CriticalCareManual 2021 Complete 020221-2

Mechanical
Circulatory Support
Devices in the
Intensive Care Unit:
Post-Implant Care and
Management
EDITORS:
JACOB ABRAHAM, MD
JOSEPH E. PARRILLO, MD, MCCM
Mechanical Circulatory Support Devices in the Intensive Care Unit: Post-Implant Care and Management 1
Copyright © 2021
All rights reserved. This book is protected by copyright. No part of this book or its supplemental videos and graphics
may be reproduced or modified in any form, including photocopying, recording, or utilized by any information storage
and retrieval system, without permission in writing from the publisher.
Care has been taken to confirm the accuracy of the information presented and to describe generally accepted
interventional practices. However, the authors, editors, and publisher are not responsible for errors or omissions or for
any consequences from application of the information in this book and make no warranty, expressed or implied, with
respect to the currency, completeness, or accuracy of the contents of the publication. Application of the information
in a particular situation remains the professional responsibility of the practitioner. Some medical devices presented
in the book may have Food and Drug Administration (FDA) clearance for limited use in restricted research settings at
the time of publication. It is the responsibility of the health care provider to ascertain the current status of each device
planned for use in clinical practice.
This publication is being published and distributed by the Society of Critical Care Medicine (SCCM) and is
supported through an educational grant from Abiomed, Inc.
Rev. 1 / Feb. 2021
CONTENTS
Preface..............................................................................................................................................................................i
About the Editors..........................................................................................................................................................ii
Authors...........................................................................................................................................................................iv
Introduction: Pathophysiology and Definitions.................................................................................................... 1
Mathew S. Lopes, MD
Steven P. Keller, MD, PhD
PART I OVERVIEW AND HEMODYNAMICS IN MECHANICAL CIRCULATORY SUPPORT

1 Overview of Mechanical Circulatory Support...................................................................................................7
Mathew S. Lopes, MD
2 Hemodynamic Assessment: Use of Right Heart Catheterization..............................................................25
Charles Hunley, MD
Craig S. Smith, MD
PART II MECHANICAL CIRCULATORY SUPPORT WITH IMPELLA® DEVICES: INSERTION,

MANAGEMENT, AND REMOVAL
3 Femoral Access and Management................................................................................................................... 37
Craig S. Smith, MD
4 Axillary Artery Access and Management........................................................................................................52
Timothy D Smith, MD
5 Percutaneous Ventricular Assist Device Console Management.............................................................. 57
Kanika P. Mody, MD
6 Team-based Care.................................................................................................................................................. 62
John Adam Reich, MD
Haval Chweich, MD
7 Anticoagulation..................................................................................................................................................... 69
Satya Shreenivas, MD
8 Blood Compatibility/Hemolysis ........................................................................................................................ 76
Jacob Abraham, MD
9 Weaning of Impella® ............................................................................................................................................ 81
Waqas Ghumman, MD
10 Impella® Removal and Closure.......................................................................................................................... 86
Timothy D Smith, MD
PART III MECHANICAL CIRCULATORY SUPPORT: OTHER DEVICES

11 Intra-aortic Balloon Pump.................................................................................................................................. 94
Arvind Bhimaraj MD, MPH, FACC, FHFSA
12 ECMO: Configurations and Management .....................................................................................................102
Samantha K. Brenner, MD, MPH
Mark Anderson, MD, MHA
Joseph E. Parrillo, MD, MCCM
Eugene Bunnell, MD
13 ECpella™: Physiological Basis and Clinical Management of Dual Mechanical
Circulatory Support with ECMO and Impella CP®.........................................................................................112
PART IV MECHANICAL CIRCULATORY SUPPORT: GENERAL MANAGEMENT ISSUES

14 Patient Transfer Considerations...................................................................................................................... 125
Brian Porvin, DO
15 Escalation of Care in Cardiogenic Shock....................................................................................................... 133
Greg Marco, MD, FCCP
16 Palliative Care.......................................................................................................................................................138
Charles Hunley, MD
17 Non-Acute Coronary Syndrome Cardiogenic Shock ..................................................................................145
Terese C. Hammond, MD
J. Christian Cash, MD
Matthew E. Powers, MD
Raymond C. Lee, MD
18 Non-Cardiac Critical Illness Management..................................................................................................... 156
Douglas M. Fetterman, MD
David H. Mandell, MD
19 Mechanical Cardiac Support Use in COVID-19..............................................................................................169
Vittorio Pazzanese, MD
Federico Pappalardo, MD
PART V MECHANICAL CIRCULATORY SUPPORT AND SYSTEMS OF CARE

20 Cardiogenic Shock Systems of Care ..............................................................................................................186
Shashank S. Sinha, MD, MSc, FACC
21 Regionalization and Protocolization of the Treatment of Cardiogenic Shock and Need for
Mechanical Circulatory Support...................................................................................................................... 192
Timothy D. Smith, MD
Kari Gorder, MD
Preface
Intense interest in improving the historically poor prognosis of cardiogenic shock (CS) provided the
impetus behind writing this eBook. Cardiogenic shock is a complex, time-sensitive cardiovascular
emergency. Over the past two decades, much attention has been directed toward the use of mechanical
circulatory support (MCS) devices to improve the high mortality rate in patients with CS.
The optimal use of MCS requires a multidisciplinary approach to manage the critically ill cardiovascular
patient. MCS patients require care from cardiologists, cardiac surgeons, critical care physicians,
anesthesiologists, advanced practice providers (physician assistants and advanced nurse practitioners),
critical care nursing personnel, pharmacists, nutritionists, respiratory therapists and, depending on type
of MCS, perfusionists. Patients commonly receive MCS devices in the cardiac catheterization laboratory
or the cardiac operating room, and these patients are then managed in the intensive care unit by
multidisciplinary teams commonly led by critical care physicians. Thus, intensivists must not only have
intimate knowledge of the diagnosis, pathophysiology, and treatment of CS; increasingly, they must also
possess an understanding of the hemodynamic effects and complications of MCS.
This eBook, Post Implant Care and Management of Mechanical Circulatory Support (MCS) Devices in the
Intensive Care Unit, was written to provide an up-to-date, concise, algorithm-heavy, review of the major
clinical issues surrounding MCS use in the ICU. It provides a reference source and review to supplement the
clinical training of residents, fellows, and attending critical care physicians. We believe that this text devoted
to the intensivist’s management of MCS will help to improve outcomes for patients with cardiogenic shock.
Although the majority of chapters in this eBook consider the specific technical procedures involved
in MCS, we have devoted chapters to pathophysiology, hemodynamic assessment, team-based care,
systems of care, regionalization, and palliative care. We believe all these topics are important to the optimal
management of the patient requiring MCS.
Percutaneous VADs of the Impella® type represent the most frequently employed technology in MCS, and
thus much of this eBook is devoted to the proper indications and management of patients supported
with Impella devices. We have, however, also included chapters considering intra-aortic balloon pumps
(IABP) and extracorporeal membrane oxygenation (ECMO), along with a chapter devoted to the COVID-19
pandemic and MCS.
We are fortunate to have attracted an exceptional group of highly experienced and accomplished clinicians
to author each chapter. We wish to thank the authors for their expertise and contributions.
We also wish to thank all those individuals who have provided the editorial and administrative input
needed to compile this eBook. Jennifer Even Melton provided expert medical writing assistance. Mary
Dyan, Lillian Palmer, and Seth Bilazarian, MD deserve special thanks for their guidance and support.
Jacob Abraham, MD
Portland, OR

Hackensack, NJ
Mechanical Circulatory Support Devices in the Intensive Care Unit: Post-Implant Care and Management i
About the Editors
Jacob Abraham, MD
Dr. Abraham is the section chief of Advanced Heart Failure for the Providence Heart Institute in Portland,
Oregon.
He graduated from Rhodes College (Memphis, TN) magna cum laude. After spending a year in Sydney,
Australia, as a Rotary Ambassadorial Scholar, he completed medical school, internal medicine residency,
and fellowship at Johns Hopkins Hospital (Baltimore, MD). He interrupted his fellowship to serve as
assistant chief of service on the Osler Medical Service (Janeway firm). He is board-certified in cardiology and
advanced heart failure/transplant cardiology.
After moving to Portland, Oregon in 2009, Dr. Abraham lead the effort to develop a mechanical circulatory
support program at Providence. In 2011 the program was granted certification by the Joint Commission.
Over the ensuing decade under his leadership, the advanced heart failure program at Providence has
grown; in 2020, Providence launched a heart transplant program.
Dr. Abraham’s academic interests include implantable hemodynamic monitoring for chronic heart failure
and cardiogenic shock.
Mechanical Circulatory Support Devices in the Intensive Care Unit: Post-Implant Care and Management ii
About the Editors
Dr. Parrillo is the chairman of the Heart and Vascular Hospital at Hackensack University Medical Center
and he holds the Justice Marie L. Garibaldi endowed chair. He is also chair and professor of the cardiology
department at the recently established Hackensack Meridian School of Medicine. Prior to Hackensack,
he was professor and founding chair of the department of medicine at Cooper Medical School of Rowan
University (Camden, NJ), Edward D. Viner chair of the department of medicine and director of Cooper
Heart Institute at Cooper University Hospital. Dr. Parrillo previously was the James B. Herrick professor of
medicine and chief of the cardiovascular program at Rush Medical Center in Chicago, IL.
A magna cum laude graduate of Dartmouth College (Hanover, NH), Dr. Parrillo received his medical degree
with honors from Cornell Medical College (New York, NY) where he was elected to Alpha Omega Alpha.
He did his post-graduate training at Massachusetts General Hospital (Boston, MA), the New York Hospital-
Cornell Medical Center (New York, NY), and the National Institutes of Health (NIH, Bethesda, MD). Dr. Parrillo
is board-certified in internal medicine, allergy and immunology, cardiovascular disease, and critical care
medicine.
Dr. Parrillo’s involvement in academia has led to significant medical advances. Examples of his research
can be found in the more than 1,080 publications he has authored or co-authored. One of Dr. Parrillo’s most
notable scientific contributions was the discovery that reversible myocardial depression was very common
in human sepsis and septic shock. This seminal research has resulted in major insights regarding the
mechanisms and treatment of serious infections and septic shock.
Dr. Parrillo received the NIH Director’s Award, the highest civil service employee honor, for “creating a
superior critical care medicine department.” He was elected to membership in the highly prestigious
American Society of Clinical Investigation (ASCI) and the Association of American Physicians (AAP), two
honorary societies recognizing the finest clinician-scientists in the nation. Dr. Parrillo was the recipient
of both the Distinguished Investigator Award and the Lifetime Achievement Award from the American
College of Critical Care Medicine. He is a past president of the Society of Critical Care Medicine (SCCM),
served as editor-in-chief of the journal Critical Care Medicine, and is the editor of one of the major standard
textbooks entitled Critical Care Medicine: Diagnosis and Management in the Adult. The fifth edition of this
textbook published in 2019.
Dr. Parrillo’s major interests have been cardiovascular performance in sepsis and cardiogenic shock; heart
failure; myocarditis; and the critically ill cardiovascular patient.
Mechanical Circulatory Support Devices in the Intensive Care Unit: Post-Implant Care and Management iii
Authors
Jacob Abraham, MD J. Christian Cash, MD
Medical Director, Advanced HF, MCS, and Heart Transplant Assistant Professor of Clinical Surgery
Providence Heart Institute Division of Cardiothoracic Surgery
Portland, OR Cardiovascular Thoracic Institute
Jacob.Abraham@providence.org Keck School of Medicine of USC
jonathan.cash@med.usc.edu
Justice Marie L. Garibaldi Endowed Chair, Chairman Haval Chweich, MD
Heart and Vascular Hospital Director of Cardiac Care Unit

Hackensack University Medical Center Tufts Medical Center/Tufts University School of Medicine
Professor and Chair, Department of Cardiology
Hackensack Meridian School of Medicine at Seton Hall
University Medical Director of Critical Care Services Anesthesiology and
Critical Care Medicine
Professor of Medicine
St Joseph’s Health Hospital Center
Rutgers New Jersey Medical School Syracuse, NY
joseph.parrillo@hackensackmeridian.org Douglas.Fetterman@sjhsyr.org
Mark Anderson, MD, MHA Waqas Ghumman, MD

Professor of Surgery Affiliated Clinical Assistant Professor of Medicine,
Hackensack Meridian School of Medicine at Seton Hall University of Miami
Nutley, NJ
Director, Mechanical Circulatory Support and Heart Failure
Chief, Division of Cardiac Surgery Program at JFK
Vice-Chair, Cardiac Surgical Services Atlantis, FL
Heart and Vascular Hospital wghumman@gmail.com
Mark.Anderson@hackensackmeridian.org
Kari Gorder, MD
Arvind Bhimaraj MD, MPH, FACC, FHFSA Cardiovascular Critical Care and Emergency Medicine
Interim Chief, Division of Heart Failure The Christ Hospital and Lindner Research Center
Medical Director, Advanced Heart Failure, MCS and Heart Cincinnati, OH
Transplant Program
Terese C. Hammond, MD
Houston Methodist DeBakey Heart and Vascular Center
University of Southern California, Dept of Surgery
Houston Methodist J.C. Walter Jr. Transplant Center
Medical Director
Houston Methodist Hospital
Providence St Johns Health Center ICU
abhimaraj@houstonmethodist.org
Terese.Hammond@providence.org
Samantha K. Brenner, MD, MPH
Charles Hunley, MD
Core Assistant Professor of Internal Medicine
Critical Care Director
Hackensack Meridian School of Medicine at Seton Hall
Nutley, NJ Orlando Regional Medical Center
Orlando Health
Intensivist, Cardiothoracic Intensive Care Unit Orlando, FL
Heart and Vascular Hospital, Hackensack Meridian Health, Charles.hunley@orlandohealth.com
Hackensack University Medical Center
Hackensack, NJ Steven P. Keller, MD, PhD
Samantha.Brenner@hackensackmeridian.org Division of Pulmonary and Critical Care Medicine
Eugene Bunnell, MD Brigham and Women’s Hospital
Harvard Medical School
Medical Director, Cardiothoracic Intensive Care Unit Boston, MA
Heart and Vascular Hospital, Hackensack Meridian Health, Institute for Medical Engineering and Science
Hackensack University Medical Center Massachusetts Institute of Technology
Hackensack, NJ Cambridge, MA
Eugene.Bunnell@hackensackmeridian.org spkeller@mit.edu
Mechanical Circulatory Support Devices in the Intensive Care Unit: Post-Implant Care and Management iv
Authors
Raymond C. Lee, MD Matthew E. Powers, MD
Assistant Professor of Clinical Surgery Assistant Professor of Clinical Surgery
Division of Cardiothoracic Surgery Division of Cardiothoracic Surgery
Cardiovascular Thoracic Institute Cardiovascular Thoracic Institute
Keck School of Medicine of University of Southern California Keck School of Medicine of USC
Los Angeles, CA Matthew.Powers@med.usc.edu
Dr.raycLee@gmail.com
John Adam Reich, MD
Raymond.Lee@med.usc.edu
Director of Cardiovascular Critical Care
Mathew S. Lopes, MD ECMO Medical Director
Division of Cardiovascular Medicine Tufts Medical Center/Tufts University School of Medicine
Brigham and Women’s Hospital jreich@tuftsmedicalcenter.org
Boston, MA Satya Shreenivas, MD
The Christ Hospital Heart and Vascular Center,
David H. Mandell, MD The Lindner Research Center
Perioperative Section Chief Cincinnati, OH
Anesthesiology and Critical Care Medicine Attending satya.shreenivas@thechristhospital.com
St. Joseph’s Health Hospital Center
David.Mandell@sjhsyr.org
Assistant Professor of Internal Medicine
Greg Marco, MD, FCCP Virginia Commonwealth University School of Medicine, Inova
Medical Director for Cardiothoracic Critical Care Campus
Frederik Meijer Heart & Vascular Institute Medical Director, Cardiac Intensive Care Unit
Grand Rapids, MI Director, Cardiovascular Critical Care Research Program
greg.marco@spectrumhealth.org Advanced Heart Failure, Mechanical Circulatory Support, and
Transplant Cardiology Program
Kanika P. Mody, MD Inova Heart and Vascular Institute
Medical Director, VAD Program Inova Fairfax Medical Campus
Heart and Vascular Hospital Falls Church, Virginia
Hackensack University Medical Center Shashank.Sinha@inova.org
Hackensack, NJ
Kanika.mody@hackensackmeridian.org Craig S. Smith, MD
Assistant Professor of Medicine,
University of Massachusetts
Department Anesthesia and Intensive Care
Medical Director, Cardiac Intensive Care
IRCCS ISMETT, UPMC Italy
Palermo, Italy Interventional Cardiologist
fedepappa@me.com Craig.smith@umassmemorial.org
Vittorio Pazzanese, MD Timothy D. Smith, MD

Intensive Cardiac Care Unit Interventional Cardiovascular and Critical Care Medicine
San Raffaele Scientific Institute Director, Farmer Family Cardiovascular ICU
Milan, Italy Director, ECMO and Shock Program
Vittorio.pazzanese@hotmail.it The Christ Hospital and Lindner Research Center
Cincinnati, OH
Brian Porvin, DO
Timothy.smith@thechristhospital.com
Vice Chairman of Internal Medicine
Honor Health Deer Valley Medical Center
Phoenix, AZ
b.porvin@pulmonaryassociates.com
Mechanical Circulatory Support Devices in the Intensive Care Unit: Post-Implant Care and Management v
TABLE OF
CONTENTS
Introduction:
Pathophysiology
and Definitions
Mathew S. Lopes, MD Steven P. Keller, MD, PhD
Division of Cardiovascular Medicine Division of Pulmonary and
Brigham and Women’s Hospital Critical Care Medicine
Harvard Medical School Brigham and Women’s Hospital
Boston, MA Harvard Medical School
Boston, MA
Institute for Medical Engineering and Science

Massachusetts Institute of Technology
Cambridge, MA
spkeller@mit.edu
Clinical definitions and metrics

TERM DEFINITION
Cardiogenic shock • Combination of:
• Low cardiac output (CO) despite adequate or elevated ventricular
filling pressures
• Hypotension
• Evidence of end-organ malperfusion9
Hypotension • Systolic blood pressure (SBP) <90 mmHg, or

• SBP >90 mmHg with the need for catecholamine infusions
(eg, norepinephrine or epinephrine) to maintain SBP >90 mmHg
Cardiac index (CI) • CO normalized to body surface area

• Facilitates comparison of perfusion between patients of differing sizes
• CI <2.2 L/min/m2 is a common threshold to identify patients with
inadequate perfusion to maintain homeostasis10
Elevated left-sided filling • Left ventricular end-diastolic pressure >18 mmHg

pressures
Introduction | Pathophysiology and Definitions Chapter 1 >>
Pathophysiology of cardiogenic shock

Cardiogenic shock is defined as cardiac dysfunction leading to end-organ malperfusion insufficient to
meet tissue metabolic demands.1–3 Common causes of cardiac impairment leading to shock include
acute myocardial infarction, progression of an underlying cardiomyopathy, arrhythmia, and valvular
heart disease.4 The onset of shock activates multiple interdependent compensatory mechanisms and
neurohormonal responses to create a dynamic and unstable physiological state.5
Decreased cardiac output triggers baroreceptor reflexes to induce peripheral vasoconstriction as a means
of maintaining systemic perfusion pressure.3 The increased afterload may be maladaptive and further
worsen cardiac dysfunction through increased metabolic demand. Progressive shock leads to ongoing
end-organ dysfunction and is evidenced by altered mental status, cool extremities and mottled skin,
decreased urine output, and elevation in laboratory markers such as lactate and liver enzymes.6
Systemic hypotension and end-organ dysfunction provoke an inflammatory response resulting in elevated
levels of interleukins and other inflammatory mediators.7 The released cytokines stimulate nitric oxide
synthase and promote release of peroxynitrite, an unstable nitrate isomer that acts as an oxidant to cause
myocardial and vascular dysfunction, leading to further cardiac impairment. Untreated, the inflammatory
response ultimately leads to pathological vasodilation before progressing to multi-system organ failure and
death.8
In clinical practice, cardiac output (CO) is commonly determined through measurements obtained via
a pulmonary artery catheter (PAC). The most frequently used methods for PAC-derived cardiac output
calculations are (1) the thermodilution technique and (2) application of the Fick equation. Both methods
provide intermittent determination of CO to guide clinical care. While the thermodilution technique
measures CO over several heartbeats, the Fick equation relates CO to oxygen consumption, as shown
in Equation 1, and is less sensitive to changes in forward flow and venous return that occur during the
respiratory cycle.
Measurement of oxygen consumption by indirect calorimetry is often not practical in the clinical setting
and standard reference values are frequently used to determine estimates of cardiac output using the
Fick equation. Assuming that a patient is at rest with a stable oxygen consumption (VO2), no evidence of
active bleeding, and is maintaining a normal arterial oxygen saturation—all reasonable assumptions for a
typical cardiogenic shock patient—Equation 1 can be further simplified such that cardiac output is shown
to be proportional to the oxygen saturation in mixed venous blood as shown in Equation 3. In health,
typical MVO2 values are greater than 70% and are consistent with adequate supply of oxygenated blood
to the body’s tissues.11 As cardiac output falls, tissues extract more oxygen from capillary blood leading to
decreased saturation levels in fully mixed venous blood with MVO2 values less than 60% corresponding
to inadequate perfusion.12 As MVO2 levels track with CO, the MVO2 can be used as an easily measured
surrogate of systemic perfusion or as a means of correlating Fick-based calculations with thermodilution-
based measurements.
EQUATION 1: FICK EQUATION
• VO2 is rate of oxygen consumption

• Ca is oxygen content of arterial blood
• Cv is oxygen content of venous blood
EQUATION 2: O2 CONTENT IN BLOOD
• [Hgb] is the concentration of hemoglobin

• O2saturation fraction is the oxygen saturation of hemoglobin
• PO2 is the partial pressure of oxygen in the blood
EQUATION 3: CO IS PROPORTIONAL TO MVO2
• CO is cardiac output
• MVO2 is the oxygen saturation of mixed venous blood
sampled from the pulmonary artery
Diagnosis and initial therapy

A high index of clinical suspicion is required to promptly diagnose and treat patients with cardiogenic
shock. In certain conditions, such as patients experiencing classic signs of a large anterior myocardial
infarction, the presenting complaint is associated with a significant risk of concomitant shock and clinical
deterioration which heightens clinical awareness and increases likelihood of prompt diagnosis.13,14
In other disease states, such as exacerbations of underlying cardiomyopathy or unrecognized cases of

viral myocarditis, patients can experience progressive shock that is difficult to detect using standard
tools of clinical assessment. In these cases, patients may express non-specific subjective complaints of
malaise with vital signs notable for normal or even elevated blood pressures accompanied by modest to
moderate tachycardia. Compensatory vasoconstrictive mechanisms and autoregulation of perfusion to
maintain blood flow to the brain may permit these patients to be conversant despite being in extremis.
Laboratory assessment performed early in clinical presentation may not yet identify evidence of end-
organ malperfusion as traditional markers are lagging indicators of shock and require hours to days of
hypoperfusion to become abnormal. It may not be until invasive assessment is performed that a below
threshold CI is appreciated and severity of shock recognized.
Duration of shock is associated with progressively worse outcomes and decreased survival which motivates
interventions to promptly restore systemic perfusion.15–17 In acute myocardial infarction complicated by
shock, time to revascularization is associated with survival rates demonstrating the need to rapidly treat
the underlying pathology in cardiogenic shock to improve clinical outcomes.9,18 The development of new
and expanded forms of mechanical circulatory support provide the clinician with new tools in the ongoing
efforts to deliver better patient survival.19 The combination of prompt diagnosis, expanded therapeutic
options, and improved metrics to guide titration of support may herald a new era in the treatment of
cardiogenic shock.
This book presents an overview of mechanical circulatory therapies in supporting patients with cardiogenic
shock with an emphasis on percutaneous ventricular assist devices (Impella®), notably the Impella CP®
and Impella family of devices. In addition to providing a detailed description of the clinical use, titration,
and weaning of Impella support, this book also presents use of the pulmonary artery catheter to diagnose
cardiogenic shock and monitor response to therapy and use of dual mechanical circulatory support with
the Impella and extracorporeal membrane oxygenation (ECMO). This book is intended as a resource for
clinicians to optimize use of mechanical circulatory support and improve clinical outcomes for patients
suffering from cardiogenic shock.
References
1. Hajjar LA, Teboul J-L. Mechanical circulatory support devices for cardiogenic shock: state of the art. Critical Care.
2019;23(76).
2. Mandawat A, Rao SV. Percutaneous mechanical circulatory support devices in cardiogenic shock. Circ Cardiovasc
Interv. 2017;10(5):1-12.
3. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: a scientific statement
from the American Heart Association. Circulation. 2017;136(16):e232–e268.
4. Berg DD, Bohula EA, van Diepen S, et al. Epidemiology of shock in contemporary cardiac intensive care units. Circ
Cardiovasc Qual Outcomes. 2019;12(3):e005618.
5. Tewelde SZ, Liu SS, Winters ME. Cardiogenic shock. Cardiol Clin. 2018;36(1):53-61.
6. Vahdatpour C, Collins D, Goldberg S. Cardiogenic shock. J Am Heart Assoc. 2019;8(8):e011991.
7. Hochman JS. Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm. Circulation.
2003;107(24):2998–3002.
8. Kohsaka S, Menon V, Lowe AM, et al. Systemic inflammatory response syndrome after acute myocardial infarction
complicated by cardiogenic shock. Arch Intern Med. 2005;165(14):1643-50.
9. Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation.
2008;117(5):686-97.
10. Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by
cardiogenic shock. SHOCK Investigators. Should we emergently revascularize occluded coronaries for cardiogenic
shock. N Engl J Med. 1999;341(9):625-34.
11. Hartog C, Bloos F. Venous oxygen saturation. Best Pract Res Clin Anaesthesiol. 2014;28(4):419-28.
12. Marx G, Reinhart K. Venous oximetry. Curr Opin Crit Care. 2006;12(3):263-8.
13. Babaev A, Frederick PD, Pasta DJ, et al. Trends in management and outcomes of patients with acute myocardial
infarction complicated by cardiogenic shock. J Am Med Assoc. 2005;294(4):448-54.
14. Kolte D, Khera S, Aronow WS, et al. Trends in incidence, management, and outcomes of cardiogenic shock
complicating ST‐elevation myocardial infarction in the United States. J Am Heart. 2014;3(1):e000590.
15. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is
the critical determinant of survival in human septic shock. Crit Care Med. 2006;34(6):1589-96.
16. Gross PA. Hypotension and mortality in septic shock: the “golden hour”. Crit Care Med. 2006;34(6):1819-20.
17. Brindley PG, Zhu N, Sligl W. Best evidence in critical care medicine: early antibiotics and survival from septic shock:
it’s about time. Can J Anesth. 2006;53:1157-60.
18. Ginsberg F, Parrillo JE. Cardiogenic shock: a historical perspective. Crit Care Clin. 2009;25(1):103-14.
19. Miller PE, Solomon MA, McAreavey D. Advanced percutaneous mechanical circulatory support devices for
cardiogenic shock. Crit Care Med. 2017;45(11):1922-29.
PART I
TABLE OF
CONTENTS
Overview and
Hemodynamics in
Mechanical Circulatory
Support
Chapter 1 Overview of Mechanical Circulatory Support........................7
Chapter 2 Hemodynamic Assessment:

Use of Right Heart Catheterization......................................... 25
Mechanical Circulatory Support Devices in the Intensive Care Unit: Post-Implant Care and Management
TABLE OF PART I Overview and Hemodynamics in Mechanical
CONTENTS
Circulatory Support
Overview
CHAPTER
1 of Mechanical
Circulatory
Support
Steven P. Keller, MD, PhD Mathew S. Lopes, MD
Division of Pulmonary and Division of Cardiovascular Medicine
Critical Care Medicine Brigham and Women’s Hospital
Brigham and Women’s Hospital Harvard Medical School
Harvard Medical School Boston, MA
Boston, MA
Institute for Medical Engineering

and Science
77 Massachusetts Avenue, Building E25-438
Cambridge, MA 02139
spkeller@mit.edu
INTRODUCTION
Cardiogenic shock is a highly morbid condition with mortality rates approaching
50% despite prompt diagnosis and initiation of appropriate medical therapy.1–3
The limitations of medical management motivated development of mechanical
means of circulatory support in an effort to restore perfusion and maintain
systemic homeostasis.4–6 The intra-aortic balloon pump (IABP) was the first
widely available mechanical circulatory support (MCS) device and was rapidly
adopted as the primary mechanical method of augmenting cardiac output
and improving coronary perfusion for cardiogenic shock patients.7 More recent
innovations have led to the development of newer MCS devices capable of
delivering expanded support with a goal to improve clinical outcomes.8
This chapter provides an overview of the operational paradigms of commonly

used percutaneous MCS devices with an emphasis on their effects on perfusion
and cardiac function. It presents the physiological rationale for providing MCS
and describes specific devices, concluding with a discussion on patient selection
and future directions.
<< Introduction Chapter 1 | Overview of Mechanical Circulatory Support Chapter 2 >>
Functional overview of MCS

The primary therapeutic function of mechanical circulatory support is to restore systemic circulation
and maintain end-organ viability. As time to shock reversal is negatively associated with survival, prompt
initiation of support and ongoing evaluation of therapeutic efficacy are key components of successful
clinical management.9,10 An additional, and often overlooked, goal of circulatory support is to both sustain
heart function and promote cardiac recovery. The ideal MCS device would:
• Restore perfusion titrated to meet end-organ metabolic demands
• Reduce cardiac work while maintaining coronary perfusion to aid heart recovery
• Provide support across a wide degree of cardiac failure
• Deploy safely and easily to facilitate quick implementation and lower threshold for use
• Provide feedback to guide titration and weaning of support to enable optimal use
While no device meets all criteria for ideal support, this list provides a framework for comparing different
modalities and emphasizing areas of ongoing investigation and innovation.
At present, a variety of MCS devices are capable of providing circulatory support deployed via percutaneous
approaches. These devices have differing operational paradigms and varying physiological effects on
cardiac function, hemodynamics, and perfusion. Many of these effects are incompletely understood
while optimal strategies for clinical management of MCS devices have yet to be determined. Pending
development of improved diagnostics and evidence-based approaches to guide titration and weaning of
support, clinicians must rely on physiological reasoning and understanding of MCS device operation to
achieve the best possible outcomes for patients.
Therapeutic benefit of MCS

Medical therapy for cardiogenic shock targets optimization of preload and afterload and augmentation
of contractility in an effort to increase cardiac output.11 When medical treatment is insufficient to provide
adequate systemic perfusion, mechanical means of circulatory support is required to meet end-organ
metabolic demand.12 The effects of shock on myocardial oxygen consumption and coronary perfusion are
particularly relevant in the setting of active myocardial ischemia in which conditions that increase myocyte
oxygen demand may exacerbate the area of injury and lead to an enlarged infarct.13
Myocardial oxygen consumption increases with elevations in ventricular wall stress, heart rate, cardiac
contractility, and cardiac work.14,15 In heart failure, ventricular systolic dysfunction and loss of intrinsic
inotropy result in a decrease in stroke volume. This physiological change leads to a compensatory increase
in end diastole ventricular volume and pressure via the Frank-Starling relationship (Figure 1).
Figure 1. Effects of Heart Failure on Cardiac State

(A) Frank-Starling relationship and effect of heart failure on LV end diastolic pressure (LVEDP); black line
represents baseline of heart with operating point A; onset of heart failure produces new relationship shown by
blue line; decrease in stroke volume produces increase in LVEDP and new operating point of heart at point B.
(B) Two pressure-volume relationships for both normal condition and loss of inotropy as occurs in heart failure;
onset of heart failure results in decreased stroke volume and increase in LVEDP
The Law of Laplace (see Box) states that wall stress

varies directly with intracardiac pressure and LAW OF LAPLACE
chamber radius and is inversely proportional to wall
thickness. The Frank-Starling relationship and the Pxr
Law of Laplace show that loss of intrinsic inotropy
T=
directly leads to increased wall stress and increased
2xh
myocardial oxygen consumption. T = Left ventricle (LV) wall stress
P = LV intraventricular pressure
Decreased blood flow in cardiogenic shock triggers
compensatory responses and increased levels of r = Chamber radius
circulating catecholamines that increase heart h = Wall thickness
rate and augment cardiac contractility.16–18 Medical
inotropic therapy mirrors these natural responses
by directly stimulating receptors that increase
calcium channel signaling to elevate heart rate
and increase myosin cycling. The cumulative effect
of both the physiological response to shock and
inotropic therapy is heightened myocyte metabolic
demand.
Mechanical support that both restores perfusion and obviates the need for inotropic therapy blunts the
physiological response to shock and reduces myocyte oxygen demand.19 Furthermore, MCS devices that
decrease ventricular volume and pressure, a process said to achieve “ventricular unloading,” (Figure 2) lead
to reduced myocardial oxygen consumption which may be a vital approach for preserving residual cardiac
function.20,21
Figure 2. Effects of Increasing

Intracardiac Pressure and Volume
on Ventricular Wall Tension
Cross-sections of heart comparing
ventricular dimensions in (A) normal
heart and (B) heart failure. Loss of
inotropy with heart failure leads
to increased LVEDP and larger
intraventricular volume at end
diastole (LVEDV). (C) MCS devices that
unload the LV act to decrease LVEDV
and may augment cardiac function.
Cardiac muscle oxygen extraction is near maximal

at rest.22 The highly efficient use of delivered oxygen CORONARY PERFUSION
demands that any increases in myocardial oxygen PRESSURE OF THE LV
consumption—as caused by increases in heart
rate, wall stress, or contractility—must be met by
a proportional increase in coronary blood flow. If
CPP = MAP – LVEDP
oxygen delivery does not match demands, ischemia CPP = coronary perfusion pressure
results, perpetuating ventricular dysfunction and
MAP = mean arterial pressure
exacerbating shock physiology.
LVEDP = left ventricular end diastolic pressure
Regulation of coronary blood flow is complex and
dictated by numerous mechanisms including
coronary perfusion pressure (CPP), tissue
compression forces, and local and hormonal
mediators of coronary vascular resistance.23
Coronary perfusion pressure of the left ventricle is
expressed by the equation shown in the Box.
Unlike most organs, in which perfusion is determined by the pressure difference between the supplying
artery and venous drainage and the vascular impedance, functional cardiac perfusion is more complex.
During systole, myocardial contraction leads to extravascular compression of the coronary circulation.
This compression decreases myocardial blood supply during systole resulting in most perfusion occurring
during myocardial relaxation in diastole. While CPP is highly variable depending on physiological state,
autoregulatory mechanisms maintain a constant blood flow across a wide range of pressure gradients. The
autoregulation range of CPP in which a constant basal blood flow is maintained is generally 60-120 mmHg
but has been reported as low as 40 mmHg in animal models.23 Outside of this range, coronary blood flow is
no longer constant and is dependent on the upstream pressure (ie, MAP).
The physiology of heart failure provides insights into the operation

of the ideal MCS device. Such a device would function not only Maintaining systemic
to maintain systemic perfusion but also to decrease myocardial
blood flow while reducing
oxygen consumption while maintaining coronary blood flow. The
intraventricular pressure is
ideal device would simultaneously:
• Increase systemic perfusion the key to maintaining global
• Maintain CPP through increased MAP and decreased LVEDP coronary perfusion and
• Decrease myocardial oxygen consumption presents a conceptual basis
for evaluating MCS devices.
To achieve lowering of myocardial metabolic demand, the ideal
MCS device would unload the ventricle to reduce ventricular
chamber size and pressure.24 Maintaining systemic blood flow
while reducing intraventricular pressure is the key to maintaining
global coronary perfusion and presents a conceptual basis for
evaluating MCS devices. Applying this framework allows for the
comparison of different forms of mechanicals support and aids
in tailoring the appropriate strategy to a patient’s physiology and
disease process.
Operational paradigms of current MCS devices

MCS devices profoundly alter normal hemodynamics and impact the physiological milieu in which the
heart functions. Key considerations in determining a mechanical support strategy for a specific patient
include:
• Familiarity with device operation
• Understanding effects of the device on cardiac loading conditions and coronary perfusion
• Ease of device deployment
• Availability of necessary personnel to implement and maintain support
• Overall goals of therapy
The first 2 considerations in particular are vital in understanding how to monitor therapy response and
guide titration of support.
MCS devices consist of mechanical pumps that can be categorized by function, flow capabilities/
characteristics, and circuit configuration (see Table 1). ECMO is increasingly being deployed as an MCS
device with highly specific effects on the heart due to its mode of operation and dependent on its titration.
Various combinations of these devices are used to support patients with biventricular failure unable to be
supported with a single device. Each device is described in further detailed below as well as elsewhere in
this e-book.
Table 1. Commonly Used Percutaneous MCS Devices

LEFT VENTRICULAR SUPPORT25 RIGHT VENTRICULAR SUPPORT26
• Intra-aortic balloon pump (IABP) • Impella RP®
• Impella® family of devices (Abiomed, Inc., Danvers, MA) • TandemHeart Protek Duo® cannula coupled with an
• TandemHeart® (LivaNova, London, UK) external pump
LV support devices
Intra-aortic balloon pump
The IABP is a counterpulsatile balloon that sits within the descending thoracic aorta and inflates during
diastole and deflates during systole.27 Figure 3 shows an example IABP device and details its hemodynamic
effects. First successfully used in clinical care in 1967, the IABP was the only MCS device widely available
for several decades and remains a common means of providing mechanical support for patients in
cardiogenic shock.28,29 Balloons vary in size from 25 to 50 mL to accommodate a range of patients and are
typically inserted into the femoral artery through an 8 Fr sheath and advanced within a few centimeters of
the aortic arch.
Balloon inflation during diastole increases aortic

pressure and augments coronary perfusion
while deflation during systole decreases afterload
and facilitates indirect LV unloading.27 Balloon
inflation-deflation is timed to the cardiac cycle via
an electrocardiogram or aortic pressure sensor.
Animal experimental data and clinical studies
demonstrate that IABPs provide an estimated 0.5
to 1 L increase in cardiac output under optimal
conditions.27,30 As device function is dependent on
the physical movement of helium gas into and
out of the balloon, patients with tachyarrhythmias
are challenging to support and may not be able to
receive support with every heartbeat.
Figure 3. Hemodynamic Effects of IABP
IABP inflates during diastole to increase diastolic
Despite its widespread adoption as a primary systemic blood pressure and improve coronary
form of MCS, IABP use has yet to translate into perfusion, and deflates during systole to decrease
mortality benefit for cardiogenic shock patients afterload and promote LV unloading.
compared to medical therapy in randomized
clinical trials.31–33 This finding is likely attributed to
severity of shock experienced by trial patients and
the relatively modest support provided by IABPs.
While IABPs may offer some physiological benefit,
current diagnostics are unable to definitively
identify patients most likely to experience improved
outcomes with IABP support. Even with these
limitations, the IABP remains the dominant MCS
device in clinical use. In addition to standard
femoral artery placement, modified IABPs for
deployment via the axillary artery are being
investigated for use in decompensated, end-stage
heart failure patients as bridge to transplantation.34
Impella
The Impella heart pump is a percutaneous catheter-mounted MCS device consisting of a microaxial flow
pump that augments systemic perfusion while simultaneously unloading the left ventricle.35 Typically
deployed via the femoral or axillary artery, the device is positioned such that the pump inlet sits within the
LV while the catheter crosses the aortic valve and the outlet resides in the ascending aorta as shown in
Figure 4. The device aspirates blood from the LV and accelerates it into the aorta to produce continuous,
non-pulsatile antegrade flow.36 By withdrawing blood throughout the cardiac cycle, the Impella decreases
LV end-diastolic volume and reduces chamber dilation to lower myocardial oxygen consumption and
directly unload the ventricle.21,24
There are currently four Impella devices available

for percutaneous support of the LV. They vary in size
and amount of flow support provided.
• Impella 2.5
• Impella CP
• Impella 5.0
• Impella 5.5
The Impella device is connected to an external

controller that provides device operational feedback
and gives the clinician the ability to determine
device support level. The Impella 2.5 and Impella
CP are smaller devices capable of percutaneous
deployment via standard catheterization
procedures. The Impella 5.0 and the newer
Impella 5.5 are larger devices typically placed into
the axillary artery which is accessed via vascular
cutdown and attachment of a vascular graft.
The effect of Impella support on cardiac function

is a complex interplay between the heart’s
physiological state and device function. As a
continuous flow pump, the Impella provides
perfusion throughout the cardiac cycle acting to Figure 4. Mechanism of Action of Impella
reduce systemic pulsatility and the component Impella CP is placed across aortic valve. Inlet
in LV draws blood from ventricle to outlet in
of forward flow supplied by the heart. During proximal aorta to directly unload LV.
profound failure, however, a reduction in ventricular
distention and a lowering of LVEDP achieved
through LV unloading may conceivably improve
cardiac function and increase heart-produced
forward flow.20,21,37 At present, similar to other
advanced MCS devices, rigorous clinical trial data
to guide the clinician in titration of Impella support
to achieve optimal clinical outcomes is lacking and
remains an area of active investigation.
The unique placement of the Impella within the LV provides the opportunity to leverage its positioning
and functional operation to provide metrics of cardiac function to guide support. Published reports detail
quantitative approaches relying on heart-device interactions and intrinsic function of the pump to provide
accurate measurements of LV end diastolic pressure (LVEDP), cardiac output, and systemic vascular
resistance.38,39 Real-time and near-continuous reporting of these metrics provides clinicians with improved
tools to guide titration of support and rapidly respond to changes in patient physiology.
TandemHeart
The TandemHeart MCS device consists of vascular cannula and an extracorporeal centrifugal pump
capable of providing flow rates up to 4 L/min.40,41 Oxygenated blood is withdrawn via a 21 Fr withdrawal
cannula inserted into the femoral vein and advanced proximally across the atrial septum and into the left
atrium as shown in Figure 5. The centrifugal pump provides retrograde systemic perfusion via a 15 to
17 Fr return cannula inserted into the femoral artery with a distal end terminating in the iliac artery or distal
aorta. Similar to other left-sided support devices, the TandemHeart requires adequate right ventricular
function to maintain cardiopulmonary circulation and delivery of blood to the left side of the heart.
Retrograde perfusion generated by the

TandemHeart has variable effects on left heart
function. Withdrawal of blood from the left
atrium decreases left ventricular filling and acts to
reduce LV distention in the setting of failure while
retrograde perfusion increases systemic blood
pressure and improves coronary blood flow. While
these factors act to improve cardiac function in the
setting of profound failure, the LV may be unable
to overcome increased afterload resulting from
retrograde perfusion. In this scenario, residual blood
within the LV may not be ejected, thereby risking
intraventricular stasis and thrombus formation with
potential for catastrophic failure.
A significant challenge in the management of

TandemHeart support is the lack of readily available
diagnostics to continuously monitor native LV
function and risk of stasis. As TandemHeart does
not directly unload the LV, support will have
variable effects on myocardial oxygen consumption.
To avoid blood stasis in profound failure, use of
inotropic therapy may be required to maintain
forward flow from the ventricle and ensure aortic
valve opening.
Figure 5. TandemHeart
Withdrawal cannula across atrial septum
withdraws oxygenated blood from left atrium.
Blood is returned via femoral artery to provide
retrograde perfusion of aorta.
A further challenge of this form of circulatory support is limited understanding of the effects of retrograde
perfusion on systemic hemodynamics and end-organ perfusion.42 Continuous perfusion supplied by the
TandemHeart collides with pulsatile antegrade perfusion from the failing heart to produce a dynamic
watershed region within the aorta. The extent of this region and its effect on distal perfusion is not well
understood.
Extracorporeal membrane oxygenation (ECMO)

ECMO is an adaptation of the cardiopulmonary bypass circuit modified for extended use in the intensive
care unit. The modern ECMO circuit (Figure 6) consists of:43
• Vascular cannula and circuit tubing
• Mechanical pump
• Gas exchange device or oxygenator
When deployed as a percutaneous circulatory

support device, ECMO withdraws deoxygenated
venous blood and returns oxygenated blood to
the systemic arterial circulation. Most commonly,
a withdrawal cannula is inserted into the femoral
vein and advanced to the inferior vena caval-right
atrial junction with the return cannula placed into
the femoral artery and advanced to the iliac artery
or distal aorta to provide continuous retrograde
perfusion of the systemic circulation. This
cannulation approach is commonly referred to as
peripheral veno-arterial (VA) ECMO to differentiate
it from central cannulation strategies used post-
cardiotomy or venous-only approaches deployed
for lung support.44 The term ECMO will be used in
this chapter to refer specifically to the peripheral
veno-arterial cannulation strategy described above.
Figure 6. Peripheral Venoarterial ECMO

