiple inotropes, supported with an IABP ○ Filtration on CPB and maintain
and dependent on renal replacement therapy by the ▪ Hb > 100 g/L
time they arrive in the operating room for VAD ▪ Base excess ± 2 mEq
placement.
○ No aortic cross- clamp during VAD cannulae implant
○ Pericardial CO2
Perioperative Management
Appropriate inotropic support for right ventricle
The perioperative strategy should be aimed at minimizing
further insult to these sick patients during VAD implant- Vasopressor infusion to maintain SVR
ation, targeting those areas that are known to result in
serious morbidities and mortality. Postoperative hemor-
rhage is the most commonly encountered complication
apart from right ventricular failure. with inotropes as required and the heart rate is opti-
Broad-spectrum prophylactic antibiotics and anti- mized with temporary pacing at 90–100 bpm; systemic
fungal agents are administered at induction of anes- vascular resistance is maintained between 800 and
thesia. Transesophageal echocardiography (TEE) is 1000 dyne.sec.cm 5 with a continuous infusion of
used to confirm an intracardiac thrombus, aortic valve vasopressors. TEE is used to confirm good positioning
competence and exclude the presence of a patent fora- of the ventricular outflow cannula and to guide deair-
men ovale or an atrial septal defect. If present, they ing of the heart before transitioning from CPB (if
require surgical closure at the time of VAD implant in used) to VAD.
order to prevent a right to left shunt following decom- The perioperative management strategy is sum-
pression of the left-sided chambers. If CPB is used, the marized in Table 14.8.
lungs can be kept ventilated throughout the bypass
period, often with the addition of nitric oxide at 5–10 Postoperative Management
parts per million (ppm) or inhaled epoprostenol to Careful hemostasis at the end of the VAD implant is
reduce PVR as much as possible. The VAD cannulae crucial. The percutaneous cannulae (in the case of
are implanted into a beating heart, avoiding aortic temporary VAD) or driveline (with durable LVAD)
cross-clamping and cardiac ischemia. The pericardial must be secured to minimize movement and trauma
space is flooded with carbon dioxide to displace air, to the exit site(s). This is the best way to encourage
allowing gas entrained into the cardiac chambers to
148 tissue healing onto the driveline and minimize exit
dissolve more readily. The right ventricle is supported site infections.

Once returned to the intensive care unit, VAD and pulmonary vasodilators. If the situation does not
patients must be closely monitored for early compli- respond rapidly to these measures, early consider-
cations. Right ventricular function often remains pre- ation should be given to the addition of a RVAD
carious in the first few days following LVAD which can be achieved using a variety of percutaneous
implantation. or surgical techniques.
Anticoagulation is device and unit specific but is
typically omitted in the first 24 hours and only intro- Complications
duced when the patient has stopped bleeding.
The early complications of temporary and durable
Rising right atrial pressure coupled with a fall in
VADs are similar and include bleeding, RV failure,
pump flow are signs of either tamponade or
renal failure, infection or thrombosis. The incidence
impending RV failure. Both can be confirmed with
of complications has reduced significantly with
TEE. In the case of RV failure, it will demonstrate full
increased experience and evolution of the devices,
right-sided cardiac chambers with empty left-sided
leading to the increased utilization of LVAD as a
chambers. The atrial and ventricular septa are seen
destination therapy. Ongoing device development
to bulge toward the left and often there is tricuspid
aims to further reduce the incidence of associated
valve regurgitation. Immediate treatment consists of
complications.
not increasing the preload further with more volume
and a combination of inotropic support for the RV
Suggested Further Reading 2013 ed. February, 2014;97

(2):610–616.
8. Borisenko O, Wylie G, Payne J
et al. Thoratec CentriMag for
1. Hajjar LA, Teboul J-L. Mechanical temporary treatment of refractory
circulatory support devices for 5. Glazier JJ, Kaki A. The Impella
device: historical background, cardiogenic shock or severe
cardiogenic shock: state of the art. cardiopulmonary insufficiency: a
Critical care. BioMed Central; clinical applications and future
directions. Int J Angiol. Thieme systematic literature review and
March 9, 2019;23(1):76–110. meta-analysis of observational
Medical Publishers; June, 2019;28
2. Schramm R, Morshuis M, (2):118–123. studies. ASAIO J. September, 2014
Schoenbrodt M et al. Current ;60(5):487–497.
perspectives on mechanical 6. Thiele H, Jobs A, Ouweneel DM
et al. Percutaneous short-term 9. Nagpal AD, Singal RK, Arora RC
circulatory support. Eur et al. Temporary mechanical
J Cardiothorac Surg. June 1, active mechanical support devices
in cardiogenic shock: a systematic circulatory support in cardiac
2019;55(Supplement_1):i31–37. critical care: a state of the art
review and collaborative meta-
3. Ali J, Vuylsteke A. Extracorporeal analysis of randomized trials. review and algorithm for device
membrane oxygenation: European heart journal. December selection. Can J Cardiol. January,
indications, technique and 14, 2017;38(47):3523–3531. 2017;33(1):110–118.
contemporary outcomes. Heart. 10. Kirklin JK, Pagani FD, Kormos
September, 2019;105 7. Subramaniam AV, Barsness GW,
Vallabhajosyula S et al. RL et al. Eighth annual
(18):1437–1443. INTERMACS report: special focus
Complications of temporary
4. Cheng R, Hachamovitch R, percutaneous mechanical on framing the impact of adverse
Kittleson M et al. Complications circulatory support for events. The Journal of Heart and
of extracorporeal membrane cardiogenic shock: an appraisal of Lung Transplantation : the official
oxygenation for treatment of contemporary literature. Cardiol publication of the International
cardiogenic shock and cardiac Ther. Springer Healthcare; Society for Heart Transplantation.
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adult patients. Ann Thorac Surg.
149

Chapter
Cardiopulmonary Bypass for Pediatric
15 Cardiac Surgery
Joseph J Sistino and Timothy J Jones
The outcomes following surgery for congenital heart Major Differences between the
disease have improved significantly in recent decades.
This has enabled a move from palliative surgical pro- Pediatric and Adult Cardiac Patients
cedures to primary surgical repair in the neonatal There are some major differences between these two
period, operating on younger and smaller patients. groups of patients. From a physiological standpoint,
With earlier repair and more successful outcomes, the metabolic rate for an infant per kilogram of body
the majority of children are surviving into adulthood. weight is approximately double that of an adult.
These developments have in part been due to Therefore, greater oxygen delivery is required per unit
advances made in our understanding and techniques of body weight or surface area. At birth, the pulmon-
of cardiopulmonary bypass (CPB). ary and systemic vascular resistance are the same and
Cardiopulmonary bypass in patients with con- very labile, meaning they can be manipulated to read-
genital heart disease has become increasingly special- ily increase or decrease pulmonary or systemic blood
ized with the choice of circuit setup, priming, flow. Pulmonary vascular resistance decreases expo-
cannulation strategies and CPB conduct being nentially over the first few months of life.
tailored to the individual patient and procedure. In neonates with single ventricles, common arter-
Pediatric perfusionists must have specialized know- ial trunks or large septal defects a critical balance
ledge related to pediatric physiology and congenital needs to be maintained between the systemic and
heart disease as well as the ability to utilize perfusion pulmonary circulations. To ensure surgical visibility
circuits adapted to a wide range of patient sizes. and protect the cerebral circulation, hypothermia is
Pediatric perfusion cases can sometimes be very often used to permit reduced blood flow by decreas-
long due to the complexity of the cardiac repairs. ing oxygen requirements. The small patient size and
Today, there is a large percentage of reoperations blood volume make minimizing hemodilution a chal-
and an increasing number of adult congenital oper- lenge. There is increased surface area contact due to
ations. As these patients grow older, they need revi- the size of the perfusion circuit relative to the patient,
sions to accommodate their increased cardiac which exacerbates the systemic inflammatory
outputs. As the mortality rates have fallen, focus is response to CPB.
now on delivering optimal perfusion to reduce
associated morbidity. Specific Pathophysiology That Affects
Over the past 40 years, the trend has been to
perform more complex, corrective and fewer pallia- Cardiopulmonary Bypass
tive procedures on younger and smaller patients. There are several conditions that are more common
Today, more than 50% of pediatric open-heart oper- in pediatric patients than adults and which need con-
ations are performed in infants less than one year of sideration during CPB. They include systemic to pul-
age with more than 20% of all pediatric heart proced- monary shunts, which at the onset of bypass can
ures performed during the first month of life. More produce flooding of the pulmonary circulation, while
than 90% of children with congenital heart disease are severely reducing systemic blood flow. Common
surviving into adulthood and there are now more examples of these shunts are a patent ductus arterio-
adults living with congenital heart disease than sus, a modified Blalock-Taussig shunt and central
150 children. shunts. These shunts should be occluded at the onset

Chapter 15: Cardiopulmonary Bypass of Pediatric Cardiac Surgery
of bypass to reduce pulmonary blood flow. Another increased ionized calcium levels during cardioplegic
source of systemic to pulmonary shunts are bronchial arrest can contribute to higher intracellular calcium
artery collaterals. Bronchial arteries normally carry levels and reperfusion injury. The perfusionist should
about 2% of the cardiac output to supply the lung maintain low normal ionized calcium levels during
parenchyma with oxygenated blood. In certain condi- arrest and only increase ionized calcium levels
tions associated with severely reduced pulmonary following cross-clamp release to ensure optimal
blood flow, the collaterals expand to increase blood contractility.
flow to the lungs in order to increase oxygenation. The immature heart has limited contractile
The net effect is reduced systemic blood flow on CPB reserve, making the cardiac output more dependent
unless the pump flow is increased to compensate. on the heart rate rather than the stroke volume. The
Another common problem is that of anomalous immature heart is also more susceptible to preload
venous drainage. The most common type is a left and afterload changes. There is also less independence
superior vena cava (SVC) draining into the coronary of the ventricles, meaning that biventricular failure is
sinus. This may require additional cannulation or more common than either isolated right or left ven-
venting of the coronary sinus and may alter plans tricular failure. These factors all need to be considered
for retrograde cardioplegia. when protecting the myocardium and when weaning
Many patients are cyanotic resulting in an a neonate from CPB.
increased red cell mass, significant collateral vessel There are several solutions currently being used
formation and sensitivity to high oxygen levels, which for cardioplegia; the most popular are del Nido and
can produce oxygen free radicals and reperfusion HTK (also known as Bretschneider solution or
injury. At the onset of bypass of these patients, oxygen Custodiol). Both solutions are depolarizing, del Nido
levels should be carefully maintained at a normal level uses potassium and lidocaine while HTK uses low-
to prevent exposure to hyperoxia, which is associated sodium. Both solutions have buffers and other com-
with poorer cardiac outcomes and increased severity ponents to protect the myocardium (see also
of ischemia/reperfusion injury. Chapter 11).
Cardioplegia delivery can be affected by the cor-
Myocardial Protection in the onary artery anatomy, aortic atresia or insufficiency,
the presence of a left superior vena cava, or sinusoids
Immature Myocardium in the right ventricle which produce a right ventricle-
Myocardial protection in the immature myocardium dependent coronary circulation (RVDCC). In all
is very different than in the adult. Compared with the these situations, cardioplegia delivery must be modi-
adult heart, there are fewer myocytes, fewer mature fied to adequately protect the ventricles during cardi-
mitochondria and an increased water content. This is oplegic arrest.
due to the increased number of capillaries which are
needed for the heart to grow at a rapid rate over the Deep Hypothermia Circulatory Arrest
next year. The primary source of energy for the neo-
natal heart is glucose, not fatty acids which become and Regional Cerebral Perfusion
the primary fuel at around two years of age and into With the availability of prostaglandin in the late
adulthood. The neonatal heart tolerates ischemia 1970s, the ductus arteriosus could be maintained
better because there are fewer contractile elements patent in neonates to increase their oxygen levels.
and mitochondria as well as decreased levels of This allowed for improved early survival in neonates
ATPase. Studies have shown that the neonatal heart with critical congenital heart disease. Since the early
can tolerate ischemia for up to one hour with good 1980s, deep hypothermia circulatory arrest (DHCA)
recovery. was the primary technique used for correcting com-
Another important consideration for the perfusio- plex defects. Cooling the patient to between 18 and
nist, related to myocardial protection and recovery, is 20°C allowed for a period of circulatory arrest, during
calcium control as there is less sarcoplasmic reticulum which cannulas could be removed to permit
in the immature heart. The immature heart is there- surgical visibility.
fore more dependent on circulating ionized calcium However, circulatory arrest was not without some
151
levels to maintain good contractility. However, long-term concerns including lower IQ, and

behavioral and physical impairments. Since the early arrest (DHCA) is going to be used to complete
2000s, regional cerebral perfusion has been used as an right-sided repairs or when surgery does not require
adjunct to deep hypothermia. Regional cerebral per- opening the heart. During periods of DHCA the
fusion provides blood flow to the brain through the aortic cannula and/or venous cannula maybe moved
innominate artery which supplies blood to the left to improve access and visibility to complete
side of the brain through the circle of Willis and the repair.
collateral vessels. Recent evidence demonstrates that In complex redo operations the femoral artery and
an average of 35 minutes of DHCA with regional vein may be cannulated in older children or the
cerebral perfusion is well tolerated; there have been carotid artery and internal jugular vein in smaller
reports of DHCA times in excess of 120 minutes children to enable safe sternal entry or if there is
followed by good cardiac and neurological recovery. uncontrollable bleeding during re-sternotomy.
Monitoring of the cerebral circulation using cerebral In patients with cyanosis or extensive collateral
oximetry has provided a real-time estimate of cerebral vessels or shunts that cannot be controlled, excessive
oxygen delivery. Both of these techniques, regional venous return to the left atrium may cause left ven-
cerebral perfusion and cerebral oxygenation monitor- tricular distension and myocardial damage. This can
ing, are widely used in clinical practice and help be managed by placing a vent in the left atrium,
improve outcomes. pulmonary vein or left ventricle.
Conduct of Cardiopulmonary Bypass Anticoagulation Management

Heparin is the primary anticoagulant used for CPB.
Cannulation Because of the larger pump prime volume in relation
The aim of cannulation is to provide adequate blood to the pediatric patient blood volume, it is important
flow with unobstructed venous drainage and an to maintain adequate circulating heparin levels by
unobstructed operating field. This presents challenges estimating circulating heparin level on CPB. For
in the pediatric patient. Both arterial and venous example, the 3 kg neonate will have a blood volume
cannulas require careful selection based on maximum of approximately 85 ml/kg 3 kg = 255 ml.
blood flow rate. The aim is to use the largest possible A heparin loading dose of 400 units/kg = 1200 units.
cannula, but this is often limited by the size of This will equal a concentration of 1200/255 =
the vessels. 4.7 units/kg. If the pump prime is 250 ml, then to
The site of arterial cannulation is determined by maintain the same heparin concentration, 1175 units
pathology and planned operation. Similar to adult of heparin need to be added to the prime. The target
surgery, the ascending aorta is the preferred site. ACT is similar to that in adult CPB, with equally big
However, access to the aortic arch in a neonate may variation between centers.
be best achieved via cannulation of a small Gortex
tube anastomosed to the innominate artery, which
can also be used for regional cerebral perfusion. Flow Rates and Oxygen Delivery
This technique may be used in patients with either Oxygen delivery is dependent on three factors: blood
an atretic aorta or interrupted aortic arch. Another flow rate, hemoglobin and pO2. The blood flow rate
strategy in such patients is cannulation through the is calculated based on the body surface area or
pulmonary artery into the patent ductus arteriosus. weight and is usually 2.6 L per minute/meter square;
Patients with an interrupted aortic arch may require blood flow rate based on kilogram weight ranges
cannulation in both the ascending and descending from 200 ml/kg/min for neonates to 125 ml/kg/min
aorta. for larger pediatric patients. After much debate, the
Bicaval cannulation for venous drainage is the current consensus is to maintain hematocrit in
most frequently used technique in pediatrics because excess of 24% during CPB in single ventricle
it allows access to the right atrium and right ventricle patients; in those with a mixed circulation it is usu-
while providing complete venous return with little ally maintained at a level above 30% during the
risk of air entrainment. A single venous cannula termination of bypass because of their low arterial
152
may be used when deep hypothermia circulatory oxygen saturation.

Table 15.1. Blood volume estimation based on weight

Monitoring
Monitoring during CPB includes arterial blood pres- Weight (kg) Blood Volume (ml)
sure, nasopharyngeal, esophageal and rectal tempera- 0–10 kg 85 ml/kg
tures, venous oxygen saturation and cerebral
10–25 kg 80 ml/kg
oximetry. Some centers also monitor central venous
pressure. During CPB, continuous monitoring of the 25–45 kg 70 ml/kg
arterial blood flow with an ultrasonic flow meter is 45 kg 65 ml/kg
critical to maintain adequate blood flow to the patient
when shunts are incorporated into the perfusion cir-
cuit. Before the termination of bypass, pressure lines
are placed in the right and left atrium to evaluate right
The inflammatory response is not dissimilar to that in
and left heart function during the weaning process
adults but is exacerbated in infants due to the large
and to assist with postoperative hemodynamic
surface area of the bypass circuit relative to the
management.
patients’ size, cardiotomy suction and certain foreign
materials which stimulate the immune system. The
Blood Gas Management inflammatory response to CPB is discussed in detail
Blood gas management during bypass can either be in Chapter 17.
one of two strategies, alpha stat or pH stat. Both
strategies are explained in detail in Chapter 9.
Oxygen management is also critical in children Hemodilution and Low Prime Circuits
with cyanosis. Because of their low pO2, they are As the pediatric patients presenting for surgery
susceptible to oxidative stress which releases oxygen became younger and smaller, it became necessary to
free radicals when exposed to high pO2. In these reduce the size of the perfusion circuit to reduce
patients it is important to start CPB at a low normal hemodilution and surface contact.
level of oxygen and then gradually increase over time Patient blood volume is estimated according to
on CPB. Table 15.1. Even today, with perfusion circuits requir-
ing prime volumes as low as 200 mL, this represents
Termination of CPB almost a 100% dilution of some patients’ blood
As with adults, termination of CPB is a very critical volume. This is in stark contrast to adult bypass
time and follows similar principles to those discussed circuits, where a standard prime volume of about
in Chapter 12. Monitoring of filling pressures is 1000ml represents a 20–30% dilution, meaning that
extremely important to avoid distension of the ven- a neonate circuit needs to be thought of as equivalent
tricles. Pediatric patients often have increased pul- to a 5 L pump prime volume in an adult patient. The
monary vascular resistance and may require severe hemodilution of clotting factors and platelets
ventilation with nitrous oxide. During this period contributes to an increased risk of postoperative
the anesthesiologist is carefully titrating inotropes to bleeding. In addition to reducing the size of the circuit
maximize the cardiac function. Good communication as much as technically possible, it is often necessary to
between the surgeon, perfusionist and anesthesiolo- add blood to the prime to maintain adequate oxygen
gist is critical during this time. Reversal of heparin delivery and oncotic pressure. The use of fresh frozen
with protamine is achieved in the same way as in plasma in the pump prime has advantages in preserv-
adults. ing coagulation in neonates. Following protamine
administration, platelet transfusion is often necessary
to increase the platelet count. Some centers have
Pathophysiology of whole blood available, which reduces the total
number of donor blood exposures.
Cardiopulmonary Bypass Neonatal oxygenators now have reduced priming
The effects of CPB in pediatric patients were first volumes around 40 ml. With the use of 1/8” tubing,
identified by Kirklin’s group in 1982 in his publica- circuit prime volumes as low as 100 ml have been
tion on whole body systemic inflammatory response.
153
reported. However, there is some variation in the way

cardioplegia solution, it is important to have a

method to remove excess crystalloid fluid in order
to maintain adequate hemoglobin levels.
Ultrafiltration reduces the levels of inflammatory
Figure 15.1
mediators IL-6 and IL-8, although the clinical utility
is still subject to debate.
that prime volume is measured. Calculation of the Zero balance ultrafiltration refers to replacing the
circuit priming volume should include venous reser- filtered off fluid with an equal amount of crystalloid
voir volume at the minimum operating level and all solution.
primed tubing lines. Figure 15.1 shows the formula Modified ultrafiltration (MUF) is a method to
for calculating the packed red cell volume needed to filter the blood after CPB. MUF has changed over
maintain a target hematocrit. the years since the early 1990s when it was first
It is essential that in the effort to reduce priming introduced by Great Ormond Street Hospital in
volume, no compromise is made in arterial line pres- London. It is important that protamine administra-
sure and venous resistance. Institutional guidelines tion is withheld until the end of MUF since blood is
about choice of oxygenator and tubing, as well as still circulating through the bypass circuit.
cannula selection, should be carefully followed for The original method was relatively simple. After
each individual pediatric patient. Arterial and venous coming off bypass, a circuit with a hemoconcentrator
cannula pressure drop should not exceed 100 mmHg was connected to the arterial cannula. The tubing
and 40 mmHg respectively at the maximum calcu- proximal to the hemoconcentrator was placed in a
lated blood flow rate for the individual patient. roller pump and the outlet tubing was connected to
a venous cannula in the right atrium. Blood was
Retrograde Autologous Prime slowly withdrawn retrograde from the aorta and
Retrograde autologous prime (RAP) is a method used pumped through the hemoconcentrator back into
to reduce the priming volume by displacing crystal- the right atrium. Numerous modifications of
loid solution with the patient’s own blood immedi- MUF circuitry and technology have been proposed
ately before going on bypass. Once heparinized and since, all of which still involve using the existing
fully cannulated, blood from the patient is slowly cannulation and pose a risk of high negative pressure
withdrawn from both the arterial and venous lines in the arterial line with the risk of cavitation or
into a collection bag. The anesthesiologist is respon- pulling air across the microporous membrane
sible for giving the patient a vasoconstrictor to main- oxygenator.
tain the patient’s blood pressure in a safe range Recently, there has been some suggestion that MUF
(usually >80 mmHg systolic). Any major change in is no longer necessary because the perfusion circuits
arterial pressure, EKG or arterial oxygen saturation is have been reduced in size, requiring smaller priming
reason to discontinue RAP. Usually about 50% of the volumes. Since it has the risk of air embolism, eliminat-
prime volume can be removed during RAP. This ing MUF avoids this potential complication.
results in an increased hematocrit during bypass
while reducing the need for blood products.
There are major challenges to accomplishing success-
Conventional and Modified Ultrafiltration ful cardiac surgery in pediatric patients. In part due to
Ultrafiltration is a method of hemoconcentration that much improved extracorporeal technology, surgical
is used both during and after CPB to increase hema- outcomes have significantly improved over the years.
tocrit, plasma proteins including clotting factors and Today, with the assistance of postoperative ECMO
platelets. As the pump volume is diluted with support, even more patients are surviving.
Suggested Further Reading pediatric perfusion practice:

2011 survey results. J Extra Corpor
2. Sistino JJ, Bonilha HS. (2012).
Improvements in survival and
1. Harvey B, Shann KG, Fitzgerald D Technol, 44(4), 186–193. neurodevelopmental outcomes in
154 et al. (2012). International surgical treatment of hypoplastic

left heart syndrome: a meta- Thorac Cardiovasc Surg, 13(1), 8. McCall MM, Blackwel, MM,
analytic review. J Extra Corpor 56–72. doi:10.1053/ Smyre JT et al. (2004). Fresh
Technol, 44(4), 216–223. stcs.2001.22738 frozen plasma in the pediatric
3. Benziger CP, Stout K, Zaragoza- 6. Sistino JJ, Atz AM, Ellis C Jr. et al. pump prime: a prospective,
Macias, E et al. (2015). Projected (2015). Association between randomized trial. Ann Thorac
growth of the adult congenital heart method of cerebral protection Surg, 77(3), 983–987; discussion
disease population in the United during neonatal aortic arch 987. doi:10.1016/j.
States to 2050: an integrative surgery and attention deficit/ athoracsur.2003.09.030
systems modeling approach. Popul hyperactivity disorder. Ann 9. Naik SK, Knight A, Elliott M.
Health Metr, 13, 29. doi:10.1186/ Thorac Surg, 100(2), 663–670. (1991). A prospective randomized
s12963-015-0063-z doi:10.1016/j. study of a modified technique of
4. Kirklin/Barratt-Boyes Cardiac athoracsur.2015.04.119 ultrafiltration during pediatric
Surgery 4th edition, by Nicholas 7. Wypij D, Jonas RA, Bellinger DC open-heart surgery. Circulation,
T. Kouchoukos, Eugene H. et al. (2008). The effect of 84(5 Suppl), III422–431.
Blackstone, Frank L. Hanley, and hematocrit during hypothermic 10. McRobb CM, Ing RJ, Lawson DS
James K. Kirklin Chapter 2: cardiopulmonary bypass in infant et al (2017). Retrospective analysis
Hypothermia, Circulatory Arrest, heart surgery: results from the of eliminating modified
and Cardiopulmonary Bypass. combined Boston hematocrit ultrafiltration after pediatric
5. Allen BS, Barth MJ, Ilbawi MN. trials. J Thorac Cardiovasc Surg, cardiopulmonary bypass.
(2001). Pediatric myocardial 135(2), 355–360. doi:10.1016/j. Perfusion, 32(2), 97–109.
protection: an overview. Semin jtcvs.2007.03.067 doi:10.1177/0267659116669587
155

Chapter
Coagulopathy and Hematological Disorders
16 Associated with Cardiopulmonary Bypass

