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CRITICAL
CARE
MEDICINE
An Algorithmic Approach
This page intentionally left blank
CRITICAL
CARE
MEDICINE
An Algorithmic Approach
Alexander Goldfarb-Rumyantzev, MD, PhD, PhD
Lecturer
Medicine
Harvard Medical School, Beth Israel Deaconess Medical Center
Boston, Massachusetts
Contributing Author
Robert Stephen Brown, MD

Associate Chief for Academic Affairs, Nephrology Division Medicine
Beth Israel Deaconess Medical Center
Associate Professor of Medicine
Harvard Medical School
Associate Editor
Martin Shao Foong Chong, MBBS, MA (Oxon), MRCP,

FRCA, FFICM, FHEA
Magill Department of Anaesthesia
Chelsea and Westminster Hospital
London, UK
Elsevier
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
CRITICAL CARE MEDICINE: AN ALGORITHMIC APPROACH, FIRST EDITION ISBN:978-0-323-696074

Copyright © 2023 by Elsevier, Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
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This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein).
Notice
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and
using any information, methods, compounds or experiments described herein. Because of rapid advances
in the medical sciences, in particular, independent verication of diagnoses and drug dosages should be
made. To the fullest extent of the law, no responsibility is assumed by Elsevier, authors, editors or con-
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Last digit is the print number: 9 8 7 6 5 4 3 2 1
Dedication
To my family, and speci¿cally to my mom Tatiana, my late uncle Veniamin,

and my children Levi and Ben – my constant source of inspiration.
Alexander Goldfarb-Rumyantzev
To my wife Judy, son Bobby, and daughter Debbie

who have always supported my hours at work
and to the late Frank Epstein –
mentor, colleague, and friend for 40 years.
Robert S. Brown
Dedicated in memory of Alexander Goldfarb-Rumyantzev, MD, PhD, PhD,
a colleague, co-author and friend,
This book is all Alex’ doing – its conception, structure and writing. His unexpected
passing on January 18th, 2021 was a loss to us all – his innovative thinking,
logic, spirit, wit and humor will not be forgotten.
Robert S. Brown, MD
Contributing Author
Robert Stephen Brown, MD
Associate Chief for Academic Aairs, Nephrology Division Medicine
Beth Israel Deaconess Medical Center
Associate Professor of Medicine
Harvard Medical School
Associate Editor
Martin Shao Foong Chong, MBBS, MA (Oxon), MRCP, FRCA, FFICM,
FHEA
Magill Department of Anaesthesia
Chelsea and Westminster Hospital
London, UK
ix
Preface
Critical Care Medicine is a broad subject that covers many areas and almost all subspecialties of
internal medicine. As one might remember from one’s years in residency, the ICU rotation is exciting
and the favorite of many. In this book we discuss practical issues of critical care medicine divided into
chapters by subspecialty. Speci¿cally, we separated the following aspects of critical care medicine:
respiratory, cardiac and circulation, infectious disease, water and electrolytes and acid-base disor-
ders, acute kidney injury and dialysis, gastroenterology, rheumatology, endocrinology, neurology,
and COVID-19. Arguably, many aspects of critical care medicine are also relevant to general internal
medicine. In eect, critical care is an internal medicine subspecialty focused on very sick people
(plus invasive procedures). As such, the chapters in this book are applicable to the practice of general
medicine as well. Therefore, the intended audience for this book includes critical care practitioners,
as well as internal medicine physicians, and fellows and residents in critical care, internal medicine,
and its subspecialties.
Let me point out what this book is NOT. First of all, it is important to note that the goal of this book
is not to give comprehensive coverage of the topics, nor to provide a fundamental understanding of
the physiology of the discussed conditions. Rather, we address the need for quick decision making
in situations where timing is of essence. This book is intended to be a source of quick reference to
provide help in approaching conditions frequently encountered in the intensive care unit, in formu-
lating the plan of care, and in making a decision regarding the next step in management of a critical
patient. In essence, this book allows the provider to alleviate the most urgent clinical matter and buy
some time to regroup, think, call consults, and obtain more detailed and comprehensive information.
By no means does it eliminates the need for a physician to read further and have a deeper understand-
ing of the subject—of special importance is the understanding of the physiology of critical illnesses.
Medicine is practiced in a rapidly changing environment and new information is coming daily. This
book does not substitute the need to be on the top of contemporary literature. Understanding of the
underlying disease process is very important, so, once the initial strategy is established and next steps
are clear in general terms, the provider should probably step back and get additional information from
more detailed sources. Along the same lines, this book cannot cover all topics, and the authors had to
be selective. Because the purpose of the book is to be a source of quick reference, we selected top-
ics representing common issues in critical care medicine, those that practitioners are dealing with on
almost a daily basis, and those that require decisive steps.
The format of this book is dierent from most textbooks in that it is based mostly on graphical
representation of information: diagrams, tables, algorithms. We believe that this format will be help-
ful to practitioners looking for concise data and references in an environment where decisions need
to be made quickly.
Most of the references used for this book are open access sources. We speci¿cally made an eort
to select appropriate sources that would be easily available to readers, unless these sources were
insucient.
Four chapters in this book (Water and electrolyte disorders, Acid-base disorders, Acute kidney
injury and dialysis, and COVID-19) were co-authored by Dr. Robert S. Brown.
We feel sure that you will ¿nd this book helpful in your daily practice and we are very much open
to suggestions how to make the next edition better.
Alexander S. Goldfarb-Rumyantzev, MD, PhD, PhD
xi
Contents
1. Respiratory Failure, 1
2. Critical Care Cardiology and Hypertension, 32

3. Renal Failure and Renal Replacement Therapy, 64

Robert Stephen Brown
4. Water and Electrolyte Disorders, 90

5. Acid-Base Disorders, 118

6. Infectious Disease in Critical Care Practice, 132

7. Critical Care Gastroenterology, 180

8. Hematology and Oncology Aspects of Critical Care, 198

9. Rheumatology, Immunology, Allergy, 223

10. Endocrinology Issues in Critical Care, 242

11. Toxicology Highlights, 260

12. Neurology Aspects of Critical Care, 265

13. COVID-19 and Critical Care, 283

14. Useful Formulae and Abbreviations, 299

Index, 309
xiii
CHAPTER 1
Respiratory Failure
Pulmonary
The chapter addresses two large areas of critical care medicine, speci¿cally, acute respiratory failure
and means of arti¿cial gas exchange, such as mechanical ventilation and extracorporeal membrane
gas exchange.
Diagnostic Tests
Chest X-Ray Assessment Algorithm
• Technical issues:
○ view (anterior-posterior/lateral), position/rotation
○ quality and penetration
○ inspiratory eort (number of ribs)
• Evaluate soft tissue

• Evaluate bones: ribs, vertebrae
• Heart, mediastinum, trachea
• Lungs contour: costo-diaphragmal angles, diaphragm, presence of pleural eusion/pneumothorax
• Lungs parenchyma:
○ dilated hila (dilated veins in congestive heart failure [CHF], dilated arteries in congenital defects,
lymph nodes, tumor masses)

○ changes in lung parenchyma (e.g., in¿ltrate, pulmonary edema)
Changes in lung parenchyma on CXR
Air space disease/ Interstitial disease

alveolar patterns (interstitial/vascular
markings)
• Solitary vs. disseminated

changes
• Consolidation of the
lung/lobe/segment
• Infiltrates/patchy infiltrates
• Cavities/nodules
Pulmonary Function Test Interpretation

The pulmonary function test is used to diagnose and stage restrictive (caused by extrathoracic or intra-
thoracic problem) or obstructive lung disease. Restrictive lung diseases cause problems that impair
lung expansion, which lead to decreased lung volume (e.g., obesity, interstitial lung disease). On the
other hand, in obstructive lung disease, lung volume is usually preserved, but there is an impairment
to air Àow, potentially caused by bronchospasm or other airway obstruction.
1
2 CHAPTER 1 Respiratory Failure
Interpretation of the results of pulmonary function test
Restrictive pattern: Obstructive pattern:

↓FEV1, ↓FVC ↓↓FEV1
Extrathoracic Intrathoracic Emphysema: Asthma:

restrictive restrictive ↓DLCO, ↓DLCO
(obesity, kyphosis): (interstitial lung ↑or N TLC
↓TLC, ↓DLCO disease):
↓TLC, ↓↓DLCO
Arterial Blood Gas Analysis

Acid-base disorder diagnostic algorithm
The following diagram provides the algorithm of interpretation of arterial blood gases (ABGs)
used in conjunction with plasma chemistry. To use this algorithm, ¿rst examine the pH and iden-
tify acidemia or alkalemia, then using the bicarbonate concentration from the serum electrolytes
and pCO2, identify whether the primary cause of the disorder is metabolic or respiratory. Finally,
perform a calculation to examine if secondary metabolic compensation for a primary respiratory
disorder or respiratory compensation for a primary metabolic disorder is appropriate. If not, there
is a second primary disorder, considered to be a “complex” (meaning more than one) acid-base
disorder, rather than a “simple” (meaning single) acid-base disorder underlying the observed
changes.
Uses four values: pH, pCO2, HCO3 , anion gap
pH—acidemia or alkalemia
Metabolic acidosis or alkalosis

(pH and pCO2 change in the opposite direction) (pH and pCO2 change in the same direction)
No difference between acute and chronic

0.08 for each 10 only about 0.04 for each 10 disorders since secondary respiratory
mm Hg change in mm Hg change in pCO2 due compensation occurs immediately
pCO2 initially to secondary metabolic
compensation taking place
over about 24 hours
However, metabolic acidosis may occur
with a normal anion gap or with an increased
anion gap, an important distinction pointing
to different etiologies
Please note that more extensive discussion on acid-base disorders is available in the Chapter 5 of
this book.
2.e1
CHAPTER 1 Respiratory Failure 3
Pleural effusion
The normal amount of pleural Àuid is about 10 mL. Pleural eusion might be formed due to sev-
eral potential causes: increased Àuid formation (increased amount of interstitial Àuid in the lungs,
increased intravascular pressure in the pleura, decreased pleural pressure, increased permeability of
the pleura, increased pleural protein level, increased amount of peritoneal Àuid disruption of blood
vessels or lymphatics in the thorax) or decreased Àuid absorption (obstruction of the lymphatics
draining pleural Àuid, disruption of the aquaporin system in the pleura, elevated systemic vascular
pressure). The ¿rst diagnostic question of pleural Àuid analysis is if it represents a transudate or an
exudate.2
Pleural effusion
Exudate Transudate
(WBC >1000, LDH fluid-to-plasma ratio >0.6, • Nephrotic syndrome
protein fluid-to-plasma ratio >0.5) • CHF
• Cirrhosis
↑ ↓Glucose (<60) ↑
• Malignant • <7.0 - Empyema • Pancreatitis • Empyema • TB
• PE • >7.2 - Benign (parapneumonic) • Malignant
• TB
• Rheumatoid arthritis
Diagnostic thoracentesis is indicated if thickness

of pleural fluid on decubitus x-ray >10 mm
Acute Respiratory Failure

Acute respiratory failure is one of the most common conditions that requires patient to be treated in
Intensive Care Unit (ICU). Unlike many other life-threatening conditions requiring ICU admission,
respiratory failure presents immediate risk and needs to be addressed promptly. In a simpli¿ed format,
respiration entails gas exchange with O2 being absorbed and CO2 excreted by the lungs. As a result,
respiratory failure could be viewed either as a de¿ciency in oxygenation or as a failure to excrete CO2.
Some look at respiratory failure in sepsis as a separate entity, whereas others classify it within either
hypoxemic or ventilatory failure. The next chart is a general algorithm describing types of respiratory
failure and their mechanisms.3 We provide more details about speci¿c conditions below.
Quick overview of types of respiratory failure
Type 1. Oxygenation failure: Type 2. Ventilatory failure: Shock: high ventilatory demand,
hypoxic pattern hypercapnic pattern (CO2 retention) increased work of breathing, hyperpnea,
↓pO2 (<60), ↓SaO2 (<90%) ↑pCO2 (>45-55), ↓pH (<7.35) tachypnea, decreased respiratory muscle
perfusion, diaphragm fatigue
Normal A-a High A-a Normal A-a High A-a