Withdrawal cannula inserted into femoral vein
and advanced to junction of inferior vena cava
and right atrium. Blood withdrawn, passed
through oxygenator, and returned via cannula to
femoral artery to provide retrograde perfusion of
aorta.
Physiologically, ECMO is similar to TandemHeart in that it increases afterload and has unpredictable effects
on myocardial oxygen consumption and myocardial blood flow.45,46 The oxygenator simplifies placement
of the withdrawal cannula, obviating the need for transeptal positioning and enabling entrainment of
deoxygenated blood into the circuit. Like the TandemHeart, ECMO produces continuous retrograde
perfusion of the distal aorta that collides with residual pulsatile perfusion from the native heart which
provides similar management challenges in the setting of profound LV failure.
Accumulating clinical evidence suggests that patients initiated on ECMO support experience better
outcomes when maintained on dual support with an IABP or Impella to augment LV unloading.47–49 While
the mechanism by which an IABP may improve LV unloading in the setting of continuous retrograde
perfusion is unclear, an Impella provides direct LV unloading and helps to reduce the risk of stasis while also
reducing myocardial metabolic demand. This dual ECMO and Impella strategy is referred to as ECpella™
support and is detailed in another chapter of this e-book.
From a management perspective, the titration of ECMO support varies depending on the indication for its
use.43 For biventricular failure or isolated LV failure, ECMO support is titrated to maintain adequate systemic
perfusion with the addition of a venting strategy if needed. In isolated RV failure, ECMO flow is titrated to
reduce RV preload with a goal to restore RV pulsatility and maintain cardiopulmonary circulation. This is of
particular importance in the setting of pulmonary embolism as ongoing forward blood flow through the
cardiopulmonary circulation is required for delivery of anticoagulants and to avoid the risk of clot extension.
Generally, cases of RV failure due to pulmonary embolism or pulmonary hypertension require less support
than patients with biventricular or LV failure.50
At present, there is limited evidence of a mortality benefit of ECMO in cardiogenic shock. A meta-analysis
of four studies using ECMO in acute myocardial infarction complicated by CS found a significant survival
benefit compared to IABP but not compared to other MCS strategies.51 Despite these limitations, the
increasing availability of ECMO and its ability to be rapidly deployed at the bedside by skilled practitioners
has led to its growing use as an MCS device.52
RV support devices
While the majority of patients presenting to cardiac intensive care units in cardiogenic shock suffer
from isolated LV dysfunction, 25% of patients have biventricular failure and 9% have isolated RV failure.53
Mechanisms of acute RV failure include: 26
• Myocardial infarction
• RV overload secondary to valvular disease
• Pressure overload secondary to left side heart failure
• Worsening pulmonary hypertension
• Acute pulmonary embolism
A small percentage of patients

develop right ventricular failure
because of isolated MCS to the LV.
Various metrics, such as the ratio
of the right atrial and pulmonary
capillary wedge pressures and the
pulmonary artery pulsatility index
(PAPi) have been validated as a means of identifying and predicting patients at risk of RV failure.
While early recognition of RV failure is an important component of successful treatment, it is only recently
that clinicians have access to dedicated MCS devices for isolated RV support. In addition to ECMO, clinicians
can deploy the Impella RP and the TandemHeart with a Protek Duo cannula, shown in Figure 7, to restore
perfusion in patients with RV failure. Whether used for isolated RV dysfunction or combined with left-sided
devices for biventricular support, these new devices give clinicians new options for providing mechanical
support.
Impella RP
Similar to the left-sided Impella support devices, the Impella RP is a continuous, non-pulsatile, microaxial
flow pump.54 The Impella RP is inserted into the femoral vein via a 23 Fr introducer and advanced
proximally through the venous circulation until the outlet is positioned in the main pulmonary artery with
the inlet residing in the inferior vena cava or right atrium. The device aspirates blood from the inlet and
ejects it directly into the pulmonary artery to achieve flow rates of 2 to 4 LPM while effectively bypassing
the failing RV.
The Impella RP functionally lowers RV filling

pressures and increase pulmonary artery pressures
while maintaining blood flow through the
cardiopulmonary circulation. Depending on the RV
functional state and titration of Impella RP support,
reduction in RV preload may result in increased RV
pulsatility or decreased pulsatility as the Impella
provides continuous perfusion with limited RV
generated forward flow.
While randomized control trials are lacking for RV-

related MCS devices, the Impella RP was studied
prospectively in the RECOVER RIGHT trial in 30
patients with medically refractory RV failure after
acute myocardial infarction or after cardiac surgery
and resulted in immediate increase in cardiac index
(CI) and decrease in CVP.54 Thirty-day mortality for
study patients was 26.7% but the study was not
designed or powered to look for mortality benefit of Figure 7. Impella RP and Protek Duo
the intervention.
(A) Impella RP ejects blood directly into
pulmonary artery bypassing failing RV.
(B) Protek Duo cannula with external centrifugal
pump propels blood into pulmonary artery to
perfuse cardiopulmonary circulation.
TandemHeart-Protek Duo
The Protek Duo is a double lumen cannula designed to be inserted via the right internal jugular vein and
advanced until the distal tip is positioned in the main pulmonary artery.55 The withdrawal lumen has inlets
that drain venous blood from the right atrium with the return lumen terminating at the distal tip of the
cannula. The cannula is manufactured in both 29 Fr and 31 Fr diameters and is capable of supporting flows
of 1 to 5 LPM. Circulatory support is provided by a centrifugal pump that withdraws blood from the right
atrium and propels it into the pulmonary artery to perfuse the cardiopulmonary circulation.
Similar to the Impella RP, extracorporeal support via the Protek Duo decreases RV preload and increases
RV afterload, which may have variable effects on RV function. The large cannula size may also distort the
RV outflow tract and impair pulmonic valve function. As an extracorporeal pump, this form of support can
be adapted to accommodate an inline oxygenator to provide lung support in the setting of concomitant
pulmonary disease.
There are no prospective randomized trials for Tandem-Heart in RV failure. Kapur and colleagues
performed a retrospective analysis of 46 patients with RV failure maintained with TandemHeart support
across 8 centers in the THRIVE registry in 2013.56 The study found that the use of TandemHeart was
associated with increased MAP, decreased right atrial pressure, and increased cardiac index. Hospital
mortality was 57% in this population, indicative of the severity of illness in patients with severe RV failure
requiring mechanical support, but the study was not designed or powered for comparative analysis to
medical therapy or other MCS options.
Table 2. MCS Summary Table
IMPELLA 2.5
ECMO TANDEMHEART
IMPELLA CP
IABP TANDEMHEART (PERIPHERAL IMPELLA RP WITH
IMPELLA 5.0
V-A ECMO) PROTEK DUO
IMPELLA 5.5
Mechanism Counterpulsatile Microaxial Vascular Vascular cannula, Microaxial Double lumen
balloon in aorta pump produces cannula and circuit tubing, pump produces cannula with
inflates during continuous, extracorporeal mechanical continuous, non- centrifugal pump
diastole and non-pulsatile centrifugal pump, and gas pulsatile flow withdraws blood
deflates during antegrade flow pump provide exchange device from inferior IVC from the RA and
systole from LV to aorta retrograde or oxygenator or RA to PA propels it into
systemic provide the PA to perfuse
perfusion from LA continuous cardiopulmonary
to aorta retrograde circulation
perfusion
of systemic
circulation
Effects Augments Augments Reduces LV filling Increases Lowers RV filling Decreases RV

coronary systemic afterload pressures preload
perfusion perfusion Reduces LV
distension Reduces preload Increases PA Increases RV
Reduces afterload Decreases LVEDP in isolated RV pressures while afterload
and LVEDV Improves failure maintaining
Facilitates indirect coronary blood blood flow
LV unloading Reduces flow Unpredictable through the
myocardial effects on cardiopulmonary
oxygen myocardial circulation
consumption oxygen
consumption and Decreases RV
Directly unloads myocardial blood preload
the ventricle flow
Increases RV
afterload
Insertion Femoral artery Femoral artery Femoral vein Femoral vein Femoral vein Internal jugular
vein
Axillary artery Axillary artery Femoral artery Femoral artery
Cannula size 7-8 Fr arterial 13-21 Fr arterial 21 Fr withdrawal 14-19 Fr arterial 22 Fr venous 29 Fr and 31 Fr
cannula cannulas
17-21 Fr venous
15-17 Fr return
cannula
Flow 0.5-1 L/min 2.5-5.5 L/min Up to 4 L/min Up to 7 L/min 2-4 L/min 1-5 L/min
Additional No mortality During profound Does not directly Watershed RECOVER Retrospective
Notes benefit for failure, may unload the LV challenges where RIGHT trial analysis by
cardiogenic shock improve cardiac continuous demonstrated Kapur et al.
compared to function and Retrograde retrograde that Impella RP demonstrated
medical therapy increase heart- perfusion has perfusion of distal increases cardiac that Tandem
in RCTs produced forward variable effects on aorta collides with index (CI) and Heart increases
flow through LV left heart function residual pulsatile decreases CVP MAP, decreases
unloading Risk of perfusion from in medically RA pressure, and
intraventricular native heart refractory RV increases CI in RV
stasis and failure after AMI failure
Limited evidence or cardiac surgery
thrombus of mortality
formation benefit of ECMO
Continuous in cardiogenic
perfusion collides shock
with pulsatile Patients
antegrade experience better
perfusion from outcomes with
failing heart to dual support
produce dynamic of ECMO with
watershed either IABP or
region in aorta; Impella (ECpella
effect on distal discussed in
perfusion not well Chapter 13)
understood
Risks of MCS and patient selection

Mechanical circulatory support can restore systemic perfusion and maintain end-organ function, but it is
not without significant risk. Large bore vascular access carries the risk of life-threatening hemorrhage and
vessel injury. Common complications across platforms include: 57–59
• Hemolysis
• Thrombocytopenia
• Limb ischemia
• Device migration
• Thrombosis
Efforts to mitigate these risks, such as use of systemic anticoagulation, carry their own risks and may
exacerbate underlying pathology and limit MCS use in patients unable to tolerate anticoagulation. All
MCS devices expose patients to non-biological materials while extracorporeal circuits expose substantial
blood flow to vascular tubing and centrifugal pumps. Blood contact with extracorporeal circuits is
known to activate platelets and leukocytes and increase circulating levels of inflammatory mediators.60
Activated platelets promote coagulation while simultaneously becoming less capable of further activation.
Combined with use of systemic anticoagulation, this translates into significant bleeding risk for patients
maintained on extracorporeal support.
Weighing the potential risks of mechanical support against the anticipated benefits for a specific patient
is a considerable challenge. A further complexity is predicting the likelihood of a positive outcome. Various
clinical scoring systems have been proposed to help clinicians identify patients at risk for poor outcomes.61
At present, these systems generally identify patients with increased severity of disease at higher risk of poor
outcome, who unfortunately, are the patients most in need of circulatory support and at risk of imminent
demise without such therapy.
The threshold for initiation of MCS is currently unknown. As detailed in this chapter, there is a physiological
basis for early initiation of mechanical support in cardiogenic shock. However, the associated risks of MCS
lead to a preferential use of medical therapy as a first line approach to be re-evaluated in the setting of
persistent shock.62 The duration of observation and severity of shock prior to MCS is uncertain and requires
ongoing investigation. A major challenge with the study of MCS is that device initiation and management
remain complex and experience dependent, which biases clinical trial results and complicates study
design.
Ultimately, multiple factors must be considered prior to initiation of mechanical support, including:
• Patient age
• Comorbidities
• Goals of support
• Cost of therapy
• Availability of support devices
Given that many patients present with limited warning and minimal time for detailed evaluation and lack
of access to complete medical records, erring on the side of initiating support to provide a window for more
consideration is often reasonable.
Summary
Cardiogenic shock remains a highly morbid disease despite advances in mechanical circulatory support.
While there is biologic plausibility that early utilization of MCS may be beneficial in patients in refractory
cardiogenic shock, available evidence for or against MCS use is observational and randomized trials have
been underpowered for meaningful clinical endpoints. Future research is needed to help identify the
right device for the right patient at the right time. Until these data emerge, careful consideration must be
weighed on a patient-by-patient basis prior to the initiation of mechanical support.
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TABLE OF PART I Overview and Hemodynamics in Mechanical
CONTENTS
Circulatory Support
Hemodynamic
CHAPTER
2 Assessment:
Use of Right Heart
Catheterization
Charles Hunley, MD Craig S. Smith, MD
Critical Care Director Assistant Professor of Medicine,
Orlando Regional Medical Center University of Massachusetts
Orlando Health Medical Director, Cardiac Intensive Care
86 W Underwood Suite 101
Orlando, FL 32726 Interventional Cardiologist
Charles.hunley@orlandohealth.com 55 Lake Ave North
Worcester, MA 01655
Craig.smith@umassmemorial.org
INTRODUCTION
Since the ESCAPE trial in 2005, right heart catheterization and hemodynamic
monitoring have been controversial in the management of critically ill patients
in whom rapid diagnosis, initiation of therapy, and management of volume
status are of paramount importance to improving survival. Over the last several
decades, advances in noninvasive imaging and the predictive accuracy of
laboratory biomarkers have contributed to a decline in the utilization of invasive
hemodynamic data in the treatment of ICU patients. A number of studies in
the late 1990s and early 2000s, both observational and randomized, failed to
show survival benefit associated with the routine use of invasive hemodynamic
assessment via pulmonary artery catheters (PACs) across medical and surgical
ICU patient populations. As a result, the use of invasive hemodynamic data has
fallen out of favor in modern critical care practice.1 However, many previous trials
have excluded or underrepresented patients with cardiogenic shock associated
with acute myocardial infarction, or those patients considered for ventricular
assist devices.
This chapter presents what we believe is the essential need to reexamine the use
of invasive hemodynamic assessment in patients with cardiogenic shock.
<< Chapter 1 Chapter 2 | Hemodynamic Assessment: Use of Right Heart Catheterization Chapter 3 >>
The evidence for PAC use today

While still a Class I indication in professional guidelines for use in decompensated heart failure with
indeterminate volume status or refractory cardiogenic shock,2 a recent registry of cardiogenic shock
patients found that PACs were used in fewer than 30% of patients who received percutaneous ventricular
assist devices (pVADs) despite studies showing a mortality benefit associated with their use in this
population.3 Invasive hemodynamics assessment with PACs has been associated with improved survival in
patients with acute heart failure syndromes with persistent hypotension as well as AMICS patients treated
with pVADs.4,5
Along with the expanding options for biventricular support and reduction in morbidity associated
with ventricular assist devices (surgical and percutaneous), the last decade has brought an increased
understanding of the essential role of right heart catheterization data in the treatment of cardiogenic
shock. Since the advent of the PAC in 1970, PAC-obtained continuous measured variables such as filling
pressures, resistances, and cardiac output have been associated with changes in therapy with prognostic
importance.6
The overall goal of hemodynamic monitoring is to modify hemodynamic parameters to ensure adequate
perfusion. While early shock trials failed to show mortality benefit based on these directly measured
parameters, our understanding of shock as a systemic circulatory and metabolic derangement has been
refined in recent years. We now understand that derived measures of cardiac work can help provide
superior clinical outcomes.
Derived measures of cardiac work include:

• Cardiac power output (CPO)
• Stroke work indexes
• Right ventricular work (PAPi)
These derived measures can be used to determine:6,7

• Timing and nature (left, right, or biventricular) of support required
• Appropriate triggers for escalating support
• Device and inotrope/vasopressor weaning strategies
While large prospective studies for the routine use of PACs in the era of mechanical support are still
required, data from device manufacturers’ databases and several patient registries suggest significant
mortality benefit to invasive data-driven clinical decisions regarding management of cardiogenic shock,
and the essential need for invasive hemodynamic assessment in the modern treatment of patients with
cardiogenic shock.8
PAC insertion and maintenance

Pulmonary artery catheter insertion can be performed in the OR, cardiac catheterization lab, or at the
bedside, although accessibility of fluoroscopy is required for femoral or antecubital approaches. For ICU
insertion, prior preparation with appropriate equipment and personnel present is vital, as average insertion
time at the bedside approaches 2 hours.9
PACs may be inserted into the right or left internal jugular veins or the subclavian, femoral, or antecubital
(basilic or brachial) veins.
• Antecubital insertion should be limited to temporary use in the cath lab and generally avoided for
long-term use due to risk of migration with arm movement and elevated risk of infection after 72
hours.
• Femoral insertion is most common in emergent cath lab procedures; however, the PAC should be
relocated for longer term monitoring in an ICU setting.
• Subclavian (left) insertion should be avoided for OR cases if possible due to the possibility of kinking
during sternotomy and subsequent difficulty with removal.
• Internal jugular insertion (R>L) is preferred for ease of placement and lower risk of infection, and this
approach allows ambulation in more stable patients.
When feasible, a proximal and distal TwistLock™ Cath-Gard® should be utilized to prevent catheter
migration or inadvertent removal through the sheath during an ICU stay. This also allows for safe
ambulation in patients on long-term mechanical circulatory support. These require a 7.5 Fr or 8 Fr PAC for
locking. With or without a lockable guard, the position of the catheter should be noted and documented
prior to transport and at the beginning of each nursing shift.
Figure 1.
Proximal and Distal
TwistLock Cath-Gard
Lockable guards secure the
PAC to prevent it from slipping
or being pulled through the
plastic sheath
Twist to lock/unlock
I = Locked
O = Open
The following should be available during the insertion and placement of PACs:
• A code cart, as insertion can cause ventricular arrhythmias or heart block in up to 5% of patients.10
A patient with a left bundle branch block (LBBB) may develop complete heart block (CHB) when the
right bundle branch is traumatized by the PAC.
• A mode of temporary pacing, such as a PAC with a pacing port.
• Ultrasound guidance for access is strongly recommended and position can be confirmed by pressure
transduction prior to dilator sheath, or stat blood gas or hematocrit (HCT) if needed.
Like all central access, sterile technique is mandated for the insertion of a PAC and wide skin preparation
to the nipple line should be performed for jugular and subclavian access. Most introducer sheaths are
8-8.5 Fr and dermotomy may be required. Smaller sheaths (5-6 Fr) with smaller caliber non-lockable PACs
may be used but are not recommended for ICU care due to migration potential and more variability in
thermodilution-derived cardiac output measures.
Nursing preparation for PAC insertion

Prior to insertion, the transducer tubing should be flushed along with all ports of the PAC catheter. The
catheter must be zeroed to atmospheric pressure and referenced, or leveled, to ensure accurate readings.
Leveling negates the effects of the weight of the tubing and the fluid column on pressure measurements.
It is essential to level the transducer with changes in patient position to ensure accurate data from which
clinical decisions are derived.
Both zeroing and leveling are typically performed with the patient in the supine position (or 30 degrees
recumbent if the patient cannot lay flat) prior to insertion. Zeroing entails opening the system to air to
establish atmospheric pressure as zero. The zeroing stopcock is then leveled to the phlebostatic axis, which
is the intersection of the 4th intercostal space and mid-axillary line and approximates the location of the
right atrium. Zeroing and leveling should be performed at least once each shift.
Transducer function and calibration

Transducer function can be confirmed by placing the PAC at heart level outside the body to confirm
0 mmHg reading and raising the catheter up and down to assess changes in pressure. After catheter
placement in the body, the dynamic response of the system can be determined. Open and close the valve
in the continuous flush port to perform a “flash flush” test. Proper damping (Figure 2) is important for
accurate measures for both hemodynamic-based insertion and for clinical decision making.
A B
C Figure 2. Determining Proper Damping

A. Normal
1-2 bounces
≤ 1 block between bounces
2nd bounce should be ≤ 1/3 amplitude of 1st bounce
B. Underdamping
Too many bounces and too many boxes in between. 2nd
bounce too high
Pressures will be overestimated
Confirm no air, leaks, loose connections, and pressure
bag is at 300 mmHg
C. Overdamping
Absent boxes
Pressure will be underestimated
Confirm no air, blood, or clots
PAC advancement
1. Prior to insertion of the PAC, test balloon inflation outside the body.
2. When past the sheath, inflate the balloon fully (1-1.5 cc) to reduce vascular injury.
3. If using a continuous cardiac output PAC with SVO2, calibration should be done to accurately reflect
oxygen consumption.
4. When floating the catheter at the bedside, communication is vital, and the distance of insertion should
be called out by the operator based on the catheter markings.
5. As most ICU-placed PACs are inserted through the internal jugular (IJ) and subclavian locations,
the right atrium is typically reached by 20 cm, with each subsequent chamber occurring in 10 cm
increments. Failure to reach a transition after 15 cm of advancement raises the possibility of coiling.
6. The right ventricular outflow tract (RVOT) is located anteromedially and caudal to the tricuspid valve, so
a gentle clockwise rotation may aid in floatation to the PA.
7. The catheter should never be left in the RV for any length of time (particularly with the balloon deflated)
due to concern for catheter-induced VT or heart block.
8. Always deflate the balloon with removal to reduce vascular injury.
Figure 3.
Advancing the PAC
RA typically reached at
20 cm
Transition to RV noted
by rise in systolic
pressure
Transition to PA noted
by rise in diastolic
pressure
If at >40 cm without PA
tracing, pull a balloon
deflated to 20 cm and
reattempt
Transition to PCWP
noted by decrease in
systolic pressure
Pulmonary artery catheter setup and insertion videos are available online.
For example: https://youtu.be/dT_ul3nvB3o
If you encounter difficulty getting the PAC past the tricuspid valve, place the patient’s head down to
aid the transition. Persistent left superior vena cava (SVC) (<1%), absent right SVC, or coronary sinus-LA
communications may bedevil normal pressure wave transitions. Oxygen saturations can help differentiate
right and left atrial tracings (in case of communications) and differentiate PA tracings from pulmonary
capillary wedge pressure (PCWP) with large V waves from severe mitral regurgitation. Transition to the
PA may be aided by placing the catheter in cold saline prior to floatation to help increase the rigidity of
the primary curve of the catheter. Repeated unsuccessful attempts to obtain PA tracings should prompt
reevaluation for placement with fluoroscopic guidance.
Once PCWP is obtained, comparison with PA diastolic (PAD) pressure should be made to assess if PAD
may be used as a surrogate in lieu of frequent PCWP advancement in prolonged ICU stays (within 4
mmHg). The presence of intrinsic lung vascular disease may mean PAD does not equate to PCWP. If less
than 1 cc of air is needed for obtaining PCWP tracing, the catheter is likely advanced too far and may lead
to vessel rupture. Withdraw the catheter 1 cm and reattempt PCWP. After final position is confirmed,
perform a stat chest x-ray (CXR).
Correct catheter position is in zone 3 of the lung. If lockable guard catheters are not used, a daily CXR
should confirm position. Any catheter with the appearance of a PCWP tracing at the bedside should be
pulled back with balloon deflated to avoid pulmonary infarction.
Complications
In addition to general complications of central venous access (eg, hemorrhage, pneumothorax, infection),
there are specific complications that arise from the intracardiac nature of the RHC. Due to the limited
use of PACs in current practice, the most common complication is data misinterpretation. All staff must
be trained in the use of the PAC with specific emphasis given to the importance of leveling, adequate
placement in the zone of the lung, and careful measurement technique. Table 1 presents some of the
complications that may arise, causes of each, and recommended interventions.
Table 1. PAC Troubleshooting Guide

PROBLEM CAUSE INTERVENTION
Deflated balloon becomes Coil of catheter straightens as the Physician or advanced practice provider
wedged catheter warms in the body causing (APP) needs to pull back the catheter
the catheter to “lengthen” and progress until “un-wedged”
further into the pulmonary system Re-secure and document new (cm)
markings
Confirm with CXR
Atrial and ventricular irritability Catheter stimulates the myocardium Physician/APP needs to reposition the
seen on insertion and during catheter
ongoing use Re-secure and document new (cm)
markings
Confirm with CXR
PA balloon rupture, noted by: Balloon may be damaged by: Cap the balloon port after removing the
Inability to wedge Over-inflation syringe and clearly label the port so other
clinicians will not use the port
Blood aspirated from the Frequent inflations
balloon port Use of syringe to deflate the balloon
PA tip migrating into the RV Cath guard unlocked; PAC pulled Physician/APP needs to reposition the
catheter or it could rupture the ventricle
wall or irritate the ventricle causing VT
PA tip migrating to the RA Cath guard unlocked; PAC pulled Notify physician/APP to reposition
Relocate infusions; infusions in the CVP
port will cause fluid in the PAC protective
sleeve
Pulmonary infarction, rupture Wedging of the catheter while in wedge; Physician/APP must remove PAC, which
(50%-75% mortality) keeping the catheter in wedge for a may require:
prolonged period of time Double-lumen endotracheal tube (DLT) to
Hypoxia secondary to bleeding
Can be thrombosis related to the catheter prevent embolization
Signs/symptoms:
Thoracotomy with hematoma evacuation,
Hemoptysis or
Cough Extracorporeal life support (ECLS) for
Dyspnea ventilation
Chest pain
Knotting seen on CXR or Knots most often occur with looping Physician/APP strongly recommended
resistance felt with removal/ of the catheter during placement with to reposition/remove PAC under imaging
withdrawal of catheter significantly greater distance noted on guidance.
the catheter relative to the pressure Knots may be stiffened allowing for easier
tracing removal with a wire or injection of cold
saline
Measurement parameters
Invasive hemodynamic assessment (PAC) provides an important adjunct in the diagnosis and continuous
evaluation of a patient with cardiogenic shock. This technique allows bedside direct and indirect
measurement of cardiac performance (ie, preload, afterload, and CO). There is relatively little data on
decisions and use of hemodynamic monitoring with cardiogenic shock, however, PACs can supply data to
assist diagnosis by showing cardiac index (CI) ≤2.2 L/min/m2 and a PCWP ≥18 mmHg with end organ failure
and support clinical decision making for initiation and titration of therapies.
Right heart catheterization also offers information regarding volume status, right heart filling pressures,
and pulmonary resistance as well as determinants of adequate oxygen delivery using CVP and SVO2. This
information can guide choices and decisions regarding initiation and titration of volume optimization,
vasodilators, vasopressors, and inotropes as well as decisions regarding whether to provide mechanical
circulatory support.
PACs are critical for the proper selection, timing, and settings of medical and mechanical support and
medical therapies in cardiogenic shock. Monitoring hemodynamic changes throughout the course of
cardiogenic shock treatment has shown prognostic importance, allowing timely escalation and de-
escalation of therapy.
The presence of RV dysfunction in AMI increases the risk of cardiogenic shock and death.11 Pulmonary
artery pulsatility index (PAPi) is a measurement that helps predict severe RV dysfunction during acute
inferior wall myocardial infarction. Many protocols use CPO and PAPi to continuously monitor therapy for
the need to escalate and deescalate.
• A PAPi <0.9 is highly specific and highly sensitive in identifying RV dysfunction, aiding clinicians in
escalating and weaning therapy.
• PAPi >0.9 and CPO >0.6 can help determine therapy course and the need to escalate and deescalate.
Utilizing advance hemodynamic monitoring to diagnose and titrate therapy in cardiogenic shock can aid
patient outcomes.
Table 2. Hemodynamic Parameters and Formulas for Assessing RV Function (adapted from Kapur et al.12)
HEMODYNAMIC PARAMETER FORMULA VALUES
• Cardiac filling pressure = RAP / PCWP • >0.63 (RVF after LVAD)13
• >0.86 (RVF in AMI)16
• Diastolic pulmonary gradient = PADP-PCWP • Undetermined19,20
• PA compliance = SV / (PASP-PADP) • <2.5 (RVF in chronic heart failure)22
• PA elastance = PASP/SV • Undetermined23
• PA pulsatility index (PAPi) = (PASP-PADP) / RAP • <1.85 (RVF after LVAD)17
• <1.0 (RVF in AMI)18
• Pulmonary vascular resistance (PVR) = mPAP-PCWP/ • >3.6 (RVF after LVAD)15
CO
• RV stroke work = (mPAP-RAP) x SV x 0.0136 • <15 (RVF after LVAD)14
• <10 (RVF after AMI)21
• RV stroke work index = (mPAP-RAP) / SV index • <0.3-0.6 (RVF after LVAD)13,17
• Transpulmonary gradient = mPAP-PCWP • Undetermined19
AMI=acute myocardial infarction; CO=cardiac output; LVAD=left ventricular assistance device; mPAP=mean pulmonary artery pressure;
PA=pulmonary artery; PADP=pulmonary artery diastolic pressure; PASP=pulmonary artery systolic pressure;
PCWP=pulmonary capillary wedge pressure; RAP=right atrial pressure; RVF=right ventricular failure; SV=stroke volume
Post-insertion and removal

Like all central access, PACs should be left in only for as long as indicated. Check the site daily with sterile
dressing changes. The PAC may be removed as a separate procedure from introducer removal.
• When removing the catheter from the jugular or subclavian access points, remove during exhalation
to prevent air embolism (or inspiration in a mechanically vented patient).
• To avoid knotting or entanglement in cardiac structures and/or devices, do not withdraw the catheter
if you encounter resistance.
• If the PAC is difficult to remove, consult with interventional cardiology.
• Remove PACs before patients undergo MRI scans to avoid the possibility of migration as well as the
risk of heating and deforming the copper thermistor at the distal tip of most PACs.
Summary
Data suggesting significant mortality benefit associated with the use of PACs in the era of mechanical
circulatory support point to the essential need for invasive hemodynamic assessment when treating
patients with cardiogenic shock. Derived measures of cardiac work—CPO, stroke work indexes, and PAPi—
help provide superior clinical outcomes in these patients. Thus, it is important for today’s clinicians to
understand concepts such as PAC insertion, advancement, and removal as well as how to troubleshoot
potential PAC complications.
References
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heart failure: The task force for the diagnosis and treatment of acute and chronic heart failure of the European
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ESC. Eur Heart J. 2016;37(27):2129-2200. Doi:10.1002/ejhf.592.
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8. Impella® Quality Assurance Program: Importance of Treatment Protocols to Improve Patient Survival and Heart
Recovery. https://www.protectedpci.com/impella-quality-assurance-program-importance-treatment-protocols-
improve-patient-survival-heart-recovery. March 21, 2017. Accessed June 23, 2020.
9. Lefrant JY, Muller L, Bruelle P, et al. Insertion time of the pulmonary artery catheter in critically ill patients. Crit Care
Med. 2000;28(2):355-9.
10. Sprung CL, Pozen RG, Rozanski JJ, et al. Advanced ventricular arrhythmias during bedside pulmonary artery
catheterization. Am J Med. 1982;72(2):203-8.
11. Mehta SR, Eikelboom JW, Natarajan MK, et al. Impact of right ventricular involvement on mortality and morbidity
in patients with inferior myocardial infarction. J Am Coll Cardiol. 2001;37(1):37-43.
Circulation. 2017;136(3):314-26.
13. Kormos RL, Teuteberg JJ, Pagani FD, et al. HeartMate II Clinical Investigators. Right ventricular failure in patients
with the HeartMate II continuous-flow left ventricular assist device: incidence, risk factors, and effect on outcomes.
J Thorac Cardiovasc Surg. 2010; 139(5):1316-24. doi: 10.1016/j.jtcvs.2009.11.020.
14. Drakos SG, Janicki L, Horne BD, et al. Risk factors predictive of right ventricular failure after left ventricular assist
device implantation. Am J Cardiol. 2010; 105(7):1030-35. doi: 10.1016/j.amjcard.2009.11.026.
15. Sheehan F, Redington A. The right ventricle: anatomy, physiology and clinical imaging. Heart. 2008; 94(11):1510-15.
doi: 10.1136/hrt.2007.132779.
16. Lopez-Sendon J, Coma-Canella I, Gamallo C. Sensitivity and specificity of hemodynamic criteria in the diagnosis of
acute right ventricular infarction. Circulation. 1981; 64(3):515-25.
17. Morine KJ, Kiernan MS, Pham DT, et al. Pulmonary artery pulsatility index is associated with right ventricular failure
after left ventricular assist device surgery. J Card Fail. 2016; 22(2):110-6. doi: 10.1016/j.cardfail.2015.10.019.
ventricular dysfunction in acute inferior myocardial infarction. Catheter Cardiovasc Interv. 2012; 80(4):593–600. doi:
10.1002/ccd.23309.
19. Aschauer S, Kammerlander AA, Zotter-Tufaro C, et al. The right heart in heart failure with preserved ejection
fraction: insights from cardiac magnetic resonance imaging and invasive haemodynamics. Eur J Heart Fail. 2016;
18(1):71–80. doi: 10.1002/ejhf.418.
20. Handoko ML, De Man FS, Oosterveer FP, et al. A critical appraisal of transpulmonary and diastolic pressure
gradients. Physiol Rep. 2016; 4(17):e12910.
21. Pouleur H, Lefevre J, van Eyll C, et al. Significance of pulmonary input impedance in right ventricular performance.
Cardiovasc Res. 1978; 12(10):617-29.
22. Dupont M, Mullens W, Skouri HN, et al. Prognostic role of pulmonary arterial capacitance in advanced heart failure.
Circ Heart Fail. 2012; 5(6):778-85. doi: 10.1161/CIRCHEARTFAILURE.112.968511.
23. Amin A, Taghavi S, Esmaeilzadeh M, et al. Pulmonary arterial elastance for estimating right ventricular afterload in
systolic heart failure. Congest Heart Fail. 2011; 17(6):288-93. doi: 10.1111/j.1751-7133.2011.00222.x.
PART II
TABLE OF
CONTENTS
Support with Impella ®
Devices: Insertion,
Management, and Removal
Chapter 3 Femoral Access and Management.......................................... 37
Chapter 4 Axillary Artery Access and Management..............................52
Chapter 5 Percutaneous Ventricular Assist Device Console

Management................................................................................... 57
Chapter 6 Team-based Care........................................................................... 62
Chapter 7 Anticoagulation............................................................................. 69
Chapter 8 Blood Compatibility/Hemolysis................................................ 76
Chapter 9 Weaning of Impella....................................................................... 81
Chapter 10 Impella Removal and Closure................................................... 86
TABLE OF PART II Mechanical Circulatory Support with Impella® Devices:
CONTENTS
Insertion, Management, and Removal
Femoral
CHAPTER
3 Access and
Management
Craig S. Smith, MD
Assistant Professor of Medicine,
University of Massachusetts
Medical Director, Cardiac Intensive Care
Interventional Cardiologist
Craig.smith@umassmemorial.org
INTRODUCTION
Percutaneous mechanical circulatory support (MCS) devices have continued to
evolve since the advent of the intra-aortic balloon pump in the 1960s allowing
for a dramatic decrease in the mortality and morbidity of patients presenting
with cardiogenic shock, undergoing high-risk coronary revascularization or
catheter ablation, and those in need of a bridge to transplantation. Increases
in hemodynamic support with MCS over time have been accompanied by
reductions in device caliber and improvements in anticoagulation regimens
and timing of device implantation. While this has translated into improved
outcomes in patients with MCS, complications are still prevalent and have
occurred at rates of 3-33% in registry data and single-center studies but appear
to be decreasing over time.8 As these devices involve the use of large bore
arterial sheaths (ECMO and TandemHeart 15-20 Fr, Impella devices 13-14 Fr),
vascular complications are foremost amongst the complications with MCS
and are associated with a significantly higher in-hospital mortality, and a near-
doubling of length of stay and cost of hospitalization.5
As access to MCS devices has become ubiquitous in cardiac catheterization

laboratories, careful access site selection, sheath insertion technique,
maintenance of distal extremity perfusion, and complication management
post procedure are key factors in differentiating high from low performing
medical centers treating the MCS patient population. This chapter discusses
femoral access and management. Axillary access is discussed in another
chapter.
<< Chapter 2 Chapter 3 | Femoral Access and Management Chapter 4 >>
Table 1. Arterial Cannula Size and Minimum Vessel Diameter of Common MCS Devices
DEVICE DEVICE SYSTEM SIZE REFERENCE ARTERY DIAMETER

IABP • 8 Fr (7 Fr sheathless) • ≥3 mm
Impella 2.5® • 13 Fr • ≥5 mm
Impella CP® • 14 Fr • ≥5 mm
TandemHeart • 21 Fr venous/ 15-19 Fr arterial • ≥5.4 mm
ECMO • 15-20 Fr • ≥5.4 mm
Access site selection

Large bore (>8 Fr) vascular access, once mandating the need for surgical cutdown, is now largely
performed percutaneously. With adequate anatomy, the femoral arterial access approach remains the
most common and is associated with less comorbidity15 in the placement of MCS devices. Alternative
access sites including axillary, subclavian, transcaval, and transapical have become increasingly utilized
as MCS device therapy has been offered to a patient population that is more elderly and with greater
prevalence of peripheral vascular disease (PVD). In addition to PVD, smaller body habitus and tortuosity
increase the risk of procedural complications and may mandate the use of alternative access sites or distal
limb reperfusion techniques.
Table 2. Clinical Factors Associated with Vascular Complications

PATIENT FACTORS PROCEDURE FACTORS POST-PROCEDURE MEDICAL CARE FACTORS
• Age >65 • Large bore sheath (>8 Fr) • IIb/IIIa receptor antagonists
• Female gender • Suboptimal puncture site (above • Heparin anticoagulation
• BMI (low or high) inguinal ligament, below femoral • Coagulopathy
bifurcation)
• PVD or small caliber common • Post procedure hypertension
femoral/iliac arteries (<5.5 cm) • Puncture without guidance
(ultrasound or Doppler) • Prolonged high dose vasopressors
• Emergent case: AMI, shock • Supratherapeutic anticoagulation
• Ipsilateral venous sheath
• Chronic kidney disease
• No prior vascular imaging
For patients in which large bore access for MCS is planned, the iliofemoral anatomy is often known. If
the anatomy is unknown, it is essential to review prior angiograms, CTA/MRAs, and medical records for
prior vascular procedures and complications. Pre-procedure imaging can significantly reduce morbidity
associated with the procedure and help ensure that the MCS sheath to artery ratio is <1.05 to minimize
distal leg ischemia and vessel injury. Table 3 lists recommended pre-procedure screening modalities to
assess the feasibility of femoral access for MCS.
Table 3. Imaging Modalities for Large bore Vascular Access (adapted from Cohen et al.16)
IMAGING MODALITY ADVANTAGES DISADVANTAGES
Angiography • May display stenosis, • Requires contrast in most laboratories
calcification, tortuosity at • 2-dimensional resolution may not adequately assess
arteriotomy and proximal calcium, tortuosity, stenosis
vasculature
• Verifies needle and/or sheath
placement
Ultrasound • Quick, real-time • Limited resolution
• Inexpensive • Does not prevent high arteriotomies
• No radiation exposure • No assessment of aorto-iliac vasculature
CT • Improved resolution • Additional radiation
• Assesses aorto-iliac • Increased cost
vasculature, aortic atheromas, • Requires stable and cooperative patient
and alternative access
• Contrast may be required
MRI • Resolution • Time-consuming
• No radiation exposure • Expensive
• Patient tolerance variable
• Inadequate calcium evaluation
• Contrast may be required
• Contraindicated for many with metallic foreign bodies
Due to hemodynamic instability or inability to safely transport the patient (eg, preexisting ECMO with need
for retrograde LV decompression), large bore access occasionally needs to be performed at the bedside
and may be achieved percutaneously or by surgical cutdown. As with fluoroscopic-guided procedures,
bedside ultrasound is recommended for femoral access with the use of a micropuncture catheter and
confirmation of placement via ultrasound, pressure transduction, or oxygen saturation. Transesophageal
echocardiography has been used to safely place MCS devices at the bedside in ICUs as reported in
several small registries and retrospective single center reports.10,11 In most cases, iliofemoral anatomy
in these patients has been known, and vascular complication rates are on par with standard-of-care
fluoroscopic guidance access. Increased rates of death, renal replacement therapy, lactate, and duration
of support are likely reflective of the increased acuity of these patients unable to be moved from the ICU.11
Echocardiographic views of the ascending aorta and arch (see Figure 1) are crucial for wire advancement
across the aortic valve with retrograde support devices such Impella. A long-axis mid esophageal view is
best for ECMO cannula placement or for confirmation of Impella positioning.
Left atrium
Aorta
Figure 1. Transesophageal Echo of

Ascending Aorta and Arch
Right
ventricle
Left
ventricle
Femoral access techniques

While bedside cannulation and access is feasible, fluoroscopic-based placement is recommended.
Combining fluoroscopic, anatomic, and ultrasound is the most reliable and safe practice for femoral access.
When assessing adequacy for femoral approach, femoral diameter must be measured without the
incorporation of calcifications. A ≥5.5 mm vessel without severe tortuosity predicts higher access success
rates, whereas a diameter of <5 mm precludes use of >10 Fr systems. If CT assessment is not available, IVUS
and bedside ultrasounds may be used to quantitate femoral access diameter. A micropuncture sheath
should be used initially, and an ipsilateral 30° angiogram obtained to confirm correct anatomic placement
prior to dilation and sheath upsizing.
The use of a “pre-close” technique for large bore access is typically recommended for short-term MCS
such as high-risk percutaneous coronary or structural interventions. In the context of emergent/urgent
placement of MCS devices, Perclose is not recommended due to the possibility of infection for prolonged
support in an ICU.
Once femoral access is obtained, a 5 Fr antegrade perfusion catheter should be placed in the ipsilateral
leg prior to sheath upsizing if compromise of the distal perfusion is suspected based on pre-procedure
vascular assessment (Figure 2). If vascular compromise is not suspected, then distal perfusion should be
assessed prior to leaving the procedural area after MCS placement as described below.
Figure 2. Antegrade Perfusion Catheter
Perfusion strategies for distal ischemia due to MCS

devices
Registry data from MCS trials have shown vascular complication rates ranging from 3-33% with more
recent data between 10-15%.5,8 The vast majority of these complications are distal vessel ischemia, bleeding,
and embolization. To ensure successful MCS device support in the ICU post procedure, it is essential to
ensure the following:
• Careful access
• Appropriate intraprocedural anticoagulation
• Adequate distal perfusion
An iliofemoral angiogram post MCS support in emergent cases is required to ensure distal perfusion (in
addition to documentation of distal pulses and/or oxygenation saturation by nursing staff). As a distal
extremity can tolerate up to 30 minutes of ischemia, high dose vasopressors required for pre-support
stabilization may be reduced and medical optimization with adjustments to antiarrhythmic therapy
and pacing performed in the procedural room prior to reassessment. Iliofemoral angiography can be
performed antegrade from an upper extremity access site, from contralateral femoral access, or via the
MCS access point if Impella devices are used. The latter is feasible due to the 14 Fr introducer sheath and
9 Fr shaft of the MCS device. A one-way valve in the introducer sheath allows for simultaneous access
with micropuncture and placement of up to a 6 Fr catheter (Figure 3). If available, digital subtraction
angiography with or without CO2-angiography is preferred for superior differentiation of vessel patency,
access vessel extravasation, and contrast minimalization (CO2).
If distal perfusion is deemed

inadequate by angiography or clinical
exam, several antegrade perfusion
strategies are available to reduce
sequalae from distal ischemia as
shown in Figures 4 through 7.
Figure 3. Single Access for High-risk PCI (SHiP) Technique
External contralateral circuit

• Establish a 5 Fr antegrade sheath in the
ipsilateral side of the MCS device.
• Place a 6-7 Fr sheath retrograde on the
contralateral side; use a male-to-male adaptor
to establish a femoral-femoral bypass circuit.
• ACT should be run higher than some MCS
device suggestions. Recommended ACT is
200-230 seconds for male-to-male connector
sheaths.
• ICU staff should perform hourly site checks and
ABIs to assess distal perfusion in addition to
biomarkers of ischemia.
• Clotting is most likely to form at sheath sidearm
sites; if totally occluded, may be exchanged
over wire, or as a last resort, aspirated with a
syringe with needle initially in the sheath and
then directed toward the sidearm.
Figure 4. External Contralateral Circuit
Internal contralateral circuit

• Use this technique for patients with pre-
existing occlusive disease or iatrogenic total
occlusion of the SFA precluding an antegrade
sheath placement at the site of the MCS device.
• Place a 7 Fr sheath on the contralateral side;
use a 5 Fr IMA or OMNI catheter to access the
profunda femoris on the side of the MCS device
with a 0.35 hydrophilic wire in an “up and over”
technique.
• Exchange the 5 Fr catheter over a wire for a 4
Fr long (45-55 cm) sheath placed through the
7 Fr sheath in a telescoping fashion. Male-to-
male connection of the sheath sidearms will
establish flow to the distal extremity ipsilateral
to the MCS device.
Figure 5. Internal Contralateral Circuit
External ipsilateral circuit

• While this technique does not require
contralateral access, use of the ipsilateral artery
for MCS device may compromise flow; a larger
caliber femoral artery is required.
• The sidearm of the MCS device should not be
used as a surrogate for the large retrograde
sheath; it will not provide sufficient flow for
distal perfusion.
• This approach requires the ability to establish
distal antegrade access with a 5 Fr sheath
(micropuncture assisted) which may be
difficult in a low flow state.
• If used with Impella, do not advance the
longer repositioning sheath in lieu of the peel-
away sheath; this will occlude the retrograde
sheath sidearm, reducing the perfusion to the
antegrade 5 Fr sheath.
• Impella is prone to migration and suction Figure 6. External Ipsilateral Circuit
alarms if the peel-away sheath is left in,
increasing the need for repositioning in the ICU.
External ipsilateral circuit

• May be placed at bedside in ICU with sterile
technique and ultrasound.
• Confirm adequate dorsalis pedis artery caliber
for a 5 Fr sheath.
• Using micropuncture technique, obtain access
to dorsalis pedis artery and place 5 Fr sheath.
• Obtain 7 Fr contralateral femoral artery access
and connect sheaths with male-to-male
connector.
• This technique will not provide adequate flow if
there is distal vascular disease proximal to the
dorsalis pedis and should only be used as a last
resort prior to resiting MCS device in the setting
of compromised distal perfusion.
Figure 7. Contralateral Distal Retrograde

Circuit
Transport considerations
The safe transport of patients with MCS devices is not a trivial consideration given the ancillary control
panels, ventilators, monitoring equipment, and personnel associated with MCS support.
• Prior to transport, map the route and have dedicated elevators (if required) held for the patient and
team.
• Have an MCS dedicated nurse, perfusionist, respiratory therapist, and additional personnel accompany
the patient.
• Continually observe the access site and control monitors for evidence for device migration.
• Securely tape the device with slack in the cannulation lines for transport.
• Place knee/extremity immobilizers with restraints for transport.
• For devices with temporary peel-away sheaths (eg, Impella), remove the peel-away sheath and replace
it with a permanent anchoring sheath at the end of the procedure. Peel-away insertion sheaths are
tapered and may result in movement of MCS device, clot formation in the tapered aspect of the
sheath, and subsequent limb ischemia.
• Bolus or increase sedation in intubated patients prior to moving to achieve a RASS sedation score of ≤3.
ICU BEST PRACTICES CHECKLIST

MONITORING
9 Continuous telemetry, pulse oximetry (ipsilateral access site if feasible) and respiratory
rate
9 1:1 nursing ratio
9 Continuous arterial BP monitoring and CVP
9 Mixed venous oxygen saturation q2h (or central venous if PA catheter data not
available) for several hours, then q4h
9 Urine output hourly
DEVICE-RELATED
9 Check device positioning on arrival with CXR and echocardiogram. Document
transversal marks on catheter shaft.
9 Have bedside echocardiography available 24/7 to confirm positioning daily
9 Sterilely flush distal perfusion catheter sidearm (if present) every shift
9 Transfer purge system and verify pressure bag if required by device protocol (eg,
Impella)
9 Secure MCS catheter to leg after position confirmed
9 Check ACT q2 hours x3 then per ICU heparin protocol based on device ACT/aPTT target
PATIENT-RELATED
9 Assess vascular access for hematoma, limb ischemia q15min x 4 upon arrival, then
q30min x 2, then hourly
9 Bedrest, log roll side to side only, HOB at 30 degrees
9 Assess for signs of hemolysis, coagulopathy at time of lab draws (hematuria, motor
current on MCS)
9 Calculate SVR, CPO, and PAPi/RV parameters with MVO2 lab draws (consider sepsis
and SIRS contribution to SVR)
9 Daily titration of MCS support to assess intrinsic cardiac function
9 Wean pressors to ensure distal limb perfusion
BIOMARKERS
9 CBC at least q4h or more frequently for large bore access/high-risk of bleeding
9 Liver function test daily
9 Serum electrolytes q6-12h, serum creatinine q12-14h
9 Lactate q1-4h (recommend q2h initially and to correlate with MVO2 data)
9 LDH, haptoglobin, and hemolysis labs (plasma-free hemoglobin) q4-6h for 24h or per
device protocol
9 Coagulation labs q4-6h or as dictated per device protocol for anticoagulation
9 Active type and screen throughout ICU stay
Best practices for MCS removal

Remove large bore arterial access for MCS devices in a procedural room or with fluoroscopy readily
available for bailout procedures. Intraoperative closure is an option if anatomy is deemed sufficiently high
risk. Due to a non-trivial rate of vascular closure device failure and/or anatomical considerations, manual
compression is sometimes required, and following best practices will increase the success rate for removal
without complications. Such best practices include:
• ACT <180 seconds
• Experienced operator
• Continuous vital signs (if noninvasive measure cuff pressure q2-3 min)
• Flushing of sheath prior to pull and brief “bleed back” post removal to remove any thrombus
• Adequate patient analgesia
• Atropine readily available for vagal reactions, particularly with concomitant aortic stenosis
• RN and extra personnel available, as large bore sheath manual compression should never be
performed alone
• For manual compression, a minimum of 3 minutes of compression per sheath size is recommended,
with distal perfusion assessed q2-3min during compression
Manual compression
The FDA has approved several devices for assisted manual compression including the FemoStop™,
C-Clamp, and hemostatic pads. The use of these devices has not been shown to reduce mortality, but has
been shown to reduce manual compression times and hematoma formation, if not reliably reducing need
for transfusion.17 The use of these devices should not preclude the use of best practices as detailed above.
Percutaneous cannulation for large bore arterial MCS access is associated with fewer local infections, and
similar rates of distal limb ischemia and sensory-motor complications but with improved 30-day mortality
when compared to surgical cutdown implantation.18 However, registry data has shown percutaneous
removal of MCS cannulas when using an assisted manual compression technique (FemoStop) is associated
with increased vascular complications requiring surgical revision (14.7% vs 3.4%).18 Recent improvements
in MCS cannula removal techniques and standardization with percutaneous closure devices (when
anatomically feasible) has resulted in significant decreases in vascular complications and should be
adopted at all centers offering MCS support.
Perform large bore sheath removal in the cath lab with the ability to perform femoral angiography
(contralateral or alternative access) post decannulation to confirm vessel patency and hemostasis. Ideally,
the procedure should be scheduled at a time when surgical intervention is available if closure device failure
occurs.
Suture-based closure devices

