PULSE OXIMETRY

Despite the absence of a demonstrable survival advantage, pulse oximetry has been identified as the single most useful monitor for the prevention of adverse patient events,⁶ and it is used routinely on virtually all patients in the ICU. Pulse oximetry utilizes the fact that the absorption spectra of blood vary depending on its oxygen saturation: oxygenated blood appears red, and deoxygenated blood appears blue. A standard oximeter probe contains two light-emitting diodes: one that emits red light (wavelength 660 nm) and one that emits near-infrared light (wavelength 940 nm). The ratio of light absorption at the two wavelengths is detected and used to calculate oxygen saturation. Light that passes through tissues is absorbed by arterial blood, capillary blood, venous blood, and nonblood components (bone, muscle, etc.). By eliminating the nonpulsatile component of light absorption, the oxygen saturation of arterial blood can be estimated. Arterial oxygen saturation obtained from a pulse oximeter is designated S_PO₂ to distinguish it from arterial oxygen saturation obtained from a blood gas analyzer, which is designated S_ao₂. In addition to S_Po₂, pulse oximeters measure heart rate and generate a pulse waveform, which provides a crude measure of peripheral perfusion. These secondary functions are useful when the pulse oximeter is used as the sole monitor.

Despite the obvious advantages of being able to rapidly and noninvasively assess arterial oxygen saturation, it must be remembered that pulse oximetry does not guarantee the adequacy of either oxygen delivery (see Equation 1-14) or ventilation (see Equation 1-17). In the presence of profound anemia, marked tissue hypoxemia can arise despite a normal S_Po₂. In patients to whom supplemental oxygen is being administered, profound hypoventilation and respiratory acidosis can be present in spite of a normal S_Po₂.

Occasionally, S_Po₂ readings are unreliable. Sources of error include poor peripheral perfusion, movement artifacts, electrical interference, dyes (e.g., methylene blue), and the presence of abnormal hemoglobin. Abnormal forms of hemoglobin include methemoglobin, which can occur in high concentrations due to nitric oxide or nitroprusside overdose, and carboxyhemoglobin, which is caused by carbon monoxide poisoning. Measurements of S_Po₂ may be unreliable in patients with extremely low arterial oxygen saturation (e.g., <70%).

ELECTROCARDIOGRAPHY

The electrocardiograph (ECG) is essential for the diagnosis of cardiac arrhythmias and is extremely useful for the identification of myocardial ischemia and infarction. Also, specific ECG abnormalities provide supporting evidence for a wide range of cardiac disorders. The physiologic basis of the ECG and its relationship to the action potential is discussed in Chapter 1. Specific ECG abnormalities are covered in the relevant chapters, particularly 8 and 21.

Leads and Electrodes

The standard 12-lead ECG involves the placement of 10 electrodes on the patient in specific positions: one on each limb and six across the chest (Fig. 8-1). To ensure good contact between skin and electrode, the skin should be first cleaned with alcohol, gently abraded with fine sandpaper and, if necessary, shaved. From these 10 electrodes, 12 leads are recorded. A lead is obtained by recording the difference in electrical potential between two electrodes. Leads may be either bipolar or unipolar. With a bipolar lead, the signal is obtained from two active electrodes: one connected to the positive pole and one connected to the negative terminal of the ECG machine. With a unipolar lead, the signal is obtained using one active electrode (connected to the positive pole of the ECG machine) and an indifferent electrode, recorded at zero potential by connecting two or three limb electrodes through a resistor to the negative terminal of the electrocardiograph.

Figure 8.1 The chest leads. The top diagram shows the correct placement of the chest leads. The bottom diagram shows the orientation of the chest leads to the heart in the horizontal plane when looking from above. The arrow identifies the net direction of current flow during ventricular depolarization in the horizontal plane.