gradient gradient gradient gradient
• Hypoventilation (opiate • R-to-L shunt (anatomic: AV • ↑CO2 production (fever, sepsis, • ↑Dead space (intrinsic
overdose, COPD, neuromuscular malformation, intracardiac seizures, increased carbo- lung disease - COPD,
disease, chest wall rigidity, upper right-to-left shunt; physiologic hydrate load, malignant asthma, cystic fibrosis,
airway obstruction) shunt that has to do with alveolar hyperthermia) pulmonary fibrosis,
• Alveolar hypoxia (low inspired filling: pulmonary edema, severe • ↓Minute ventilation emphysema, ARDS,
O2 _ high altitude, inhalation of ARDS; increased flow in the • Decreased respiratory drive pulmonary embolism
toxic gases, scuba diving mishap, alveolar capillaries) (drug overdoses) • Chest wall disorders
combustion within a close space) • Ventilation-perfusion mismatch • Neuromuscular weakness (scoliosis, trauma,
• Increased extraction (e.g., in low (flow obstruction - COPD, (CNS disorder, peripheral massive ascites, or
cardiac output state, anemia, asthma; vascular obstruction nerve disease, metabolic/ pleural effusion)
which produces low mixed [pulmonary embolism]), electrolyte abnormalities,
venous oxygenation) pneumonia, ARDS, cardiogenic severe fatigue)
pulmonary edema, • Upper airway obstruction,
hepatopulmonary syndrome dynamic airway obstruction4
• Interstitial inflammation with
↓diffusion (pneumonia, ARDS,
sarcoidosis)
Correct with FiO2, PEEP Correct with tidal volume and rate
Ventilatory Failure
Asthma and Chronic Obstructive Pulmonary Disease
Although pathophysiologies of asthma and chronic obstructive pulmonary disease (COPD) are dier-
ent, the end result leading to ventilator failure is similar and is based on hypoventilation. Therefore
whereas approaches to treatment of noncritical stable asthma and COPD might be dierent, once it
reaches the stage of respiratory failure, the focus in both conditions is to relieve bronchospasm and
provide adequate ventilation. However, one has to be cautious about gas trapping which can precipi-
tate hemodynamic instability and barotrauma.5 6
Asthma Vs. COPD
No lung destruction, Underlying lung

idiopathic attacks, disease
airway hypersensitivity
Long-term suppression of airway inflammation See figure below

and relief of symptoms with quick-acting
bronchodilators (primarily aerosolized
beta-agonists)
Inhaled corticosteroids
The most effective agents available for the
symptomatic control of asthma and
improvement in pulmonary function
Long-acting beta-agonists, theophylline, and

leukotriene antagonists
• Diminishing the production of IgE through

effects on interleukin-4 or on IgE itself:
soluble recombinant IL-4 receptor,
recombinant humanized monoclonal
antibody that forms complexes with free
IgE (rhuMAB, -E25' or omalizumab), blocks
the interaction of IgE with mast cells and
basophils
• Conventional allergen immunotherapy
• DNA vaccines and other molecular methods
of down-regulating antigen-specific
Th2-mediated responses
PO prednisone for 2
weeks, then:
• inhaled steroids
Indications for home O2 • alternative days
• Ht ≥55 prednisone
• pO2 ≤55 • minimal effective daily
• O2 sat ≤85 dose of prednisone
Theophylline Theophylline
Anticholinergics Antocholinergics Antocholinergics Metered

dose
β-agonists prn β-agonists prn β-agonists prn β-agonists inhalers
Dyspnea episodes: <1 h

FEV1 ≤80% FEV1 - 60%–80% FEV1 <60%
duration, <2 times/week
Treatment of exacerbations and

ventilatory failure in asthma
• Beta-2-adrenergic agonists
• Corticosteroids (systemic or inhaled)
• Anticholinergic agents
• Magnesium
• Aminophylline
• Systemic catecholamines
• Theophylline
• Leukotriene antagonists
If not better
Alternative therapies
• Heliox
• Ketamine
• Glucagon
• Leukotriene inhibitors
• Nebulized clonidine
• Nitroglycerin
• Nebulized calcium channel blockers
• Nebulized lidocaine
• External chest compression
If not better–consider NIPPV
Contraindications to NIPPV?
altered consciousness, hemodynamic instability,
excessive secretions, patient is
uncooperative, high risk of aspiration
No
Yes
NIPPV starting at 10/5 and titrate up as needed
No improvement
Indications for intubation
Clinical Laboratory
• Cardiac arrest • Severe hypoxemia despite maximal oxygen delivery
• Respiratory arrest/impending arrest or profound bradypnea (pO2 <60 mm Hg on 100% O 2 mask)
• Tachypnea of >40/min • Worsening respiratory acidosis or failure to reverse
• Altered sensorium (lethargy or agitation) interfering severe respiratory acidosis despite intensive therapy
with O2 delivery Of note: it is not hypercapnia but respiratory acidosis
• Progressive exhaustion, fatigue that triggers the intubation.
• Silent chest • ABG criteria: pH <7.2, pCO2 increasing
• Complicated barotrauma (or >65 mm Hg) with abnormal pH
• Unresolving acidosis
Yes
Intubate, might start with volume control

ventilation, set low respiratory rate, paralyze
for air trapping and increased pressures
Initial ventilator setting for asthmatic patient

• Controlled mechanical ventilation at 10 breaths/min
• Tidal volume at 7–8 mL/kg of ideal body weight
• Peak inspiratory flow at 60 L/min (constant flow) or 80–90 L/min (decelerating flow)
• Fraction of inspired oxygen at 1.0
• Auto-PEEP and Pplat should be followed during mechanical ventilation
• Hypercapnia is preferable to hyperinflation (not in the context of increased intracranial
pressure). Acceptable hypercapnia: pH as low as 7.15 and a PaCO 2 of up to 80 mm Hg
Issues with managing intubated patient with asthma
• Volume of gas exhaled during • Consequence of dead space

prolonged apnea (lung volume at • Minute ventilation. Increased minute ventilation (caused by alveolar
inspiration VEI). VEI is affected by ventilation increases the risk of overdistension)
severity of airflow obstruction and hypotension and barotrauma (when • Serious consequences of
ventilator settings. VEI is the most increased from 10 to 16 to 26 L/min). hypercapnia are uncommon
reliable predictor of ventilator-related • Minimal PEEP ≤5 cm H2) is • Neuro: increased cerebral blood
complications. recommended flow, intracranial pressure →
• Plateau airway pressure (Pplat; in cerebral edema and subarachnoid
acute severe asthma average 24–26 cm hemorrhage.
H2O, acceptable up to 30) • Cardiac: decreased intracellular
• Auto-PEEP (10–15 cm H2O in severe pH → reduced contractility
asthma) during volume-cycled ventilation. • Consider alkalinizing agent when
• Peak airway pressure (Ppk), target <50 cm pH is persistently below 7.15−7.2
H2O. Ppk depends on inspiratory (Na bicarbonate or tromethamine).
flow-resistive properties in addition to
hyperinflation. Ppk >50 cm H2O does
not predict increased risk of barotrauma.
• Systemic corticosteroids: anti-inflammatory effect (2.5 mg/kg/day of methylprednisolone)

• Inhaled beta-agonists (MDI or nebulizer): albuterol 2.5 mg Q4 or Q6, ipratropium
• Other bronchodilators (IV theophylline)
• Deep sedation: combination of propofol (or benzodiazepine) and fentanyl
• Neuromuscular blocking agent is sometimes necessary (intermittent boluses rather than continuous infusion)
Additional measures (not supported by strong evidence):
• Heliox (a mixture of helium and oxygen)
• Inhalational anesthetics (isoflurane)–should the effect right away, and if not then discontinue
• Ketamine IV
• Bronchoscopic removal of impacted mucus
• Extracorporeal life support (membrane oxygenation and CO 2 removal)
See mechanical ventilation section for details on managing intubated and ventilated patient
Medical Management of Asthma in the Intubated Patient Additional Measures (not Supported by Strong Evidence)
•  Systemic corticosteroids: antiinammatory effect (2.5 mg/kg •  Heliox (a mixture of helium and oxygen)
per day of methylprednisolone) •  Inhalational anesthetics (isourane)—the effect should be
•  Inhaled beta-agonists (MDI or nebulizer): albuterol 2.5 mg right away; if not, then discontinue
Q4 or Q6, ipratropium •  Ketamine IV
•  Other bronchodilators (IV theophylline) •  Bronchoscopic removal of impacted mucus
•  Deep sedation: combination of propofol (or benzodiazepine) •  Extracorporeal life support (membrane oxygenation and
and fentanyl CO2 removal)
•  Neuromuscular blocking agent is sometimes necessary
(intermittent boluses rather than continuous infusion)
MDI, Metered dose inhaler.
See Mechanical Ventilation section for details on managing intubated and ventilated patient
Hypoxemic Respiratory Failure

A number of mechanisms can lead to hypoxemic respiratory failure, resulting either from oxygen
delivery problems (acute respiratory distress syndrome [ARDS], pneumonia, pulmonary edema, high
altitude) or lung perfusion problems (pulmonary embolism, shunting).
Below is the general approach to treatment of hypoxemic respiratory failure; we also discuss spe-
cial cases (ARDS, pulmonary embolism) in more detail.
Oxygenation failure (hypoxemia)
Pneumonia or ARDS
V-Q mismatch,
Impaired gas exchange and
Cardiogenic pulmonary edema e.g., pulmonary embolism
V-Q mismatch, (decreased
(decreased perfusion)
ventilation)
NIPPV, start with 12/8−10,

titrate up PEEP
Decision point: intubation/IPPV vs. NIPPV based on clinical

impression, if patient is quickly deteriorating, lethargic, clearly
If persistent hypoxemia, infected, produces lots of secretion and otherwise have unfavorable
worsening fatigue—intubate clinical indicators—do not delay intubation and IPPV. There is no
and ventilate proven evidence for clinical benefit of NIPPV in ARDS or pneumonia.
NIPPV, titrate up PEEP Intubate, lung protective strategies,

Although there is no evidence of benefit titrate PEEP, FiO2
of NIPPV in ARDS and pneumonia, PEEP is more physiologic than
and suggestions of worse outcomes7 FiO2 as it “recruits” lung
some still advocate it.
No improvement or clinical If ARDS–increase PEEP

deterioration; specifically after If refratory hypoxemia–try other
2 hours of NIPPV: stategies: intrapulmonary
PEEP >10 percussive ventilation, airway
FiO2 >0.6 pressure release ventilation,
PaO2 <100 paralysis, proning, NO
PaO2/FiO2 (P/F ratio) <200
If no improvement—ECMO
Other than ventilator failure and hypoxemic respiratory failure, some separate respiratory failure
in sepsis into a separate entity, whereas in fact it is for the most part a multifactorial combination.
Intubation and invasive positive pressure ventilation (IPPV) is the treatment of choice for the respira-
tory failure in sepsis.
Respiratory failure in sepsis
Intubate, IPPV, volume-control

ventilation, RR 15−18/min
ARDS
ARDS is characterized by increased permeability of the alveolar capillary membrane, diuse alveolar
damage, and accumulation of proteinaceous alveolar edema. Mortality remains very high (>40%) and
does not seem to decrease between 1994 and 2006.8 That, in addition to high incidence and relatively
limited therapeutic options, makes ARDS a serious and mostly unresolved issue in critical care.1 3 9–12
1. Acute onset, presence of inciting event

2. PaO2/FiO2 ≤200 (regardless of PEEP level)
3. Bilateral infiltrates seen on frontal chest radiograph
4. PCWP ≤18 mm Hg or no clinical evidence of left atrial hypertension
Classification by PaO2/FiO2 ratio

• Acute lung injury (ALI) or mild ARDS: <300
• Moderate >100−200
• Severe ≤100
• Rule out other similar presentations: interstitial lung disease,

malignancy presenting similar to ARDS, acute eosinophilic
pneumonia, diffuse alveolar hemorrhage, hypersensitivity
pneumonitis, and pulmonary alveolar proteinosis
• Consider BAL: identify infectious causes (e.g., bacterial or viral)
• Consider lung biopsy if
o high clinical suspicion for a “contributive result” (results leading to
additional therapy)13
o the risk of empirical therapy is too high
o when empirical therapy has been unsuccessful 14
o note that lung biopsy presents substantial risk in ventilated patient
on high PEEP and benefits must clearly outweigh risks
• Lung protective ventilation (lower tidal volume and airway pressures)