Perclose ProGlide® 6 Fr and Prostar™ XL Percutaneous Vascular Surgical System 10 Fr (Abbott Vascular) are
associated with reduced mortality, fewer blood transfusions, and shorter length of stay when compared
to open surgical removal.19 The pre-close technique utilizing the Perclose ProGlide has been the most
commonly used technique for closing large bore access in cardiac catheterization. Two 6 Fr Perclose
ProGlides are deployed in the vessel prior to upsizing and placement of the MCS device. Sutures are
secured outside the body and kept wet to prevent suture fracture. The pre-deployed suture knots are
sequentially advanced and tightened post MCS device removal.
The pre-close technique must be used with caution in cardiogenic shock patients as the suture material
may act as a nidus for infection with prolonged (2-3 day) duration of mechanical support. Instead, dry-
closure techniques with deployment of suture devices after MCS removal have been adopted to achieve
the superior outcomes seen with percutaneous closure devices while reducing the risk of infection
associated with the pre-close approach.
The use of a temporary cross-over balloon tamponade dry-closure technique allows for control of access
site bleeding while suture or plug-based devices are used to close the arteriotomy site. This approach has
a high success rate and has been shown to reduce vascular complications and bleeding as well as increase
earlier mobilization and cost savings.20 Most commonly, this approach consists of contralateral femoral
artery access with a 7 Fr sheath and a 5 Fr catheter engages the ipsilateral common iliac artery. After wiring
past the MCS sheath into the ipsilateral SFA, a peripheral balloon (typically 8-9 mm x 20-40 mm) is inflated
to occlude flow in the external iliac artery proximal to the large bore sheath which is then removed (see
Figure 8).
If pre-closure has not been utilized,

placement of two Perclose devices
through two 8 Fr sheaths may be
used while balloon tamponade
is maintained in a post-closure
technique. Collagen-based plugs may
also be used to achieve hemostasis
(Angio-Seal®, Terumo Corporation,
MANTA® closure system, Essential
Medical, Exton, PA) but are associated
with the inability to rewire the vessel
if the closure devices fail to achieve
hemostasis.
Dry-closure allows for a prolonged

inflation to assist with low-pressure
tamponade until hemostasis is
achieved, access for a covered stent if
vessel rupture occurs, or stabilization
for operative repair in emergency
situations.
Figure 8. Temporary Cross-over Balloon Tamponade Dry

Closure Technique
Complications
It is not surprising that large caliber arterial access for MCS devices translates into higher rates of vascular
complication compared with other percutaneous procedures. With the wide adoption of MCS devices
for the support of CS patients, increasingly pLVADs are being placed in lower volume centers where prior
experience in dealing with vascular complications may be limited. While most single center reports are
biased to centers with high volume and experienced operators, the problem remains substantial with the
larger bore ECMO cannulas consistently showing higher rates of vascular complications when compared
to Impella or TandemHeart devices.4
Vascular complications in ECMO circuits, most commonly distal limb ischemia and access site bleeding,
are highly correlated and an independent risk factor for mortality and the presence of DIC2 with a hazard
ratio over 2 for survival—second only to neurologic compromise (hazard ratio 7). Lower extremity ischemia
appears to have a greater impact on survival than bleeding. Mild lower extremity ischemia managed
conservatively has the approximate contribution to mortality as a major bleed (>3 U PRBC) whereas limb
ischemia requiring procedural intervention doubles this risk (hazard ratio 3).2 The greatest predictor of limb
ischemia is the failure to place a distal perfusing catheter at the time of ECMO cannulation.
Rates of significant vascular complications with percutaneous MCS such as Impella and TandemHeart
(pLVADs) are lower than ECMO but remain stubbornly in the mid-teens despite a dramatic increase in the
use of these devices over the last decade (over 1500% increase vs 100% in non-pLVAD devices).5,12 Unlike
ECMO, limb ischemia is less frequent than bleeding events in pLVAD patients. However, of those patients
with bleeding events, approximately 30% are severe enough to require transfusion (3.7% of all patients with
pLVADs).5
Emergent placement of pLVADs for cardiogenic Table 3. Registry Data of Vascular Complications
with Impella® and TandemHeart® Devices
shock are highly predictive of vascular (adapted from Patel et al.5)
complications, as is placement in lower volume
VASCULAR COMPLICATION WITH PLVAD RATE
centers and teaching hospitals. This latter point
suggests that lack of either institutional or personal Any vascular complication 13.5%
experience in the management of these devices • Vascular complication requiring surgery • 7.5%
post implantation plays a large role in complications
• Transfusion-dependent bleeding • 3.7%
as trainees are often directly involved in the post-
placement access care of these patients despite • Lower extremity embolism • 2.4%
the larger volume that tertiary referral centers often
• Critical limb ischemia • 0.5%
fulfill.
• AV fistula • 0.06%
• Retroperitoneal bleed • 0.02%
• Other vascular complication • 2.1%
Transfusion
Centers performing any large bore access should be prepared to resuscitate patients due to massive
blood loss with a protocol-driven process. A massive transfusion protocol (defined as >4U PRBCs in 1
hour, replacement of 50% of blood volume in 3 hours) is required to improve response time and ideally is
subject to a QA committee review for timeliness to activation and product availability, appropriateness, and
outcome. As MCS patients cannot augment cardiac output to improve perfusion, the body’s metabolic
demands must be met by adequate resuscitation in these circumstances.
MASSIVE TRANSFUSION CHECKLIST

MONITORING
9 2 large bore IVs (14-16 gauge); if central line, use multiport trauma line for rapid fluid
resuscitation and pressure monitoring
9 Continuous arterial BP monitoring, CVP, pulse oximetry and core temperature
9 If not placed previously, PA catheter if LV compromise present
9 Urine output hourly
PATIENT-RELATED
9 Warming devices: inline fluid warmers and cutaneous
9 Forewarning to blood bank about trauma-level blood need
9 Personnel for rapid transport of blood products
9 Rapid infusion pumps
9 Intubation (likely needed for compromised LV compensatory mechanisms and volume
overload)
9 Each transfusion pack has 4 U PRBC, 2 U FFP; 1 U platelets and 3g CaCL after each
transfusion pack)
9 Anticipate 1 pack every 20 minutes until ordered to stop by ICU/procedural attending
9 Clinical targets:
• MAP at least 60 mmHg, Hgb >7 g/dL
• INR <1.5, aPTT ≤45 s, platelets >50K
• Core temp target >35C
• Base deficit <3 and lactate <2mEq/L
BIOMARKERS
9 ABG with hemoglobin, lactate, electrolytes with calcium hourly until stabilized
9 DIC labs – decrease in clotting factors for every 500 cc blood loss
9 If PT, aPTT, and fibrinogen >1.5x normal, 2+ units of FFP transfused
Summary
The use of MCS devices continues to revolutionize the care for patients with cardiogenic shock. The routine
adoption of best practices in obtaining large bore access and its management in the ICU will play a key role
in improving patient outcomes for this increasingly utilized option for patient support.
References
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Cardiology. Archives of Cardiovascular Disease. 2018;111(10):601-12.
10. Pieri M, Pappalardo F. Bedside insertion of Impella percutaneous ventricular assist device in patients with
cardiogenic shock. International Journal of Cardiology. 2020;316:26-30. https://doi.org/10.1016/j.ijcard.2020.05.080
11. Crowley J, Cronin B, Essandoh M, et al. Transesophageal echocardiography for Impella placement and
management. J Cardiothorac Vasc Aneth. 2019;33(10):2663-8.
support: incidence, outcomes, and cost analysis. J Am Coll Cardiol. 2014;64(14):1407-15.
13. Wollmuth J, Korngold E, Croce K, Pinto DS. The single-access for hi-risk PCI (SHiP) technique. Catheter Cardiovasc
Interv. 2020;96(1):114-6.
14. Sandoval Y, Burke MN, Lobo AS, et al. Contemporary arterial access in the cardiac catheterization laboratory. J Am
Coll Cardiol Interv. 2017;10(22):2233-41.
15. Chitwood RW, Shepard AD, Shetty PC, et al. Surgical complications of transaxillary arteriography: a case-control
study. J Vasc Surgery. 1996;23(5):844-9.
16. Cohen M, Panakos A. Large Bore Access: Adjunctive Imaging for Access in Vascular Access, Management, and
Closure Best Practices. Shroff A, Pinto D ed. 2019. The Society for Cardiovascular Angiography and Interventions.
17. Jones T, McCutcheon H. Effectiveness of mechanical compression devices in attaining hemostasis after femoral
sheath removal. Am J Crit Care. 2002;11(2):155-62. Epub 2002/03/13. PubMed PMID: 11888128
18. Danial P, Hajage D, Nguyen L, et al. Percutaneous versus surgical femoro-femoral veno-arterial ECMO: a propensity
score matched study. Intensive Care Med. 2018;44(12):2153-61.
19. Schneider DB. Perclose ProGlide versus surgical closure outcomes-real world evidence. Presented at: The Leipzig
Interventional Course (LINC) 2018; January 30, 2018-February 2, 2018; Leipzig, Germany.
20. Genereux P, Kodali S, Leon MB, et al. Clinical outcomes using a new crossover balloon occlusion technique for
percutaneous closure after transfemoral transcatheter aortic valve implantation. Catheter Cardiovasc Interv.
2011;4(8):861-7.
CONTENTS
Axillary Artery
CHAPTER
4 Access and
Management
Timothy D Smith, MD
Interventional Cardiovascular and Critical Care Medicine
Director, Farmer Family Cardiovascular ICU
Director, ECMO and Shock Program
The Christ Hospital and Lindner Research Center
Medical Office Building
2123 Auburn Ave, Suite 136
Cincinnati, Ohio
INTRODUCTION
The field of interventional cardiology has throughout its history evolved to
optimize catheter-based therapies and to meet the evolving needs of patient
care. Moreover, the interventionalist must now more than ever be adept at
percutaneous arterial access and closure from other vascular sites. Despite
the common femoral artery remaining the most commonly used site of
access, advanced peripheral vascular disease could otherwise limit the ability
to support a patient’s cardiometabolic needs in times of hemodynamic
deterioration or complex, high-risk intervention. Inasmuch, the axillary artery
has become an alternative site of interest. In a retrospective analysis by Tayal et
al. of 110 CT scans done at a single institution, the mean diameter of the axillary
artery was 6.38 mm on the right and 6.52 mm on the left.1 Notwithstanding
the common femoral artery being more than 6 mm in diameter, the axillary
arteries demonstrated substantially lower rates of stenosis, calcification, and
size variation compared with the iliofemoral arteries.2
Although techniques may vary slightly, in this chapter I will describe the
techniques that I prefer for axillary access and axillary removal.
<< Chapter 3 Chapter 4 | Axillary Artery Access and Management Chapter 5 >>
Axillary access technique

1. Prep the patient in a supine position with the arm abducted at 120 degrees. The axillary artery (AA) is
typically easy to palpate in the deltopectoral groove.
2. Using fluoroscopy to identify the inferior border of the glenoid cavity, place a hemostat as an anatomic
landmark. Anatomically, the AA is divided into 3 parts depending on their relation to the pectoralis
minor muscle. As shown in Figure 1, the posterior, lateral, and medial cords of brachial plexus embrace
the second part of the AA, as per their names. Contrary to conventional teaching, I suggest accessing
the AA in its second portion to lessen the risk of brachial plexus injury. As an added precaution,
ultrasound should be utilized to identify the surrounding nerves.
Figure 1. Anatomy of the Axillary Artery
3. Use an additional access point to image the axillary artery. I prefer the ipsilateral radial artery or in cases
where the ipsilateral artery isn’t an option, the common femoral arteries can be substituted. From the
additional access site, we use a multipurpose catheter to selectively engage the subclavian artery on
the side of access.
4. If a baseline computed tomography scan is available, the axillary artery can be sized from those
images. However, in a majority of cases, the characteristics of the anatomy will often be unknown.
In this more common scenario, perform baseline angiography or obtain a digital subtraction image
of the subclavian, axillary, and high brachial arteries. Identify key vascular branches in relation to the
previously placed hemostat (see Figure 2) and ideally measure the artery diameter using quantitative
analysis or peripheral intravascular ultrasound for a more specific caliber. In addition, you may place
a micropuncture or traditional needle as a marker in the subcutaneous tissue after administration of
local anesthetic.
Again, ultrasound may be used to readily identify the artery and the surrounding nerve structures of
the brachial plexus and correlated with fluoroscopy depending on operator preference.
Figure 2. Key
Vascular Branches
5. Use a micropuncture needle to access the second portion of the axillary artery using fluoroscopic
guidance and ultrasound imaging. This approach is akin to best practice techniques for common
femoral arteries. Place a 4 Fr micropuncture sheath followed by access site angiography to confirm
appropriate sheath positioning within the axillary artery. Additional digital subtraction imaging can be
employed to assure there is no extravasation.
6. Advance a standard 0.035″ J-tip wire into the subclavian artery. In obese patients, a more supportive,
soft tip wire can also be used. Remove the 4 Fr micropuncture sheath while applying manual pressure
to the site and place an 8 Fr dilator through the tract to the artery. Once the dilator is removed, deploy
a Perclose ProGlide™ (Abbott) suture-mediated closure device in a well-described pre-close fashion.3 A
second Perclose may be deployed at the discretion of the operator. At this point, if not already done,
exchange the wire should for a standard support wire.
7. Serially expand the arteriotomy with dilators before introducing the 14 Fr Impella® sheath. Repeat
angiography to ensure proper placement of the large bore sheath, no extravasation, and adequate flow
to the distal arm. If angiography reveals questionable distal perfusion, place a pulse oximetry probe on
the affected fingers and perform a Barbeau test. If this confirms poor blood flow to the distal arm, use
the radial sheath for a short-term retrograde bypass from the axillary sheath sidearm or identify a more
durable bypass site.
8. Place a pigtail catheter into the left ventricle using routine methods to cross the aortic valve. Obtain an
LV end diastolic pressure and then advance a 0.018″ wire fashioned to have a large, curved tip through
the catheter into the ventricle. Insert the Impella over the wire and through the sheath. Advance the
Impella under fluoroscopic guidance into the left ventricle using standard technique. Remove the wire
and initiate hemodynamic support. PCI and/or hemodynamic support can now be performed.
9. For longer term support, if necessary, I prefer to attach the device to the patient’s arm and use a sling to
secure the arm.
Axillary removal technique

When support is no longer required, we recommend that an interventionalist or surgeon who is
credentialed and facile with endovascular techniques remove the device in the cardiac catheterization lab
or a hybrid lab for optimal safety.
1. Following PCI, carefully remove the Impella and pass a 0.035″ wire from the large bore arteriotomy
sheath into the aorta. Then reengage the subclavian artery from the common femoral artery using a 7
Fr sheath or, for more advanced users, the ipsilateral radial artery with either a 6 Fr or 7 Fr sheath.
2. Advance an exchange-length 0.035″ or 0.018″ wire, depending on your peripheral inventory (we prefer
a Glidewire Advantage [Terumo]), well beyond the axillary artery sheath into the brachial artery. If an
ipsilateral radial approach is being utilized, position the wire well into the descending aorta.
3. Advance an appropriately sized 6 x 20 mm or larger balloon over the wire proximal to the arteriotomy
into the subclavian artery and inflate (see Figure 3). Under fluoroscopic guidance, slowly withdraw the
large-bore arteriotomy sheath over the Impella sheath wire with the Perclose cinched to the axillary
artery arteriotomy site.
Figure 3. Balloon Inflated for “Dry Closure”

While Removing the Impella Sheath
4. Completely remove the Impella sheath over the 0.035″ wire already in place and complete the pre-close
technique by sequentially cinching and locking the previously deployed Perclose ProGlide sutures. This
“dry closure” limits blood loss and allows the operator time to adequately complete the arteriotomy
closure in a controlled manner.
5. Deflate the balloon in the subclavian artery and perform digital subtraction angiography through the
balloon wire-lumen to confirm there is no leak at the large-bore arteriotomy site. If there is no evidence
of extravasation, remove the balloon and apply light manual pressure for 5-10 minutes to ensure
complete hemostasis.
6. If significant extravasation is noted from the arteriotomy site following closure, re-inflate the subclavian
balloon and apply manual pressure. Have a self-expanding covered stent (Viabahn® [Gore]) available as
a bailout strategy in case you have difficulty obtaining hemostasis (see Figure 4).
Axillary artery extravasation Balloon to seal arteriotomy Covered stent placement
Figure 4. Extravasation and Covered Stent Placement
Summary
Axillary artery access offers an alternative to large-bore femoral access. Despite what is typically a smaller
diameter, the axillary artery may be less susceptible to atherosclerotic disease than the iliofemoral system
and axillary access may reduce bedrest time and associated morbidities. Axillary “dry closure” removal
techniques can help limit blood loss and prevent complications. Peripheral endovascular techniques are an
important skill set when performing alternate access in sites such as the axillary artery.
References
1. Tayal R, Iftikhar H, LeSar B, et al. CT angiography analysis of axillary artery diameter versus common femoral artery
diameter: implications for axillary approach for transcatheter aortic valve replacement in patients with hostile
aortoiliac segment and advanced lung disease. Intl J Vasc Med. 2016;2016: 3610705.
2. Arnett DM, Lee JC, Harms MA, et al. Caliber and fitness of the axillary artery as a conduit for large-bore
cardiovascular procedures. Catheter Cardiovasc Interv. 2018;91(1):150-6. doi: 10.1002/ccd.27416. Epub 2017 Nov 11.
PMID: 29130612.
3. Lee, WA. Percutaneous access for TEVAR: the Preclose technique and the Proglide device offer safe and effective
percutaneous access for thoracic endovascular aortic repair. Endovascular Today. 2008 Sept:48-55.
CONTENTS
Percutaneous
CHAPTER
5 Ventricular Assist
Device Console
Management
Kanika P. Mody, MD
Medical Director, VAD Program
Heart and Vascular Hospital
Hackensack University Medical Center
Hackensack, NJ 07601
Kanika.mody@hackensackmeridian.org
INTRODUCTION
The Impella® heart pump is a percutaneous ventricular assist device (pVAD)
commonly used to support patients with ventricular dysfunction both in the
setting of cardiogenic shock and during high-risk percutaneous coronary
intervention (HRPCI). The Impella console provides parameters to help ensure
proper Impella placement and function. To help minimize unrecognized device
malfunction, alarms are built into the programming of the console to alert the
care providers of important issues that may alter efficacy of the pump, as well
as cause potential harm to patients.
This chapter provides a brief overview of the ways in which the Impella console
helps clinicians with positioning, suction, and purge pressure management.
<< Chapter 4 Chapter 5 | Percutaneous Ventricular Assist Device Console Management Chapter 6 >>
Console overview
The Impella console screen provides placement signal tracings, a motor current tracing, performance level
(P-level) with corresponding flow, and purge pressure and purge flow with normal or expected values
that are unique for each device. Figure 1 illustrates how the console may display this information for the
Impella CP® with SmartAssist®.
Figure 1.
Impella Console Display
for Impella CP with
SmartAssist
Ao placement signal waveform
LV placement signal waveform
Motor current waveform
Impella flow
Purge Flow and Purge Pressure
Positioning
When the Impella is correctly positioned, both the placement signal and motor current signal should be
pulsatile as shown in Figure 1. Loss of pulsatility of the motor current suggests malposition of the pump.
When the Impella is not correctly positioned, an “Impella Position Wrong”, “Impella Position in Aorta”, or
“Impella Position in Ventricle” alarm appears on the top on the console display. This alarm should prompt
imaging with either transthoracic or transesophageal echocardiography to evaluate Impella positioning.
To reposition the pump, reduce the flow rate to P-2 and reposition the pump so that the inlet area is 3.5 cm
below the aortic valve annulus for the Impella 2.5®, Impella CP®, Impella 5.0®, and Impella LD® pumps and
5 cm below the annulus for the Impella 5.5® pump. Perform imaging and repositioning in a timely manner.
Persistent positioning issues, either too shallow or too deep into the ventricle, may cause hemolysis, or in
rare cases, structural damage to the heart.
Suction
A suction alarm may indicate decreased blood flow through the Impella pump. The clinical team should
troubleshoot this alarm with patient specific data. Suction may suggest low Impella inflow due to
hypovolemia or right ventricular (RV) failure, or Impella obstruction due to malposition. In rare instances,
suction at high P-levels may indicate ventricular recovery. Hemodynamic data along with echo imaging
can be useful to help identify and address the underlying cause of suction.
Troubleshoot suction events in a timely manner. When addressing suction, reduce the P-level by 2-3 levels
if tolerated to allow for better LV filling and Impella function while the underlying cause is determined.
Continued suction can result in ventricular arrhythmias, hemolysis, as well as inadequate Impella support
in the cases of malposition or RV failure.
Monitoring purge pressure

The Impella console displays purge flow and purge pressure parameters, which ensure proper function of
the motor when in normal range. When purge pressure is elevated, clear the purge tubing, sidearms, and
catheter of any potential kinks to prevent high pressure in the system. If the pressure remains elevated,
reduce the concentration of dextrose in the purge fluid. If there is no contraindication, increase the heparin
concentration up to a maximum of 50 IU/mL. Consider replacing the Impella pump if low purge flow is not
resolved, the alarm persists, or motor current rises.
Low purge pressure may signal a leak in the purge tubing. Check and tighten all connections. Inspect
and replace the purge cassette if there is purge fluid leakage. If the purge fluid concentration is too low,
increase to D5 or D10 solutions. If the alarm persists, there may be damage to the pump. Pull the Impella
back into the descending aorta until it can be safely removed.
SmartAssist technology ®
Impella heart pumps with SmartAssist technology have an optical sensor that provides more accurate
placement and flow data to the console. The console displays an aortic placement signal, an LV placement
signal, and the motor current waveform. When the Impella is correctly positioned, the LV and aortic
(Ao) tracing peaks overlap suggesting optimal unloading. Alterations in the LV and Ao placement signal
relationship may indicate hemodynamically significant issues (see Figure 2).
TYPE HOW TO RECOGNIZE HOW TO RESOLVE
• After reducing P-level:

Diastolic 1. Check filling and
Suction volume status
2. Check Impella position
• After reducing P-level:

Continuous 1. Check Impella position
Suction 2. Check filling and
volume status
Figure 2. Diastolic and Continuous Suction as Displayed for Impella with SmartAssist
If the LV and aortic peaks on the console are not overlapping and the LV tracing reveals significantly
negative diastolic pressures, this may indicate hypotension and continuous suction. Evaluate the patient
for malposition of the Impella. If imaging confirms good placement, use clinical data to differentiate
hypovolemia from right ventricular dysfunction, and treat the underlying cause. The flow may need to be
adjusted to allow for proper LV filling while the underlying etiology is corrected.
If the aortic and LV peaks are properly overlapping and the LV diastolic pressure is negative, but recovers
by end diastole, this may indicate intermittent suction without significant hypotension and suggest
hypovolemia. If the LV volume status is adequate but intermittent suction persists, use imaging to
interrogate placement. Again, based on clinical data, determine and treat the underlying etiology and
temporarily reduce the flow if tolerated.
Summary
It is important to understand the parameters displayed on the Impella console in order to ensure proper
Impella placement and function. Respond to alarms in a timely manner to prevent reduced efficacy and
potential harm to the patient.
For more information about the Impella console and alarms refer to the appropriate Instructions for Use
manuals on the Abiomed website or call the Abiomed clinical support hotline.
References
1. Impella CP® with SmartAssist® For Use During Cardiogenic Shock and High-Risk PCI Instructions for Use and
Clinical Reference Manual, Abiomed Inc., 2020.
2. Improved Troubleshooting Suction Management, Impella CP®, Abiomed Inc., 2020. Available at: https://www.
impellasmartassist.com/impella-cp-smartassist/. Accessed 8/24/2020.
CONTENTS
Team-based
CHAPTER
6 Care
John Adam Reich, MD
Director of Cardiovascular Critical Care
ECMO Medical Director
Tufts Medical Center / Tufts University School of Medicine
jreich@tuftsmedicalcenter.org
Haval Chweich, MD
Director of Cardiac Care Unit
Tufts Medical Center/ Tufts University School of Medicine
INTRODUCTION
A patient is admitted to the cardiac intensive care unit (CICU) and a team is
assembled to review the case and set the course for managing the patient.
A resident presents a systemic review of history and presentation. A bedside
nurse presents an update on pain, agitation, delirium, vasoactive infusions, and
access. A respiratory therapist presents ventilation settings. An ECMO specialist
presents circuit update, flows, and pre- and post- gasses. A pharmacist presents
medical reconciliation and medication updates. The plan is then set with the
cardiologist and intensivist who are rounding together at the bedside.
In today’s CICU, the sheer volume of data and information that needs to be
processed and the number of tasks to be completed to manage a patient are
more than any one clinician can manage. The following case represents the
complexity of care delivered in the CICU and illustrates the benefits of team-
based care.
<< Chapter 5 Chapter 6 | Team-based Care Chapter 7 >>
CASE STUDY
A 35-year-old male with nonischemic cardiomyopathy, ejection fraction (EF) 10%, loses
consciousness while working at a grocery store and his implantable cardioverter defibrillator
(ICD) discharges. He is transported by EMS to a community hospital and found to have
repeated discharges for ventricular tachycardia. Amiodarone bolus and drip is started, but the
patient’s blood pressure begins to drop. Norepinephrine infusion is started and the patient is
intubated followed by a brief—less than 10 minutes—cardiac arrest from sustained ventricular
tachycardia. He is transported by helicopter to our tertiary care hospital.
The patient is now on multiple vasoactive infusions (norepinephrine, epinephrine, vasopressin)

and is taken directly to the catheterization laboratory where right heart catheterization reveals
a cardiac index of 1.1, an RA pressure of 25 mmHg, pulmonary capillary wedge pressure of
38 mmHg, and a lactate of 10 mmol/L. An echocardiogram confirms biventricular dysfunction
and absence of tamponade.
Given the patient’s advanced state of hemometabolic shock and elevated LVEDP, the shock
team recommends placement of VA-ECMO plus Impella CP® for unloading the left ventricle.
The interventional cardiology team completes cannulae and percutaneous VAD implants and
the patient is transported to the CICU.
Over the next 72 hours, the patient’s cardiogenic shock and multiple organ system failure are
treated with ECpella™, with continual renal replacement therapy for aggressive decongestion.
Lactate clearance occurs, transaminitis from ischemic hepatitis improves, and his neurologic
status is found to be reassuring. Rib/sternal fractures from CPR and resultant hemothorax are
addressed and drained by the trauma surgery service. Our palliative care team engages and
supports the family, along with pastoral care during this dramatic period of uncertainty. The
vascular surgery team addresses the antegrade perfusion catheter failure, which resulted in
critical leg ischemia. His VAD and transplant workup continue, and he is cleared for either, but
he is unable to be successfully weaned from ECMO over the next 14 days due to severe right
ventricular failure.
The team elects to transition to a percutaneous VAD strategy in hopes of deescalating and
rehabilitating before bridging directly to transplant. A percutaneous RVAD is placed in
right IJ (Protek Duo) and an Impella 5.5® is placed in right axillary approach at time of ECMO
decannulation. Patient is able to stand within days and begins to ambulate the unit.
Teams of specialists continue to optimize his care. A dietician ensures that his protein and
caloric needs are being met and that his glycemic control is managed so that he is able to
heal and perform prehabilitation for his eventual transplant. The heart transplant team social
worker ensures he has the family support in place to help him manage at home and that his
family is supported through the process. The patient successfully receives a heart transplant 18
days later and is discharged home on postoperative day 8.
Rationale and emerging trends for the

team-based approach
During the first 48 hours of care, a remarkable number of healthcare providers (see Figure 1) gather patient
information, make recommendations, and provide care to patients such as the one described in the case
study above. The review and synthesis of clinical information and the coordination of delivery of care plan is
incredibly complex and needs to be integrated into a team-based plan. An efficient, flexible, and responsive
team-based care model is the optimal way of caring for patients in the modern CICU.
MEDICAL VASCULAR
SOCIAL SURGEON
WORKER
SHOCK
DIETICIAN TEAM
PALLIATIVE EP
CARE PHYSICIAN
PHYSICIAN
CA
ST RD
I
V
TRAUMA
IO
SI
RADIOLOGIST SURGEON
INTEN
LO
GIST
ADVANCED
HEART FAILURE
PATIENT INTERVENTIONAL
CARDIOLOGIST CARDIOLOGIST
SPIRITUAL CI
COUNSELOR CU TEA M NEPHROLOGIST
CRITICAL CARE RESPIRATORY

TECHNICIAN THERAPIST
PHYSICAL ECMO
THERAPIST BEDSIDE SPECIALIST
NURSE
Figure 1. Sphere of Care Provided by Multidisciplinary Team-based Approach in the CICU
The cardiac care unit (CCU) of the past was a post procedural suite for care of post STEMI patients who
received interventions. The most common occurrence was arrhythmia management. Now with advances
of care, we are having more and more survivors with comorbidities and organ system failures that require
a full-service cardiac intensive care unit (CICU). Each CICU should be set up with team-based care that
derives success from its local strengths.
The current literature does not provide a clear recommendation for integrating team-based care in the
CICU. Each institution must choose its own approach based on available resources, and in many instances,
advocate for additional resources. While there is no single, definitive approach, trends are emerging. Here
we highlight some of the key players we’ve identified for team-based care in the CICU.
The intensivist
In a retrospective review of 2,239 admissions to a cardiac care unit with a multidisciplinary team,
researchers examined outcomes 12 months before and 12 months after the inclusion of an intensive care
physician on that team.1 The original multidisciplinary team consisted of cardiologists, cardiology fellows,
medical residents, nurses, a respiratory therapist, and an ICU pharmacist. Adding an intensivist to the team
resulted in significant improvement in outcomes, including reductions in time on the ventilator, length of
stay, and mortality (Figure 2).
Before intensivist
added to CCU team
91/820
12
(11.1) After intensivist
added to CCU team
10
8 7.5±4.5
7.0±4.5
48/820
(5.9)
6 63/1419
(4.4) 4.3±2.5
50/1419
4 (3.5)
2.9±2.0
2.5±2.0 2.0±1.0
2
0
CCU Hospital Average CCU Average Hospital Average Ventilator
Mortality (%) Mortality (%) Length of Stay (d) Length of Stay (d) Days
P < .01 P < .01 P < .01 P < .01 P < .01
Figure 2. Outcomes Before and After Adding Intensivist to Multidisciplinary CCU Team
(adapted from Fanari et al., 20171)
Just having an intensive care physician consult on the patients may not be enough to provide the optimal
results. Intensive care physicians can interface with the patient/family in a low intensity or high intensity
manner.
• With low intensity involvement the intensivist sees the patient daily in a consultative format, not
during multidisciplinary rounds, and is available for phone calls or procedures later if necessary.
• With high intensity involvement, the intensivist is involved as a primary driver of patient care,
being present on multidisciplinary rounds, and continuously evaluating and adjusting treatments
throughout the day.
Changing the intensivist involvement with teams caring for patients admitted to the CICU to the high
intensity model dramatically reduced hospital mortality (10.7% to 6.1% p=0.009)2 from both cardiac causes
and noncardiac causes, as shown in Figure 3. These results illustrate that in specialty cardiac intensive care
units, adding an intensivist to the team likely results in improvement in care, and a high intensity-staffing
model is ideal.
Before High-intensity Staffing Model: After High-intensity Staffing Model:

Patients managed only by their individual physicians Dedicated cardiac intensivist responsible for
patient assessment and all aspects of patient care in
CICU with multidisciplinary team rounding
12
Noncardiovascular death
4.1
10
Cardiovascular death
2.9
8
MORTALITY (%)
6.8
6
1.9
6.0
4
1.1 4.2
3.0
2
0
CCU Hospital CCU Hospital
Figure 3. Significant Reductions in CICU and In-hospital Mortality Associated with

Cardiac Intensivist-directed Care (adapted from Na et al., 20162)
The clinical pharmacist

Another essential addition to multidisciplinary team-based care is a clinical pharmacist, who is present
and participates on rounds with each patient. A recent review and meta-analysis showed striking results.
Pharmacists being present and active on multidisciplinary rounds were associated with:3
• Decreased mortality (odds ratio, 0.78; 95% CI, 0.73–0.83; p < 0.00001)
• Decreased length of stay (95% CI, –1.75 to –0.90 days; p < 0.00001)
• Profound reduction in adverse drug events
It is clear that having a pharmacist on the CICU team should be a mandate for optimal team-based care.
Physical therapists, occupational therapists, and speech-

language pathologists
Gone are the days when patients in the ICU were kept sedated for weeks until the problem list was
completely resolved. It is clear now that rehabilitation can safely start early and physical therapy,
occupational therapy, and early speech and language pathology assessments are important.
Given the increasing prevalence of acute mechanical circulatory devices in the ICU, it helps to have a small-
dedicated team of therapists familiar with safe care and mobilization to help patients achieve a higher
functional state sooner during critical illness. With guidance from our physical therapy teams, we now
frequently mobilize patients with axillary IABPs, percutaneous VADs, external VADs, and ECMO. Research
is revealing that achieving a higher maximum mobility score after Impella 5.0® implantation may be
associated with improved survival.4 Bridging a patient from ECMO to axillary Impella is described as a way
to de-escalate support and ambulate patients before bridging to durable VAD.5 This time period is crucial
to rehabilitating patients and preparing them for the next surgery.
The shock team

A shock team is important to team-based care as well. At our institution, our physician shock team consists
of heart failure and interventional cardiology specialists, transplant and VAD cardiothoracic surgery
specialists, and ECMO directors. The team discusses each cardiogenic shock patient and makes a group
decision in conjunction with the bedside team as to the type of support needed and best implantation
strategy. Many institutions have also protocolized care to limit variability and attempt to avoid delays in the
decision-making process. Part of team-based care involves being able to activate this shock team at any
time so that the bedside team never has to make difficult decisions without consultation.
Summary: Specialist interplay in team-based care

The optimal approach to caring for patients in the modern CICU is an efficient, flexible, and responsive
team-based care model. The interplay of specialists in team-based care is a carefully orchestrated process.
The severity of illness lends little room for cognitive or procedural delays or errors.
In our unit, the cardiologist ensures integration and coordination of all cardiology subspecialty decisions
and interventions, and the critical care intensivist coordinates and drives the decisions and interventions
regarding the other organ systems. This is done in concert with joint rounds in the morning and night. It is
essential that all members of the team know that they are essential, and have their voices heard regarding
the care of the patient. It is imperative that cardiac units transition from the old open and low intensity
CCUs of the past to high functioning full service CICUs with a multidisciplinary team-based structure to
best serve the complex demographic of critically ill cardiac patients.
References
1. Fanari Z, Barekatain A, Kerzner R, et al. Impact of a multidisciplinary team approach including an intensivist
on the outcomes of critically ill patients in the cardiac care unit. Mayo Clin Proc. 2016;91(12):1727-34. doi:10.1016/j.
mayocp.2016.08.004
2. Na SJ, Chung CR, Jeon K, et al. Association between presence of a cardiac intensivist and mortality in an adult
cardiac care unit. J Am Coll Cardiol. 2016;68(24):2637-48. doi:10.1016/j.jacc.2016.09.947
3. Lee H, Ryu K, Sohn Y, et al. Impact on patient outcomes of pharmacist participation in multidisciplinary
critical care teams: a systematic review and meta-analysis. Crit Care Med. 2019;47(9):1243-50. doi:10.1097/
CCM.0000000000003830
4. Esposito ML, Jablonski J, Kras A, et al. Maximum level of mobility with axillary deployment of the Impella 5.0 is
associated with improved survival. Int J Artif Organs. 2018;41(4):236-39. doi:10.1177/0391398817752575
5. Bertoldi LF, Pappalardo F, Lubos E, et al. Bridging INTERMACS 1 patients from VA-ECMO to LVAD via Impella 5.0:
de-escalate and ambulate. J Crit Care. 2020;57:259-63. doi:10.1016/j.jcrc.2019.12.028
CONTENTS
CHAPTER
7 Anticoagulation
Satya Shreenivas, MD
The Christ Hospital Heart and Vascular Center
The Lindner Research Center
Cincinnati, OH
satya.shreenivas@thechristhospital.com
INTRODUCTION
Patients treated with mechanical circulatory support (MCS) are
at high risk for both thrombosis and bleeding. Careful utility and
monitoring of anticoagulation is key to achieving successful
clinical outcomes. In this chapter we review the possible risks
for thrombosis and bleeding in this patient population, outline
suggested anticoagulation regimens, and discuss ways to
troubleshoot thrombotic and bleeding complications.
<< Chapter 6 Chapter 7 | Anticoagulation Chapter 8 >>
Risk of thrombosis and bleeding with MCS

Patients treated with MCS devices, such as extracorporeal membrane oxygenation (ECMO) and
percutaneous ventricular assist devices such as the Impella® heart pump, are at high risk for
hypercoagulability for several reasons.
• Patients are already in a hyperinflammatory state, either due to the underlying medical disorder
(cardiogenic shock, recent myocardial infarction, severe decompensated heart failure) or recent
procedure (percutaneous coronary intervention or surgery).
• Patients are frequently hospitalized and bedbound for numerous days leading to stasis.
• There is endothelial dysfunction due to vessel trauma from the insertion of percutaneous devices
including possible concomitant procedures such as percutaneous coronary intervention.
• The patient-device interaction involves contact of bloodborne hypercoagulable proteins with non-
biologic device surfaces that can become the nidus of thrombus formation.
• There is potential stasis if the Impella sheath is not peeled away and the repositioning sheath inserted,
which may lead to diminished flow in the limb distal to where the device has been placed (Figure 1).
Thrombosis
resulting in
Figure 1.
ischemia Sheath Thrombosis
with Failure to Remove
Clinical thrombotic complications Peel-away Sheath
can result in lower extremity ischemia Large thrombus removed
from the Impella peel-
or an embolic stroke. Monitoring away sheath after 2
of clinical thrombosis is done by days of support without
careful and sequential extremity and removing the peel-away
sheath as recommended
neurologic exams. Some centers in the Instructions for
have adopted protocols of baseline Use manual.15 Despite
lower extremity ultrasound imaging adequate anticoagulation
(ACT consistently >160)
to help establish vascular baselines in and an antegrade sheath
anticipation of future difficulties with to help with distal limb
perfusion, the risk for
clinical exams in patients that might thrombosis is high in
be on vasopressors, undergoing these critically ill patients.
hypothermia (post-cardiac arrest for
example), or might have underlying
severe peripheral vascular disease.
However, such a regimen of baseline
vascular imaging has not been
studied and should be considered
on a case-by-case basis for patients
on whom serial exams might prove
difficult.
Cerebrovascular accidents (CVA) are a dreaded complication with MCS. Risks for CVA include
thrombocytopenia, anticoagulation intensity, and duration of support.1 Treatment of new embolic CVA
is difficult in this patient population due to the high risk for bleeding with systemic tissue plasminogen
activator (tPA) but mechanical thrombectomy or catheter delivered local tPA have been used in these
patients with resolution of symptoms. Usually a neurologic event is managed by attempting to wean and
remove circulatory support to forestall subsequent events, or if the stroke is severe, a discussion about goals
of care.
Thrombotic complications resulting in pump

dysregulation
During MCS support, adequate anticoagulation should be utilized to prevent thrombotic complications
which can result in pump dysfunction. Sources of emboli during venoarterial (V-A) ECMO include the
ECMO circuit itself, along with potential formation of clot in the oxygenator.2 During Impella support, an
elevation in purge pressures may indicate denatured protein build-up in the small purge gaps of the
motor. The Impella should be used with a continuous purge infusion that maintains a countercurrent,
creating a pressure barrier and preventing blood from interacting with the main Impella motor
component (Figure 2). Heparin in the purge solution enhances protection against ingress and coagulation
of blood components and may improve bearing working life.3
Figure 2. Importance
of Impella Purge Flow
(Courtesy of Abiomed)
The retrograde flow of a
continuous purge infusion
counteracts the antegrade
flow of blood and creates a
pressure barrier preventing
blood contact with many of
the more sensitive Impella
motor components.
Elevation in lactate dehydrogenase (LDH) and plasma free hemoglobin can suggest increased hemolysis,
which can have multiple etiologies, including thrombotic complications.4 Similar to serial exams, the key
to both of these parameters is understanding temporal change, especially when it comes to biomarker
elevation. LDH is an acute phase reactant, and in critically ill patients, normal LDH levels are not the same
as reference LDH values for a healthy adult. LDH can increase in response to tissue injury, including during
myocardial infarction and cardiogenic shock, common indications for MCS, and it is not recommended
to use in isolation to assess for hemolysis. Rather, an abrupt increase in LDH levels in the setting of
rising plasma free hemoglobin could suggest subclinical thrombosis in patients on MCS. Best practice
recommendations are to monitor biomarkers every 4 to 8 hours, and in light of appropriate change in
biomarkers and pump readings, consider increasing anticoagulation targets or even consider a pump
exchange.
Bleeding
Patients supported with MCS are also at risk for bleeding at the site of device insertion (usually related
to vessel trauma) or more generalized bleeding such as gastrointestinal bleeding or hemorrhagic
stroke, complications that are known to occur in patients who are critically ill. The underlying disorder
(shock) can result in severe disruptions in the coagulation cascade, especially if liver derangements are
also present. These patients are also frequently on additional antiplatelet medications due to recent
coronary interventions. Finally, insertion of the MCS device or subsequent interventions (central line
placement for example) carries high risk for vessel trauma and subsequent bleeding. Careful monitoring of
anticoagulation is key to achieving good outcomes with MCS.
Following best practice guidelines for prevention of vessel injury and trauma during device insertion is
key to limiting bleeding complications. Using MCS devices without anticoagulation is not recommended;
however, in cases of life-threatening bleeding this difficult decision will need to be made. Specifically, in
the setting of Impella support, in cases where anticoagulation is stopped, the preference would be to stop
systemic anticoagulation prior to stopping purge anticoagulation, which is used to protect the motor
against rising purge pressures. If both anticoagulants need to be stopped, the purge infusion should still be
continued with a dextrose infusion to help maintain pump function.
Anticoagulation guidelines
Heparin is the recommended anticoagulant during MCS due to wide availability, physician and nurse
familiarity, short half-life of 1 to 2 hours, and the availability of protamine as a reversal agent. Specifically
for the Impella, suggested dosing of heparin is based on a combination of systemic infusion and a purge
infusion that prevents denatured protein buildup (Table 1, Figure 3).
Table 1. Heparin Dosing Recommendations for Impella

Monitoring • Activated clotting time (ACT)
Goal • ACT of 160-180 seconds
Recommended Anticoagulation • Intravenous heparin
Method of Delivery Total heparin = Systemic infusion + Purge infusion through the Impella
• Total heparin rate delivered to patient to achieve an ACT of 160-180 is based on
hospital protocol
• Once total rate has been determined, subtract the Impella delivered heparin rate
from the total heparin rate to determine systemic heparin rate
• Impella delivered heparin rate = Heparin in the purge (25 U/mL or 50 U/mL) x
Purge flow rate (mL/hr)
Total Heparin Delivered

to Patient (Rate) Recommended by
Impella Delivered Heparin Rate + hospital protocol or
(U/hr) pharmacy
Systemic IV Heparin Rate = Total Heparin Delivered to Patient (Rate)
Total Heparin Delivered to Patient
Impella Delivered x =
Heparin Rate (U/mL) (mL/hr) (U/hr)
Heparin Concentration Purge Flow Rate Impella Delivered
in Purge from AIC from AIC Heparin Rate
Systemic IV
Heparin Rate
– =
Abiomed recommends using a heparin
concentration of 25 U/mL in the purge system. (U/hr) (U/hr) (U/hr)
Total Heparin Delivered Impella Delivered Systemic IV
D5W with heparin 25 U/mL or 50 U/mL is
to Patient (Rate) Heparin Rate Heparin Rate
acceptable.
Figure 3. Heparin Rate Calculator (Courtesy of Abiomed)

Monitoring of anticoagulation should include activated clotting time (ACT), but activated partial
thromboplastin time (aPTT) and anti-Xa levels can also be monitored.5-7 Each of these monitoring
parameters has limitations; patient factors such as thrombocytopenia, variation in anti-thrombin levels,
hypothermia, and hemolysis can all affect these levels.8 The Society of Cardiovascular Angiography and
Intervention (SCAI) has developed comprehensive recommendations for the monitoring of anticoagulants
during cardiac procedures that incorporate the benefits and limitations of various monitoring assays (Table
2).9
Table 2. Monitoring Anticoagulation (adapted from SCAI recommendations)9

ASSAY MECHANISM PRO CON
ACT • Point of care test assessing • Easy to perform (point of care, • Highly variable based on device,
whole blood clotting time, quick turnaround) operator, and patient factors
mostly by monitoring anti-IIa • Useful test for rapid assessment such as platelet levels and
levels of degree of anticoagulation ambient temperature
• Useful for moderate to high • Useful first test if used by • Check aPTT or anti-Xa levels if
dose anticoagulant monitoring trained staff, with careful ACT levels are not responding to
attention paid to monitoring changes in anticoagulation
device standardization
aPTT • Monitors both the common • Can monitor direct thrombin • Similar to ACT, point of care
and intrinsic pathways of inhibitors as well as heparin results are more variable
coagulation by measuring the • Can be done as point of care or • Can be affected by abnormal
time from activation of factor XII laboratory based liver function
to the formation of fibrin
• Widely available test with nurse • Must be calibrated for each
and physician familiarity of institution’s reagents so
results and titration therapeutic goal varies by
institution
Anti-Xa • Direct monitoring of Xa • Less affected by physiologic • Not point of care
inhibition variables (compared to ACT and • Not available at all hospitals
aPTT)
• Not able to monitor direct
thrombin inhibition
• Can be falsely elevated in cases
of hemolysis
No large-scale studies have been done that show superiority of one monitoring regimen. Each center
should develop standardized protocols based on local expertise and have alternative monitoring options
for patients with certain comorbidities (eg, severe liver failure) that might make a single monitoring
strategy inaccurate. In addition, care should be taken with titrating anticoagulation based on point of care
tests. These tests are frequently less reliable than laboratory testing and titration of heparin, which has a
steady state half-life of 6 hours, and should be done with caution if frequent monitoring is occurring.
Impella support may be used concomitantly with ECMO, a technique often referred to as ECpella™.
Competing anticoagulation goals are common in the setting of multiple devices. For example, the
Extracorporeal Life Support Organization (ELSO) recommends an ACT goal of 180-220, much higher than
the Impella guidelines.10 Risks for bleeding and thrombosis increase in the presence of multiple MCS
devices, but no studies have examined either the optimal anticoagulation regimen or monitoring strategy,
and individual centers should approach these complicated patients with their own expert guidelines.
In our opinion, patients with higher risk for bleeding (eg, large size, difficulties with cannulation,
concomitant antiplatelet medications) might benefit from lower ACT goals. However, increased duration
of support or other hypercoagulable disorders might predispose physicians to aim for higher ACT goals.
Regardless of which level of anticoagulation is chosen, it is important to carefully monitor ACT levels,
hemoglobin, possible bleeding complications, purge pressure, biomarkers, and extremities as well as
neurologic exam.
Alternative anticoagulants
In the setting of heparin-induced thrombocytopenia (HIT), alternative anticoagulants such as direct
thrombin inhibitors can be considered (Table 3).
Table 3. Alternative Anticoagulation Dosing Recommendations

