The Intensive Care Manual - part 1 pdf

Contributors ix1 The Critically Ill Patient: Overview of Respiratory Failure and Oxygen Delivery 6 Approach to Infectious Disease 7 Approach to Nutritional Support 8 Approach to Cardiac

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The Intensive Care

Manual

Medicine is an ever-changing science As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required The editors and the publisher of this work have checked with sources believed to be reliable in their ef- forts to provide information that is complete and generally in accord with the stan- dards accepted at the time of publication However, in view of the possibility of human error or changes in medical sciences, neither the editors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or com- plete, and they are not responsible for any errors or omissions or for the results ob- tained from use of such information Readers are encouraged to confirm the information contained herein with other sources For example and in particular, read- ers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this book

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Contributors ix

1 The Critically Ill Patient: Overview of Respiratory Failure

and Oxygen Delivery

6 Approach to Infectious Disease

7 Approach to Nutritional Support

8 Approach to Cardiac Arrhythmias

ANDREWCORSELLO, JOSEPHM DELEHANTY,ANDDAVIDHUANG 185

Contents

vii

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9 Approach to Acute Myocardial Infarction: Diagnosis and Management

10 Approach to Endocrine Disease

11 Approach to Gastrointestinal Problems in the Intensive Care Unit

JAMESR BURTON, JR.ANDTHOMASA SHAW-STIFFEL 243

12 Approach to Hematologic Disorders

Rochester, NY

C H A P T E R 2 :

APPROACH TO INTRAVASCULAR ACCESS AND HEMODYNAMIC MONITORING

J AMES E S ZALADOS , MD, MBA, MHA, FCCP, FCCM

Attending in Critical Care Medicine, Anesthesiology

and Hospitalist Medicine Unity Health System Rochester, NY

at Genesee College Rochester, NY

Contributors

ix

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Strong Memorial Hospital Rochester, NY

Winston-Salem, NC

x Contributors

C H A P T E R 8 :

APPROACH TO CARDIAC ARRHYTHMIAS

A NDREW C ORSELLO , MD

Instructor in Medicine University of Rochester School of Medicine and Dentistry

Rochester, NY

J OSEPH M D ELEHANTY , MD

Associate Professor of Medicine Director, Cardiovascular ICU University of Rochester Medical Center

J OSEPH M D ELEHANTY , MD

Associate Professor of Medicine Director, Cardiovascular ICU University of Rochester Medical Center

APPROACH TO GASTROINTESTINAL PROBLEMS

IN THE INTENSIVE CARE UNIT

Contributors xi

J AMES R B URTON , J R , MD

Resident in Internal Medicine Department of Medicine University of Rochester School of Medicine and Dentistry Strong Memorial Hospital Rochester, NY

T HOMAS A S HAW -S TIFFEL , MD, CM, FRCPC, FACP

Associate Professor of Medicine Director of Hepatology University of Rochester Medical Center

Rochester, NY

C H A P T E R 1 2 :

APPROACH TO HEMATOLOGIC DISORDERS

J ANICE L Z IMMERMAN , MD, FCCM, FCCP, FACP

Professor of Medicine Director, Department of Emergency Medicine Ben Taub General Hospital Houston, TX

P ETER J P APADAKOS , MD, FCCP, FCCM

Associate Professor of Anesthesiology Professor of Respiratory Care SUNY University of Rochester Medical Center

Rochester, NY

xii Contributors

The ICU Manual was developed as a bedside reference for house officers,

fellows, and attendings who care for patients in ICUs The book is ized in organ-specific chapters This was done to increase the utility of andsimplify the use of this manual The organ specific approach parallels the waypatients in the ICU are cared for This approach enables the clinician to organizethe diagnosis and management of complicated critically ill patients The book hasnumerous illustrations, tables, and figures to ease information transfer A variety

organ-of authors, each with their own areas organ-of expertise, were utilized to improve thebook’s perspective and overall character We feel you will find the ICU Manualinformative and helpful in your care of critically ill patients

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MICHAELJ APOSTOLAKOS

OXYGEN DELIVERY OXYGEN CONSUMPTION SUMMARY

Copyright 2001 The McGraw-Hill Companies Click Here for Terms of Use

The care of the critically ill patient is complex and, at times, overwhelming Manyorgan systems may be affected simultaneously Each of these organ systems andthe approach to their dysfunction is discussed in subsequent chapters This chap-ter focuses on respiratory failure (hypoxemic and hypercapnic) and oxygendelivery: the underlying concepts are central to what we do in the intensive careunit (ICU)