Pathophysiology of Coagulopathy After stimulus of thrombin formation. In these

conditions endothelial cells rapidly shift from
Cardiopulmonary Bypass being anti-thrombotic to being prothrombotic.
CPB as well as surgical trauma have a significant Cardiotomy suction blood carries cell debris and
impact on the usually well-balanced coagulation tissue factor directly into the circulating blood,
system. This often leads to bleeding complications, causing thrombin and fibrin generation via the
and interventions to restore this balance are fre- extrinsic pathway.
quently attempted perioperatively. The coagulation The platelet count decreases during CPB through
and inflammatory systems are so complex that restor- hemodilution and mechanical destruction. A degree
ation of homeostatic balance cannot be achieved by of platelet dysfunction is caused by hypothermia, but
giving blood products alone. this is partially reversible with rewarming. They
Major known causes of CPB-associated coagulopa- undergo reversible aggregation during CPB, show
thy are dilution, complex and variable platelet dysfunc- more and more changes in morphology with increas-
tion, fibrinolysis, the effects of heparin and protamine, ing length of bypass and degranulate partially.
hypocalcemia, hypothermia, as well as activation of the Even high doses of heparin do not “paralyze” the
coagulation system after contact with artificial surfaces hemostatic system. Thrombin generation is ever pre-
and from tissue factor release from the endothelium in sent during CPB and heparin combined with anti-
response to ischemia and reperfusion. thrombin merely blocks the formation of fibrin.
The priming volume of a standard adult CPB Thrombin triggers fibrinolysis, which in turn can lead
circuit leads to 20–30% hemodilution, while loss of to the breakdown of clots; the resulting fibrin degrad-
activity for isolated clotting factors becomes clinically ation products (particularly D-dimers) further impair
significant at 30–50% of normal activity. The import- fibrin polymerization.
ance of minimizing hemodilution can therefore not Residual heparin can cause bleeding after cardio-
be overstated. Today, many centers make efforts to pulmonary bypass and needs to be reversed with
reduce hemodilution by using smaller CPB circuits protamine. Non-heparin-bound protamine has anti-
and by retrograde autologous priming. Chapters 2, 7 coagulant effects, and high protamine-heparin ratios
and 8 discuss circuit design and other strategies to should be avoided as much as incomplete reversal of
decrease priming volume. heparin. Heparin rebound might occur by redistri-
Historically, artificial surfaces were considered the bution from tissue or cell surfaces even hours after
primary activators of coagulation. Today we know initial reversal.
that ischemia reperfusion injury, endothelial release
of thrombin and the presence of tissue factor may
outweigh extrinsic activation: Role of Preoperative Medication
Endothelial cells at rest are highly anti- in Coagulopathy
inflammatory and anti-thrombotic; when stressed, Cardiac patients are prescribed a wide range of medi-
however, they become active exporters cations for a variety of underlying conditions. Many
of thrombin. of these drugs have effects on platelets, vascular
Arteriolar microemboli may lead to localized reactivity, hepatic or renal function and may be linked
156 ischemia and reperfusion, which is a potent to bleeding or thrombosis risk. Some commonly

Chapter 16: Coagulopathy and Hematological Disorders Associated with Cardiopulmonary Bypass
prescribed drugs, such as cephalosporin antibiotics, and its major metabolite are active. Although the
can have anti-platelet effects. What makes a patient half-life is 7–9 hours, restoration of platelet
bleed is likely to be a complex combination of drugs, activity takes significantly longer.
effects of acute and chronic inflammation, oxidative There is very strong evidence that discontinuation of
stress, inflammation on CPB and the patient’s own clopidogrel prior to elective cardiac surgery is not just
genetic makeup. preferable but is a must. A European Society of
Cardiology meta-analysis, including 54 separate stud-
Genetic Factors ies and over 50,000 patients, showed that preoperative
Genetic predilection for disease is complex as is the dual anti-platelet therapy with clopidogrel and aspirin
response to drugs. Examples are that: significantly increased major bleeding and transfu-
patients with angina are more hypercoagulable sion as well as increasing the risk of re-exploration
than the general population for bleeding 2.5-fold, while not conferring an advan-
tage by decreasing the incidence of perioperative
blood group O patients have more bleeding,
transfusion and postoperative chest tube output myocardial infarction when compared to patients
than those with groups A, B or AB whose clotting had been allowed to return to baseline.
Another meta-analysis comprising of 30 studies
anti-platelet (P2Y12) agents and aspirin have a
showed that mortality increased 47% if dual anti-
significant proportion of non-responders.
platelet therapy was continued to surgery. It is con-
jectured that much of the increased risk of death was
Anti-platelet Agents due to bleeding and excessive use of allogeneic blood
Glycoprotein IIb/IIIa inhibitors and monoclonal products.
antibodies – the success of cardiology interventions The use of single, dual or even triple anti-platelet
has relied for years on acutely blocking the therapy creates a therapeutic dilemma in patients with
fibrinogen receptor on the platelet surface with recently fitted coronary stents. Dual anti-platelet ther-
short acting drugs, such as eptifibatide and apy is recommended up to six months immediately
tirofiban, or longer acting monoclonal antibodies, after stent placement and for up to 12 months in
such as abciximab, and other IIb/IIIa inhibitors. patients who have had an acute coronary event. As
Abciximab has a 10–30 minute redistribution half- seen above, it is recommended to stop dual therapy
life, but its terminal half-life and effects on platelets for 5–7 days prior to elective surgery. Unfortunately,
may last up to 15 days. there are reports of acute coronary events soon after
Aspirin – functions by acetylating cyclooxygenase stopping these drugs and there is some evidence that
enzymes in platelets. Cyclooxygenase-1 (COX-1) acute hypercoagulable state occurs after withdrawing
is involved in the formation of thromboxane, a the therapy. In cases where an operation becomes
prostaglandin signaler for platelets to partially urgently necessary after a percutaneous intervention
activate. Following even low dose aspirin the anti-platelet effects can be overcome by transfus-
administration, COX-1 is irreversibly inhibited ing platelet concentrates, so that the platelet number
within megakaryocytes and as such will “poison” overwhelms any residual drug.
growing platelets for their life span of 7–10 days. It Table 16.1 summarizes the characteristics of com-
takes 3–7 days after aspirin discontinuation to monly encountered anti-platelet drugs.
increase non-aspirin tainted platelets. Aspirin
does not appear to lead to a higher incidence of
bleeding complications after CAGB and the Vitamin K Antagonists
current recommendation is not to stop it prior to Vitamin K coagulation proteins are involved with the
surgery. extrinsic cascade (Factor VII) and the final common
P2Y12-blockers – these drugs affect platelet pathway (II, IX and X). Carefully titrated and moni-
activation via the ADP receptor and include the tored, warfarin therapy provides a 30–50% reduction
thienopyridines (clopidogrel, prasugrel and in the risk of pulmonary embolism and/or stroke in
ticlopidine) and ticagrelor. Clopidogrel acts for atrial fibrillation. However, it comes with a 3–5% risk
the life of the platelet, i.e. 7–10 days. Ticagrelor of major bleeding per year. 157

Table 16.1. Summary of commonly encountered anti- and fully correct after CPB while others do not give
platelet drugs
any reversal until the patient has been weaned.
Plasma Time to Reversal agent
half-life effect available Novel Oral Anticoagulants
offset
This group of new and evolving pharmaceutical
Aspirin 15–30 7–10 days no agents block either factor Xa or factor II (thrombin).
minutes Novel oral anticoagulants (NOACs) or direct acting
Clopidogrel 8 hours 7–10 days no oral anticoagulants (DOACs) are utilized today for
treatment of hypercoagulable states such as venous
Prasugrel 7 hours 7–10 days no
thromboembolism and for prevention of clot with
Ticagrelor 7 hours 5 days yes (PB2452, in atrial fibrillation. NOACs/DOACs have a similar
clinical stage effectiveness at reducing the incidence of VTE as
trials) warfarin but come with an enhanced safety profile.
Abciximab 10–15 12 hours no Most NOACs have a half-life of 7–14 hours, minim-
minutes izing the risk of bleeding once patients have been off
Eptifibatide 2.5 hours 2–4 hours no the drug for 24–48 hours. There does not seem to be a
rebound hypercoagulability with NOACS.
Tirofiban 2 hours 2.5 hours no
The management of patients coming to the oper-
ating room without having stopped their NOAC or
DOAC is controversial. These agents block the final
common coagulation pathway and FFP seems the
logical treatment. Unfortunately, FFP has, at best,
The therapeutic window of warfarin is 2–3 times the same level of proteins as normal plasma and a
international normalized ratio (INR). Cardiac huge volume would be required to overcome the
patients are at risk of sudden and rapid increases in effects of these drugs. Several direct binding agents
INR without altering the dose. This is especially true are approved for NOAC reversal in acute bleeding:
for those: Andexanet-α will within 30 minutes fully reverse
with right sided heart failure, tricuspid the effects of Rivaroxaban and Apixaban and
insufficiency and vena cava congestion where liver the monoclonal antibody idarucizumab can
protein synthesis is reduced and reverse the effect of dabigatran.
with acute or chronic heart failure where gut These two direct reversal agents are very
absorption of vitamins as well as the microbiome expensive. 4FPCC appears to at least partially reverse
are changed. NOACs and could present an alternative in cases
With INR levels above 1.2 associated with excess where no specific reversal agent is available. It must
bleeding most practices agree there is no “safe” INR be noted, though, that it does not have a specific
elevation for bleeding risk in the operating room. indication for that use.
Accordingly, most surgical teams aim to correct the
INR close to 1.0.
The most appropriate way to acutely reverse war- Assessment of Coagulopathy
farin is to administer 4 factor prothrombin complex Coagulopathy after cardiopulmonary bypass should
concentrate (4FPCC). The use of PCC has been found ideally be treated in a goal-oriented manner. The ideal
to be superior to fresh frozen plasma (FFP) in restor- bleeding/coagulation assessment tool is currently elu-
ing a normal INR as well as maintaining it for 24–48 sive but should have the features summarized in
hours. Most institutions will co-administer Vitamin Table 16.2. Timely test results are critical to effective
K to use this 24–48 hour window to support the treatment success as coagulopathy is a dynamic pro-
hepatic synthesis of Vitamin K dependent coagulation cess, made worse by ongoing blood loss.
factors. There is no clear guidance about the timing of Standard laboratory tests (SLT), such as platelet
158 intraoperative 4FPCC administration. Some teams count, fibrinogen levels, aPTT or PT, usually have a
opt to give a 50% dose after anesthetic induction turnaround time of 30–90 minutes. In addition, SLTs

Table 16.2. The ideal coagulation test

Therapeutic Interventions and
Features Areas of
Assessment
Management of Bleeding Patients
There are no simple answers and there is no magic
Point-of-care test Plasmatic bullet when it comes to treatment of bleeding in heart
coagulation surgery. Blood coagulation is a cellular event taking
Fast results Platelet function place at a specific site of endothelial cell dysfunction,
Easy to use by non-laboratory Fibrinogen activity i.e. the site of surgical disruption of capillaries and
staff small vessels.
Temperature: Besides using coagulation tests, tem-
Unprocessed whole blood Clot stabilization
perature control is of utmost importance as blood
Able to neutralize heparin Fibrinolysis does not coagulate below 30–32°C. It is not the central
effect core temperature that matters but wound tempera-
Able to correct for Drug effects ture. Measuring the temperature at a patient’s sternal
hypothermia edge in a cold operating room can yield surprising
results. This might explain why more often than not
the bleeding markedly slows down once the chest is
closed and the wound is no longer exposed to a 20°C
are poor discriminators – an abnormal aPTT or ACT environment.
does not differentiate between factor deficiency and Platelets: Platelet transfusions are obtained from
residual heparin effect. Having to wait for blood pooled donors or from apheresis (single donor). They
results for an hour after giving protamine often leads are the scarcest of blood products and in very
to initial blind, empiric treatment of any bleeding high demand.
after CPB. Platelets are the part of the coagulation system
The alternative approach is to assess whole blood that is most affected by CPB and by inflammation.
coagulation with viscoelastic tests (VET), such as VETs are poor at picking up platelet dysfunction and
thromboelastography/elastometry (e.g. ROTEM™, the post-CPB platelet count currently provides the
TEG™, ClotPro™) or resonance technology (e.g. best guidance for transfusion. Institutional thresholds
TEG6s™, Quantra™). These point-of-care devices vary but generally are between 50.000 and 100.000/l.
(POC) utilize whole blood samples with draw-to- Unfortunately, a large proportion of packed plate-
result times of around 20 minutes. They offer assays lets are dysfunctional, dying or apoptotic and can act
sensitive and insensitive to heparin, which allow early as prothrombotic microparticles. Platelet transfusions
testing while still on bypass and fully heparinized, as carry large concentrations of cytokines and can be a
well as detection of residual heparin when testing major risk for septic/bacterial transfusions with an
after protamine. Results include clotting time (integ- incidence of approximately 1/2000 transfusions.
rity of clotting factors), total clot firmness with FFP and Cryoprecipitate: FFP contains all the pro-
fibrinogen and platelet contribution and fibrinolysis tein coagulants found in circulating plasma at normal
(lysis index). Figure 16.1 gives an overview of the levels unless it has been processed at 1–6°C to pro-
information that can be gained from VET. Recent duce cryoprecipitate. Cryoprecipitate is rich in Factor
practice guidelines strongly recommend VET over VIII, von Willebrand Factor and fibrinogen. At first
SLT in the management of excess bleeding after glance it appears logical to use FFP to replenish pro-
cardiac surgery. teins consumed by coagulopathy during bypass.
VET should be used in conjunction with an insti- When taking the dilution in the patient’s circulation
tutionally agreed algorithm for the treatment of into account, at least 15 ml/kg body weight of FFP are
post-CPB bleeding (see Figure 16.2). There is increas- necessary to achieve a meaningful rise toward normal
ing evidence that the judicious use of VET and bleed- levels of coagulation factors. Transfusing such a large
ing algorithms reduce transfusion requirements, amount of volume will lead to a significantly
particularly when clinicians accept that an abnormal decreased platelet and red cell count, and further
test result by itself should not prompt treatment if transfusion with associated risks and significant 159
there is no clinical evidence of coagulopathic bleeding. volume overload.

100
Amplitude in mm (Firmness)
80
60
40 MCF ML
A10
20 alpha LI 30
0
CT Clotting time
CFT Clot formation time
alpha Alpha-angle
CFT A10 Amplitude 10 min after CT
MCF Maximum clot firmness
LI30 Lysis index 30 min after CT
CT
ML Maximum lysis
0 10 20 30 40 50 60
Time in min
Figure 16.1 Picture of typical Temogram.
CT (s) – The CT parameter facilitates the decision to substitute clotting factors or to reverse anticoagulation.
CFT (s) – The CFT parameter facilitates the decision to substitute with platelets, fibrinogen or both. A shortened CFT is indicative for
hypercoagulation (as well as increased MCF parameter)..
MCF (mm) – A low MCF indicates a low clot firmness. The MCF value is used to facilitate the decision for substitution therapy with platelets or
fibrinogen. A high MCF value may indicate a hypercoagulable state.
A (x)-values represent the clot firmness. An A(x)-value is the amplitude after a certain time x after CT (e.g. A10 after 10 min)..
LOT (s) - The time span from CT to the start of significant lysis in s. Significant lysis is defined as a decrease of the amplitude of 15% as
compared to MCF.
ML (%) – The parameter of maximum lysis (ML) describes the degree of fibrinolysis relative to maximum clot firmness (MCF) achieved during
the measurement (% clot firmness lost). Image provided courtesy of Werfen.
160
Figure 16.2 Typical ROTEM based algorithm for managing post-CPB bleeding with POC tests.

Unfortunately, the use of coagulation products effect of residual heparin should be excluded by com-
from the blood bank is over-utilized in many clinical paring intrinsically activated coagulation times on
practices. Unguided transfusion does not decrease VET with heparin insensitive assays and treated with
bleeding and increases adverse events, including additional protamine if necessary.
length of hospital stay, pneumonia, renal failure and If coagulopathic bleeding persists after the “first
mortality. The data from combat casualty and major round” of tests and products, the above cycle starting
trauma, promoting 1:1:1 transfusion of red cell to FFP with viscoelastic testing should be repeated until safe
to platelet after a full blood volume loss, cannot be transfer to the ICU is possible.
extrapolated to cardiac surgery and CPB
coagulopathy.
Factor concentrates: Today both cryoprecipitate Blood Conservation Techniques
and FFP can be replaced with prothrombin complex Anemia as well as red blood cell transfusion have both
concentrate (PCC) and fibrinogen concentrate. been linked to unfavorable outcomes after cardiac
Factor concentrates are available as single factors surgery. Perioperative blood and coagulation man-
(Factor VIIa, VIII, IX and others) or as a combination agement needs to strike the right balance between
of three or four factors. The latest iteration are the avoiding low hemoglobin concentrations and
4FPCCs, which do not just contain pro-coagulant avoiding unnecessary transfusion.
factors but also Protein C, S, Anti-Thrombin III and
a very small amount of heparin. Modern 4FPCCs
contain the 25-fold concentration of pro-coagulant
Antifibrinolytic Agents
proteins compared to FFP. Fibrinolysis is triggered by thrombin activation and
PCC and fibrinogen concentrate figure prominently physiologically occurs in parallel to clotting and leads
in difficult bleeding after CPB, particularly in algo- to balanced hemostasis. This process is governed by
rithms based on viscoelastic testing. Concentrates, how- physiological activators (tissue and urinary plasmino-
ever, should not be given prophylactically. There are gen activator) and inhibitors (plasminogen activator
several reports of catastrophic thromboembolic compli- inhibitor-1 and -2 and alpha-2-antiplasmin).
cations following aggressive treatment of post-CPB Despite the presence of high dose heparin, thrombin
bleeding with PCC, especially with older 3-Factor PCCs. and fibrin are constantly formed within the CPB circuit.
1-desamino-8-D-arginine-vasopressin (DDAVP): Unsurprisingly, this is accompanied by activation of
DDAVP is a synthetic analogue of vasopressin, which fibrinolysis, as demonstrated by elevated levels of tissue
has no or little vascular contractility effect. DDAVP plasminogen activator during CPB, using up fibrinogen
can enhance platelet function through the release of and potentially impairing clot formation after reversal
vWF and multimeric building blocks of vWF. The use of heparin. Blocking antifibrinolytic activity has been
of DDAVP after CPB in patients with renal failure shown to reduce postoperative blood loss in cardiac
and uremia has gained some attraction but data are surgical patients. The prophylactic administration of
scarce. antifibrinolytic agents has become a standard practice
Practical management: Coagulation testing with and is recommended in current guidelines.
VET within a structured algorithm is recommended The synthetic lysine-analogues tranexamic acid
as best practice (Figure 16.2). Assessment should start (TXA) and epsilon-aminocaproic acid (EACA) are
prior to coming off CPB using tests that neutralize the most commonly used antifibrinolytics in cardiac
heparin in vitro. They should be done with enough surgery. They prevent the activation of plasminogen
time to arrange for the necessary coagulation products to plasmin by reversibly blocking its lysine-binding-
to arrive in the operating room should coagulopathic site. There does not seem to be an increased risk of
bleeding develop following protamine administration. prothrombotic events with both substances but high
In case of deranged VET results, coagulation doses of TXA have been linked to an increased inci-
factors should be substituted using 4FPCC. Keeping dence of seizures. Lower dose regimens, with either:
in mind the potential for thromboembolic events, a single bolus of up to 25 mg/kg or
starting with a low dose approach is recommended. a bolus of up to 10 mg/kg followed by an infusion
Fibrinogen concentrate and platelets should be trans- of typically 1 mg/kg/h for the duration of the 161
fused in accordance with a bleeding algorithm. The operation

are currently recommended. Higher dose regimens from the blood. This requires the venous reservoir
have not shown further decreases in blood usage. to be well filled to still be able to run bypass safely
Until 2008 the non-specific serine protease inhibi- without triggering a level alarm. Patients most likely
tor aprotinin was the antifibrinolytic of choice in to benefit from ultrafiltration are those with decom-
cardiac surgery. It has been shown to significantly pensated heart failure or renal failure and volume
reduce blood loss in numerous studies. Following a overload. It can also be useful where high volume
series of controversial studies raising concerns of crystalloid cardioplegia techniques with Custodiol or
higher rates of renal and cardiovascular complications Brettschneider are employed. Residual volume in the
with aprotinin, it was withdrawn from the United pump after separating the patient from bypass can be
States market. In recent years there has been a resur- concentrated using an ultrafilter. Cell salvage systems
gence in interest in aprotinin. Its marketing license (“cell saver”) can be used to minimize the loss of red
has been reinstated by Health Canada and by the blood cells before, during and after CPB. These auto-
European Medicines Agency and registry data re- mated systems heparinize blood during collection
evaluating its safety are eagerly awaited. into a reservoir, filter it and process it by centrifuging
and washing it to produce a red cell concentrate.
Fluid, plasma with clotting factors, platelets and the
Avoiding Hemodilution anticoagulant heparin are largely removed during the
Surgical misadventure aside, one of the main threats washing process. Cell saved blood helps to maintain a
to hemoglobin concentration is hemodilution. sufficient hematocrit, but additional replacement of
Excessive iv fluids and, more importantly, the CPB coagulation factors and platelets is likely to be neces-
priming solution can cause significant dilution. sary to treat coagulopathy.
Strategies such as optimizing the circuit, using min-
imal invasive extracorporeal circulation (MiECC), or
retrograde autologous priming are discussed in Special Conditions
Chapter 8. Although the conditions discussed below are infre-
Acute normovolemic hemodilution (ANH), where quently encountered in normal practice, they can
whole blood is removed into a blood storage bag create problems for clinicians who are unaware of
before heparinizing and replacing it with the same them. It is worth having a working knowledge of
amount of crystalloid or colloid fluid, has fallen out them and developing locally agreed protocols on
of favor in recent years. ANH has theoretical advan- how to deal with them.
tage that not only red cells but also coagulation
factors and platelets are spared the exposure to bypass Jehovah’s Witnesses
and are available to support coagulation at the end of
surgery. While ANH has been shown to reduce the There are more than 7 million followers of the
risk of bleeding and transfusion, it is most effective Jehovah’s Witness (JW) faith worldwide. Since
when larger volumes of up to 800 ml of blood are 1945 the majority of members of this community
removed. Only a very limited number of patients will refuse allogeneic blood transfusion, even in life-
have a high enough Hb (>150 g/l) to tolerate ANH threatening situations.
without the risk of significant hemodynamic JW patients do not accept whole blood, red blood
instability. cell, platelet or plasma transfusion. Some other treat-
Cardiotomy suction reduces the actual blood loss ments are left to the individual’s decision and may be
as shed blood is returned from the surgical field to the accepted:
CPB reservoir. This blood is filtered to remove cell derivatives of blood: albumin, coagulation factors,
debris but remains potentially highly activated with immunoglobulins, interferons, hemoglobin,
inflammatory mediators and coagulation products, cryoprecipitate
potentially accelerating the cycle of clotting recombinant factors: erythropoietin, rFVIIa
and fibrinolysis. procedures: cardiopulmonary bypass, cell salvage,
Ultrafiltration during CPB helps to increase normovolemic hemodilution, hemofiltration or
hematocrit, concentration of clotting factors and dialysis, provided continuity with the patient’s
162
platelets indirectly by removing extracellular water circulation is maintained at all times.

It is essential to have an informed discussion with the Cardiac surgery can be performed in JW patients with
patient to determine their wishes, which are generally outcomes comparable to those of routine cases, des-
detailed in an advance directive document, prior to pite the limited therapeutic options with blood trans-
surgery and to meticulously document the consent pro- fusion and treating coagulopathy. This has not only
cess. The question whether the refusal of transfusion been shown for patients undergoing CABG surgery,
extends to life-threatening situations should be asked but also for more complex procedures including
explicitly and the answer needs to be documented. LVAD implantation and heart transplantation, espe-
If Jehovah’s Witnesses present for cardiac surgery cially where a preoptimization protocol was used.
their acceptance of extracorporeal circulation is usu- This demonstrates the effectiveness of blood conser-
ally tied to there being continuity at all times between vation techniques as a holistic concept to decrease
the bypass circuit and the patient’s own circulation. blood usage in cardiac surgery without increasing
The same principle applies to cell salvage. risk.
It is paramount to the successful management of
JW patients to avoid situations of anemia and coagu- Sickle Cell Anemia
lopathy. All accepted measures of modern patient
Sickle cell anemia is an autosomal genetic hemoglo-
blood management should be part of a multidisciplin-
binopathy with mutations of the β-globin gene, which
ary institutional treatment protocol for JW patients
results in abnormal β-chains, leading to abnormal
undergoing cardiac surgery.
hemoglobin S (HbS) rather than the normal HbA.
Preoperative optimization – Treatment with Due to a relative resistance of HbS to malaria, preva-
(intravenous) iron and erythropoietin is essential lence of the sickle cell gene is highest in African and
to aim for a high-normal hemoglobin level of at Middle Eastern populations. Depending on the geno-
least 140–150 g/dL. Cardiac catheterization should type, there is the heterozygous (HbAS) sickle cell trait
happen weeks before surgery, if possible, to avoid with around 40% HbS and the homozygous (HbSS)
an inadvertent loss of Hb too close to surgery. All sickle cell disease with only abnormal HbS.
medication potentially impairing coagulation Combination with other haemoglobinopathies is also
(platelet inhibitors, warfarin, DOAC, etc.) should possible (e.g. HbSC, β-thalassemia). Diagnosis
be stopped early, and bridged where necessary. includes HbS-screening test, full blood count for
Tolerance of anemia – Oxygen delivery (DO2) can assessing anemia, and hemoglobin electrophoresis to
be improved during CPB by maintaining confirm and quantify the HbS fraction in sickle cell
normovolemia, increasing the cardiac output (i.e. trait patients.
pump flow), fully oxygenate the available Deoxygenated HbS is decreased in solubility and
hemoglobin and potentially utilize dissolved forms polymers, creating the typical sickle-shaped
oxygen transport with high partial pressures of erythrocytes. As a consequence, blood viscosity
oxygen (0.3 ml O2/100 mmHg). Oxygen increases and capillaries are blocked, often leading to
consumption (VO2) can be reduced by sufficiently embolic-like organ infarction. Typical clinical features
deep anesthesia, including muscle relaxation, are anemia, acute and chronic pain, bone pain and
and hypothermia. necrosis, splenic sequestration, pulmonary hyperten-
Intraoperative management of cardiopulmonary sion, stroke and vaso-occlusive or aplastic crises.
bypass may include acute ANH, RAP, the use of Sickle cell crises can be triggered by hypoxemia, hypo-
vasopressors over volume to maintain blood thermia and acidosis, which are all conditions fre-
pressure, hypothermic bypass (32–34°C), cell quently encountered during cardiopulmonary
salvage and ultrafiltration. Residual pump blood bypass. HbS polymerizes at around PaO2 of 40–50
should be reinfused via the aortic cannula to keep mmHg, which means sickling can occur under
a closed circulation. Meticulous surgical physiological conditions in HbSS patients.
hemostasis is of the essence including the use of Characterization of the genotype and knowing the
topical hemostatic agents. Antifibrinolytic agents percentage of HbS are crucial for choosing the man-
are a standard of care and in case of coagulopathic agement plan for operations involving CPB.
bleeding the early use of accepted hemostatic General principles for management of patients
agents should be considered. with sickle cell disorders are: 163

Avoiding hypothermia (use of warm cardioplegia a primary form, which is associated with
where necessary), dehydration, acidosis and most lymphoproliverative disorders and
importantly hypoxemia a secondary form, which is part of an immune
Blood transfusion with HbS-negative blood while response to various viral and bacterial infections
avoiding cell salvage and retransfusion of residual (e.g. mycoplasma pneumonia, EBV, CMV,
pump blood influenza, HIV, chlamydia) or a neoplastic process
If hypothermia is unavoidable (in operations such (e.g. adenocarcinoma) and is usually less severe
as pulmonary thrombendarterectomy, see and self-limiting.
Chapter 9) exchange transfusion aiming for an In preparation for cardiac surgery, patients with CA
HbS of less than 30%, ideally three to five days need to have their titer and the thermal amplitude
prior to surgery, is necessary. evaluated. A titer below 1:32 and an amplitude below
Accepting a lower hematocrit might improve blood 20°C is considered low risk for cardiac surgery.
viscosity and perfusion during CPB in these patients. A significant titer is thought to be over 1:64 and a
thermal amplitude of above 30°C seems relevant in
Cold Agglutinins patients undergoing cardiopulmonary bypass.
The patient temperature needs to be kept above
Cold agglutinins (CA) are mostly IgM-antibodies
the threshold temperature, CPB should be conducted
against surface antigens of red blood cells.
with normothermic perfusion and warm cardioplegia
Antibody-antigen interaction only becomes relevant
should be used. If cold crystalloid cardioplegia is
below a certain threshold temperature, the so-called
used, the coronary system should be flushed out
CA antibody specific thermal amplitude. Because of
with a warm crystalloid solution to remove red
the pentameric structure of IgM, CA antibodies can
blood cells prior to administering the cold solution.
bind to multiple erythrocytes causing hemagglutina-
In preparation for procedures where hypothermia
tion below their thermal amplitude, potentially
cannot be avoided (e.g. aortic arch surgery), preo-
leading to occlusion of small blood vessels and tissue
perative treatment with plasmapheresis or monoclo-
damage. Even though the agglutination resolves when
nal antibodies (rituximab) can reduce the antibody
temperature rises again, the antibody-antigen inter-
titer.
action triggers a non-reversible complement acti-
The perfusionist is often the first person to spot
vation, which leads to hemolysis.
cold agglutination in patients that have not been
The incidence of cold agglutinin disease is low.
diagnosed. Agglutination generally occurs first in the
A study screening nearly 15,000 cardiac surgical
cardioplegia circuit when cold cardioplegia is mixed
patients found true antibodies in only 0.13%. Two
with the patient’s own blood.
forms of cold agglutinin disease have been described:
Suggested Further Reading on patient blood management for

adult cardiac surgery.
7. Tanaka A, Ota T, Uriel N et al.
Cardiovascular surgery in
1. Besser MW, Klein AA. The J Cardiothorac Vasc Anesth. 2018; Jehovah’s Witness patients: The
coagulopathy of cardiopulmonary 32: 88–120. role of preoperative optimization.
bypass. Crit Rev Clin Lab Sci. J Thorac Cardiovasc Surg. 2015;
2010; 47: 197–212. 4. Ortmann E, Besser MW, Klein
AA. Antifibrinolytic agents 150: 976-83.e1–3.
2. Hofer J, Fries D, Solomon C et al. in current anaesthetic 8. Vaislic CD, Dalibon N, Ponzio O
A snapshot of coagulopathy after practice. Br J Anaesth. 2013; 111: et al. Outcomes in cardiac surgery
cardiopulmonary bypass. Clin 549–563. in 500 consecutive Jehovah’s
Appl Thromb Hemost. 2016; 22: Witness patients: 21 year
505–511. 5. RCoS. Caring for patients who
refuse blood – a guide to good experience. J Cardiothorac Surg.
3. Task Force on Patient Blood practice. 2016. 2012; 7: 95.
Management for Adult Cardiac 9. Patel PA, Ghadimi K, Coetzee E
Surgery of the European 6. Jassar AS, Ford PA, Haber HL
et al. Cardiac surgery in Jehovah’s et al. Incidental cold agglutinins in
Association for Cardio-Thoracic cardiac surgery: Intraoperative
S, the European Association of Witness patients: ten-year
164 Cardiothoracic A, Boer C et al. experience. Ann Thorac Surg. surprises and team-based
2012; 93: 19–25. problem-solving strategies during
2017 EACTS/EACTA Guidelines cardiopulmonary bypass.