TYPE BIVALIRUDIN ARGATROBAN
Monitoring • aPTT 1.5–3 x normal • aPTT 1.5–3 x normal
Method of • In purge (50-100 mcg/mL) and depending • In purge (20 mcg/mL) and depending on
delivery on clinical factors and the aPTT, a systemic clinical factors and the aPTT, a systemic
infusion as well infusion as well
Concerns • Avoid in severe renal dysfunction • Avoid in severe hepatic dysfunction
Half life • Normal renal function: 25 minutes • Normal hepatic function: 30-50 minutes
• Severe renal dysfunction: >3 hours • Severe hepatic dysfunction: >3 hours
There are case series of patients successfully treated with both argatroban and bivalirudin in ECMO11, 12 as
well as in Impella, both as a systemic infusion and in only the purge infusion, although with diminished
protection of the motor against rising Impella purge pressures compared to using heparin in the purge.
The concentration of argatroban in the purge solution ranged from 50–100 mcg/mL with goal aPTT of
1.5–3 times normal levels.13,14 Our institution and others have also developed protocols to use bivalirudin for
patients with HIT and at extremely high risk for bleeding with argatroban (such as severe liver dysfunction).
The advantages for bivalirudin include a short half-life of 25 minutes. In patients with HIT and the need for
anticoagulation our practice is to employ argatroban in cases of severe renal dysfunction and bivalirudin in
cases of severe hepatic dysfunction.
References
1. Hassett CE, Cho SM, Hasan S, et al. Ischemic stroke and intracranial hemorrhages during Impella cardiac support.
ASAIO J. 2020;66(8):e105-e109.
2. Keebler ME, Haddad EV, Choi CW, et al. Venoarterial extracorporeal membrane oxygenation in cardiogenic shock.
JACC Heart Fail. 2018;6(6):503-16.
3. Anticoagulation FAQ. Available at: https://www.protectedpci.com/faq/what-causes-thrombus-formation-among-
blood-contacting-medical-devices-and-what-can-be-done-to-prevent-thrombosis/. Accessed November 10, 2020.
4. Esposito ML, Morine KJ, Annamalai SK, et al. Increased plasma-free hemoglobin levels identify hemolysis in
patients with cardiogenic shock and a transvalvular micro-axial flow pump. Artif Organs. 2019;43(2):125-31.
5. Sieg A, Mardis BA, Mardis CR, et al. Developing an anti-Xa based anticoagulation protocol for patients with
percutaneous ventricular assist devices. ASAIO J. 2015;61(5):502-8.
6. Jennings DL, Nemerovski CW, Kalus JS. Effective anticoagulation for a percutaneous ventricular assist device using
a heparin-based purge solution. Ann Pharmacother. 2013;47(10):1364-7.
7. Bembea MM, Annich G, Rycus P, et al. Variability in anticoagulation management of patients on extracorporeal
membrane oxygenation: an international survey. Pediatr Crit Care Med. 2013;14(2):e77–84.
8. Esper SA. Extracorporeal Membrane Oxygenation. Advances in Anesthesia. 2017;35(1):119-43.
9. Beavers CJ, Bagai J. Anticoagulation monitoring during cardiac procedures: Considerations for anticoagulation
safety. https://scai.org/anticoagulation-monitoring-during-cardiac-procedures-considerations-anticoagulation-
safety. Accessed on 10/10/2020.
10. Extracorporeal Life Support Organization (ELSO). ELSO Guidelines for Cardiopulmonary Extracorporeal Life
Support. ELSO General Guidelines. 2017;Version 1.4.
11. Sanfilippo F, Asmussen S, Maybauer DM, et al. Bivalirudin for alternative anticoagulation in extracorporeal
membrane oxygenation: a systematic review. J Intens Care Med. 2017;32(5):312–9.
12. Rouge A, Pelen F, Durand M, Schwebel C. Argatroban for an alternative anticoagulant in HIT during ECMO. J
Intensive Care 2017;5:39.
13. Blum EC, Martz CR, Selektor Y, et al. Anticoagulation of percutaneous ventricular assist device using argatroban-
based purge solution: a case series. J Pharm Pract. 2018;31(5):514-8.
14. Laliberte B, Reed BN. Use of an argatroban-based purge solution in a percutaneous ventricular assist device. Am J
Health Syst Pharm. 2017;74(9):e163-e169.
15. Impella Ventricular Support Systems for Use During Cardiogenic Shock and High-Risk PCI: Instructions for Use and
Clinical Reference Manual. Available at: https://www.abiomed.com/impella-device-instructions-for-use. Accessed
November 11, 2020.
CONTENTS
Blood
CHAPTER
8 Compatibility/
Hemolysis
Jacob Abraham, MD
Medical Director, Advanced HF, MCS, and Heart Transplant
Providence Heart Institute
Portland, OR
Jacob.Abraham@providence.org
INTRODUCTION
All axial and centrifugal mechanical circulatory support devices (MCSD) cause
mechanical trauma to blood components. Low levels of background hemolysis
are expected as MCSD can subject red blood cells (RBCs) to high shear stresses,
contact with non-biologic materials, cavitation, and non-laminar flow.1 More
severe hemolysis may result from obstruction of the MCSD blood flow path,
excessively high rotational speeds, prolonged device support, or unfavorable
hemodynamic loading conditions.
The clinical consequences of intravascular hemolysis include anemia, acute

kidney injury from pigment nephropathy, and need for MCSD removal.
Prevention and monitoring for hemolysis are therefore paramount to improve
outcomes for patients supported by MCSD.
<< Chapter 7 Chapter 8 | Blood Compatibility/Hemolysis Chapter 9 >>
Hemolysis and hemolysis biomarkers

Serum biomarkers commonly used to detect hemolysis include plasma-free hemoglobin (PFHb), lactate
dehydrogenase (LDH), and haptoglobin. Each biomarker has limited specificity and sensitivity (Table 1).
Table 1. Hemolysis Biomarkers
BIOMARKER BIOLOGIC RELEVANCE BIOMARKER RELEVANCE

Plasma free hemoglobin (PFHb) Unbound PFHb depletes vascular Not readily available in all hospital
endothelial nitric oxide and causes laboratories
vasoconstriction; activates platelets; and
causes glomerular and tubular injury2
Lactate dehydrogenase (LDH) Sources of LDH include cardiac muscle, Often elevated in cardiogenic shock
skeletal muscle and liver due to organ injury prior to MCSD
deployment
Haptoglobin Produced by liver and forms complexes Most specific marker for intravascular
with PFHb that are removed by hemolysis
reticuloendothelial system
The Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) defines minor
hemolysis and major hemolysis.3
• Minor hemolysis is defined as PFHb greater than 20 mg/dL or a serum LDH greater than 2.5 times the
upper limits of the normal (ULN) range at the implanting center occurring after the first 72 hours post-
implant in the absence of clinical symptoms or findings of hemolysis or abnormal pump function.
• Major hemolysis is defined as PFHb greater than 20 mg/dL or LDH greater than 2.5 times ULN at
the implanting center occurring after the first 72 hours post-implant and associated with clinical
symptoms or findings of hemolysis or abnormal pump function. Major hemolysis requires the
presence of one or more of the following conditions:
▶ Hemoglobinuria (“tea-colored urine”)
▶ Anemia (decrease in hematocrit or hemoglobin level that is out of proportion to levels explainable by
chronic illness or usual post-VAD state)
▶ Hyperbilirubinemia (total bilirubin above 2 mg/dL, with predominantly indirect component)
▶ Pump malfunction and/or abnormal pump parameters
The INTERMACS definitions were developed for durable MCSD. There is no consensus definition of
hemolysis developed for temporary MCSD. A small retrospective analysis reported that change in PFHb
by >27 mg/dL within 24 hours of Impella® implantation had greater specificity than change in LDH for
predicting hemolysis.4 In the Impella Registry, site-reported hemolysis rates were 8.47%, 10.81%, and 8.33%,
respectively, for the Impella 2.5®, Impella CP®, and Impella 5.0®.5
Comparison of rates of hemolysis among MCSD is challenging due to lack of standard definitions and
varying duration of support. Table 2 summarizes reports of hemolysis for various MCSD used in cardiogenic
shock.
Table 2. Reported Incidence of Hemolysis in Cardiogenic Shock for MCSD
CLINICAL INCIDENCE OF
DEVICE HEMOLYSIS DEFINITION
CONDITION HEMOLYSIS
Impella 2.5 Hemolysis requiring transfusion AMICS 7.5%6
PFHb >40 or hematuria AMICS 10.3%7
Impella CP Biomarkers CS 46.8%8
Hemolysis requiring transfusion or AKI requiring CS 9.7%8

dialysis
Hemolysis requiring device removal AMICS 8%9
VA-ECMO Hemolysis requiring transfusion or AKI requiring CS 40%8

dialysis
PFHb 11-50 mg/dL CS 41%10
Circuit thrombosis or hemolysis requiring exchange CS 0.78%11
VA-ECMO with Impella CP Hemolysis requiring transfusion or AKI requiring CS 43%8

or Impella 5.0 dialysis
AMICS = acute myocardial infarction complicated by cardiogenic shock; CS = cardiogenic shock; VA-ECMO = veno-arterial extracorporeal
membrane oxygenation
Management recommendations
For all MCSD, serial monitoring of LDH, PFHb, and haptoglobin is recommended to identify and monitor
hemolysis.
Impella devices
In vitro testing of the Impella device has shown that outlet obstruction creates more hemolysis than
obstruction at the inlet area or within the cannula itself. As shown in Figure 1, the optimal position of the
Impella device is characterized by:
• Inlet area approximately 3.5 cm distal to the aortic valve
• Inlet area free from mitral valve structures
• Outflow well above the aortic valve
Tips for avoiding hemolysis include:
• Use frequent echocardiographic and/or radiographic imaging in conjunction with laboratory
monitoring to screen for hemolysis due to device malposition.
• Take steps to minimize device migration during transport or patient repositioning.
• Avoid excessively high flow rates and adjust the performance level to the minimum setting required to
maintain hemodynamic stability.
• Optimize volume status, using pulmonary

artery catheter guidance when possible, to A
avoid hemolysis from inadequate LV filling
pressures or low end-systolic LV volume.
• Watch for increases in motor current, which
may indicate obstruction within the pump
from ingested thrombus.
ECMO
Elevated levels of hemolysis biomarkers are
common during extracorporeal membrane
oxygenation (ECMO) support. Clinically apparent
hemolysis is rare and is significantly more likely with
veno-venous (VV) ECMO than veno-arterial (VA)
ECMO. Hemolysis is associated with:11 B
• Pump head or oxygenator thrombosis
• High flow velocities in small cannulas that can
increase shear stress
Conclusion
To improve outcomes in patients supported
by mechanical circulatory support devices, it
is important to monitor for hemolysis. Serum
biomarkers, such as PFHb, LDH, and haptoglobin
can help identify and monitor hemolysis associated
with MCSD. For Impella, ensuring optimal
positioning of the device, avoiding excessively high
flow rates, optimizing volume status, and watching C
for increases in motor current can help minimize
hemolysis. For ECMO, particularly VV ECMO, watch
for pump head or oxygenator thrombosis and high
flow velocities in small cannulas.
Figure 1. Echo Images of Impella Positioning

A. Optimal Impella position
B. Impella inlet positioned in papillary muscle (too
deep)
C. Impella in sub-aortic position (too shallow)
References
1. Olia SE, Maul TM, Antaki JF, Kameneva MV. Mechanical blood trauma in assisted circulation: sublethal RBC damage
preceding hemolysis. Int J Artif Organs. 2016;39(4):150-159.
2. Gladwin MT, Kanias T, and Kim-Shapiro DB. Hemolysis and cell-free hemoglobin drive an intrinsic mechanism for
human disease. J Clin Invest. 2012;122(4):1205-1208.
3. Interagency Registry for Mechanically Assisted Circulatory Support, National Heart Lung and Blood Institute.
INTERMACS Adverse Events Definitions: Adult and Pediatric Patients. https://www.uab.edu/medicine/intermacs/
images/protocol_4.0/protocol_4.0_MoP/Appendix_A_INTERMACS_AE_Definitions__05152013.docx. Accessed
January 2, 2019.
4. Esposito ML, Morine KJ, Annamalai SK, et al. Increased plasma-free hemoglobin levels identify hemolysis in
patients with cardiogenic shock and a transvalvular micro-axial flow pump. Artif Organs. 2019;43(2):125-131.
5. Summary of Safety and Effectiveness Data. https://www.accessdata.fda.gov/cdrh_docs/pdf14/P140003S004B.pdf.
Accessed January 4, 2020.
6. Lauten A, Engström AE, Jung C, et al. Percutaneous left-ventricular support with the Impella-2.5-assist device in
acute cardiogenic shock: results of the Impella-EUROSHOCK-registry. Circ Heart Fail. 2013;6(1):23-30.
7. O’Neill WW, Schreiber T, Wohns DH, et al. The current use of Impella 2.5 in acute myocardial infarction complicated
by cardiogenic shock: results from the USpella Registry. J Interv Cardiol. 2013;27(1):1-11.
8. Tehrani BN, Truesdell AG, Sherwood MW, et al. Standardized team-based care for cardiogenic shock. J Am Coll
Cardiol. 2019;74 (3):1659-69.
in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2017;69(3):278-87.
10. Saeed O, Jakobleff WA, Forest SJ, et al. Hemolysis and nonhemorrhagic stroke during venoarterial extracorporeal
membrane oxygenation. Ann Thorac Surg. 2019;108(3):756-63.
11. Pan KC, McKenzie DP, Pellegrino V, et al. The meaning of a high plasma free hemoglobin: retrospective review of
the prevalence of haemolysis and circuit thrombosis in an adult ECMO centre over 5 years. Perfusion. 2016;31(3):223-
31.
CONTENTS
Weaning of
CHAPTER
9 Impella®
Waqas Ghumman, MD
Affiliated Clinical Assistant Professor of Medicine,
University of Miami
Director, Mechanical Circulatory Support and
Heart Failure Program at JFK
180 JFK Drive
Atlantis, FL 33462
wghumman@gmail.com
INTRODUCTION
Throughout the management of a patient with an Impella® device in place, it
is important to continually evaluate the patient’s hemodynamic and metabolic
status. At each reassessment, decide whether it is appropriate to escalate
mechanical support, continue the current level of support, or initiate weaning.
There are no randomized controlled trials or firmly established protocols to
guide the weaning of an Impella, but there are general principles of weaning
based on established practice patterns.5 This discussion of weaning is based on
the use of Impella for the support of cardiogenic shock and low cardiac output
states and, although some principles are similar, this is not meant as a guideline
for weaning of an Impella that has been used successfully for high-risk PCI.
<< Chapter 8 Chapter 9 | Weaning of Impella® Chapter 10 >>
Initiating weaning
While there is no established minimal duration of support, many sites advocate for an Impella to remain
in place for a minimum of approximately 48 hours, although weaning may be initiated as soon as certain
conditions allow.
1. When deciding to attempt weaning, completely withdraw or minimize vasoactive drugs as ongoing
use of vasoactive drugs is associated with poor prognosis.3,5
2. Optimize hemodynamics with the use mechanical circulatory support as opposed to the use of
vasoactive medications. Hemodynamic optimization includes evidence of adequate left ventricular (LV)
cardiac support including:
• Cardiac power output (CPO) > 0.6 watts5
• Cardiac index (CI) > 2 L/min/m2
• Wedge pressure (PWCP) < 15 mmHg
• Pulmonary artery pulsatility index (PAPi) > 1.05
• Central venous pressure (CVP) < 15 mmHg6
3. Consider fluid status as optimization of fluid balance will be necessary to achieve hemodynamic
optimization.
4. Once hemodynamic status is optimized, stabilize metabolic status and correct evidence of organ
dysfunction2,4 prior to weaning.
• Physical exam and laboratory analysis should provide evidence of adequate end organ perfusion and/
or recovery of function. Specifically, the exam should reveal:
▶ Appropriate mental status
▶ Adequate urine output
▶ Warm and well perfused extremities with good capillary refill
• Laboratory data should indicate recovery or, at a minimum, improvement in renal and hepatic
function. Biochemical markers of organ resuscitation include:
▶ Lactate < 21
▶ Mixed venous oxygen saturation (SVO2) > 601
▶ Normalization of acid-base status, as evidenced by normalization of pH and bicarbonate;
minimization of base deficit should be obtained prior to weaning
5. If possible, correct the cause of the insult to the myocardium prior to weaning.2 This may entail:
• Revascularization in the setting of ischemia
• Correcting arrhythmic insults
• Correcting valvular or other anatomic issues
Once hemodynamic parameters are optimized, organ function is restored, and correctable cardiac insults
are addressed, it is the ideal time to initiate weaning.
Weaning strategy
A conscientious weaning strategy requires patience and diligence. Ideally, as the mechanical circulatory
support device is being down titrated, continue to optimize hemodynamics, organ function, and
symptoms.
Decrease P level
With an Impella, weaning is achieved by decreasing device speed, or performance level (P level), which
ranges from P9 to P0. Higher P levels (eg, P9) indicate higher flow and a greater degree of cardiac support.
There is institutional variation, but a typical weaning strategy involves a stepwise decrease in P level
combined with evaluation of patient tolerance as the level of mechanical support is decreased.
The weaning strategy utilized at JFK Medical Center begins with decreasing P levels by 2 levels no more
frequently than every 6 hours, for example P9 to P7 within a 6-hour timeframe. During each reduction in P
level, we determine successful weaning by the patient’s ability to maintain adequate LV support as noted
by CPO > 0.6 watts, cardiac index > 2 L/min/m2, PAPi > 1.5, and a CVP < 15 mmHg. If we are not able to attain
such hemodynamics, we increase hemodynamic support, allow more time for recovery, and retry later. If
such hemodynamic criteria are met with decreasing mechanical support, we then assess the adequacy
of organ perfusion by reassessing SVO2 on pulmonary artery catheter and keeping it above 60 as well as
assessing lactates and keeping them below 2.
Closely follow biochemical markers

We also closely follow biochemical markers of organ injury, such as renal and hepatic function. If SVO2,
lactate, or biochemical markers indicate evidence of worsening organ dysfunction, we increase support
again. If, however, hemodynamic parameters are maintained and organ function remains adequate,
we assess the patient’s symptoms and continue to wean. Often patients are intubated and sedated and
symptom assessment may be difficult, but if we are able, we assess the patient’s pulmonary function for
any evidence of congestion, and we assess urine output as we wean Impella support.
Look for signs of myocardial recovery

During the process of weaning the patient from mechanical circulatory support, we may encounter
varying levels of myocardial recovery. In the most successful weaning scenario, we will be able to decrease
Impella support to P2 while maintaining optimal hemodynamics, organ function, and symptomatology.
At this point, we make sure the patient is fully anticoagulated when the Impella level reaches P2 and
we perform an echo ramp study to look for evidence of anatomic preservation of function. We are
assessing whether the LV or RV dilate as well as whether LV and RV systolic function are maintained. We
also assess for worsening valvular regurgitation as it may limit our ability to wean from the mechanical
circulatory device. A successful echo ramp study would be one where, while decreasing Impella support,
LV and RV dimensions do not dilate and LV and RV function is maintained without worsening of valvular
regurgitation. If these conditions are met, we proceed with removing the Impella once anticoagulation
is stopped and an adequate ACT or PTT is obtained. We consider this a case with successful myocardial
recovery.
In other cases, we may see no evidence of myocardial recovery and be unable to wean the mechanical
circulatory device without hemodynamic compromise and/or organ dysfunction. In such a situation, we
may consider escalation of support, with a device such as an Impella 5.0®, or palliative care2 if no other
options are available. Alternatively, we may consider transferring the patient to an advanced mechanical
circulatory support center that may be able to evaluate the patient for a durable left ventricular assist
device (LVAD) and/or heart transplantation2 once support is re-established and optimized.
HEMODYNAMIC PARAMETERS
• Cardiac power output (CPO) = (CO x MAP)/451 in Watts
• Pulmonary artery pulsatility index (PAPi) =
(Systolic PA pressure - Diastolic PA pressure)/(CVP or right atrial pressure)
We may also encounter a situation in which myocardial recovery is inadequate. In such a case, we typically
continue support and/or frequent clinical reassessments. If we see signs of heart recovery, as described
above, we attempt weaning. If, however, after 48 to 72 hours we continue to see inadequate recovery, we
consider palliative care,2 device escalation, or transfer for evaluation for a durable LVAD/heart transplant.2
Predictors of 30-day mortality and successful weaning

Many groups have established predictors for successful mechanical circulatory support weaning and/or
increased 30-day mortality. Utilization of a pulmonary artery catheter for hemodynamic tailoring has been
associated with improved outcomes in registries. Predictors of 30-day mortality include 1 or more of the
following:5
• Hemodynamic parameters
• Biochemical markers of poor perfusion
• Organ dysfunction
Hemodynamic parameters, such as CPO < 0.6

watts at 24 hours and/or PAPi < 1 at 24 hours
are associated with increased mortality. Other CARDIOGENIC RISK PREDICTORS
parameters associated with poor prognosis are FOR INCREASED 30-DAY
lactate > 3 mmol/L at 24 hours and/or need for MORTALITY
dialysis or ongoing pressor requirements past 36 • Lactate >3 mmol/L at 24 hours
hours. Age > 71 years and diabetes mellitus are also • Pressor duration from diagnosis >36 hours
markers for poor likelihood to recover.
• CPO <0.6 W at 24 hours
• PAPi <1 in 24 hours
Strategies to successfully wean mechanical
circulatory support devices need to incorporate and • Diabetes mellitus
utilize a multitude of parameters to predict and • Dialysis
optimize outcomes. Risk stratification scores can • Age >71 years
be created by such parameters as demonstrated by
the Inova Heart and Vascular Institute group.5
Conclusion
Weaning from a mechanical circulatory support device, such as Impella, can be a very challenging
aspect of patient care. With no formalized or trial proven protocols, individual institutions create
their own weaning strategies. These strategies commonly include achieving patient stability prior to
weaning attempts, performing a stepwise decrease in support, and evaluating for tolerance of weaning
hemodynamically, metabolically/biochemically, and symptomatically.
References
1. Vahdatpour C, Collins D, Goldberg S. Cardiogenic shock. J Am Heart Assoc. 2019;8(8):e011991. doi:10.1161/
JAHA.119.011991.
2. van Diepen S, Katz JN, Albert NM et al. Contemporary management of cardiogenic shock: a scientific statement
3. Thayer K, Newman S, Ayouty M et al. Abstract 15943: Phenotypes of cardiogenic shock associated with increasing
in-hospital mortality: a report from the National Cardiogenic Shock Working Group Registry. Circulation. 2019;140.
doi: 10.1161/circ.140.suppl_1.15943.
4. Vallabhajosyula S, Dunlay SM, Prasad A et al. Acute noncardiac organ failure in acute myocardial infarction with
cardiogenic shock. J Am Coll Cardiol. 2019;73(14):1781–1791.
5. Tehrani BN, Truesdell AG, Sherwood MW et al. Standardized team-based care for cardiogenic shock. J Am Coll
Cardiol. 2019;73(13):1659-1669. doi: 10.1016/j.jacc.2018.12.084.
6. Davila C, Morine K, Esposito M et al. TCT-817 changes in right atrial pressure are associated with outcomes in
patients with cardiogenic shock receiving acute mechanical circulatory support devices: insights from the
Cardiogenic Shock Working Group. J Am Coll Cardiol. 2019;74(13 Suppl):B800. doi: 10.1016/j.jacc.2019.08.963.
CONTENTS
Impella ®
CHAPTER
10 Removal and
Closure
Timothy D Smith, MD
Interventional Cardiovascular and Critical Care Medicine
Director, Farmer Family Cardiovascular ICU
Director, ECMO and Shock Program
The Christ Hospital and Lindner Research Center
Cincinnati, OH
INTRODUCTION
The removal of the Impella® heart pump is critical to the overall
success of the procedure as well as the safety of the patient.
Depending on the clinical scenario, the device may be weaned
and removed at the conclusion of the procedure or secured
in place for an extended duration of mechanical support.
Regardless, an effective and well-planned removal strategy is
compulsory.
<< Chapter 9 Chapter 10 | Impella® Removal and Closure Chapter 11 >>
Impella CP and Impella 2.5 removal

® ®
Removal techniques for the Impella CP and Impella 2.5 are essentially identical.
1. Decrease power to P-1.
2. Pull the device across the aortic valve into the descending aorta.
3. Turn off the device at the console.
4. Remove the Impella through the vascular sheath.
• The Impella CP has a 14 Fr motor and thus requires a 14 Fr vascular sheath
• The Impella 2.5 has a 13 Fr motor that calls for a 13 Fr sheath
• At this point the primary focus is safe removal of the vascular sheath.
Regardless of the manner of closure, consider employing a “dry field” environment using a contralateral
femoral approach to deliver a 1-to-1 size matched balloon to the external iliac artery. Inflate the balloon
while the sheath is removed. Although it is possible to accomplish this maneuver with radial access, the
maneuver is limited by distance, diameter, and the ability to deliver a covered stent. Dry closure offers the
advantage of limited blood loss with access site control. Possible disadvantages include direct vascular
injury and an additional arterial access site. By connecting the sidearm of the large bore sheath to a
pressure transducer, one can dampen the arterial waveform with balloon inflation to ensure adequate
hemostatic control.
Figure 1. Balloon
Inflated for Dry
Closure Hemostatic
Control
Arteriotomy closure
Depending on individual preference and device availability, dry field closure of the arteriotomy can be
achieved using several techniques, including:
• Manual pressure with adjunctive pressure devices
• Perclose ProGlide™ pre-close technique
• MANTA® vascular closure
• Post close technique
Manual pressure with adjunctive pressure devices

Although manual compression has long been the gold standard for hemostasis, large bore access makes
this approach more challenging as well as time and labor intensive. It can also be very uncomfortable for
the patient. However, manual compression can typically be performed safely in the cardiac catheterization
lab or at the patient’s bedside. Mastery of proper technique is essential for patient safety (see Box).
TIPS FOR MASTERING MANUAL COMPRESSION TECHNIQUE

• Adjust height of the patient’s bed to allow optimal positioning for manual pressure to
be applied.
• Wait for an activated clotting time (ACT) of less than 180 seconds.
• Position a FemoStop® band beneath the patient.
• Administer 10-15 mL of lidocaine around the arteriotomy site.
• Have medications available for any possible vagal reaction as well as good IV access.
• Ensure control over the arteriotomy site with one hand while removing the sheath with
the other hand.
• Allow some back bleeding to ensure no thrombotic occlusion of the vessel.
• Apply pressure for 2 minutes per French size or until complete hemostasis is achieved.
• Apply a supervised FemoStop to aid with hemostasis. Keep the duration of pressure
application to a minimum to decrease the risk of complications such as nerve injury,
venous thrombosis, or limb ischemia.
• Following hemostasis, an additional 6-12 hours of bedrest is recommended.
Figure 2. Manual Compression with

FemoStop
Pre-close technique with Perclose

If 1 or 2 Perclose ProGlide vascular closure devices were placed prior to the insertion of the Impella, the
sheath can be removed and the Perclose simply cinched into position. In the case of Perclose failure, apply
manual pressure, or if wire access was maintained, deploy an Angio-Seal® vascular closure device as a
means of added hemostasis.
Figure 3. Perclose Pre-closure

Technique
MANTA vascular closure

The MANTA vascular closure device is specifically designed for large bore vascular closure. In fact, it is
the first commercially available biomechanical closure device designed for this purpose. It features a
resorbable collagen and footplate design.
MANTA has 2 platforms:

• 14 Fr system for closure of 10-14 Fr arteriotomies
• 18 Fr system for closure of 14-22 Fr arteriotomies
Figure 4. MANTA Vascular Closure
Post close technique

Although the pre-close technique is frequently utilized, unfortunately, there will be circumstances when no
pre-closure was performed and access to newer large bore closure devices is limited. Yet, the risks of sheath
removal will require an alternative approach for hemostasis beyond that of manual pressure.
The post close technique can be employed as follows:

1. Use two 0.035″ wires through the large bore sheath.
2. Remove the sheath.
3. Place two 8 Fr sheaths (one over each wire).
4. Deploy a Perclose in standard fashion via each 8 Fr sheath.
Figure 5. Post Close Technique
Removal of the Impella RP ®
The Impella RP has a 22 Fr pump motor and requires a 23 Fr sheath for insertion. The device is weaned in
standard fashion with removal through the sheath. The sheath can then be removed by utilizing manual
pressure, which can be quite prolonged. An easier alternative is to place 1 or 2 figure of eight sutures
around the sheath, remove the sheath, and cinch the sutures into position. Typically, a larger size braided
suture is best suited for this task. The figure of eight sutures are routinely left in place for 48 hours.
Figure 6. Figure of
Eight Technique
Removal of the Impella 5.0 and Impella 5.5 ® ®
The Impella 5.0 and Impella 5.5 require a 23 Fr sheath for insertion. Although there have been isolated cases
where the Impella 5.0 has been inserted percutaneously using femoral access, the standard approach is to
use a surgical cut-down with a beveled graft attached to the artery. As such, the Impella 5.0 and 5.5 should
be removed surgically and discussion of such surgical removal is beyond the scope of this discussion.
Summary
It is vital to have a plan for safely removing Impella when the patient no longer requires mechanical
circulatory support. A “dry field” environment can facilitate arteriotomy closure. Depending on individual
preference and device availability, closure techniques may involve manual pressure with adjunctive
pressure devices, Perclose pre-close technique, MANTA vascular closure, or post close technique.
PART III
TABLE OF
CONTENTS
Support: Other Devices
Chapter 11 Intra-aortic Balloon Pump......................................................... 94
Chapter 12 ECMO: Configurations and Management............................102
Chapter 13 ECpella: Physiological Basis and Clinical

Management of Dual Mechanical Circulatory
Support with ECMO and Impella CP®.....................................112
TABLE OF PART III Mechanical Circulatory Support: Other Devices
CONTENTS
Intra-aortic
CHAPTER
11 Balloon Pump
Arvind Bhimaraj MD, MPH, FACC, FHFSA

Interim Chief, Division of Heart Failure
Medical Director, Advanced Heart Failure, MCS and Heart Transplant Program
Houston Methodist DeBakey Heart and Vascular Center
Houston Methodist J.C. Walter Jr. Transplant Center
Houston Methodist Hospital
abhimaraj@houstonmethodist.org
INTRODUCTION
The intra-aortic balloon pump (IABP) is a cardiac mechanical
circulatory support (MCS) device that works on the principle of internal
counterpulsation. First used in 1967 by Adrian Kantrovitz,1 IABP is possibly
the oldest percutaneous MCS available. The major advantages of this
device are its ease of implantation and universal availability. While
IABP has been used steadily over many decades across various clinical
situations, recent clinical evidence has questioned its utility in certain
indications.
<< Chapter 10 Chapter 11 | Intra-aortic Balloon Pump Chapter 12 >>
Physiology and anatomy of the pump

The IABP is a catheter-based device with a 22-27.5 cm long balloon with a 34-55 cc volume capacity.
Inflated, the diameter of the balloon is between 15 and 18 mm. It is most commonly inserted in a
percutaneous manner through the femoral artery, although it may also be placed in a percutaneous
manner through the axillary artery as a strategy for prolonged use.3 In addition, IABP can be placed in
an open surgical approach through a vascular access graft in the axillary or subclavian artery, which, like
percutaneous axillary insertion, promotes ambulation.2
The IABP catheter has a port that connects the balloon to the external console which houses a helium tank
that inflates and deflates the balloon. The catheter also has a central lumen port that opens as a fluid filled
system at the distal end of the catheter inside the body allowing transduction of arterial blood pressure.
Some pumps have an additional fiberoptic tip to reflect intra-aortic blood pressure. While early studies
used air and carbon dioxide, helium became the choice of gas because it allows faster gas exchange and
maintains a larger volume within the balloon for a longer time. Helium also dissolves faster in case of entry
into the bloodstream, hence minimizing embolization consequences.
The timing of balloon inflation is based on the input chosen on the console. The input is used to
synchronize inflation and deflation of the balloon with the cardiac cycle so that the balloon inflates during
systole and deflates during diastole. This input may be:
• ECG
• Blood pressure
• A-paced
• V/AV-paced
• Internal
The physiological impact of balloon timing is to unload the heart with a reduction in systemic vascular
resistance during systole as blood is pumped into the systemic circulation, and increase coronary perfusion
by displacing blood back into the ascending aorta during diastole as shown in Figure 1. ECG input is used
most commonly for the timing. In situations where the rhythm is paced, it might be relevant to use the
appropriate setting to pick up the pacing in the atrium and/or ventricle. In situations of tachycardia where
augmentation is not easy to achieve, a 1:2 ratio might facilitate appropriate hemodynamic impact. The
pressure trigger can be used when there might be artifact interfering with ECG input. An internal trigger
means there is no external timing trigger and the IABP cycles at its own constant rate. Such a trigger is
used in the setting of cardiac resuscitation efforts.
Figure 1. Physiologic Impact of IABP Timing
The IABP appears to augment cardiac output by 0.5 to 1 L/min and can be set to assist every beat, every
other beat, or 1 in 3 cardiac beats. IABP is considered to be a mechanical support device for the left ventricle
in the context of augmenting cardiac output and has no role in primary right ventricular failure apart from
improving right coronary artery perfusion.
Indications and clinical evidence for IABP placement

Cardiogenic shock is the most common indication for IABP use and some of the common clinical settings
are:
• STEMI
• Acute new onset heart failure
• Acute on chronic heart failure
• Peri-operative support
• Cardiac arrest
Utilization of IABP in the setting of STEMI has been studied most extensively with trials suggesting a
lack of benefit when used routinely or as an assistance to revascularization.4 Although guidelines have
downgraded the routine utilization of IABP in the STEMI setting and as an assistance to PCI, there still
seems to be a role for IABP in the setting of cardiogenic shock supported by retrospective assessment of
real world data5-8 suggesting that there may be cohorts of patients who might still benefit, especially in the
setting where another mechanical support device is not available.
It is possible that a device that depends on native cardiac contractility might not be sufficient in a setting
like STEMI and percutaneous intervention where the impact on native contractility is substantial not just
due to coronary occlusion but also due to unavoidable procedure related injury. Studies have suggested
that cardiac power output (reflective of native cardiac abilities) can predict success of an IABP.9 There is
also accumulating evidence that using a transaortic mechanical assist device such as the Impella® heart
pump to unload the left ventricle may provide a protective effect on revascularization injury in the setting
of a STEMI.10 Interestingly, at the same time a small study comparing transaortic percutaneous mechanical
support and IABP did not show any difference in outcomes.11
The utility of IABP in other clinical settings has not been well studied in a systematic fashion. While IABP
augmentation of cardiac output in the setting of cardiogenic shock is minimal, it appears the response of
individuals is variable depending on the clinical setting. Due to chronicity and neurohormonal changes,
there could be a distinct difference between an acute setting like STEMI and myocarditis compared to
acute on chronic heart failure. Also, in the setting of advanced heart failure, percutaneous axillary IABP
provides support for a prolonged period. This can help patients stabilize and recuperate as well as provide
time for complex decision making for advanced therapies and eventually bridge to a heart transplant or
durable mechanical device.3,12
IABP placement and removal

An IABP can be placed percutaneously using a standard Seldinger technique for access. The IABP is
placed over a wire through the 7-8 French (Fr) IABP sheath and positioned below the left subclavian and
above the celiac artery using fluoroscopic guidance. This technique makes it convenient to insert an IABP
at beside in an emergency. A similar technique, with some modifications, is used for percutaneous IABP
placement in the axillary artery.3 A surgical implantation with a cut-down and a graft placement is used
less commonly, typically in the axillary position but requires general anesthesia.
The IABP can be removed at the patient’s bedside with proximal manual compression of the artery for
approximately 45 minutes. Once the IABP is ready to be removed, pull the catheter out until it reaches (and
feels stuck in) the sheath. Then pull the sheath and the IABP together as an entity while holding proximal
compression. Due to the possibility of thrombi on the balloon surface, hold distal compression while letting
out some blood for a few beats before applying complete compression proximally as shown in Figure 2.
Figure 2. Technique for IABP

Removal
A. Pull IABP until deflated
balloon lodges in introducer
sheath.
B. Remove IABP while holding
pressure on vessel.
C. Let some blood out for 2 to
3 beats, maintaining mild
proximal pressure and strong
distal pressure (with a finger
or other hand).
D. Maintain 45 minutes of
proximal pressure on the
artery to enable coagulation.
IABP patient management

Key IABP patient management tips include the following:
• When the IABP is placed in the femoral artery the patient must lie flat with minimal incline of the head
to avoid kinking and injury of the IABP entry site. This issue can be overcome with axillary placement
either percutaneous or with a surgical graft.
• Use systemic anticoagulation for IABP especially if the ratio is set less than 1:1 to avoid stasis on the
IABP membrane.
• Access site complications including hematomas and aneurysms have been reported at 1-3% and
infection and bacteremia range from 2-14% depending on duration of support.13
• Unique complications of IABP kinking and displacement have been seen when IABP is placed
percutaneously through the axillary artery.3 Less migration and movement of the IABP is seen when it
is implanted through a graft as the IABP is tied within the graft.
• Balloon rupture can occur with a sudden stoppage of the IABP with appearance of blood in the
helium port. Stop the IABP immediately and remove or exchange the IABP utilizing a wire exchange
technique.3
Percutaneous axillary IABP: a special mention

The option to place an IABP through the upper extremity arterial circulation has been available as an open
surgical technique with a graft placement. To avoid risk of general anesthesia and open vascular surgery in
tenuous advanced heart failure patients, the heart failure and interventional teams at Houston Methodist
have used a percutaneous technique to implant IABP. Initially we used a technique in the subclavian artery
similar to one used for subclavian vein access, but aiming for the artery. We later modified this technique
further laterally to access the axillary artery. Over the past several years we have used such a technique to
perform more than 200 axillary IABP implants,3 the majority of which were a bridge to advanced therapy or
decision making.
Axillary access can be obtained under either ultrasound or fluoroscopic guidance with a wire placed in
the axillary artery through left radial, brachial, or femoral artery access.3 The left axillary is preferred over
the right for percutaneous placement due to the high incidence of proximal displacement of the balloon
during maintenance of the IABP. In such a scenario, proximal displacement in a right axillary position will
place the balloon in the arch hence predisposing the major anterior circulation of the brain to risk.
Longer term maintenance of counterpulsation devices in ACC Stage D heart failure patients seems
to enable patients to recuperate physically and mentally while being optimized for an LVAD or heart
transplant. While right ventricular parameters could predict the ability of IABP to provide adequate
support, systematic studies are lacking. In our practice, if hemodynamics reveal that individuals with a
groin IABP are receiving suboptimal support, we assess these individuals for an axillary Impella 5.0® or
Impella 5.5® instead of an axillary IABP. In the setting of worsening hemodynamics, it is also important to
assess the need to upgrade support after axillary IABP placement.
During maintenance of IABP support,

while individuals are ambulating,
the IABP is prone to being pulled
back, requiring simple bedside
repositioning. As shown in Figure
3, the IABP may move into the arch
of the aorta, or the distal tip into
the abdominal branches. Timely
recognition of such displacement is
key to preventing untoward negative
consequences.
Figure 3. IABP Arch Malposition (video)
Longer maintenance can also lead to a need for

IABP exchange due to fracture of the helium port
in the catheter (as shown in Figure 4) and balloon
rupture. A replacement can be performed while
maintaining the same access site by exchanging
the failed balloon using a stiff wire through the
arterial port of the IABP and removing the IABP
and the sheath as a single entity and replacing the
sheath. Such an exchange technique can also be
used in the groin.
While percutaneous axillary IABP placement

is not highly prevalent, its use is increasing in
many centers. The ability to safely perform and
maintain percutaneous axillary IABP requires a
more concerted effort to educated implanters and
utilizers as well as innovation in troubleshooting the
nuances that are unique to axillary placement.
Conclusion
Despite many controversies about the role of IABP
in the setting of myocardial infarction, it remains a
widely available mechanical support device with a
significant role in the armamentarium for treating
cardiogenic shock, especially in the setting of ACC
Stage D heart failure. While axillary placement is a
good option for prolonged use, maintenance of the
unique nuances of such a strategy requires special
attention. Further studies are needed to assess
appropriate utilization of IABP in an algorithmic
Figure 4. Axillary IABP Air Leak (video)
approach of early MCS utilization and appropriate
and timely escalation of MCS with more robust
support as needed.
References
1. Parissis H, Graham V, Lampridis S, et al. IABP: history-evolution-pathophysiology-indications: what we need to
know.
J Cardiothorac Surg. 2016;11:122.
2. Cochran RP, Starkey TD, Panos AL, Kunzelman KS. Ambulatory intraaortic balloon pump use as bridge to heart
transplant. Ann Thorac Surg. 2002;74:746-51; discussion 751-2.
3. Bhimaraj A, Agrawal T, Duran A, et al. Percutaneous left axillary artery placement of intra-aortic balloon pump in
advanced heart failure patients. JACC Heart Fail. 2020;8(4):313-23.
4. Thiele H, Zeymer U, Neumann FJ, et al. Intraaortic balloon support for myocardial infarction with cardiogenic shock.
N Engl J Med. 2012;367:1287-96.
5. Zheng XY, Wang Y, Chen Y, et al. The effectiveness of intra-aortic balloon pump for myocardial infarction in patients
with or without cardiogenic shock: a meta-analysis and systematic review. BMC Cardiovasc Disord. 2016;16(1):148.
6. Levine GN, Bates ER, Blankenship JC, et al. 2011 ACCF/AHA/SCAI guideline for percutaneous coronary intervention.
A report of the American College of Cardiology foundation/American Heart Association task force on practice
guidelines and the Society for Cardiovascular Angiography and Interventions. J Am Coll Cardiol. 2011;58:e44-122.
7. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation
myocardial infarction: a report of the American College of Cardiology foundation/American Heart Association task
force on practice guidelines. J Am Coll Cardiol. 2013;61:e78-e140.
8. Authors/Task Force members, Windecker S, Kolh P, et al. 2014 ESC/EACTS guidelines on myocardial
revascularization: the task force on myocardial revascularization of the European Society of Cardiology (ESC) and
the European Association for Cardio-Thoracic Surgery (EACTS) developed with the special contribution of the
European Association of Percutaneous Cardiovascular Interventions (EAPCI). Eur Heart J. 2014;35(37):2541-619.
9. Sintek MA, Gdowski M, Lindman BR, et al. Intra-aortic balloon counterpulsation in patients with chronic heart
failure and cardiogenic shock: clinical response and predictors of stabilization. J Card Fail. 2015;21(11):868-76.
10. Kapur NK, Alkhouli MA, DeMartini TJ, et al. Unloading the left ventricle before reperfusion in patients with anterior
ST-segment-elevation myocardial infarction. Circulation. 2019;139:337-46.
pump in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2017;69(3):278-87.
12. Macapagal FR, McClellan E, Macapagal RO, et al. Nursing care and treatment of ambulatory patients with
percutaneously placed axillary intra-aortic balloon pump before heart transplant. Crit Care Nurse. 2019;39(2):45-52.
13. Elahi MM, Chetty GK, Kirke R, et al. Complications related to intra-aortic balloon pump in cardiac surgery: a decade
later. Eur J Vasc Endovasc Surg. 2005;29:591-4.
CONTENTS
ECMO: Configurations
CHAPTER
12 and Management
Samantha K. Brenner, MD, MPH Joseph E. Parrillo, MD, MCCM
Core Assistant Professor of Internal Medicine Justice Marie L. Garibaldi Endowed Chair, Chairman
Hackensack Meridian School of Medicine at Heart and Vascular Hospital
Seton Hall Hackensack University Medical Center
Nutley, NJ Professor and Chair, Department of Cardiology
Intensivist, Cardiothoracic Intensive Care Unit Hackensack Meridian School of Medicine at Seton Hall
Heart and Vascular Hospital University
Hackensack Meridian Health, Hackensack Professor of Medicine
University Medical Center
Hackensack, NJ Rutgers New Jersey Medical School
Samantha.Brenner@hackensackmeridian.org joseph.parrillo@hackensackmeridian.org
Mark Anderson, MD, MHA Eugene Bunnell, MD

Professor of Surgery Medical Director, Cardiothoracic Intensive Care Unit
Hackensack Meridian School of Medicine at Heart and Vascular Hospital
Seton Hall Hackensack Meridian Health,
Nutley, NJ Hackensack University Medical Center
Hackensack, NJ
Chief, Division of Cardiac Surgery
Eugene.Bunnell@hackensackmeridian.org
Vice-Chair, Cardiac Surgical Services
Heart and Vascular Hospital
Mark.Anderson@hackensackmeridian.org
INTRODUCTION
Extracorporeal membrane oxygenation (ECMO) is a centrifugal mechanical circulatory
support (MCS) device that is employed as a rescue strategy in the setting of urgent need
for the management of life-threatening pulmonary or cardiac failure or some combination
of the two. ECMO is typically employed either as temporary supportive care in service of
organ recovery or as a bridge to permanent devices or surgeries such as organ transplant.
Management of ECMO patients requires coordination of a team of providers to ensure proper
monitoring of the patient and the circuit. The goal is to prevent and minimize frequent and
common complications, such as renal failure and coagulation disorders—both bleeding and
clotting.
TRADITIONAL ECMO NOMENCLATURE

FIRST LETTER = Source of deoxygenated blood from body to pump
SECOND/THIRD LETTER = Destination of oxygenated blood from pump to body
For example:
• Veno-arterial (V-A) commonly used for cardiac failure
• Veno-venous (V-V) commonly used for respiratory failure
<< Chapter 11 Chapter 12 | ECMO: Configurations and Management Chapter 13 >>
ECMO circuit components

ECMO was developed as a modified cardiopulmonary bypass circuit. A centrifugal pump removes blood
from the venous system through a large-bore cannula. Blood passes through the pump and then through
a membrane oxygenation system, which also extracts carbon dioxide via fresh gas flow. The oxygenated
blood returns to the patient’s circulatory system either through different ports of the same cannula or
through a separate large-bore cannula.1 Consideration must be given to adequate cannula sizing for the
expected amount of flow required, while also seeking to minimize complications from large-bore vascular
access.2
Common configurations
ECMO is typically deployed in one of three common configurations depending on indication. V-A ECMO
is generally considered for patients with cardiogenic shock, while V-V ECMO is generally considered for
patients with respiratory failure. Figure 1 illustrates the most common cannulation set-ups:
• Femoral V-V ECMO cannulation
• Central V-A ECMO cannulation
• Peripheral V-A ECMO cannulation
Figure 1. Typical
ECMO Cannulation
Configurations
(adapted from
Murphy et al.18)
Cannulation
configurations
and common sites
where mixing of
oxygenated and
deoxygenated blood
occurs.
(A) V-V ECMO with
venous femoral
drain and right atrial
return;
(B) Central V-A
ECMO with right
atrial drain and left
atrial return;
(C) Peripheral V-A
ECMO with femoral
venous drain and
femoral arterial
return
Alternative configuration
In addition to the common configurations, a newer setup for V-V ECMO has been designed, simplifying
cannulation with a single dual lumen catheter inserted into the right internal jugular vein. Blood can be
removed from ports in the superior and inferior vena cava, then returned to the right atrium with careful
positioning using transesophageal echocardiography or fluoroscopy so that the flow is directed toward the
tricuspid valve.
Single cannula V-V ECMO setup (Figure 2) maximizes right ventricular filling with oxygenated blood while
providing two key advantages:2
• Reduced vascular complications
• Increased patient mobility if clinical circumstances allow for ambulation2
Figure 2. Single Cannula

V-V ECMO
Access obtained through the
right internal jugular vein.
Cannula has several external
drain ports that flow to the drain
line with a single return port to
the tricuspid valve, which serves
as the return limb
Indications for use

Clinicians should consider V-A ECMO for patients with cardiogenic shock and V-V ECMO for patients with
respiratory failure. In cases where both cardiac and pulmonary failure are present, V-A ECMO should be
considered. The combination of V-A ECMO with a left ventricular Impella® device (a combination referred to
as ECpella™) can also be considered with V-A ECMO. The advantage of ECpella is that it provides unloading
of the left ventricle to help avoid left ventricular distension that can be a side effect of the increased
afterload associated with the return of oxygenated blood to the aorta. An ECpella configuration also has
the advantage of facilitating pump weaning if cardiac function is slow to recover.3,4
Table 1. Common V-A and V-V ECMO Indications
COMMON V-A ECMO INDICATIONS1 COMMON V-V ECMO INDICATIONS1
• Post-cardiotomy (unable to come off cardiopulmonary • Adult respiratory failure distress syndrome (ARDS)
bypass following cardiac surgery) • Pneumonias (most commonly, bacterial or viral)
• Post-heart transplant in the setting of primary graft • Trauma
failure
• Severe air leak syndromes
• Decompensated cardiomyopathy
• Primary graft failure in lung transplant patients
• Myocarditis
• Pre-transplant for those awaiting a donor match for lung
• Acute coronary syndrome with cardiogenic shock transplant
• Profound cardiac depression due to drug overdose or
sepsis
• Witnessed in-hospital cardiac arrest (E-CPR)5,6
Patient selection
ECMO is a resource-intensive strategy, which like other advanced medical treatment tools and strategies
can support a patient’s life even when there is little chance for meaningful recovery. Therefore, patient
selection is paramount. One of the central considerations for ECMO placement is the likelihood of organ
recovery. Placing ECMO in patients with single organ dysfunction remains preferable to placing ECMO in
patients with multi-system organ failure and diminished likelihood of recovery. The best candidates for
EMCO are patients with hemodynamically or physiologically devastating temporary, reversible single organ
failure in need of organ rest.1,2,7
Specific V-V ECMO considerations

In general, V-V ECMO is considered when predicted patient mortality is greater than 80% despite optimal
use of less invasive strategies.2 Several different guidelines and clinical opinions have been put forth as
common clinical scenarios in which V-V ECMO should be considered; however, clinical consideration
should be given not just to absolute values but to the rate of clinical demise. Table 2 presents specific
parameters to be considered in the decision to initiate V-V ECMO.
Table 2. Parameters Indicating Refractory Hypoxic and Hypercarbic Respiratory Failure and Consideration for
V-V ECMO
CONSIDER V-V ECMO FOR REFRACTORY HYPOXIC CONSIDER V-V ECMO FOR REFRACTORY HYPERCARBIC
RESPIRATORY FAILURE IF: RESPIRATORY FAILURE IF:
• PaO2/FiO2 ratio <50-8020 • pH <7.25 for >6 hours2,7,21