(see mechanical ventilation box below)
• Neuromuscular blockade15,16
cisatracurium should be considered for short-term use (<48 h) in
patients with severe ARDS (defined as PaO 2/FiO2 <120 mm Hg)
until further studies are available17
• Esophageal pressure to adjust PEEP (improves oxygenation)
• Fluid conservative vs fluid-liberal therapy (see fluid management box below)
• Extracorporeal membrane oxygenaton (see ECMO section for details)
No proven benefit:
• High PEEP
• High frequency ventilation
• Early prone positioning
• Continuous administration of surfactant has no effect on 30-day
survival, duration of mechanical ventilation, or physiologic function
• Activated protein C (APC)
• GM-CSF
• Pulmonary artery catheter
• Methylprednisolone/steroids (questionable benefit). Some recommend
7−14-day trial of 2−4 mg/kg prednisone in patients with severe ARDS who
show no clinical signs of improvement. Rule out or treat systemic infections.
• Omega-3 fatty acid (may be harmful)
• Beta-2 agonists
• Antioxidants
• Vasodilator therapy (liposomal prostoglandin E1, nitric oxide). Liposomal
PGE1 blocks platelet aggregation, downregulates neutrophil-mediated
inflammation, produce vasodilatation.
• Ketoconazole inhibits tromboxane synthesis and biosynthesis of leukotriens
• N-acetylcysteine
Details of some specific therapeutic approaches

Details of mechanical ventilation
• Excessive fluid administration may lead to an increased amount • Optimize sedation and analgesia.
of pulmonary edema and a worsening of oxygenation. On the • Lower initial tidal volume (6−8 mL/kg), do not produce a
other hand, inadequate intravascular volume may create transpulmonary pressure that exceeds 30−35 cm H2O.
decreased cardiac output and inadequate perfusion of the • Titrate PEEP to maintain an arterial oxygen saturation of >90%
organs. Monitor biochemical markers of organ dysfunction at an FiO2 <60% (usually PEEP 5−12 cm H2O).
and lactate. • Low volume-low pressure ventilation (plateau pressure <30 cm
• If the patient is anemic (Hct <21), transfusion of packed RBC H2O) to reduce mechanical stretch improves outcome in ARDS,
can be used as a volume expander. but might lead to hypoxemia, poor lung compliance, severe
• Otherwise crystalloids or colloids should be utilized. respiratory acidosis.11
• Volume depletion may be accomplished with diuretics. • Avoid oxygen toxicity if possible (FiO2 <0.6).
• Inverse ratio ventilation (strategy, when the amount of time the
lungs are in inhalation is greater than the amount of time they
are in exhalation) may enhance recruitment at the expense of
ventilation. The resultant effect on PaCO2 is “permissive
hypercapnia” (keep static peak airway pressure <40 cm H2O,
maintain O2 saturation >90%, while tolerating pH as low as
7.15 before initiating IV buffering agents bicarbonate or THAM.
Higher doses of propofol are required to sedate patients
managed with permissive hypercapnia).
• Consider mechanical ventilation in the prone position.1
• Inhaled nitric oxide at 10 parts per million to improve VQ
matching and oxygenation but has not been shown to alter
outcome
• High-frequency oscillatory ventilation (see10 for specific
severity criteria)
• Airway pressure (release) ventilation (alternative approach
to open lung)
• ECMO
Outcome: resolution might be slow and mortality remains very high
Resolution mechanism Causes of death15
• reabsorbtion of alveolar edema • underlying illness or injury

• repair of epithelial and endothelial barriers • sepsis
• removal of inflammatory cells and exudate from distal • irreversible respiratory failure
airspaces • associated multi system organ failure due to unremitting hypoxia
Interstitial Lung Disease and Pulmonary Fibrosis

Underlying interstitial lung disease (ILD) might be a cause of hypoxemic respiratory failure. ILD
refers to lung diseases aecting the interstitium of the lungs (alveolar epithelium, pulmonary capillary
endothelium, basement membrane, and perivascular and perilymphatic tissues).19 Detailed discussion
of ILD management is outside the scope of this chapter; however, we brieÀy discuss the causes and
diagnostic approach to ILD below.
Interstitial lung disease
Chronic interstitial lung disease Acute interstitial lung changes
Granulomatous diseases
• Unknown cause (sarcoid, • Bacterial or viral pneumonia
Langerhans cell granulomatosis, etc) • Sepsis due to non-pulmonary infections
• Known cause (hypersensitivity • Aspiration of gastric content
pneumonitis, some drugs, inhalation • Major trauma with shock
causes) • Less common: acute pancreatitis,
transfusions, drug reactions, fungal
and parasitic lung infections
Inherited causes
• Tuberous sclerosis Risk factors:
• Neurofibromatosis • Chronic alcohol abuse
• Metabolic storage disorders • Multiple organ failure in septic shock
• Other: pancreatitis, near-drowning, post
cardiopulmonary bypass.
Inhalation causes • Cigarette smoking exposure (quantified
• Occupational by plasma level of cotinine)
• Environmental • Variants in more than 25 genes have an
• Domestic (birds, pets) and other association
20
tissue diseases • History, physical, labs

• SLE • Thoracic imaging (high resolution CT)
• Broncoscopy if indicated with BAL tests,
endoscopic lung biopsy
• Surgical lung biopsy (e.g., VATS)
Other
• Bronchiolitis obliterans
• Eosinophilic pneumonia
• Iatrogenic (drugs, irradiation)
• Lymphangioleiomyomatosis
• Respiratory bronchiolitis
• GERD
Treatment for specific forms of ILD20
Supportive care, anti-reflux measures,

N-acetylcysteine, lung transplantation
Sarcoidosis:
Corticosteroids, methotrexate, influximab,
lung transplantation
Corticosteroids, mycophenolate, other immunosuppression,

Corticosteroids, other immunosuppression, macrolides
Hypersensitivity pneumonitis:
Corticosteroids, other immunosuppression,
Corticosteroids, other immunosuppression
Connective tissue disease associated ILD:

Corticosteroids, mycophenolate, other
DMARD agents, anti-reflux therapy, treatment
of pulmonary hypertension, lung transplantation
Corticosteroids, cytotoxic drugs
Pulmonary Embolism
After establishing the diagnosis of pulmonary embolism, therapeutic options are (1) anticoagulation,
(2) thrombolysis/thrombectomy, or (3) if anticoagulation is contraindicated—placement of intrave-
nous ¿lter. Treatment of pulmonary embolism is discussed in the diagram below.21
Pulmonary embolism treatment
Serious contraindications to systemic anticoagulation
No Yes
Systemic anticoagulation (use Consider placement of a filter

unfractionated heparin if thrombolysis
is contemplated)
If massive PE If sub-massive PE If none of the above is true

(Definition: hypotension, shock, (Definition: evidence of right
cardiac arrest, or respiratory ventricular dysfunction with a
failure due to the embolism) normal blood pressure)
Use of thrombolytics Utility of thrombolytics

is recommended is controversial
Presence of contraindications
Major contraindications to thrombolysis

• Active bleeding
• Bleeding diathesis
• Risk of intracranial bleed (previous intracranial hemorrhage,
structural intracranial disease, ischemic stroke within 3 months,
recent brain or spinal surgery, and recent head trauma)
Yes
Relative contraindications to thrombolytics Continue systemic anticoagulation only
• Recent bleeding
• Risk of bleeding other than intracranial (recent surgery, recent
invasive procedure, anticoagulation, traumatic cardiopulmonary
resuscitation, pericarditis, or pericardial fluid)
• Pregnancy
• Hypertension SBP >180 mm Hg or DBP >110 mm Hg
• Ischemic stroke (>3 months prior)
• Age >75 years
No
Proceed with thrombolysis
Choice of thrombolytic
• Alteplase is the agent of choice
o Dose: 100 mg infused over 2 hours intravenously (IV; 10 mg
bolus, then 90 mg infused over 2 hours). In cardiac arrest the
entire dose is given as bolus
• Tenecteplase (not FDA approved for treatment of PE, but has Anticoagulation during thrombolysis
been studied for it) • Heparin should be administered in full therapeutic doses
o Administered as single dose over 5 to 10 seconds prior to administering thrombolytic therapy
o For weight <60 kg−30 mg; • The heparin infusion is most often suspended during infusion
o for weight 61 to 70 kg−35 mg; of the thrombolytic
o for weight 71 to 80 kg−40 mg; • Check PTT immediately after thrombolytic infusion and every
o for weight 81 to 90 kg−45 mg; 4 hours, restart heparin (without a bolus and at the same
o and for weight >90 kg−50 mg infusion rate as prior) when PTT <80 seconds
Mechanical Ventilation
Noninvasive Positive Pressure Ventilation
Noninvasive positive pressure ventilation (NIPPV) is an alternative to intubation and invasive venti-
lation that can be used for both ventilatory (COPD, asthma) and hypoxemic (cardiogenic pulmonary
edema) failure.22 It is a cost-eective and less invasive modality, but current evidence only supports
its use in obstructive pulmonary disease and in cardiogenic pulmonary edema.
• Lower risk of nosocomial infections (pneumonia, UTI, and catheter related)

• Less antibiotic use
• Shorter length of stay in the ICU
Benefits compared to invasive ventilation • Lower mortality
• No need for sedation/analgesia
• More comfortable to patient
• More rapid weaning
• Clinical: progressive dyspnea, tachypnea, increased work of breathing

• Respiratory acidosis and hypercapnea (pCO 2 >45 mm Hg, pH <7.35)
• Hypoxemia (PaO2/FiO2 <200)
• The use of NIPPV is well supported in the treatment of chronic
obstructive pulmonary disease exacerbations, decompensated
congestive heart failure, and in immunocompromised patients; but
there is lack of evidence to support it in respiratory failure NOT
caused by COPD or CHF
Indications
• Other acute respiratory failure scenarios where it can be used:
facilitation of weaning/extubation and extubation failure,
immunosuppressed patient, DNI status, palliative in end-stage patients,
community acquired pneumonia (with or without COPD), asthma, obesity
hypoventilation, post-op respiratory failure, and more
• Current data about the use of NIPPV in acute respiratory distress
syndrome and pneumonia (hypoxemic respiratory failure) demonstrate
poor outcomes
• Respiratory arrest
• Aspiration risk: inability to protect airway, swallowing impairment,
excessive secretion
Contraindications • Recent upper airway or GI surgery
• Technical issues: inability to fit the mask, uncooperative patient
• Medically unstable (shock, GIB, uncontrolled ischemia/arrhythmia) or
multiorgan failure
• Set pressures at low levels initially (PEEP 4–5 cm H 2O, pressure

support ~8 cm H2O)
• Set FiO2 aiming at SaO2 >90%
Initial setting • Reset pressures (increase PEEP to get SaO 2 >90%, pressure support
to get expired tidal volume ≥6 mL/kg
• ABG at baseline and 1 hour after start
• Humidification if applied for >6 hours
• Helmet
• Total face mask
• Full face mask
Devices for NIPPV • Nasal mask
• Mouthpiece
• Nasal pillows
Bilevel ventilation (combination of pressure support and PEEP)