J Cardiothorac Vasc Anesth. 2017; shall find – but then what do you agglutinin screening before
31: 1109–1118. do? Cold agglutinins in cardiac surgery. Transfus Med
10. Jain MD, Cabrerizo-Sanchez R, cardiopulmonary bypass and a Rev. 2013; 27: 65–73.
Karkouti K et al. Seek and you single-center experience with cold
165

Chapter
Inflammation and Organ Damage during
The transition from physiological circulation to car- Inflammatory Response Syndrome (SIRS) in sepsis.
diopulmonary bypass (CPB) represents a major Unfortunately, the SIRS criteria are widely regarded
change to the homeostasis of the body including as too non-specific to add any discriminant value to
alterations in the distribution of blood flow and the systemic inflammatory response, with moderate
oxygen delivery to organs (see Figure 17.1a). Tissue tachycardia and pyrexia >38°C qualifying a patient
oxygen delivery is influenced to a large extent by with the syndrome. SIRS has de facto been abandoned
CPB flow rate (see Figure 17.1b). During CPB cere- in the field of cardiopulmonary bypass, with a small
bral and systemic oxygen saturation are significantly minority of papers (<14%) on this topic even men-
reduced by lower blood flow regardless of systemic tioning SIRS and even fewer reporting on the four
arterial pressure. Moreover, vasopressors, frequently criteria necessary to define SIRS.
administered to restore blood pressure, are associ- Despite the lack of a practical definition, there is
ated with a further decrease in cerebral and systemic acceptance that an iatrogenic inflammatory response
oxygen saturation. Organ dysfunction on CPB may is most likely triggered to a greater or lesser extent in
thus be in part attributed to changes in the regional all patients undergoing cardiac surgery with CPB and
distribution of blood flow and the dependence of that this contributes to the perioperative complica-
oxygen delivery on the maintenance of adequate tions summarized in Table 17.1. This chapter focuses
CPB flow rates. on CPB-associated gastrointestinal, pulmonary and
Layered on top of disturbances in oxygen delivery myocardial dysfunction. Renal and cerebral compli-
to the tissues is a systemic inflammatory response cations are discussed in further detail in Chapters 18
triggered by contact of leukocytes and other blood and 19.
components with the artificial surfaces of the extra-
corporeal circuit. This results in a storm of cytokine Table 17.1. Complications after cardiac surgery
and protease release from leukocytes in addition to
Renal failure 3.1 %
activation of complement, kallikrein, coagulation and
fibrinolytic pathways. While most of these host Stroke or coma 2.8 %
responses are appropriate and desirable in the con- Gastrointestinal complications 2.5 %
text of a localized injury or infection, they are not
Re-op for bleeding 2.3 %
desirable systemically and contribute to the morbid-
ity and mortality associated with cardiopulmonary Sternal infections 1.4 %
bypass. Periop myocardial infarction 1.1 %
Acute respiratory distress syndrome 0.9 %
Systemic Inflammatory Response Dialysis 0.9 %
There is some controversy over the definition of the Multisystem failure 0.6 %
systemic inflammatory response, which has evolved
Patients after first time coronary artery bypass in the USA (Society
as an amalgam of formal and informal definitions. of Thoracic Surgeons, 1997 Database; 161,018 patients). Adopted
The only formal definition is borrowed from critical from Hessel; Seminars in Cardiothoracic and Vascular Anesthesia
care and the 1992 diagnostic criteria of the Systemic 2004.
166

Chapter 17: Inflammation and Organ Damage during Cardiopulmonary Bypass
Figure 17.1 (a) Regional O2 delivery with onset cardiopulmonary bypass, (b) Change in organ DO2 with changes in CPB flow rate. (Adapted
from Boston US, Slater JM, Orszulak TA, Cook DJ. Hierarchy of regional oxygen delivery during cardiopulmonary bypass. Ann Thorac Surg. 2001 Jan;71(1):260–264.)
From Teflon to Velcro: How Endothelial studies have shown that the endothelium lining
microvascular beds (e.g. in the brain and kidneys)
Lining Links the Systemic Inflammatory can become activated by periods of ischemia/reperfu-
Response to Organ Injury sion. Such activated endothelium becomes prothrom-
Endothelial cells have been recognized as gatekeepers, botic, is open to solute exchange and supports the
separating the activated milieu in the circulation from transport of activated leukocytes into organs
the tissues (Figure 17.2a). Even modest hypoxia can (Figure 17.2b). This mode of organ injury occurs in
activate endothelial cells, thereby forming a nexus for addition to more direct hypoxic injury to tissues, such
prothrombotic events and exudation of inflammatory as to the sensitive medullar region of the kidney.
mediators and leukocytes into the tissues. Several Maintaining optimal and continuous tissue perfusion 167

therefore takes on further importance from the per- to-skin time (>240 minutes) and prolonged cardiopul-
spective of the systemic inflammatory response. monary bypass time (>121 minutes). Acute kidney
failure and pneumonia were identified as postoperative
Dysfunction of Specific Organ Systems risk factors. Interestingly, the type of surgery and new
onset postoperative atrial fibrillations were not found
Gastrointestinal Dysfunction to be risk factors.
Gastrointestinal (GI) complications post cardiac surgery
Pathogenesis of GI Complications
are relatively uncommon with an incidence of 2–4 %, but
a mortality rate of 15–60%. This represents about Depressed systemic hemodynamics: CPB causes profound
11 times (range 4–32 times) the mortality in patients reductions in blood flow in the splanchnic circulation
not experiencing GI complications. The median time intraoperatively and for up to several hours postopera-
for presentation of GI complications is eight days. tively. Severe intestinal ischemia may occur during CPB
Despite improvements in surgical techniques and even when the indices of global body perfusion remain
perfusion strategies, the incidence and the normal. This may be due to the release of a variety of
mortality rate have not changed in the last two decades. endogenous vasoactive factors, such as vasopressin, cat-
The clinical assessment of patients with GI complica- echolamines and thromboxanes, and to the administra-
tions is often delayed because patients might be sedated, tion of vasopressors to maintain perfusion pressure. Both
partially unresponsive, mechanically ventilated or the of these lead to a redistribution of regional blood flow
classical symptoms and signs are masked by other car- away from the mucosa of the GI tract.
diac and pulmonary complications. Table 17.2 sum- SIRS: The combination of reduced splanchnic
marizes the most common GI complications. blood flow and the CPB-induced SIRS reduce the
In a study of 4,883 patients who underwent cardiac efficacy of both the absorptive and barrier functions
surgery, several risk factors were identified as predis- of the GI tract. The increase in gastrointestinal muco-
posing for GI complications, including prolonged skin- sal permeability results in the translocation of bacterial
(a)
Barrier Anti-thrombotic Anti-adhesive

function surface surface
NO (nitric oxide) mediates endothelial dependant relaxation
AT-III inhibits thrombin

tPA promotes fibrinolysis
PGI2 inhibits platelet activation
Absence of inducible selectin and intercellular adhesion

molecules required for leukocyte recruitment
Figure 17.2 Contrasting properties of resting versus activated or denuded endothelium. Diagram depicts a cut away section of a blood
vessel lined with (a) resting intact endothelium or (b) activated or denuded endothelium. Resting, intact endothelium provides barrier
function, an anti-thrombotic surface, an anti-adhesive surface and nitric oxide mediated vasorelaxation. Vascular beds or grafted vessels that
have been activated by inflammatory mediators, transient ischemia, anaerobic metabolism or endothelial denudation lose their homeostatic
barrier properties and promote thrombosis, solute exchange, adhesion and extravasation of cytodestructive neutrophils, and loss of nitric oxide
mediated vasodilation.
Key: NO = nitric oxide; At-III = antithrombin-III; tPA = tissue plasminogen activator; PI2 = prostaglandin I2; PAI-1 = plasminogen activator
168 inhibitor-1; ICAM-1 = intercellular adhesion molecule-1.

endotoxins from the GI tract into the bloodstream, cardiac output, which are also often associated with
amplifying SIRS and subsequent organ damage. mechanical ventilation, this may result in splanchnic
Prolonged mechanical ventilation > 24 hours: hypoperfusion and mucosal injury.
Mechanical ventilation using large tidal volumes with Table 17.3 gives an overview of the risk factors for
high airway pressures may lead to release of proin- GI complications.
flammatory cytokines. In conjunction with stimula-
tion of the sympathetic nervous system and decreased Specific GI Complications
GI bleeding – bleeding from the upper GI tract is
Table 17.2. Visceral complications after cardiac surgery far more common than bleeding from the lower
GI tract. Lower GI tract bleeding is usually
Incidence (%) Mortality (%)
associated with bowel ischemia or preexisting
Gastrointestinal 30.7 26.9 large bowel disease.
bleeding Bowel ischemia or perforation – bowel ischemia
Ischemic bowel 17.7 71.3 after cardiac surgery is one of the most serious
complications in the postoperative period. It
Pancreatitis 11.2 27.5
accounts for 18 % of all GI complications and is
Cholecystitis 10.9 26.9 associated with a mortality rate of >70%. It is
Paralytic ileus 4.5 10.8 more common in advanced age, females,
emergency surgery, complex surgery, end stage
Perforated peptic ulcer 4.2 43.8
renal disease, prolonged bypass and perioperative
Hepatic failure 3.5 74.4 use of IABP and vasopressors. The earliest
Diverticulitis 2.6 17.1 presenting signs are progressive metabolic
acidosis, leukocytosis and ileus. Early diagnosis
Small bowel 2.0 18.5
obstruction and intervention, for example CT scan or
laparotomy, may be lifesaving.
Pseudo-obstruction of 1.9 21.4
Hepatic dysfunction – as a result of reduced
colon
splanchnic perfusion, hepatic metabolism is
Adapted with modifications from: Hessel; Seminars in reduced during CPB. Hepatic blood flow has been
Cardiothoracic and Vascular Anesthesia 2004
reported to decrease by 19% after CPB is
(b)
Loss of Pro-thrombotic Pro-adhesive

barrier function surface surface
↓AT-III ↓tPA ↑P-selectin

NO ↓PGI2 ↑PA-1 ↑ICAM
Loss of nitric oxide/loss Thrombus formation/ Neutrophil

of vascular tone platelet aggregation recruitment/
cytodestruction
Elastase
myeloperoxidase
oxygen radical
secretion
Figure 17.2 (cont.)

169

Table 17.3. Risk factors associated with GI complications post ○ Impaired ability to generate heat and regulate
cardiac surgery
temperature
Preoperative Age > 75 years ○ Impaired glucose metabolism.
History of congestive heart failure or
ejection fraction < 40%
Renal insufficiency
Pancreatitis – overt pancreatitis, characterized by
Increased preoperative total bilirubin
a rise in serum amylase to over 1000 IU/l, occurs
>1.2 mg/dl in 0.1–1% of cases following cardiac surgery and
Preoperative partial thromboplastin time accounts for 11% of GI complications.
(PTT) >37 seconds Uncomplicated pancreatitis carries a mortality of
Type of cardiac surgery 5–10%, but cases progressing to necrotizing
Emergency pancreatitis or to the development of a pancreatic
Reoperation abscess or a pseudocyst usually result in death.
Valve or combined procedure Lesser degrees of pancreatic cellular injury with
Cardiac transplantation mild elevations in serum amylase concentrations
Intraoperative Intraoperative circulatory failure are common. The etiology is probably related to
CPB duration > 100 minutes perioperative reduction in splanchnic blood flow
Aortic cross-clamp duration > 55 causing pancreatic ischemia. Calcium, frequently
minutes used to treat intraoperative hypotension, has not
Transfusion of packed red blood cells been identified clearly as an independent risk
Postoperative Low cardiac output factor.
Use of inotropes or vasopressors or intra-
aortic balloon pump (IABP)
Reoperation for bleeding
Pulmonary Dysfunction
Loss of normal sinus rhythm Pulmonary complications remain a leading cause of
Ventilation > 24 hours morbidity after cardiac surgery. The incidence is 7.5%
Intensive care unit stay > 1 day and the mortality rate is 21%. The spectrum of pul-
monary complications ranges from atelectasis to
acute respiratory distress syndrome (ARDS). The
incidence of post-CPB ARDS is <2%. The mortality
commenced. There may be a transient rise in the rate associated with post-CPB ARDS, however, is
levels of hepatic enzymes, which usually peaks >50%.
early in the postoperative period. Only a small Median sternotomy results in more than a 50%
number of patients show clinically evident postoperative reduction in vital capacity (VC) and
jaundice, although bilirubin levels can rise in forced expiration (FEV1) from preoperative values.
about 20% of cases. Moderate or severe degrees of These changes last for about four months postopera-
hepatic dysfunction are rare and usually occur in tively and are caused by poor coordination of rib cage
concert with multi-organ failure. expansion following sternotomy, pleural effusion and
Risk factors for hepatic dysfunction post pain. The use of the internal mammary artery for
cardiac surgery include female gender, congestive grafting exacerbates these changes. There is no differ-
heart failure, valvular heart surgery, combined ence between on-pump versus off-pump surgery with
surgical procedures, postoperative bleeding and regard to these changes except that CPB may be
transfusion. Consequences of hepatic dysfunction associated with the release of bronchoconstricting
relevant to CPB specifically include: mediators causing an increase in expiratory
○ Impaired drug metabolism resistance.
○ Reduced plasma protein concentrations Table 17.4 provides an overview over the most
leading to reduced plasma oncotic pressure common causes of respiratory failure after
and alteration in the volume of distribution cardiac surgery.
of drugs Although some of the factors listed relate to car-
170 ○ Impaired coagulation due to reduction in diac surgery in general and are not specific to CPB,
production of clotting factors the combined effect is the development of

Table 17.4. Common causes of postoperative During these periods the heart is subjected to insults
respiratory failure
from microemboli, SIRS, regional hypoperfusion,
Atelectasis complete ischemia and reperfusion injury. The injuri-
ous effects incurred from these insults, together with
Increase in lung water content as a result of increased
capillary permeability caused by SIRS
the potential for inadequate myocardial protection
and distension of the flaccid heart during the period
Impaired hemodynamics in the immediate of cross-clamping, result in myocardial edema and
postoperative period reduced ventricular contractility, which may persist
Additional fluid load during CPB into the postoperative period. Furthermore, if the
Altered production of surfactant heart is subject to excessive preload or high afterload
lung collapse during CPB during weaning from CPB, left ventricular end-
SIRS causing decreased static and dynamic lung diastolic volume, myocardial wall stress and oxygen
compliance consumption are all increased, further contributing to
Transfusion-related acute lung injury (TRALI)
deterioration in cardiac function.
Altered chest wall mechanics resulting from sternotomy

Pneumothorax or hemothorax
Therapeutic Strategies for Attenuating
Phrenic nerve injury impairing diaphragmatic function
the Systemic Inflammatory Response
How to Measure Anti-inflammatory
intrapulmonary shunts that cause a mismatch Interventions?
between ventilation and perfusion. This manifests as There is no practical working definition of the sys-
a higher inspired oxygen concentration requirement temic inflammatory response. The only formal defin-
to maintain an acceptable level of blood oxygenation. ition of SIRS does not provide discriminant value,
This mismatch tends to resolve gradually postopera- with moderate tachycardia and pyrexia >38°C quali-
tively, but patients may require supportive measures fying for the syndrome. In the absence of a workable
such as positive endexpiratory pressure (PEEP) during definition, different scoring systems, such as ODIN
mechanical ventilation or continuous positive airway (Organ Dysfunctions and/or Infection) or APACHE
pressure (CPAP) when spontaneously breathing until (Acute Physiology and Chronic Health Evaluation),
resolution occurs. In mechanically ventilated patients, have been adopted by different groups to link the
tidal volumes in excess of 10 ml/kg were found to be a CPB-associated systemic inflammatory response to
risk factor for organ failure and prolonged intensive clinical endpoints, providing better discriminant
care unit stay. Diuretics, as an adjunct to careful fluid value.
balancing, may help to reduce interstitial lung water. In An alternative approach put forth by the
hemodynamically stable patients, with adequate gas “Outcomes” Consensus Panel in 2010 is to measure
exchange and no evidence of neurologic insults or “softer” outcomes, such as time to extubation, renal
bleeding, adequate pain control and early extubation and cardiac injury biomarkers, length of ICU stay and
allow early ambulation and the ability to cough and neurocognitive deficits tailored to heart surgery, as
clear pulmonary secretions, which reduces the inci- surrogate but still clinically meaningful endpoints.
dence of pulmonary complications.
Myocardial Dysfunction Anti-inflammatory Interventions

Using the “Outcomes” Consensus Panel’s surrogate
The period of CPB during cardiac surgery can be endpoints, a multidisciplinary consortium of sur-
divided into three phases: geons, anesthetists, perfusionists and basic scientists
– Onset of CPB until application of the cross-clamp synthesized the evidence covering the complete spec-
– The period of cross-clamping and cardioplegic or trum of anti-inflammatory interventions deployed in
fibrillatory arrest the setting of cardiopulmonary bypass. This included
– The reperfusion period following removal of the pharmacological, perfusion-related and surgical/peri- 171
cross-clamp and ultimately separation from CPB. operative management interventions. Ninety-eight

anti-inflammatory interventions including off-pump gastrointestinal bleeding and hyperglycemia

surgery, minimized circuits, biocompatible circuit requiring insulin infusion. The routine
coatings, leukocyte filtration, complement C5 inhib- administration of prophylactic corticosteroids is
ition, preoperative aspirin and corticosteroid prophy- thus not recommended.
laxis were part of the analysis. Unfortunately no single Statins – are primarily used in the treatment of
intervention was supported by strong level A evidence hypercholesterolemia. They also have anti-
(multiple randomized controlled trials [RCTs] or inflammatory effects with a reduction in post-CPB
meta-analysis) of clinical benefit. The somewhat renal and cerebrovascular complications. Statins
gloomy conclusions from the review were consistent may have a potential benefit on graft patency and
with the fact that there are few statistically well reduction in mortality and equivocal benefit on
powered studies and meta-analyses examining hard reduction of postoperative atrial fibrillation. For
endpoints. A Cochrane review concluded that corti- these reasons, continuation of perioperative
costeroids had no effect on mortality, cardiac or pul- statins may be recommended pending more
monary complications in cardiopulmonary bypass definitive evidence of efficacy.
patients, while meta-analyses investigating leukocyte Angiotensin converting enzyme inhibitors (ACE-
filtration and ultrafiltration strategies found that these I) – ACE-I are antihypertensive agents that are
were sometimes associated with heightened leukocyte used as an adjunct in the treatment of heart failure
activation. with beneficial effects on cardiac remodeling.
A secondary analysis of the “Outcomes” criteria They have anti-inflammatory effects as shown by
revealed that suppression of a single inflammatory attenuation of the IL-6 rise in the postoperative
biomarker was insufficient to confer clinical benefit. period and antifibrinolytic effects that might
This is consistent with a “multiple hit” hypothesis, in decrease the incidence of graft thrombosis. Long-
which clinically effective suppression of the systemic term survival benefits and reduction in cardiac
inflammatory response will require combinations of adverse events are still controversial, particularly
treatments and interventions to hit multiple targets in in patients with normal ejection fraction.
the multiple pathways activated. The evidence there-
fore points toward the fact that narrowly targeted
interventions fail to demonstrate clinical benefit when
Perfusion Strategies
used on their own. This is hardly surprising if we take Heparin-bonded circuitry – proponents of bonded
into account the broad array of host defense path- circuits used them with the intention of reducing
ways – complement, coagulation, kinins, fibrinolysis, the degree of complement activation. Despite high
leukocytes, platelets, hemolysis, and inflammatory initial hopes they have not been proven to be
mediators – activated across the surgical population. effective in attenuating coagulation disorders or
The mechanisms of the currently most plausible fibrinolysis.
interventions are summarized below. Hemofiltration/ultrafiltration – convection and
osmosis under hydrostatic pressure have been
Pharmacological Strategies incorporated into CPB circuits to remove low-
Steroids – administrating pre-CPB corticosteroids molecular-weight substances from plasma with
may attenuate the inflammatory response by the aim of reducing the circulating levels of
inhibiting the release of the inflammatory proinflammatory mediators. Current techniques
cytokines IL-6, IL-8 and enhancing the release of are more effective in the pediatric than the adult
the anti-inflammatory cytokine IL-10. In one population.
study this was associated with a decrease in ICU Leukocyte depletion – such filters are often
and hospital stay and in the incidence of incorporated into the CPB circuit to reduce the
postoperative atrial fibrillation. This did not number of circulating activated white cells. Their
translate into survival benefits or a reduction in value is presently unclear, but leukocyte depletion
the cardiac or pulmonary complications. On the may have a protective effect in reducing the
contrary, there was an increase in the incidence of severity of lung, renal and myocardial injury after
172

CPB. The most consistent benefit is found in endogenous vasoconstrictors and platelet
higher risk patients with preexisting lung disease activation leading to local cellular damage. On the
and ventricular dysfunction as well as patients other hand, pulsatile flow has the theoretical
undergoing transplantation or procedures with advantage of delivering more surplus
prolonged CPB duration. Leukocytes in allogenic hemodynamic energy (SHE) to the
blood transfusions have important microcirculation. This should result in
immunomodulatory effects in the recipient. The preservation of the microcirculation, improved
use of leukocyte depleted stored blood has been blood flow to vital organs and attenuation of
shown to decrease mortality in some cardiac the systemic inflammatory response. Despite
surgical patients. This is predominantly due to a these potential advantages, the use of pulsatile
decrease in non-cardiac causes of death, in flow on CPB is controversial because of the
particular multi-organ failure. However, a number absence of data showing clinically significant
of studies have shown that leukocyte adhesion to benefits.
filters may cause their activation and subsequent Avoiding CPB – off-pump CABG (OPCABG) is
release of inflammatory proteases and cytokines. an alternative technique for coronary
Maintaining ventilation and pulmonary artery revascularization, which is still controversial and
perfusion – keeping the lungs ventilated and, where highly dependent on institutional experience and
possible, perfused during CPB decreases the preference. Clinical reports have shown that
incidence of postoperative atelectasis and lung oxidative stress and markers of inflammation
ischemia-reperfusion injury and hence decreases (particularly IL-8, IL-6, TNF and E-selectin) are
the incidence of post-CPB pulmonary dysfunction. significantly reduced during OPCABG when
Although this strategy has been associated with compared to CABG performed on CPB. OPCABG
lesser inflammatory and proteolytic response, its has also been shown to be associated with a
clinical benefit is still to be proven. reduction in blood transfusion. Full
Minimal invasive extracorporeal circulation heparinization may not be necessary and this,
(MiECC) – recently, there has been growing together with the avoidance of hemodilution
interest in the use of MiECC to replace through the CPB priming volume, may be more
conventional cardiopulmonary bypass circuits. important in reducing transfusion requirements
The use of MiECC circuits has been shown to lead than any advantageous effects from ameliorating
to less thrombin generation due to improved the systemic inflammatory response. Despite these
biocompatibility, elimination of the blood-air potential advantages, large-scale studies failed to
interaction in the reservoir and exclusion of show benefits in long-term survival or
unprocessed shed blood reinfusion. Despite some neuropsychological outcomes after OPCABG
studies showing potential clinical advantages, such compared to on-pump CABG. On the contrary,
as lower incidence of postoperative AF and renal OPCABG patients have poorer graft patency at
dysfunction and a reduction in blood transfusion, one year.
MiECC circuits have not gained wide clinical
acceptance yet. See Chapter 8 for more detail.
Pulsatile flow – most cardiac centers use non- Disturbances in blood flow and its distribution, along
pulsatile roller or centrifugal pumps to drive with systemic inflammatory responses, are character-
circulation during CPB. Though the exact istics of CPB which put vital organs at risk. While the
mechanism is not fully understood, it is believed specific injury patterns of various organs have
that non-pulsatile laminar flow, as opposed to become better elucidated, methods to mitigate
physiological pulsatile flow, causes deterioration damage for many of these remain elusive. It is likely
of microcirculatory perfusion and shedding of the that clinically effective suppression of the systemic
endothelial glycocalix. Proponents of pulsatile inflammatory response will require combinations of
flow argue that as a result of non-pulsatile, treatments and interventions to hit the multiple path-
laminar flow there is an increase in endotoxins, ways activated.
173