• FiO2 ≥0.820 • PaCO2 ≥60 mm for >6 hours7
• Duration (hours) >3-6 hours2,20 • Pplat ≥31 to 33 cmH2O2
• Failure of prior adjunctive therapies such as:20 • Failure of prior adjunctive therapies such as:20
▷ iNO or inhaled prostaglandins ▷ Set RR of 35/min
▷ Recruitment maneuvers ▷ Vt reduction by steps of 1 mL/kg, to reach a goal of
▷ Prone positioning 4 mL/kg
▷ Neuromuscular blockade ▷ PEEP reduction to a minimum of 8 cmH2O
FiO2 = fraction of inspired oxygen; iNO = inhaled nitric oxide; PaCO2 = partial pressure of carbon dioxide;
PaO2/FiO2 = partial pressure of oxygen to fraction of inspired oxygen ratio; Pplat = plateau pressure; RR = respiratory rate; Vt = tidal volume
Relative contraindications
Although some authors site specific absolute contraindications for ECMO, there is no consensus. Clinical
conditions for which serious consideration should be given as to whether ECMO is a viable circulatory
support strategy include: 2,8
• Clinical frailty scale score ≥3
• Significant comorbidities
• Mechanical ventilation >7 days (for V-V ECMO only)
• Disseminated malignancy
• Advanced age (≥65 years)
• Graft vs host disease
• Immunocompromised
• Multi-organ failure
• Existing brain injuries
• RESP score ≤39,10
• Contraindications to anticoagulation
Management principles
The Extracorporeal Life Support Organization (ELSO) provides detailed guidelines for the management of
ECMO circuits.11 Table 3 presents some general management principles.
Table 3. General Management Principles for ECMO Circuits2,11

CLINICAL PARAMETER RECOMMENDED INDICATIONS
Circuit flow 50-100 mL/kg/min
Patient weight Attempt to achieve patient’s dry weight
Anticoagulation Activated partial thromboplastin time 1.2-1.8 times above normal
Hemoglobin Normal, or 8-9 g/dL if SaO2 >85%
Platelets (in non-bleeding patients) >20 x109/L
Platelets (for bleeding patients) 50-100 x109/L
<0.5-1.0 g/L
Plasma-free hemoglobin If not at goal, consider re-evaluating anticoagulation, cannula position, pump
speed, and long-term viability of pump
V-V ECMO SPECIAL CONSIDERATIONS1,2
• SaO2 >80%
• PaCO2 within normal limits
• Inspiratory pressure <25 cmH2O
• Plateau pressure <30 cmH2O
• PEEP 5-10 cmH2O
PaCO2 = partial pressure of carbon dioxide; SaO2 = oxygen saturation
A team of trained clinicians and ECMO specialists should carefully coordinate management of ECMO
cases within an institution, as this model may improve outcomes.12,13 Visually inspect the circuit and pump
for signs of thrombosis at regular intervals at least once daily. A physical examination of the patient and
regular x-ray monitoring can ensure the cannulas remain in good position without signs of bleeding.2
Of particular concern in peripheral V-A ECMO cannulation is the mixing point where the oxygenated
blood from the ECMO circuit meets the variably oxygenated blood flow from the heart (refer to Figure 1).
This mixing point, which represents the interplay between the native cardiac pump and ECMO, occurs
somewhere in the aorta and depends on the flow from each pump. Since the carotid arteries branch
from the aortic arch, these vessels may have a disproportionate flow from the heart, which may lead to
suboptimal oxygenation of the brain. This mixing point can vary over time. Therefore, right radial arterial
cannulation is preferred for monitoring and ensuring adequate perfusion from this cardiac component of
cerebral blood flow. When arterial access is a challenge, right upper extremity oximetry (eg, either ear lobe)
or central nervous system oxygenation monitoring systems may offer an alternative.1
Accomplishing physiologic rest to allow recovery is an important mechanism by which ECMO is thought
to benefit patients. In V-A ECMO cases the goal is to minimize inotrope usage while maintaining enough
cardiac contractility to ensure left ventricular emptying. For V-V ECMO cases this entails minimizing any
iatrogenic barotrauma or volutrauma by employing minimal ventilator settings.1
In general, hypoxia should be treated by either increasing the FiO2 of the ECMO circuit or increasing the
rate of flow on the ECMO rather than increasing ventilator parameters. Likewise, hypercarbia should
be managed by increasing the ECMO fresh gas flow, also known as the sweep, and not by increasing
ventilator parameters.1 In difficult to manage cases, neuromuscular blockade can be added to assist in
reaching the physiologically acceptable goals as described in Table 3.2
Weaning
V-A ECMO
There are several indications of cardiac recovery including:
• Increasing blood pressure
• Increasing (or return of) pulsatility on the arterial pressure waveform
• Improving PaO2, specifically in a right radial arterial line
While institutional guidelines regarding the specifics of timing and amount vary considerably, the
commonly accepted test for assessing native cardiac function is to decrease the ECMO flows. During
the weaning procedure, visually assess physiologic function with echocardiography or calculate function
using the Fick equation and mixed venous saturation. Perform weaning in the setting of therapeutic
anticoagulation.1,11
V-V ECMO
The weaning of V-V ECMO is not flow dependent. Instead, decrease the gas flow through the ECMO
circuit to low levels such as <30% FiO2 and fresh gas flow rates, sweep, of <2 L/min.2 Patients are likely to be
weanable from the circuit if they can be adequately oxygenated and ventilated with reasonably moderate
ventilator settings (eg, tidal volume 6 mL/kg, <25 breaths/min, FiO2<0.6, PEEP <15 cmH2O), and plateau
pressures remain <30 cmH2O.1,2,11
Withdrawal of care
Some studies have suggested that there should be no limit on the amount of time a patient receives
ECMO support.2,14 However, in practice most institutions give patients on ECMO about 2-3 weeks on circuit
before considering withdrawal, unless the patient’s survivability comes into question before that time.2
Complications
International organizations such as ELSO track ECMO cases and monitor complication rates in
participating ECMO centers.
Historically, thrombosis was the greatest concern with ECMO. Over time, advances in ECMO design have
rendered the circuitry less thrombogenic and activating;2,15 however ECMO still poses a thrombotic risk so
anticoagulation of patients on an ECMO circuit is advised.
Conversely, ECMO can result in the consumption and dilution of clotting factors, and therefore, bleeding
is also a common complication in patients with these large bore cannulas.1 Systematic reviews of ELSO
database patients reveal that elevated activated partial thromboplastin times were associated with
bleeding while on ECMO, suggesting that at least some of the bleeding events may be iatrogenic and
therefore preventable with careful monitoring and administration of anticoagulation.16
Examining complication rates overall, data from a meta-analysis conducted with over 1700 ECMO cases
has identified the three most frequent complications from newer, improved ECMO circuits:17
• Renal failure requiring renal replacement therapy (52%)
• Bacterial pneumonia (33%)
• Bleeding (29%)
In the case of acute kidney injury, ultrafiltration can be directly spliced into the ECMO circuit, which some
clinicians prefer to decrease the incidence of competing blood flow.2 In a large review of hematologic
complications using patients in the ELSO database from 1986 to 2013, Murphy and colleagues found high
rates of oxygenator clots, systemic thrombosis, and cannula site bleeding.18 Of the bleeding complications,
intracranial hemorrhage (ICH) remains a rare but important complication. ICH is estimated to occur in
about 1.8-2.1% of ECMO cases with an elevated relative risk of mortality of 1.27-4.43 when compared to non-
ICH ECMO patients.19 Local peripheral cannulation site complications, most commonly leg ischemia, can
be prevented with the addition of a limb-perfusion catheter to ensure leg circulation regardless of cannula
size.2
Summary
ECMO is a versatile MCS device that can be employed as a rescue strategy in the setting of an
emergent, life-threatening pulmonary or cardiac failure. ECMO remains resource intensive, with
common complications. ECMO requires a specialized treatment team focused on implementing sound
management practices to promote good patient outcomes and ensure patient safety.
References
1. Marasco SF, Lukas G, McDonald M, et al. Review of ECMO (extra corporeal membrane oxygenation) support in
critically ill adult patients. Heart Lung Circ. 2008;17S:S41-7. doi:10.1016/j.hlc.2008.08.009
2. MacLaren G, Combes A, Bartlett RH. Contemporary extracorporeal membrane oxygenation for adult respiratory
failure: life support in the new era. Intensive Care Med. 2012;38(2):210-20. doi:10.1007/s00134-011-2439-2
3. Patel SM, Lipinski J, Al-Kindi SG, et al. Simultaneous venoarterial extracorporeal membrane oxygenation and
percutaneous left ventricular decompression therapy with Impella is associated with improved outcomes in
refractory cardiogenic shock. ASAIO J. 2019;65(1):21-8. doi:10.1097/MAT.0000000000000767
4. Sayer GT, Baker JN, Parks KA. Heart rescue: The role of mechanical circulatory support in the management of
severe refractory cardiogenic shock. Curr Opin Crit Care. 2012;18(5):409-16. doi:10.1097/MCC.0b013e328357f1e6
5. Avalli L, Maggioni E, Formica F, et al. Favourable survival of in-hospital compared to out-of-hospital refractory
cardiac arrest patients treated with extracorporeal membrane oxygenation: An Italian tertiary care centre
experience. Resuscitation. 2012;83(5):579-83. doi:10.1016/j.resuscitation.2011.10.013
6. Chen Y-S, Lin J-W, Yu H-Y, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus
conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and
propensity analysis. Lancet. 2008;372(9638). doi: 10.1016/S0140-6736(08)60958-7.
7. Zochios V, Brodie D, Parhar KK. Towards precision delivery of ECMO in COVID-19 cardiorespiratory failure. ASAIO J.
Published online 2020:1-11. doi:10.1097/MAT.0000000000001191
8. Zochios V, Brodie D, Charlesworth M, Parhar KK. Delivering extracorporeal membrane oxygenation for patients
with COVID-19: what, who, when and how? Anaesthesia. Published online 2020:1-5. doi:10.1111/anae.15099
9. Schmidt M, Bailey M, Sheldrake J, et al. Predicting survival after extracorporeal membrane oxygenation for severe
acute respiratory failure: The Respiratory Extracorporeal Membrane Oxygenation Survival Prediction (RESP) score.
Am J Respir Crit Care Med. 2014;189(11):1374-82. doi:10.1164/rccm.201311-2023OC
10. Brunet J, Valette X, Buklas D, et al. Predicting survival after extracorporeal membrane oxygenation for ARDS: An
external validation of RESP and PRESERVE scores. Respir Care. 2017;62(7):912-19. doi:10.4187/respcare.05098
11. Extracorporeal Life Support Organization (ELSO) Guidelines. Accessed June 16, 2020. https://www.elso.org/
Resources/Guidelines.aspx
12. Dalia AA, Ortoleva J, Fiedler A, et al. Extracorporeal membrane oxygenation is a team sport: Institutional survival
benefits of a formalized ECMO team. J Cardiothorac Vasc Anesth. 2019;33(4):902-7. doi:10.1053/j.jvca.2018.06.003
Cardiol. 2019;73(13):1659-69. doi:10.1016/j.jacc.2018.12.084
14. Lindén V, Palmér K, Reinhard J, et al. High survival in adult patients with acute respiratory distress syndrome
treated by extracorporeal membrane oxygenation, minimal sedation, and pressure supported ventilation. Intensive
Care Med. 2000;26(11):1630-7. doi:10.1007/s001340000697
15. Thomas J, Kostousov V, Teruya J. Bleeding and thrombotic complications in the use of extracorporeal membrane
oxygenation. Semin Thromb Hemost. 2018;44(1):20-9. doi:10.1055/s-0037-1606179
16. Aubron C, DePuydt J, Belon F, et al. Predictive factors of bleeding events in adults undergoing extracorporeal
membrane oxygenation. Ann Intensive Care. 2016;6(1). doi:10.1186/s13613-016-0196-7
17. Zangrillo A, Landoni G, Biondi-Zoccai G, et al. A meta-analysis of complications and mortality of extracorporeal
membrane oxygenation. Crit Care Resusc. 2013;15(3):172-8.
18. Murphy DA, Hockings LE, Andrews RK, et al. Extracorporeal membrane oxygenation-hemostatic complications.
Transfus Med Rev. 2015;29(2):90-101. doi:10.1016/j.tmrv.2014.12.001
19. Fletcher-Sandersjöö A, Thelin EP, Bartek J, et al. Incidence, outcome, and predictors of intracranial hemorrhage
in adult patients on extracorporeal membrane oxygenation: A systematic and narrative review. Front Neurol.
2018;9(JUL):1-10. doi:10.3389/fneur.2018.00548
20. Combes A, Hajage D, Capellier G, et al. Extracorporeal membrane oxygenation for severe acute respiratory distress
syndrome. N Engl J Med. 2018;378(21):1965-75. doi:10.1056/NEJMoa1800385
21. Peek GJ, Mugford M, Tiruvoipati R, et al. Efficacy and economic assessment of conventional ventilatory support
versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre
randomised controlled trial. Lancet. 2009;374(9698):1351-63. doi:10.1016/S0140-6736(09)61069-2
CONTENTS
CHAPTER
ECpella : ™
13 Physiological Basis and

Clinical Management
of Dual Mechanical
Circulatory Support with
ECMO and Impella CP ®

Division of Pulmonary and Critical Care Medicine
Brigham and Women’s Hospital
Boston, MA
Institute for Medical Engineering and Science

Cambridge, MA
spkeller@mit.edu
INTRODUCTION
“ECpella” denotes concurrent use of both extracorporeal membrane oxygenation
(ECMO) and an Impella® heart pump to provide mechanical circulatory support
(MCS) for patients in cardiogenic shock.1,2 This approach is used for patients with
profound left ventricular or biventricular failure and typically arises in 1 of 2 clinical
scenarios:
• Initiation of ECMO in a patient with persistent shock already supported by an
Impella, or
• Placement of an Impella for venting the left ventricle (LV) in a patient
supported on ECMO
While ECpella support can be performed with any of the left-sided Impella
devices, the Impella CP® is most commonly employed and will be used as the
paradigmatic device for this chapter.
<< Chapter 12 Chapter 13 | ECpella™: Physiological Basis and Clinical Management of Dual Chapter 14 >>
Mechanical Circulatory Support with ECMO and Impella CP®
Dual mechanical support with ECpella presents complex management challenges as the clinician must
simultaneously titrate 2 interdependent MCS devices, determine support for concomitant organ failure,
and provide appropriate medical therapy. At present, there is a paucity of research on ECpella support
and limited clinical studies available to guide the optimal approach to device and patient management.
Pending new studies to support the development of evidence-based guidelines, clinicians must rely on
physiological reasoning and understanding device operation to optimally manage patients with existing
resources.
The goal of this chapter is to provide clinicians with insights into the effects of ECpella support on cardiac
function and hemodynamics and present a physiology-grounded approach to management and weaning
of ECpella support.
Physiology of ECMO support and LV venting

ECMO is rapidly being adopted to provide circulatory support despite limited understanding of its effects
on cardiac function and how to titrate support to achieve optimal patient outcomes.3–5 Deployed as an MCS
device, ECMO shunts venous blood through an oxygenator via a centrifugal pump to return oxygenated
blood to the systemic arterial circulation.6 Peripheral cannulation is the most common approach with the
return cannula inserted into the femoral artery and advanced until the tip terminates in the iliac artery or
distal aorta. For this chapter, the term ECMO will refer to this specific cannulation strategy.
ECMO support profoundly alters physiological blood

flow and effectively decouples the arterial system
from the left ventricle. Continuous retrograde
perfusion from the ECMO circuit collides in the
aorta with residual pulsatile flow generated by
the failing heart to create a dynamic watershed
region whose size and position varies over the
cardiac cycle.7 The perfusion provided by the ECMO
circuit increases afterload which acts to increase
myocardial oxygen demand while requiring
increased cardiac work.8 In severe heart failure, the
LV may be unable to overcome ECMO-generated
afterload resulting in lack of aortic valve opening
and risking blood flow stasis in the cardiopulmonary
circulation, LV distention and reduced coronary
perfusion, and intracardiac thrombus formation.6,9
Figure 1. Peripheral Veno-Arterial (V-A) ECMO

(adapted from Murphy et al.32)
Methods to either directly or indirectly augment

LV emptying (see Box) are termed “venting” and
are initiated in an effort to reduce the catastrophic
consequences of inadequate LV ejection that can
occur during ECMO support.10,11 LV distention can
occur either slowly, over hours or days, or within
minutes of initiating ECMO depending on titration
of support and severity of underlying heart function.
While the specific criteria used to determine the
timing of initiating LV venting is an area of active
investigation, accumulating clinical studies suggest
early LV venting may yield improved patient
outcomes.2,10
Figure 2. ECMO Support and

Watershed Region
LV VENTING APPROACHES
Indirect LV venting methods:11–13
• Atrial septostomy: provides outlet for drainage when LV pressures are elevated
• Intra-aortic balloon pumps (IABP): appears to improve LV ejection although

mechanism is unclear in setting of continuous retrograde perfusion from ECMO
Direct LV venting methods:

• Transventricular drainage: surgical placement of a drainage cannula into the LV that is
then connected to ECMO drainage cannula
• Transvalvular drainage: use of an Impella to promote forward flow through
cardiopulmonary vascular system and direct emptying of LV
The Impella heart pump provides multiple potential advantages over other LV venting strategies including
the following:
• Impella achieves unloading even in profound heart failure, unlike indirect approaches that still require
some basal level of heart contractility
• Impella, like the IABP, is placed via minimally invasive percutaneous vascular access and does
not require injury to the heart—as is required for atrial septostomy and surgical ventricular drain
placement—to achieve LV venting
• Impella provides titratable mechanical support and enables a staged de-escalation approach not
easily achievable with other forms of venting
Potential disadvantages of Impella as an LV venting strategy include increased risk of hemolysis with
dual mechanical support and traditional contraindications such as the presence of a mechanical aortic
valve prohibiting placement of the Impella.14,15 Although additional studies are required, retrospective
clinical studies suggest improved survival for patients maintained on ECpella support over ECMO-only
approaches.2,10
Physiology and clinical management of ECpella support

ECpella support requires coordinated titration of 2 distinct yet interdependent MCS devices. Unlike ECMO-
only support, in which uptitration of circuit flow is limited by deleterious effects on LV function, ECpella
provides both:
• Mechanical support of systemic perfusion
• LV protection to promote cardiac recovery
The presence of the Impella enables titration of ECMO support to meet end-organ perfusion
demands while simultaneously acting to reduce cardiac work and maintain forward flow through the
cardiopulmonary circulation. However, the operational state of each device alters the physiological milieu
for the other and requires an integrated management approach to ensure optimal patient outcome.
ECpella perfusion and hemodynamics

Total perfusion of the aortofemoral vascular tree
during ECpella support consists of varying levels of
3 interconnected sources:7
• Pulsatile antegrade flow from the heart
• Continuous antegrade flow from the Impella
• Continuous retrograde flow from the ECMO
circuit
Figure 3. ECpella Support
Compared with ECMO-only support, during which all antegrade perfusion derives from residual function
of the failing heart, the Impella in ECpella-supported patients produces forward flow through the
cardiopulmonary circulation and across the aortic valve even in profound LV failure. Although watershed
dynamics are yet to be described during ECpella support, Impella-generated continuous antegrade
perfusion likely decreases variation and movement of the watershed region over the cardiac cycle due to
reduction in pulsatile flow from the heart. The effects of this are unknown but may lead to a reduction in
chaotic blood flow domains within the aorta and more stable end-organ perfusion.
ECpella hemodynamics are determined by vascular tone and the total and relative blood flow generated
by the 3 sources of systemic perfusion. Pulsatility is created by the pressure wave produced during LV
contraction, whose magnitude is a function of the contractility and loading state of the ventricle.16 LV
unloading by the Impella generally reduces pulsatility as the blood volume ejected during ventricular
contraction is decreased.17 In profound cardiogenic shock, severely reduced contractility may lead to an
absence of pulsatility with all perfusion provided by continuous flow from the ECMO circuit and Impella.
The loading state of the heart is partially a function of titration of both Impella and ECMO support. A
relative increase in Impella support decreases LV preload while increasing afterload by directly ejecting
blood from the LV into the aorta. An increase in ECMO flow in ECpella support decreases LV preload by
shunting more blood away from cardiopulmonary circulation while simultaneously increasing afterload.
The flow produced by both the ECMO circuit and the Impella is partially determined by afterload.18,19
Avoiding elevated blood pressures is a means to therefore optimize mechanical circulatory support
and increase systemic flow. Although the safe lower bound of blood pressure during MCS is unknown,
maintaining a goal mean arterial pressure of 65 to 80 mmHg is a reasonable target within standard
approaches to shock management.20,21
Figure 4. Perfusion Provided by ECpella Support
Patient monitoring
The major goals of patient monitoring are to ensure adequate end-organ perfusion and oxygenation
and maintenance of target systemic blood pressure. Patient monitoring is challenging in the setting of
ECpella support given the non-physiological blood flow generated and limitations of existing diagnostics
to precisely determine total systemic perfusion. While modern ECMO circuits and the Impella provide
estimated flow measurements, the primary means of determining adequacy of current support is through
the serial measurement of systemic lactate levels and assessment of end-organ function.
The range of useful metrics supplied by pulmonary artery catheters (PACs) during ECpella support is
limited by entrainment of venous blood into the ECMO circuit. While PACs provide measurements of right
atrial pressure and pulmonary artery pressures, they cannot provide reliable estimates of cardiac output
on ECMO support. The primary value of the PAC is during weaning of ECMO support as the catheter can
then provide insight into right ventricle function and the effect of decreasing support on pulmonary artery
pressures.
A persistent challenge in any form of ECMO support, including ECpella, is risk of differential oxygenation
in the setting of coexistent lung disease.22,23 While the ECMO circuit provides oxygenation to the distal
aorta, antegrade blood flow from the heart depends on the lungs for gas exchange. Tissues perfused
by antegrade flow from the heart require close monitoring to ensure adequate oxygenation and guide
titration of mechanical ventilation or supplemental oxygen delivery. As the right brachiocephalic artery
is the first branching vessel off the aortic arch, monitoring tissue oxygenation on the right arm through
blood gas analysis or tissue oximetry is a means to ensure adequate cerebral oxygenation and appropriate
respiratory support.
An approach to initial titration of ECpella support

Following institution of ECpella support, the clinician must determine initial support settings to restore
systemic perfusion and maintain end-organ function. The general approach to ECpella support is to rely
on the ECMO circuit as the predominant source of perfusion while using the Impella to protect the LV and
maintain forward flow through the cardiopulmonary circulation. As venous return is entrained into the
ECMO circuit, less blood is available to enter into the cardiopulmonary circulation. Practically, this results
in less ventricular filling and limits uptitration of Impella support. The following is a stepwise approach to
determine initial ECpella device parameters.
1. Initiate Impella support at P-1. If there are retrograde flow alarms, increase by 1 step until retrograde
flow alarms cease.
2. Increase ECMO flow until target flow is reached or flow is limited by either suction events (or
withdrawal cannula “chatter”) or reaching threshold for safe pump RPMs. Assume ECMO flow provides
70%-90% of total perfusion while on ECpella support.
3. Maintain goal MAPs of 65 to 80 mmHg. Initiate and titrate vasopressor or vasodilator therapy as
needed to maintain MAP target. Re-assess ECMO flow if initial titration occurred with MAPs out
of target range. Wean inotrope support to reduce myocardial oxygen consumption and rely on
mechanical support to maintain systemic perfusion.
4. Re-assess Impella P-level. Goal is to maintain stable forward flow through cardiopulmonary circulation
while limiting Impella suction events. Use bedside echocardiogram if available to guide increase in
P-level support until intraventricular septum is midline. Initial P-level settings typically range from P-1 to
P-3. If suction events occur at P-1, attempt gradual decrease in ECMO support to increase flow through
the cardiopulmonary circulation.
5. Administer volume therapy if ECMO flows are below target and are limited by suction events.
6. Obtain serial lactate measurements to monitor for adequate end-organ perfusion and reversal of
shock.
Initiation of mechanical support may be a very dynamic clinical management period for the cardiogenic
shock patient. It is common for patients to experience varying degrees of reperfusion injury and an
increase in circulating inflammatory mediators following restoration of blood flow in addition to the
leukocyte activation that occurs on blood contact with the extracorporeal circuit.24 Volume administration
is often required to maintain adequate extracorporeal flows and vasopressors may be needed in the setting
of vasoplegia. Patients experiencing prolonged shock prior to mechanical support may never become
stably supported and demonstrate the need for prompt reversal of shock to improve clinical outcomes.
For patients stably maintained on mechanical support, restoration of perfusion may be followed by gradual
recovery of end-organ function. This often requires several days of full support as inflammation recedes and
vascular tone recovers. As vasopressor requirements lessen, patients may tolerate volume removal either
via diuretic administration or use of renal replacement therapy depending on kidney function. As patients
regain homeostasis, the primary focus of care is to create the physiological milieu to promote weaning
of ECMO support though optimization of cardiac loading conditions and treatment of the underlying
etiology of the presenting cardiac dysfunction.
It is important to note that patients experience a wide variety of trajectories and that no proposed
approach to support can encompass all clinical scenarios. Rather, the proposed approach is intended
to demonstrate a specific process for the titration of support that can then be applied and modified for
each patient’s specific physiology. Advancements in diagnostics and device function will further alter the
approach to support as new information enables tailored support and provides the clinicians with new
tools in guiding and titrating therapy.
Weaning and de-escalation of ECpella support

Weaning of MCS is an ongoing area of investigation requiring further experimentation to optimally identify
patient readiness to be withdrawn safely from support.25,26 The presence of dual mechanical support
provides a particular challenge as there are 2 devices to titrate and assess in determining readiness to
wean.
Key factors to evaluate for deciding when to withdraw support include:

• Systemic homeostasis and recovery of end-organ function
• Underlying etiology of cardiogenic shock and evidence of cardiac recovery
• Overall goals of care and options for durable long-term support if weaning is unsuccessful
Use of a staged de-escalation approach provides for a controlled reduction in mechanical support that
provides for ongoing support while assessing recovery and determining need for durable support. Because
the ECMO circuit is more invasive and profoundly alters physiological blood flow, removal of ECMO is the
primary initial step in de-escalation of support. As with overall management and support, there are no
evidence-based guidelines to determine the optimal weaning strategy. In an effort to provide guidance on
the weaning of ECpella support, a physiology-based approach is suggested to assess readiness for ECMO
weaning.
The purpose of weaning criteria is to identify patients who may be ready to tolerate withdrawal of ECMO
support. One approach prior to advancing to a more formal weaning study is to first perform a rapid
bedside screening test. This test consists of gradually reducing ECMO flow to 2.5 LPM and assessing
hemodynamics and pulmonary arterial pressures. Withdrawal of ECMO supports requires the right
ventricle to rapidly accommodate the entire venous return and maintain adequate cardiac output without
support. Ideally, patients will have an indwelling PAC to allow for simultaneous assessment of right-sided
filling pressures and pulmonary artery pressures. The rapid screen determines if both the right and left
heart can tolerate the increase venous return directed to the cardiopulmonary circulation and are able to
maintain hemodynamics. Patients who tolerate this can advance to a more formal bedside study.
Variable approaches to ramp studies for ECMO supported patients are described in the literature.27,28 In
general, the approaches consist of a gradual decrease in support while monitoring the physiological
response. Practically, this can be performed by a gradual decrease in ECMO flow by 0.5 LPM until a low flow
of 1 LPM is reached. The patient may require a modest increase in Impella support or low dose inotrope
support to maintain forward flow and systemic hemodynamics. Decreasing support performed with
simultaneous echocardiogram imaging is preferred as it provides observation of ventricular changes with
decreasing ECMO support. While quantitative cutoffs have yet to be definitely determined, qualitative
changes that lead to concern about the tolerability of ECMO weaning include RV or LV dilation or evidence
of valvular dysfunction.
The optimal duration of the ramp trial prior to determination of decannulation is unknown but typically
on the order of 60 minutes or less as the reduced flow through the ECMO circuit is a significant clotting
risk. The low flow also leads to blood recirculation in the pump which risks hemolysis.29 Bolus dosing of
anticoagulation prior to ramp study performance is common practice to reduce risk of peri-procedural
clotting. The ramp study is important to predicting post-decannulation clinical course as it provides the
clinician with insight into how the patient’s heart will tolerate a return to sustaining full flow through
the cardiopulmonary circulation and maintenance with only a left-sided support device. Although
bedside decannulation is possible, the preferred approach for long-term patency of the femoral artery is
decannulation with a formal transesophageal echocardiogram followed by surgical repair of the femoral
artery.
The goal of maintaining the patient on minimal to low dose inotropes and vasopressors and low Impella
P-level prior to ECMO decannulation is to provide the clinician with therapeutic options to increase support
following decannulation. While the overall goal of MCS is to reduce need for inotropic therapy, transient
use of inotropes may be required at the time of decannulation as the heart adapts to return of physiologic
venous return.
ECpella complications and management challenges

Dual mechanical support presents additional complications and management challenges beyond those
found with solitary use of either ECMO or Impella. Both devices individually can induce blood cell damage
and cause hemolysis which can be worsened when the devices are used in combination. The presence of
large cannula in the femoral arteries also increases the risk of lower extremity ischemia. This is a particular
problem in ECMO support and is typically managed with use of a distal perfuser.30 Rarely, this may also
occur in the side in which the Impella is placed. Depending on anatomical constraints, use of alternative
arterial access sites such as the axillary artery may be required for Impella placement.
Anticoagulation and hemorrhage

Blood exposure to extracorporeal circuits is a persistent clotting risk and requires therapeutic
anticoagulation.31 Patients with profound shock frequently experience hepatic dysfunction and
coagulopathies that complicate safe administration of anticoagulation. Depending on the duration of
shock prior to initiation of support, patients may be at risk for mesenteric ischemia and the potential
for catastrophic hemorrhage. These patients are often pro-thrombotic despite active hemorrhage
which makes their management particularly challenging. One approach is to normalize the INR while
maintaining a therapeutic PTT or Anti-Xa with the goal to ensure adequate levels of Protein C and S in
addition to adequate clotting factors. As the Impella requires anticoagulation administration, appropriate
accounting for multiple sites of anticoagulation administration must be done during ECpella support.
Ventilator management
Patients with profound shock requiring ECpella support are frequently intubated and maintained on
mechanical ventilation during initial management. Ventilator interactions with ECpella support have
yet to be described and are an area of potential complication. Decreasing blood flow through the
cardiopulmonary circulation alters ventilation-perfusion matching in unpredictable ways. Positive pressure
from the ventilator increases alveolar pressure which may overcome pulmonary arteriolar pressure and
significantly alter the distribution of perfusion in the lung. Ventilation-perfusion mismatch is further
produced by shunting of blood away from the cardiopulmonary circulation by the ECMO circuit. For
patients with persistent Impella suction alarms due to low flow in the cardiopulmonary circulation, PEEP
titration may be required to promote additional forward flow.
Summary
ECpella support is an MCS strategy for cardiogenic shock patients that provides for both restoration
of systemic perfusion and protection of the LV from the deleterious effects of ECMO. Pending the
development of evidence-based guidelines for management of dual mechanical support, achieving
optimal patient outcomes requires an approach relying on physiological reasoning and understanding of
device operation. Dual mechanical support is a viable strategy to support patients with profound shock
while staged de-escalation provides for a pathway enabling both survival and cardiac recovery.

References
1. Vallabhajosyula S, O’Horo JC, Antharam P, et al. Venoarterial extracorporeal membrane oxygenation with
concomitant Impella versus venoarterial extracorporeal membrane oxygenation for cardiogenic shock. ASAIO J.
2020;66(5):497-503. doi: 10.1097/MAT.0000000000001039.
membrane oxygenation may improve survival of patients with cardiogenic shock. Eur J Heart Fail. 2017;19(3)404-12.
doi: 10.1002/ejhf.668.
support: incidence, outcomes, and cost analysis. J Am Coll Cardiol. 2014;64(14):1407-15. doi: 10.1016/j.jacc.2014.07.958.
4. Karagiannidis C, Brodie D, Strassmann S, et al. Extracorporeal membrane oxygenation: evolving epidemiology and
mortality. Intensive Care Med. 2016;42(5):889-96. doi: 10.1007/s00134-016-4273-z.
5. Lequier L, Horton SB, McMullan DM, Bartlett RH. Extracorporeal membrane oxygenation circuitry. Pediatr Crit Care
Med. 2013;14:S7-12. doi: 10.1097/PCC.0b013e318292dd10.
6. Keller SP. Management of peripheral venoarterial extracorporeal membrane oxygenation in cardiogenic shock. Crit
Care Med. 2019;47(9):1235-42. doi: 10.1097/CCM.0000000000003879.
7. Nezami FR, Khodaee F, Edelman ER, Keller SP. A computational fluid dynamics study of the extracorporeal
membrane oxygenation-failing heart circulation. ASAIO J. 2020. doi:10.1097/MAT.0000000000001221
8. Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of mechanical circulatory support. J Am Coll Cardiol.
2015;66(23):2663-74. doi: 10.1016/j.jacc.2015.10.017.
9. Xie A, Forrest P, Loforte A. Left ventricular decompression in veno-arterial extracorporeal membrane oxygenation.
Ann Cardiothorac Surg. 2019;8(1):9–18. doi: 10.21037/acs.2018.11.07.
10. Piechura LM, Coppolino A, Mody GN, et al. Left ventricle unloading strategies in ECMO: A single-center experience.
J Card Surg. 2020;35(7):1514-24. doi: 10.1111/jocs.14644.
11. Meani P, Gelsomino S, Natour E, et al. Modalities and effects of left ventricle unloading on extracorporeal life
support: a review of the current literature. Eur J Heart Fail. 2017;19:84–91. doi: 10.1002/ejhf.850.
12. Camboni D, Akay B, Sassalos P, et al. Use of venovenous extracorporeal membrane oxygenation and an
atrial septostomy for pulmonary and right ventricular failure. Ann Thorac Surg. 2011;91:144-9. doi: 10.1016/j.
athoracsur.2010.07.036.
13. Griffin JM, Restaino S, Takeda K, Garan AR. Left ventricular decompression on veno-arterial extracorporeal
membrane oxygenation with intra-aortic balloon counterpulsation. J Cardiothorac Surg. 2019;14(1):153. doi: 10.1186/
s13019-019-0970-3. doi: 10.1097/MAT.0000000000000290.
14. Badiye AP, Hernandez GA, Novoa I, Chaparro SV. Incidence of hemolysis in patients with cardiogenic
shock treated with Impella percutaneous left ventricular assist device. ASAIO J. 2016;62(1):11-4. doi: 10.1097/
MAT.0000000000000290.
15. Patel SM, Lipinski J, Al-Kindi SG, et al. Simultaneous venoarterial extracorporeal membrane oxygenation and
percutaneous left ventricular decompression therapy with Impella is associated with improved outcomes in
refractory cardiogenic shock. ASAIO J. 2019;65(1):21-8. doi: 10.1097/MAT.0000000000000767.
16. Mitchell GF. Aortic stiffness, pressure and flow pulsatility, and target organ damage. J Appl Physiol. 2018:125(6):1871-
80. doi: 10.1152/japplphysiol.00108.2018.
17. Chera HH, Nagar M, Chang NL, et al. Overview of Impella and mechanical devices in cardiogenic shock. Expert Rev
Med Devices. 2018;15(4):293-9. doi: 10.1080/17434440.2018.1456334.
18. Driessen JJ, Fransen G, Rondelez L, et al. Comparison of the standard roller pump and a pulsatile centrifugal
pump for extracorporeal circulation during routine coronary artery bypass grafting. Perfusion. 1991;6(4):303-11. doi:
10.1177/026765919100600411.
19. Chang BY, Keller SP, Bhavsar SS, et al. Mechanical circulatory support device-heart hysteretic interaction can
predict left ventricular end diastolic pressure. Sci Transl Med. 2018;10(430):eaao2980. doi: 10.1126/scitranslmed.
aao2980.
20. Gross PA. Hypotension and mortality in septic shock: the “golden hour”. Crit Care Med. 2006;34(6):1819-20. doi:
10.1097/01.CCM.0000220054.95214.7D.
21. Mann HJ, Nolan PE. Update on the management of cardiogenic shock. Curr Opin Crit Care. 2006;12(5):431-6. doi:
10.1097/01.ccx.0000244122.62118.da.
22. Stevens MC, Callaghan FM, Forrest P, et al. A computational framework for adjusting flow during peripheral
extracorporeal membrane oxygenation to reduce differential hypoxia. J Biomech. 2018;79:39-44. doi: 10.1016/j.
jbiomech.2018.07.037.
23. Rupprecht L, Lunz D, Philipp A, et al. Pitfalls in percutaneous ECMO cannulation. Heart Lung Vessel. 2015;7(4):320-6.
24. Millar JE, Fanning JP, McDonald CI, et al. The inflammatory response to extracorporeal membrane oxygenation
(ECMO): a review of the pathophysiology. Crit Care. 2016;20(1):387. doi: 10.1186/s13054-016-1570-4.
25. Pappalardo F, Pieri M, Corada BA, et al. Timing and strategy for weaning from venoarterial ECMO are complex
issues. J Cardiothorac Vasc Anesth. 2015;29(4):906-11. doi: 10.1053/j.jvca.2014.12.011.
26. Guglin M, Zucker MJ, Bazan VM, et al. Venoarterial ECMO for adults: JACC expert panel. J Am Coll Cardiol.
2019;73(6):698-716. doi: 10.1016/j.jacc.2018.11.038.
27. Aissaoui N, Luyt CE, Leprince P, et al. Predictors of successful extracorporeal membrane oxygenation (ECMO)
weaning after assistance for refractory cardiogenic shock. Intensive Care Med. 2011;37(11):1738-45. doi: 10.1007/
s00134-011-2358-2.
28. Ortuno S, Delmas Diehl J, et al. Weaning from veno-arterial extra-corporeal membrane oxygenation: which
strategy to use? Ann Cardiothorac Surg. 2019;8(1):E1–E8. doi: 10.21037/acs.2018.08.05.
29. Gross-Hardt S, Hesselmann F, Arens J, et al. Low-flow assessment of current ECMO/ECCO2R rotary blood pumps
and the potential effect on hemocompatibility. Crit Care. 2019;23(1):348. doi: 10.1186/s13054-019-2622-3.
30. Jou YY, Skancke M, Sanaiha Y, et al. Efficacy of distal perfusion cannulae in preventing limb ischemia during
extracorporeal membrane oxygenation: a systematic review and meta-analysis. Artif Organs. 2017;41(11):E263–E273.
doi: 10.1111/aor.12942.
31. Murphey DA, Hockings LE, Andrews RK, et al. Extracorporeal membrane oxygenation—hemostatic complications.
Transfus Med Rev. 2015;29(2):90–101. doi: 10.1016/j.tmrv.2014.12.001.
32. Murphy DA, Hockings LE, Andrews RK, et al. Extracorporeal membrane oxygenation-hemostatic complications.
Transfus Med Rev. 2015;29(2):90-101. doi:10.1016/j.tmrv.2014.12.001
PART IV
TABLE OF
CONTENTS
Support: General
Management Issues
Chapter 14 Patient Transfer Considerations............................................. 125
Chapter 15 Escalation of Care in Cardiogenic Shock............................. 133
Chapter 16 Palliative Care................................................................................138
Chapter 17 Non-Acute Coronary Syndrome Cardiogenic Shock.......145
Chapter 18 Non-Cardiac Critical Illness Management...........................156
Chapter 19 Mechanical Cardiac Support Use in COVID-19...................169
TABLE OF PART IV Mechanical Circulatory Support: General Management Issues
CONTENTS
Patient Transfer
CHAPTER
14 Considerations
Brian Porvin, DO
Vice Chairman of Internal Medicine
Honor Health Deer Valley Medical Center
Phoenix, AZ
b.porvin@pulmonaryassociates.com
INTRODUCTION
Interhospital transfer of critically ill patients is a safe and effective
method of matching patients with advanced healthcare needs
to the institutions and clinicians that have the resources to care
for them. This chapter reviews several aspects of patient transfer
for patients with cardiogenic shock and/or patients who are
supported with mechanical circulatory support devices.
<< Chapter 13 Chapter 14 | Patient Transfer Considerations Chapter 15 >>
Hub and spoke model

The “hub and spoke” model describes a network of hospitals that care for patients with a diverse range
of clinical needs. This model categorizes variable clinical, surgical, and technological staffing capabilities
in over 6000 hospitals within the continental United States. Patients are initially evaluated, triaged, and
treated at a spoke hospital and then transferred to a hub if the needs of the patient exceed the resources or
capabilities of the spoke hospital.
Each hospital within a regionalized care system has unique capabilities. Regionalized care systems
currently exist for stroke, out-of-hospital cardiac arrest (OHCA), trauma, STEMI, and aortic dissection and will
likely improve outcomes in patients with cardiogenic shock.6-13
It is important that every institution:

• Understand its own capabilities and the capabilities of other hospitals within their care system
• Have clear criterion for transfer to other hospitals
• Develop relationships, protocols, and benchmarks for appropriate and safe patient transfer when
required
Pathway for patients in cardiogenic shock

Safe and effective transfer of patients in cardiogenic shock (CS) or with mechanical circulatory support
(MCS) devices such as Impella® catheters in place starts with appropriate patient selection. Early transfer of
patients prior to prolonged shock and multiorgan dysfunction is paramount to improve patient outcomes.
Once a patient is identified as requiring transfer, all efforts must be made to optimize and stabilize
the patient to facilitate safe transfer and to minimize the risk of decompensation while en route to the
accepting facility. Finally, ongoing communication with the accepting institution is necessary so that the
patient is triaged to the appropriate level of care with the resources required to care for that patient.
Figure 1 illustrates a proposed cardiogenic shock pathway. Understanding this pathway is key to
understanding the capabilities required to care for patients in cardiogenic shock. Notably, it is important
to understand how lactate and cardiac power output (CPO) measurements at 12 to 24 hours predict
outcomes in cardiogenic shock (Figure 2). Therapy escalation is needed for patients who fail to clear lactate
and improve CPO.
RESCUSCITATION AND MEDICAL THERAPY FOR CARDIOGENIC SHOCK

• Inotropes, vasopressors • Mechanical ventilation • Medical therapy for specific etiology
TEMPORARY MCS*
• IABP
• Peripheral VAD
• Implantable VAD
REPERFUSION (ACS only)*

• PCI
• CABG
• Fibrinolysis
RECOVERY PALLIATIVE CARE
TRANSPLANT DURABLE VAD DESTINATION VAD
Figure 1. Proposed Cardiogenic Shock Care Pathway (adapted from van Diepen et al.1)
*Whether temporary MCS or reperfusion comes first may vary; however in cases of refractory cardiac arrest or shock,
consider temporary MCS before reperfusion
CARDIAC POWER OUTPUT

>0.6 ≤0.6
63% Survival 30% Survival

≥4
(n=5/8) (n=3/10)
LACTATE
<4 96% Survival 80% Survival

(n=45/47) (n=8/10)
Figure 2. Lactate and CPO as Predictors of Survival at 12 and 24 Hours (adapted from Basir et al.2)
Hospital capabilities
When considering whether to transfer a patient, it is important to understand hospital capabilities
(Table 1). There has been a push that all cardiogenic shock regional centers should meet a minimum level
1 unit organizational and staffing criteria as outlined by international scientific statements.14-17
Table 1. Hospital Capabilities
CATH LAB CAPABILITIES
• Diagnostic
• Interventions including stenting/rotablation
• Percutaneous MCS (eg, Impella 2.5®, CP®, RP®, or IABP)
• Right heart catheterization (RHC)
SURGICAL CAPABILITIES
• Impella 5.0/LD
• ECMO/ECPR
• Other surgical VADs (eg, Centrimag, TandemHeart)
• Durable VAD
• Transplant
CRITICAL CARE CAPABILITIES
• 24/7 intensivist coverage

• 24/7 echo
• Nursing ratios and skill sets
• Perfusionist
• Invasive hemodynamic monitoring; Swan Ganz, CVP, ScvO2, SvO2
• Hemodialysis, continuous renal replacement therapy
SUB-SPECIALTY AVAILABILITY
• Advanced heart failure

• Cardiothoracic surgery
• Vascular surgery
• Nephrology
• Hematology
• Neurology
• Formalized palliative care
• Critical care
Care options
There may be several care options to consider for a patient with AMI complicated by cardiogenic shock.
• Immediate transfer or bypass hospital by emergency services
• Stabilize and transfer
• Stabilize and treat
• Academic or hub hospital
Table 2 describes the capability considerations for each of these options.
Table 2. Capability Considerations for Various Care Options

CARE OPTIONS CAPABILITY CONSIDERATIONS
Immediate transfer • No PCI capabilities available
or bypass hospital by • Studies have shown significant improvement in mortality when patients with AMI shock
emergency services are transferred to hospitals with direct revascularization capabilities3,4
Stabilize and transfer • Primary PCI capabilities available

• May or may not have MCS capabilities available
• May or may not have hemodynamic monitoring capabilities
Stabilize and treat • Primary PCI capabilities available

• Percutaneous MCS capabilities available
• May or may not have surgical MCS capabilities
• Advanced hemodynamic monitoring available
• 24/7 critical care coverage available
• Subspecialty consultation available
• May or may not have ECMO available
• Transfer if the patient declines or needs escalation of therapy (see Figure 2)
Academic or hub • Hub and academic centers may require relationships with regional centers outside of their
hospital hospital system for therapies that may not be available, such as durable VAD or transplant
Modes of transfer
Modes for transferring patients from one hospital to another include:
• Ground transport
• Fixed wing transport
• Helicopter transport
No mode of transport has been shown to be superior in transporting critically ill patients. When choosing
the mode, consider the following factors:
• Distance
• Availability of local resources
• Regional protocols
• Stability of the patient
Preparing the patient for transfer

When preparing a patient for transfer to another hospital, communication and patient preparation are key.
Table 3 describes some key patient transfer considerations.
Table 3. Key Patient Transfer Considerations

Communicate with the accepting facility and clinical team regarding:
• Patient’s current clinical condition
COMMUNICATION
• Potential complications of transfer
• Anticipated resources required by accepting hospital
• Secure airway prior to transport

AIRWAY
• Low threshold for intubation if not already ventilated
• Optimize ventilator settings

• Limit mean and peak airway pressures to limit barotrauma and volutrauma
VENTILATION • Consider low tidal volume ventilation at 6-8mL/kg ideal body weight
• Keep plateau pressure (Pplat) <30 cm H2O if possible
• Ensure adequate blood gas exchange; maintain blood pH >7.15; PaO2 >60 mmHg
VASCULAR ACCESS • Ensure adequate vascular access with at least 2 large bore IVs or central venous access
Obtain current labs just prior to transport including:

• Lactate
• Metabolic panel
LABS
• Hemoglobin
• Markers of hemolysis
Transfuse prior to transfer if required or anticipated ongoing blood loss
• Optimize hemodynamics including titration of vasopressors and inotropes