RESPIRATORY FAILURE

Respiratory failure may be divided into two broad categories: hypoxemic (type 1)and hypercapnic (type 2) Hypoxemic respiratory failure is defined as a partialpressure of oxygen in arterial blood (PaO2) of less than 55 mm Hg when the frac-tion of inspired oxygen (FIO2) is 0.60 or more Hypercapnic respiratory failure isdefined as a partial pressure of carbon dioxide in arterial blood (PaCO2) of morethan 45 mm Hg Disorders that initially cause hypoxemia may be complicated byrespiratory pump failure and hypercapnia (Table 1–1) Conversely, diseases thatproduce respiratory pump failure are frequently complicated by hypoxemia re-sulting from secondary pulmonary parenchymal processes (e.g., pneumonia) orvascular disorders (e.g., pulmonary embolism)

Hypoxemia

Hypoxemia may be broadly divided into four major categories

1 Hypoventilation and low FIO2

2 Diffusion limitation

3 Ventilation/Perfusion (V/Q˙ ) mismatch

4 Shunt

2 The Intensive Care Manual

TABLE 1–1 Common Causes of Hypoxemia and Hypercapnia

HYPOVENTILATION AND F IO 2Hypoventilation and a low FIO2are rare causes

of hypoxemia in ICU patients Hypoventilation should be suspected as the cause

of hypoxemia in patients with an elevated PaCO2 Oversedation or hypercapnicrespiratory failure are common causes of this condition Low FIO2should not be

a cause of this condition unless there is an inadvertent oxygen disconnection on apatient receiving oxygen Hypoventilation and a low FIO2may be separated fromthe other causes of hypoxemia in that they are the only ones associated with anormal alveolar-aterial (A-a) oxygen gradient

The alveolar-arterial (A-a) gradient is the difference between PAO2and PaO2.The A-a gradient may be calculated from the following equation:

Where

FIO2is the fraction of inspired oxygen

PBis the barometric pressure

PH2Ois the partial pressure of water

R is the respiratory quotient

The A-a gradient is normally less than 10 mm Hg on room air In adults over age

65, normal values may extend up to 25 mm Hg

Case Example

An example of the usefulness of calculating the A-a gradient is demonstrated inthe following case: A 21-year-old patient was admitted to the ICU from theemergency department (ED) with a drug (narcotic) overdose On presentation

to the ED, the respiratory rate was 4/min Initial arterial blood gas (ABG) valueswere pH, 7.1; PaCO2, 80 mm Hg; PaO2, 40 mm Hg; O2sat, 70% The patient wasintubated and transferred to the ICU To calculate the patient’s A-a gradientfrom the equation previously given (Normal value is 10 mm Hg or less on roomair):

A-a gradient = 21 (747 mmHg − 47 mmHg) − 80 mmHg/.8 − 40 mmHg

= 147 mmHg − 100 mmHg − 40 mmHg = 7 mmHgThe normal A-a gradient value supports the hypothesis that this patient’s hypox-emia was caused solely by hypoventilation and that no other cause of hypoxemia,such as pneumonia, needs to be investigated The normal A-a gradient value sep-arates this category of hypoxemia from the other three categories

DIFFUSION LIMITATION Diffusion limitation is a rare cause of hypoxemia in

ICU patients The alveolar capillary unit has about 1 second in which to exchange

4 The Intensive Care Manual

FIGURE 1–1 Physiology of oxygenation in lung under normal circumstances (a), during

V/Q˙˙ mismatch (b), and shunt (c).

(a)

1 / Respiratory Failure and Oxygen Delivery 5

6 The Intensive Care Manual

I

FIGURE 1–1 (continued)

I

(c)

carbon dioxide for oxygen This normally occurs within the first 0.3 second Thisleaves approximately 0.7 second as a buffer, which protects against hypoxemiaduring exercise (which increases cardiac output and decreases time available forgas exchange) or when necessary to overcome diseases that cause diffusion limi-tation Except for severe end-stage lung disease (e.g., fibrosis, emphysema), this is

a rare occurence and, therefore, a rare cause of acute hypoxemia Diffusion tation, in general, is handled by the pulmonary specialist over a long period

limi-VENTILATION/PERFUSION MISMATCH Ventilation/perfusion (V/Q˙ ) match is the most common cause of hypoxemia seen in the ICU Only perfusionwith reduced or absent ventilation leads to hypoxemia Ventilation without per-fusion is simply dead-space ventilation, and by itself, does not lead to hypoxemia

mis-If severe, ventilation without perfusion may lead to carbon dioxide retention Tounderstand this completely, call to mind the following equations:

VEˆ = VO+ VA

PaCO2= k × VCO2/VA

Where

VEis total minute ventilation

VDis dead space minute ventilation

VAis alveolar minute ventilation

VCO2is carbon dioxide productionNormally VDand VAare 30% and 70%, respectively, of minute ventilation k

is a constant and VCO2can generally be considered constant Therefore, PaCO2isinversely proportional to VA(i.e., PaCO2∼ 1/VA) This becomes important whenadjusting ventilator settings

SHUNT A shunt is simply one extreme of ventilation/perfusion mismatch in

which there is perfusion but absolutely no ventilation Because of this, genated blood is shunted from the right side of the heart back to the left side ofthe heart causing profound hypoxemia As there is absolutely no ventilation tothis shunted area, increasing the FIO2will not improve the oxygenation This ishow V/Q˙ mismatch may be separated from shunt in that V/Q˙ mismatch will im-prove with increasing FIO2, but shunt will not It should be noted that there areintrapulmonary shunts caused by underlying lung disease such as pneumonia,but there are also extra pulmonary shunts, most commonly a patent foramenovale When there is a patent foramen ovale and right-sided heart pressure is in-creased, blood can be shunted across the atria from the right side of the heart tothe left side of the heart causing shunt and hypoxemia This can be diagnosed by

unoxy-a contrunoxy-ast echocunoxy-ardiogrunoxy-am

1 / Respiratory Failure and Oxygen Delivery 7

ASSESSMENT OF HYPOXEMIA When assessing hypoxemia, an understanding

of the normal physiology of the lung is necessary (Figure 1–1a) The pulmonary

artery is the only artery in the body that delivers unoxygenated blood A normalABG obtained from the pulmonary artery is pH, 7.35, PCO2, 45 mm Hg, PO2, 40

mm Hg, and O2sat, 75% The PAO2is approximately 110 mm Hg (obtained fromthe A-a gas equation) and alveolar PACO2is 40 mm Hg A perfectly matchedalveolar-capillary unit produces pulmonary venous blood with a pH of 7.4, PCO2,

40 mm Hg; PO2, 110 mm Hg; and O2SAT, 100% However, “normal” ABG valuesobtained peripherally yield about: pH, 7.4; PaCO2, 40 mm Hg; PaO2, 95 mm Hg;

O2 sat, 98% The difference between the pulmonary venous and the arterialblood values is the result of an anatomic shunt Approximately 2% of venous re-turn from the systemic circulation is to the left side of the circulation, withoutgoing through the pulmonary circuit Two major contributors to this shunt arethe bronchial circulation and the thebesian veins of the heart A combination of98% of pulmonary venous blood and 2% shunted (systemic venous) blood yieldsnormal peripheral ABG values

Ventilation/perfusion (V/Q˙ ) mismatch leads to hypoxemia when perfusedalveolar units have reduced oxygen levels in the alveolar space because of reducedventilation, which is generally the result of some obstruction (e.g., bronchiolaredema or mucus related to infection, bronchospasm secondary to asthma) V/Q˙mismatch, however, may be overcome by an increase in FIO2 (Figure 1–1b).

Shunt is simply the extreme of V/Q˙ mismatch, in which there is no ventilationbut perfusion persists (Remember that ventilation without perfusion is dead-space ventilation) Shunt is not overcome by an increase in FIO2(Figure 1–1c).

TREATMENT OF HYPOXEMIA Quite simply, there are two major ways to

im-prove oxygenation:

1 Increase FIO2

2 Increase mean airway pressure

Increasing FIO2is simple and can only be done one way Increasing mean airwaypressure can be done a multitude of ways An increase in mean airway pressure im-proves oxygenation by recruiting partially or fully collapsed alveoli, thus bettermatching ventilation to perfusion and reducing shunt The easiest way to increasemean airway pressure is to increase positive end-expiratory pressure (PEEP) In-verse ratio ventilation also increases MAP by increasing the normal inspiratory-ex-piratory ratio from 1:2 to 1:1 or 2:1.1This change keeps the positive pressure in thechest for a longer time Some believe that this technique simply adds to the PEEP bynot allowing enough time for exhalation This has led to the term “sneaky PEEP”being used in reference to IRV High-frequency ventilation and oscillating ventila-tion are “high-tech” ways of increasing mean airway pressure and oxygenation.2

Two less commonly used ways to improve oxygenation—prone positioning andinhaled nitric oxide—work by improving V/Q˙ matching.3,4

8 The Intensive Care Manual