Suggested Further Reading cardiac surgery: effects of

cardiopulmonary bypass and
13. Butler J, Rocker GM, Westaby S.
Inflammatory response to
1. Prondzinsky R, Knupfer A, anesthesia. Ann Thorac Surg 2009 cardiopulmonary bypass. Ann
Loppnow H et al. Surgical trauma November;88(5):13961403. Thorac Surg 1993 February;55
affects the proinflammatory status (2):552–9.
after cardiac surgery to a higher 7. Litmathe J, Boeken U, Bohlen G
degree than cardiopulmonary et al. Systemic inflammatory 14. Landis RC, Arrowsmith JE,
bypass. J Thorac Cardiovasc Surg response syndrome after Baker RA, et al. Consensus
2005 April;129(4):760–766. extracorporeal circulation: a Statement: minimal criteria for
predictive algorithm for the reporting the systemic
2. Dieleman JM, van Passen J, van patient at risk. Hellenic J Cardiol inflammatory response to
Dijk D et al. Prophylactic 2011 November;52(6):493–500. cardiopulmonary bypass. Heart
corticosteroids for Surg Forum 2010 April;13(2)
cardiopulmonary bypass in adults. 8. Hessel, EA 2nd. Abdominal organ
injury after cardiac surgery. Semin E116–123.
Cochrane Database Syst Rev 2011;
(5):CD005566. Cardiothorac Vasc Anesth, 2004. 8 15. Shann KG, Likosky DS, Murkin
(3):243–263. JM, et al. An evidence-based
3. Warren O, Alexiou C, Massey R review of the practice of
et al. The effects of various 9. Weissman, C. Pulmonary
complications after cardiac cardiopulmonary bypass in adults:
leukocyte filtration strategies in a focus on neurologic injury,
cardiac surgery. Eur surgery. Semin Cardiothorac Vasc
Anesth 2004. 8(3):185–211. glycemic control, hemodilution,
J Cardiothorac Surg 2007 April;31 and the inflammatory response. J
(4):665–676. 10. Buggeskov KB, Grønlykke L, Thorac Cardiovasc Surg 2006
4. Zhu X, Ji B, Wang G et al. The Risom EC et al. Pulmonary artery August;132(2):283–90.
effects of zero-balance perfusion versus no perfusion
during cardiopulmonary 16. Landis RC, Brown JR, Fitzgerald
ultrafiltration on postoperative D, et al. Attenuating the Systemic
recovery after cardiopulmonary bypass for open heart surgery in
adults. Cochrane Database Syst Inflammatory Response to Adult
bypass: a meta-analysis of Cardiopulmonary Bypass: A
randomized controlled trials. Rev 2018 February 8;2:CD011098.
critical Review of the Evidence
Perfusion 2012 September;27 11. Ng CS, Wan S. Limiting Base. J Extra Corpor Technol 2014
(5):386–392. inflammatory response to September;46(3):197–211.
5. Ranucci M, Balduini A, Ditta A cardiopulmonary bypass:
pharmaceutical strategies. Curr 17. Myers GJ, Wegner J.
et al. A systematic review of Endothelial Glycocalyx and
biocompatible cardiopulmonary Opin Pharmacol 2012. 12
(2):155–159. Cardiopulmonary Bypass. J
bypass circuits and clinical Extra Corpor Technol 2017
outcome. Ann Thorac Surg 2009 12. Dvirnik N, Belley-Cote E, Hanif H September;49(3):174–181.
April;87(4):13111319. et al. Steroids in cardiac surgery: a
systematic review and meta- 18. Landis RC, Durandy Y “Dear
6. De Backer D, Dubois MJ, SIRS . . . unfaithfully yours”.
Schmartz D et al. analysis. Br J Anesth 2018 120 (4):
657–667. Anaesth Intensive Care 2017
Microcirculatory alterations in March;45(2):274–275.
174

Chapter
Neuromonitoring and Cerebral Morbidity
18 Associated with Cardiopulmonary Bypass

Etienne J Couture, Stéphanie Jarry and André Y Denault
Neurological complications after a cardiac surgery are clamping and cannulation are likely to play a huge
common and have a large impact on patient outcomes. role in the shedding of atheromatous emboli from the
They are the result of a combination of numerous ascending aorta.
factors, many of them associated with cardiopulmon-
ary bypass (CPB). Blood pressure control is essential to Blood Pressure Control
reduce the incidence of cerebral hypoperfusion and
Blood pressure control during CPB is important to
ischemic stroke during and after cardiac surgery.
ensure appropriate perfusion of end-organ tissues
Cerebral oxygen saturation can be tracked using
such as the brain, the kidneys and the gastrointestinal
near-infrared spectroscopy to assess cerebral perfusion
tract. Organ perfusion pressure, defined as arterial
and oxygenation. Careful temperature management
minus venous pressure, is a key factor to assuring
plays a key role in preventing cerebral morbidity.
adequate blood flow, oxygenation and metabolic
Despite multiple attempts to find pharmacologic strat-
function. The “tools” built into the CPB machine
egies to prevent neurologic injury, no such solution has
provide control of multiple parameters, such as blood
been found to reduce the burden of neurologic compli-
temperature, flow and carbon dioxide, all of which
cations associated with cardiac surgery.
can be used to optimize cerebral blood flow (CBF).
Hypotension during CPB can be the result of hemo-
Risk Factors dilution or of vasodilatation due to pro-inflammatory
The incidence of stroke after cardiac sugery has been processes, anesthetic drugs and preoperative use of
reported to be as high as 6%. Unfortunately, post- angiotensin-converting enzyme inhibitors (ACEI) or
operative neurocognitive dysfunction is even more calcium channel blockers. Hypotension may comprom-
common with a rate of up to 60%. Numerous studies ise the clearance of emboli and reduce cerebral perfu-
have identified independent predictors of periopera- sion, especially to the watershed areas of the brain.
tive stroke, the most commonly named variables are Hypertension, on the other hand, can result from
summarized in Table 18.1. inadequate levels of anesthesia or analgesia, endogen-
Different surgical procedures come with different ous release of catecholamines or vasoconstriction due
risks of stroke. Figure 18.1 shows the results of a to hypothermia. Hypertension may lead to cerebral
retrospective review of 16,184 patients undergoing hyperperfusion and hyperemia.
various cardiac procedures. It is interesting to note Good blood pressure control is very important to
that the operations done without CPB, i.e. off-pump ensure optimal neurologic outcomes as both hypoten-
coronary artery bypass grafting (OPCABG) and min- sion and hypertension can be deleterious. The
imal invasive direct coronary artery bypass grafting, 2019 European guidelines on the conduct of CPB
show the lowest incidence of stroke. This gives cre- recommend adjusting mean arterial pressure (MAP)
dence to the theory that the majority of cerebral to within the range of 50–80 mmHg with the use of
infarcts are embolic in nature. In the majority of vasoconstrictors and vasodilators, after ensuring
studies, the lesions identified by computed tomog- adequate depth of anesthesia and optimal pump flow.
raphy (CT) were indicative of a macroembolic eti- A MAP less than 50 mmHg is not recommended as
ology with the culprit lesion most commonly located this may fall below the lower limit of cerebral auto-
in the distribution of the major cerebral arteries, regulation, commonly estimated to be around that
mainly the middle cerebral artery. Aortic cross- point despite the wide interindividual variety. 175

Etienne J Couture, Stéphanie Jarry and André Y Denault
Blood Pressure Control and Stroke as multiple trials to find the optimal target MAP
during CPB have yielded conflicting results.
Stroke with clinical symptoms occurs with an inci-
A retrospective study of 7,457 patients demonstrated
dence of 1–2% after cardiac surgery; neurologic
the effects of a sustained MAP < 65 mmHg during
injury, however, occurs in up to 50% of patients and
CPB on postoperative stroke. Every 10-minute period
can be silent or only exhibit subtle symptoms such as
of MAP between 55 and 64 mmHg was associated
mild postoperative neurocognitive dysfunction. The
with a 13% increase in the odds of having a stroke;
optimal MAP during CPB remains a focus of inquiry
every 10-minute period of MAP < 55 mmHg was
associated with a 16% increase. The study is not able
Table 18.1. Patient and operation factors associated with to recommend an ideal MAP target but suggests that
increased risk of perioperative stroke the MAP should be kept at least at 65 mmHg in order
to reduce the incidence of postoperative neurological
History of cerebrovascular disease
complications. A randomized controlled trial of
Any grade of internal carotid artery stenosis 248 patients undergoing coronary artery bypass
Peripheral vascular disease grafting (CABG) reported significantly higher rates
of cardiac and neurological events with a low MAP
Age > 70 years
strategy (50–60 mmHg) when compared with a high
Diabetes mellitus MAP strategy (80–100 mmHg) (12.9 versus 4.8%, p =
Hypertension 0.026). The incidence of permanent neurologic injury
was also higher in the low MAP group (7.2 versus
Infective endocarditis
2.4%). Conversely, another study targeting a high
Emergency/urgent operation MAP (70–80 mmHg) and comparing it to a low
Redo surgery MAP (40–50 mmHg) at similar pump flow did not
show any difference between the two groups in the
CPB time > 2 hours
volume or number of new perioperative cerebral
High transfusion requirement infarcts detected by magnetic resonance imaging
(MRI) or the incidence of postoperative cognitive
dysfunction. However, this study showed a trend
12
10
Incidence of Stroke (%)
0
Total CABG Beating OPCAB MIDCAB MV AV DV COMB
Heart Surgery Surgery Surgery
Figure 18.1 Incidence of stroke in relation to different surgical procedures. CABG = coronary artery bypass grafting, beating heart = OPCABG
+ MIDCABG, MV = mitral valve surgery, AV = aortic valve surgery, DV = double valve surgery, COMB = any other combined procedure. (From
176 Bucerius J, Gummert JF, Borger MA et al. Stroke after cardiac surgery: a risk factor analysis of 16,184 consecutive adult patients. Ann Thorac Surg. 2003 Feb;75
(2):472–4788.)

Chapter 18: Neuromonitoring and Cerebral Morbidity Associated with Cardiopulmonary Bypass
toward a higher rate of stroke (7.0% versus 1.1%; p = 1 when CBF falls outside the limits of autoregulation,
0.06) and death (4.1% versus 0%; p = 0.06) in the high meaning that any change in MAP will be associated
MAP group. A different study comparing an on- with a linear change in CBF; when the correlation
pump MAP based on preoperative values versus a coefficient is 0, the autoregulation is preserved and
set MAP of 80 mmHg has shown the same rates of there is no correlation between MAP and CBF. The
mortality, major neurological or cardiac complica- lower limit of autoregulation is defined as the MAP
tions, deterioration of cognitive function and decline where the correlation between cerebral oximetry and
in functional status. CBF mean velocity increases above a threshold of 0.4,
The ultimate individual approach is to use con- meaning that any decrease in MAP is associated with
tinuous cerebral blood flow autoregulation assess- a decrease in CBF. The upper limit of autoregulation
ment on the operating table to personalize blood is defined in a similar fashion.
pressure management during CPB. Despite the poten- Ultrasound-tagged NIRS to determine the limits
tial benefits, the current evidence does not support the of autoregulation showed no difference in the amount
hypothesis that basing the MAP during CPB on cere- of blood pressure excursions above and below the
bral autoregulation monitoring reduces the frequency optimal MAP during CPB and in the first three hours
of stroke or delayed neurocognitive recovery after after ICU admission in patients with or without delir-
surgery compared with usual care. However, person- ium at postoperative days one and three. However,
alized MAP management using a cerebral autoregula- there were more blood pressure excursions above the
tion approach does reduce the incidence of delirium optimal MAP in patients with delirium and this was
and alterations in memory after surgery. positively correlated with the severity of delirium on
postoperative day two.
Blood Pressure Control and Delirium In a similar study using the concept of optimal
blood pressure based on CBF autoregulation derived
The impact of hypotension on the incidence of post-
from cerebral oximetry, the same group found a sig-
operative delirium and cognitive dysfunction remains
nificant difference in the rate of postoperative delir-
subject to debate. In a randomized controlled trial of
ium in patients whose MAP exceeded the upper limit
92 patients undergoing CABG, those in the high MAP
of autoregulation compared to patients whose MAP
group (80–90 mmHg) had less delirium (0 versus 13%)
did not. The magnitude and duration of MAP above
and a smaller reduction in Mini-MentalStatus score
the upper threshold during CPB was associated with
(1.1±1.9 versus 3.9±6.5) when compared to a low
an increased risk of delirium, while MAP below the
MAP group (60–70 mmHg). On the other hand, a
autoregulation threshold was not.
prospective cohort study based on 734 cardiac surgical
The Cerebral Autoregulation Study Group from
patients did not find an association between intrao-
Johns Hopkins University compared CPB patients with
perative hypotension – defined by MAP lower than 50
a local standard MAP target of 60 mmHg or higher
mmHg, MAP decreased by more than 30% relative to
with a group of patients with a target MAP above the
the baseline or even a MAP decrease by more than 40%
lower limit of autoregulation based on systemic arterial
relative to the baseline – and postoperative delirium.
and middle cerebral artery pressure. Despite an only
marginally higher MAP in the autoregulation group
Cerebral Blood Flow (73.9 mmHg versus 71.3 mmHg, p = 0.01), the inci-
In recent years, CBF autoregulation has been pro- dence of postoperative delirium was lower compared
posed as a new parameter that can be personalized to the standard of care group (37.9% versus 52.7%, p =
from patient to patient. Different tools have been used 0.04). These results highlight the importance of indi-
in order to find the best MAP during CPB. Among vidualizing the MAP target during CPB in order to
them are the mean velocity index (Mx) and the cere- avoid hypoperfusion and hyperemia.
bral oximeter index (Ox). The lower and upper limit
of autoregulation can be defined using a Pearson’s
correlation coefficient calculated from MAP and cere- Cerebral Oxygen Saturation
bral oximetry using near-infrared spectroscopy The balance between cerebral oxygen consumption
(NIRS) or mean CBF velocity using transcranial and supply can be assessed by cerebral oxygen satur- 177
Doppler. The correlation coefficient approaches ation, which is measured using NIRS and is the result

of the local change in the concentration of oxyhemo- and tissue metabolism. NIRS also lacks the ability to
globin over total hemoglobin. NIRS optodes are com- differentiate the causes of low rSO2 (i.e. emboli versus
monly applied to the forehead to measure the regional hypoperfusion). Despite the absence of unequivocal
cerebral oxygen saturation (rSO2) in the evidence to suggest that its use reduces the incidence
frontal cortex. and severity of postoperative neurological complica-
There are three different mechanisms of cerebral tions, NIRS is widely used in deep hypothermic cir-
desaturation: culatory arrest (DHCA) to assess cerebral
altered cerebral metabolism oxygenation during cooling, arrest and rewarming.
decreased blood oxygen content and Measuring cerebral oxygen saturation during car-
compromised cerebral blood supply. diac surgery is best utilized as one component of multi-
modal neurologic and hemodynamic monitoring and
Cerebral desaturation is generally defined as a decrease interpreted in the context of the patient’s pathology
of 20% from baseline or an absolute value of less than and the operation. NIRS can only access a small area of
50%. These thresholds were defined during clamping the frontal cortical area. The use of this technology is
for carotid endarterectomy, using transcranial Doppler, not intended to detect or lower the incidence of stroke,
electroencephalography or somatosensory evoked which is more associated with embolic phenomena.
potential as they are able to detect ipsilateral cerebral Emboli detected using transcranial Doppler can often
ischemia during carotid artery clamping with a sensi- go undetected by cerebral oximetry (see Figure 18.3).
tivity of 44–100% and a specificity of 44–82%. Light transmission and absorption used for NIRS takes
The usefulness of cerebral oximetry during car- place in arteries, capillaries and veins and thus does not
diac surgery has been evaluated in multiple trials. One differentiate between arterial and venous blood. NIRS
multicenter study found that 61% of patients experi- monitoring algorithms assume a fixed distribution of
ence at least one episode of cerebral desaturation venous and arterial blood, between 70:30 and 75:25,
during CPB. 34% of these resolved with usual care, depending on the manufacturer. The internal algo-
while 66% resolved in response to an intervention rithms of these devices do not take into account any
based on a management algorithm. Only 5% of variation in blood flow or distribution caused by
cerebral desaturations remained unresolved. A multi- changes in CO2 levels or temperature, as are com-
center Canadian study evaluated the use of cerebral monly encountered during CPB.
saturation by randomizing patients into either an Monitoring venous oxygen saturation at the jugu-
intervention group where the clinician was aware of lar bulb (SJVO2) using a fibreoptic catheter provides a
the cerebral saturation and a control group where the continuous measure of the global balance between
cerebral saturation was recorded but blinded to the cerebral oxygen supply and demand. Retrograde inser-
clinician. 63% of patients had at least one episode tion of the SJVO2 catheter comes with the attendant
of cerebral desaturation, which was successfully risk of vascular injury and typically requires fluoro-
reversed in 97% in the intervention group. These scopy to ensure correct placement. The normal range
studies highlight that cerebral oxygen desaturation is for SJVO2 is quoted to be 55–75% but may be as high as
common during cardiac surgery and these episodes 85% in some normal individuals. SJVO2 < 50% is
can be appropriately reversed in more than 95% of the indicative of inadequate cerebral oxygenation.
time using an intervention algorithm (see A normal or near-normal SJVO2 value may, however,
Figure 18.2). These studies, however, do not show mask regional cerebral ischemia. SJVO2 monitoring
any advantages in neurological outcome conferred has high specificity but low sensitivity for the detection
by using NIRS. of cerebral ischemia. SJVO2 monitoring has been used
There are several factors that contribute to the low to assess the adequacy of cerebral cooling prior to
sensitivity and specificity of NIRS for diagnosing DHCA using a target SJVO2 of >95%.
cerebral ischemia. Its sensitivity is limited by the small
sampling window over the frontal cortex, and its
inability to monitor global cerebral oxygenation. Its Pharmacologic Options for
specificity is limited by the fact that rSO2 can be Neuroprotection
influenced by a variety of factors such as systemic Despite an improved understanding of the mechan-
178 and regional hemodynamics, blood oxygen transport isms underlying neuronal injury after cardiac surgery,

Figure 18.2 Intervention algorithm to manage decreases in cerebral oxygen saturation.

Step 1: Verify head position and position of vascular catheters. Step 2: Adjust blood pressure to within 20% of baseline values. Step 3: Increase
inspired oxygen fraction to correct low oxygen saturation values. Step 4: Adjust ventilator parameters to increase arterial end tidal carbon
dioxide levels within normal ranges (35–45 mmHg). Step 5: Consider giving blood transfusions to patients with low hemoglobin level when
steps 1–4 have not increased cerebral oxygen saturation within 20% of baseline values. Step 6: Consider improving ventricular function in the
presence of low output state. Step 7: Rule out hypothermia, seizures and light anesthesia. Step 8: Consider cerebral edema and increased
intracranial pressure. Abbreviations: ETCO2, end tidal carbon dioxide; Hb, hemoglobin; MAP, mean arterial pressure; O2, oxygen; PaCO2, arterial
carbon dioxide tension; SaO2, arterial oxygen saturation; SvO2, mixed venous oxygen saturation. (Adapted from Deschamps et al.)
there are currently no recommendations regarding Inhalational anesthetic agents induce both pre- and
pharmacologic neuroprotection. post-conditioning neuroprotection via intracellular
There is some evidence that the use of volatile mechanisms. These include activation of adenosine
anesthetics in cardiac anesthesia is associated with receptors, KATP channels and protein kinase C, inhib-
lower mortality compared to intravenous agents. ition of NF-kB activation and pro-inflammatory IL-1B
A meta-analysis including 549 patients found that cytokine production, as well as inhibition of N-Methyl
both calcium-binding protein S100β serum levels D-aspartate (NMDA) receptors.
and cerebral oxygen metabolic rate were decreased Ketamine is an NMDA receptor antagonist that
after CPB in the group receiving inhaled anesthetic decreases the intracellular calcium concentration,
agents compared to those having total intravenous thereby reducing cerebral apoptosis. The exact mech-
anesthesia. Patients in the inhalational anesthesia anism remains unclear, but the neuroprotective effect
group had a higher intraoperative CBF and better of ketamine may be explained by the inhibition of
postoperative Mini-Mental State Examination scores. inflammatory responses to surgery and CPB. 179

Figure 18.3 Hemodynamic monitoring including cerebral oximetry and transcranial Doppler. (a) Hemodynamic parameters prior to
cardiopulmonary bypass (CPB). Pulmonary and systemic hypertension is present, with an abnormal systemic-to-pulmonary mean arterial
pressure ratio (106/37 = 2.9; normal >4). The right ventricular (RV) pressure waveform (Prv, blue trace) shows an abnormal diastolic slope
suggesting RV diastolic dysfunction. (b) Significant portal vein pulsatility ([19cm/s–9cm/s]/19cm/s = 52%; normal < 30%) was present in this
patient initially. (c) Cerebral and somatic oxygen saturation monitoring using near-infrared spectroscopy (NIRS) during CPB. Baseline cerebral
saturation was 72% on the right side and somatic saturation 73% on the right lower limb with an arterial carbon dioxide partial pressure
(PaCO2) of 39 mmHg (point 1). Cerebral desaturation to 66% upon initiation of CPB with unchanged somatic value (point 2) pointed to
hypocapnia (PaCO2 of 31 mmHg) as seen on subsequent arterial blood gas analysis; ventilation was corrected, and the cerebral saturation
returned to baseline (point 3; PaCO2 of 45 mmHg). (d) Hemodynamic parameters and transtemporal transcranial Doppler (TCD) ultrasound
monitoring of both middle cerebral artery (MCA) blood velocities. (e) During the first CPB separation attempt. Note the significant gradient
(mean of 25 mmHg) between the mean femoral arterial pressure (Pfa) and radial arterial pressure (Pra). The increase in the pulmonary artery
pressure (Ppa) was secondary to aortic prosthetic valvular dysfunction. Transtemporal TCD velocities of both MCA after the first (e) and second
(f) separation from CPB. Note the absence of high-intensity transient signals (HITS) upon the first separation attempt (59 and 125). (f)
A significant increase in HITS was present upon the second CPB separation attempt (671 and 1062). This preceded the development of right
ventricular dysfunction and implicated air embolization to the right coronary artery. Abbreviations: AUC, area under the curve; CVP, central
180 venous pressure; EDV, end-diastolic velocity; HR, heart rate; MV, mean velocity; PaCO2, arterial carbon dioxide partial pressure; PI, pulsatility
index; PSV, peak systolic velocity; RF, baseline reference value; SaO2, arterial oxygen saturation. (Adapted from Azzam et al.)

Ketamine also suppresses NF-kB expression and may undergoing cardiac surgery with CPB, low doses of
therefore reduce the expression of genes encoding intravenous lidocaine seem to have a protective effect
pro-inflammatory cytokines such as interleukin in non-diabetic patients, while diabetic patients were
(IL)-6 and IL-8. A prospective randomized controlled more likely to develop postoperative neurocognitive
study of 58 patients undergoing cardiac surgery with dysfunction if they received lidocaine. The authors
CPB proposed that the use of an intravenous bolus of hypothesize that this detrimental effect in diabetic
ketamine (0.5 mg/kg) during anesthetic induction patients may be linked to lidocaine metabolism, more
attenuates postoperative delirium. The authors specifically its elimination through demethylation
hypothesize that ketamine may trigger a prolonged pathways, which are deficient in patients with dia-
effect that renders NMDA receptors less susceptible betes. In a small randomized controlled study of
to activation by ischemia and reperfusion injury 65 patients undergoing CABG, patients who had
during the postoperative period. These results were received a lidocaine infusion at the induction of anes-
not supported in a larger multicenter, double-blind thesia had less cognitive dysfunction after surgery.
trial of 672 patients undergoing cardiac and non- A follow-up study of 158 patients was not able to
cardiac surgery under general anesthesia. Ketamine confirm any of the previous findings. Preliminary
was administered at low dose or high dose and com- results of a larger trial currently underway suggest
pared to a placebo group. This second study did not that an intraoperative lidocaine infusion does not
demonstrate an effect on the incidence of postopera- confer any neuroprotective effects.
tive delirium but showed an increase in the incidence It is well known that surgery on CPB generates a
of postoperative hallucinations and nightmares in cascade of inflammatory reactions due to activation of
both ketamine groups compared to the placebo the complement system, leukocytes and pro-
group. inflammatory cytokines. Corticosteroids given prior
The neuroprotective effects of propofol remain to commencing CPB or as part of the prime may help
unclear. Some of the evidence suggests that propofol suppress systemic inflammation and have been shown
protects neurons against mild ischemic injury by to reduce postoperative neuron-specific enolase and
decreasing activity via gamma-aminobutyric acid S100β serum levels. As with other CPB related indi-
(GABA) receptor activation, inhibition of NMDA cations, the usefulness of glucocorticoids as a neuro-
receptors and reduction of calcium, sodium and protective agent remains subject to debate.
potassium ion channel transport. In a prospective Barbiturates are used as intravenous anesthetic
study of patients undergoing CABG on CPB, induction agents. In some centers they are given as
40 patients were randomized to receive either propo- neuroprotective agents during DHCA. Barbiturates
fol or desflurane during the anesthetic induction. The decrease the cerebral metabolic rate, lower cerebral
authors demonstrated that patients receiving propofol oxygen consumption, and therefore provide protec-
had lower S100β serum levels compared to desflurane tion during ischemia. The use of thiopental
anesthesia and suggest that propofol may thus reduce during DHCA seems to provide cerebral protection.
cerebral injury. When administered prior to DHCA, however, the
Calcium channel blockers such as nimodipine are available evidence suggests that thiopental may
thought to confer some neuroprotective effects by deplete the cerebral energy state before arrest,
decreasing vasospasm after subarachnoid hemor- which may lead to ischemia and poorer neurological
rhage. Conversely, in one study including patients outcome.
undergoing valve replacement surgery, nimodipine Over the past decades, perioperative statin therapy
was believed to promote intracerebral hemorrhagic before cardiac surgery has garnered interest.
events through vasodilatation and antiplatelet effects. A retrospective study of 6,813 patients undergoing
Animal and in vitro studies suggest that lidocaine coronary artery bypass surgery concluded that
may protect against brain hypoxia and ischemia patients who were given the combination of statin
through multiple mechanisms. These include reduc- and beta-blockers before surgery had lower odds of
tion of residual metabolism, decreased neuronal postoperative stroke. Conversely, two retrospective
membrane depolarization, preservation of cerebral studies including 9,430 patients did not find an asso-
blood flow and modulation of excitotoxic cascades. ciation between statin use and reduced rates of neu- 181
In a randomized controlled trial of 277 patients rologic complications following cardiac surgery.