• Pressure-control: fluctuates between high inspiratory and low expiratory
pressures; ventilator switch to expiration only after preset inspiratory time
Ventilation modalities is reached (patient is unable to control the duration of inspiration)
• Proportional-assist ventilation: targets spontaneous inspiratory flow rate
as a surrogate of patient’s effort
Positive pressure
• CPAP: constant positive pressure is applied (to raise functional residual capacity and open flooded alveoli)
• Pressure-support ventilation: preset positive pressure boost triggered by the patient; pressure applied until
inspiratory flow falls below a target pressure (patient controls breathing rate, duration of inspiration and expiration)
Endotracheal Intubation
Intubation is one of the most frequent procedures in critically ill patients. Whereas some indications
are very clear, certain situations represent a gray area, where the decision might not be straight-
forward, mostly based on uncertainty whether the patient is going to deteriorate. As any invasive
procedure, it carries a burden of complications and entails a commitment to mechanical ventilation,
sedation, and sometimes paralysis, which should also be considered in the risk-bene¿t analysis.5
• Clinical
o Respiratory arrest or profound bradypnea
Indications for intubation and IPPV o Cardiac arrest
• Laboratory: hypercapnea or hypoxia
o Severe hypoxemia with maximal oxygen delivery (pO2 <60 mm Hg on
100% O2 mask) e.g., ARDS, pulmonary edema
o Failure to reverse severe respiratory acidosis despite intensive therapy
(progressively increasing pCO2 unresponsive to therapy) or high pCO2
associated with altered mental status (hypoventilation, )
o ABG criteria: pH <7.2, pCO2 increasing by 5 mm Hg or >55–70 mm Hg
• Impending respiratory failure
o Tachypnea of >40/min
o Altered sensorium (lethargy or agitation) interfering with O2 delivery
o Complicated barotrauma
o Progressive exhaustion
o Silent chest
o Unresolving lactic acidosis
o Respiratory burns
o Anaphylaxis
o Failed trial of extubation
Other indications
• Airway protection: diminished mental status or decreased ability to
maintain airway and clear secretions
• Secretion management/ pulmonary toilet
• To facilitate bronchoscopy
• Sepsis to minimize O2 consumption and increase O2 delivery
• Circulatory shock
• Terminate seizure
• Temperature control (e.g., serotonin syndrome)
• Pharyngeal instability
• Etomidate, intravenous push, 0.3 mg/kg, with a time to effect of 15–45

seconds, and a duration of action of 3–12 minutes
• Midazolam 0.1–0.3 mg/kg IV push, with a time to effect of
approximately 30–60 seconds, and a duration of action of 15–30 minutes
• Ketamine 1–2 mg/kg IV, provides analgesia along with its amnestic,
Sedation and neuromuscular sedative, as well as bronchodilatory effects. Time to effect of 45–60
blockade for intubation seconds, and a duration of action of 10–20 minutes. It is
contraindicated in ischemic heart disease, HTN, preeclampsia,
increased intracranial pressure
• Propofol acts at the GABA receptor causing sedation and amnesia as
well as bronchodilatory effect. Induction doses of 1.5–3 mg/kg IV, time
to effect of approximately 15–45 seconds, and a duration of action of
5–10 minutes. Propofol does not provide analgesia
Neuromuscular blockade
• Succinilcholine 1–1.5 mg/kg; rapid onset and short duration of action.
Potentially greater histamine release → bronchospasm. Also might
cause hyperkalemia
• Vecuronium—no hyperkalemia, but longer duration of paralysis
Post-intubation medication
• Sedation: Propofol (can lead to seizures, hypertriglyceridemia, increased
CO2 production, “propofol infusion syndrome”) or benzodiazepine
Sedation, analgesia, and (e.g., lorazepam)
neuromuscular blockade after intubation • Narcotic: fentanyl or alfentanil
• Neuro-muscular blocade: (reduce the risk for barotrauma, avoids coughing,
avoids dyssynchronous breathing, allows respiratory muscles to rest)
For longer-term paralysis: cisatracurium (Nimbex) 0.8–1.2 mcg/kg/min drip
• Chest wall movements

• Condensed water vapor in ETT
• Auscultation of breath sounds (in both axillae)
• Carbon dioxide detector and capnography
Confirming placement
• Adequate oximeter readings, and chest radiography
• Visualizing trachea or carina through fiberoptic bronchoscope
• Chest radiography will determine the depth of intubation but not
esophageal intubation with the patient breathing ‘‘around the tube’’
Complications of Intubation and Mechanical Ventilation
Complications of IPPV
•  Ventilator-associated pneumonia •  Central Nervous System (CNS) injury (cerebral anoxia due to
•  Sepsis cardiorespiratory arrest prior to intubation)
•  Venous thromboembolism •  Muscle weakness due to acute myopathy (possibly effect
•  Barotrauma of glucocorticoids and neuromuscular paralysis or due to
•  Hypotension (by decreasing venous return, increase in right prolonged near-total muscle inactivity)
ventricular afterload risk related to degree of hyperination): •  Pneumothorax (chest tubes should be placed by blunt dis-
30–60-second apnea trial is recommended, rapid infusion of section to avoid piercing hyperinated lung)
uid, then if not better consider pneumothorax or myocar-
dial depression
Some of the speci¿c complications of intubation and mechanical ventilation are discussed in more
detail below.
(With permission from Henderson JJ, Popat MT, Latto IP, Pearce AC, Difcult Airway Society 2004.)
Respiratory complications: persistent or worsening hypoxemia after intubation
Check for tube misplacement or displacement (e.g., accidental intubation

of the esophagus, endobronchial intubation), right main stem intubation
Is endotracheal tube OK?
(proper endotracheal tube placement is generally 21 cm at the incisors in
a woman and 23 cm in a man)
No oxygen, failure of the ventilator, disconnected tubing, or leakage of air

around the endotracheal tube
Is there any equipment failure?
Check for mucous plug, kinking, biting of tube, progressive bronchospasm,

oropharyngeal trauma, or broken teeth or dentures
Is there airway obstruction?
Aspiration, respiratory system compliance problems (e.g., gastric

distention), pneumothorax, or perfusion defect (PE, cardiac arrest, or shock)
Is there other respiratory system issues?
Hemodynamic complications: hypotension
Yes
Relative or actual dehydration? Give IV bolus
Hyperinflation and increase in intrathoracic Prevent increase of intrathoracic pressure (e.g.,

pressure caused by mechanical ventilation hyperinflation, gastric distention, and tension
leads to decreased systemic venous return, pneumothorax); decrease the respiratory rate
potentially leading to a decrease in cardiac and adjusting the ventilatory cycle to allow for a
Yes
output (measure auto-PEEP and Pplat and shorter inspiratory cycle and longer expiratory
apply reduction measure). cycle are typical strategies. In critical hypotension
(SBP <90 mm Hg or drop of >40 mm Hg), a trial
of hypopnea (2−3 breaths/min) or apnea in a
preoxygenated patient for 30–60 seconds
Other causes
• Medications used for sedation or medical
management
• Pneumothorax
• Myocardial infarction and sepsis
Cardiac arrest in an intubated/ventilated patient
• Hyperinflation: → decreasing preload to the right ventricle, increasing

pericardial pressure and tamponade physiology, increasing total
pulmonary vascular resistance and right ventricular strain predisposing
Identify the cause to tension pneumothorax
• Hypoxemia (e.g., endotracheal tube displacement, kinking, or plugging);
see algorithm above
• Other metabolic causes: acidemia, electrolyte abnormalities (including
lethal hyperkalemia if succinylcholine was used for intubation of a patient
with respiratory acidosis)
• Myocardial ischemia (particularly if high-dose beta-agonists were used
systemically)
• Use of illicit drugs, such as heroin or crack cocaine
• Trial of apnea or hypopnea for no more than 30 to 60 seconds

• External chest compressions
Initiate treatment • Volume challenge
• Epinephrine
• Consider tension pneumothorax early
• Barotrauma (possibly related to airway pressure, PEEP, andtidal volume).

Other complications of intubation and For example, in asthma volume at end inspiration (Vei) of greater than
mechanical ventilation 20 mL/kg correlates with barotrauma
• Myopathy (corticosteroids, and neuromuscular blocking agents)
Difficult Airway
Dicult airway refers to two dierent clinical scenarios: dicult mask ventilation and dicult endo-
tracheal intubation.7,23,24
Difcult Tracheal Intubation •  Anatomic abnormalities (distortion or narrowing of larynx or

trachea)
•  Difculty in visualization of the larynx (difcult direct laryngo-
scopy)
Prediction: Conditions Associated With Difcult Airway  o Tumor

 o Subglottic stenosis
•  Abnormal facial anatomy/development
 o Anatomical abnormality of epiglottis
 o Small mouth, large tongue, dental abnormality
 o Obesity, advanced pregnancy, acromegaly Other predictors
•  Inability to open mouth •  Past airway difculty
•  Cervical immobility/abnormality •  Age >55 years
 o Short neck/obesity •  Body mass index >26 kg/m2
 o Poor cervical mobility •  Presence of beard
•  Pharyngeal and laryngeal abnormality •  Lack of teeth
 o High or anterior larynx •  History of snoring
 o Deep vallecula
Does patient have predictors of difficult intubation and airway is anticipated to be difficult
Yes
Options for anticipated difficult airway

• Awake intubation
o Fiberoptic (technique of choice)
o Retrograde intubation: introducing cannula and wire with ETT tube
placed over the wire
• Under anesthesia without neuromuscular blockade
No, but found difficult airway in the process of intubation
Strategy for unanticipated difficult airway—difficulty during intubation

• Maintain oxygenation and avoid hypercapnia
• Let patient recover consciousness
• Cricoid cartilage pressure or bimanual laryngoscopy
• Using stylet (to shape the tube) or gum elastic bougie (place bougie
first and introduce the ET tube over bougie)
• Chose different laryngoscope blade
• Lighted stylet (blind tracheal intubation, light is visible through
anterior soft tissues, ET tube introduced over stylet)
• Fiberoptic intubation
• Supraglottic airway devices (e.g., laryngeal mask airway)
• Cricothyrotomy (needle, wire-guided percutaneous, surgical)
Extubation
Early weaning seems to be bene¿cial. There is higher mortality, increased rate of pneumonia, and
longer hospital stay observed in the group with delayed discontinuation of mechanical ventilation.
Although there is still a possibility of selection bias, if the patient seems to be ready to be extubated
and meets the criteria, the extubation and discontinuation of mechanical ventilation should not be
delayed. While that is true, approximately 15% of all patients who have been extubated and in whom
mechanical ventilation has been discontinued require reintubation within 48 hours. Below are the
approaches to weaning and extubation.25
Strategies to Reduce the Duration of Mechanical Ventilation •  Early physical therapy

•  Conservative uid management
•  Low TV (6 mL/kg of ideal body weight) in patients with ARDS
•  Strategies to reduce ventilator-associated pneumonia
•  Sedation
 o Wake up (interrupt sedation) patient daily and prior to
spontaneous breathing trial
 o No use of sedatives
Typical Readiness Criteria • 

pH 7.33–7.48 with acceptable PaCO2
• 
Respiratory rate (RR) of 25 or less
•  Hemodynamic stability
• 
Vital capacity of 10 mL/kg or more
•  Ratio of PaO2 (mm Hg) to FiO2 >200 with PEEP of 5 or less
• 
Maxim inspiratory pressure force <−25 cm H2O
•  Improvement in underlying condition causing respiratory
• 
TV >5 mL/kg
failure
Ratio of RR (breaths/min) to TV (liters) 105 or less during
Other criteria
1-minute trial with T-piece (also called rapid shallow breathing
•  Improved clinical status index or RSBI)
•  Adequate oxygenation
PEEP, Positive end-expiratory pressure.
If patient meets these criteria – spontaneous breathing trial

• Switch ventilator to pressure support or CPAP or T-piece
• Should tolerate for 30 minutes without any of the following:
o Respiratory rate >35/min for more than 5 min
o O2 saturation less than 90%
o HR >140 or sustained change in HR of 20%
o SBP >180 mm Hg or less than 90 mm Hg
o Increased anxiety or diaphoresis
Successful Unsuccessful
• Weaning: progressive reduction in ventilator assistance

Unable to
(diminishing level of pressure support, progressive
protect
• Quantity of airway secretions duration of spontaneous breathing trials)
• The strength of cough, peak cough flow • Tracheostomy
• Mentation
Able to protect
Additional risk factors

• Increased rate/tidal volume ratio at the end of
spontaneous breathing trial
• Positive fluid balance
• Diagnosis of pneumonia
• Chronic heart failure
• Upper airway stridor at extubation
• Age >65 years
• Pneumonia is the cause of respiratory failure
• Higher comorbidity: APACHE score >12, more than one
coexisting condition other than heart failure
• Failure of 2 or more trials
No Yes
Extubate Extubate, consider higher risk of reintubation
• Reintubation might be more difficult than the original

intubation
• Before extubation have a plan and strategy for reintubation
• Airway exchange catheter (placed through ETT prior to
extubation and remains in place in case reintubation is
necessary)
• Consider tracheostomy
Details of Mechanical Ventilation