Six leads view the heart in the frontal plane (I, II, III, aVR, aVL, aVF) and six leads (V₁ through V₆) view the heart in the horizontal plane. The three standard leads (I, II, III) are bipolar leads; each lead records the potential difference between two limbs (Fig. 8-2). The augmented limb leads (aVR, aVL, aVF) are unipolar leads that record the potential difference between one limb and an indifferent composite electrode: aVR is obtained from the right arm; aVL from the left arm, and aVF from the left leg. The standard and augmented limb leads record the magnitude of the electrical signal in specific directions within the frontal plane, as shown in Fig. 8-3. The chest leads are unipolar leads that record the potential difference between the surface of the chest and an indifferent composite electrode. The orientation of the chest leads to the heart in the horizontal plane is shown in Figure 8-1.

Figure 8.2 The standard bipolar limb leads (I, II, and III). Each lead records the potential difference between two limbs. With lead I, the negative terminal of the ECG machine is connected to the right arm (RA) and the positive terminal, to the left arm (LA). With lead II, the negative terminal of the ECG machine is connected to the right arm and the positive terminal to the left leg (LL). With lead III, the negative terminal of the ECG machine is connected to the left arm, and the positive terminal is connected to the left leg.

Figure 8.3 The axes of the three bipolar standard limb leads (I, II, and III) and three unipolar augmented limb leads (aVL, aVF, and aVR). The direction from which each lead “looks” at the heart in the frontal plane is shown. If the direction of ventricular depolarization is toward a lead (i.e., toward the arrow), the QRS complex in that lead is positive. The size of the QRS deflection is dependent on the magnitude and direction of ventricular depolarization.

Interpretation of the 12-Lead ECG

ECGs are recorded onto a grid pattern composed of large and small squares. Large squares have dimensions of 5 mm by 5 mm and represent 0.5 mV on the vertical axis and 0.2 sec on the horizontal axis, assuming standard sweep and gain settings. Small squares have dimensions of 1 mm by 1 mm and represent 0.04 sec in the horizontal axis and 0.1 mV in the vertical axis. The various components of an individual ECG complex are shown in Figure 8-4. A normal 12-lead ECG is shown in Figure 8-5.

Figure 8.4 The waves, segments, and intervals of the ECG. See text for details.

Figure 8.5 A normal 12-lead ECG. The frontal plane axis is 30 degrees; see text for details.

(Image modified from Wagner GS: Marriot’s Practical Electrocardiography, ed. 9. Fig. 2.10, p. 30. Philadelphia, Lippincott Williams and Wilkins, 1994.)

Heart Rate

Heart rate is determined by dividing 300 by the number of large squares between each QRS complex (each large square represents 0.2 seconds, and there are 300 lots of 0.2 seconds in a minute). Once the heart rate is greater than 100, the number of small squares should also be considered, and the rate is calculated by dividing 1500 by the number of small squares.

P Wave

The P wave represents atrial contraction. P waves are normally evenly rounded and either positive or negative in all leads except V₁, where a biphasic wave is sometimes seen. Its duration should be less than 0.12 seconds and its amplitude less than 0.25 mV. Right atrial hypertrophy (e.g., due to pulmonary hypertension) results in peaked P waves. This is known as P-pulmonale and is best seen in leads II, III, and aVF. Left atrial hypertrophy (e.g., due to mitral stenosis) results in bifid P waves. This is known as P-mitrale and is also best seen in leads II, III, and aVF. Abnormalities of P-wave morphology also occur with atrial arrhythmias.

PR Interval

The normal PR interval is 0.10 to 0.22 seconds and is determined by the speed of conduction through the atrioventricular node. The PR interval varies inversely with heart rate and gradually lengthens with increasing age. A short PR interval is seen in some preexcitation syndromes, and a long PR interval is seen in first-degree and Wenckebach-type second-degree heart block (see Chapter 21).

QRS

The Q wave is a small negative deflection that precedes the R wave. Small Q waves (<0.03 seconds in duration) are a normal finding in all leads except V₁ through V₃, where they are always pathologic. Q waves of any size may be normal in leads III and aVR. Pathologic Q waves are indicative of transmural myocardial infarction (see Chapter 18). They develop within a few hours of infarction and are permanent.

The R wave is the first upward deflection that appears in the QRS complex. From leads V₁ through V₄ the R wave normally increases in amplitude and duration. Loss of this normal progression is indicative of loss of left ventricular muscle mass. The S wave is a downward deflection that follows the R wave and also reflects ventricular mass. The S wave is normally large in V₁, larger in V₂, and then decreases in size from V₃ through V₆.