Table 18.2. Summary of the recommendations for temperature management during cardiopulmonary bypass from the Society of
Thoracic Surgeons, the Society of Cardiovascular Anesthesiologists and the American Society of ExtraCorporeal Technology
1. Optimal site for temperature monitoring

1.1. The oxygenator arterial outlet blood temperature is recommended to be used as a surrogate for cerebral
temperature measurement during CPB. (Class 1, Level C)
1.2. To accurately monitor cerebral perfusate temperature during warming, it should be assumed that the oxygenator
arterial outlet blood temperature underestimates cerebral perfusate temperature. (Class 1, Level C)
1.3. Pulmonary artery or nasopharyngeal temperature recording is reasonable for core temperature measurement.
(Class Ila, Level C)
2. Avoidance of hyperthermia
2.1. Surgical teams should limit arterial outlet blood temperature to less than 37°C to avoid cerebral hyperthermia.
(Class 1, Level C)
3. Peak cooling temperature gradient and cooling rate
3.1. Temperature gradients between the arterial outlet and venous inflow on the oxygenator during CPB cooling
should not exceed 10°C to avoid generation of gaseous emboli. (Class 1, Level C)
4. Peak warming temperature gradient and rewarming rate
4.1. Temperature gradients between the arterial outlet and venous inflow on the oxygenator during CPB rewarming
should not exceed 10°C to avoid outgassing when warm blood is returned to the patient. (Class 1, Level C)
4.2. Rewarming when arterial blood outlet temperature 30°C:
4.2.1. To achieve the desired temperature for separation from bypass, it is reasonable to maintain a temperature
gradient between the arterial outlet and the venous inflow temperature of 4°C or less. (Class IIa, Level B)
4.2.2. To achieve the desired temperature for separation from bypass, it is reasonable to maintain a rewarming
rate of 0.5°C/min or less. (Class Ila, Level B)
4.3. Rewarming when arterial blood outlet temperature < 30°C:
4.3.1. To achieve the desired temperature for separation from bypass, it is reasonable to maintain a maximal gradient of
10°C between the arterial outlet and venous inflow temperature. (Class IIa, Level C)
Magnesium is a non-competitive blocker of the support mannitol administration, there is some evi-
NMDA glutamate receptor that modulates calcium, dence that it lowers 30-day mortality after acute type
sodium and potassium ion influx. Magnesium sulfate A aortic dissection. Many centers routinely use man-
decreases inflammatory cytokine levels and reduces nitol as part of their priming fluids for every cardiac
the effect of hypoxia, therefore preventing cell death. case done on CPB.
A systematic review of seven studies with a total of
1,164 patients was conducted to present evidence of Temperature Management and
the neuroprotective effects of magnesium in adults
with cardiac arrest or undergoing cardiac surgery. Cerebral Morbidity
This review concludes that magnesium administra- Most elective cardiac surgery are done at mild hypo-
tion during cardiac surgery may improve functional thermia, between 34 and 36°C, or at normothermia;
neurological outcomes in patients who undergo car- more complex cases are often done at moderate hypo-
diac surgery on CPB. The dosing regimen of magne- thermia, 28–32°C, to improve end-organ tolerance
sium varied between studies, with a maximum of 5 g to ischemia.
in a 24-hour period. Although there are various sites to measure core
Mannitol is a potent osmotic diuretic and reduces or cerebral temperature, it is now recommended to
182
cerebral edema. It is also a free radical scavenger that use the oxygenator arterial outlet blood temperature
may be beneficial after cerebral ischemia. Data as a surrogate for cerebral temperature. During

cooling, the difference between arterial outlet and increasing number of surgeons advocate using epiaor-
venous inflow blood temperature should not exceed tic ultrasound (EAU) to identify areas of the
10°C to discourage the formation of gaseous micro- ascending aorta that are free of disease and to allow
emboli. During rewarming, the arterial outlet blood safe cannulation and placement of clamps in adjacent
temperature should be limited to 37°C to avoid cere- disease free areas. A recent review including 11,496
bral hyperthermia. Rapid rewarming and cerebral patients showed the rate of stroke in CABG patients
temperature in excess of 37°C are known to cause who underwent EAU to be significantly improved
poor neurological outcomes. Table 18.2 summarizes compared to those who did not (0.6% versus 1.9%).
the recommendations on temperature management
from the Society of Thoracic Surgeons, the Society
of Cardiovascular Anesthesiologists and the Neurological complications after cardiac surgery are
American Society of ExtraCorporeal Technology. unfortunately common and generally the result of a
Chapters 7 and 9 provide more in-depth discussion combination of multiple factors. Both embolic and
of this topic. ischemic etiologies can adversely impact neurological
outcome. Blood pressure control is essential to reduce
Epiaortic Ultrasound Scanning of the the incidence of cerebral hypoperfusion and ischemic
Ascending Aorta stroke, as is good temperature management during
cooling and rewarming as well as careful manipula-
The necessity of manipulating the ascending aorta for
tion of the ascending aorta for placement of cannulas
cannulation as well as complete cross-clamping, par-
and clamps. Despite some significant limitations,
tial clamping or both has long been recognized as a
cerebral oxygen saturation can be utilized to assess
significant source of cerebral emboli during cardiac
cerebral perfusion and oxygenation. Multiple
surgery. In some cases atherosclerotic changes can be
attempts to find a pharmacologic treatment to pre-
detected by carefully palpating the vessel, however
vent neurologic injury have been unsuccessful.
this method is unreliable. For this reason an
Suggested Further Reading surgery patients: a randomized

controlled trial. Circulation 2018;
inhalation anaesthesia and total
intravenous anaesthesia in
1. Liu Y, Chen K, Mei W. 137: 1770–1780. patients undergoing cardiac
Neurological complications after surgery with cardiopulmonary
cardiac surgery: anesthetic 5. Hogue CW, Brown CH 4th, Hori
D et al. Personalized blood bypass: a systematic review and
considerations based on outcome meta-analysis. BMJ Open 2017; 7:
evidence. Curr Opin Anaesthesiol pressure management during
cardiac surgery with cerebral e014629.
2019; 32: 563–567.
autoregulation monitoring: a 9. Hudetz JA, Patterson KM, Iqbal Z
2. Joshi B, Ono M, Brown C et al. randomized trial. Semin Thorac et al. Ketamine attenuates
Predicting the limits of cerebral Cardiovasc Surg 2021; 33: delirium after cardiac surgery
autoregulation during 429–438. with cardiopulmonary bypass.
cardiopulmonary bypass. Anesth J Cardiothorac Vasc Anesth 2009;
Analg 2012; 114: 503–510. 6. Lewis C, Parulkar SD, Bebawy J
et al. Cerebral neuromonitoring 23: 651–657.
3. Sun X, Lindsay J, Monsein LH during cardiac surgery: a critical 10. Engelman R, Baker RA, Likosky
et al. Silent brain injury after appraisal with an emphasis on DS et al. The Society of Thoracic
cardiac surgery: a review: near-infrared spectroscopy. Surgeons, The Society of
cognitive dysfunction and J Cardiothorac Vasc Anesth 2018; Cardiovascular Anesthesiologists,
magnetic resonance imaging 32: 2313–2322. and The American Society of
diffusion-weighted imaging ExtraCorporeal Technology:
findings. J Am Coll Cardiol 2012; 7. Biancari F, Santini F, Tauriainen
T et al. Epiaortic ultrasound to Clinical practice guidelines for
60: 791–797. cardiopulmonary bypass –
prevent stroke in coronary artery
4. Vedel AG, Holmgaard F, bypass grafting. Ann Thorac Surg. temperature management during
Rasmussen LS et al. High-target 2020 January;109(1): 294–301. cardiopulmonary bypass.
versus low-target blood pressure J Cardiothorac Vasc Anesth 2015;
management during 8. Chen F, Duan G, Wu Z et al. 29: 1104–1113.
Comparison of the 183
cardiopulmonary bypass to
prevent cerebral injury in cardiac cerebroprotective effect of

Chapter
Renal Morbidity Associated with
Acute kidney injury (AKI) is the most common major injury. Abnormal serum creatinine is also con-
complication after cardiac surgery. The incidence of founded by its dependence on tubular secretion and
cardiac surgery-associated AKI (CSA-AKI) varies its relationship to muscle mass, catabolism and fluid
between 5 and 40% and leads to dramatically worse status. Fluid overload may negatively confound serum
outcomes. The incidence of CSA-AKI requiring renal creatinine’s ability to indicate AKI. CPB priming
replacement therapy (RRT) after coronary artery volume and/or heart failure often lead to fluid over-
bypass grafting (CABG) alone is roughly 1%. After load in the perioperative period, which might result in
valve surgery or combined CABG plus valve surgery, an underestimate of the incidence and severity of AKI
the risk of requiring RRT increases to 1.7 and 3.3% by falsely lowering serum creatinine.
respectively. Regardless of its reversibility, CSA-AKI Several other biomarkers for the detection of AKI
has been associated with increased mortality and risk have been proposed:
of developing chronic or end-stage renal disease, and The increase of the serum and urine neutrophil
consequently generating substantial cost as well. gelatinase-associated lipocalin (NGAL) precedes
an increase in creatinine by over two days. NGAL
is an excellent predictor of AKI in the pediatric
Definitions cardiac surgical population, and recent data has
AKI is the abrupt decline in the glomerular filtration suggested that NGAL may also be of value in adult
rate (GFR), resulting in the accumulation of meta- patients in the perioperative period.
bolic waste products and in the dysregulation of The combination of urine metalloproteinases-2/
extracellular volume and electrolytes that normally insulin-like growth factor-binding protein 7
would be excreted by the kidney. (TIMP-2/IGFBP7) is FDA approved to assess the
For many years there was neither a standard def- risk of moderate or severe AKI in critically ill
inition nor staging system for AKI. In 2004, Bellomo adults post cardiac surgery.
et al proposed the RIFLE criteria (Risk, Injury,
Failure, Loss and End-Stage Kidney Disease). They
were revised in 2012, when the Acute Kidney Injury Epidemiology and Outcomes
Network (AKIN) proposed a more sensitive defin-
ition for AKI, taking into account that even small Associated with AKI
elevations in serum creatinine are associated with Depending on the adopted definition, the incidence of
increased mortality. In 2012 a multidisciplinary group CSA-AKI is up to 30% after cardiac surgery, while the
proposed “The Kidney Disease: Improving Global requirement for RRT ranges between 1 and 6%. Any
Outcomes (KDIGO) definition and staging system,” AKI occurring in the perioperative period carries an
which is now widely used in research and clinical increased risk of short and long-term mortality (see
practice. Criteria for the diagnosis and staging of Figure 19.1).
AKI are summarized in Table 19.1 Even slight decreases in GFR imply an increased
These standard criteria are limited by their reli- mortality risk: an increased mortality risk of four to
ance on creatinine as the serum marker of decreased five-fold with any increase in serum creatinine has
renal function (i.e. decreased GFR). Serum creatinine been reported among patients followed for one year.
is a suboptimal biomarker for AKI recognition as it A 30% decrease in GFR during the perioperative
184
often lags 48–72 hours behind the onset of kidney period is associated with a 6% overall mortality over

Chapter 19: Renal Morbidity Associated with Cardiopulmonary Bypass
Table 19.1. Overview over the most commonly used renal failure scores
Classification Definition of AKI Stage Serum Creatinine Criteria for AKI Staging
RIFLE Increase in SCr 50% within 7 days Risk Increased creatinine x 1.5 or GFR decrease
>25% or UO < 0.5 ml/kg/h for 6 h
Injury Increased creatinine x 2 or GFR decrease
>50% or UO < 0.5 ml/kg/h for 12 h
Failure Increased creatinine x 3 or creatinine 4
mg/dL (Acute rise of 0.5 mg/dL) or GFR
decrease >75% or anuria for 12 h
Loss Persistent ARF – complete loss of
kidney function> 4 weeks
End- End-stage kidney disease > 3 months
Stage
Kidney
Disease
AKIN score Increase in SCr by 0.3 mg/dl or 1 Increase of 0.3 mg/dl or to 1.5–1.9 times
50% within 48 h baseline or UO < 0.5 ml/kg/h for 6 h
2 To 2–2.9 times baseline or UO < 0.5 ml/kg/h
for 12 h
3 To 3 times baseline or 0.5 mg/dl
increase to at least 4.0 mg/dl or the
initiation of RRT or UO < 0.3 mL/kg/h for
24 h or anuria for 12 h
KDIGO score Increase in SCr by 0.3 mg/dL within 48 1 Increase in SCr 0.3 mg/dl within 48 h or to
hours, or increase in SCr to 1.5 times 1.5–1.9 times baseline or UO <0.5 ml/kg/
baseline, or UO <0.5 mL/kg/hour for 6 h h for 6–12 h
2 Increase in SCr to 2.0–2.9 x baseline or UO <
0.5 ml/kg/h for 12 h
3 Increase in SCr to 3.0 x baseline or at least
4.0 mg/dl or UOP <0.3 mL/kg/hour for
24 h, or anuria for 12 h, or initiation of
RRT
1.00 the subsequent year, as compared with 0.4% mortality

Proportion Survived
No AKI
AKI for
without an accompanying AKI. When RRT is
0.75 1-2 Days
required for AKI, recovery of renal function sufficient
3-6 Days
0.50 27 Days
to discontinue chronic RRT occurs in less than
half of these patients, leading to a dramatic decrease
0.25 in quality of life and longevity (20% mortality rate
0.00 per year).
0 1 2 3 4 5
Years
Pathophysiology
Figure 19.1 Survival by duration of acute kidney injury (AKI). The
proportion of patients surviving from the time of cardiac surgery is The underlying mechanisms of CSA-AKI remain poorly
plotted by the categories for the duration of AKI. From Giovanni understood and appear to be multifactorial. Cardiac sur-
Mariscalco, Roberto Lorusso, Carmelo Dominici et al. Acute Kidney Injury: a 185
relevant complication after cardiac surgery; The Annals of Thoracic Surgery;
gery often leads to renal hypoperfusion due to CPB
Volume 92; Issue 4; pages 1539–1547 (October 2011) induced free radical production, increase in inflammatory

mediators, pigment nephropathy after hemolysis, Table 19.2. Risk factors for postop AKI
activation of the complement cascade, low flow and hypo- Patient- CKD
perfusion, or activation of the sympathetic and renin- related Diabetes mellitus
angiotensin-aldosterone (RAA) system. Cardiac surgery Female sex
is often complicated by bleeding and vasodilatory shock, Advanced age
both of which are associated with reduced renal perfusion. Obesity
If renal hypoperfusion persists long enough struc- Preop heart failure
tural tubular injury will occur. Paradoxically, improv- Poor preop functional state
ing renal perfusion can perpetuate renal damage by Peripheral vascular disease
inducing ischemia-reperfusion injury. Restoring renal Anemia
perfusion in already injured renal cells induces Procedure- CPB
opening of the mitochondrial permeability transition related Urgent or emergency surgery
pore and increases the production of reactive oxygen Postop cardiogenic shock
species, the release of pro-inflammatory cytokines, Bleeding (Hct < 24%)
neutrophils, macrophages and lymphocytes, causing Transfusion
renal parenchymal cellular infiltration. Type of surgery:
Valve < valve + CABG < redo surgery
Pulsatile blood flow is important to achieve adequate
< aortic surgery other than ascending
renal blood flow in the renal cortex and to preserve aorta
oxygen delivery to cortical and medullary areas of the
kidney. Non-pulsatile perfusion increases renin secre- Perfusion- CPB duration
tion, leading to elevation of the systemic vascular resist- related Hemodilution
Rewarming
ance and redistribution of intra-renal blood flow.
Oxygen delivery
However evidence supporting a clinical benefit is limited.
Damage to red blood cells is common during
pulsatile CPB, often seen as “pink urine.” Hemolysis
and increased levels of plasma-free hemoglobin
risk of requiring RRT increases to nearly 28% with a
encourage the production of reactive oxygen species
preoperative serum creatinine greater than 4 mg/dl.
and deposits of Tamm Horsfall protein in the renal
Even subclinical CKD is an independent risk
collecting system. Patients developing CSA-AKI can
factor for RRT in cardiac surgical patients. Patients
have up to double the level the plasma-free hemo-
with moderately reduced creatinine clearance (CrCl
globin at the end of CPB compared to those with no
<60 ml/minute) have a similar risk as those undergo-
renal injury, suggesting that hemolysis significantly
ing redo sternotomy, considered by many a profound
contributes to the incidence of renal failure.
risk factor for perioperative RRT.
Other patient-related risk factors include preexist-
Risk Factors ing diabetes mellitus, female gender, increased age,
Generally, the risk factors for developing AKI can obesity, preoperative congestive heart failure and
be separated into those that are patient-related low ejection fraction, peripheral vascular disease, pre-
versus those that are procedure and perfusion- operative balloon pump requirements, hypoalbumi-
related. Table 19.2 provides a summary of the nemia, chronic obstructive pulmonary disease,
main risks. emergency surgery, anemia and, although somewhat
controversial, decreased serum ferritin level (see
Table 19.2)
Patient-Related Factors
The single most important patient-related factor pre- Procedure-Related Factors
dicting AKI is preexisting chronic kidney disease The type of cardiac surgical procedure plays a sub-
(CKD). There is an overall 10–20% risk of AKI stantial role in renal outcomes and the need for RRT
requiring RRT among cardiac surgical patients with after surgery. Procedures such as valve replacement,
a preoperative serum creatinine of 2–4 mg/dl. The valve repair, combined valve and coronary surgery,
186

redo surgery and aortic arch surgery are associated 260–300 ml/min/m2 is reported to reduce the risk
with a substantially higher risk of CSA-AKI and a of developing kidney injury.
greater incidence of the need for RRT. As expected, Duration of CPB – Longer CPB times are
patients undergoing urgent or emergency surgery associated with a higher incidence of developing
have a higher incidence of AKI and need for RRT. CSA-AKI. A meta-analysis of nearly 12,500
Low hematocrit values (<23%) during CPB are patients showed that the mean difference of CPB
associated with an increased incidence of postopera- duration between the AKI and non-AKI group
tive renal failure. Paradoxically, blood transfusion was 25.65 minutes. A recent analysis of nearly
during bypass is also associated with developing renal 4000 patients confirmed these findings and
failure. Both seem to be confounders to each other – demonstrated that the risk increased exponentially
the risk of renal failure doubles when hematocrit for patients with an estimated GFR of <30 ml/
levels <23% occur in transfused patients. min/1.73m2 (see Figure 19.2).
Hemolysis – Blood cells’ exposure to artificial
Perfusion-Related Risk Factors surfaces and to shear forces during CPB can lead
Despite preserving cardiac output, the use of CPB is to varying degrees of cell lysis, potentially more so
associated with CSA-AKI. with pulsatile than with non-pulsatile flow. The
The risks and benefits of several perfusion related mechanical destruction of erythrocytes and
interventions need to be considered: subsequent release of plasma-free hemoglobin can
cause the occlusion of renal tubules and ultimately
Temperature management – Hypothermia is often
tubular cell necrosis.
being used for organ protection during CPB
through reduction of metabolic activity and Pulsatile/non-pulsatile flow – Pulsatile flow
amelioration of ischemic stress. However, there is during CPB has been advocated in some quarters
evidence that hypothermia, particularly when the as a means to reduce the incidence of CSA-AKI.
CPB inflow temperature is <27°C, may contribute There is an equipoise of low-grade evidence
to renal injury. It is also suggested that the showing advantages and no change in renal
temperature of the perfusate, rather than naso- outcomes when compared to laminar flow CPB.
pharyngeal or bladder temperature, is the A 2019 retrospective review of 2,500 patients,
determining factor. however, found that there is either no association
between pulsatile flow and reduced kidney injury
Rewarming – Returning the patient to
or that the difference is extremely small.
normothermia before weaning from CPB appears
to equally influence the risk of renal injury. Pressure/flow – To this day the argument whether
A large cohort study of nearly 8,500 patients blood pressure or pump flow is more important to
demonstrated that an oxygenator arterial outlet decrease the incidence of renal or other organ
temperature of >37°C was independently injury is not settled. There is an equipoise in the
associated with developing AKI, while evidence and research is ongoing. An emerging,
temperatures of 36 and 36.5°C were not. experimental concept is measuring bladder urine
PO2 and adjusting flow and/or pressure according
Hemodilution – As seen above, a low hematocrit
to its value.
during CPB is an independent risk factor for
developing AKI postoperatively. The relative risk
increases by 7% for each 1% decrease of nadir
hematocrit on-pump. Strategies to minimize Blood Flow and Oxygen Delivery to
prime volume and other blood conservation the Kidneys
techniques are discussed in Chapters 5, 8 and 16. Autoregulation in the kidneys keeps blood flow con-
Oxygen delivery – Low oxygen delivery while on stant despite variations in blood pressure in the range
bypass has been demonstrated to be an from 80 to 200 mmHg. The kidneys receive approxi-
independent risk factor of the development mately 20% of the total cardiac output (about 1 L/minute).
of CSA-AKI. Ensuring that the NADIR Oxygen delivery thus exceeds 80 ml/minute/100 g tissue.
oxygen delivery index (DO2i) is kept above The distribution of blood flow within the kidney is not 187

Association between Cardiopulmonary Bypass (CPB) Time and

Predicted Probability of Acute Renal Failure (ARF)
Stratified by Preoperative Renal Function
0.8 GFR <30

GFR 30–60
GFR >60
Predicted Probability of ARF
0.6
0.4
0.2
0
30 60 90 120 150 180 210 240 270 300
CPB Time (min)
At Risk:
GFR <30 100 52 5 0
GFR 30–60 1010 450 34 5
GRF >60 2757 1246 87 7
Figure 19.2 From correlation of cardiopulmonary bypass duration with acute renal failure after cardiac surgery. (Axtell, Andrea L et al. The Journal
of Thoracic and Cardiovascular Surgery, Volume 159, Issue 1, 170–178.e2.)
uniform, with the cortex receiving more than 90% (about exceeds demand and that there should be an adequate
5 ml/minute/g) of total blood flow; therefore, there is oxygen reserve. However, the kidney is highly sensitive
lower blood flow (about 0.03 ml/minute/g) to the renal to reduction in perfusion with AKI being a frequent
medulla. Although a high percentage of blood goes to the complication of hypotension. The sensitivity of the
cortex, the cortex extracts only about 18% of total oxygen kidney to damage as a result of hypoperfusion, despite
delivered to it. On the other hand, the medullary its low overall oxygen consumption, is related to the
region has a far smaller blood flow, but has a far greater physiological intra-renal oxygen gradient. Within the
extraction (about 79% of the delivered oxygen), as a result kidney, the cortex and medulla have widely disparate
of the high oxygen requirement for tubular reabsorption blood flows and patterns of oxygen extraction (see
of sodium and chloride ions. Renal medullary hypoxia is Figure 19.3).
an obligatory part of the process of urinary concentration Medullary oxygenation is normally strictly bal-
as oxygen diffuses from arterial to venous vasa recta and anced by a series of control mechanisms which match
the medullary thick ascending limb requires a large regional oxygen supply and consumption. Failure of
amount of oxygen to generate an osmotic gradient to these controls renders the medullary region suscep-
maximize the concentration of the urine. These cells are tible to acute or repeated episodes of hypoxic injury,
therefore uniquely vulnerable to anoxic damage. Total which may lead to acute tubular necrosis (ATN). The
renal oxygen consumption is less than 10% of total body differing requirements of cortex and medulla for
utilization, and thus there is a low arteriovenous oxygen blood flow and oxygen result in oxygen tension in
content difference (1.5 ml O2 /100 ml blood). The low the cortex of about 50 mmHg higher than that of the
188 oxygen extraction by the kidney suggests that supply inner medulla. This explains why renal tubules are

Figure 19.3 Distribution of renal blood flow and oxygen levels throughout the kidney. (From Scholz, H, Boivin, FJ, Schmidt-Ott, KM et al. Kidney
physiology and susceptibility to acute kidney injury: implications for renoprotection. Nat Rev Nephrol 17, 335–349 (2021).)
189

extremely vulnerable to hypoxic injury and why ATN some issues related to CPB, such as the systemic
can be induced by as little as a 40–50% decrease in inflammatory response, non-pulsatile flow and the
renal blood flow. impact of endothelial damage. A recent systematic
review of 33 randomized controlled trials (17,322
Prevention of AKI patients) evaluated the use of off-pump coronary
artery bypass (OPCABG) grafting surgery.
Any strategies to minimize the risk of CSA-AKI need
OPCABG was associated with a 14% relative risk
to focus on avoiding decreased oxygen delivery to the
reduction of CSA-AKI compared to on-pump
kidney, as it is the major mechanism of renal injury in
CABG surgery. However, no difference was noted
patients undergoing cardiac surgery. The KDIGO
in the risk of RRT or death. Long-term renal
guidelines recommend a bundle comprising of:
outcomes have also been studied showing no
discontinuation of nephrotoxic agents benefit from OPCABG. Current guidelines, such
optimization of blood glycemic control as the 2018 guidelines from the European Society
close monitoring of serum creatinine level and of Cardiology and European Association for
urine output Cardio-Thoracic Surgery, suggest that OPCABG
maintaining hemodynamic stability. should be considered for subgroups of high-risk
The PrevAKI trial published in 2017 showed that patients and performed by experienced off-
implementation of the KDIGO guidelines bundle pump teams.
compared against standard care resulted in a 23% Pulsatile flow during CPB has been advocated as a
relative reduction in CSA-AKI frequency. The imple- means to reduce the incidence of CSA-AKI. There
mentation of the bundle led to significantly improved is an equipoise of low-grade evidence showing
hemodynamic parameters, higher inotrope use, less advantages and no change in renal outcomes when
hyperglycemia and reduced use of renin-angiotensin compared to laminar flow CPB.
system (RAS) blockers compared to controls. Remote ischemic preconditioning (RIPC): RIPC
However, there was no difference in secondary out- was initially considered a great promise, but later
comes such as RRT requirements, ICU and hospital yielded conflicting results. RIPC is the induction
stay or all-cause mortality at 30, 60 and 90 days. of brief episodes of ischemia and reperfusion in
The discontinuation of nephrotoxic agents for distal tissues to induce the natural defenses to
AKI prevention has been previously investigated. ischemia in the kidney and other organs to
A systematic review of six studies with 1,663 enrolled prevent further damage during the surgery.
participants found low quality evidence that discon- A Cochrane review including 28 RCTs with 6,851
tinuing ACE inhibitors or angiotensin receptor patients showed that, disappointingly, RIPC leads
blockers prior to coronary angiography and cardiac to minimal or no difference in the incidence of
surgery may reduce the incidence of AKI. CSA-AKI, need for RRT, length of hospital stay
As the causes of AKI are multifactorial, a single or mortality.
intervention is unlikely to demonstrate significant Renal replacement therapy: Prophylactic RRT has
benefits, but a combination of different non- been proposed for patients with preexisting
pharmacological and pharmacological interventions advanced kidney disease. A small pilot RCT
is likely to offer better results in reducing the risk of evaluated 88 non-dialysis dependent CKD
CSA-AKI. patients and randomized them to either receiving
hemodialysis three times before surgery or
standard of care. The trial showed a 10-fold
Non-pharmacological Interventions decrease in mortality but it did not affect the
As in any other type of AKI, ensuring adequate renal development of postoperative morbidities.
perfusion and adjusting potentially nephrotoxic Due to the small sample size and some
medications are general measures to prevent CSA- methodological limitations further studies are
AKI and need to be assessed for every patient required for a more accurate assessment of
individually. the effects of prophylactic dialysis in
190 Avoidance of cardiopulmonary bypass: Off-pump patients with underlying CKD undergoing cardiac
cardiac surgery has been advocated to mitigate surgery.