Ventilation Modalities
The ventilation modality is determined by three factors26:
• Trigger: spontaneous (describes the patient eort) or machine (machine or patient initiates the
breath): assist control (AC) or intermittent mandatory ventilation (IMV). Variable Àow shapes indi-
cate IMV.
• Target: pressure control (PC) (pressure is the target) or volume control (VC). If various pressures
are in dierent breaths, then it is volume controlled; if volume is dierent in dierent breaths, it is
pressure controlled (pressure should be stable in each breath).
• Cycle: what turns the breath o: time, volume, or Àow criteria/pressure.
Ventilator breath can be achieved in two ways:

flow/volume targeting (volume control [VC])
or pressure targeting (or pressure control [PC])
Volume control ventilation: target specific delivered Pressure control ventilation: target specific plateau
volume pressure (7%–20% use as initial modality, preferential
modality after 48 hours) of mechanicalventilation.
Because it controls the volume—make sure
pressures are OK Because it controls pressures, make
sure TV is OK
For each of these two modalities there are three basic breath sequences
Continuous mandatory ventilation (CMV):

also known as assist-control ventilation Intermittent mandatory Continuous spontaneous
VC-CMV (used in 4%–60% of critically ill ventilation (IMV) ventilation
patients) and PC-CMV
CMV: Continuous Mandatory Ventilation SIMV: Synchronized Intermittent Mandatory Ventilation

(on new machines triggered by the patient and delivers preset Delivers preset number of breaths with preset volume,
volume each time patient tries to take a breath) patient allowed to take own breaths. Similar to CMV,
mandatory breath can be patient triggered with SIMV;
however, if patient effort is not sensed—the ventilator
delivers a mandatory breath
Other PC Modalities in Addition to PC-CMV and PC-IMV

• Pressure support ventilation: patient determines inflation volume and respiratory frequency (but not pressure, as this is
pressure-controlled), used to augment spontaneous breathing to overcome the resistance of ventilator, especially during
weaning. It is different from PCV that in PCV breaths are initiated by the machine.
• Airway Pressure Release Ventilation (APRV)
• Biphasic Positive Airway Pressure
• Pressure-regulated VC Ventilation (PRVC) is combination of two: Pressure Control and Volume Control
Other PC Modalities in Addition to PC-CMV and PC-IMV different from PCV in that in PCV breaths are initiated by the
•  Pressure support ventilation: patient determines ination machine.
volume and respiratory frequency (but not pressure, as •  Airway pressure release ventilation (APRV)
this is pressure controlled), used to augment spontaneous •  Biphasic positive airway pressure
breathing to overcome the resistance of ventilator, especially •  Pressure-regulated VC ventilation (PRVC) is combination of
during weaning, or to augment spontaneous breathing. It is two: PC and VC
PC-CMV, Pressure control–continuous mandatory ventilation.

PC vs. VC
Pressure Control Volume Control

Trigger Patient triggered or time triggered Patient triggered or time triggered
Set ventilatory variables Inspiratory pressure TV Vt, ventilator uses the same ow-time waveform in
Pressure rise time every breath
RR RR
Inspiratory time (Ti) or fraction (I:E ratio) Ti or fraction (I:E ratio)
Set variables that affect oxygenation: PEEP Set variables that affect oxygenation: PEEP and FiO2
and FiO2
Dependent variables Volume and ow; vary with both respiratory Airway pressure
mechanics and patient effort
Pressure and ow wave- The pressure waveform during inspiration Inspiratory ow pattern in VC-CMV is most frequently
forms is virtually constant (square) and the ow a square ow; other ow patterns can be used (e.g.,
waveform is one of decelerating ow ramp [accelerating or decelerating] or sinusoidal)
Cycling Determined by time or ow Time or volume
Ppk With PC-CMV, the Ppk is guaranteed by the Ppk in VC-CMV is the sum of the elastic and resistive
ventilator and will not exceed the preset pressures plus the initial pressure in the system dur-
pressure limit ing ow delivery
TV Depends on driving pressure, resistance/com- Preset
pliance of respiratory system, and Ti
Ppk, Peak airway pressure; VC-CMV, volume control–continuous mandatory ventilation.
PC Ventilation
• Limits the maximum airway pressure delivered to the lung
• May result in variable tidal and minute volume
• Clinician titrates the inspiratory pressure to the measured tidal volume (TV)
• Inspiratory Àow and Àow waveform are determined by the ventilator (as it attempts to maintain a
square inspiratory pressure pro¿le)
VC Ventilation
• Safety of a preset TV and minute ventilation
• Clinician needs to appropriately set the inspiratory Àow, Àow waveform, and inspiratory time
• Airway pressure increases in response to reduced compliance, increased resistance, or active exha-
lation and may increase the risk of ventilator-induced lung injury
The bene¿cial characteristics of both volume-controlled ventilation (VCV) and pressure-controlled
ventilation (PCV) may be combined in dual-control modes, which are volume targeted, pressure lim-
ited, and time cycled.27
Pressure Control Volume Control

Mechanism Set inspiratory pressure level, PEEP, I:E ratio, RR, and FiO2 Set TV, PEEP, RR, FiO2 inspiratory pres-
The TV can be variable depending on patient characteristics sure level, PEEP, I:E ratio, RR, and FiO2
(compliance, airway/tubing resistance) and driving pressures
(difference between the plateau pressure of the airways at end-
inspiration and PEEP; also be expressed as the ratio of TV to
respiratory system compliance. Evidence suggests we should
keep driving pressure below 14 cm H2O)
Advantages PC favors the control of oxygenation28 VC favors the control of ventilation28
•  Increased mean airway pressure, which improves oxygenation •  Guaranteed TVs produce a more sta-
•  Increased duration of alveolar recruitment (alveoli are opened ble minute volume
earlier and remain open for longer) •  The minute volume remains stable
•  Protective against barotrauma (prevents exposure to extremely over a range of changing pulmonary
high pressures) characteristics
•  Work of breathing and patient comfort may be improved (initial •  The initial ow rate is lower than in
high ow rate prevents the “ow starvation”) pressure-controlled modes, i.e., it
•  Limits the maximum airway pressure delivered to the lung avoids a high resistance-related early
•  PCV may offer lower work of breathing and improved comfort pressure peak28
for patients with increased and variable respiratory demand27
Disadvantages •  TV and minute volume are variable and dependent on respira- •  The mean airway pressure is lower
tory compliance •  Recruitment may be poorer in lung
•  Uncontrolled volume may result in “volutrauma” (overdistension) units with poor compliance
•  A high early inspiratory ow may breach the pressure limit if •  In the presence of a leak, the mean
airway resistance is high28 airway pressure may be unstable
•  PCV offers no advantage over VCV in patients who are not •  Insufcient ow may give rise to
breathing spontaneously27 patient-ventilator dyssynchrony28
Specic cases
when to use
ACV/CMV
SIMV Ventilator
delivered breaths
Spontaneous
breaths
CPAP
Clinical Objectives of Mechanical Ventilation

•  To reverse hypoxemia •  To permit sedation and/or neuromuscular blockage
•  To reverse acute respiratory acidosis •  To decrease systemic or myocardial oxygen consumption
•  To relieve respiratory distress •  To reduce intracranial pressure
•  To prevent or reverse atelectasis •  To stabilize the chest wall
•  To reverse respiratory muscle fatigue
Initial Ventilator Setting for Ventilatory Failure Patient

•  Controlled mechanical ventilation, e.g., assist controlled, •  Fraction of inspired oxygen at 1.0 initially, and then adjust to
occasionally other modes (e.g., PRVC, CMV) provide adequate oxygenation
•  Rate: 10 breaths/min (8–16 is acceptable rate initially), •  PEEP—supports expiratory pressure to prevent closure of
depending on desired PaCO2 (PaCO2 target/PaCO2real = edematous small airways, indicated when oxygenation is
Rate_target/Rate_real) inadequate (start at 5, increase by 2–5 to maintain oxygena-
•  TV = 6–8 mL/kg of ideal body weight, calculate ideal body tion PaO2³ 60 mm Hg, PEEP >12 sometimes requires an
weight rst: males: 50 + 2.3* (height in inches: 60); females: S-G catheter)
45.5 + 2.3* (height in inches: 60) •  Pressure support = supports inspiratory pressure (=peak
•  High peak inspiratory ow such as 80–90 L/min to minimize airway pressure/3)
inspiratory time and enhance expiratory time
S-G, Swan-Ganz.
Troubleshooting of Common Ventilator Issues
Desaturation D—displacement of the tube, air leak/broken cuff (difference in TV in and out)
O—obstruction (tube or lter): elevated peak pressure
P—pneumothorax (feel pressure while bagging, elevated peak, and plateau pressure),
PE, parenchymal disease (worsening of CXR), intrapulmonary shunt
E—equipment failure (rare)
R—rigidity of chest wall (increased pressures)
Action: examine the tube, pressure cuff, check ventilator parameters (peak and plateau
pressures, TV in and TV out), disconnect ventilator and bag, see if there is resistance
(tube obstruction, pneumothorax, rigidity), and if O2 saturation improves with bagging
(suggests machine setting issues). If ARDS is the cause—prone and paralyze
Elevated peak pressure29 30 •  If patient is hypotensive—think elevated intrathoracic pressure: critical auto-PEEP or
tension pneumothorax. Remove ventilator and bag (if auto-PEEP) hypotension im-
proves. If patient does not improve –think tube obstruction or pneumothorax: consider
needle decompression and then chest tube
•  If hemodynamically stable
 o If high difference between peak and plateau (>5 cm H2O)—increase resistance of
airways (e.g., bronchospasm, ET tube obstruction, ventilator circuit obstruction,
anaphylaxis, or inappropriately high inspiratory ow >60 L/min): inline suctioning,
bronchodilators
 o If low difference—acute decrease in lung compliance (e.g., pneumothorax, ARDS,
evolving pneumonia, pulmonary edema, auto-PEEP caused by “breath staking,”
chest wall rigidity, abdominal distention, right main stem intubation)
Hypotension in ventilated patient31 •  Relative hypovolemia (reduction in venous return exacerbated by positive intrathoracic
pressure)
•  Drug-induced vasodilation and myocardial depression (all anesthetic induction agents
have some short-lived vasodilatory/myocardial depressant effects)
•  Gas trapping (dynamic hyperination)
•  Tension pneumothorax
Patient-ventilator dyssynchrony See below
ET, Endotracheal tube.

Troubleshooting for Ventilator Issues

•  Air leak: discrepancy between set TV and delivered TV:  o If both peak and plateau pressure increased—decreased
check tubing for leak compliance (e.g., pneumothorax, tube migrated to right
•  Disconnected airway: check for continuity of tubing bronchus, pulmonary edema)
•  TV issues in PC mode (TV drops): check for decreased  o If only peak pressure elevated—increased resistance
compliance or increased resistance (e.g., mucous plug)
•  Increased pressures in VC mode:
Quick Algorithm and Checklist of Ventilator Setting Assessment/Adjustment

•  If settings are adequate: look at ABG: PaO2 goal 55–80 mm  • Pressures:
Hg or SpO2 88%–95%, pH goal 7.3–7.45. FiO2 and PEEP ■ Peak pressure reect resistance in the entire circuit
affect pO2, while TV and rate affect pCO2 from ventilator to alveolus
 o If pH 7.15–7.3 (respiratory acidosis): increase RR until pH ■ Pplat (goal <30 cm H2O) reects on resistance to lung
>7.3 or PaCO2 <25 (max RR 35) ination (e.g., restrictive lung disease, too high TV)
 o If pH <7.15 (respiratory acidosis): increase RR to 35; if ■ Transpulmonary pressure (Pplat minus Pesoph) of
pH remains <7.15: increase TV in 1-mL/kg steps until pH 25–30 cm H2O
>7.15 (maintain Pplat not higher than 30) ■ Driving pressure (Pplat minus PEEP), should be 15–18,
 o If ↓ pCO2—hyperventilation—decrease rate or TV if higher—reduce TV32
 o If ↑ pCO2—CO2 retention—increase rate or TV ■ O2 and PEEP: pO2 goal 55–80 mm Hg or SpO2
 o If hypoxemic—increase FiO2 or PEEP 88%–95%, use a minimal PEEP of 5 cm H2O
 o I:E ratio: duration of inspiration ≤ expiration ■ Is there potentially intrinsic PEEP (auto-PEEP)
•  If settings are safe: look at the •  If patient is comfortable (look for tachypnea, asynchrony):
 • TV (not more than 6 mL/kg), calculate ideal body weight one way to improve comfort and synchrony—control pres-
rst: males: 50 + 2.3* (height in inches: 60); females: 45.5 sure. More on asynchrony—see below
+ 2.3* (height in inches: 60). If you are concerned about •  If possible, extubate
TV, then control the ow/volume.
I:E ratio, Inspiratory-to-expiratory ratio; Pesoph, esophageal pressure; Pplat, plateau pressure.
Ventilator Asynchrony Management