HEMODYNAMICS
• For patient supported with Impella, titrate to a MAP rather than SBP
• Ensure adequate distal perfusion of the leg if large bore arterial access is in place
DISTAL PERFUSION
• Consider distal catheter for retrograde perfusion of the leg
TRANSFER CONSIDERATIONS SPECIFIC TO IMPELLA ®
Specific pre-transfer considerations for patients supported with an Impella catheter include:
• Pre-determined team of transport personnel
• Transport equipment list, including a backup Automated Impella Controller (AIC) console
and defibrillator
• Transport monitoring plan with pre-set intervals for documentation of patient vitals and
Impella position as well as monitoring for clinical signs of hemolysis, including urine color
and output
• Preparation for potential loss of pulsatility during transport (see CPR considerations
below)
• Post-transfer checklist
Considerations for CPR during transport in critically ill patients with Impella in place:
• CPR is not necessarily required for loss of pulsatility in a patient who is on support but has
maintained peripheral perfusion and mean arterial pressure. Focus on rapidly improving
native cardiac function with fluids, inotropes, aggressive management of electrolyte
abnormalities, and correction of acidosis.
• If the patient’s hemodynamics are not maintained and there is a loss of pulsatility, turn
Impella down to P2 and initiate CPR while aggressive resuscitation efforts proceed.
• If there is a return of spontaneous circulation (ROSC), increase to the appropriate Impella
P-level and reconfirm placement, initially with appropriate waveforms on the AIC and
subsequently with echocardiography.
Summary
Many hospitals utilize a hub and spoke model in which critically ill patients, such as those with cardiogenic
shock, are evaluated at a spoke hospital and then transferred to a hub hospital with the resources to meet
patients’ advanced healthcare needs. When interhospital transfer is considered, clinicians must evaluate
and understand hospital capabilities, care options, modes of transfer, and how to prepare the patient for
transfer.
Studies demonstrate a positive correlation between operator and hospital volume with mortality in
primary PCI, surgery, and cardiogenic shock.5 In cardiogenic shock specifically, clinical volume has been
directly associated with improved mortality and high-volume centers tend to be academic, urban, and
serve as referral hub hospitals. High volume centers with expertise in cardiogenic shock more frequently
utilized early revascularization, MCS, ECMO, and hemodialysis.
References
1. van Diepen S, Katz JN, Albert NM, et al. Contemporary management of cardiogenic shock: A scientific statement
from the American Heart Association. Circulation. 2017;136(16):e232-68. doi.org/10.1161/ cir.0000000000000525
2. Basir M, Isseh I, Schreiber T, et al. TCT-83 lactate and cardiac power output measurements at 12-24 hours reliably
predict outcomes in cardiogenic shock: Insights from the National Cardiogenic Shock Initiative. J Am Coll Cardiol.
2018;17(13 Supplement):B37.
cardiogenic shock. N Engl J Med. 1999;341:625-34. DOI: 10.1056/NEJM199908263410901
4. Le May MR, Wells GA, So DY, et al. Reduction in mortality as a result of direct transport from the field to a receiving
center for primary percutaneous coronary intervention. J Am Coll Cardiol. 2012;60(14):1223–30. doi: 10.1016/j.
jacc.2012.07.0
5. Shaefi S, O’Gara B, Kociol RD, et al. Effect of cardiogenic shock hospital volume on mortality in patients with
cardiogenic shock. J Am Heart Assoc. 2015;4(1):e001462. doi: 10.1161/JAHA.114.001462.
6. Alberts MJ, Latchaw RE, Selman WR, et al. Recommendations for comprehensive stroke centers: a consensus
statement from the Brain Attack Coalition. Stroke. 2005;36(7):1597–1616. doi: 10.1161/01.STR.0000170622.07210.b4
7. Celso B, Tepas J, Langland-Orban B, et al. A systematic review and meta-analysis comparing outcome of
severely injured patients treated in trauma centers following the establishment of trauma systems. J Trauma.
2006;60(2):371–78. doi: 10.1097/01.ta.0000197916.99629.eb.
8. Graham KJ, Strauss CE, Boland LL, et al. Has the time come for a national cardiovascular emergency care system?
Circulation. 2012;125:2035–44. doi: 10.1161/CIRCULATIONAHA.111.084509
9. Granger CB, Henry TD, Bates WER, et al. Development of systems of care for ST-elevation myocardial infarction
patients: the primary percutaneous coronary intervention (ST-elevation myocardial infarction-receiving) hospital
perspective. Circulation. 2007;116(2):e55–e9. doi: 10.1161/CIRCULATIONAHA.107.184049
10. Harris KM, Strauss CE, Duval S, et al. Multidisciplinary standardized care for acute aortic dissection: design
and initial outcomes of a regional care model. Circ Cardiovasc Qual Outcomes. 2010;3(4):424–30. doi: 10.1161/
CIRCOUTCOMES.109.920140
11. Henry TD, Sharkey SW, Burke MN, et al. A regional system to provide timely access to percutaneous
coronary intervention for ST-elevation myocardial infarction. Circulation. 2007;116(7):721–28. doi: 10.1161/
CIRCULATIONAHA.107.694141
12. MacKenzie EJ, Rivara FP, Jurkovich GJ, et al. A national evaluation of the effect of trauma-center care on mortality.
N Engl J Med. 2006;354:366–78. doi: 10.1056/NEJMsa052049
13. Mooney MR, Unger BT, Boland LL, et al. Therapeutic hypothermia after out-of-hospital cardiac arrest: evaluation of
a regional system to increase access to cooling. Circulation. 2011;124:206–14. doi: 10.1161/CIRCULATIONAHA.110.986257
14. Hasin Y, Danchin N, Filippatos GS, et al. Recommendations for the structure, organization, and operation of
intensive cardiac care units. Eur Heart J. 2005;26(16):1676–82. doi: 10.1093/eurheartj/ehi202
15. Le May M, van Diepen S, Liszkowski M, et al. From coronary care units to cardiac intensive care units:
recommendations for organizational, staffing, and educational transformation. Can J Cardiol. 2016; 32(10):1204–13.
doi: 10.1016/j.cjca.2015.11.021
16. Morrow DA, Fang JC, Fintel DJ, et al. Evolution of critical care cardiology: transformation of the cardiovascular
intensive care unit and the emerging need for new medical staffing and training models: a scientific statement
from the American Heart Association. Circulation. 2012; 126(11):1408–28. doi: 10.1161/CIR.0b013e31826890b0
17. Garan AR, Kirtane A, Takayama H. Redesigning care for patients with acute myocardial infarction complicated by
cardiogenic shock: the “shock team.” JAMA Surg. 2016;151(7):684–85. doi: 10.1001/jamasurg.2015.5514
CONTENTS
Escalation
CHAPTER
15 of Care in
Cardiogenic
Shock
Greg Marco, MD, FCCP
Medical Director for Cardiothoracic Critical Care
Frederik Meijer Heart & Vascular Institute
100 Michigan Street NE | MC 031
Grand Rapids, MI 49503
greg.marco@spectrumhealth.org
INTRODUCTION
Despite advances in the management of acute coronary syndromes,
cardiogenic shock complicating acute myocardial infarction remains a
condition associated with high mortality. Over the past 2 decades, mortality
in these patients has remained relatively constant at around 50%.1 Recent
data from the National Cardiogenic Shock Initiative (NCSI) utilizing a protocol
that emphasizes early recognition, early hemodynamic support, advanced
hemodynamic surveillance, and rapid escalation of therapy has reported
survival rates exceeding 70% in this patient population.2 This discussion focuses
on the role of early recognition, high level surveillance, and early escalation of
therapy in patients with acute myocardial infarction and cardiogenic shock
(AMICS).
<< Chapter 14 Chapter 15 | Escalation of Care in Cardiogenic Shock Chapter 16 >>
Early recognition of AMICS

When a patient presents with acute myocardial infarction, timely recognition and therapeutic intervention
of shock or impending shock is imperative. Therapeutic goals include:
• Supporting blood pressure and organ perfusion
• Restoring myocardial perfusion
• Unloading the injured left or right ventricle
Delays in restoring adequate organ perfusion risk progression to irreversible end organ failure, in which
case rescue therapies are less likely to be effective. Likewise, restoring organ perfusion utilizing a strategy
that may compromise cardiac recovery risks development of advanced stage heart failure either in the
acute setting or in subsequent months.3
Patients presenting
with hypotension or the
need for vasopressors
EXCLUSION CRITERIA
NATIONAL CARDIOGENIC SHOCK INITIATIVE  Evidence of Anoxic Brain Injury
 Unwitnessed out of hospital cardiac arrest or any cardiac arrest in which ROSC is not
ALGORITHM
to treat hypotension
achieved in 30 minutes
 IABP placed prior to Impella
 Septic, anaphylactic, hemorrhagic, and neurologic causes of shock
and evidence of organ

 Non-ischemic causes of shock/hypotension (Pulmonary Embolism, Pneumothorax,
INCLUSION CRITERIA Myocarditis, Tamponade, etc.)
 Active Bleeding
Acute Myocardial Infarction: STEMI or NSTEMI
hypoperfusion should
 Recent major surgery
 Ischemic Symptoms
 Mechanical Complications of AMI
 EKG and/or biomarker evidence of AMI (STEMI or NSTEMI)
 Known left ventricular thrombus
Cardiogenic Shock
be considered for  Hypotension (<90/60) or the need for vasopressors or inotropes to maintain systolic
blood pressure >90
 Patient who did not receive revascularization
 Contraindication to intravenous systemic anticoagulation
 Mechanical aortic valve
 Evidence of end organ hypoperfusion (cool extremities, oliguria, lactic acidosis)
pre-PCI mechanical
circulatory support ACCESS & HEMODYNAMIC SUPPORT
 Obtain femoral arterial access (via direct visualization with use of ultrasound and fluoro)
(MCS). In patients ACTIVATE CATH LAB



Obtain venous access (Femoral or Internal Jugular)
Obtain either Fick calculated cardiac index or LVEDP
developing these signs IF LVEDP >15 or Cardiac Index < 2.2 AND anatomy suitable, place IMPELLA
during or immediately
following PCI, right Coronary Angiography & PCI
 Attempt to provide TIMI III flow in all major epicardial vessels other than CTO
heart catheterization ** QUALITY MEASURES **  If unable to obtain TIMI III flow, consider administration of intra-coronary
vasodilators
(RHC) is recommended  Impella Pre-PCI

 Door to Support Time
for hemodynamic Perform Post-PCI Hemodynamic Calculations
< 90 minutes 1. Cardiac Power Output (CPO): MAP x CO
assessment and  Establish TIMI III Flow 451
surveillance.  Right Heart Cath
2. Pulmonary Artery Pulsatility Index (PAPI): sPAP – dPAP
 Wean off Vasopressors & RA
Inotropes
Figure 1 presents  Maintain CPO >0.6 Watts
the NCSI algorithm  Improve survival to
Wean OFF Vasopressors and Inotropes
If CPO is >0.6 and PAPI >0.9, operators should wean vasopressors and inotropes and determine if Impella
emphasizing this
can be weaned and removed in the Cath Lab or left in place with transfer to ICU.
discharge to >80%
Escalation of Support
approach. If CPO remains <0.6 operators should consider the following options:
 PAPI is <0.9 consider right sided hemodynamic support
 PAPI >0.9 consideration for additional hemodynamic support
NATIONAL
Local practice patterns should dictate the next steps:
 Placement of more robust MCS device(s)
 Transfer to LVAD/Transplant center
If CPO is >0.6 and PAPI <0.9 consider providing right sided hemodynamic support if clinical suspicion
for RV dysfunction/failure
CARDIOGENIC
Vascular Assessment
 Prior to discharge from the Cath Lab, a detailed vascular exam should be performed including femoral
angiogram and Doppler assessment of the affected limb.
 If indicated, external bypass should be performed.
SHOCK ICU Care

 Daily hemodynamic assessments should be performed, including detailed vascular
INITIATIVE
assessment
 Monitor for signs of hemolysis and adjust Impella position as indicated
Device Weaning
Impella should only be considered for explantation once the following criteria are met:
 Weaning off from all inotropes and vasopressors
NationalCSI@hfhs.org  CPO >0.6, and PAPI > 0.9
Bridge to Decision
www.henryford.com/cardiogenicshock Patients who do not regain myocardial recovery within 3-5 days, as clinically indicated, should
be transferred to an LVAD/Transplant center. If patients are not candidates, palliative care
NationalCSI – Algorithm – v1.5 – 11/2017 options should be considered.
Detroit CSI Flowsheet - v5.0 – April 2017
Figure 1. NCSI Algorithm
Hemodynamic assessment
In patients who develop hypotension or need for vasopressors during or following PCI, RHC is
recommended to tailor therapy as well as provide objective criteria to assess the need for escalation of
support. Reasonable initial goals are:
• MAP >60-65 mmHg
• CI ≥2.2 L/min/m2
• SVO2 >60%
• Cardiac power output (CPO) >0.6 W
Frequent hemodynamic reassessments (every 2-4 hours) are recommended with an eye toward need for
escalation to initial MCS or alternative MCS.
The NCSI has identified need for combinations of multiple vasopressors, an elevated lactate, and a low
cardiac power output as predictors of mortality and potential need for escalation. Achieving hemodynamic
goals utilizing a strategy that increases myocardial demand while limiting coronary perfusion (vasoactive
induced coronary arterial constriction) may limit short term survival as well as put ischemic and peri-
ischemic myocardium at risk, which may limit optimal myocardial recovery.4
Prompts for escalation

Low cardiac power output, ongoing or escalating need for vasopressor support, elevated lactate, and
low pulmonary artery pulsatility index (PAPi) are prompts to consider escalation of support (Figure 2).
Frequently monitor these clinical variables (every 2-4 hours) to assess adequacy of therapy and to prompt
multidisciplinary discussions regarding the need to escalate therapy by progressing to mechanical
circulatory support or transfer to another facility. Figure 3 shows an example of one institution’s approach
to cardiogenic shock.
Figure 2.
Prompts for
considering Admission to ICU/CCU
escalation of
support from
NCSI data
AMICS: Monitor CPO, PAPi, Lactate
CPO < 0.8 CPO < 0.8 CPO > 0.8

Lactate > 4 Lactate < 4 Lactate < 4
PAPi < 1.0 PAPi < 1.0 PAPi > 1.0
EARLY CLOSE WEAN

ESCALATION OBSERVATION PRESSORS
Goals of Care Consider Escalation Wean MCS
In-hospital Survival Post Impella PCI Based on Predictors of In-hospital Survival 12-24 Hours
CPO and Inotrope Use4 Postprocedure Based on Lactate and CPO4
Number of Inotropes Cardiac Power Output Post MCS and PCI

CPO (watts) Lactate
0 1 ≥2 >0.6 ≤0.6
≤0.6 ≥4 50% Survival 31% Survival

67% 57% 33%
(n=9/18) (n=4/13)
0.6 to <0.8 100% 60% 50% <4
95% Survival 65% Survival
≥0.8 85% 79% 57% (n=58/61) (n=11/17)
Figure 3.
Inova
Cardiogenic CARDIOGENIC SHOCK TEAM MANAGEMENT
Shock
Management Cardiogenic Shock Management in the CICU
• Wean vasopressors/inotropes
Algorithm • Early escalation for refractory shock
• Heart recovery
IS THERE REFRACTORY SHOCK?*

Serial Assessment q4hr x 24hrs
• Lactate
• Fick CO/Cl
• CPO and PAPi
YES NO
• Continuous hemodynamics
CPO > 0.6
and if PMCS: PAPi > 1.5
• LDH & Haptoglobin
RA < 15
• Neurovascular checks Bi-V CS LV-dominant CS RV-dominant CS PCWP < 15
• Limited Echo Daily
• IVF to keep RA >10, PCWP >12 CPO < 0.6 CPO < 0.6 CPO < 0.6
PAPi < 1.0 PAPi > 1.0 PAPi < 1.0
*Criteria for Refractory Shock RA > 15 RA < 15 RA > 15
• Lactate >3 PCWP > 15 PCWP > 15 PCWP < 15
• UOP <30cc/hr
• CPO <0.6
• Increasing pressor requirement
• Evidence of organ hypo-perfusion HYPOXEMIA? HYPOXEMIA? HYPOXEMIA?
Critera for RV Dysfunction

• PAPi <1.0 YES NO YES NO YES NO
• RA >15mmHg
• RA/PCWP ratio >0.63
TH + TH + TH +
Oxygenator Oxygenator Impella RP Wean PMCS
Bi-Pella Oxygenator Impella CP
or or or and
or or or
VA-ECMO + VA-ECMO +/- ProtekDuo assess for
CPO = MAP x CO/451 TH/ProtekDuo VA-ECMO + Impella 5.0
LV vent LV vent heart recovery
PAPi = (sPAP-dPAP)/RA LV vent
Earlier chapters have emphasized the value of a shock team, use of RHC for hemodynamic-tailored
therapy, and ability to employ various forms of MCS. It is recognized that all centers performing PCI do
not have these capabilities. In situations where the shock state does not rapidly resolve, consider transfer
to a center with the ability to rapidly escalate care when indicated.5 As previously mentioned, once
hemodynamic shock has progressed to multi-organ failure, the deployment of advanced therapies is less
likely to be of benefit. Delays in transfer may negatively affect survival and/or optimal myocardial recovery
following AMICS.
The persistent need for temporary mechanical support beyond 72 hours should also prompt discussions
of candidacy for durable ventricular assist devices or transplant. As with all therapies, medical treatment
should be centered around the patient’s goals and desires. Frequent effective communication is essential
to ensure medical and patient goals remain aligned.
Conclusion
Treatment protocols for cardiogenic shock, such as presented in the NCSI, have contributed to significant
increases in survival in patients with AMI cardiogenic shock. Key elements of these protocols include:
• Early recognition of cardiogenic shock
• Hemodynamic surveillance
• Early escalation of therapy when necessary
References
1. Miller L. Cardiogenic shock in acute myocardial infarction: the era of mechanical support. J Am Coll Cardiol.
2016;67(16):1881-4.
2. Basir MB, Schreiber T, Dixon S, et al. Feasibility of early mechanical circulatory support in acute myocardial
infarction complicated by cardiogenic shock: The Detroit cardiogenic shock initiative. Catheter Cardiovasc Interv.
2018;91(3):454-61.
3. Kapur NK, Paruchuri V, Urbano-Morales JA, et al. Mechanically unloading the left ventricle before coronary
reperfusion reduces left ventricular wall stress and myocardial infarct size. Circulation. 2013;128(4):328-36.
4. Basir MB, Kapur NK, Patel K, et al. Improved outcomes associated with the use of shock protocols: Updates from
the National Cardiogenic Shock Initiative. Catheter Cardiovasc Interv. 2019;93(7):1173-83.
5. Rab T, Ratanapo S, Kern KB, et al. Cardiac shock care centers. J Am Coll Cardiol. 2018;72(16):1972-80.
CONTENTS
Palliative Care
CHAPTER
16
Charles Hunley, MD
Critical Care Director
Orlando Regional Medical Center
Orlando Health
86 W Underwood Suite 101
Orlando, FL 32726
Charles.hunley@orlandohealth.com
INTRODUCTION
Today there is a growing need to integrate palliative care (PC) decision
making into a team-based treatment plan for acute myocardial infarction
(AMI) and cardiogenic shock. With advances in reperfusion therapy,
survival is improving; however, there are disparities in care and in-
hospital mortality remains high (27%–51%).9 The use of PC with AMI and
cardiogenic shock has been controversial. Notably, papers demonstrate
a lack of knowledge of optimal delivery of PC in the cardiogenic shock
population with significant variability in implementation.6
In this chapter we explore some of the data on the use of palliative

care in AMI and cardiogenic shock as well as barriers to and challenges
associated with PC. We then look to lessons learned from PC in heart
failure to create a roadmap for our vision for PC in AMI with cardiogenic
shock.
<< Chapter 15 Chapter 16 | Palliative Care Chapter 17 >>
Low use of PC in AMI with cardiogenic shock

In 2019 an American Heart Association study outlined the utilization of PC for cardiogenic shock
complicating AMI.9 The study analyzed 15 years of data and trends to determine that despite a trend toward
increasing adoption of PC, its use in AMI with cardiogenic shock was low.
A study published by Elgendy and colleagues in 2020 using data from the National Inpatient Sample
from 2002 to 2016 noted an increase in penetration of PC over the study period for both STEMI and
NSTEMI patients.3 Yet despite this increase the use of PC remained low, with use seen in just 3.9% of STEMI
patients in 2016 and 2.7% of NSTEMI patients. Most of the increase was seen in patients who died during
hospitalization, with 30% of those who died in the hospital having PC consults in 2016 compared with just
1.5% in 2002.3,6
Ando et al.5 showed that the use of PC in STEMI complicated by cardiogenic shock increased significantly
between 2005 and 2014, yet there remained a lack of consensus regarding when and how PC consults
are prescribed. The study demonstrated significant variations in PC consultation from hospital to
hospital, highlighting the need for quantitative and qualitative research on providers’ beliefs and biases of
integrating PC in patients with acute cardiogenic shock.
Barriers to and challenges of PC

Engaging palliative care with acute AMI in cardiogenic shock can be challenging due to several factors
including delayed recognition, waxing and waning clinical symptoms, and an acute shortage of PC
physicians. There is often a misrepresentation or lack of understanding of what PC can do in a system-
based practice with the physicians taking care of this population of patients. Just as a provider’s perception
can be a barrier to PC consults, the patient’s and family’s perception of the disease condition and prognosis
can be a barrier as well.
CHALLENGES TO PALLIATIVE CARE WITH ACUTE AMI IN

CARDIOGENIC SHOCK INCLUDE:
• Delayed recognition
• Waxing and waning clinical symptoms
• Acute shortage of PC physicians
• Lack of understanding of what PC can do
• Patient and family perception of the disease condition
In one study, heart failure (HF) providers were interviewed to assess knowledge, attitudes, and perceptions
about PC. They reported:8
• Limited knowledge of PC
• Confusion between palliative and hospice care
• Uncertainty about the differences between standard therapy and PC
Ando et al. demonstrated that socioeconomic factors, the type of procedures performed, and hospital
resources were associated with an increase in PC consults, elucidating the need to develop research and
care systems to improve these barriers. Even in advanced HF without cardiogenic shock, despite chronic
severe symptoms and multiple comorbidities, only 6% to 10% of patients are referred for PC services during
hospitalization.4 Nakagawa et al.7 showed that PC consultation was used roughly half the time in patients
with cardiogenic shock requiring short term mechanical support,3 demonstrating the need to standardize
processes for a team-based approach.
PC in heart failure as a roadmap to PC in AMI and

cardiogenic shock
It is beneficial to look at palliative care in the heart failure population when attempting to envision
PC in AMI and cardiogenic shock. In 2003 the European Society of Cardiology recommended PC as a
treatment modality for HF patients. The American Heart Association followed in 2013. The International
Society of Heart and Lung Transplant has also recommended that PC should be an integral part of the
multidisciplinary team.9
In the heart failure population, most palliative care advances have included a team-based consulting
modeling based on cancer care models. Given the high prevalence and substantial morbidity and
mortality associated with heart failure, care for these patients will benefit from:
• Interdisciplinary collaboration
• Shared decision-making with objective evidence
• A team-based approach
Interdisciplinary collaboration is critical to providing optimal care for patients throughout the full spectrum
of HF. A cohort study2 of more than 50,000 patients with HF showed they were enrolled to PC later in
their disease severity than patients with cancer. Fewer patients with HF were referred for symptom
management compared to the cancer population but had similar rates of symptom improvement after
referral.1 This demonstrates the need for strategic assessment of patients’ severity and clinical trajectory.
With advanced HF patients the predictors of all-cause mortality are:

• Reduced ejection fraction
• Low systolic blood pressure (SBP)
• Increased creatinine and N-terminal pro–B-type natriuretic peptide
• New York Heart Association (NYHA) class III – IV heart failure
• Inpatient status
• History of ischemic heart disease
• Atrial fibrillation
• Prolonged heart failure
• Multiple hospital admissions
• Noncompliance
Multiple studies suggest the benefits of PC consults for earlier stages of HF. These studies demonstrated
a reduction in symptom burden and improved quality of life at 1 month with no difference in early re-
hospitalization, hospice use, or death.10, 11 This highlights the need to have a systematic way of triggering PC
consults.
Successful implementation of acute cardiogenic shock teams has resulted in a reduction in mortality.
However, there is a need to integrate PC systematically into the teams. Several articles have demonstrated
concepts of introduction of shared decision-making with objective evidence and a team-based approach.12
Yet a lack of empirical evidence remains regarding how and when to implement PC with acute
cardiogenic shock and AMI. Most of the evidence for a team-based approach in PC has come from the
field of heart failure where data demonstrates a benefit to an early team-based approach for improving
symptoms and morbidity by integrating PC earlier in the patient’s clinical course with HF.
Vision for PC for AMI cardiogenic shock

The patient population with AMI and cardiogenic shock faces a unique set of challenges when it comes
to palliative care, notably challenges with timing of PC consultation. Unlike heart failure, the acute nature
of cardiogenic shock provides little time for patients, families, and healthcare professionals to prepare for
discussions about prognosis, advance directives, care transitions, quality of life, and treatments aimed at
symptomatology. Yet a study of qualitative interviews showed that such future care planning was highly
valued by patients, care providers, and family physicians.13
Therapeutic trials in the AMI and cardiogenic shock patient population have had little success, partially
because some patients were “too sick” to benefit from the studied intervention and needed PC consults.
Multidisciplinary collaboration and communication between experts is critically important to define the
groups of patients who suffer from cardiogenic shock.
As a systematic approach to treating and evaluating cardiogenic shock is developed, a team approach
should be integrated into the decision-making process of when PC should be triggered. Studies have
demonstrated that there is a lack of consensus and a bias of when PC consults are made.
Dr. David Baran and a multidisciplinary group of experts convened by the Society for Cardiovascular
Angiography and Interventions (SCAI) published a simple classification system describing the stages
of cardiogenic shock (Figure 1).14 The multidisciplinary bedside team can use this common language to
facilitate communication regarding prognosis, interventions, treatment decisions, and early PC consults.
EXTREMIS
E
A patient with circulatory collapse, frequently (but not always) in refractory cardiac arrest with ongoing
cardiopulmonary resuscitation (CPR) or are being supported by multiple simultaneous acute
interventions including ECMO-facilitated CPR. These are patients with multiple clinicians at bedside
laboring to address multiple simultaneous issues related to the lack of clinical stability of the patient.
D
DETERIORATING/DOOM
A patient that is similar to category C but is getting worse. They have failure to respond to
initial interventions.
CLASSIC CARDIOGENIC SHOCK

C A patient that manifests with hypoperfusion that requires intervention (inotrope,
pressor or mechanical support, ECMO) beyond volume resuscitation to restore
perfusion. These patients typically present with relative hypotension.
BEGINNING CARDIOGENIC SHOCK

B A patient who has clinical evidence of relative hypotension or tachycardia
without hypoperfusion.
AT RISK
A A patient who is not currently experiencing signs or symptoms of
cardiogenic shock, but is at risk for its development. These
patients may include those with acute myocardial infarction,
acute and/or acute on chronic heart failure symptoms.
STAGE
Figure 1. SCAI Cardiogenic Shock Stage Descriptions14
The American Heart Association outlined triggers and indicators of PC readiness derived from advanced
heart failure (Table 1). However, these factors are associated with poor outcomes. Therefore, these indicators
should be viewed conservatively due to the fact that patients with PC consults were older, sicker, and had
more heart failure diagnosis on admission.9
Table 1. Indicators of Readiness for Palliative Care Derived from Advanced Heart Failure
(adapted from American Heart Association9)
INDICATORS OF READINESS FOR PALLIATIVE CARE
• Age over 80 years with 2 or more life-threatening medical issues
• Worsening comorbidities
• Renal function
▷ Need to initiate dialysis
▷ High admission blood urea nitrogen (43+ mg/dL)
▷ High serum creatinine (2.75+ mg/dL)
▷ Escalation of diuretics to maintain volume status
• Low hemoglobin
• Hyponatremia due to fluid overload
• Presence of comorbidities of the Gold Standards Framework Prognostic Indicator Guidance
• Multisystem organ failure involving ≥3 organs
• Persistent hypotension (low admission systolic BP ≤115 mmHg)
• Persistent tachycardia (heart rate >130 bpm)
• Persistent significant dyspnea

• Respiratory rate >25 breaths per minute
• Increased work of breathing
• Breathlessness at rest
• Persistent pulmonary congestion by ultrasound
• Respiratory Distress Observation Scale (RDOS)-8 items:

• Increased heart rate
• Increased respiratory rate
• Restlessness/non-purposeful movements
• Neck muscle use during inspiration
• Abdominal paradox (abdomen moves in on inspiration)
• Grunting or guttural sound at end-expiration
• Nasal flaring
• Look of fear
Although treatment modalities and clinical prognostic tools have improved for cardiogenic shock,
variability in treatment plans has been a barrier to initiate PC consults. The prognosis for patients with
cardiogenic shock who receive mechanical support remains guarded. The need is great to blend
cardiogenic shock therapy and PC modalities.
Summary
Clinicians and patients value palliative care, and palliative care is feasible in acute high risk cardiac
conditions such as AMI and cardiogenic shock. However, with the inability to accurately identify which
patients with cardiogenic shock will require palliative treatment, curative therapies may need to be
blended with PC early in the course of treatment in a team-based approach to optimize care.
References
1. von Schwarz ER, He M, Bharadwaj P. Palliative care issues for patient with heart failure. JAMA Netw Open.
2020;3(2):e200011. doi:10.1001/jamanetworkopen.2020.001
2. Lui AY, O’Riordan DL, Marks AK, et al. A comparison of hospitalized patients with heart failure and cancer referred
to palliative care. JAMA Netw Open. 2020;3(2):e200020. doi:10.1001/jamanetworkopen.2020.0020
3. Elgendy IY, Elbadawi A, Sardar P, et al. Palliative care use in patients with acute myocardial infarction. J Am Coll
Cardiol. 2020;75(1):113-117.
4. Braun LT, Grady KL, Kutner JS, et al. Palliative care and cardiovascular disease and stroke: a policy statement
from the American Heart Association/American Stroke Association. Circulation. 2016; 134(1):e198–e225. doi: 10.1161/
CIR.0000000000000438
5. Ando T, Akintoye E, Uemura T, et al. Palliative care referral in ST-segment elevation myocardial infarction
complicated with cardiogenic shock in the United States. Heart Lung. 2020;49(1):25-9. doi: 10.1016/j.
hrtlng.2019.10.005
6. Vallabhajosyula S, Prasad A, Dunlay SM, et al. Utilization of palliative care for cardiogenic shock complicating acute
myocardial infarction: A 15-year national perspective on trends, disparities, predictors, and outcomes. J Am Heart
Assoc. 2019;8(15):e011954. doi:10.1161/JAHA.119.011954
7. Nakagawa S, Garan AR, Takeda K, et al. Palliative care consultation in cardiogenic shock requiring short-
term mechanical circulatory support: A retrospective cohort study. J Palliat Med. 2019;22(4):432-6. doi: 10.1089/
jpm.2018.0393
8. Kavalieratos D, Mitchell EM, Carey TS, et al. “Not the ‘grim reaper service’”: an assessment of provider knowledge,
attitudes, and perceptions regarding palliative care referral barriers in heart failure. J Am Heart Assoc.
2014;3(1):e000544. doi: 10.1161/JAHA.113.000
10. Gavazzi A, De Maria R, Manzoli L, et al. Palliative needs for heart failure or chronic obstructive pulmonary disease:
results of a multicenter observational registry. Int J Cardiol. 2015;184:552–8. doi: 10.1016/j.ijcard.2015.03.056
11. Sidebottom AC, Jorgenson A, Richards H, et al. Inpatient palliative care for patients with acute heart failure:
outcomes from a randomized trial. J Palliat Med. 2015;18(2):134–42. doi: 10.1089/jpm.2014.0192
12. Vreugdenhil G. Shared decision making plus early palliative care-implications for use in clinical decision making.
Acta Oncol. 2019;58(2):225-6. doi: 10.1080/0284186X.2018.1502468
13. Denvir MA, Cudmore S, Highet G, et al. Phase 2 randomised controlled trial and feasibility study of future care
planning in patients with advanced heart disease. Sci Rep. 2016;6:24619. doi: 10.1038/srep24619
14. Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic
shock. Catheter Cardiovasc Interv. 2019;94(1): 29–37. https://doi.org/10.1002/ccd.28329
CONTENTS
CHAPTER
Non-Acute
17 Coronary Syndrome
Cardiogenic Shock
Terese C. Hammond, MD Matthew E. Powers, MD

University of Southern California, Assistant Professor of Clinical Surgery
Dept of Surgery Division of Cardiothoracic Surgery
Medical Director, Providence St Johns Cardiovascular Thoracic Institute
Health Center ICU Keck School of Medicine of USC
Terese.Hammond@providence.org Matthew.Powers@med.usc.edu
J. Christian Cash, MD Raymond C. Lee, MD

Assistant Professor of Clinical Surgery Assistant Professor of Clinical Surgery
Division of Cardiothoracic Surgery Division of Cardiothoracic Surgery
Cardiovascular Thoracic Institute Cardiovascular Thoracic Institute
Keck School of Medicine of USC Keck School of Medicine of University of
Southern California
jonathan.cash@med.usc.edu Los Angeles, CA
Dr.raycLee@gmail.com
Raymond.Lee@med.usc.edu
INTRODUCTION
While cardiogenic shock due to acute coronary syndrome (ACS) is the primary
indication for mechanical circulatory support (MCS)—with percutaneous
left ventricular assist devices such as venoarterial extracorporeal membrane
oxygenation (VA-ECMO); axial flow pumps such as Impella 2.5®, Impella CP®,
Impella 5.0®, Impella LD®, and TandemHeart®; or intra-aortic balloon pump
(IABP)—other non-ACS indications have increasingly emerged. For example,
medically refractory heart failure, acute valvular failure, acute fulminant
myocarditis, overwhelming sepsis, acute right heart failure (RHF) due to massive
pulmonary embolism (PE), or takotsubo cardiomyopathy are among the life-
threatening conditions present in approximately 20% of patients who receive
MCS and the utility of these devices for temporary cardiovascular support
continues to expand.1
<< Chapter 16 Chapter 17 | Non-Acute Coronary Syndrome Cardiogenic Shock Chapter 18 >>
Introduction (continued)
The underlying mechanism in non-ACS cardiogenic shock, as it is in acute myocardial infarction (AMI)
associated decompensation, is acute hypoperfusion and concomitant end-organ failure due to profoundly
reduced cardiac output.2 Mortality is extremely high, approximately 50%, in cardiogenic shock, even in
those aggressively treated with advanced heart failure pharmacotherapy and MCS.2
Life-threatening conditions, other than ACS cardiogenic shock,

present in approximately 20% of patients who receive MCS include:1
• Medically refractory heart failure
• Acute valvular failure
• Acute fulminant myocarditis
• Overwhelming sepsis
• Acute RHF due to massive PE
• Takotsubo cardiomyopathy
Cardiogenic shock is a form of circulatory shock that is associated with a cardiac etiology. Circulatory shock
is characterized by systolic blood pressure below 90 mmHg or mean arterial blood pressure less than 65
mmHg for more than 30 minutes, in addition to evidence of end-organ hypoperfusion, such as altered
mental status, decreased urine output (< 0.5 mL/kg/hour), cold/clammy skin, and elevated serum lactate
levels (>1.5 mmol/L).2 Cardiogenic shock may coexist with other forms of circulatory shock, such as septic
shock, which can make clinical management extremely difficult.
Since the Centers for Medicare and Medicaid Services (CMS) mandated real time quality reporting of
compliance with its sepsis bundle (SEP-1), hospitals have been under increasing pressure to ensure
all hypotensive patients receive the required 30 cc/kg intravenous fluid infusion, sequential lactic acid
determinations, and broad spectrum antibiotics within 3 hours. However, this simplified SEP-1 protocol,
which was implemented in 2017, does not incorporate a method for adjusting for patients’ comorbidities
and volume status risks.3 Hence, patients are at risk for under or over-resuscitation and this is a particular
peril for patients with underlying cardiomyopathies.
Fluid over-resuscitation in patients with cardiogenic shock can lead to further hemodynamic
decompensation as it overdistends an already stressed left ventricle by further increasing left ventricular
end diastolic volume (LVEDV) and end diastolic pressure (LVEDP).4 This effect, potentially in combination
with other non-ACS conditions such as acute pulmonary embolism (PE), can lead to acute right heart
failure and further volume resuscitation in the context of a failing right ventricle, and can increase right
sided filling pressures to the point of interventricular septal displacement into the left ventricular outflow
tract (LVOT), leading to further decreases in CO/CI. This vicious cycle3 often results in refractory shock,
and additional efforts to use volume or pressor support fall short, leading to the downward spiral into
biventricular failure. Broader availability of MCS has the potential to mitigate this decline and potentially
decrease mortality in these highly complex patients. However, many questions remain to be answered
regarding flexibility, cost, timing, and overall effectiveness of MCS for non-ACS cardiogenic shock.
CASE STUDY
A 63-year-old obese male, with a history of non-ischemic cardiomyopathy

and ejection fraction (EF) 18%, presented to our Emergency Department with
3 days of intensifying abdominal pain, severe lactic acidosis, and presumed
septic shock. General surgery was consulted, but the patient became
increasingly unstable and the ICU shock team was consulted. He was moved
emergently to the ICU for endotracheal intubation, central, arterial, and Swan
Ganz catheter placement, and additional volumes resuscitation. Bedside
echocardiogram confirmed EF 15%. Initial hemodynamics demonstrated
CVP 15 mmHg, PA pressure 41/27 mmHg, and mean pulmonary pressure
32 mmHg. Initial mixed venous saturation (SvO2) was 50%. He was
resuscitated and then taken emergently to the operating room.
After a low anterior resection with colostomy and draining of liver abscess,
patient returned to the ICU and continued to be unstable. Post-operative
hemodynamics on full pressor and ventilator support: CVP 12 mmHg,
PAP 31/20 mmHg, PAM 25 mmHg, cardiac output/index (CO/CI) 3/1.3 L/min,
CI 1.9-2.1, SVR 1440 dynes/sec/cm-5. Cardiothoracic surgery was consulted for
combined cardiogenic and septic shock and need for mechanical circulatory
support (MCS).
Patient was transferred back to the operating room for Impella 5.0® placement
via an axillary graft. He returned on P-9 setting with flow of 4.7-4.8 L and, over
the course of his first pre-operative day, his pressors were titrated down and his
CO/CI was 6.0/3 L/min. He was extubated to high flow nasal cannula on post-
operative day 1. By post-operative day 7, he was off all pressors, briskly diuresing,
and slowly titrating off Impella support.
Left ventricular support devices have advantages and limitations, which are detailed in prior chapters.
With regard to cardiogenic shock, each device has a unique impact on the pressure-volume loop (Figure
1).4 IABP, with its modest augmentation of cardiac output, is being increasingly displaced by newer
technologies.4 ECMO with its increased availability, and percutaneously placed axial devices (eg, Impella
5.0® and Impella 5.5®) with their improved cardiac output and risk profiles, are increasingly used as first
line interventions in cases where MCS is required. While 80% of MCS is currently deployed in the setting of
AMI or prophylaxis for high-risk percutaneous coronary intervention (PCI), non-ACS indications for MCS are
expanding.
Figure 1. Pressure-Volume Loops Reveal Cardiac Effects of MCS Devices

A. Activation of intra-aortic balloon pump (IABP) reduces peak LV systolic and diastolic pressures and
increases LV stroke volume.
B. Activation of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) increases LV systolic and
diastolic pressure without a venting strategy, and reduces LV stroke volume, thus increasing the ratio of
LVEDP to stroke volume.
C. Activation of percutaneous left ventricular assist devices (pLVAD), such as Impella and TandemHeart,
significantly reduces LV volumes and pressures as well as LV stroke volume, resulting in a significant
reduction in cardiac workload.
Severe heart failure in the setting of non-ischemic

cardiomyopathy
Appropriately deployed MCS can mitigate the pressure and volume overload driving the decline in
myocardial function in patients with acutely decompensated heart failure and lead to improvements in
CO/CI. MCS may also help avoid the negative effect of cardiac remodeling as a patient transitions back
from acute to more chronic heart failure and improve long-term cardiac recovery.5 Long-term destination
therapy with ventricular assist devices has demonstrated promise in the management of this complex
and costly population of patients and is addressed in another chapter. The National Heart, Lung and
Blood Institute (NHLBI) is actively studying short-term intervention with MCS with the promise of creating
rational, cost-effective guidelines for the implementation, use, and discontinuation of these devices.5
Acute, fulminant myocarditis is an inflammatory condition affecting the myocardial muscle.6 It is a

relatively rare cause of cardiac failure, representing approximately 10% of those diagnosed with acute
cardiac failure and accounting for 8-12% of sudden cardiac death.7 Of note, young female patients are
disproportionally affected.7 A variety of agents have been implicated as causes of fulminant myocarditis
(see Table 1), including emerging evidence of newer triggers including checkpoint inhibitors used in
cancer therapy, such as nivolumab (OPDIVO®).6,8,9 Although the incidence of checkpoint inhibitor related
myocarditis is estimated at only 1-2% of patients treated, increased use and availability of these newer drugs
will presumably increase these numbers.
Table 1. Etiologies of Myocarditis6,8,9
INFECTIOUS ETIOLOGIES INFLAMMATORY ETIOLOGIES OTHER ETIOLOGIES

• Enterovirus (Coxsackie B) • Kawasaki disease • Toxins
• Adenovirus • Rheumatologic disease • Cocaine
• Parvovirus B19 • Iron (hemochromatosis)
• Human herpesvirus 6 (HHV-6) • Copper (Wilson disease)
• Lyme disease (Borrelia) • Arsenic
• Cytomegalovirus (CMV) • Cardiotoxic effects of immune
• Epstein-Barr virus (EBV) checkpoint inhibitors
(eg, ipilimumab, pembrolizumab,
• Hepatitis C nivolumab, atezolizumab, avelumab,
• Chagas disease durvalumab)
(Central and South America,
presents with right heart failure)
Accumulating evidence suggests that MCS may provide a “bridge to recovery” for patients with fulminant
myocarditis, although the heterogenous nature of this population of patients makes it difficult to study.
In one recent retrospective, single center study (n=30), aggressive use of MCS for fulminant myocarditis
was associated with 83.3% long-term survival.6 Of interest, successful conversion of short-term MCS to
longer-term VAD support was strongly associated with total bilirubin rise, which helped identify the 20% of
participants in this study who were referred for destination LVAD therapy. A multi-institutional cohort study
(n=56) also found survival advantages to early initiation of VA-ECMO in this population of patients.7
Acute right heart failure from massive pulmonary

embolism
Venous thromboembolism (VTE) and its most lethal manifestation, massive PE, is a common cause of
hospitalization, morbidity, and mortality. The incidence of acute PE is approximately 60 to 70 per 100,000 in
adults and mortality is estimated at 15% within the first 3 months of presentation. PE remains a significant
contributor to sudden death.10
The primary indication for MCS in patients with acute PE is refractory shock or cardiac arrest.10 PE
combined with evidence of end-organ dysfunction, such as increased serum lactate, blood urea nitrogen,
creatinine, or liver function enzymes, may ultimately prove to be a better early indicator for the use of MCS
in PE.
Device selection varies by institutional experience, availability, and device-specific features.10,11,12 The principal
aim of MCS in acute PE is to reduce right atrial pressure and provide adequate circulatory support of 4-5
liters/min. Table 2 provides a comparison of the 3 most widely used devices.10
Table 2. Mechanical Circulatory Support Devices for High-risk Pulmonary Embolism

(adapted from Elder et al., Interv Cardiol Clin. 2018)10
IMPELLA RP® TANDEMHEART PROTEK VA-ECMO (CENTRIMAG)
Device description • Micro-axial pump • Centrifugal pump • Centrifugal pump
• 24 Fr peel away, 9 Fr • 29-31 Fr dual lumen • 14-16 Fr arterial, 18-21 Fr
catheter • Dual-lumen internal venous
• Single femoral vein jugular (IJ) vein insertion • Peripheral or central
insertion; 9 Fr catheter insertion
remains in vein
Overall Pros • Single access site • Patients can ambulate • Provides hemodynamic
• BiVAD possible with (neck insertion) support
escalation • Provides significant
oxygenation
Overall Cons • No intrinsic oxygenator • Long insertion time • LV distension
• Hight transfusion rates • Vascular complications
• Transseptal left atrium- • Systemic inflammatory
femoral artery (LA-FA) response syndrome (SIRS)
bypass may occur after ECMO
decannulation
• Transfusion (bleed)
Hemodynamic support >4 L/min maximum flow Up to 5 L/min 5 L/min
Duration of use Days Months Weeks
Hemodynamic effects Change from baseline after device placement:
Right atrial pressure Reduces RAP Reduces RAP Reduces RAP
(RAP)
Pulmonary artery Increases mean PAP Increases mean PAP Little to no reduction in
pressure (PAP) mean PAP
Pulmonary capillary Increases PCWP Increases PCWP Reduces PCWP
wedge pressure (PCWP)
LV afterload No change in LV afterload No change in LV afterload Significantly increases LV
afterload
Cardiac output Increases CO Increases CO Little to no reduction in CO
Device preparation time + ++ +++
Implantation time + +++ ++
Anticoagulation ++ +++ ++
Postimplant + ++ +++
management
Hemolysis risk ++ ++ +
Respiratory support No Yes Yes
Cost $$ $$$$ $$$
Implementation of MCS in acute PE is highly time sensitive as patients with massive or submassive PE
can decompensate rapidly.10 More recently, MCS has been employed increasingly as a bridge to surgical
endarterectomy.13
Takotsubo and other stress-induced cardiomyopathies

Takotsubo cardiomyopathy (aka “apical ballooning syndrome” or “broken heart syndrome”) is a condition
characterized by transient, global left ventricular dysfunction, typically in the setting of an emotional or
physical trigger.14 It is generally considered a manifestation of neurocardiogenic myocardial stunning
and, while reversible over a period of days to weeks in the majority of patients, it is now considered a very
serious form of cardiogenic shock. Takotsubo cardiomyopathy is frequently associated with complications
such as ventricular arrhythmias, thromboembolism, left ventricular outflow tract obstruction (LVOT),
intramyocardial hemorrhage/rupture, and even death.15 Although the mortality rate for stress-induced
cardiomyopathy is lower than that for cardiogenic shock from other causes (15% vs. 35%, odds ratio: 0.32;
95% confidence interval: 0.25 to 0.39; p <0.001),16 takotsubo cardiomyopathy is probably underdiagnosed in
a variety of conditions where it manifests, especially septic shock.15
The mechanisms underlying takotsubo and other stress-induced cardiomyopathies are similar. The
primary trigger appears to be an increase in cerebral blood flow to deep brain structures including the
hippocampus, brainstem, and basal ganglia, which leads to activation of noradrenergic neurons and
release of stress-related neuropeptides such as neuropeptide Y.16 These substances may have a direct
cardiodepressant effect in addition to a postulated indirect effect through perturbation of microvascular
perfusion leading to supply-demand uncoupling and myocardial stunning.16 A variety of factors, including
anxiety, depression, substance abuse, asthma/COPD, diabetes, and female gender, may predispose
patients to takotsubo cardiomyopathy. Variable echocardiographic manifestations, as shown in Table 3, can
make the diagnosis tricky.16
Table 3. Anatomic Variations in Patients with Stress Cardiomyopathies16

(adapted from Medina de Chazal et al, J Am Coll Cardiol. 2018)
APICAL BALLOONING FOCAL

MIDVENTRICULAR BASAL OR INVERTED BIVENTRICULAR
(TYPICAL) DYSFUNCTION
75% - 80% of cases 10% - 20% of cases 5% of cases <0.5% of cases Rare
• Can be associated • Severe LV • Less severe • Severe • Benign course

with LVOT dysfunction hemodynamic hemodynamic • More commonly
obstruction and/ • Acute HF syndrome compromise compromise and associated with
or apical thrombus is common cardiogenic shock chest pain
formation
• Variable prognosis
Treatment for stress-induced cardiomyopathy is mainly supportive, although recent efforts have
focused on identifying patients at increased risk of mortality or developing serious complications.16
These “at risk” patients may receive the most benefit from early initiation of MCS. Increasingly, novel
MCS devices are being deployed to provide short-term support to recovery in these patients.17 A small,
retrospective, multicenter study (n=15) utilizing the Impella 2.5®, Impella CP®, or Impella 5.0® for MCS
recently demonstrated decreased mortality, with 11/15 (73.3%) surviving to discharge and 100% of the
survivors experiencing myocardial recovery as evidenced by significant improvement in LVEF at discharge
compared to baseline (18.1% ± 6.5% on admission vs. 60.9% ± 4.8% before discharge, p<0.001).18
Sepsis associated stress-induced cardiomyopathy is of increasing interest, especially in terms of early MCS
implementation. Septic shock with cardiovascular dysfunction has a mortality rate of 70-90% compared to
a mortality rate of 20-30% in patients with sepsis and preserved cardiac function.20 Interestingly, a lower EF
and higher end diastolic volume (EDV) confers a survival advantage in early sepsis. Defacto LV dilation may
represent a compensatory mechanism that helps maintain cardiac output and makes the myocardium
less susceptible to circulating myocardial depressant factors such as interleukin-1, interleukin-6, nitric oxide,
tumor necrosis factor alpha, and endothelin-1.21,22
The early phase of septic shock, known as “warm” shock, is associated with an increase in cardiac output,
warm extremities, and decreased systemic vascular resistance. Patients successfully resuscitated in the
early “warm” phase of septic shock appear to have a survival advantage over those who progress to the
later phase of septic shock, known as “cold” shock. “Cold” shock is characterized by low cardiac output, poor
peripheral perfusion (persistently low SvO2), increasing lactic acidosis, and cool extremities.20
It is increasingly apparent that early initiation of MCS (<96 hours) in patients unresponsive to traditional
treatments for sepsis and at risk for proceeding to “cold” or late stage shock confers a survival benefit.23
Other factors associated with improved survival are gram positive infections (HR, 0.20, 95% CI, 0.08-0.57),
acute myocarditis (HR, 0.12, 95% CI, 0.06-0.27), pneumonia (HR, 0.54, 95% CI, 0.30-0.90), early effective
antibiotic therapy (HR, 0.57, 95% CI, 0.37-0.89), and short door to ECMO times (≤96 hrs, 59% vs 15%,
P<.0001).23 Numerous additional questions remain to be answered, specifically whether early initiation of
MCS in septic shock can ameliorate other highly lethal associations, such as cardiorenal and hepatorenal
syndromes.
Other non-ACS indications for MCS