The QRS complex represents ventricular depolarization and has a normal duration of 0.07 to 0.10 seconds. A wide QRS indicates abnormal conduction within the ventricles (e.g., bundle branch block) or a ventricular origin of an impulse (e.g., ventricular pacing or complete heart block).

The QRS amplitude has wide normal limits, ranging from as low as 5 mm in obese subjects to as high as 30 mm in slim males. Causes of large QRS amplitude include physical fitness and ventricular hypertrophy. Causes of low QRS amplitude include obesity, emphysema, and pericardial effusion.

QRS Axis

The net direction of current flow in the heart at any moment can be represented as a vector. If the vector is directed toward a particular lead during ventricular depolarization, the QRS complex is predominantly positive (R wave > S wave). If the vector is directed away from that lead, the QRS is predominantly negative (S wave > R wave). If the vector is perpendicular to the lead, the R wave and S wave are equal. The direction of depolarization through the ventricles in the frontal plane is called the QRS axis and is determined by examination of the six limb leads (I, II, III, aVL, aVR, aVF). The following steps can be used to determine the frontal-plane QRS axis (see Fig. 8-3):

1. The transitional lead, in which the positive and negative deflections are approximately equal, is identified. In Fig. 8-5, this is lead III.

2. The lead perpendicular (90 degrees) to the transitional lead is identified (lead aVR in Fig. 8-5). If the predominant direction of the QRS complex in this lead is positive, the axis is equal to the positive pole of this lead. If the direction is negative (as in Fig. 8-5), then the axis equals the negative pole of that lead (i.e., about 30 degrees in Fig. 8-5).

Figure 8-6 shows the normal range for the frontal-plane QRS axis along with the criteria for the diagnosis of left, right, and extreme axis deviation. Common causes of axis deviation are listed in Table 8-1.

Figure 8.6 Sectors indicating normal and abnormal frontal plane QRS axis. NA = normal axis. LAD = left axis deviation. RAD = right axis deviation. EAD = extreme axis deviation.

(Image redrawn from Galen S, Wagner GS: Marriot’s Practical Electrocardiography, ed. 9. Fig. 3.9, p. 45. Philadelphia, Lippincott Williams and Wilkins, 1994.)

Table 8-1 Causes of Deviation in the Frontal Plane QRS Axis

Left Axis Deviation

Left anterior hemiblock (Table 21-1)

Inferior myocardial infarction

COPD

Left ventricular hypertrophy

Wolff-Parkinson-White syndrome

Right Axis Deviation

Left posterior hemiblock (Table 21-1)

Right ventricular hypertrophy (including COPD)

Lateral or apical myocardial infarction

Wolff-Parkinson-White syndrome

Extreme Axis Deviation (rare)

Practical

Ventricular tachycardia

Right ventricular hypertrophy

Apical myocardial infarction

Hyperkalemia

COPD, chronic obstructive pulmonary disease.

Ventricular Hypertrophy and Strain

Given that the net direction of current flow during ventricular systole is from the base to the apex of the heart and is dominated by the left ventricle, then based on Figure 8-1 it can be appreciated that the QRS complexes in leads V₁ and V₂ are normally negative, and the QRS complexes in leads V₅ and V₆ are normally positive. With right ventricular hypertrophy, the electrical axis in the horizontal plane shifts rightward, resulting in a progressive increase in R wave amplitude in leads V₁ and V₂ such that with severe right ventricular hypertrophy, the QRS becomes positive in these leads. In contrast, with left ventricular hypertrophy there is accentuation of the normally dominant R wave in V₅ and V₆ and the development of deep S waves in V₁ and V₂. Ventricular hypertrophy may also result in ST segment depression and T wave inversion (strain pattern), which may be difficult to distinguish from ischemia. The ECG findings in right and left ventricular hypertrophy are summarized in Table 8-2.