Disrupted or poor interaction between the patient and ventilator leads to asynchrony between
ventilator-delivered breaths and patient’s breathing. This eventually results in patient discomfort and
fatigue.33 Asynchronous ventilator pattern should be avoided.
Asynchrony management
Solutions for trigger asynchrony

• Missed triggers or delayed trigger: patient effort not recognized by the In volume assist-control (VAC):
ventilator secondary to intrinsic PEEP, weak effort, or inappropriate • In the older generation ventilators flow trigger
sensitivity setting (if the patient is having difficulty triggering the ventilator would, at times, reduce trigger asynchrony.
despite a sensitive setting—consider that auto-PEEP causing dynamic • Increase sensitivity
hyperinflation is the problem) • Reduce auto PEEP
• Auto-triggering: breaths delivered in the absence of patient effort secondary • Apply extrinsic PEEP
to leaks or inappropriate sensitivity setting
• Double triggering: continued patient effort following breath delivery,
resulting in a second triggered breath: volume control continuous
mandatory ventilation and neurally adjusted ventilatory assist (NAVA)
• Reverse triggering: activation of respiratory muscles by mandatory, time
triggered breaths
Solutions for flow asynchrony

• Flow mismatch or flow asynchrony (patient demand does not match • VAC
ventilator output): volume control o Increase set flow (decrease Ti)
• Insufficient pressurization rate (rise time too slow): pressure support o Switch to a pressure target mode
• Mode asynchrony: active effort during adaptive pressure ventilation, o Square wave of flow (decrease Ti)
resulting in insufficient support: use of intermittent mandatory ventilation • Pressure assist-control (PAC)/PSV
with interspersed volume and pressure breaths, precluding sufficient o Adjust the rise time
respiratory muscle unloading o Increase the inspiratory pressure
(watch for increase in Vt)
Solutions for Cycle Asynchrony

• Premature cycling: neuromechanical asynchrony: mechanical inspiratory Premature cycling in VAC
time shorter than neural inspiratory time • Decrease flow/Vt in VAC
• Late cycling: neuromechanical asynchrony: mechanical inspiratory time Premature cycling in PAC
longer than neural inspiratory time • Increase Ti
• I:E ratio: 1:2 ratio is close to a normal breathing pattern and is more • Switch to PSV
comfortable Premature cycling in PSV
• Adjust flow termination %
• Mode of ventilation
o Spontaneous modes are more comfortable
than control modes
o BIPAP might be more comfortable and
improves synchrony
Adjustment of Ventilator Parameters Based on Compliance and Resistance

Decreased compliance and increased resistance might give additional insight and dictate further
adjustment of ventilator parameters.5 6
Diagnostic value of compliance and resistance 34
Resistance
• Definition • Definition: Resistance = (Paw – Pplat)/Peak
o Static compliance = TV/(Pplat – PEEP) normally 60 and below cm H 2O inspiratory flow rate
o Dynamic compliance = TV/(Ppeak – PEEP) normally 100 and below • Diagnostic value: increased resistance presents
cm H2O as increased peak pressure and increased
• Diagnostic value: decreased compliance presents as increased both peak difference between peak and plateau): ≥6 cm H2O
pressure and plateau pressure: ≥30 mL/cm H2O • Increased resistance will “lose” tidal volume;
• Stiffer lungs will show shallow volume curve check TV in pressure control ventilation
• Decreased compliance is observed in: • Increased resistance:
o Pulmonary edema o Bronchospasm
o Fibrosis o Mucous plugging
o ARDS
o Pneumothorax
Ppk—peak inspiratory pressure (<25–35 cm H2O)

Pplat—plateau pressure (<30 cm H2O)
↑Ppk, ↑Pplat ⇒ resistance at the alveolar level—non-compliance,

pneumothorax, auto-PEEP, mainstem bronchus intubation, atelectases
↑Pplat, normal Ppk—too high tidal volume set on the ventilator
↑Ppk, normal Pplat ⇒ resistance to flow (e.g. tube occlusion, thick

secretion, bronchospasm)
Dynamic Static phase
More Details on Managing Intubated/Ventilated Patient in Specific Conditions

Mechanical Ventilation in Obstructive Lung Disease (COPD, Asthma)5 6
Potential Issues With Ventilating Patient With Obstructive Disease

Assess for pulmonary hyperination (see below) Assess compliance and resistance and adjust ventilator pa-
Manage hypercapnia (see below) rameters
Address asynchrony
Assess for pulmonary hyperinflation

• Assess for hyperinflation: check volume of gas exhaled during prolonged
apnea (lung volume at inspirationVEI). The Vei includes the tidal volume
Hyperinflation and the additional volume of gas due to dynamic hyperinflation.VEI is
affected by severity of airflow obstruction and ventilator settings. VEI is
the most reliable predictor of ventilator-related complications.
• Assess auto-PEEP (intrinsic PEEP, PEEPi) or dynamic autoinflation
(10–15 cm H2O in severe asthma) during volume-cycled ventilation.
Intrinsic PEEP one of the biggest contributors to asynchrony. It makes
it harder for the patient to take/trigger a breath. How to detect intrinsic PEEP:
o Expiratory flow does not return to baseline
o Flow over time curve is probably easiest—might not help if some units are
totally occluded
o Occlusion of expiratory circuit of the ventilator during exhalation
o Difficult to obtain accurate measurement in spontaneously breathing
patient
o Esophageal balloon
• Consider decreasing minute ventilation (increased minute ventilation from

10 to 16 to 26 L/min increases the risk of hypotension and barotrauma).
Shorter inspiratory time, longer exhalation time and longer cycle length
(respiratory rate as low as possible) help to minimize hyperinflation
• Set peak flow rates relatively high
• Set lower tidal volumes (6–8 mL/kg)
• Plateau airway pressure (Pplat; in acute severe asthma average 24–26 cm
H2O, acceptable up to 30)
• Peak airway pressure (Ppk), target <50 cm H2O. Ppk depends on inspiratory
flow-resistive properties in addition to hyperinflation. Ppk >50 cm H2O does
not predict increased risk of barotrauma.
• Titrate PEEP: PEEP can be titrated up to minimize dyssynchrony
o Titrate PEEP according to Pplat and associated hypoxia
o Match PEEPi
• Attempt to achieve end-expiratory flow of “0”
• Hypercapnia is a consequence of dead space ventilation (caused by

alveolar overdistension)
Hypercapnia
• Hypercapnia is preferable to hyperinflation (not in the context of increased
intracranial pressure). Permissive hypercapnia appropriate in most patients.
Acceptable hypercapnia: pH as low as 7.15 and a PaCO2 of up to 80 mm Hg
• Serious consequences of hypercapnia are uncommon
o Neuro: increased cerebral blood flow, intracranial pressure → cerebral
edema and subarachnoid hemorrhage).
o Cardiac: decreased intracellular pH → reduced contractility
o Although generally the use of HCO3 in hypercapnia is discouraged, consider
alkalinizing agent when pH is persistently below 7.15–7.2 (Na bicarbonate
or tromethamine)
o Pulmonary arterial hypertension
Management of hypercapnia
In a ventilated patient hypercapnia is managed by increased TV or respiratory rate

In addition to that there are other therapeutic strategies to manage hypercapnia
Lower CO2
• Fever and/or shivering (control temperature
• Systemic corticosteroids: anti-inflammatory and shivering) • Heliox (a mixture of helium and
effect (2.5 mg/kg/day of methylprednisolone) • Increased work of breathing (support oxygen)
• Inhaled beta-agonists (MDI or nebulizer): ventilation and ensure synchrony) • Inhalational anesthetics (e.g.,
albuterol 2.5 mg Q4 or Q6, ipratropium • Nutritional support isoflurane)—should the effect right
• Other bronchodilators (IV theophylline) • Adequate sedation away, and if not then discontinue
• Deep sedation: combination of propofol • Discourage use of HCO3 • Ketamine IV
(or benzodiazepine) and fentanyl • Bronchoscopic removal of impacted
• Neuromuscular blocking agent is sometimes mucus
necessary (intermittent boluses rather than • Extracorporeal life support
continuous infusion) (membrane oxygenation and
CO2 removal)
Mechanical Ventilation in Parenchymal Lung Disease (e.g., ARDS)
Strategies to adjust PEEP

• Optimal PEEP in patients with ARDS remains an area of active investigation
• The easiest approach to select PEEP might be according to the severity of the disease: 5–10 cm H 2O PEEP in mild ARDS, 10–15 cm
H2O PEEP in moderate ARDS, and 15–20 cm H 2O PEEP in severe ARDS35
• Several methods of selecting optimal PEEP are available: increasing or decreasing PEEP trial (see below), ARDSnet study tables
(see below)36
• Consider recruitment maneuvers37
• Optimal PEEP may depend on the tidal volume (so if TV is changed optimal PEEP might need to be established again) 38
• Increase PEEP and check plateau pressure, if increased by less than PEEP addition, then it means some lung volume has been
recruited
• Be cognizant of RV function: PEEP affects RV function in acute respiratory failure patients 39
• Use measurements to adjust PEEP:
o Stress index (a parameter derived from the shape of the pressure-time curve, can identify injurious mechanical ventilation)
o Esophageal pressure
o Pressure volume curve
PEEP trial
• Establish level of PEEP at which oxygen delivery is optimal or that
maximizes lung compliance
• If a pulmonary artery catheter is in place, oxygen delivery (DO 2) is
calculated with each change in PEEP: DO 2 = (Hb x SaO2 × 1.34 +
PaO2 × 0.003) × CO
o Note: DO2 declines if the drop in CO caused by PEEP outweighs the
rise in arterial O2 content. Therefore, the best PEEP may be less than
the amount that achieves the highest SaO 2
• If a pulmonary artery catheter is not available, the best PEEP may be
approximated by determining the level which results in the highest
compliance for a given tidal volume, using the formula: compliance
= TV / (Ppl - PEEP)
o Note: cardiac output may fall independently of changes in thoracic
compliance
ARDSnet study tables40

OXYGENATION GOAL: PaO2 55–80 mm Hg or SpO2 88%–95%
Use a minimum PEEP of 5 cm H2O. Consider use of incremental
FiO2/PEEP combinations such as shown below (not required) to achieve
goal
Lower PEEP/higher FiO2

FiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7
PEEP 5 5 8 8 10 10 10 12
FiO2 0.7 0.8 0.9 0.9 0.9 1.0

PEEP 14 14 14 16 18 18.24
Higher PEEP/lower FiO2

FiO2 0.3 0.3 0.3 0.3 0.3 0.4 0.4 0.5
PEEP 5 8 10 12 14 14 16 16
FiO2 0.5 0.5–0.8 0.8 0.9 1.0 1.0