Mechanical complications such as ventricular septal rupture (VSR, 4%) or free wall rupture (2%) and acute
severe mitral regurgitation (7%) are less frequent causes of cardiogenic shock, specifically after ACS. Other
non-ACS related triggers for cardiogenic shock include decompensated valvular heart disease (eg, aortic
valve stenosis or regurgitation) or non-perfusing arrhythmias.24
MCS may improve survival in the period prior to operative intervention for ventricular septal repair in
post-myocardial infarction VSR.25 Although observational studies show a trend toward improved survival
with both IABP and ECMO support, statistical significance is variable due to the small number of study
participants.25
Acute valvular emergencies, such as acute mitral regurgitation due to chordae rupture or cardiogenic
shock as a complication of transaortic valvular replacement (TAVR), have anecdotally been addressed
with MCS.26 However, the overall mortality rate remains high when MCS is deployed for acute valvular
emergencies associated with cardiogenic shock. At a mean follow up of 18.2 months, the all‐cause
cumulative mortality for MCS + TAVR was 41% (27% for elective and 71% for emergency cases).26 Mortality is
similarly high when MCS is utilized in the setting of acute mitral regurgitation/valve prolapse.27
Although relatively uncommon, the use of MCS in the setting of severe post-partum cardiomyopathy is
excellent. For these patients, MCS has been successfully used as a bridge to transplant as well as a bridge to
recovery.28
Conclusions
It is increasingly clear that the keys to successful implementation of MCS include:
• Appropriate patient selection
• Early initiation of MCS in patients at risk for evolution of their cardiogenic shock
• Careful, multidisciplinary management of other key factors associated with survival from critical illness,
such as optimization of volume status, low tidal volume ventilation, early mobilization, appropriate
nutrition, infection prevention, and mitigation of delirium
Markers for more systemic severe disease that might trigger early initiation of MCS are also being
investigated. Exotic markers such as bioactive adrenomedullin, growth differentiation factor 15, and
various micro-RNAs are actively being investigated as mortality risk stratifiers for cardiogenic shock.22 Even
relatively common measurements such as serum albumin, lactate, or bilirubin might play a role in triaging
patients in cardiogenic shock.28 Early effectiveness of MCS may eventually be quantifiable through the use
of metrics such as total bilirubin rise/fall and lactic acid clearance.29
In conclusion, the efficacy of MCS is being demonstrated in an expanding variety of patients with non-ACS
cardiogenic shock. Successful use of MCS in these patients depends on properly defining who to target
for these advanced therapies, when best to initiate MCS, and how to ethically discontinue MCS in patients
whose disease is refractory to even these devices.
Relatively common measurements may

play a role in triaging patients in cardiogenic
shock and quantifying early effectiveness of
MCS:28.29
• Serum albumin
• Lactate/Lactic acid clearance
• Bilirubin
References
1. Hritani A, Allaqaband S, Jan MF. Cardiogenic shock. In: Akin I, ed. Interventional Cardiology. IntechOpen; 2017:141-
63.
2. Reyentovich A, Barghash MH, Hochman JS. Management of refractory cardiogenic shock. Nat Rev Cardiol.
2016;13(8):481-92.
3. Pepper DJ, Sun J, Cui X, et al. Antibiotic-and fluid-focused bundles potentially improve sepsis management, but
high-quality evidence is lacking for the specificity required in the Centers for Medicare and Medicaid Service’s
sepsis bundle (SEP-1). Crit Care Med. 2019;47(10):1290-1300.
4. Rihal CS, Naidu SS, Givertz MM, et al. 2015 SCAI/ACC/HFSA/STS clinical expert consensus statement on the use of
percutaneous mechanical circulatory support devices in cardiovascular care: endorsed by the American Heart
Association, the Cardiological Society of India, and Sociedad Latino Americana de Cardiologia Intervencion;
affirmation of value by the Canadian Association of Interventional Cardiology-Association Canadienne de
Cardiologie d’intervention. J Am Coll Cardiol. 2015;65(19):e7-e26.
5. Drakos SG, Pagani FD, Lundberg MS, Baldwin JT. Advancing the science of myocardial recovery with mechanical
circulatory support: a working group of the National Heart, Lung and Blood Institute. JACC Basic Transl Sci.
2017;2(3):335-40.
6. Saito S, Toda K, Miyagawa S, et al. Diagnosis, medical treatment, and stepwise mechanical circulatory support for
fulminant myocarditis. J Artif Organs. 2018;21(2):172-9.
7. Lorusso R, Centofanti P, Gelsomino S, et al. Venoarterial extracorporeal membrane oxygenation for acute fulminant
myocarditis in adult patients: a 5-year multi-institutional experience. Ann Thorac Surg. 2016;101(3):919-26.
8. Savorgnan F, Checchia PA. Medical management of acute fulminant myocarditis. In: Mastropietro CW, Valentine
KM, eds. Pediatric Critical Care: Current Controversies. Cham, Switzerland: Springer; 2019:85-96.
9. Chen DY, Huang WK, Chien-Chia Wu V, et al. Cardiovascular toxicity of immune checkpoint inhibitors in cancer
patients: A review when cardiology meets immuno-oncology. J Formos Med Assoc. 2019.
10. Elder M, Blank N, Shemesh A, et al. Mechanical circulatory support for high-risk pulmonary embolism. Interv
Cardiol Clin. 2018;7(1):119-128.
11. Elder M, Blank N, Kaki A, et al. Mechanical circulatory support for acute right ventricular failure in the setting of
pulmonary embolism. J Interv Cardiol. 2018;31(4):518-24.
12. Shokr M, Rashed A, Mostafa A, et al. Impella RP support and catheter-directed thrombolysis to treat right
ventricular failure caused by pulmonary embolism in 2 patients. Tex Heart Inst J. 2019;45(3):182-5.
13. Iaccarino A, Frati G, Schirone L, et al. Surgical embolectomy for acute massive pulmonary embolism: state of the
art. J Thorac Dis. 2018;10(8):5154-61.
14. Nakamura M, Nakagaito M, Hori M, et al. A case of Takotsubo cardiomyopathy with cardiogenic shock after
influenza infection successfully recovered by IMPELLA support. J Artif Organs. 2019;22(4):330-3.
15. Nabzdyk CS, Couture EG, Shelton K, et al. Sepsis induced cardiomyopathy: pathophysiology and use of mechanical
circulatory support for refractory shock. J Crit Care. 2019;54:228-34.
16. Medina de Chazal H, Del Buono MG, Keyser-Marcus L, et al. Stress cardiomyopathy diagnosis and treatment: JACC
state-of-the-art review. J Am Coll Cardiol. 2018;72(16):1955-71.
17. Spratt JR, Raveendran G, Liao K, John R. Novel percutaneous mechanical circulatory support devices and their
expanding applications. Expert Rev Cardio Therapy. 2016;14(10):1133-50.
18. Napp LC, Moeller JE, Ibrahim K, et al. First series of Impella mechanical circulatory support for takotsubo syndrome
with shock. European Heart Journal. 2018;39(suppl_1):ehy566.P5691.
19. Vallabhajosyula S, Dunlay SM, Murphree DH, et al. Cardiogenic shock in takotsubo cardiomyopathy versus acute
myocardial infarction: an 8-year national perspective on clinical characteristics, management, and outcomes. JACC:
Heart Failure. 2019;7(6):469-76.
20. Kakihana Y, Ito T, Nakahara M, et al. Sepsis-induced myocardial dysfunction: pathophysiology and management.
J Intensive Care. 2016;4(1):22.
21. Aneman A, Vieillard-Baron A. Cardiac dysfunction in sepsis. Intensive Care Med. 2016;42(12):2073-76.
22. Sergi C, Shen F, Lim DW, et al. Cardiovascular dysfunction in sepsis at the dawn of emerging mediators. Biomed
Pharmacother. 2017;95:153-160.
23. Cheng A, Sun HY, Tsai MS, et al. Predictors of survival in adults undergoing extracorporeal membrane oxygenation
with severe infections. J Thorac Cardiovasc Surg. 2016;152(6):1526-36.
24. Holger T, Ohman EM, Desch S, et al. Management of cardiogenic shock. European Heart Journal. 2015;36(20):1223–
30.
25. Liebelt JJ, Yang Y, DeRose JJ, Taub CC. Ventricular septal rupture complicating acute myocardial infarction in
the modern era with mechanical circulatory support: a single center observational study. Am J Cardiovasc Dis.
2016;6(1):10-6.
26. Singh V, Damluji AA, Mendirichaga R, et al. Elective or emergency use of mechanical circulatory support devices
during transcatheter aortic valve replacement. J Interv Cardiol. 2016;29(5)513-522.
27. Pahuja M, Singh M, Patel A, et al. Utilization of mechanical circulatory support devices in chordae tendinae and
papillary muscle rupture complicating ST-elevation myocardial infarction: insights from nationwide inpatient
sample. JACC. 2018;71(11): A219.
28. Sertic F, Mathelier H, Lewey J, et al. Long-term outcomes with the use of mechanical circulatory support in patients
with severe peripartum cardiopulmonary failure. Circulation. 2019;140(Suppl_1):A13685.
29. Jäntti T, Tarvasmäki T, Harjola VP, et al. Hypoalbuminemia is a frequent marker of increased mortality in
cardiogenic shock. PLoS ONE. 2019;14(5):e0217006.
30. Singh S, et al. TCT-551 Lactate clearance is a prognostic marker for survival in cardiogenic shock receiving early
percutaneous mechanical circulatory support. JACC. 2017;70(18)Suppl B:B228.
CONTENTS
Non-Cardiac
CHAPTER
18 Critical Illness
Management
Medical Director of Critical Care Services
Anesthesiology and Critical Care Medicine
St Joseph’s Health Hospital Center
Syracuse, NY
Douglas.Fetterman@sjhsyr.org
David H. Mandell, MD
Perioperative Section Chief
Anesthesiology and Critical Care Medicine Attending
St. Joseph's Health Hospital Center
David.Mandell@sjhsyr.org
INTRODUCTION
The cardiac intensive care unit (CICU) is not a coronary care unit (CCU).
Following percutaneous coronary intervention (PCI), most patients no longer
need a CCU due to the combination of improved PCI skills and earlier time to
intervention. Most post PCI patients can go to the floor after the procedure
while a smaller proportion will require the CICU.
The CCU from a generation ago is not the same as today’s CICU. Patients who
go to the CICU are more complex, often with multisystem organ failure and
concomitant medical problems such as sepsis, neurological compromise, renal
failure, liver dysfunction, and respiratory failure.
<< Chapter 17 Chapter 18 | Non-Cardiac Critical Illness Management Chapter 19 >>
Managing modern CICU patients

To manage the modern CICU patients, clinicians must understand how to:
• Manage sepsis
• Conduct targeted temperature management
• Use advanced modes of ventilation
• Use advanced modes of mechanical circulatory support
• Understand both invasive and non-invasive cardiac monitoring techniques
Intensivists are most likely to deliver care in today’s ICU. For years, studies have been conducted comparing
“open” versus “closed” models of intensive care management. The “closed” model, one in which the
intensive care physician is the attending of record, has become the primary model. This evolution has
occurred not only because of the preponderance of supporting evidence, but also because of third party
organizations such as The Leapfrog Group, a national nonprofit organization that reports on hospital
performance. Leapfrog judges the quality of an ICU based on the delivery model, giving higher marks to
those units led by intensivists.
The terms “open” and “closed” have created unnecessary friction around control of the patient. In the
CICU, the intensivist should appreciate the knowledge and preferences for management that the
cardiologist brings, while the cardiologist should appreciate how the intensivist balances decisions
against the backdrop of myriad patient conditions. The primary function of the intensivist is to coordinate
care recommendations from a variety of consultants and allied health professionals, ensuring safe and
evidenced-based critical care practices. In these complex patients it is important that a multidisciplinary
team be involved. The team, in addition to other physician consultants, should consist of respiratory
therapists, pharmacists, nurses, nutritionists, social workers, and family members. The intensivist integrates
and synthesizes the information provided by these team members to formulate and execute the best care
plan.
What if you don’t have the support of an intensivist at your hospital? First, set patient care guidelines that
detail when escalation and transfer should occur. The American Heart Association has proposed defining
CICU in terms of levels of care,1 such as the levels illustrated in Figure 1. Each CICU level has criteria for
therapeutic and monitoring technology, nursing ratios, and intensivist physician management. These
proposed CICU levels are in lock step with the 2018 publication in The Journal of The American College of
Cardiology review article, “Cardiac Shock Care Centers.”2
LEVEL LEVEL LEVEL
3 TRIAGE & TRANSFER

2 CULPRIT PCI
1 ADVANCED MCS
Non-PCI capable hospital, STEMI receiving and PCI Dedicated cardiac

typically rural capable hospital without shock care center
advanced MCS
Figure 1. Levels of Care for Cardiac Shock (adapted from Rab et al.2)
Whether you choose to keep the

patient at your home institution ASSESS, PREVENT, AND
or transfer to a higher level of MANAGE PAIN
care, this chapter provides some • Assess pain with Critical Care Pain Observation Tool
introductory insights into critical care (CPOT) or Behavioral Pain Scale (BPS) to ensure adequate
pain control
management of the most common • Use regional anesthesia and nonopioid adjuncts
non-cardiac considerations for the • Employ analgesia-based sedation techniques with
non-intensivist managing patients in fentanyl
the CICU.
Delirium in the BOTH SAT & SBP

ICU: ICU liberation • Use daily linked spontaneous awakening trial (SAT) and
spontaneous breathing trial (SBP)
strategy using the • Employ multidisciplinary coordination of care
• Aim for faster liberation from mechanical ventilation (MV)
A-F bundle
Delirium is one of the most frustrating
problems that can derail great patient CHOICE OF SEDATION
outcomes. Whether hyperactive or • Use targeted light sedation when sedation is necessary
hypoactive, delirium affects nearly • Avoid benzodiazepines
80% of patients in the ICU. The
• Use dexmedetomidine for high delirium risk, cardiac
incidence may seem lower due to the surgery, and MV weaning
fact that just over half of the patients
with delirium have the hyperactive
form.
DELIRIUM MONITORING &
Delirium has many risk factors, MANAGEMENT
however only a few of them are • Assess with routine Confusion Assessment Method
modifiable. Identifying these risk for the intensive care unit (CAM-ICU) or Intensive Care
Delirium Screening Checklist (ICDSC)
factors, such as poor pain control, use • Employ nonpharmacologic intervention, including sleep
of benzodiazepines, deep sedation, hygiene
sleep disturbance, and the use of • Use dexmedetomidine or antipsychotic for hyperactive
symptoms
steroids, has led to the development
of the ICU Liberation strategy.3
The Society of Critical Care Medicine’s

(SCCM) ICU Liberation initiative seeks
EARLY MOBILITY & EXERCISE
• Do physical and occupational therapy assessment
to improve patient outcomes by
• Coordinate activity with SAT or periods of no sedation
ridding patients of the harmful effects
• Progress through range of motion, sitting, standing,
of pain, agitation, and delirium in walking, activities of daily living (ADLs)
the ICU. The initiative was born out
of evidence that evolved into the A-F
bundle of care (see Figure 2). FAMILY ENGAGEMENT &
EMPOWERMENT
• Provide emotional and verbal support for reorientation
• Use cognitive stimulation and participate in mobilization
• Participate in multidisciplinary rounds
Figure 2. Society of Critical Care Medicine’s A-F Bundle of Care

(adapted from Hayhurst et al.3)
The use of the A-F bundle has been shown to reduce:4,5,6

• ICU length of stay
• Ventilator days
• Ventilator associated events (ie, pneumonia)
• Incidence of delirium
• Incidence of post-traumatic stress disorder (PTSD) following ICU admission
The era of deeply sedating every mechanically ventilated patient in the ICU now resides in the history
books. Today, it is clear that deep sedation, even initially, increases the risk of mortality.7 Instead, sedation
should be lightened to the lowest level possible while maintaining a safe patient condition.8 When feasible,
intermittent boluses are preferred over continuous sedation.8 In CICU patients supported with mechanical
support devices, light sedation can be accomplished. Deeper levels of sedation should only be considered
in patients in the following conditions:
• Status epilepticus
• Alcohol withdrawal
• Unrelenting agitation putting the patient at risk of self harm
• High dose vasopressors or frequent upward titrations of vasopressors resulting from unstable
hemodynamics (hemodynamics often improve with less sedation)
• Acute respiratory distress syndrome (ARDS)/unstable oxygenation or ventilation
• Increased intracranial pressure
• Ongoing myocardial ischemia
• Ongoing neuromuscular blockade
While sedation level has been thoroughly studied, sedative choice remains a topic of intense research.
Dexmedetomidine (an alpha-2 agonist), benzodiazepines (eg, lorazepam and midazolam), propofol, and
opioids are the most studied agents. In a 2013 meta-analysis,9 the use of an alpha-2 agonist or propofol was
superior to the use of benzodiazepine-based sedation. Dexmedetomidine resulted in less delirium and
fewer ventilator-days than midazolam or lorazepam but did not reduce ICU or hospital length of stay.
Despite conflicting studies on the side effects of dexmedetomidine, my practice has revealed a higher
incidence of bradycardia and hypotension, although side effects rarely result in a need to change therapy.
The side effects of both dexmedetomidine and propofol are either easily mitigated or rare. If propofol is the
main sedative used for extended periods, pay attention to triglyceride levels. Propofol infusion syndrome
(PRIS), a rare, often fatal, condition of unknown etiology, is defined by development of lipemic serum,
metabolic acidosis, rhabdomyolysis, hepatomegaly, cardiac arrhythmias, and acute renal failure.
The SCCM published sedation guidelines in 2018.8 Recommendations include:

• Propofol or dexmedetomidine are recommended as first line agents over benzodiazepines for
maintaining light sedation.
• Pain can be managed initially with acetaminophen, and then either a low dose infusion of fentanyl or
intermittent doses as needed.
• Morphine is typically avoided in the ICU due to the higher incidence of renal failure and the potential
buildup of active metabolites.
The adage that an ounce of prevention is worth a pound of cure is fittingly applied to delirium. Beyond
the A-F bundle, no pharmacologic agent has been shown to decrease the incidence of delirium. Studies
involving antipsychotics, such as haloperidol and risperidone, have had mixed results. In the CICU
population, prolongation of QT interval needs to be monitored when using such medications. Preliminary
evidence supports the use of statins in prevention10, but further studies are needed.
In the treatment of delirium, the hyperactive delirium patient is most often recognized, while hypoactive
delirium is missed. CAM-ICU scoring is key to understanding the true incidence in your ICU. The most
common mistake in the treatment of hyperactive delirium is the use of benzodiazepines, which
can create a vicious cycle of deep sedation followed by awakening with worsening delirium. While
haloperidol, quetiapine, and dexmedetomidine have all been studied for the management of delirium,
dexmedetomidine is typically preferred because it can decrease the hyperactive component while not
leading to over sedation. Dexmedetomidine also reduces ventilator times and ICU length of stay.3
Respiratory failure: respiratory support and

antibiotic choices
In the CICU, patient respiratory failure can develop for a multitude of reasons. Many patients with heart
conditions have comorbidities such as obesity and COPD, which increase the likelihood of developing
respiratory distress and failure. Acute heart failure can result in pulmonary edema, challenging a patient’s
ability to oxygenate. In states of profound shock, acute ischemic liver injury and acute kidney injury can
worsen acid clearance. In turn, this acidosis may lead to tachypnea as a respiratory compensation for
the acid-base disturbance. Acidosis, hypercapnia, and hypoxemia can worsen right and left heart failure
through increases in pulmonary artery pressures and poor coronary oxygenation.
Physicians typically choose between 2 types of respiratory support for patients:

• Invasive mechanical ventilation (MV) with an endotracheal tube, or
• Non-invasive positive pressure ventilation (NIPPV), or BiPAP, via a face mask
Many factors figure into the decision of which course to take, including the physician’s estimation of how
rapidly the respiratory distress is likely to resolve.
BiPAP uses a tightly fitting face mask connected to a ventilator to assist the patient in breathing. Because
BiPAP supports an actively breathing patient, many clinicians fail to understand that this NIPPV method is
still a “ventilator.” With the ability to set respiratory rate and tidal volume on most newer machines, the only
difference between NIPPV and MV is the use of the face mask versus an endotracheal tube. NIPPV is the
equivalent of pressure support ventilation when a patient is intubated, where the pressure support level
is equal to the inspiratory pressure (IPAP) on the NIPPV machine and the positive end-expiratory pressure
(PEEP) and expiratory pressure (EPAP) are synonymous in function.
When choosing between NIPPV and MV, it’s important to understand the risks and the benefits of each
method of support. First and foremost, patients on NIPPV must be awake and able to protect their
airway. Conditions that place the patient at higher risk of aspiration, such as upper GI bleeding or an
acute intraabdominal process, are absolute contraindications to NIPPV. Patients with acute or chronic
neurological conditions must also be assessed for aspiration risk. Recent facial trauma or head or neck
surgery can prohibit the use NIPPV from a technical perspective.
In the settings of myocardial ischemia, arrythmias, and hemodynamic instability, physicians should decide
whether NIPPV is appropriate on a case by case basis by considering the likelihood of the condition
resolving without compromising the patient’s airway and risking aspiration. For refractory arrythmias
where frequent cardioversions are required, intubation and MV with sedation may be most comfortable for
the patient without risking development of untoward psychiatric sequelae in the long term.
NIPPV is most appropriate for respiratory support in patients with rapidly reversible causes of hypoxemia
or hypercarbia. For example, NIPPV would be a good choice of support for acute hypoxemia related
to pulmonary edema in an awake patient in whom diuretic therapy has a high likelihood of success. If
the patient’s condition cannot be improved within a short timeframe, then intubation and mechanical
ventilation is likely the better choice.
NIPPV is also the mainstay of treatment for COPD exacerbation where hypercapnic respiratory failure can
be reversed while treatments such as antibiotics, intravenous steroids, and inhaled bronchodilators can
work to reverse the cause.
When using NIPPV for hypercapnia, having a baseline ABG, and then repeating within 1 to 2 hours, is
crucial to understanding the direction in which the patient is headed. When hypoxemia or respiratory
distress is the indication, pulse oximetry and patient observation usually suffice. A respiratory therapist is
a key member of the healthcare team for mechanical respiratory support and it is vital to understand how
much support the machine is providing and what effect that is having on the patient.
For patients on respiratory support, order:

• Inspiratory pressure (IPAP)
• Expiratory pressure (EPAP), and
• Fraction of inspired oxygen (FiO2)
An IPAP of 10-15 cm H2O and an EPAP 4-5 cm H2O are good starting points with the goal of achieving a
tidal volume of 6-8mL/kg ideal body weight. Set oxygen settings based on patient condition and baseline
PaO2/SaO2. If a patient requires IPAP over 15 cm H2O, consider intubation.
Intubation and MV are standard for patients who fail to meet the criteria for ongoing NIPPV use or present
in arrest with shock. Because hemodynamic changes during the induction phase can be quite profound,
place an arterial line prior to intubation. Medications used to anesthetize the patient for intubation affect
vasomotor tone and changes in intrathoracic pressure can impact left ventricular filling as well as right
ventricular afterload. Hypoxia, hypercarbia, and the patient’s resultant stress response often artificially
elevate arterial blood pressure, giving a false sense of robust hemodynamics. Once a patient is sedated for
intubation, the patient’s true underlying hemodynamic instability can be unmasked. Being prepared with
vasopressors at the ready is an important part of intubation.
Interventional cardiologists often receive patients who were given CPR prior to arrival and may have
aspirated oral secretions or gastric contents into the airway. The question of whether to use antibiotics for
empiric pneumonia coverage in these patients is often debated. A 2019 study in the New England Journal
of Medicine reported that the use of amoxicillin-clavulanate for 2 days in patients treated with targeted
temperature management post cardiac arrest reduced the incidence of ventilator associated pneumonia.11
The choice to start antibiotics should be based on the likelihood of infection. Risk factors for bacterial
aspiration include chronic use of gastric suppression agents and small bowel obstructions. Given the risk
of Clostridium difficile, the use of any antibiotic in the ICU should be judicious. Therefore, in most cases of
mild to moderate aspiration, even with infiltrate, withhold antibiotics and follow the patient clinically over
the first 48 hours.12
Prevention of a ventilator associated pneumonia (VAP) is important, regardless of antibiotic usage. The key
elements of VAP prevention include:
• Raising the head of the bed to 30-45 degrees
• Daily assessments of sedation and readiness for extubation
• DVT and GI prophylaxis
The risk of aspiration and new pneumonia remains after extubation. In patients intubated longer than 48
hours with risk factors such as age, acute and chronic neurological conditions, COPD, and chronic reflux,
it is important to consider a formal swallow evaluation. In these patients, or other patients with risk factors
for impaired swallowing, a standard protocol for assessment by speech and language pathologists can be
useful. Although identification of impaired swallowing can help prevent aspiration during eating, the silent
aspiration of oral and pharyngeal secretions may still occur leading to aspiration pneumonia. Standard
therapies such as lung expansion therapy, daily oral hygiene, and getting out of bed are important as well.
Sepsis management: Surviving Sepsis Campaign

General medical ICUs (MICU) consider sepsis and septic shock a bread and butter diagnosis. Remembering
the medical proverb, “When you hear hoof beats in the hallway, think horses, not zebras,” be mindful from
which viewpoint you look at patients. Cardiogenic shock can be misdiagnosed as septic shock in the MICU,
and, conversely, in the CICU the signs of sepsis may be ignored or dismissed as signs cardiogenic shock.
Sepsis continues to be the deadliest of all illnesses, yet it garners less public attention than acute
myocardial infarction and cancer. As a result of its high cost of treatment and high mortality, public
domains such as state and federal governments have implemented sepsis requirements for hospitals and
physicians to follow.
Sepsis can be difficult to identify in the CICU. The systemic inflammatory response syndrome (SIRS) criteria
provide a starting point (Table 1). Patients with 2 or more of the SIRS criteria should be investigated further
for sepsis.
Table 1. SIRS Criteria (adapted from Alsulaiman 2017)13

Temperature Fever: >38.3°C (101°F)
Hypothermia: <36.0°C (96.8°F)
Respiration Tachycardia: >90 beats/minute
Tachypnea: >20 breaths/min or PaC02 <4.3 kPa (32 mmHg)
WBC count Leukocytosis: WBC count >12 x 109/L (12,000 mL), or
Leukopenia: WBC count <4 x 109/L (4000 mL), or
Normal WBC count with >10% immature neutrophils
Unfortunately, most patients with acute myocardial infarction and cardiogenic shock also present with
similar physiologic and laboratory perturbations. Therefore, it is important for clinicians to rigorously assess
a patient’s history, physical exam, and laboratory values for features that could indicate infection. Although
the biologic plausibility and potential harm of overprescribing antibiotics is debated,14 clinical investigations
have supported the idea that for every hour antibiotics are delayed, mortality worsens.15 When it is not
clear whether there is bacterial infection or other non-bacterial or non-infectious illness, check serum
procalcitonin level as the next step. Procalcitonin concentrations of >1 ng/mL can have up to an 89%
sensitivity and 94% specificity for the diagnosis of sepsis.16 Another benefit of measuring a procalcitonin
level is the ability to use it to trend patient response to antibiotics. Serial measurement can safely support
decreased antibiotic use.17
The management of sepsis forever changed in 2001 when Dr. Emanuel Rivers published his landmark
study in the New England Journal of Medicine.18 This single center study showed a reduction in mortality
from 46.5% to 30.5% with the use of early goal-directed therapy (EGDT) in patients with severe sepsis
and septic shock. The ProCESS, ProMISe, and ARISE trials published in 2014 along with their subsequent
combined meta-analysis, called PRISM, showed that early fluid resuscitation and antibiotics were similar in
outcome to the use of EGDT. In other words, the use of dobutamine and blood transfusions to target pre-
specified central venous saturations have not subsequently been proven important in the treatment of
sepsis.
The initial Surviving Sepsis Campaign and current CMS guidelines support the use of a 3 hour and 6 hour
bundle. More recently, the Surviving Sepsis Campaign has called for an even more aggressive approach in
the “1 hour bundle.”19
Table 2. Surviving Sepsis Campaign: Hour-1 Bundle (from Surviving Sepsis Campaign)19
INITIAL RESUSCITATION FOR SEPSIS AND SEPTIC SHOCK:
1. Measure lactate level. Remeasure if initial lactate is elevated (>2 mmol/L).
2. Obtain blood cultures before administering antibiotics.
3. Administer broad-spectrum antibiotics.
4. Begin rapid administration of 30 mL/kg crystalloid for hypotension or lactate ≥4 mmol/L.
5. Apply vasopressors to maintain a mean arterial pressure of 65 mmHg or higher if patients are hypotensive during or
after fluid resuscitation.
Fluid management in patients with heart failure and end stage renal disease is an often-contested area of
sepsis management. However, studies to date continue to show that early resuscitation in patients with
heart failure and sepsis with hypotension is imperative to lessen mortality.20 Management of sepsis while
a patient is in cardiogenic shock with the potential for inserting a peripheral ventricular assist device is
much more complicated. Although early antibiotics are still paramount, the use of IV fluids must be based
on clinical assessment such as pulmonary artery catheter values, vasopressor titrations, systolic pressure
variation, or stroke volume variation, as well as suction alarms on the mechanical support devices. Although
surviving sepsis calls for trending lactates, in the patient with AMI or cardiogenic shock, the information the
lactate provides must be evaluated to determine whether it represents worsening cardiogenic shock, gut
or limb ischemia, epinephrine use, thiamine deficiency, or severe, acute, ischemic liver injury.
MANAGING SEPSIS
• Early identification using clinical judgement, SIRS, and procalcitonin is invaluable.
• Once sepsis is known or suspected, blood cultures, with or without respiratory or

urinary cultures, followed by broad spectrum antibiotics is key.
• Fluid resuscitation must be based on myriad clinical parameters but, unless
absolutely contraindicated, an early fluid bolus should be given.
Neurological injury after cardiac arrest: prognostication

and mitigation
Cardiac arrest remains a major health issue, although survival rates with good neurological recovery have
increased with improved access to emergent medical care and progress in critical care. However, cardiac
arrest remains a frequent cause of coma leading to ICU admission.
In addition, new clinical dilemmas have arisen in the ICU with improved survival after cardiac arrest.
Notably, clinicians are presented with the questions:
• Has there been a neurological injury?
• How severe is the injury?
• How can I further mitigate any neurological injury?
The immediate assumption post-arrest is that there has been a neurological injury due to global cerebral
hypoperfusion; however, the severity of the anoxic injury is extremely hard to characterize immediately
post-arrest. Therefore, immediate management should be directed toward mitigating further extra-
cerebral insults and attempting to identify and/or correct the cause of the arrest.
Targeted temperature management (TTM) has become a mainstay for improving neurological recovery
in patients post-arrest. Therapeutic hypothermia (TH) with TTM at 32º-34º C for 24 hours has been shown
to improve functional neurological outcome and survival (Level A) in patients with cardiac arrest caused
by pulseless ventricular tachycardia (VT)/ventricular fibrillation. Alternatively, TTM with a goal of 36º C post-
arrest has been shown to have similar efficacy regardless of initial rhythm (VT/VF vs. asystole or pulseless
electrical activity (PEA)) (Level B). In addition, aggressive supportive care to prevent secondary injury and
maintain optimal perfusion pressures for all organ systems, including avoidance of hyperglycemia, is a key
part of managing of these patients.
Cerebral performance categories (CPC) are commonly used to describe neurological recovery and
outcome after post-arrest coma.
• CPC 1 – Back to baseline or minimal impairment
• CPC 2 – Moderate impairment
• CPC 3 – Severe impairment
• CPC 4 – Vegetative/Comatose
• CPC 5 – Brain dead, circulation preserved
CPC 1 and 2 are typically considered “good” outcomes, whereas CPC 3-5 are considered poor outcomes.
Of all the categories, CPC 3 is considered the most heterogeneous with a wide variety of cerebral
abnormalities.
Neurological prognostication begins almost immediately in the post-arrest patient once spontaneous
circulation has been regained.
• A baseline neurological exam and non-contrast CT scan of the head can help guide further
interventions/management. These initial tests, which may identify patients with no chance for good
neurological recovery, may also impact the decision whether to pursue TH or TTM.
• A baseline EEG within 12-24 hours post-arrest can help assess background rhythm and presence of
epileptiform discharges.
• Neuron-specific enolase is a biomarker that can indicate severe neuronal damage.
• Somatosensory evoked potentials can also be useful in prognostication.
• Repeat brain imaging (either CT or MRI) can be very useful to assess the evolution and/or severity of
the initial injury.
Table 3 describes a sample prognostication algorithm for all comatose patients.
Table 3. Sample Prognostication Algorithm for Comatose Patients Following Cardiac Arrest
(adapted from Sandroni et al.)21
DAYS AFTER CARDIAC ARREST APPROACH TO TREATMENT
Days 1-2 Controlled temperature and rewarming following cardiac arrest
If the patient remains unconscious with a Glasgow Motor Score (M) of 1 or 2 after
recovery of spontaneous circulation (ROSC) and excluding confounders, particularly
residual sedation:
A. Are pupillary and corneal reflexes If YES to A and/or B:
absent? • Poor outcome very likely
B. Is N20 somatosensory evoked • (False positive rate (FPR) <5%, narrow
potential (SSPE) wave bilaterally 95% CIs)
absent?
If NO to A and B:
• Wait at least 24 hours and reassess
Days 3-5
C. Did status myoclonus start ≤48 hours If YES to 2 or more of C-F:

after ROSC? • Poor outcome likely
D. Are neuron specific enolase (NSE)
levels high?
If NO to more than 2 of C-F:
E. Does EEG reveal unreactive burst-
suppression or status epilepticus? • Observe and re-evaluate;
indeterminate outcome
F. Does CT or MRI reveal diffuse anoxic
injury on brain?
Summary
Today, patients in the CICU tend to be complex patients with multisystem organ failure. Delirium,
respiratory failure, sepsis, and neurological injury are some of the most common non-cardiac
considerations for clinicians managing patients in the CICU.
• Delirium affects nearly 80% of patients in the ICU, but effective strategies, such as those proposed by
SCCM, can reduce ICU LOS, ventilator days, and ventilator associated events, as well as the incidence of
delirium and PTSD following ICU admission.
• Respiratory failure, common among patients with heart conditions, requires strategies for deciding
whether to support patients with MV or NIPPV and when and how to use antibiotics.
• Sepsis, a deadly illnesses that can derail cardiogenic recovery, requires early identification and
appropriate management and the Surviving Sepsis Campaign provides useful guidance.
• Timely prognostication and mitigation of neurological injury following cardiac arrest is also vital to
understand.
References
1. Morrow DA, Fang JC, Fintel DJ, et al. Evolution of critical care cardiology: transformation of the cardiovascular
intensive care unit and the emerging need for new medical staffing and training models: a scientific statement
from the American Heart Association. Circulation. 2012;126(11):1408-28. Epub 2012 Aug 14.
2. Rab T, Ratanapo S, Kern KB, et al. Cardiac shock care centers. J Am Coll Cardiol. 2018;72(16):1972-80.
3. Hayhurst CJ, Pandharipande PP, Hughes CG. Intensive care unit delirium: a review of diagnosis, prevention, and
treatment. Anesthesiology. 2016;125(6):1229-41.
4. Trogrlić Z, van der Jagt M, Bakker J, et al. A systematic review of implementation strategies for assessment,
prevention, and management of ICU delirium and their effect on clinical outcomes. Crit Care. 2015;19:157.
5. Klompas M, Anderson D, Trick W, et al. The preventability of ventilator-associated events: the CDC prevention
epicenters wake up and breathe collaborative. Am J Respir Crit Care Med. 2015;191(3):292-301.
6. Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired sedation and ventilator weaning protocol for
mechanically ventilated patients in intensive care (Awakening and Breathing Controlled trial): a randomized
controlled trial. Lancet. 2008;371(9607):126-34.
7. Balzer F, Weiss B, Kumpf O, et al. Early deep sedation is associated with decreased in-hospital and two-year follow-
up survival. Crit Care. 2015;19(1):197.
8. Devlin JW, Skrobik Y, Gélinas C, et al. Executive summary: clinical practice guidelines for the prevention and
management of pain, agitation/sedation, delirium, immobility, and sleep disruption in adult patients in the ICU.
Crit Care Med. 2018;46(9):1532-48.
9. Fraser GL, Devlin JW, Worby CP, et al. Benzodiazepine versus nonbenzodiazepine-based sedation for mechanically
ventilated, critically ill adults: a systematic review and meta-analysis of randomized trials. Crit Care Med. 2013;41(9
Suppl 1):S30-8.
10. Morandi A, Hughes CG, Girard TD, et al. Statins and brain dysfunction: A hypothesis to reduce the burden of
cognitive impairment in patients who are critically ill. Chest. 2011;140(3):580-85.
11. François B, Cariou A, Clere-Jehl R, et al. Prevention of early ventilator-associated pneumonia after cardiac arrest.
N Engl J Med. 2019;381:1831-42.
12. Mandell LA, Niederman MS. Aspiration pneumonia. N Engl J Med. 2019;380(7):651-63.
13. Alsulaiman D, Kubiak DW. Criteria for sepsis: systemic inflammatory response syndrome (SIRS) and quick sepsis-
related organ dysfunction assessment (QSOFA). Current Emergency and Hospital Medical Reports. 2017;5:28-32.
14. Singer M. Antibiotics for sepsis: does each hour really count, or is it incestuous amplification? Am J Resp Crit Care
Med. 2017;196(7):800-02.
15. Liu VX, Fielding-Singh V, Greene JD, et al. The timing of early antibiotics and hospital mortality in sepsis. Am J
Respir Crit Care Med. 2017;196(7):856-63.
16. Müller B, Becker KL, Schächinger H, et al. Calcitonin precursors are reliable markers of sepsis in a medical intensive
care unit. Crit Care Med. 2000;28(4):977–83.
17. Kalil AC, Van Schooneveld TC. Is procalcitonin-guided therapy associated with beneficial outcomes in critically ill
patients with sepsis? Crit Care Med. 2018;46(5):811-12.
18. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock.
N Engl J Med. 2001;345:1368-77.
19. Surviving Sepsis Campaign. Hour-1 Bundle Pocket Card and Infographic. Available at: https://www.sccm.org/
getattachment/SurvivingSepsisCampaign/Guidelines/Adult-Patients/Surviving-Sepsis-Campaign-Hour-1-Bundle.
pdf?lang=en-US. Accessed March 4, 2020.
20. Kuttub HI, Lykins JD, Hughes MD, et al. Evaluation and predictors of fluid resuscitation in patients with severe
sepsis and septic shock. Crit Care Med. 2019;47(11):1582–90.
21. Sandroni C, Cariou A, Cavallaro F, et al. Prognostication in comatose survivors of cardiac arrest: an advisory
statement from the European Resuscitation Council and the European Society of Intensive Care Medicine.
Intensive Care Med. 2014;40(12):1816-31. doi: 10.1007/s00134-014-3470-x. Epub 2014 Nov 15.
CONTENTS
Mechanical
CHAPTER
19 Cardiac Support
Use in COVID-19
Vittorio Pazzanese, MD
Intensive Cardiac Care Unit
San Raffaele Scientific Institute
Milan, Italy
vittorio.pazzanese@hotmail.it
Department Anesthesia and Intensive Care
IRCCS ISMETT, UPMC Italy
Palermo, Italy
fedepappa@me.com
INTRODUCTION
The COVID-19 global pandemic has, as of mid-September 2020, affected
more than 28 million patients worldwide and led to more than 900,000
deaths.1 Cardiovascular disease is commonly observed among patients with
symptomatic COVID-19 infection.2,3 While the interplay between the SARS-
CoV-2 virus and cardiovascular system is very compelling, the exact mechanism
of cardiac involvement in COVID-19 remains under investigation.
This chapter reviews the cardiovascular consequences of COVID-19 and

describes mechanical circulatory support (MCS) use in this disease state.
<< Chapter 18 Chapter 19 | Mechanical Cardiac Support Use in COVID-19 Chapter 20 >>
COVID-19 disease background

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-
CoV-2). SARS-CoV-2 is a member of the genus Betacoronavirus like the 2 other coronaviruses that have
caused pandemic diseases: SARS in 2002 (SARS-CoV) and MERS (Middle East Respiratory Syndrome) in
2012 (MERS-CoV).
SARS-CoV-2 is a positive-sense, single-stranded RNA virus.4 It has a crown-like morphology and uses
angiotensin I converting enzyme 2 (ACE2) as an attachment receptor to enter host cells through structural
spike (S) proteins. Two entry pathways are described with different therapeutic implications:
• Virus attaches to ACE2 through receptor-binding domain on the surface subunit S1 of the S protein
and subsequent S protein priming by the transmembrane serine protease TMPRSS2 and the fusion of
the viral membrane with the membrane of the host cell
• ACE2–virus complex is translocated to endosomes and S protein priming is performed by the
endosomal proteases cathepsin B and cathepsin L5
SARS-CoV-2 causes a respiratory infection. Data from the Chinese Center for Disease Control and
Prevention report that 5% of patients develop uncontrolled SARS-CoV-2 infection that can trigger a
cytokine storm and multiple organ dysfunction or failure.6 (See Figure 1)
Among patients with symptoms, 14% experienced severe symptoms, including:

• Dyspnea
• Respiratory rate ≥30 breaths per minute
• Blood oxygen saturation ≤93%
• Partial pressure of arterial oxygen to fraction of inspired oxygen ratio <300
• Lung infiltrates >50% within 24 to 48 hours
COVID-19
14%
Severe
symptoms 5%
Cytokine
storm
Figure 1. COVID-19
Symptoms
ASYMPTOMATIC MILD MODERATE SEVERE DISEASE MOF
Cardiovascular consequences of SARS-CoV-2

The prevalence of cardiovascular disease among patients with symptomatic COVID-19 infection is 10%2-3
and cardiovascular disease is associated with a high rate of death. While the exact mechanism of cardiac
involvement in COVID-19 remains under investigation, the following is known: (see Figure 2)
• COVID-19 is a systemic disease that primarily injures the vascular endothelium and consequently
can cause cardiovascular disorders such as arrhythmias, acute coronary syndrome (ACS),
thromboembolism, and myocarditis, although the true prevalence of COVID-19 acute myocarditis is
unknown.
• Acute myocardial injury, defined as elevated cardiac biomarkers or electrocardiogram abnormalities, is
common (7-20% of patients7-8) and associated with a worse prognosis.9
• The rise in hs-cTnI or hs-cTnT with other inflammatory biomarkers (D-dimer, ferritin, interleukin-6,
lactate dehydrogenase) can reflect systemic inflammatory syndrome.
• Wang et al. reported that common complications among the 138 patients included shock (8.7%), ARDS
(19.6%), arrhythmia (16.7%), and acute cardiac injury (7.2%).8
• A study of 150 patients with COVID-19 reported 68 deaths. Among these 7% were attributed to
myocarditis with circulatory failure.10
• In a German cohort of patients with recent COVID-19 illness, CMR revealed cardiac involvement in 78%
and ongoing myocardial inflammation in 60%.11
• Histological evidence of myocardial involvement is scarce and the data on direct damage caused
by the virus are conflicting.12 Mild lymphocytic myocarditis and signs of epicarditis were described in
autopsy findings.13
• Myocardial injury could at least partially explain the reported incidence of arrhythmias together with
other mechanisms such a hypoxia, coronary perfusion impairment, direct tissue injury, scar-mediated
injury, inflammatory response, or medication-induced electrolyte abnormality.
ARDS
19.6%
ACUTE
MYOCARDITIS CORONARY
prevalence unknown
SYNDROME
ACUTE
MYOCARDIAL
ARRHYTHMIA INJURY
16.7%, 44.4% SHOCK
in ICU patients (7–20%) 8.7%
HEART PULMONARY
FAILURE EMBOLISM
Figure 2. Cardiovascular Consequences 24% 4/12 patients in
autopsy study
of COVID-19 Infection
Acute coronary syndrome

As with other viral infectious diseases, COVID-19 can cause acute coronary syndrome (ACS). Among
COVID-19 patients who presented with ST-elevation on ECG, case series from the United States and Italy
reported a 44% and 60% incidence, respectively, of myocardial infarction requiring revascularization.14,15 The
true incidence of ACS in patients with COVID-19, however, is still unknown. Many mechanisms for COVID-
19-induced ACS have been suggested such as plaque rupture (Type I MI) due to collagenases and tissue
factor released by activated macrophages or myocardial oxygen supply/demand mismatch (Type II MI).16
Direct vascular injury

The possibility of direct vascular injury (Figure 3) is an important issue for understanding the systemic
manifestations of COVID-19.17 Direct endothelial involvement could explain the dynamic coronary
circulation and coagulation abnormalities. In studies from Wuhan China, elevated levels of D-dimer (>1
mg/L) were observed in 42% of patients (81% of those who died)18 while reduced platelet counts and
prolonged prothrombin were less common.7 The cross-talk between endothelium and activation of the
inflammatory and coagulation cascade could explain the hypercoagulable state and the high thrombotic
burden.
In one autopsy study, deep vein thrombosis was revealed in 7 of 12 patients and pulmonary embolism in
4 of the 12 patients who died with COVID-19 in whom diagnosis was not made before death.19 Other series
report large-vessel ischemic stroke and acute limb ischemia in COVID-19 patients.20,21
SARS-CoV-2
Spike Protein (S)
Activation Attachment
TMPRSS2 ACE2
DIRECT
VASCULAR
DAMAGE
ENDOTHELIAL DAMAGE
PROCOAGULANT VASOCONSTRICTION PROINFLAMMATORY
• Tissue factor
• Thromboxane • Decrease NO • Increase in ferritin,
• Leukocyte adhesion • Thromboxane LDH, IL-1, IL-6
Figure 3. COVID-19 and
molecules • Endothelial death
Direct Vascular Injury
• Increase in D-dimer
Acute heart failure

Patients affected by COVID-19 are at risk of acute heart failure. According to some data, heart failure is one
of the most common complications with an incidence of 24% in all patients and 49% in patients who died.18
As shown in Figure 4, two different mechanisms may explain the high rate of decompensation in COVID
patients.
• Acute myocardial injury, myocarditis, sustained/repetitive cardiac arrhythmia, and COVID-19 induced
ACS can provoke myocardial dysfunction.
• In critically ill patients with advanced stages of COVID-19, inflammatory response through induction
of iNOS, oxidative stress, and persistent activation of sphingomyelinase dependent pathway induce
a more prolonged delayed phase that demonstrates depression of both basal and stimulated
contractility.
SARS-CoV-2 INFECTION
DIRECT
Lung failure/ Prothrombotic Inflammatory Renal
MYOCARDIAL
ARDS activity response impairment
INJURY
Hypoxia, pulmonary Ischemia, myocardial

embolism, pulmonary contractility Volume overload
hypertension depression
Right ventricular
dysfunction Left ventricular dysfunction
Figure 4. Heart Failure Mechanisms in COVID-19
Acute respiratory illness and shock