Table 8-2 ECG Findings in Ventricular Hypertrophy

Abnormality	Left Ventricular Hypertrophy	Right Ventricular Hypertrophy
QRS conduction	Partial or complete left bundle branch block	Partial or complete right bundle branch block
Strain pattern (ST segment depression and T wave inversion)	Leads V3-V6	Leads V1-V3
Vertical plane	Leftward shift in QRS axis	Rightward shift in QRS axis
Horizontal plane	Large S waves in V2 and V3	Large R waves in V1 and V2 with severe hypertrophy, the QRS complex may become positive
	Large R waves in V5 and V6
Atrial hypertrophy	P-mitrale: bifid P waves in II, II, aVF	P-pulmonale: peaked P waves in II, II, aVF

T Wave

The T wave represents ventricular repolarization. T waves are normally positive, but negative T waves are normal findings in leads aVR and V₁ (and in young people, in V₂). The causes of pathologic T-wave inversion include myocardial ischemia and infarction, ventricular strain, and treatment with digoxin. Following a myocardial infarction, T-wave inversion develops within 12 to 48 hours and is usually permanent. There is a wide variation in both the duration and the amplitude of the T wave. Flattening T waves are seen with hypokalemia, and peaked T waves are seen with hyperkalemia.

ST Segment

The ST segment is measured from the J point (the point where the ST segment meets the QRS complex) to the beginning of the T wave (see Fig. 8-4). Slight (<1 mm) upsloping, downsloping, or horizontal ST segment depression is a normal variant. Up to 4 mm of ST segment elevation in leads V₁ through V₃ may also be a normal finding, especially in young males.

Pathologic ST segment elevation may indicate myocardial infarction, left ventricular aneurysm, pericarditis, or bundle branch block. With myocardial infarction, ST segment elevation usually develops within a few minutes and resolves within 24 to 48 hours. The distribution of ST segment elevation can be used to help localize the zone of infarction (see Chapter 18). ST segment elevation across a wide range of leads is common following cardiac surgery and probably represents a pericardial reaction. A clue to this diagnosis is that the ST segment elevation is usually mild and is not limited to a specific coronary territory.

ST segment depression is commonly associated with myocardial ischemia but is also seen with ventricular strain, digoxin therapy, hypokalemia, and conduction abnormalities such as bundle branch block. Mild upsloping ST segment depression is seen with tachycardia. ST segment depression due to ischemia is typically horizontal or downsloping (Fig. 8-7). Upsloping ST depression is not usually indicative of ischemia. Unlike ST segment elevation, the distribution of ST segment depression does not reliably localize the region of ischemia.

Figure 8.7 ST segment depression. See text for details.

U Wave

The U wave is a small positive deflection that follows the T wave. It may be present or absent, and its significance is uncertain.

QT Interval

The QT interval varies inversely with heart rate, and measurements should be corrected for this. The corrected QT interval (QTc) is the measured QT interval adjusted to a heart rate of 60 beats/min and is obtained by dividing the measured QT interval by the square root of the preceding RR interval:

8-1

Thus, a measured QT interval of 0.35 seconds at a heart rate of 90 beats/min yields a QTc:

The upper limit of normal for the QTc is 0.44 seconds for males and 0.46 seconds for females. Prolongation of the QT interval usually indicates delayed ventricular repolarization (i.e., prolongation of the QT segment) but may also reflect delayed depolarization (i.e., QRS prolongation). QT prolongation due to delayed repolarization may be congenital or acquired and predisposes to torsades de pointes ventricular tachycardia.

Cardiac Rhythm

The assessment of cardiac rhythm is discussed in Chapter 21.

INVASIVE ARTERIAL PRESSURE MONITORING

Invasive arterial pressure monitoring provides real-time measurement of blood pressure and is indicated in patients at risk for hemodynamic instability and those receiving infusions of vasoactive drugs. Modern single-use transducer kits are easy to set up and are less prone to damping and drift of the zero point than the older reusable systems. The pressure transducer should be zeroed to the level of the right atrium, which is taken to be the fifth intercostal space in the midaxillary line. Transducers should be rezeroed each time the patient’s position is changed and routinely every to 12 hours.