Pharmacological Interventions including 6,105 patients undergoing cardiac

surgery showed that inhaled anesthetics were
Numerous pharmacological interventions to reduce
associated with lower mortality, minimal
the incidence and/or severity of CSA-AKI have been
reduction of the cardiac index and less vasoactive
investigated over the years but for the most part
support compared to propofol. Another similar
showed no benefit. Levosimendan, statins, N-
review in 2014 showed that inhaled anesthetics are
acetylcysteine, sodium bicarbonate, erythropoietin,
potentially protective against CSA-AKI.
theophylline, anti-oxidant supplements (selenium,
Dexmedetomidine is a highly selective α2
zinc, vitamin C and vitamin B1), dexamethasone,
adrenoceptor agonist, used for perioperative
pentoxyphyline, clonidine, diltiazem, dopamine, and
anxiolysis, sedation and analgesia. A number of
melanocyte-stimulating hormone are among the
small trials suggest that it reduces the incidence
interventions that have been studied but all have
and severity of CSA-AKI after cardiac surgery.
failed to demonstrate a reduction on CSA-AKI. It is
A recent randomized controlled trial evaluated the
important to highlight that hydroxyethyl starch has
effects of dexmedetomidine on renal function in
not only been associated with no benefits but an
patients undergoing valve replacement against a
increase in mortality after CABG. A recent systematic
placebo group. It found that the drug significantly
review showed that the perioperative use of statins
increased intraoperative urine output and
may be associated with an increased risk of CSA-AKI.
decreased postoperative incidence of AKI,
Glycemic control: Intraoperative hyperglycemia is however it did not report on the incidence of RRT.
an independent risk factor for complications, Fenoldopam: Fenoldopam is a selective agonist of
including death, and increased ICU and hospital dopamine D1 receptors and is responsible for
stay. Avoiding hyperglycemia with moderate, relaxation of smooth muscle, vasodilatation and
rather than tight, glycemic control, is inhibition of tubular reabsorption of sodium in
recommended for patients undergoing the kidney. The evidence supporting its use is
cardiac surgery. equivocal. Some studies demonstrate that
Fluid management: The difficulty in achieving the intraoperative fenoldopam may reduce CSA-AKI,
right balance between fluid administration to others demonstrated no benefit but showed an
optimize preload and preserve cardiac output on increased number of hypotensive episodes.
one side, and avoidance of fluid overload with Avoiding potential nephrotoxins:
pulmonary edema and excessive extracellular fluid
accumulation on the other side, is key to avoiding ○ RAS blockers – The perioperative use of RAS
CSA-AKI. Fluid overload worsens CSA-AKI and blockers is controversial. Two systematic
is associated with a higher risk for pulmonary reviews found 29 and 13 observational studies
edema and organ dysfunction. demonstrating that patients who were
continued on RAS blockers on the day of
Liberal fluid administration pre-CPB has been
surgery had an increased risk of CSA-AKI,
shown to exacerbate bypass associated
more episodes of intraoperative hypotension
hemodilution to hematocrit <23% and leads to a
and higher mortality. Another review of three
higher rate of blood transfusion and postoperative
randomized controlled and three observational
renal failure.
trials found low quality evidence that
Diuretics and mannitol: Currently the
withdrawal of RAS at least 24 hours prior to
recommendation is to avoid intraoperative loop
cardiac surgery may reduce the incidence of
diuretics as they increase oxygen consumption in
CSA-AKI. These facts plus the unlikely risk of
the renal medulla.
increasing cardiovascular events after a short,
A recent systematic review found that the
temporary suspension of RAS blockers led
intraoperative use of mannitol, which is widely
experts to recommend stopping these drugs
added to CPB priming fluids, cannot be
24 hours before cardiac surgery.
considered an evidence-based intervention to
○ iv contrast – Early cardiac surgery after
prevent AKI.
contrast administration is also controversial.
Inhaled anesthetics, propofol and 191
Several observational studies found a higher
dexmedetomidine: A systematic review of 58 trials

incidence of CSA-AKI when surgery was immediate postoperative period to manage fluid bal-
commenced within 24 hours of coronary ance as well as biochemical parameters.
angiography. It seems widely accepted that There is no need to use normal saline instead of
surgery should be delayed for 24–72 hours balanced solutions such as Lactated Ringer’s to prime
after contrast administration, the clinical the CPB pump for patients with end-stage renal dis-
situation permitting. There is some ease. The small amount of extra potassium (4–5 mEq/
observational data suggesting that cardiac L) is unlikely to generate significant hyperkalemia,
surgery can be performed safely within a day particularly compared to the large potassium load
of contrast administration in appropriately administered through cardioplegia. Also, large
selected patients with a low risk of AKI. volumes of normal saline are associated with causing
○ Nonsteroidal anti-inflammatory drugs a hyperchloremic acidosis that in turn will aggravate
(NSAIDs) – It is generally recommended that any hyperkalemia.
NSAIDs should be avoided perioperatively in
patients undergoing cardiac surgery. There is,
however, more recent data showing that their Patients with Non-RRT-dependent CKD
use in CABG patients might be safe. Patients with chronic renal impairment, but who do
not have sufficiently advanced renal disease to war-
rant RRT, may benefit from intraoperative hemofil-
tration/ultrafiltration while on CPB to optimize acid-
Management of Patients with Chronic base and electrolyte status during surgery. Such
Kidney Disease patients, as discussed above, have a higher likelihood
of developing AKI in the postoperative period and
The number of patients with chronic kidney disease
may require RRT postoperatively until their renal
or on dialysis presenting for cardiac surgery has
function returns to a viable level.
steadily increased in the last decade. Their periopera-
tive management is challenging, both clinically and
logistically.
CSA-AKI portends a grave outcome both acutely and in
the long-term. As non-remediable demography and
RRT-dependent Patients preexisting illnesses play such a large role in the devel-
Cardiac surgical patients with CKD who are already opment of perioperative kidney injury, appropriate
RRT-dependent should be dialyzed close to the time identification of high-risk patients and preoperative
of operation; generally, this is best done in the 1–2 counseling are critically important. All efforts should
days preceding surgery, to optimize their metabolic be undertaken to prevent adverse outcomes by maxi-
and volume status. Arrangements should also be mizing general supportive measures and specifically
made for RRT to recommence in the early postopera- avoiding nephrotoxins. Application of panels of bio-
tive period. Intraoperative ultrafiltration can be used markers of AKI may offer some hope of earlier recogni-
in case of emergency surgery or if additional fluid tion and intervention. Prompt, but not rushed,
removal is needed. Zero balance ultrafiltration can initiation of medical and extracorporeal therapy, coord-
help with removing toxins, electrolytes (particularly ination of care among the multiple care teams and
potassium after cardioplegia administration) or avoidance of further iatrogenic complications will
drugs. In some cases, RRT may be required in the maximize positive outcomes in these high-risk patients.
Suggested Further Reading analysis of randomized controlled

trials. Nephrology. October
3. Cole SP. Stratification and risk
reduction of perioperative acute
1. Cheungpasitporn W, 2015;20(10):727–735. kidney injury: an update.
Thongprayoon C, Anesthesiol Clin. December
Kittanamongkolchai W et al. 2. Chew STH, Hwang NC. Acute
kidney injury after cardiac 2018;36(4):539–551.
Comparison of renal outcomes in
off-pump versus on-pump surgery: a narrative review of the 4. Hoste EAJ, Vandenberghe W.
192 coronary artery bypass grafting: a literature. J Cardiothorac Vasc Epidemiology of cardiac surgery-
systematic review and meta- Anesth. August 7, 2018. associated acute kidney injury.

Best Pract Res Clin Anaesthesiol. Initiative) Group. J Am Heart 9. Ranucci M, Biagioli B, Scolletta S
September 2017;31(3):299–303. Assoc. June 1, 2018;7(11). et al. Lowest hematocrit on
5. Kim WH, Hur M, Park SK et al. 7. Wang Y, Bellomo R. Cardiac cardiopulmonary bypass impairs
Pharmacological interventions for surgery-associated acute kidney the outcome in coronary surgery:
protecting renal function after injury: risk factors, nn Italian multicenter study from
cardiac surgery: a Bayesian pathophysiology and treatment. the National Cardioanesthesia
network meta-analysis of Nat Rev Nephrol. November Database. Tex Heart Inst J.
comparative effectiveness. 2017;13(11):697–711. 2006;33(3):300–305.
Anaesthesia. August 2018;73 8. Whiting P, Morden A, Tomlinson 10. Newland RF, Baker RA, Mazzone
(8):1019–1031. LA et al. What are the risks and AL et al. Perfusion downunder
6. Nadim MK, Forni LG, Bihorac A benefits of temporarily collaboration. rewarming
et al. Cardiac and vascular discontinuing medications to temperature during
surgery-associated acute kidney prevent acute kidney injury? cardiopulmonary bypass and
injury: The 20th International A systematic review and meta- acute kidney injury: a multicenter
Consensus Conference of the analysis. BMJ open. April 7, 2017;7 analysis. Ann Thorac Surg. May
ADQI (Acute Disease Quality (4):e012674. 2016;101(5):1655–1662.
193

Chapter
Common and Uncommon Disasters during
Cardiopulmonary bypass (CPB) is highly technical and (the holes in cheese slices) need to be in alignment for
complex. No matter the degree of team preparedness, adverse events to occur. He also advocated that
accident and error can occur due to malfunction of “Incident reporting allows us to be aware of mishaps,
equipment and/or human factors. Since its first suc- incidents, near misses and are in fact ‘free lessons’ on
cessful clinical use in 1953 by John Gibbon, incremen- safety.” For over 20 years the Australian and New
tal improvements in the heart lung machine (HLM) – Zealand College of Perfusionists (ANZCP) has been
such as the introduction of low-level and bubble running a voluntary, de-identified perfusion incident
alarms, one-way valves, servo regulation of pump con- reporting system (PIRS) for perfusion accidents
trollers along with the acceptance of a culture centered (Australian and New Zealand Perfusion Incident
around safety – have resulted in a decline of perfusion- Reporting System Version 1). This was first developed
related accidents. In contrast to aviation, however, after the publication in 1997 of a survey, which found
where many secondary systems are available should that incidents in the field of perfusion occur at a rate
one fail, the modern day HLM is not designed with of 1:2,500 and are 10-fold more prevalent than inci-
sufficient internal redundancy to compensate for many dents in anesthesia. Similar perfusion incident surveys
potential primary device failures. It is therefore have followed and the frequency of common and
imperative that a support system is in place and that uncommon incidents seems to be fairly similar across
countermeasures are practiced and employed to min- continents and cultures. Recently the ANZCP
imize any potential negative impact on our patients. updated PIRS, to incorporate the Safety 2 concept
These safety practices need to be constantly with a focus on what went well, rather than what went
reviewed and their implementation should be regularly wrong (PIRS-2, https://anzcp.org/pirs-ii). Figures
rehearsed by all members of the intraoperative team and 20.1–20.4 give an overview of the most recent PRIS
not only by the perfusion team. Safety practices such as findings. Similarly, the Society of Clinical Perfusion
the use of protocols, bypass checklists, failure modes Scientists of Great Britain and Ireland maintain a web
and effects analyses (FMEAs) have been demonstrated based incident reporting system with archived safety
to reduce the incidence of error and equipment fault. reports documented.
Where an error or a fault is detected, the repetitive Incident reports, while providing valuable insight
nature of perfusion practice and the high degree of into adverse events, are based on random events and
competency of trained perfusionists often lead to a cannot be used to measure safety (error rates) due to
“good catch” before patients actually come to harm. inherent potential bias. Event reports are low in
Still, unforeseen events occur, no matter how much number, submitted from a limited number of
preparation is undertaken. Institutional protocols, reporters and represent a snapshot of activity.
compliance with instructions for use (IFUs) of equip- These reports, however, highlight the error type
ment and step-by-step processes to deal with error and and incidents that do occur. While the variety of
unforeseen events will minimize their impact. errors that can occur is vast, this chapter includes a
discussion of the most commonly reported perfusion
incidents along with potential prevention strategies
Incident Reporting and Safety Culture and treatment options.
In 2000, James Reason devised a Swiss cheese model A culture of safety dictates that all common and
194 of accidents which portrays that multiple contributors uncommon disasters that occur during

Chapter 20: Common and Uncommon Disasters during Cardiopulmonary Bypass
100%
Oxygenator Failures
80% The first sign of failure to oxygenate is usually the
60% arterial blood appearing dark. The surgeon may com-
ment on this as often they notice this first because the
40%
operating room lights shine on the lines. Blood gas
20% analysis or online measurements will confirm a low
0%
pO2; the SaO2 measured by the pulse oximetry probe
2019 2018 2017 2016 2015 on the patient’s finger or earlobe is generally unreli-
Near miss No harm Harmful able on CPB.
Figure 20.1 Incident type reported to ANZCP PIRS -2 for the
Failure to oxygenate during CPB has numerous
period 2015–2019. Incidents are categorized into “a near miss event,” potential etiologies, some of which will be further
a “no harm incident” and “harmful.” ANZCP.org/PIRS-ii. explored in subsequent sections. The two main cat-
egories of oxygenation failure are gas supply issues
and membrane oxygenator failures. While uncom-
cardiopulmonary bypass should be treated with a mon, as with anesthesia gas supply issues, errors in
team approach. Several broad general principles based hospital and/or tank supplies have been reported.
on a team approach should be followed in any identi- With the introduction of pipeline supply low-pressure
fied or evolving safety event during CPB: alerts and pin-indexing of oxygen and other gas con-
Notify everyone in the room that the potential nectors, many such errors have been avoided over the
safety issue exists past several decades. The inclusion of oxygen sensors
Get help (from another perfusionist preferably: can mitigate against delivering hypoxic or even nor-
two sets of eyes are better than one) moxic mixtures when supplemental oxygen is
Consider coming off bypass if possible (if near the intended. Issues related to gas supply will be discussed
beginning or end of the CPB) within Clinical Events later in this chapter.
If the cause is not immediately reversible, change Membrane oxygenator failure may similarly result
out faulty equipment if possible (need appropriate from several causes. Diffusion membrane oxygen-
backup and properly maintained devices) ators utilize hollow-fiber technology or a folded sili-
cone membrane. A countercurrent flow of oxygen-
Minimize risk of harm to the patient
rich gas is typically passed across the oxygenator,
Pre-bypass checklists will help to reduce the incidence allowing the perfusionist to control the patient’s
of error and equipment fault but must be undertaken PaO2 by setting the FiO2 and the PaCO2 by adjusting
diligently as a perform/verify process. the rate fresh gas flow, or “sweep,” to accomplish
Simulation can be a valuable part of ongoing ventilation. The FiO2 is set using a gas blender that
training for all perfusionists as it fosters critical think- mandates a supply of oxygen and air. Failure at the
ing and provides the ability to practice the response to blender (connections, inlet or outlet patency, or cali-
common and uncommon events in a non-clinical bration) may result in hypoxemia. Any leak along the
environment. Simulation and training for the whole pathway, from the wall source through the blender
intraoperative team has been validated as an effective (including the in-line anesthetic gas vaporizer) to the
tool for improving the response time to the resolution oxygenator may result in insufficient gas exchange at
of many catastrophic emergencies. the membrane oxygenator. Occlusion or impairment
of efferent gas exhaust from the oxygenator can cause
Common and Uncommon Disasters the same issues.
Any minor issue may lead to one of many common Oxygenators vary in size in accordance with the
and uncommon disasters during CPB. Although there surface area of the gas/fluid interface, which allows
is significant overlap between sections they are matching supply and demand with patients’ sizes and
grouped into: needs. The advantage of size-matched oxygenators is
i. oxygenator failures that the priming volume is directly proportional to
ii. equipment failures the size of the oxygenators, allowing for judicious
blood conservation in smaller patients. Conversely, 195
iii. clinical events.

Table 20.1. Prevention and recognition of failure to oxygenate
Complete pre-bypass checklist Verify oxygen/air source

Review patient size and reference IFU to choose
appropriately sized oxygenator
Ensure all gas supply pathways are connected, secured
and patent.
Ensure gas analyzers are calibrated
Record pump settings/line pressures/flows to recognize
serial changes for progressive oxygenator failures
Monitor serial blood gases to determine adequacy of
oxygenation/ventilation
Countermeasures
If immediate failure upon bypass initiation, determine if Add a gas line from a spare oxygen cylinder or from the
CPB can be safely discontinued while solving the anesthetic machine
problem Hold volume in the right heart to allow RV ejection and
pulmonary blood flow (partial bypass) and ventilate
lungs to reduce shunt
Gas supply interruption Start from one end of the gas circuit, i.e. from the wall
gas, work along toward the oxygenator, to methodically
find where the issue is
Consider incorrectly seated anesthetic gas vaporizer
Blender failure Obtain a spare blender from another machine
Oxygenator failure Consider oxygenator changeout versus pump exchange
○ Cognitive aids/checklists may prevent errors or
omissions in steps
○ Simulation and training will improve efficiency, sterility,
success rates and decrease stress
choosing an oxygenator of insufficient surface area to typically at 20–30 minute intervals, is imperative as
support full CPB of a larger individual leads to multiple factors (consumption, redistribution, hemo-
tissue hypoxia. dilution, heparin resistance, volume loss) can lead to
Prolonged mechanical support can lead to pro- the need to readminister anticoagulant medications
gressive oxygenator failure, as can insufficient sys- (see Chapter 6).
temic anticoagulation. Fibrin clot deposition may Similarly, occlusion (cannula position, tubing
develop insidiously and may be evidenced by a pro- kinked, air lock) or visible thrombus in the venous
gressive decline in the ability to oxygenate/ventilate, inflow and/or the reservoir can prevent blood flow to
requiring a steady increase of FiO2 or sweep. Visible the oxygenator, while any outflow occlusion
fibrin deposits may appear and the pressure on the (occluded downstream filter, kinked line, malposi-
pre-oxygenator line from the pump may increase for tioned arterial cannula) can prevent oxygenated blood
any set speed of the pump. from reaching the patient.
The appearance of water condensation in the oxy- Violation of the integrity of the gas/fluid mem-
genator may indicate oxygenator failure and, while brane interface, either from a manufacturing defect or
uncommon with newer oxygenators, plasma leak inappropriate handling, can predispose to cata-
through the membrane can occur. Periodic monitor- strophic arterial gas embolism or diminish the mem-
196 ing of the adequacy of systemic anticoagulation, brane’s ability to transfer oxygen and CO2. Table 20.1

Table 20.2. Prevention and recognition of failure to achieve adequate flow
Complete pre-bypass checklist Ensure the cardiopulmonary bypass circuit is

continuous, free of air and unobstructed prior to
clamping and dividing lines
Review cannulation strategies during time-out process
and prior to institution of CPB
Ensure appropriate tubing, connectors and splitters are
present and available for planned cannulation strategies
Verify position of cannulas, test arterial cannula prior to
initiating bypass for patency and pressure (“good
swing”)
Record pump settings/line pressures/flows to recognize
serial changes
Countermeasures
If immediate failure upon bypass initiation, determine if Start from one end of the CPB circuit, visually inspect
CPB can be safely discontinued while solving the pathway for air, clamps, kinks, occlusions
problem
○ Remove obstructions and/or occlusions
○ “Milk” air along venous line back to venous reservoir if
an air lock has occurred; secure cannula snares to
prevent further air entrapment
○ Determine whether cannulas remain appropriately
positioned (surgeon: visually and by palpation;
anesthesiologist: imaging if present)
summarizes strategies for prevention and convincing evidence that cerebral oximetry is sensi-
recognition of the problem and suggests appropriate tive or specific enough to determine the absolute
countermeasures. value of cerebral oxygen saturation or if a certain
percentage decline from baseline mandates the need
Blood Path Obstruction for an intervention, although case reports of ipsilat-
Arterial blood path obstruction can lead to the inabil- eral decreases in RSO2 may indicate issues related to
ity to provide adequate flow of oxygenated blood to cannula misplacement or venous obstruction. Several
the patient during CPB. Venous blood path obstruc- randomized controlled studies investigating all-cause
tion can lead to impaired venous drainage of the head, morbidity and mortality or the association of low
heart and visceral organs. Impaired drainage of the intraoperative RSO2 values with postoperative delir-
pulmonary venous system, either directly or through ium have returned mixed results. See Table 20.3 for
a vent in the pulmonary artery, the left atrium or the suggested troubleshooting when cerebral saturation
left ventricle, can result in pulmonary edema. drops.
Table 20.2 provides an overview of prevention, recog-
nition and countermeasures. Equipment Failure
Falling Cerebral Saturation Errors with and failure of equipment are either of a
technical nature (related to equipment and/or soft-
Institutions use cerebral oximetry (RSO2) with vary-
ware) or are due to human factors (error or violations
ing frequency and for varying indications and apply
in practice). Equipment failure can occasionally be
different thresholds for intervention if cerebral satur-
attributed to conditions prevalent within the system
ation drops. Measuring RSO2 during CPB is currently
they need to function in. These are usually organiza- 197
not considered universal standard of care. There is no
tional and result from inadequate policies, procedures

Table 20.3. Potential causes of falling cerebral 70%

oximetry saturation
60%
Exclude Devices functioning properly?
50%
monitoring Sensors properly affixed
failure (symmetrically and not 40%
overlying superior
sagittal sinus)? 30%
Patient issues Extracranial tissue edema? 20%

Shift in patient position? 10%
O2 supply Arterial cannula position? 0%
impaired Aortic dissection?
Knowledge based Skill based
Venous/SVC cannula
obstructed or poor venous Rule based Team based Violation
drainage (increasing CVP will
Figure 20.3 Human factor reports may be divided into different
decrease cerebral blood flow at human factor types. The breakdown of report types, associated with
any given MAP)? the incidents for the period 2010–2020 are shown. ANZCP.org/PIRS-
CPB flow adequate? ii.
Physiological Hypocapnia (may lead to

issues cerebral vasoconstriction)? is not always possible, there should be a documented
Low hemoglobin? contingency plan when there is no backup. An extra
Methemoglobinemia? perfusion staff member (or other adequately trained
Light anesthesia? staff ) is also advisable to improve safety and to help
Temperature effect? out in a crisis. All equipment, including backup
○ Rewarming (increased O2 devices, have to be properly maintained and serviced,
demand)? uninterrupted power supply systems need to be
checked and charged routinely.
The following should be accessible and readily
available as backup:
Spare HLM with all monitoring devices (n + 1 for
100%
the number of cardiac operating rooms in use)
90% Spare heater/cooler
80% Spare gas cylinders/regulators and gas lines
70% Hand-cranks for centrifugal and roller pumps –
60% easily accessible and operable
50% Spare oxygenators/tubing/change out kit with
40% sterile scissors
30% Portable lighting and flashlights (inexpensive
20% “head lights” allow for freeing up hands when
10% needed)
0% Spare disposable tubing and connectors for
Management Equipment circuit disruptions.
Figure 20.2 The reports of incidents may be grouped into either An ECMO circuit may also be used if no backup HLM
management or equipment failure. Management can be due to is available. Although there is no reservoir, a patient on
protocol, managerial or organizational failures. ANZCP.org/PIRS-ii.
CPB can be transferred onto ECMO until the failed
CPB system is fixed or an alternative has been found.
and/or protocols or pressure on clinicians (see
Figures 20.2 and 20.3). Circuit Disruption
Ideally, “backup” equipment should be available Circuit disruption is the most commonly reported
198 for all devices used in the operating room. While this incident in surveys (see recent PIRS-2 reporting in