Acute respiratory illness is the main presentation of COVID-19 which may lead to acute respiratory distress
syndrome (ARDS), manifested as ground-glass opacities on chest imaging and hypoxemia in about 20% of
patients. Shock is the most dramatic clinical manifestation but the hemodynamic profiles in these patients
are unclear. ARDS and shock were more common in ICU-hospitalized patients and it’s unclear whether
shock occurs independently of respiratory failure.
Although distributive shock is the most common form, some patients may experience mixed forms in
which myocardial dysfunction occurs. Radiological features are not conclusive and may be seen in the case
of de novo or coexisting cardiogenic pulmonary edema.
Echocardiography should be performed in patients with hemodynamic characteristics such as decreased

systemic arterial blood pressure (mean arterial pressure <60 mmHg) and/or patients who require high-
doses of inotropic and vasoactive agents to achieve a normal-range systemic arterial blood pressure. When
serum brain natriuretic peptide (BNP) and echocardiography do not help clarify the diagnosis, consider
right heart catheterization to assess pulmonary capillary wedge pressure and to guide clinical decision
making.22,23
Invasive assessment with pulmonary artery (PA) catheters is the gold standard in deteriorating patients to
obtain cardiac output and index, LV power/cardiac power output, as well as PA pulsatility index. Preload-
recruitable stroke work or stroke work (SW) index is the gold-standard index for the assessment of LV
systolic function. For a given LVEDV, a particular stroke work may be used as an isolated data point. Cardiac
power output is the correlate of stroke work, calculated as mean arterial pressure multiplied by cardiac
output.
Although the left ventricular ejection fraction (LVEF) is not a good index of true contractility because it is
related to afterload and preload, it is generally a useful tool to determine whether MCS is reasonable. MCS
should not be used in distributive shock phenotype with a normal LVEF. MCS should be considered if the
LVEF is low, with a normal LVEDV and heart rate because the cardiac output is reduced despite optimal LV
preload (see Figure 5).
Acute respiratory failure due to When necessary,

COVID-19 causes a severe evaluate pulmonary and
ventilation-perfusion (V/Q) cardiac function:
mismatch which may require:
Noninvasive support SBP<90 mmHg or vasopressor;

lactates<2; Sv02<65%
Early intubation
Suspected cardiogenic or
mixed shock
Muscular paralysis
Echocardiogram and, if necessary,

pulmonary artery catheter
Proning
ADVANCED RESPIRATORY AND/OR CIRCULATORY SUPPORT
Figure 5. Mechanical Pulmonary and/or Circulatory Support and COVID-19
Mechanical pulmonary and/or cardiac support and

COVID-19
In management of acute pulmonary failure related to COVID-19, pulmonary and cardiac function should
guide the choice of mechanical support and its appropriateness and correct timing. It is essential to
determine when a concomitant cardiogenic component is present.
Acute respiratory failure due to COVID-19 causes a severe ventilation-perfusion (V/Q) mismatch,
represented by severe hypoxemia with normal lung compliance. Several groups suggest that this can be
explained, in part, by microvascular thrombosis in several tissue beds.18 Noninvasive mechanical ventilation
(MV) with a continuous positive airway pressure can be an initial strategy in patients with hypoxemia
suboptimally treated by high-flow supplemental oxygen systems. Transition to invasive MV remains
patient-specific. Lung-protective mechanical ventilation (tidal volumes <6 mL/kg ideal body weight,
plateau airway pressures <30 cm H2O, and FIO2 titrated to achieve adequate systemic arterial oxygen
saturations) and prone-positioning should be used. However, the increase in PEEP to treat refractory
hypoxemia may have some detrimental effects such as alveolar overdistension and increase in pulmonary
vascular resistance with a decrease in systemic venous return and cardiac output.
Modality of mechanical circulatory support

Role of extracorporeal membrane oxygenation (ECMO)
ELSO recommends against starting new ECMO centers for the sole purpose of treating patients with
COVID-19. V-V ECMO is not an alternative to mechanical ventilation or proning and it should only be
considered when mechanical ventilation is failing.
According to a recent recommendations document from ASAIO24 and a COVID-specific ELSO ECMO
Guidance Document,25 the decision to implant ECMO is the result of several factors and cannot be
considered until after a clear and timely evaluation of invasive MV failure.
The Extracorporeal Life Support Organization (ELSO) guidance document25 recommends immediate
consideration of ECMO in patients who have a high risk of mortality. However, results from the EOLIA trial
group26 demonstrated that 60-day mortality in patients assigned to immediate ECMO was not significantly
lower than mortality in patients treated with conventional MV with the option of crossover to ECMO. A
study by Xin Li et al. reported a survival rate below 50% in 8 COVID-19 patients treated with ECMO. In this
study, 7 of these patients were supported with V-V ECMO and 1 with V-A ECMO during cardiopulmonary
resuscitation and of the 8 patients, 5 patients died.27
As of October 29, 2020, the ELSO registry reported that 3026 COVID-19 patients underwent ECMO
implantation and 2253 initiated ECMO at least 90 days ago. Of these patients, 2149 (95%) were treated for
respiratory support, 80 (4%) for circulatory support, 24 (1%) for ECPR. The most important complications
were stroke (1%), intracranial hemorrhage (6%), oxygenator failure (10%) and circuit change (15%). Survival
was reported to be 57%.28 (Figure 6).
ELSO REGISTRY
Patients with COVID-19 on ECMO Major complications:

for at least 90 days required:
• Stroke (1%)
• Respiratory support (95%)
• Intracranial hemorrage (6%)
• Circulatory support (4%)
• Oxygenator failure (10%)
• ECPR (1%)
• Circuit change (15%)
• 22% discharged alive to home or

acute rehabilitation
• 17% discharged alive to
long-term acute care
57%
• 13% discharged alive to another REPORTED
hospital
SURVIVAL
• 1% discharged from ICU
• 6% remain in ICU
• 42% in-hospital death
Figure 6. ELSO Registry Report of COVID-19 Patients as of October 29, 2020
Current unpublished data from more than 50 COVID-19 patients in Japan and South Korea reported
approximately 50% recovery and survival with ECMO.
New evidence is emerging from EuroELSO registry of patients with COVID-19 that have required ECMO
support. As of September 14, 2020, there are 1531 confirmed COVID-19 cases recorded of which 91% were
supported with V-V ECMO, 5% with V-A ECMO, and 4% other.29 (Figure 7)
91% V-V ECMO
5% V-A ECMO
4% Other
Figure 7. EuroELSO Registry Report of

ECMO in 1531 Patients with COVID-19
(September 14, 2020)
When considering whether to implement ECMO, consider the following:

• Restricting use to patients with isolated single organ system (pulmonary) dysfunction
• Risks of cannulation-related complications
• Preexisting coagulopathy that increases local and systemic bleeding
• Local availability and practitioner expertise
• Exclusion of patients affected by terminal disease, severe central nervous system damage, and
significant comorbidities
• Exclusion of patients on invasive mechanical ventilation for more than 7 days
• Balancing resource availability with the potential to improve outcomes with older age
• Potential for cross-contamination of staff in the risk-to-benefit ratio of performing ECPR in COVID-19
patients
Peripheral cannulation is most commonly percutaneous. It has lower periprocedural bleeding risks
although it is associated with higher incidence of ischemic extremity complications and may result in
differential hypoxemia. Central cannulation is technically more complex and requires cardiothoracic
surgeons to perform it. Dual lumen cannulae should be avoided if possible.
Role of short-term left ventricular assist devices

Selected COVID-19 patients will be considered for short-term left ventricular (LV) assist device support.
Short-term LV support may be considered for cardiogenic shock due to direct acute myocardial injury (eg,
ACS or myocarditis) or it may be selected instead of or in addition to V-A ECMO in shock to provide direct
LV unloading. (Figure 8).
The combination of ECMO and short-term LV support with an Impella® heart pump (Abiomed, Danvers,
MA) has been shown to improve survival over the use of ECMO alone.30 There has been experience with this
combination of ECMO with Impella, often referred to as ECpella™, in compromised COVID-19 patients.31
V-A ECMO ensures high flow support, typically about 3 to 4 L/min. Although V-A ECMO decreases right
ventricular preload, it does not decrease pulmonary congestion. ECMO increases blood pressure related
to increase in arterial flow. The left ventricle must be able to generate enough pressure to overcome the
ECMO-induced increase in arterial pressure. Moreover, persistent residual flow through the pulmonary
circuit, Thebesian drainage of coronary blood flow, and aortic regurgitation produce blood return to the left
ventricle.
According to the Frank-Starling mechanism, the increase in LV filling pressure ensures that LV outflow
equals the flow returning into the LV.32 PCWP, and pulmonary artery diastolic pressure as its surrogate, are
determined by LV end-diastolic filling pressure. PCWP is an important parameter for monitoring LV filling
pressure.
Mechanical circulatory support (MCS) approaches, which ensure direct unloading through inflow cannula
within the left ventricle, are more effective in achieving LV unloading than those which employ right-
sided circuit inflow. Impella heart pumps can achieve a wide range of delivered volumetric flow rates. In
the setting of persistent profound LV dysfunction, once the lungs are decongested and adequate blood
oxygenation achieved, pVADs capable of 3.5 or 5.0 L/min generally provide sufficient flow so that ECMO can
be fully weaned. The Impella 5.0 and 5.5 heart pumps, each of which may be introduced via side grafts on
the axillary artery, are capable of providing flows of 5.0 and 5.5 L/min respectively.
Microaxial transaortic ventricular assist devices (pVADs) such as Impella offer advantages that include:
• Percutaneous transfemoral placement that can be performed at the bedside under
echocardiographic guidance.33
• Direct unloading of the LV so that stasis of blood within the LV because of aortic valve closure is not a
concern.
• Increase in total blood flow when Impella and ECMO are used together.
• Initiation of ECMO weaning if blood is adequately oxygenated.
• Patient mobility and ambulation while on support with axillary pVAD implantation in combination
with appropriate ECMO configurations.34
• Potentially safer proning position when the newest introducer sheaths are used with axillary artery
placement.
Direct acute myocardial injury

(eg, ACS or myocarditis)
REFRACTORY RESPIRATORY FAILURE CARDIOGENIC SHOCK
Biventricular LV unloading Left and/or right

dysfunction during V-A ECMO ventricular
support dysfunction
Impella and/or
V-V ECMO V-A ECMO ECpella Impella RP
Figure 8. Mechanical Circulatory Support for Patients with COVID-19
Right ventricle mechanical support

A recent study revealed right ventricular (RV) dilation, diminished RV function, and elevated pulmonary
arterial systolic pressure in non-survivors of COVID-19 without known cardiomyopathy.35 RV function
could be considered a predictor of mortality in COVID-19 patients. Rapid hemodynamic deterioration,
arrhythmias, and sudden death in patients with COVID-19 and right ventricular dysfunction may be
explained by increases in PVR due to ARDS and pulmonary embolism, negative inotropic effect related
to cytokine storm, and microvascular and direct damage from SARS-CoV-2 through macrovascular
dysfunction and ACE2.
In some cases, respiratory failure causes acute right ventricular failure due to an increase in the pulmonary
vascular impedance and RV afterload. Reduced right ventricle output can further cause V-V ECMO
recirculation and efficiency. Therefore, strategies that support the RV are justified. RVADs using femoro/
atrial/jugular to pulmonary artery approaches can be used with an oxygenator.
A peripheral percutaneous approach with the Impella RP® can ensure high flow rates. The Impella RP has
been approved for the treatment of right ventricular failure due to pulmonary embolism in COVID-19.
Infection risk during ECMO support

Immunological status of patients should be considered when selecting candidates for ECMO. Significantly
lower lymphocyte counts and higher IL-6 values were reported among COVID-19 patients who died
compared to survivors.15 During ECMO, a decrease in the number and function of some lymphocytes and
an increase in IL-6 levels has been observed.36
Pharmacologic agents in COVID-19 patients receiving

ECMO
Several antiviral drugs are used, albeit with limited evidence, in the treatment of COVID-19. It’s important to
understand the potential interactions and cardiovascular effects of these drugs.
ECMO can reduce the bioavailability of drugs due to sequestration in the circuit and can induce
pharmacokinetic alterations. For lipophilic drugs, significant uptake in the ECMO circuit could lead to low
initial plasma concentrations and higher loading dose requirements. Absorption seem to be influenced by
circuit size and/or type of oxygenator.37
Some reports describe lower than expected concentrations of ritonavir in patients during ECMO treatment.
To date the suggested dosages of remdesivir are the same in patients with or without ECMO.38
Patients with severe COVID-19 might have a cytokine storm syndrome that manifests as hemophagocytic
lymphohistiocytosis (sHLH), characterized by a fulminant and fatal hypercytokinemia with multiorgan
failure.7 In these cases immunosuppression is likely to be beneficial. Therapeutic options include steroids,
intravenous immunoglobulin, selective cytokine blockade (eg, anakinra or tocilizumab) and JAK inhibition.
ECMO can increase systemic activation of coagulation and inflammation pathways because of the
continuous contact surface between blood and the extracorporeal circuit. Ultimately this can lead
to an unbalance between procoagulant and anticoagulant factors and may lead to thrombosis and
disseminated intravascular coagulation.
At present we do not have solid data from the literature, but it could be assumed that immunosuppression
can counteract inflammatory activation. Blood purification techniques—such as blood adsorber devices
(eg, CytoSorb) with a highly porous biocompatible polymer able to bind hydrophobic compounds with
a molecular weight between 10 and 55 kDa—could provide a nonpharmacological option for COVID-19
complicated by cytokine storm.39
Optimal anticoagulation strategy

V-A ECMO is associated with a prothrombotic state that increases the risk of thromboembolic
complications. Guidelines recommend using unfractionated heparin targeting an activated clotting
time (ACT) of 180 to 220 seconds.40 The use of anti-Xa, which monitors heparin levels, has become the
gold standard because there are few conditions interfering with its accuracy. Antithrombin III (ATIII) binds
heparin for its activity. COVID-19 may induce variations in heparin sensitivity secondary to reduced ATIII
levels. If ATIII assay is <70% it should be administered for a goal functional activity of 80% to 120%.
Severe COVID-19 may predispose to disseminated intravascular coagulation (DIC) and it is associated with
poor outcome.41 COVID-19 may induce a hypercoagulable state (elevations of D-dimer, fibrin degradation
products, prothrombin time, and aPTT) and variations in heparin sensitivity secondary to reduced ATIII
levels.42 Some evidence recommends targeting higher-than-typical anticoagulation intensity with
concurrent potential benefit from antiplatelet agents in ECMO patients with COVID-19.43
Furthermore, COVID-19 is characterized by a procoagulant state that results in a massive production of

thrombin. This mechanism can upregulate formation of microthrombi at the endothelial level.44 Bivalirudin
is a direct thrombin inhibitor that produces transient inhibition of thrombin at the terminal step in the
cleavage of fibrinogen. The potential advantage of bivalirudin, especially during ECMO, is its ability to
directly attach and inhibit both freely circulating and fibrin-bound thrombin. Much evidence has emerged
regarding the use and safety of bivalirudin in mechanical circulatory support. These reports cite many
advantages such as a reduced incidence of supratherapeutic aPTT and need for transfusion, as well as
reduction in bleeding events.45
Heart transplantation during COVID-19 pandemic

Currently data show a dramatic reduction (up to 60%) in the number of organs recovered due to the lack
of available critical care beds.46 An effort should be made to maximize the number of lives saved through
management of resources in intensive care and better selection of patients who could become organ
donors.
An interesting Consensus Statement47 distinguishes multiple phases of the pandemic and we can
consider how these phases affect treatment strategies for advanced heart disease. When the number
of hospitalized patients with COVID-19 is low but expected to increase, the most important serious risk
is underutilization of available resources. In the later stages, resources need to be reallocated, organ
donation may decline, and underutilization of available resources and transmission of infection is the most
important risk.
Criteria determining transplant urgency before the pandemic may not still apply during the current
pandemic. This may increase the expected benefit of durable MCS and conservative treatment modalities
compared with listing for transplant.
Whereas MCS implants in non-inotrope-dependent patients may be safely deferred, transplantation

or MCS for patients in critical care may liberate resources. The reduced availability of organs may justify
increased use of durable MCS or strategies that previously may have been considered inferior to transplant.
A provocative question with ethical implications arises: Is there a role for COVID-19 positive donation
after brain death (DBD) and donation after cardiac death (DCD) donors to COVID-19 patients awaiting
transplantation?
Summary
COVID-19 is a systemic disease that can cause cardiovascular disorders such as arrhythmias, acute coronary
syndrome (ACS), thromboembolism, and myocarditis. Cardiovascular disease is common among patients
with COVID-19, although the exact mechanism of cardiac involvement remains under investigation. In this
chapter we’ve examined the cardiovascular consequences of SARS-CoV-2 in acute coronary syndrome,
direct vascular injury, and acute heart failure. We’ve also discussed the role of ECMO, short-term LV assist
devices (alone or in combination with ECMO) and RV mechanical support in patients with COVID-19 as
well as topics related to infection risk, pharmacologic treatments, anticoagulation strategies, and heart
transplant during COVID-19.
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PART V
TABLE OF
CONTENTS
Support and Systems of
Care
Chapter 20 Cardiogenic Shock Systems of Care......................................186
Chapter 21 Regionalization and Protocolization of the

Treatment of Cardiogenic Shock and
Need for Mechanical Circulatory Support...........................192
TABLE OF PART V Mechanical Circulatory Support and Systems of Care
CONTENTS
Cardiogenic
CHAPTER
20 Shock Systems
of Care
Assistant Professor of Internal Medicine
Virginia Commonwealth University School of Medicine, Inova Campus
Medical Director, Cardiac Intensive Care Unit
Director, Cardiovascular Critical Care Research Program
Advanced Heart Failure, Mechanical Circulatory Support, and Transplant
Cardiology Program
Inova Heart and Vascular Institute
Inova Fairfax Medical Campus
Falls Church, Virginia
Shashank.Sinha@inova.org
INTRODUCTION
Cardiogenic shock (CS) is one of the primary indications for admission to the
cardiac intensive care unit (CICU).1,2 However, the landscape of CICUs in the
United States shows substantial heterogeneity:3
• Only 8.2% of institutions have dedicated CICUs
• 14.7% have dual boarded cardiac intensivists
• 25.8% have unit-based staffing models
While it is unlikely that a “one-size-fits-all” approach will be effective, the

optimal organizational structure for managing cardiogenic shock patients
suggests a role for regionalized systems of critical care delivery, similar to
programs developed for acute ST-elevation myocardial infarction (STEMI),
stroke, and out-of-hospital cardiac arrest care.
This chapter describes cardiogenic shock center characteristics, a tiered

structure for CS care centers, CS management strategies, and organizational
staffing models for care of patients with CS.
<< Chapter 19 Chapter 20 | Cardiogenic Shock Systems of Care Chapter 21 >>
Cardiogenic shock center characteristics

In 2017, an American Heart Association (AHA) scientific statement proposed a classification system for
regionalized systems of care for CS management, colloquially known as a “hub” and “spoke” model.4 The
major goals of the hub and spoke model include:
• Early identification and treatment in the management of cardiogenic shock
• Coordinated consultation of the multidisciplinary team, including but not limited to:
▶ Interventional cardiologists
▶ Cardiac surgeons
▶ Advanced heart failure specialists
▶ Intensivists
▶ ECMO specialists
• Early hemodynamic characterization and optimization with temporary mechanical circulatory support
In this model, all CS regional destination (“hub”) referral or destination centers should meet minimum
organizational and staffing criteria as outlined in Table 1.
Table 1. Characteristics of Cardiogenic Shock Centers (adapted from van Diepen et al.4)
HIGH-VOLUME CARDIOVASCULAR CENTERS TERTIARY CARE CENTERS
Critical care unit • 24/7 in-house unit coverage by MD, PA, NP, or • CICU or ICU
resident
• 1:1 nurse-to-patient ratio
• Vasoactive infusions
• Mechanical ventilation
• Invasive cardiac and hemodynamic monitoring
• CRRT
• Temporary transvenous pacing
Medical and • Cardiac surgery • 24/7 primary PCI

technological • IABP
capabilities
• Percutaneous VAD
• Implantable VAD
• Mobile ECMO team and eCPR capabilities
• Echocardiography
Onsite medical • Cardiologist-intensivist or intensive care • Cardiology:

consultants • Cardiac surgery › Interventionalists
• Nephrology › Echocardiographers
• Palliative care › Advanced heart failure/transplantation
specialists
› Electrophysiology
• Palliative care
• Neurology
HIGH-VOLUME CARDIOVASCULAR CENTERS TERTIARY CARE CENTERS
Professional • Social work • Pharmacy

consultants • Respiratory therapist
• Physical therapist
• Occupational therapist
• Dietician
• Pharmacy
Academic • Quality improvement and auditing • Cardiogenic shock research or participation in

characteristics • Trainee education national registries
CICU=cardiac intensive care unit; CRRT=continuous renal replacement therapy; ECMO=extracorporeal membrane oxygenation;
eCPR=extracorporeal membrane oxygenation-facilitated cardiopulmonary resuscitation; IABP=intra-aortic balloon pump; ICU=intensive care
unit; MD=medical doctor; NP=nurse practitioner; PA=physician assistant; PCI=percutaneous coronary intervention; VAD=ventricular assist
device
High-volume cardiovascular centers are designated as CS receiving (“hub”) centers and receive patients
from lower acuity CS hospitals (“spoke” centers). Ultimately, the goal is for complex CS patients to be
transferred to an advanced CICU that can provide invasive hemodynamic monitoring and provide the
aforementioned on-site advanced mechanical circulatory support (MCS) and cardiothoracic surgical
capabilities.
Tiered structure for cardiogenic shock care centers

Dr. Tanveer Rab and colleagues embellished upon the AHA conceptual model for cardiac shock care
centers based on 3 tiers:5
• Level 1 consists of dedicated cardiac shock care centers (similar to AHA proposed tertiary care centers
described above) that include:
▶ Cardiac catheterization and angioplasty facilities with advanced MCS available 24 hours/7 days per
week, with on-site cardiothoracic surgery capabilities
▶ A multidisciplinary cardiogenic shock team comprised of an interventional cardiologist,
cardiothoracic surgeon, critical care specialists, and advanced heart failure specialists
▶ Established protocols for targeted temperature management for out-of-hospital cardiac arrest
patients
• Level 2 consists of STEMI receiving and percutaneous coronary intervention (PCI)-capable hospitals
without advanced MCS, which typically have:
▶ Cardiac catheterization and angioplasty facilities available 24 hours/7 days per week, but no on-site
cardiothoracic surgery capabilities
▶ Intra-aortic balloon pump (IABP) devices, but not advanced MCS capabilities; thus transfer to a Level
1 center is recommended as soon as possible
• Level 3 consists of non-PCI capable hospitals, which typically are Advance Cardiovascular Life Support
(ACLS) capable and should have a written plan for prompt transfer to a Level 1 dedicated shock care
center
LEVEL LEVEL LEVEL
3 TRIAGE & TRANSFER

2 CULPRIT PCI
1 ADVANCED MCS
Non-PCI capable hospital, STEMI receiving and PCI Dedicated cardiac

typically rural capable hospital without shock care center
advanced MCS
Figure 1. Three-Tiered Structure for Cardiac Shock Care Centers (adapted from Rab et al.5)
In this proposed framework, comprehensive CS services should be provided at a Level 1 center, which
should include dedicated critical care specialists (cardiologists or intensivists) along with nursing teams
that are familiar with escalation and weaning protocols for mechanical circulatory support. The majority of
CS patients, however, currently present to less well-resourced Level 2 or Level 3 centers. Early recognition
of CS is essential, and emergency medical services should collaborate closely with Level 1/2/3 centers in
the triage, identification, and stabilization of CS patients. Expedited transfer to a Level 1 center should
be encouraged whenever possible. Ideally, these referral calls should be directed to a single center that
activates a multidisciplinary shock team, if available, to provide an initial assessment regarding diagnostic
evaluation and management.
Cardiogenic shock management strategies

Emerging data supports
the implementation
of cardiogenic shock Cardiogenic Shock Management in the CICU
teams,6, 7, 8 which have
been associated with TREATMENT OBJECTIVES
• Wean vasopressors/inotropes • Early escalation for refractory shock • Heart recovery
improved clinical
outcomes. A shock
team with serial DOES THE PATIENT HAVE
REFRACTORY SHOCK?*
multidisciplinary • CPO < 0.6
• Cl < 2.2 L/min/m2
assessments by key • Lactate levels increasing
consultants may
help facilitate timely YES NO
escalation strategies
for mechanical Multidisciplinary shock team consultation Wean vasopressors/inotropes
circulatory support and to assess candidacy for temporary MCS and assess for heart recovery
best support patients

during the initial acute
or refractory phases Biventricular CS LV-dominant CS RV-dominant CS
CPO < 0.6W CPO < 0.6W CPO < 0.6W
of their critical illness PAPi < 1.0 PAPi > 1.0 PAPi < 1.0
RA > 15 mmHg RA < 15 mmHg RA > 15 mmHg
(Figure 2). PCWP > 15 mmHg PCWP > 15 mmHg PCWP < 15 mmHg
HYPOXEMIA? HYPOXEMIA? HYPOXEMIA?
YES NO YES NO YES NO
R+L pVAD with L pVAD with R pVAD with

oxygenator oxygenator oxygenator
or R+L pVAD or L pVAD or R pVAD
VA ECMO +/- VA ECMO + VA ECMO +/-
LV vent LV vent LV vent
Figure 2. Proposed CICU Algorithm for Management of Cardiogenic Shock

(adapted from Tehrani et al.8)
The team of specialists should

consider and discuss appropriate
LEVEL
exit strategies, including a durable
ventricular assist device, heart 3 TRIAGE & TRANSFER
transplantation, myocardial recovery, LEVEL

or palliative care. 1 ADVANCED MCS
LEVEL
Putting all of this together, the
following Shock Care pathway 2 CULPRIT PCI
facilitates comprehensive
management of these vulnerable CS
IDENTIFICATION AND CLASSIFICATION
patients (Figure 3). OF SHOCK STATE
• SBP <90 mmHg for >30 minutes or intropes/vasopressors
to maintain SBP >90 mmHg
Organizational • Evidence of end-organ hypoperfusion

• Lactate >2 mmol/L
staffing model
Finally, a brief comment on the
STABILIZATION
optimal organizational staffing model
for the care of critically ill cardiac
patients, including those with CS.
CORONARY REVASCULARIZATION (AMI CARDIOGENIC SHOCK)
Two overarching models have been
proposed:
• A cardiac intensivist model COMPREHENSIVE HEMODYNAMIC ASSESSMENT
• A collaborative cardiologist- • Cl <1.8L/min/m2 without vasopressors/inotropes or <2.2 L/min/m2
intensivist co-management with vasopressors/inotropes
model • CPO <0.6W

• PCWP and PAPi to identify CS phenotype
Cardiac intensivist model

EARLY, SELECTIVE, TAILORED CIRCULATORY SUPPORT
The cardiac intensivist model
was evaluated in a pre-and-post
observational study of more than
CICU CARE WITH MULTIDISCIPLINARY SHOCK TEAM
2400 patients admitted over a 4-year
period to a single 12-bed CICU in a
tertiary center in South Korea. The Figure 3. Shock Care Pathway Algorithm
findings of Na et al. suggest that (adapted from Tehrani et al.8)
the transition from an open, low-
intensity care model to a closed unit
model with care led by a dual-trained
cardiologist-intensivist was associated
with a 47% lower CICU mortality
after a propensity-matched analysis.9
However, given the observational
design, it is not possible to discern
the independent contribution from
staffing, physician training, and
restructuring of the multidisciplinary
team.
Collaborative cardiologist-intensivist co-management model

Kapoor and colleagues conducted a pre-and-post study of 363 patients at a single U.S. academic center in
which a collaborative cardiologist-intensivist model improved CICU length of stay, hospital length of stay,
ventilator-free days, and risk-adjusted mortality.10
Summary
Cardiogenic shock is a devastating disease that requires an effective regional systems of care network for
timely and appropriate management. While further research is needed, the proposed best practices for
systems of critical care delivery for management of CS will help inform the rapidly evolving literature.
References
1. Bohula EA, Katz JN, van Diepen S, et al. Demographics, care patterns, and outcomes of patients admitted to
cardiac intensive care units: the Critical Care Cardiology Trials Network prospective North American multicenter
registry of cardiac critical illness. JAMA Cardiology. 2019;4(9):928-35.
2. Berg DD, Bohula EA, van Diepen S, et al. Epidemiology of shock in contemporary cardiac intensive care units:
data from the Critical Care Cardiology Trials Network registry. Circulation: Cardiovascular Quality and Outcomes.
2019;12(3):e005618.
3. van Diepen S, Fordyce CB, Wegermann ZK, et al. Organizational structure, staffing, resources, and educational
initiatives in cardiac intensive care units in the United States: an American Heart Association acute cardiac care
committee and American College of Cardiology critical care cardiology working group cross-sectional survey.
Circulation: Cardiovascular Quality and Outcomes. 2017;10(8):e003864.
from the American Heart Association. Circulation. 2017;136(16):e232-e268.
5. Rab T, Ratanapo S, Kern KB, et al. Cardiac shock care centers: JACC review topic of the week. J Am Coll Cardiol.
2018;72(16):1972-80.
Cardiol. 2019;73(13):1659-69.
7. Taleb I, Koliopoulou AG, Tandar A, et al. Shock team approach in refractory cardiogenic shock requiring short-term
mechanical circulatory support: a proof of concept. Circulation. 2019;140(1):98-100.
8. Tehrani BN, Truesdell AG, Psotka MA, et al. A standardized and comprehensive approach to the management of
cardiogenic shock. J Am Coll Cardiol Heart Failure. 2020. (in press).
9. Na SJ, Chung CR, Jeon K, et al. Association between presence of a cardiac intensivist and mortality in an adult
cardiac care unit. J Am Coll Cardiol. 2016;68(24):2637-48.
10. Kapoor K, Verceles AC, Netzer G, et al. A collaborative cardiologist-intensivist management model improves cardiac
intensive care unit outcomes. J Am Coll Cardiol. 2017;70(11):1422-23.
TABLE OF PART V Mechanical Circulatory Support and Systems of Care
CONTENTS
Regionalization and
CHAPTER
21 Protocolization of the
Treatment of Cardiogenic
Shock and Need for
Support
Timothy D. Smith, MD Kari Gorder, MD

Interventional Cardiovascular and Cardiovascular Critical Care and
Critical Care Medicine Emergency Medicine
Director, Farmer Family Cardiovascular The Christ Hospital and Lindner Research
ICU Center
Director, ECMO and Shock Program Cincinnati, OH
The Christ Hospital and Lindner Research
Center
Cincinnati, OH
INTRODUCTION
Cardiogenic shock (CS), defined as a low-output cardiac state resulting in
severe end-organ hypoperfusion, is a life-threatening condition requiring
prompt recognition and intervention. While the differential etiology for a
cardiogenic shock state is broad, acute coronary syndrome (ACS) remains
a leading cause, with CS complicating up to 10% of acute myocardial
infarction (AMI) presentations.1 Despite improvements in the recognition and
management of ACS throughout the years, including early revascularization,
the incidence of CS has increased over the last decade,1 and in-hospital
mortality remains high.
<< Chapter 20 Chapter 21 | Regionalization and Protocolization of the Treatment of Cardiogenic
Shock and Need for Mechanical Circulatory Support
Mechanical circulatory support (MCS) devices are utilized for patients who, despite mechanical
revascularization and medical management, remain in a profound shock state. The implementation of
MCS devices in this patient population has increased throughout the last decade.1 When implemented in
the appropriate patient, MCS therapies have the potential to meaningfully decrease the mortality rate for
patients in cardiogenic shock. In many instances, advanced care for patients with CS may require transfer
to a regional referral hospital with advanced MCS options.
This chapter reviews the evidence for a stepwise, algorithmic heart team approach to patients with
cardiogenic shock, including those who would benefit from MCS therapies, and discusses the value of a
regionalization approach for integrated care.
Recognition and initial management of cardiogenic shock

Definitions and recognition
While the exact definition of what constitutes cardiogenic shock varies by source, most clinical trial
definitions of CS include either:
• Systolic hypotension (SBP <90 mmHg) for a prolonged time, or
• The requirement of vasopressors to achieve SBP >90 mmHg, in conjunction with signs of end-organ
hypoperfusion, such as cool extremities or urine output <30 mL/hr
Some definitions also include hemodynamic criteria such as: 2,3

• Cardiac index (CI) ≤2.2 L/min
• Elevated pulmonary capillary wedge pressure (PCWP) ≥15 mmHg
• Lactate >2.0 mmol/L
However, as various presentations of CS patients have been described,4 these criteria may miss some of the
less classic phenotypes, such as the “warm and wet” patient with profound systemic inflammation. Indeed,
up to 25% of patients with ST-elevation myocardial infarctions (STEMIs) will present with signs of systemic
inflammatory response, and many patients with CS are frequently suspected of having or are diagnosed
with concomitant septic shock,5 highlighting the potential heterogeneity in this critically ill patient
population.
Historically, the clinical diagnosis of CS was often made in the catheterization laboratory, as up to 81% of
patients presenting with CS do so secondary to AMI. Indeed, many of the major landmark CS trials only
included AMI patients.36 However, only 5-10% of all AMI patients present with cardiogenic shock, and it
is increasingly recognized that up to one-fifth of CS cases arise from other etiologies,46 such as acute on
chronic heart failure, acute valvular disorders, and myocarditis. Additionally, even among AMI patients, the
majority of patients with CS do not present initially to the healthcare system in shock. In one study, 62%
of patients developed cardiogenic shock within 24 hours of admission, whereas only 24% of patients had
shock upon presentation.6
As our understanding of the nuanced presentation and diagnosis of cardiogenic shock improves, and as
the incidence of CS continues to rise,1 it is clear that this diagnosis may be made with increasing frequency
in locations outside of the catheterization laboratory, such as intensive care units, emergency departments,
outlying care facilities without access to catheterization laboratories or advanced treatment options, and
even the outpatient setting. Consequently, a high index of suspicion for cardiogenic shock is paramount
to timely recognition and initiation of initial treatment, followed by clear pathways forward for referral to
advanced therapeutics in this critically ill population.
Initial management and treatment of cardiogenic shock

Once cardiogenic shock is suspected as the etiology for a patient’s presentation or decompensation,
expedient diagnosis, treatment, and potential escalation of care are paramount to improving survival.
After the landmark SHOCK trial, early revascularization became the standard of care initial management
strategy for shock secondary to ACS.2 For non-ACS patients with CS, very little randomized trial data exists
regarding management, and as such, recommendations for this population have been extrapolated from
the AMI data. Interestingly, while early revascularization efforts have decreased overall mortality in AMI
patients with shock, the mortality rate for patients with ACS-derived CS remains higher than for those with
a non-ACS etiology.6 Regardless, for the vast majority of patients with CS, initial management will invariably
involve coronary angiography and often right heart catheterization. While there remains debate regarding
the best initial PCI strategy, an early invasive approach with revascularization for appropriate patients has
been previously described and is recommended as best practice based on randomized trial data and
consensus statements.4
Early recognition of need for mechanical circulatory support

Unfortunately, for many patients with CS revascularization alone is not sufficient to improve end-organ
perfusion and will not immediately improve the shock state. Despite application of maximal medical
management, which may include intravenous fluid resuscitation, addition of vasopressors or inotropes, and
placement of advanced monitoring devices such as pulmonary artery catheters (PACs) to guide therapy,
the short- and long-term mortality rates for these patients remain unacceptably high. In fact, the use of
inotropes alone has been associated with higher mortality for CS patients in some studies7,8 reflecting
some of the limitations of medical management in this complex population.
Advanced mechanical circulatory support offers additional therapeutic options for the failing heart. Indeed,
timely utilization of MCS is associated with improved mortality for CS patients in the setting of AMI.9 While
the intra-aortic balloon pump (IABP) remains a common initial support modality, its benefit is often
limited, with studies showing no mortality benefit with its use in the CS population.10 In fact, IABP use has
been shown to be inferior to percutaneous left ventricular assist device use with regard to hemodynamic
support for patients in cardiogenic shock.11
Options for advanced MCS include:

• Percutaneous axial flow left and right ventricular support devices such as the Impella CP®, Impella 5.0®,
and Impella RP® (Abiomed)
• Centrifugal flow devices such as the TandemHeart® transseptal bypass system (TandemLife)
• Centrally placed support devices such as the CentriMag™ (Abbott)
• Extracorporeal membrane oxygenation (ECMO)
While these MCS options have unique applicability criteria and potential significant side effects,
appropriate patient and device selection for those requiring temporary or more long-term cardiac support
is of the utmost importance, and often requires resources beyond what an initial receiving hospital may
possess. As time to stabilization is key in the CS population, local partnerships and regionalization efforts
with clear clinical escalation algorithms can facilitate more timely application of advanced MCS options for
these patients.
Regionalization of cardiogenic shock treatment

While access to care has expanded over the last several decades, there is increasing evidence that higher
volume centers and operators are directly linked to improved outcomes. While this has been seen across
medical subspecialties, within the realm of cardiac emergencies, many studies have shown a direct
correlation between operator and institutional volume and outcomes for both PCI and CABG.12,13 This
remains true in the most high-risk subgroups. For patients presenting with AMI, there is a significant
decline in mortality if PCI is performed by experienced operators at high-volume institutions. This also was
borne out in other high-risk subgroups such as patients with heart failure, multivessel disease, or other
comorbid conditions.14
Based on this data, it is logical to conclude that mortality and outcomes for patients with CS may be
improved at regional high-volume centers, and indeed this is supported by the data. In a recent large trial
reviewing over 500,000 admissions for cardiogenic shock,15 it was demonstrated that large volume centers
are more likely to appropriately treat this complex patient population. Compared to lower volume centers,
high-volume centers were more likely to offer standard of care revascularization strategies, as well as apply
more aggressive, specific advanced mechanical circulatory support options. The authors also noted an
increase in receipt of complementary therapeutic options for patients with end-organ dysfunction, such
as dialysis, at higher volume facilities. Most importantly, a lower annual hospital case volume for patients
with CS was associated with a significantly increased odds of in-hospital mortality. The authors’ conclusion
raised the question as to whether lower volume centers should consider early stabilization and transfer to
higher volume centers for patients in cardiogenic shock.
Regionalization of care involves establishing systems of care delivery where higher-volume, specialized
facilities receive patients from outlying regional hospitals using clearly-defined criteria and established
transfer protocols to facilitate the timely triage of these patients. Historically regionalized care has been
successfully implemented for other emergent medical conditions, such as trauma, STEMI, and stroke,
and has been associated with improved outcomes. For example, a large meta-analysis found that the
establishment of a national trauma center system resulted in a 15% improvement in mortality for this
patient population.16 Similarly, for cardiac emergencies, multiple studies have shown the feasibility and
benefit of the regionalization of care for patients suffering from STEMIs, out-of-hospital cardiac arrest
(OHCA), and aortic dissection. 17-19
At the same time as these regionalization efforts have improved delivery of care in other realms, the
standard of care for definitive management of patients with cardiogenic shock has improved. Recognizing
the increasing complexity of patients with acute cardiac pathologies, various international organizations
have recommended certain resource, organizational, and staffing requirements for the best delivery of
cardiac critical care.20,21 This often involves a multidisciplinary shock team that includes:
• Interventional cardiologists
• Advanced heart failure cardiologists
• Cardiothoracic surgeons
• Intensivists
• Advanced support staff
• Ancillary services, such as emergency care and transport services
Research, quality, and education are also integral parts of improving delivery of care to this patient
population. To this end, the American Heart Association has proposed designation for levels of cardiac
intensive care units (CICU) analogous to the system used in the designation of trauma centers, with a level 1
CICU representing the most comprehensive and advanced care unit for patients with CS and other cardiac
emergencies.21
Given the value of referral networks as discussed above, it stands to reason that CS patients represent a
key patient population that would benefit from a “hub-and-spoke” model of regionalized care. This was
formally recognized in 2017, when in a scientific statement the American Heart Association proposed
regionalization of CS patients in a similar fashion to STEMI and OHCA patients. This proposed regional
system of care would require the receiving “hub” hospital to have a level 1 CICU with 24/7 access to:4
• Consultations
• Referrals
• Application of MCS technologies
Similarly, it recognized the varying capabilities of the outlying “spoke” hospitals, highlighting the
importance of creating CS treatment algorithms to:4
• Standardize regional management practices
• Provide futility parameters
• Determine the timing of transfer once the diagnosis of refractory CS is established
An algorithmic approach to escalation of care for patients

with cardiogenic shock
To improve the delivery of care to these complex patients, individual hospitals must form partnerships
within a regional referral network. While the acuity and therapeutic capabilities of the “spoke” hospitals
may vary, the cornerstone of regionalization efforts entails:
• Establishing agreed upon management strategies
• Delineating clear criteria for application of advanced MCS
• Acknowledging predefined triggers for consideration for transfer
Diagnostic and treatment algorithms are common in medicine, have been validated in the heart failure
population,22 and often involve both objective and subjective patient criteria. Many of the clinical expert
consensus guidelines for cardiogenic shock, such as the Society for Cardiovascular Angiography &
Intervention (SCAI) statement on CS,23 use both objective hemodynamic criteria such as CI and PCWP
as well as biomarkers or other laboratory data, in conjunction with patient-specific bedside findings,
increasing the applicability and utility of these classification schema to a variety of clinical settings and
practitioners. Extending this structure to the treatment of CS, an algorithm for management should
include hemodynamic and clinical trigger points with a clear actionable path forward.
Figure 1 presents one example of a management approach for patients with a decompensated heart and
cardiogenic shock.
Figure 1. Proposed
Comprehensive Shock
Team Approach to
Cardiogenic Shock
Approach based
on hemodynamic
parameters of specific
phenotypes, with a focus
on when to refer for
mechanical circulatory
support
CO: cardiac output. CI: cardiac index. CPO: cardiac power output. PCWP: pulmonary capillary wedge pressure.
PAPi: pulmonary artery pulsatility index. SVR: systemic vascular resistance. MCS: mechanical circulatory support.
In this algorithm, which utilizes the common “warm/dry” and “cold/wet” phenotypes previously discussed
and described elsewhere, 1,5,23 hemodynamic parameters and clinical scenarios are described with clear
recommendations for medical management, consideration for escalation for MCS options, and activation
of the shock team. This multidisciplinary team approach to cardiogenic shock has been shown to decrease
mortality in this patient population.24 Given the resources required for escalation of care in these patients,
for many facilities this will require transfer to a high-volume center as previously discussed.
For CS patients who are failing medical management, the decision to escalate to MCS and the choice
of MCS strategy is a complex yet critical one. It requires a fundamental understanding of the individual
patient’s hemodynamics and clinical presentation, as well as a familiarity with the variety of MCS options
available. Figure 2 represents a proposed algorithm for MCS application in the CS population.
Figure 2. Proposed
Approach to Selection of
Support Options
This approach is based
on the degree of left and
right ventricular failure
as predicted by CPO and
PAPi, respectively.
CPO: cardiac power output. PAPi: pulmonary artery pulsatility index
This algorithm uses 2 main hemodynamic parameters to capture the complex interplay between the right
and left heart in CS and facilitate appropriate MCS device selection:
• Cardiac power output (CPO)
• Pulmonary artery pulsatility index (PAPi)
CPO estimates the left heart’s pumping ability through measurements of pressure and flow and is the
product of cardiac output and mean arterial blood pressure. In a multivariate analysis of the SHOCK trial,
CPO was found to be the strongest hemodynamic predictor of mortality in cardiogenic shock patients,25
with interval changes in CPO linearly tied to outcome.
Similarly, for the right ventricle, PAPi is a validated hemodynamic parameter that predicts mortality for
patients with acute right ventricular failure, specifically within the setting of AMI. In an analysis of the
ESCAPE trial, PAPi was shown to be a strong independent predictor for mortality in patients with CS,
leading the authors to suggest using the value to improve patient selection for advanced therapies.26 In
other studies, PAPi has demonstrated superior sensitivity and specificity for predicting mortality in patients
with AMI compared to traditional metrics of the RV, such as RA to PCWP ratio or the RV stroke work index.27
Conclusion
Cardiogenic shock is a complex hemodynamic shock state that, despite improvements in treatment
modalities and delivery of care, remains challenging to diagnose, frequently fails medical management
alone, and confers a high mortality rate. Mechanical circulatory support offers additional treatment options
for patients with CS, improving end-organ recovery and affording time for additional decisions about a
patient’s care. Timely application of advanced strategies, including MCS, is of the utmost importance for
this complex and critically ill patient population. A system of regionalized care for patients with cardiogenic
shock may facilitate earlier recognition, treatment, and transfer, with the potential to improve outcomes.
This requires close collaboration with high-volume centers that offer advanced cardiovascular care in a
multidisciplinary fashion. This relationship can be facilitated by established algorithms for the recognition,
diagnosis, treatment, and escalation of care for CS patients, with a special focus on clear decision points
and triggers for transfer from regional facilities.
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Mechanical

Rev. 1 / Feb. 2021

PART I OVERVIEW AND HEMODYNAMICS IN MECHANICAL CIRCULATORY SUPPORT

PART II MECHANICAL CIRCULATORY SUPPORT WITH IMPELLA® DEVICES: INSERTION,

PART III MECHANICAL CIRCULATORY SUPPORT: OTHER DEVICES

PART IV MECHANICAL CIRCULATORY SUPPORT: GENERAL MANAGEMENT ISSUES

PART V MECHANICAL CIRCULATORY SUPPORT AND SYSTEMS OF CARE

Joseph E. Parrillo, MD, MCCM

Joseph E. Parrillo, MD, MCCM

Heart and Vascular Hospital Director of Cardiac Care Unit

Mark Anderson, MD, MHA Waqas Ghumman, MD

Vittorio Pazzanese, MD Timothy D. Smith, MD

Institute for Medical Engineering and Science

Clinical definitions and metrics

Hypotension • Systolic blood pressure (SBP) <90 mmHg, or

Cardiac index (CI) • CO normalized to body surface area

Elevated left-sided filling • Left ventricular end-diastolic pressure >18 mmHg

Pathophysiology of cardiogenic shock

EQUATION 1: FICK EQUATION

• VO2 is rate of oxygen consumption

EQUATION 2: O2 CONTENT IN BLOOD

• [Hgb] is the concentration of hemoglobin

EQUATION 3: CO IS PROPORTIONAL TO MVO2

Diagnosis and initial therapy

In other disease states, such as exacerbations of underlying cardiomyopathy or unrecognized cases of

Chapter 2 Hemodynamic Assessment:

Institute for Medical Engineering

This chapter provides an overview of the operational paradigms of commonly

Functional overview of MCS

Therapeutic benefit of MCS

Figure 1. Effects of Heart Failure on Cardiac State

The Law of Laplace (see Box) states that wall stress

Figure 2. Effects of Increasing

Cardiac muscle oxygen extraction is near maximal

The physiology of heart failure provides insights into the operation

Operational paradigms of current MCS devices

Table 1. Commonly Used Percutaneous MCS Devices

Balloon inflation during diastole increases aortic

There are currently four Impella devices available

The Impella device is connected to an external

The effect of Impella support on cardiac function

Retrograde perfusion generated by the

A significant challenge in the management of

Extracorporeal membrane oxygenation (ECMO)

When deployed as a percutaneous circulatory

Figure 6. Peripheral Venoarterial ECMO

A small percentage of patients

The Impella RP functionally lowers RV filling

While randomized control trials are lacking for RV-

Table 2. MCS Summary Table

Effects Augments Augments Reduces LV filling Increases Lowers RV filling Decreases RV

Risks of MCS and patient selection

The evidence for PAC use today

Derived measures of cardiac work include:

These derived measures can be used to determine:6,7

PAC insertion and maintenance

Nursing preparation for PAC insertion

Transducer function and calibration

C Figure 2. Determining Proper Damping

Table 1. PAC Troubleshooting Guide

Post-insertion and removal

Chapter 4 Axillary Artery Access and Management..............................52

Chapter 5 Percutaneous Ventricular Assist Device Console