The determinants of the arterial pressure are complex, but in essence, mean arterial pressure (MAP) is determined mainly by stroke volume and systemic vascular resistance, and pulse pressure is determined mainly by stroke volume and arterial compliance. The normal arterial pressure waveform changes in shape as it progresses through the arterial tree (Fig. 8-8) due to alterations in the arterial compliance and reflected pressure waves from the periphery.

Figure 8.8 The arterial waveform at various sites. As the monitoring site is moved peripherally, there is a progressive change in the arterial waveform, characterized by a steeper upstroke, a higher peak systolic pressure, a lower end-diastolic pressure, and a later dicrotic notch.

(Image modified from Bedford RF: Invasive blood pressure monitoring. In Blitt CD, ed: Monitoring in Anesthesia and Critical Care, p. 505. New York, Churchill Livingstone, 1985.)

Abnormal Waveforms

Damping

An overdamped trace manifests as a narrow pulse pressure with a blunted upstroke and loss of the dicrotic notch. Overdamping is usually caused by problems in the arterial catheter (kinking, thrombus formation) rather than in the transducer system. Overdamping results in a falsely low systolic pressure, but MAP is usually displayed accurately. Underdamping typically occurs in patients who have very noncompliant arterial systems and results in an arterial waveform that overestimates systolic pressure. An underdamped trace may also contain several artefactual peaks, causing an overestimation of MAP. Even in the absence of underdamping, the reduction in arterial compliance that occurs in elderly patients results in an arterial waveform with a widened pulse pressure and a high systolic peak.

Cardiac Disease

With aortic regurgitation, the reflux of blood back into the left ventricle during diastole results in a low diastolic pressure. Stroke volume is increased due to overfilling of the left ventricle. These effects result in an increased systolic peak and widened pulse pressure (Fig. 8-9). A widened pulse pressure with diastolic hypotension also occurs in pregnancy, patent ductus arteriosus, and vasodilatation. Conditions associated with a low stroke volume, such as pericardial tamponade and cardiogenic shock, result in a narrow pulse pressure, which can be easily mistaken for a problem with the arterial catheter. Aortic stenosis is associated with a slow upstroke and a narrow pulse pressure (see Fig. 8-9). Alterations in the arterial pressure waveform due to an intraaortic balloon pump are described in Chapter 22.

Figure 8.9 Alterations in the arterial waveform with various disease states. See text for details.

(Redrawn from AC Guyton AC, Hall JE: Textbook of Medical Physiology, ed 10. Fig. 15.4, p. 154. Philadelphia, WB Saunders, 2000.)

Pulsus alternans is an abnormality in which there are regular alternating amplitudes of the systolic pressure. The condition is uncommon but is occasionally seen in association with severe left ventricular dysfunction and aortic stenosis.

Respiratory Changes

During normal breathing there is a slight fall in systolic pressure with inspiration (mainly due to pooling of blood within the pulmonary circulation) and a slight increase in systolic pressure during expiration. With positive pressure ventilation, systolic pressure normally increases slightly during late inspiration (due to enhanced left ventricular emptying as a result of reduced afterload and direct chamber compression) and falls slightly during late expiration. Large fluctuations (>10 to 15 mmHg) in systolic pressure with respiration are termed pulsus paradoxus (Fig. 8-10). Pulsus paradoxus is associated with a number of conditions encountered in the ICU, including hypovolemia, cardiac tamponade, raised intrathoracic pressure (bronchospasm, pneumothorax, ventilator dysynchrony), raised intraabdominal pressure, and extreme obesity. Pulsus paradoxus is predictive of fluid responsiveness (see later material).

Figure 8.10 Respiratory changes in the systemic arterial, pulmonary arterial (PAP), and central venous (CVP) pressure waveforms during mechanical ventilation.

(Modified from Magder S: Clinical usefulness of respiratory variations in arterial pressure. Am J Respir Crit Care Med 169:151-155, 2004.)