Venous reservoir
Vascular injury
Temperature
Pump servoregulation
Oxygenator
Myocardial protection
IABP/assist
Hypo/hyper fusion
Heater cooler unit
Gas supply
Gas exchange
Fatigue
Electrical/electronic
ECMO
Drug/medication
Donor blood
Communication
Cold agglutinin
Coagulation
Clerical/data entry
Circuit error
Circuit disruption
Circuit contamination
Cardioplegia
Cannulation
Blood loss
Blood gas
Arterial filter
Air in circuit
Air embolism
0 10 20 30 40 50
Good catch near miss Good catch no harm Harmful
Figure 20.4 Incident category and severity of PIRS 2 reports for the 10-year period 2010 to 2020 are shown. Each subgroup is divided into
good catch near miss, good catch no harm, harmful events. The large number of good catch events highlights that most incidents are “caught”
before they can cause harm. ANZCP.org/PIRS-ii.
Figure 20.4). The CPB circuit is complex and has Split tubing from roller pump raceways, in
many components that can disconnect or leak. The particular pump boots
use of checklists during setup and priming can help Reservoir ports snapped off
identify errors during setup. Securing connections Temperature thermistors leaking
with cable ties and having spare connectors in the Taps snapping off, destroying the threaded Luer-
room in case of failure helps mitigate against avoid- lock connection
able accidents. Finally, having a second perfusionist Lines blown apart due to over-pressurization
verify the use of a checklist and the circuit setup helps Excessive use of suckers or vents connected to an
against making easily rectifiable mistakes. unvented reservoir can cause pressure to build up
The most common sources of leaks are: and will eventually blow the lid off the reservoir.
Faulty components (filters, vent valves, gas/
hemoglobin saturation cells) Air in Circuit
Connections not secure (cable ties and cross The third most common, and potentially disastrous,
threading, non-heat sealed) event that occurs during CPB is air entrainment into 199
Lines not connected in setup the circuit. Macrobubbles, or visible gross collections

of air in the arterial circuit, can result in occlusion of with resultant purge of arterial gas into the
major arteries and arterioles, resulting in end-organ arch effluent.
ischemia. Air in the coronary arteries presents as Treatment with IV methylprednisolone has been
acute ST-elevation ischemia and may result in pro- considered with the goal of minimizing the
found myocardial dysfunction and inability to separ- inflammatory damage secondary to ischemia and
ate from CPB, while cerebral arterial gas embolism subsequent reperfusion, although the efficacy is
may result in stroke, seizure, or impaired neurocog- not clear.
nitive function postoperatively. Any microbubbles Intravenous lidocaine may be beneficial.
can transfer directly into the patient’s microcircula- Definitive treatment for cerebral arterial gas
tion with the potential to cause harm through diffuse embolism includes hyperbaric oxygen therapy.
impairment of gas exchange in the capillary bed. Air
In addition to decreasing oxygen demand, the other
in the venous lines can cause an air lock, preventing
goal in this situation is to maintain adequate oxygen
venous drainage and necessitating a rapid reduction
delivery to tissues, which can be achieved with nor-
of forward flow in order to prevent emptying of the
movolemia and adequate perfusion pressure.
venous reservoir.
Hemodilution to a hematocrit of ~30% may be bene-
Air embolism during cardiac surgery is a compli-
ficial. The most common causes leading to air in the
cation with potentially severe or fatal consequences.
CPB circuit are summarized in Table 20.4.
Even if recognized and treated immediately, it can
cause significant and irreversible neurological injury. Electrical Failure
A sudden and rapid drop in the cerebral oximetry
All hospitals should have multiple levels of power
readings without an obvious alternative explanation
supplies, with backup generators that switch in with-
should give rise to a high index of suspicion for
out delay when mains power fails. While the inci-
cerebral arterial gas embolism. Transesophageal echo-
dence of multi-level power failures is rare, they do
cardiography can potentially help in identifying air in
occur, and strategic planning needs to be included in
the aorta.
local protocols.
The primary goal for managing this complication
Most contemporary HLMs have a battery backup
is protecting the brain. Measures include:
built into the system. These need to be maintained to
Identifying the location of air entry and assure best battery performance. Keeping a hand
preventing further air from entering crank on each HLM is mandatory in case of total
the circulation. electrical failure. Although practices such as making
Supine positioning. Steep Trendelenburg sure the HLM’s battery is fully charged, that the
positioning had previously been thought to help machine is plugged into a wall socket that is fed by
expel air bubbles from the cerebral circulation, the hospital backup system and that the hand crank is
however, this is now not recommended, as placing present seem totally intuitive, it is advised to include
the patient head-down can exacerbate them in the pre-CPB checklist to assure high
cerebral edema. reliability.
Decreasing cerebral oxygen demand, which can be On occasions where a single pump dies, a spare
achieved pharmacologically with medications pump module should be available for immediate use.
such as propofol, as well as by actively cooling the Clinicians need to make sure during setup that the
patient. Cerebral oxygen demand decreases by tubing is long enough to be moved to a different
approximately 7% for each degree Celsius that the module. Failure of the electronic control panel or
patient is cooled (see also Chapter 18). Active the recording system are mostly software issues and
cooling is easily achieved on CPB once the source can often be dealt with by rebooting the system.
of air has been identified and eliminated and flow Modern HLMs should be able to be run with just
has been reestablished. Emergent initiation of manual control, independent of the electronic system.
deep hypothermia has also been successfully
supplemented with retrograde cerebral perfusion Heater Cooler Failure
in several cases, whereby oxygenated blood is run The heating/cooling device is a major component of
200 retrograde via superior vena cava cannulation cardiopulmonary bypass. A backup device or an

Table 20.4. Causes of air entrainment into CPB circuit Table 20.5. Common drug errors
Vent tubing backwards Incorrect drug labeling

Purge lines open Out of date drugs used
Failure/inactivation of low-level alarm or bubble Heparin not given or given in wrong dose or at
detectors; venous line occlusion with subsequent inappropriate time
draining of reservoir
Protamine given while pump suckers activated
Membrane fiber leak
Cardioplegia solution with too much/too little
Vacuum drainage with excessive negative pressure potassium
Inattention/distraction of perfusionist Cardioplegia delivered systemically before cross-
clamping of aorta
Countermeasures
Incompatible blood group transfusion
Vent tubing Pre-bypass checklist
Check suckers with Anesthetic gas vaporizer on HLM left open after CPB
blood/saline before
Countermeasures
commencing CPB
One-way valve in Double-check drugs including reading label and dates on
all vents vials and syringes, use of appropriate labeling system
Level alarm, bubble Tested, connected and Commence CPB only after all team members have
detectors servo regulated confirmed safe ACT
Positive and negative Suckers are turned off and removed from chest when
pressure valves intact anesthesiologist announces that protamine is about
to start
Positive and negative
pressure is measured Confirm blood/cardioplegia ratio before operation; check
and alarmed when potassium concentration with blood gas analysis
vacuum is used Use end-of-CPB checklist to ensure HLM is stripped
Decrease venous embolic Snare venous down correctly
load cannula to prevent
(further) air from
entering
Partially clamp
venous line
Clinical Events
Numerous clinical events may result in CPB disasters.
The following are summaries of some of the more
prevalent clinical events that have been previously
alternative method to rewarm a patient should be reported in the Australian and the UK perfusion
available. These devices must be maintained in incident reporting systems.
accordance with their IFU to minimize mycobacterial
growth. Meticulous maintenance is particularly Drug and Medication Error
important, highlighted by the impact of mycobacter- This topic represents the second highest number of
ium chimaera, as continual disinfection may cause incidents reported to PIRS-2 (Figure 20.4). Teamwork
faults due to the corrosive nature of chemicals used. and excellent communication, preferably in the form
A backup heater/cooler or similar device from an of closed loop communication, are important so each
ECMO circuit should be available at all times. If this is member of the team is aware of allergies, religious
not the case a roller pump with a loop of tubing beliefs (e.g. Jehovah’s Witness) and when drugs are
attached to 2 Hansen connectors, sitting in a bucket given (especially heparin and protamine). Table 20.5
of warm water can allow some temperature control compiles a select few of the more common drug 201
until a more permanent solution has been found. errors and ways to prevent them.

Heparin Resistance reported in preoperative assessment. When a malig-

Heparin is the most common anticoagulant used for nant hyperthermia crisis is triggered, a hypermeta-
cardiopulmonary bypass. The standard heparin dose bolic state is induced in which there is a massive
is 300–500 IU/kg, the target ACT varies between and unchecked release of calcium from the sarcoplas-
institutions but generally is somewhere between mic reticulum of skeletal muscle. This triggers a cas-
400 and 550 seconds. Failure to achieve the ACT goal cade of derangements, including hyperthermia,
despite repeated heparin doses up to 600 IU/kg is tachycardia, hyperkalemia, hypercapnia, muscular
defined as heparin resistance. In the event of an inad- breakdown and metabolic acidosis. It is often noticed
equate response to heparin, it is a Class 1A recom- first by the surgeon, noticing unusual chest wall rigid-
mendation of the Society of Thoracic Surgeons and ity or that the patient feels warm. Blood gases confirm
Society of Cardiovascular Anesthesiologists that that CO2 rises fast despite increasing sweep gas flow.
recombinant antithrombin III be used to improve Metabolic acidosis, excessive temperature despite
heparin sensitivity. If not treated adequately, heparin cooling and hematuria are also typical warning signs.
resistance could result in subtherapeutic anticoagula- In cases of preoperatively known or suspected
tion, potentially leading to oxygenator failure, throm- malignant hyperthermia the anesthesiologist and per-
boembolic phenomena and patient death. Alternative fusionist should discuss the anesthetic plan, including
anticoagulants such as bivalirudin or argatroban avoidance of all triggering agents such as succinylcho-
should be considered in cases where heparin resist- line and volatile anesthetic agents, as well as flushing
ance is not due to inadequate antithrombin III levels the anesthesia machine with O2 and removing the
(see also Chapter 6 for more detail). vaporizer from HLM.
In the event of a MH crisis all potential triggering
agents have to be stopped immediately and removed
Cold Agglutination
from continuity with the patient. The ventilator cir-
Cold agglutinins are IgM antibodies directed against cuit and CO2 absorber canister should be replaced
red blood cells. They are inert at physiological body with new components, the patient has to be treated
temperatures and have a variable temperature thresh- with dantrolene and the surgical procedure should be
old below which they become active (thermal ampli- terminated as soon as reasonably possible. The
tude). Depending on this threshold they might Malignant Hyperthermia Association of the United
become activated during hypothermic bypass. Once States maintains a 24-hour hotline and additional
activated they agglutinate erythrocytes, which in turn resources to help prepare for and provide real time
fix to activated complement, leading to irreversible assistance to acutely manage a malignant hyperther-
cell damage. Severe hemolysis occurs when the blood mia crisis. Similar helplines are available in most
temperature is (i) cold enough for the antibody to be countries around the world.
active and (ii) warm enough for complement to be
active. Surgeons wearing magnifying loops or perfu- Vasoplegic Shock
sionists observing their cold cardioplegia circuit are Systemic vasodilation, often refractory to standard
often the first ones to spot any agglutination. therapies, is a dangerous complication of cardiopul-
Normothermia, avoiding cold cardioplegia and flush- monary bypass. It is thought to be associated with a
ing the coronaries with warm cardioplegia before systemic inflammatory response that can be precipi-
removing the aortic cross clamp are the mainstays tated by the patient’s circulation interacting with the
of managing patients with known cold agglutinins foreign materials of the bypass circuit. It may also
or sudden onset of hemolysis (see Chapter 16 for result from a reaction of common anesthetics with
more detail). certain drug classes, including but not limited to
angiotensin converting enzyme inhibitors and angio-
Malignant Hyperthermia
tensin II receptor blockers. The vasoplegic patient is
Malignant hyperthermia (MH) is the result of a reac- unable to achieve adequate end-organ perfusion due
tion to specific triggering agents in patients with to hypotension in spite of adequate or supra-normal
myopathies typically affecting the type 1 ryanodine cardiac output. In some cases, this can make it impos-
receptor. This condition is hereditary and transmitted sible to safely separate from CPB if not adequately
202 in an autosomal dominant pattern. There often is a treated. Treatment options include vasopressors, such
family history of malignant hyperthermia that will be as norepinephrine, vasopressin, intravenous

methylene blue and vitamin B12 (hydroxycobalamin), the aortic root during antegrade cardioplegia can
as well as newer agents such as angiotensin II. result in direct injury to the aortic root or valve. The
root is typically monitored visually by the surgeon
Aortic Dissection and a Y-connector can be used to vent the root when
Manipulation or instrumentation of the aorta can needed. Anterograde cardioplegia catheters with inte-
cause disruption of the intima and acute dissection grated overpressure relief valves are commercially
of the vessel. This occasionally occurs during aortic available.
cannulation or at proximal coronary graft anasto-
mosis sites. It is critical to identify this complication Inadvertent Cannulation of Hepatic Vein during
early. As a consequence of cannulating a dissected Bi-caval Venous Cannulation
aorta, there may be loss of radial arterial line wave- Advancing the inferior vena cava cannula too far
form or elevated line pressure when attempting to go during bi-caval cannulation is not uncommon.
on bypass and the aorta may begin to appear dilated Inadvertent placement into the hepatic vein can lead
and discolored. Intraoperative transesophageal echo- to poor venous drainage, hepatic venous congestion
cardiography, as well as epiaortic ultrasound, can be with potential hepatic dysfunction and efferent
used to identify or confirm this diagnosis. venous obstruction of visceral organs and the kidneys.
This complication needs to be treated immedi- Transesophageal echocardiography can be used to
ately. Depending on the extent of the damage done confirm proper cannula placement and assist with
this can require surgery ranging from an ascending repositioning.
aortic interposition graft to a complete aortic arch
replacement.
This chapter highlights commonly reported incidents
Over-pressurization during Cardioplegia in current perfusion practice. New forms of compli-
Over-pressurization during anterograde or retrograde cations arise as our HLMs become more complex and
cardioplegia can occur. Monitoring the pressure in feature integration with monitoring and electronic
the delivery system and taking the pressure drop in medical records. In order to run a highly reliable
the aortic root or the coronary sinus into account can perfusion service it is essential that protocols and
avoid cardiac injury. Consequences of over- procedures for dealing with accidents and unforeseen
pressurization of the retrograde system include cor- events are regularly updated to include new equip-
onary sinus rupture, and more commonly, epicardial ment or technology as it is added to our arsenal of
petechiae and myocardial edema from extravasation tools.
of high pressure cardioplegia. Over-pressurization of
Suggested Further Reading controlled trial examining

neurocognitive and perioperative
The Society of Cardiovascular
Anesthesiologists and The
1. Reason J. Human error: models outcomes. J Thorac Cardiovasc American Society of
and management. BMJ. 2000; 320 Surg 2020; 159(3):943–953.e3 ExtraCorporeal Technology:
(7237):768–770. Clinical practice guidelines –
5. Ferraris VA, Brown JR, Despotis
2. Wilcox TW, Baker RA. Incident GJ et al. Special report: STS anticoagulation during
reporting in perfusion: current workforce on evidence based cardiopulmonary bypass. Ann
perceptions on PIRS-2. surgery. 2011 update to the Thorac Surg. 2018;105
J Extracorp Tech 2020; 52:7–12. Society of Thoracic Surgeons and (2):650–662.
3. Darling E, Searles B. Oxygenator the Society of Cardiovascular 7. Gulabani M, Gurha P, Ahmad S
change-out times: the value of a Anesthesiologists blood et al. Intra-operative post-
written protocol and practice conservation clinical practice induction hyperthermia, possibly
simulation exercises. Perfusion guidelines * The Society of malignant hyperthermia:
2010 May; 25(3):141–143; Thoracic Surgeons Blood anesthetic implications, challenges
discussion 144–145. Conservat. ATS. 2011;91 and management. J Anaesthesiol
4. Uysal S, Lin HM, Trinh M et al. (3):944–982. Clin Pharmacol. 2014;30
Optimizing cerebral oxygenation 6. Shore-lesserson L, Baker RA et al. (4):555–557.
203
in cardiac surgery: a randomized The Society of Thoracic Surgeons,

8. Still RJ, Hilgenberg AD, Akins 9. Assaad S, Geirsson A, Rousou L in the diagnosis of intraoperative
CW et al. Intraoperative aortic et al. The dual modality use of iatrogenic type-a aortic dissection.
dissection. Ann Thorac Surg. epiaortic ultrasound and J Cardiothorac Vasc Anesth. 2013
1992;53(3):374–379. transesophageal echocardiography Apr;27(2):326–328.
204

Index
abciximab, 157–158 weaning from CPB, 115 arterial line filters, 21–22, 35–36
abdominal tumors, 126 angiotensin converting enzyme arteriovenous (AV) loop, 35–36
acetate, 46 inhibitors (ACE-I), 172, 190 aspartate, 107
acid-base management, 85, 94, angiotensin receptor blockers, 190 aspirin, 157–158
115–116 antegrade cardioplegia, 108–109 AT3 deficiency, 53
activated clotting time (ACT), 30–31, antegrade cerebral perfusion (ACP), atherosclerosis, 58–59, 175, 178, 180,
50–52 87–88 183
acute aortic syndrome, 58 anterior mediastinal mass, 125–126 autologous blood priming, 42–44, 154
acute kidney injury (AKI), 184 anti-arrhythmic drugs, 113–114, 117 autoregulation
CKD management, 192 anticoagulation, 49. See also heparin cerebral, 86, 177
definitions and scores, 184–185 direct thrombin inhibitors, 54–55 kidney, 187–190
epidemiology and outcomes, future, 55–56 axillary arterial cannulation, 13–14, 60
184–185 MiECC, 73
extracorporeal life support, 136 monitoring, 30–31, 50–52 barbiturates, 86, 181
pathophysiology, 185–186 novel oral anticoagulants, 158 battery backup unit, 35
prevention, 190–192 pediatric patients, 152 benzodiazepines, 99
risk factors, 186–188 reinstitution of CPB, 119 bicaval cannulation, 14–15, 61–62, 152,
acute normovolemic hemodilution reversal, 53–54, 118 203
(ANH), 83–84, 162 vitamin K antagonists, 157–158 biocompatible tubing, 11–12, 172
acute respiratory distress syndrome anti-diuretic hormone (ADH), 121 bivalirudin, 54–55
(ARDS), 123, 170–171 antifibrinolytic agents, 85–86, 161–162 bleeding
adrenaline, 119 anti-inflammatory interventions assessment, 158–161
after-drop, 63–64, 85 perfusion strategies, 172–173 causes, 156–158
afterload, during weaning from CPB, pharmacological strategies, 172 gastrointestinal, 169
118 antiplatelet agents, 157–158 management, 159–161
air bubble detectors, 28–29, 35–36 anti–Xa activity, 51–52 blood, 162
air embolism aortic aneurysm, 81–82, 126–129 cold agglutinins, 164, 202
during aortic root cannulation, aortic cannulation, 12–13 Jehovah’s Witnesses, 162–163
59–60 aortic cross-clamping, 110, 183 sickle cell anemia, 163–164
with centrifugal pumps, 18 aortic dissection, 203 blood cardioplegia, 105–107
in circuit, 199–201 aortic root cannulation, 58–60, blood conservation, 85–86, 156,
de-airing for prevention, 112–113 108–109 161–162
filters and bubble traps, 20–22 apixaban, 158 antifibrinolytic agents, 85–86,
priming, 42 aprotinin, 85–86, 161–162 161–162
with reservoir emptying, 18 argatroban, 54–55 cardiotomy suction, 66–68, 162
with venous cannulation, 61–62 argipressin, 121 cell salvage, 21, 68, 71, 97–98, 118,
air lock, 14, 61–62 arrhythmia, during weaning from CPB, 162
Air Protection System (APS), 40 113–114, 117 MiECC, 73–74
alarms, heart-lung machine, 28–29, 115 arterial blood path obstruction, 197 blood flow. See also flow rates
albumin priming solution, 45 arterial cannula, 12–14 cerebral, 86, 175, 177
Allen formula, 43–44 designs, 12–13 hemodilution, 42–43
alpha agonists, 93–94 flow profiles, 13 kidney, 187–190
altered heparin resistance, 53 performance index, 57–58 monitoring, 25–26
Andexanet-α, 158 arterial cannulation, 57–58 obstruction, 197
anemia, 161–164 complications, 59–60 parameters for adequate perfusion,
anesthesia connection, 58–59 92–93
gas scavenging system, 35 DHCA, 81, 83 splanchnic, 168–170
myocardial protection, 111 pediatric patients, 152 blood gas analysis, 29–30, 94–95, 100, 205
neuroprotection, 86, 179, 181 peripheral, 60 180, 195–197

Index
blood gas management temperature, 110 monitoring, 30, 177–180

alpha stat management, 85, 100 cardiopulmonary bypass (CPB). See pharmacological cerebral protection,
during DHCA, 85 also weaning from CPB; specific 178–182
parameters for adequate perfusion, topics risk factors, 175–176
93–94 conduct, 57 temperature management, 182–183
for pediatric patients, 153 connection of patient to circuit, cerebral metabolic rate (CMRO2), 86,
pH-stat, 20, 100, 153 62–63 99
temperature effects on, 100 initiation, 63 cerebral oxygen saturation
blood pressure, 175 monitoring, 64–68 CPB changes, 166–167
AKI risk, 186–187 pediatric patients, 152–153 during DHCA, 84, 88
cerebral blood flow, 177 pressure management, 64–68 monitoring of, 30, 177–180
delirium, 177 rewarming, 63–64 neurological complications, 177–180
stroke, 176–177 temperature management, 63–65 cerebral perfusion strategies
blood priming, 42–44, 154 venous cannulation, 61–63 intermittent cerebral perfusion,
bowel ischemia, 169 history, 9–10, 123 86–87
Bretschneider’s solution, 105–107 MiECC practical lessons, 77–78 for pediatric patients, 151–152
briefing, preoperative, 7 registries, 33 retrograde cerebral perfusion, 59–60,
bubble detectors, 28–29, 35–36 cardiopulmonary bypass (CPB) circuit 87–88
bubble traps, 20–22 air in, 199–201 selective antegrade cerebral
carbon dioxide flushing, 36 perfusion, 87–88
calcium, 46, 97, 115, 121, 151 components, 11, 34 cerebrospinal fluid (CSF) drainage, 89
calcium channel blockers, 181 filters and bubble traps, 20–24, checklist, 37–38
calibration, monitoring systems, 29 172 chloride, imbalances, 97–98
cannulation. See also arterial hemofilters, 23–24, 154, 162, 172 chronic kidney disease (CKD),
cannulation; venous suckers and vents, 22, 36, 68–69 186–187, 192
cannulation tubing, 9–12, 35–36, 172 chronic thromboembolic pulmonary
aortic, 12–13 typical configuration, 9–10 hypertension (CTEPH), 90
aortic root, 58–60, 108–109 disruption, 198–199 circuit pressures, 27–28
axillary arterial, 13–14, 60 failure, 197–198 citrate-phosphate-dextrose (CPD), 107
bicaval, 14–15, 61–62, 152, 203 MCS, 123–125 clopidogrel, 157–158
cavo-atrial, 14–15, 61–62 priming, 36–37 clot formation, 49
coronary sinus, 65–67, 109 hemodilution with, 42–44, 162 clotting factors, 43, 49–50
femoral, 13–14, 60, 62 solutions, 42–47 coagulopathy
inferior vena cava, 62 setup, 34–36, 40 assessment, 158–161
peripheral arterial, 60 DHCA modifications, 82–83 blood conservation techniques,
peripheral venous, 62–63 human factors, 37 85–86, 156, 161–162
right atrial, 61–62, 65–67 minimally invasive extracorporeal pathophysiology, 156
subclavian, 13–14 circulation, 40 preoperative medication, 156–157
superior vena cava, 62 pre-bypass checklist, 37–40 antiplatelet agents, 157–158
carbon dioxide (CO2) flushing, 36 pre-bypass patient concerns, 38, novel oral anticoagulants, 158
carbon dioxide production (VCO2), 30, 40 vitamin K antagonists, 157–158
95–96 cardiopulmonary bypass (CPB) therapeutic interventions and
cardiac arrest. See also cardioplegia machine. See heart-lung management, 159–161
accidental hypothermic cardiac machine cold agglutinins, 164, 202
arrest, 134–135 cardiotomy suction, 66–68, 162 colloid priming solutions, 45
cardiogenic shock, 135–136, 138 cavitation, 61–62 communication
cardioplegia, 103–104, 111 cavo-atrial cannulation, 14–15, 61–62 solutions to improve, 5
delivery, 22–23, 107–108 cell salvage, 21, 68, 71, 73–74, 97–98, preoperative briefing and
antegrade, 108–109 118, 162 postoperative debriefing, 7
minimal access surgery, 109–110 central venous pressure (CVP), 65 standardized conversations, 5
preparation and setup, 35 centrifugal pump, 16–18, 73–74, during weaning from CPB, 112
retrograde, 109 123–125 congenital heart disease, 150. See also
through vein grafts, 109 CentriMag, 147 pediatric patients
history, 102–103 cerebral blood flow (CBF), 86, 175, 177 cooling, 84
in MiECC, 73–74, 109–110 cerebral cooling, 84 coronary air embolism, 112–113
monitoring, 27–28 cerebral embolism, 112–113, 175, 178, coronary artery bypass graft (CABG),
over-pressurization during, 203 180, 183 110, 173, 190
pediatric patients, 151 cerebral ischemia, 175, 183 coronary sinus cannulation, 65–67, 109
206 physiology, 103–105 blood pressure control, 176–177 corticosteroids, 47, 172, 181