PEEP 18 20 22 22 22 24
35
• Multiple methods have been described

• 40 cm H20 for 40–60 seconds
• 3 consecutive sighs/min with a plateau pressure of 45 cm H 2O
• 2 minutes of peak pressure of 50 cm H2O and PEEP above upper
inflection point (obese/trauma patients may require >60–70 cm H 2O)
• Long slow increase in inspiratory pressure up to 40 cm H 2O (RAMP)
• Stepped increase in pressure (e.g., staircase recruitment maneuver)
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RESPUESTA DE VASQUIRAN
INTERROGANDO
Á FLAMIANO
Bien me plaze hauerte oydo lo
que dizes. Veamos agora,
Flamiano, ¿tu mal e tu passion no
es e nace del demasiado amor
que a Belisena tienes? Si. Tú no
dizes qu'el bien que la quieres en
estremo te trae en lo que estas?
Si. Tu desseo que es galardon de
tus seruicios? Si. Y este galardon
que desseas que se ver cumplida
tu voluntad? Si. De qué te
quexas, de que su voluntad va
lexos de lo que la tuya queria? Si.
Tú no quieres, segun dizes y es
razon, más a ella que a ti? Si.
Pues desta manera o tú no sabes
lo que quieres o es falso lo que
dizes. No dizes, como es, que en
ella está el fin e medio comienço
de toda la virtud, e nobleça e
perficion? Si. Pues si tal es, como
es, e tu voluntad e desseo
fuessen buenos, no
desconformaria dello su voluntad,
por consiguiente, o ella no es qual
tú dizes, o tu desseo es malo; si
es malo, ¿cómo dizes que bien la
quieres e le desseas mal?
Hagamos agora que tu voluntad
fuesse buena y la suya buena
como es, no dizes que la quieres
mas que a ti? Pues si más que a
ti la quieres, razon es que quieras
más lo qu'ella quiere que lo que tú
quieres, pues si lo qu'ella quiere,
quieres, no ternás de quexarte; no
teniendo quexa no ternás mal, no
teniendo mal, ganado haure yo la
question.
FLAMIANO A VASQUIRAN
No me contenta lo que dizes
porque no satisfaze a lo que digo;
yo te digo que ninguna cosa se
haze sin esperança de algun fin,
como vemos claramente.
Dexando agora lo de arriba que
no es razon que en ello
hablemos, pero en lo de acá;
¿porqué seruimos al rey a quien
deuida obligacion nos obliga? ¿no
le seruimos por lo que somos
obligados? Si. Si pues le somos
obligados, ¿porqué nos
quexamos si de nuestros
seruicios algun seruicio no nos
haze, e si de nuestros fauores
algun galardon no alcançamos? Y
por consiguiente de nuestros
mismos padres lo mismo
queremos e si no lo hazen lo
mismo quexamos, y aun como el
vulgo dize, a los santos no querria
seruir si galardon no esperasse,
pues para seruir a estos no nos
fallesce amor, pero si satisfecha
no es nuestra voluntad no nos
falta quexa, e quanto mal
nuestros seruicios e voluntad han
sido, tanto más nos da pena e
congoxa lo poco que nos es
agradecido. Luego ¿qué hare
qu'en satisfacion de lo que bien
quiero soy aborrecido que es el
mayor mal, en pago de mis
seruicios e passion no alcanço
mas de disfauores, menosprecios,
desdenes e mill ultrajes? Pues si
mi querer no puede mudarse, mi
passion no puede afloxar,
esperança de más no la espero,
remedio no le hay ni le hallo, qué
mayor mal quieres quel mio?
VASQUIRAN A FLAMIANO
Harto es poco tu mal si más razon
no tienes de la que dizes para él;
muy lexos van tus palabras e
razones de tus congoxas, pero o
hagamos que sea como dizes, o
llevemos las cosas por razon;
digamos lo que dizes que sea
razon, que sin la razon que nos
obliga seruir al rey deuamos
esperar mercedes e satisfacion
de nuestros seruicios e hagamos
ygual este seruir con lo que a
Belisena sirues; yo quiero que
assi sea como dizes e ansi te
mostraré como en una manera no
tienes razon de quexarte y en otra
te mostraré como eres satisfecho.
Digo que no has razon desta
manera. Los seruicios que tú al
rey hazes en que le sirues? O le
sirues en sus guerras y
conquistas en guarda e defension
de su persona y estado, o en
acrecentamiento de sus reynos
con peligro de la tuya, o le sirues
en la paz acompañandole e
siguiendo su corte con mucha
costa que te cuesta, de manera
que todos tus seruicios son
buenos e merecen hauer bien.
Pues veamos a Belisena si la
sirues en nada de esto. Digo que
no. ¿Pues en qué la sirues?
¿Sabes en qué? En apocar su
honrra, en alterar su fama, en
poner en juyzio de mal
sospechantes su bondad, en
todas las cosas que peor juyzio le
pueden hazer, en dessear por tu
bien su mal, o por tu voluntad su
mengua. Y quiereslo ver? El
mayor bien e mas honesto que en
tu desseo pudiesse hauer seria
que sin cargo alcanzasses lo que
de otra dama que ygual te fuesse
alcançar podrias; pues eso no se
podria hazer sin que ella de su
estado al tuyo baxase, luego mal
le desseas. Podrias dessear que
Dios te subiesse a tanto que
ygual le fuesses? La pena que
desto recibirias no te la da ella
sino lo que en ti falta. Luego sin
razon te quexarias. Tornando al
proposito digo que si al rey
siruiesses en cosa que le
perjudicasse, ni él te lo deueria
agradecer, ni tú quexarte de su
ingratitud. Pero aun de otra
manera digo que eres satisfecho
de lo que te quexas; bien sabes tú
que hay muchas maneras de
seruicios en las quales hay
algunas que en la misma obra
dellas está el galardon, estas son
aquellas de que obrandolas
ganamos honrra, pues que esta
es la cosa mas desseada como
sea señalarse el hombre en una
batalla de campo o de tierra, en
otra semejante afrenta hecha en
seruicio de señor o persona tal o
de que el que la haze, assi por
señalarse, como por la calidad de
aquel a quien sirue, queda
honrrado. Pues parecete a ti que
solo este nombre sea poca gloria
e fama e honrra? tú sabes que es
mucha ser seruidor de quien eres
siendo más publico que oculto, no
pueden tanto merecer tus
teruicios que esto no sea más; no
seran jamas tan grandes tus
passiones e tormentos que esta
gloria mayor no sea; ningun dia
puedes tanto penar que su vista
no te dé mas descanso, ninguna
congoxa te puede dar tu desseo
que tu pensamiento no te dé
mayor gloria. Mi mal es de doler
por que en él no hay remedio; en
los plazeres agenos yo peno; en
las passiones e males de los
otros, los mios se doblan, y esto
te basta para que esta question
baste, e acabo.
RESPUESTA DE FLAMIANO
Poco a poco me echarias de la
tierra con tus argumentos de
logico, ante que lo fagas quiero
tornar al comienço de nuestra
question e digo que nunca mis
males menos de grandes los
senti, ni nunca los tuyos más de
pequeños los juzgué; desta
manera que a mi se me figura
como nunca otra cosa conoci, que
mal es que ningun mal con el mio
se yguala.
La lengua es vn instrumento en
qu'el dolor del coraçon suena, e
desta manera la mia haze el son
que oyes. A ti como el plazer has
perdido figurasete que tienes
mucha raçon e que pues que la
raçon es mucha que la causa es
grande; assi que te quexas como
quien mucho bien ha perdido, yo
me quexo como quien mucho mal
ha passado e passa y el bien
nunca vió. Pues si tú has habido
bien e grande, yo mal e grande, tú
has sabido qué es bien, yo sé que
es mal; agora tú sabes qué es
bien e mal; yo mal e mal; claro
está qué más mal es el mio que el
tuyo. A mi me parece qu'es tanta
mi pena que con el más penado
trocaria, creyendo que no es tanta
la suya. Tú goçando tu bien tan
contento estauas, que con el más
gozoso no trocaras, creyendo que
no hauia más bien que goçar. Yo
querria saber a qué sabe por
juzgar tu perdida quanto es
grande, porque a mi se me figura
que el mayor daño mio es el mal
con que tú lo hazes menor,
diziendo que pues nunca tuve
bien, que no puedo sentir qué es
mal; yo digo que harto mal es
saber qué es bien, despues
passar mal, pero mayor es nunca
saber qué es sino mal, y aun te
digo vna cosa, pues los consuelos
que tú me das bastarian para vn
rustico que nunca de ningun bien
gozó e poco del le pareceria
mucho, o para un grosero que en
su entendimiento no entra ni lo
que dessear se deue, ni lo que
penar se puede, que este con
cualquier cosa que le acaeciesse
seria satisfecho como tú quieres
que yo haga, pero para mi que
desseo lo que dessearse puede
de bien e padezco lo que padecer
se puede de mal, no me parece
que yerro como dizes, ante que
tengo raçon de llorar de mis
males su dolor e de los bienes
agenos su enuidia. E assi estó
puesto en el estremo que vees
para no poder venir en
conocimiento de tu raçon, porque
todo lo que hablamos tiene dos
sentidos; tú les das el que te
parece ó sientes, yo les doy el
que parece o siento, e assi seria
insoluble nuestra porfia. Ponerla
en manos de quien la determine
no la consiente su causa, mejor
seria dexarla suspensa.
No quiero, Flamiano, que
suspensa quede, sino que se
determine e que tú seas el juez, e
no quiero sino en breve darte la
determinacion que has de hazer,
y es que juzgues qual de nosotros
más mal padece, que esto es
todo el fin desta question. Tu mal
no puede ser mucho sino siendo
grande el amor que a Belisena
tienes, e si tal no es, no es tal tu
mal como dizes. Si tal no es,
como dizes, fingido seria, e assi
seria mayor el mio. Pues si tú
quieres mucho como yo creo e
creo que tu passion es grande,
mas digo que la mia es mayor. Tú
dizes que querrias saber a qué
sabe mi mal por mejor juzgarlo;
bien sé que no lo dizes por lo que
agora yo padezco sino por lo que
he gozado. Mal has hablado,
porque no podrias saber lo vno e
lo otro sino passando por todo,
pero pues que dicho lo has,
sobr'esto quiero hazerte juez de la
causa. Hagamos agora que la
uentura te ayudasse para que de
Belisena gozasses ni mas ni
menos que yo de Violina; que tu
gozo y el tiempo e vuestras
voluntades conformes fuessen
tanto e con tanto contentamiento
como el nuestro fue, con tal
condicion que Dios dende agora
te contentasse, e que a cabo de
otro tanto tiempo tu señora en tu
poder muriesse en tu presencia y
tú sin ella quedasses como yo sin
la mia he quedado qual me vees,
aceptarlo yas? Di la verdad e
conoceras que si mi gozo fue
grande, que mi mal es grande, e
que si tú agora tan gran gozo
alcançabas que seria mayor tu
bien que agora es tu mal; pues
desta manera quando tan gran
bien perdiesses, quál seria mayor
mal, el que entonces sentirias en
perderlo, o el que agora sientes
en dessearlo? No te quiero mas
dezir; juzga lo que querras, que si
esto niegas, quanto has dicho
negarás e seria fengido de lo que
padeces.
RESPUESTA DE FLAMIANO
Mejor seria, Vasquiran, qu'esta
question no houiessemos
començado, que no que a este
paso houiessemos llegado,
porque temo que la ponçoña de
nuestras passiones nuestras
amistades alteren.
No puedo responderte a esta
partida porque en mi boca no
puede caber tal raçon, ni quisiera
que en la tuya houiera cabido; no
ha hecho Dios los dias de
Belisena para que en nuestras
lenguas termino les pongamos,
no por comparacion como agora
has hecho. Baste esto, que
todauia me parece segund lo que
siento que es verdad lo que digo;
creo que lo mismo hazes. El mal
de los infernados tenemos, qu'el
menos penado trocaria con el que
más pena, juzgando mayor la
suya que la del otro; yo me refiero
a lo que he dicho e tú no menos.
Dexemos nuestro processo
abierto, determinenlo los que lo
leyeren, pues que ya está
determinado que cada vno de
nosotros tiene tan poca alegria,
que no nos cabe llorar duelos
ajenos.
Mudemos la platica en otras
cosas, que pues que tan poco
plazer tenemos, pesar no nos
faltará sin que le busquemos.
Bien sé que sabes que tu mal
más que a nadie me duele, bien
sé que mi descanso mas que otro
lo desseas. El dia que fuymos a
casa de la señora duquesa me
parece que te vi hablar con la
señora Yssiana; no me soy
acordado agora de pedirte qué
passaste con ella; agora que me
acuerdo, te aviso que te guardes,
que tiene mala mano. Podria ser
que si mucho la mirasses, que
como agora de tu mal plañes que
del mio llorasses, e quiça
entonces juzgarias de nuestra
question lo que agora no
conosces.
Bien sabia que a tal estrecho te
hauia de traer como has llegado.
En tu alteracion conozco lo que
en mi passion conoces, hacerte
quiero contento, mudasme de
nuevas, quiero te responder a lo
que pides. Lo que con essa
señora passé, fue que
hallandome la señora Belisena,
ella se llegó con nosotros e
dixome que me esforçase e me
allegrase, que no juzgaba menos
discrecion en mi seso, que dolor
en mi pesar, e que la fortuna me
pudo quitar lo que pudo, pero no
la virtud que en mí quedaua que
era más. Yo le respondi que Dios
le diesse tanta parte del bien en la
tierra, quanto de su hermosura le
hauia dado de la del cielo, pues
que estaua en ella más aparejado
el merecer para ello, que en mí el
consuelo para ser alegre, e que
bien sabia yo que si possible
fuera que en mí pudiera haber de
remedio para mi tristeça
esperança, que della a solas la
esperaua, pero que no solo me
faltaua remedio, mas esperança
dél. Respondiome que no hauia
cosa sin remedio viniendo, e que
lo mucho que le dolia verme tal, y
el desseo que tenia de verme con
menos tristeça le offrecia a
consentirme que la siruiesse, e
que dello seria contenta, e que
assi me aceptaua por su seruidor
con prometimiento de
fauorecerme de manera que sin
perjuicio suyo que algo de mi
congoxa afloxaria. Yo le respondi
que lo hauia por impossible. E por
no poderle más responder al
presente, la enbié despues estas
coplas sobre el caso mesmo.
COPLAS QUE VASQUIRAN