CENTRAL VENOUS PRESSURE MONITORING

Interpreting Central Venous Pressure

The Waveform

The CVP waveform is explained in Figure 8-11. Atrial fibrillation results in loss of the A wave, whereas atrial flutter causes regular flutter A waves on the CVP trace. Atrioventricular dissociation or junctional rhythm with retrograde atrial conduction can cause large (cannon) A waves due to atrial contraction occurring against a closed tricuspid valve. Irregular cannon waves are seen with atrioventricular dissociation; regular cannon waves, occurring with each heartbeat, are seen with junctional rhythm. Tricuspid regurgitation may cause exaggerated ventricular (V) waves due to elevated atrial pressure during ventricular systole.

Figure 8.11 The relationship between the central venous pressure (CVP) waveform and the ECG. The A wave occurs at end-diastole and is caused by atrial contraction. The A wave is followed by the C wave, which is caused by ventricular contraction and closure of the tricuspid valve. The pressure falls steadily throughout the remainder of systole (the X descent), principally because of atrial relaxation. The V wave occurs in late systole and is caused by atrial filling prior to the opening of the tricuspid valve. It is followed by the Y descent as the valve opens and blood flows into the relaxing ventricle.

(Redrawn from Mark JB: Central venous pressure monitoring: clinical insights beyond the numbers. J Cardiothorac Vasc Anesth 5:163-173, 1991.)

Measurement of Central Venous Pressure

To minimize the effects of ventilation, CVP should be measured at end-expiration. The transducer should be zeroed to the level of the right atrium: the fifth intercostal space in the midaxillary line. For simplicity, the averaged pressure throughout the cardiac cycle is normally used. However, when an abnormal waveform is present, the pressure at right ventricular end-diastole (the A wave) should be used because this is the time when the tricuspid valve is open and there is no flow across the valve—that is, when CVP is indicative of right ventricular end-diastolic pressure.

Values for Central Venous Pressure in Cardiac Surgery Patients

Although there is no absolute value for CVP that predicts fluid responsiveness,^8,9 the following comments are generally true. First, if cardiac function is relatively normal, a CVP of 6 to 12 mmHg is appropriate for most cardiac surgery patients during their early postoperative course. Second, a CVP greater than 15 mmHg is usually indicative of a significant cardiac or respiratory problem and warrants investigation (see Chapter 20). Third, a patient who has a CVP less than 6 mmHg but is otherwise stable requires no intervention. Finally, trends in CVP in response to a fluid challenge are more useful than absolute values. In hypovolemic patients, the usual response to a fluid bolus is a sustained increase in MAP and cardiac output with no change, or only a transient increase, in CVP. The causes of increased CVP are listed in Table 8-3.

Table 8-3 Causes of High Central Venous Pressure

Hypervolemia

Increased venous tone

Right ventricular systolic dysfunction

Right ventricular diastolic dysfunction

Elevated pulmonary vascular resistance

Severe left ventricular dilatation causing impairment of right ventricular diastolic filling

Tricuspid valve stenosis or regurgitation

Pulmonary valve stenosis

High pericardial pressure (tamponade, constriction)

High intrathoracic pressure (ventilatory dysynchrony, bronchospasm, pneumothorax)

High intraabdominal pressure

Respiratory Changes in Central Venous Pressure

The CVP normally fluctuates slightly throughout the respiratory cycle. With positive pressure ventilation, CVP increases slightly during inspiration and falls during expiration (see Fig. 8-10). These changes are reversed with normal spontaneous breathing. An inspiratory fall in CVP of more than 1 mmHg has been shown to be predictive of fluid responsiveness in extubated patients.⁸ However, respiratory variations in CVP can also occur with abnormal patterns of breathing. In particular, large respiratory swings in CVP are seen in patients with partial airway obstruction, chronic obstructive airways disease, and marked obesity. CVP is often very difficult to interpret in grossly obese patients, particularly following extubation.

THE PULMONARY ARTERY CATHETER

The balloon-tipped, flow-directed PAC was originally described by Swan and Ganz in 1970,¹⁰ and it remains in widespread use today. Multiple measured and derived variables can be obtained from a PAC. Measured parameters are: (1) CVP; (2) pulmonary artery pressure; (3) pulmonary artery wedge pressure (PAWP); (4) stroke volume and cardiac output; (5) mixed venous oxygen saturation (S_vo₂); (6) right ventricular ejection fraction (some catheters only); (7) temperature. Some PACs provide continuous measurements of cardiac output and S_vo₂. Derived values include the transpulmonary gradient, pulmonary and systemic vascular resistances (Equations 1-5 and 1-6), and left and right ventricular stroke work. Cardiac output and vascular resistances are usually indexed to body-surface area.