Index
cryoprecipitate, 159–161 direct thrombin inhibitors (DTIs), ex vivo lung perfusion (EVLP),
crystalloid cardioplegia solutions, 54–55 129–132
105–107 disasters during CPB, 194–195, 203 extracellular cardioplegia solutions,
crystalloid priming solutions, 43–45 air in circuit, 199–201 105–107
culture of safety, 194–195, 198–199 blood path obstruction, 197 extracorporeal cardiopulmonary
custodiol solution, 105–107 circuit disruption, 198–199 resuscitation (ECPR), 134
cyclosporine, 111 electrical failure, 200 extracorporeal circuit. See
equipment failure, 197–198 cardiopulmonary bypass circuit
dabigatran, 158 falling cerebral oxygen saturation, extracorporeal life support (ECLS), 71
de-airing, heart, 112–113 197–198 accidental hypothermic cardiac
deep hypothermic circulatory arrest heater cooler failure, 200–201 arrest, 134–135
(DHCA), 80, 90, 99 incident reporting and safety culture trauma patients, 135–136
indications, 80–81 in prevention, 194–195, extracorporeal membrane oxygenation
monitoring during, 80–81, 85, 88–90 198–199 (ECMO). See also veno-arterial
neuroprotection during, 86 oxygenator failures, 195–197 extracorporeal membrane
hypothermia alone, 86–88 dobutamine, 119 oxygenation
intermittent cerebral perfusion, donation after brain stem death (DBD), backup during equipment failure,
86–87 129 197–198
pharmacological, 86, 181 donation after cardiac death (DCD), centrifugal pumps in, 18
retrograde cerebral perfusion, 129–131 failure to wean from CPB, 122
87–88 donor organs history, 9–10, 123
selective antegrade cerebral heart, 129–131 MCS with, 123–125, 140
perfusion, 87–88 lung, 129–132 emergent or bail-out applications,
spinal cord, 88–90 dopamine, 119 133–136
pediatric patients, 151–152 drug bioavailability, 43 lung transplantation, 132–133
perfusion considerations drug error, 201 thoracic surgeries using, 125–126
acid-base management, 85 drug metabolism, 98–99
blood conservation, 85–86 factor concentrates, 157–158, 161
circulatory arrest, 84–85 echocardiography. See transesophageal factor II inhibitors, 158
cooling, 84 echocardiography factor Xa inhibitors, 158
extracorporeal circulation, 82–83 elastometry, 158–159 femoral cannulation, 13–14, 60, 62
glucose management, 85 electrical failure, 200 fenoldopam, 191–192
hemodilution, 83–84 electrocardiogram (ECG), 31, 65 fibrillation induction, 110
rewarming, 85 electroencephalography (EEG), 84 fibrinogen concentrate, 161
temperature management, 84–85 electrolyte management, 45–47, 96–98, fibrinolysis, 156, 161–162
physiological effects, 80, 82 115–116 filters, 20–24, 172
preoperative considerations, 80–81 electronic perfusion data, 31–33 filtration, 23–24, 36–37, 154, 162, 172
pulmonary (thrombo) embolism. See also air embolism flow rates
endarterectomy, 86–87, 90 aortic root cannulation and acid-base management, 116
safe duration, 86 atherosclerotic, 58–59 AKI risk, 186–187
spinal cord protection during, 88–90 cerebral, 112–113, 175, 178, 180, 183 heart-lung machine monitoring of,
surgical considerations, 81–83 detection, 178, 180 25–26
Del Nido Cardioplegia (DNC), pulmonary, 90 oxygen delivery, 166–167
106–107 endothelial activation, 167–168 pediatric patients, 152
delirium, postoperative, 177 endotoxins, 168–169 targets for adequate perfusion, 92–93
1-desamino-8-D-arginine-vasopressin enoximone, 119–121 fluid overload, 191–192
(DDAVP), 161 epiaortic ultrasound (EAU), 58–59, 183 flushing, CPB circuit, 36
descending thoracic aortic aneurysm epicardial pacing, 114 fresh frozen plasma (FFP), 157–161
(DTAA), 81–82, 126–129 epinephrine, 119
dexmedetomidine, 191–192 epsilon-aminocaproic acid (EACA), gas exchange
diastolic augmentation, 138, 141 161–162 monitoring, 29
difficult airway, 125–126 eptifibatide, 157–158 cerebral oxygen saturation, 30,
direct acting oral anticoagulants error, 37. See also disasters during CPB 177–180
(DOACs), 158 human factors perspective on, 2–3, in-line blood gas analysis, venous
direct current cardioversion (DCCV), 37 saturation and hematocrit
117 Safety 1 and Safety 2 perspectives on, monitors, 29–30, 94
direct ostial cardioplegia, 109 1–2 oxygen delivery and carbon
direct procurement and perfusion esmolol, 107 dioxide extraction, 30
(DPP), 129, 131 evoked potential monitoring, 89–90 oxygenator, 19–20 207

Index
gas scavenging system, 35 parameters for adequate perfusion, hypothermic cardiac arrest;
gas supply system, 20 93–94 rewarming
gaseous microemboli (GME), 61–62 hemodilution, 42 adverse effects, 100
gastrointestinal (GI) dysfunction, AKI risk, 186–187 AKI risk, 186–187
168–170 avoidance, 156, 162 bleeding management with, 159
GDP ratio, 96 blood flow, 42–43 blood gas management, 85, 100
Gelofusine priming solution, 45 clotting factors, 43 coagulopathy associated with, 156
glucose control, 43–44 drug metabolism effects, 98–99
management, 85, 98, 116, 191–192 during DHCA, 83–84 metabolic management, 99–101
priming solution, 46–47 drug bioavailability, 43 monitoring, 26–27, 65, 80–81, 85
glutamate, 107 drug metabolism effects, 98–99 myocardial protection, 102, 110–111
glyceryl trinitrate (GTN), 121 in pediatric patients, 153–154 neuroprotection, 86–88
glycoprotein IIb/IIIa inhibitors, hemodynamic monitoring, 31, 73, 76, physiological effects, 80, 82
157–158 178, 180 sickle cell anemia, 163–164
goal-directed perfusion (GDP), 95–96 hemofilters, 23–24, 154, 162, 172 venous saturation, 94–95
gravity siphoning, 61 hemoglobin, during weaning from hypothermic cardiac arrest (HCA),
Gritten Report, 34, 37 CPB, 116 134–135
hemolysis, 18, 28, 66–67, 92–93,
Haemaccel priming solution, 45 185–187, 202 idarucizumab, 158
Harlequin Syndrome, 143 heparin, 49, 54–56 Impella, 138–139, 146
heart, damage during CPB, 171. See dosing, 49–51 incident reports, 194–195, 198–199
also myocardial protection monitoring, 30–31, 50–52 inferior vena cava (IVC), 62, 126
heart failure, stratification of, 144–145 neutralization, 53–54, 118 inflammation. See systemic
heart-lung machine (HLM), 194 for pediatric patients, 152 inflammatory response
alarms, 28–29, 115 pharmacology, 49–50 inhalational anesthetic agents. See
components, 11, 34 in priming solution, 47 volatile anesthetic agents
development, 9–10 rebound, 54, 156 in-line blood gas analysis, 29–30, 94
failure, 197–198 resistance to, 53, 202 inotropic support, 115, 117–121
gas supply system, 20 thrombocytopenia induced, 54–55 insulin, 46–47, 98, 116
MCS with, 123–125 tubing containing, 11–12, 172 insulin resistance, 85
monitoring, 25–29 heparin-induced thrombocytopenia Interagency Registry of Mechanically
oxygenators, 19–20, 35, 195–197 (HIT), 54–55 Assisted Circulatory Support
preparation and setup, 34–36, 40 hepatic dysfunction, 169–170 (INTERMACS), 144–145
human factors, 37 hepatic vein, inadvertent cannulation intercostal artery perfusion, 127–129
minimally invasive extracorporeal of, 203 intermittent cerebral perfusion, 86–87
circulation, 40 histidine-tryptophan-ketoglutarate intermittent cross-clamping/fibrillation
pre-bypass checklist, 37–40 (HTK), 105–107 (ICC), 110
pre-bypass patient concerns, 38, homeostasis, 92, 166–167. See also international normalized ratio (INR),
40 metabolic management 157–158
priming, 36–37 human factors, 1–3, 37, 194, 198 intra-aortic balloon pump (IABP),
hemodilution with, 42–44, 162 hydroxyethyl starch (HES), 45, 65–66, 68, 117
solutions, 42–47 191–192 failure to wean from CPB, 122
pump heads, 14–18 hyperchloremia, 97–98 MCS with, 138–140
reservoirs, 18–19 hyperglycemia, 46–47, 85, 98, 116, complications, 140
heart rate, during weaning from CPB, 191–192 indications, 140
113–114 hyperkalemia, 46, 96–97, 115 management of patients with, 139
heart transplantation, 129–132 hyperlactatemia, 95 physiological effects, 141
heart venting, 68–69 hyperoxia, 150–151 intracellular cardioplegia solutions,
heart-lung transplantation, 132 hypertension, 175 105–107
HeartMate 3, 147 hyperthermia, 85, 100–101, 182–183 intrathecal pressure (ITP), 89
HeartWare HVAD, 147 hypocalcemia, 46, 97 ischemia. See also cerebral ischemia
heat exchanger, 19–20, 22, 34–35 hypoglycemia, 116 gastrointestinal, 168–169
heater cooler failure, 200–201 hypokalemia, 46, 96–97, 115 myocardial, 102–103, 151
hematocrit (Hct) hypomagnesemia, 46, 97 pancreatic, 170
AKI risk, 186–187 hyponatremia, 45–46 ischemia-reperfusion injury
deep DHCA, 83–84 hypophosphatemia, 97 coagulopathy, 156
factors affecting, 43–44 hypotension, 175, 177 cold reperfusion for prevention, 85
monitoring, 29–30, 94 hypothermia. See also deep lung, 173
208 optimal values, 42–43 hypothermic circulatory arrest; myocardial, 102–103

Index
in pediatric patients, 150–151 outside of operating room, conventional CPB lessons learned
ischemic preconditioning, 102, 133–136 from, 77–78
110–111, 190 perioperative, 133 evidenced-based clinical advantages,
equipment selection, 123–125 76–77
Jehovah’s Witnesses, 162–163 failure to wean from CPB, 121–122 modular design advantages, 74–75
jugular venous oxygen saturation, 88 historical perspective, 123 physiological perfusion quest, 76
intra-aortic balloon pump, 138–141 systemic inflammatory response
ketamine, 179–181 during organ implant management with, 173
kidney, blood flow and oxygen delivery heart and heart-lung team approach to, 73
to, 187–190 transplantation, 132 anesthesiologist, 73
kidney injury. See acute kidney injury liver transplantation, 133 perfusionist, 73–74
kinetic-assisted venous drainage lung transplantation, 132–133 surgeon, 73
(KAVD), 28, 73–74 thoracic aortic surgeries using, 126 training programs, 74–75
left heart bypass, 81–82, 126–127 miniplegia, 106–107
lactate, 46, 93, 95, 116 partial or complete CPB, 127 mitochondrial based protection, 103
latent failures, 1–2 selective spinal and reno-visceral mitochondrial permeability transition
latex rubber tubing, 11 perfusion, 127–129 pore (mPTP), 103
leaks, CPB circuit, 198–199 thoracic surgeries using, 125 mixed venous oxygen saturation
left atrial (LA) pressure, 65 anterior mediastinal masses and (SVO2), 93–95
left heart bypass (LHB), 81–82, difficult airways, 125–126 modified ultrafiltration (MUF), 154
126–127 thoracic and abdominal tumor modular MiECC systems, 72–75
left ventricle (LV) distension, 65–66, surgery, 126 monitoring, 25
68–69 types of devices, 138–139 anticoagulation, 30–31, 50–52
left ventricular assist device (LVAD), mechanical ventilation, 115, 169 application of electronic data from,
146–148 mediastinal masses, 125–126 32–33
leukocyte depletion, 172–173 mental workload, 4–5 during conduct of CPB, 64–68
levosimendan, 121 metabolic acidosis, 97–98, 116 during DHCA, 80–81, 88–90
lidocaine, 181 metabolic management, 92 documentation, 31–32
liver dysfunction, 169–170 CPB challenges, 92 ECG, 31, 65
liver transplantation, 133 drug metabolism, 98–99 gas exchange, 29–30, 94
low level alarm, 28–29 effective bypass and circuit design, heart-lung machine parameters,
low-molecular-weight heparin 92 25–29
(LMWH), 54 electrolytes, 96–98 hemodynamic, 31, 73, 76, 178, 180
lung. See also heart-lung machine goal-directed perfusion parameters left ventricle distension, 65–66, 68
CPB effects on, 170–171 in, 95 metabolic, 92–96
ischemia-reperfusion injury, 173 CO2-derived parameters in, during MiECC, 73, 76
transplantation, 129–133 95–96, 96 neuro-, 175
during weaning from CPB, 115 DO2 parameters in, 95–96 cerebral oxygen saturation, 30,
O2 and CO2 ratios in, 96 177–180
magnesium, 46, 97, 107, 115–116, 182 markers of adequate, 92 during DHCA, 88–90
malignant hyperthermia, 202 acid-base balance, 94 pediatric patients, 153
mannitol, 47, 65, 105–107, 182, blood flow, 92–93 pressure, 27–28, 64–68, 80–81
191–192 blood gases, 93–94 standards and recommendations, 26
mean arterial pressure (MAP) blood lactate, 93, 95 TEE, 31, 65–68
heart-lung machine monitoring, hematocrit, 93–94 temperature, 26–27, 65, 80–81, 85
27–28 mean arterial pressure, 93–94 urine output, 65
management, 64–65 mixed venous oxygen saturation, during weaning from CPB, 115
optimization, 175–177 93–95 monoclonal antibodies, antiplatelet,
parameters for adequate perfusion, urine output, 93, 95 157–158
93–94 temperature effects on, 99–101 motor evoked potential (MEP), 89–90
mechanical circulatory support (MCS), metabolism muscle relaxants, 99, 121
123. See also veno-arterial cerebral, 86 myocardial damage during CPB, 171
extracorporeal membrane drug, 98–99 myocardial protection, 102–103. See
oxygenation; ventricular assist milrinone, 119–121 also cardioplegia
devices minimal invasive extracorporeal hypothermia, 102, 110–111
during donor organ procurement circulation (MiECC), 24, 40, 43, intracellular modulators of cell
heart transplantation, 129–131 71–72 survival, 103
lung transplantation, 129–132 cardioplegia in, 73–74, 109–110 mitochondrial based, 103
emergent or bail-out applications of classification, 71–73 myocardial ischemia, 102–103, 151 209

Index
myocardial protection (cont.) noradrenaline (norepinephrine), 121 pediatric patients, 150, 154
myocardial oxygen demand, normothermic regional perfusion conduct of CPB, 152–153
103–104 (NRP), 129 DHCA and regional cerebral
non-cardioplegic methods, 110 novel oral anticoagulants (NOACs), perfusion, 151–152
cyclosporine, 111 158 differences between adult cardiac
intermittent cross-clamping/ patients, 150
fibrillation, 110 obesity, 92–93 myocardial protection in, 151
ischemic preconditioning, 102, occlusion pathophysiology of CPB in, 153–154
110–111 blood path, 197 pathophysiology specific to, 150–151
off-pump surgery, 110 pumps, 14–16, 35 percutaneous temporary ventricular
remote ischemic preconditioning, off-pump coronary artery bypass graft assist devices (VADs), 145–146
111 (OPCABG), 110, 173, 190 perfusion pumps. See pumps
sodium hydrogen exchanger one lung ventilation (OLV), 132–133 perfusion record, 31–33
isoform-1, 111 opioids, 99 peripheral arterial cannulation, 60
volatile anesthetic agents, 111 optimized extracorporeal circulation peripheral venous cannulation, 62–63
in pediatric patients, 151 (opECC), 77–78 peristaltic pump. See roller pumps
reperfusion injury role in, 102–103 organ damage during CPB, 166–167, pH. See acid-base management
173 pharmacokinetics, 43, 98–99
near infrared spectroscopy (NIRS), 84, endothelial lining effects in, 167–168 pharmacological neuroprotection, 86,
88, 177–180 gastrointestinal dysfunction, 178–182
nephrotoxic agents, 190–192 168–170 phenylephrine, 93–94
neurological complications, 175, 183 myocardial dysfunction, 171 phosphate, 97
blood pressure control, 175–177 pulmonary dysfunction, 170–171 phosphodiesterase-III (PDE III)
cerebral oxygen saturation, 177–180 therapeutic strategies, 171–173 inhibitors, 119–121
epiaortic ultrasound of ascending organ perfusion pressure, 175 pH-stat management, 85, 100
aorta, 183 organ transplantation physiological perfusion, 76
pharmacological protection, heart, 129–132 platelet dysfunction, 156
178–182 heart-lung, 132 platelet factor 4 (PF4), 51
risk factors, 175–176 liver, 133 platelet inhibition, 54
temperature management, 182–183 lung, 129–133 platelet transfusions, 159
neuromonitoring, 175 osmolarity, priming solution, 46 point-of-care tests, 52, 158–161
cerebral oxygen saturation, 30, over-pressurization, during polymethylpentene (PMP)
177–180 cardioplegia, 203 oxygenators, 19
during DHCA, 88–90 oxidative stress, in pediatric patients, polypropylene (PPL) oxygenators, 19
neuroprotection, 178–182 153 polyvinylchloride (PVC) tubing, 11
during DHCA, 86 oxygen consumption (VO2), 95–96 porcelain aorta, 58
hypothermia alone, 86–88 oxygen delivery (DO2) postoperative cognitive dysfunction,
intermittent cerebral perfusion, AKI risk, 186–187 176–177
86–87 CPB changes to, 166–167 postoperative debriefing, 7
pharmacological, 86, 181 goal-directed perfusion parameters, potassium, 46, 96–97, 102–105, 115
retrograde cerebral perfusion, 95–96 prasugrel, 157–158
87–88 hemodilution, 42–43 pre-bypass filtration, 36–37
selective antegrade cerebral kidney, 187–190 pre-CPB checklist, 37–40
perfusion, 87–88 monitoring, 30 preoperative briefing, 7
spinal cord, 88–90 optimization, 64–65 pressure
newborns, 150. See also pediatric for pediatric patients, 152 management, 64–68
patients oxygen extraction ratio (O2ER), 96 monitoring, 27–28, 64–68, 80–81
nimodipine, 181 oxygen saturation, 29–30, 88, 177–180. priming, 36–37
nitric oxide (NO), 121 See also cerebral oxygen autologous blood, 42–44, 154
nitrous oxide, 98 saturation hemodilution with, 42–44, 162
NMDA receptor antagonists, 179–181 oxygenators, 19–20, 35, 195–197 minimally invasive extracorporeal
non-cardiac surgical functions of CPB. circulation, 43
See mechanical circulatory P2Y12-blockers, 157–158 for pediatric patients, 153–154
support pacing, during weaning from CPB, 114 solutions, 42, 44, 47
non-pulsatile flow, 92–93, 173, pancreatitis, 170 colloids, 45
185–187, 190 paraplegia, 88–90 crystalloids, 43–45
nonsteroidal anti-inflammatory drugs partial CPB, 127 electrolyte management, 45–47
(NSAIDs), 191–192 patient concerns, pre-CPB review of, volume, 42–43, 153–154
210 nontechnical skill (NTS), 7 38, 40 propofol, 99, 181, 191–192

Index
protamine, 53–54, 118, 156 selective antegrade cerebral perfusion nontechnical skills, 7
protamine titration, 52 (SACP), 87–88 repair, recovery and resilience, 5
prothrombin complex concentrate selective spinal and reno-visceral solutions to improve, 5
(FPCC), 157–158, 161 perfusion, 127–129 preoperative briefing and
pulmonary artery catheter (PAC), 31 shunts, in pediatric patients, 150–151 postoperative debriefing, 7
pulmonary artery (PA) perfusion, 173 sickle cell anemia, 163–164 standardized conversations, 5
pulmonary artery (PA) pressure, 65 Sieving coefficient, 23–24 team creation and training, 7–8
pulmonary dysfunction, 170–171 silicone rubber tubing, 11 temperature, 26–27, 65, 80–81, 85. See
pulmonary embolism, 90 siphon effect, 61 also hypothermia
pulmonary (thrombo) endarterectomy sodium bicarbonate (NaHCO3) bleeding management with, 159
(PTE), 86–87, 90 as cardioplegia solution additive, 107 management, 63–65
pulmonary hypertension, 90 priming solution, 46–47 cardioplegia, 110
pulsatile flow, 92–93, 173, 185–187, 190 during weaning from CPB, 116 cerebral, 182–183
pumps, 9, 14, 35. See also flow rates sodium hydrogen exchanger isoform-1 during DHCA, 84–85
centrifugal, 16–18, 73–74, 123–125 (NHE-1), 111 metabolic management, 99–101
roller, 14–16 somatosensory evoked potentials weaning from CPB, 112
(SSEPs), 89–90 temperature coefficient (Q10), 99
RAS blockers, 191–192 spallation, 11 thiopental, 86, 181
regional cerebral perfusion, 151–152 spinal cord perfusion pressure (SCPP), thoracic surgery, 125–126
remote ischemic preconditioning 89 thoracoabdominal aortic aneurysm
(RIPC), 111, 190 spinal cord protection, 88–90 (TAAA), 81–82, 126–129
renal morbidity. See acute kidney splanchnic circulation, 168–170 thrombin, 49–50, 156, 161–162
injury St Thomas’ Solution, 105–107 thrombocytopenia. See heparin-
renal replacement therapy (RRT), 136, standardized conversations, 5 induced thrombocytopenia
184–187, 190, 192 statins, 172, 181 thromboelastography, 158–159
reno-visceral perfusion, 127–129 “sterile cockpit” concept, 4 ticagrelor, 157–158
reperfusion, weaning from CPB, 113 steroids, 47, 172, 181 time-out phase, 37
reperfusion injury. See ischemia- stroke, 175 tirofiban, 157–158
reperfusion injury blood pressure control, 176–177 tranexamic acid (TA), 161–162
reservoirs, 18–19, 35 detection, 178, 180 transactional leaders, 5
levels for weaning from CPB, 116 risk factors, 175–176 transcranial Doppler (TCD), 88, 178,
monitoring, 28–29 subclavian cannulation, 13–14 180
residual blood management, 118 sucker bypass, 22, 66 transducer levels, weaning from CPB,
resonance technology, 158–159 suckers, 22, 36 116
respiratory failure, postoperative, cardiotomy suction with, 66–68, 162 transesophageal echocardiography
170–171 suction blood, reservoir segregation of, (TEE)
respiratory quotient (RQ), 96 19 monitoring with, 31, 65–68
retrograde autologous prime (RAP), superior vena cava (SVC), cannulation in weaning from CPB, 114, 118
43–44, 154 of, 62 transformational leaders, 5
retrograde cardioplegia, 109 systemic inflammatory response, 166, transition of care, 5–6
retrograde cerebral perfusion (RCP), 171–173 Transmedics Organ Care System, 129,
59–60, 87–88 endothelial lining effects in, 167–168 131
rewarming, 63–64, 112, 200–201 gastrointestinal effects, 168–169 trauma patients, 135–136
AKI risk, 186–187 in pediatric patients, 153 tris (hydroxymethyl) aminomethane
cerebral temperature during, systemic to pulmonary shunts, (THAM), 107
182–183 150–151 tubing, 9–12
from DHCA, 85 Systems Engineering Initiative to biocompatible coatings, 11–12, 172
metabolic management, 100–101 Patient Safety (SIEPS), 2–3 preparation and setup, 35–36
right atrial cannulation, 61–62, size, 12
65–67 TandemHeart, 138–139, 145–146 tumor resection, 126
right atrial (RA) tumors, 126 teamwork ultrafiltration, 23–24, 154, 162, 172
right ventricular assist device (RVAD), communication, 1, 3–6
146–148 human factors in, 1–3, 37 unfractionated heparin (UFH), 49, 54.
right ventricular (RV) failure, 147, 149 leadership, 5 See also heparin
rivaroxaban, 158 mental workload, 4–5 uninterruptible power supply (UPS), 35
roller pumps, 14–16 during MiECC, 73 urine output (UO), 65, 93, 95
anesthesiologist perspective, 73
Safety 1 and Safety 2, 1–2 perfusionist perspective, 73–74 vacuum-assisted venous drainage
safety culture, 194–195, 198–199 surgeon perspective, 73 (VAVD), 18–19, 28, 62 211

Index
vasodilators, during weaning from MiECC, 73–74 metabolism, 98–99

CPB, 115 pediatric patients, 152 myocardial protection, 111
vasoplegic shock, 202–203 peripheral, 62–63 neuroprotection, 179
vasopressin, 121 TEE monitoring, 65–67
vasopressors, 93–94 venous drainage, 92, 150–151 warfarin, 157–158
failure to wean from CPB, 119–121 venous saturation, 29–30, 93–95 weaning from CPB, 112
side effects, 121 veno-venous extracorporeal membrane checklists, 112–113
during weaning from CPB, 115, oxygenation (VV ECMO), 123, alarms, 115
117–118 140 anesthesia, 115
vein grafts, cardioplegia delivery ventilation, 115, 169, 173 de-airing, 112–113
through, 109 ventricular assist devices (VADs), 18, electrolytes and acid-base balance,
veno-arterial extracorporeal membrane 146–148 115–116
oxygenation (VA ECMO), 123 failure to wean from CPB, 122 inotropes, 115
failure to wean from CPB, 122 MCS with, 138–139, 144–145 levels, 116
MCS with, 138–140, 143–144 complications, 146, 149 pacing, 114
circuit designs, 140–146 patient management, 148 rate/rhythm/contractility, 113–114
complications, 143 perioperative management, 148 reperfusion, 113
contraindications to, 141–143 postoperative management, temperature, 112
emergent or bail-out applications, 148–149 ventilation, 115
133–136 types, 145–148 failure, 119–122
indications, 141, 143 percutaneous temporary, 145–146 pediatric patients, 153
weaning from, 144 vents, 22, 36, 68–69 prediction of difficulty, 117
venous autologous prime (VAP), 43–44 viscoelastic tests (VET), 158–161 residual blood management, 118
venous blood path obstruction, 197 vitamin K antagonists, 157–158 reversal of anticoagulation, 118
venous cannula, 14–15 volatile anesthetic agents separation mechanics, 117–118
venous cannulation, 61 AKI prevention, 191–192 TEE in, 114, 118
complications, 63 gas scavenging system, 35 weaning from ECMO, 144
connection, 61–62 heart-lung machine monitoring, whole blood clotting time (WBCT),
DHCA, 81 25–26 50–51
212

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Cardiopulmonary Bypass

Cambridge University Press is part of Cambridge University Press & Assessment,

We share the University’s mission to contribute to society through the pursuit of

James H. Abernathy III Helena Argiriadou

Simon Anderson Christiana Burt

Amanda Crosby Joanne F. Irons

Erik Ortmann Center; Medical Director, Cardiothoracic Intensive

Michael Poullis Pascal Starinieri

Teams are especially critical for avoiding errors

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Table 1.1. Overview of Safety 1 and 2

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Briefing and Debriefing providing recognized programs to integrate team-

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PROFESSIONAL TEAM BEHAVIOUR

Suggested Further Reading statement from the American

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2 Simon Anderson and Amanda Crosby

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DLP® Flexible Arch Cannulae EOPA® Arterial Cannulae

Pressure Loss (mm Hg)

Pressure Drop (mm Hg)

Figure 2.2 Cannula flow profiles.

internal diameter, they achieve lower resistance to

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Blood leaves Figure 2.6 Line drawing of a

Rollers force blood

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3/8” Blood inlet with two barbs for Durable bearing

Durable, chemical resistant

Ceramic pivot shaft

Six low-profile impeller fins for Smooth cone for

Internal molded magnet for torque

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which can occur if the suckers are left running at a

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Filters and Bubble Traps

Figure 2.10 LivaNova S5W Electronic Gas Blender,

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Manufacturer Filter type Fiber material Filter size (μm)

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Table 2.7. Cardioplegia delivery systems

Manufacturer Integrated Air Delivery System

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Suggested Further Reading Circulation. 2000;102: Iv-87–Iv-93

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3 Richard F Newland and Pascal Starinieri

A fundamental area of responsibility for the perfusio- Heart Lung Machine

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Temperature rate and oxygen consumption reduce by 50% for

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(a) Low level detector (b) Bubble detector

Inability to introduce Adventitia occluding the Trauma to the vessel