EMBIÓ
A YSSIANA SOBRE QUE LE
MANDÓ QUE LE SIRUIESSE
Tan llagada está mi vida
de los males de mi mal
que por ser la causa tal
no ay do quepa otra herida,
de manera
que si mi mal tal no fuera,
solo veros
me forçara de quereros
por cuya causa viuiera.
Mas estoy como el herido
que la raçon e natura
le descubren en la cura
no poder ser guarecido,
bien que cierto
vuestra beldad e concierto
daran vida
a quien la tenga perdida,
pero ya passo de muerto.
Porque si'l morir recrece
do la vida se dessea,
con la muerte se pelea
pues llegado s'aborrece,
pero quando
vive el viuo desseando
s'el morir,
aquel tal es de dezir
que es más que muerto
penando.
Desta suerte, dama,
muestro,
siendo vuestras gracias tales,
que la sobra de mis males
no m'an dexado ser vuestro,
ni soy mio,
porque mi franco albedrio
es verdad
que no'stá en mi libertad
mas está en el daño mio.
Pues si vos no me sanays
yo no quiero guarecer,
no quiero querer poder
aunque vos, dama, querays;
¿sabeys porqué?
Porque ya murió mi fe,
e pues no es viua
no será jamas captiua
sino de quien siempre fue.
No, porque mi desuentura
con su mucha crueldad
a mi fe e mi libertad
las metió en la sepultura
con aquella
por quien viue mi querella
assi penando,
yo la muerte desseando
más que no viuir sin ella.
LO QUE SE CONCERTO
ACABADO LA HABLA
ENTRE ELLOS DOS
Assi pussieron silencio por
entonces en su contienda,
mudando en otras cosas su
passatiempo, e dende a pocos
dias, estando vn dia sobre tabla
razonando el vno con el otro,
Flamiano con muy ahincados
ruegos rogo a Vasquiran que
quissiese ser contento que los
dos tuviessen vna tela de justa
real, pues que avnque cosa de
fiesta e plazer fuesse para los
atribulados del mal que ellos lo
estauan, tanto para publicar sus
apassionados dolores daua
aparejo como a los alegres e
contentos de plazer les abria
camino. Porque no holgauan
menos los vnos en manifestar su
mal, que los otros en publicar su
bien con sus intenciones, e que
en esto no solo él haria señalada
gracia e merced, mas aun a todas
las damas haria gran seruicio. A
lo qual Vasquiran le respondio:
Verdaderamente, Flamiano, más
aparejo hay en mi para llorar
como vees, que no para justar
como quieres, pero pues que el
amistad nuestra me forço en tal
tiempo venir a verte, e el amor
que te tengo me obliga a
complazerte en todo lo que
possible me será. Assi que
ordena lo que te parecera, que de
aquello sere contento, no en esto
que es poca cosa, mas donde la
vida e honrra en todo peligro se
pussiese lo seria. En especial que
yo recibo tanta pena en ver la que
con la mia te doy, que desseo
hallar algo con que te pueda
complazer. Flamiano
agradeciendoselo mucho,
respondio: Si tan complido te
hiziera la fortuna de ventura como
de virtud, jamas viuieras
descontento. E assi los dos
caualgaron disfraçados e se
fueron a casa del cardenal de
Brujas que era vn notable
cauallero e mancebo, e tan
inclinado a las cosas de la
caualleria, aunque perlado,
quanto en el mundo lo houiesse,
e assi llegados a su posada,
retraydos todos tres a solas, su
pensamiento e a lo que eran
ydos, le hizieron saber, de lo qual
él holgo demasiadamente. Pues
en la misma hora, todos tres
vestidos de mascara, al palacio
del visorey se fueron. El qual con
mucho plazer los recibio, e assi
todos quatro en la camara de su
guarda ropa sentados a vna
ventana que sale sobre la mar,
hablaron todo el caso porque alli
eran venidos, e con mucho
contentamiento e plazer fue dello
contento. E hauiendo assi estado
vna gran pieça de la tarde, los
tres se tornaron a casa del
cardenal, donde cenaron con
muchos otros caualleros que alli
acostumbrauan venir a comer, y
en la cena se publicó la tela que
querian tener, lo qual puso en
mucho plazer e regocijo a todos.
E hauiendo cenado, en presencia
de todos, se ordenó el cartel con
las condiciones siguientes e
diosse a vn albardan que la
pregonasse.
LAS CONDICIONES DEL

CARTEL
Dado fue el cartel a vn albardan
para que lo pregonasse, el qual
con muchos atabales e trompetas
e menestriles, fue publicado en
todos aquellos lugares que les
parecio que publicarse deuia. En
el qual cartel se contenian las
condiciones siguientes:
Primeramente se daua al que
mas gentil cauallero a la tela
saliesse con paramento e cimera,
vna cadena de oro de dozientos
ducados. Dauase mas seys canas
de brocado al cauallero que con
lanças de fiesta mejores quatro
carreras haria, e que no pudiesse
justar a este prez quien al otro no
tirasse, esto es, sin paramentos ni
cimera. Dauase mas a la dama
que mejor e mas galanamente
vestida aquel dia a la fiesta
saliesse, vn diamante de cien
ducados de peso[288]. Mas al
galan que a la noche a la fiesta en
casa del señor visorey saldria
mejor e mas galan vestido, vn rico
rubí. A este precio de la noche los
tablajeros tirauan. Fueron juezes
de los caualleros el señor Visrey y
el principe de Salusana y el
almirante Vilander y el conde
Camposalado. Juezes de las
damas fueron la señora Reyna e
Nobleuisa e la señora duquesa de
Meliano e la duquesa de
Francouiso, todas tres viudas.
Tuuose el renque dia de Santiago,
que hauia quarenta dias desd'el
dia que el cartel se publicó hasta
aquel dia. En el qual tiempo todos
los caualleros e damas se
adereçaron de la manera que
adelante se dirá. De lo que en
este tiempo se siguio ninguna
cosa aqui se cuenta hasta el dia
de la tela.
COMO LAS DAMAS SALIERON

EL DIA
DE LA TELA
En el dia de la fiesta la señora
Reyna con sus damas, e la
señora duquesa de Francouiso se
vinieron a comer con la señora
duquesa de Meliano, porque assi
juntas se fuessen a la tela, donde
houo muchos galanes e muy
ricamente vestidos que hasta alli
las acompañaron e de alli hasta la
tela. De los quales atauios aqui
no se haze mencion, saluo que
hauiendo comido todas tres
caualgaron con sus damas e
salieron desta manera. La señora
Reyna salio vestida de negro
como siempre va; verdad es que
en vna gorra y en vnas mangas
de vna saya de terciopelo que
lleuaua, hauia muchas pieças de
oro e joyeles muy ricos e muchas
perlas.
Lleuaua vn cauallo blanco con
vna guarnicion rica e veynte
moços de espuelas vestidos con
sayos de grana guarnecidos de
terciopelo negro sobre raso
amarillo, con jubones de damasco
naranjado, vna calça negra e otra
azul e amarilla.
La señora duquesa de Meliano
salio su persona vestida de negro
con vn cauallo morcillo con vna
guarnicion de terciopelo negro;
doze moços d'espuelas vestidos
con sayos morados guarnecidos
de raso pardillo. Jubones de raso
negro con vna calça negra, otra
negra e morada.
La señora duquesa de Francouiso
salio vestida de negro. Los moços
d'espuelas vestidos todos de
leonado.
Salio la señora Belisena con vna
saya de brocado raso blanco
cubierta de raso negro, cortado
todo el raso de vnas cortaduras
muy espessas que se hazia dellas
vna obra como vnos manojos,
atadas todas las cuchilladas con
vnos torçales de oro, e de seda
encarnada con los cabos hechos
de perlas; vn collar de oro hechas
las pieças a manera de las
cortaduras de la saya, esmaltadas
todas las pieças de negro. Hauia
en la saya en cada pieça de
terciopelo vna pieça de oro de
martillo que hazia la obra de las
cortaduras, vna gorra de raso
encarnado guarnecido de las
pieças del collar; vn cauallo
blanco con vna guarnicion de
plata toda esmaltada con muchos
floques de oro y encarnado que
salian por las pieças de la
guarnicion muy largos. Doze
moços d'espuelas vestidos de
amarillo y encarnado.
La señora Yssiana sacó vna saya
de terciopelo leonado e brocado
pardillo hecha a tableros como vn
marro; estauan las costuras
juntadas con pestañas de tafetan
amarillo. Hauia en cada pieça de
la seda e del brocado vna cifra
trocada de lo vno en lo otro
bordadas con cordones de plata.
Vna gorra de raso leonado llena
de cabos de oro hincados a
manera de vn erizo, muy llena
con collar de pieças de manera
delas cifras.
Sacó la señora Graciana vna
saya de raso azul con vna reja
encima de terciopelo azul sobre
pestañas de raso amarillo, e con
vnas lazadas de vnas madexas
de hilo de oro que ataua las
juntas de la reja. Vna gorra de
terciopelo azul llena delas mismas
madexas trauadas vnas de otras;
vn collar hecho de madexas de
hilo de oro tirado muy rico.
Todas las otras damas de la
señora duquesa salieron vestidas
con saya de raso morado, con
barras de brocado negro sobre
pestañas de tafetan blanco; con

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Critical Care Medicine: An Algorithmic

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CRITICAL CARE MEDICINE: AN ALGORITHMIC APPROACH, FIRST EDITION ISBN:978-0-323-696074

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To my family, and speci¿cally to my mom Tatiana, my late uncle Veniamin,

To my wife Judy, son Bobby, and daughter Debbie

Alexander S. Goldfarb-Rumyantzev, MD, PhD, PhD

2. Critical Care Cardiology and Hypertension, 32

3. Renal Failure and Renal Replacement Therapy, 64

4. Water and Electrolyte Disorders, 90

5. Acid-Base Disorders, 118

6. Infectious Disease in Critical Care Practice, 132

7. Critical Care Gastroenterology, 180

8. Hematology and Oncology Aspects of Critical Care, 198

9. Rheumatology, Immunology, Allergy, 223

10. Endocrinology Issues in Critical Care, 242

11. Toxicology Highlights, 260

12. Neurology Aspects of Critical Care, 265

13. COVID-19 and Critical Care, 283

14. Useful Formulae and Abbreviations, 299

○ quality and penetration

○ inspiratory eort (number of ribs)

• Evaluate soft tissue

lymph nodes, tumor masses)

Changes in lung parenchyma on CXR

Air space disease/ Interstitial disease

• Solitary vs. disseminated

Pulmonary Function Test Interpretation

Interpretation of the results of pulmonary function test

Restrictive pattern: Obstructive pattern:

Extrathoracic Intrathoracic Emphysema: Asthma:

Arterial Blood Gas Analysis

Uses four values: pH, pCO2, HCO3 , anion gap

Metabolic acidosis or alkalosis

No difference between acute and chronic

Diagnostic thoracentesis is indicated if thickness

Acute Respiratory Failure

Quick overview of types of respiratory failure

Normal A-a High A-a Normal A-a High A-a

Asthma Vs. COPD

No lung destruction, Underlying lung

Long-term suppression of airway inflammation See figure below

Long-acting beta-agonists, theophylline, and

• Diminishing the production of IgE through

Anticholinergics Antocholinergics Antocholinergics Metered

Dyspnea episodes: <1 h

Treatment of exacerbations and

If not better–consider NIPPV

Indications for intubation

Intubate, might start with volume control

Initial ventilator setting for asthmatic patient

Issues with managing intubated patient with asthma

• Volume of gas exhaled during • Consequence of dead space

• Systemic corticosteroids: anti-inflammatory effect (2.5 mg/kg/day of methylprednisolone)

Hypoxemic Respiratory Failure

Oxygenation failure (hypoxemia)

NIPPV, start with 12/8−10,

Decision point: intubation/IPPV vs. NIPPV based on clinical

NIPPV, titrate up PEEP Intubate, lung protective strategies,