In the following section the interpretation of PAWP and cardiac output are discussed. The implications of raised pulmonary artery pressure and the transpulmonary gradient are discussed in Chapter 24. S_Vo₂ is discussed in Chapter 1.

PULMONARY ARTERY WEDGE PRESSURE

The PAWP waveform is obtained by inflating the balloon at the tip of the PAC such that flow beyond the balloon is interrupted (see Chapter 40). In this situation, the pressure recorded at the catheter tip should be the same as that within the left atrium. At end-diastole, when the mitral valve is open and diastolic filling has ceased, the wedge pressure is the same as the left ventricular end-diastolic pressure (LVEDP). LVEDP is used as a surrogate for LVEDV (preload). (The definition and determinants of preload are discussed in Chapter 1.) However, for PAWP to reflect preload accurately, several assumptions must hold true.

Interpreting the Pulmonary Artery Wedge Pressure

Waveform

The PAWP waveform is similar to the CVP waveform shown in Figure 8-11. Abnormal waveforms are analogous to those described for the CVP: large V waves with mitral regurgitation and cannon A waves with nodal rhythm or complete heart block. Large A waves may also occur in patients with left ventricular diastolic dysfunction.

With mitral valve disease, the magnitude of a V wave does not correspond to the severity of the mitral regurgitation. With chronic mitral regurgitation, in which there is a dilated, highly compliant left atrium, even severe regurgitation may not produce visible V waves. Conversely, with acute mitral regurgitation, in which the left atrium is small and noncompliant, large V waves may occur despite only moderate regurgitation.

Measurement of the Pulmonary Artery Wedge Pressure

The technique of obtaining a PAWP waveform is described in Chapter 40. The PAWP is taken as the average value throughout the cardiac cycle, but if an abnormal waveform is present, the measurement should be timed to the A wave because that is when the mitral valve is open and LVEDV is equivalent to left atrial pressure. With respect respiratory oscillations in the waveform, PAWP is measured at end-expiration using a value averaged over several breaths. End-expiration occurs at the lowest point of the respiratory oscillation in ventilated patients and at the highest point in extubated patients (Fig. 8-12).

Figure 8.12 Respiratory variations in the pulmonary capillary wedge pressure trace during spontaneous and mechanical ventilation. See text for details.

(Image redrawn from Reich DL, Moskowitz DM, Kaplan JA: Hemodynamic monitoring. In Kaplan JA, Reich DL, Konstadt SN, eds. Cardiac Anesthesia, ed 4. Fig. 11.4, p. 342. Philadelphia, WB Saunders, 1999.)

Values for Pulmonary Artery Wedge Pressure in Cardiac Surgery Patients

The usual range for PAWP in postoperative cardiac surgery patients is 6 to 15 mmHg, but there is no absolute value that predicts fluid responsiveness.^8,9 Indeed, in the presence of diastolic dysfunction, patients may be fluid responsive despite having a PAWP of more than 18 mmHg.¹⁸ As with CVP, trends in PAWP in response to a fluid challenge are more useful than the absolute value. The causes of an elevated PAWP are listed in Table 8-4.

Table 8-4 Causes of High Pulmonary Artery Wedge Pressure

Hypervolemia

Left ventricular systolic dysfunction

Left ventricular diastolic dysfunction

Severe right ventricular dilatation causing compression of the left ventricle

Mitral regurgitation or stenosis

Increased left ventricular afterload

Pulmonary venous obstruction

Malposition of catheter tip in West zone 1 or 2 in association with raised intrathoracic pressure

MEASUREMENT OF CARDIAC OUTPUT

Cardiac output is a critical determinant of global tissue oxygen delivery (Equation 1-14) and as such is of great interest to clinicians caring for cardiac surgery patients. The average value for cardiac output in awake normotensive subjects is 2.7 l/min/m², with a range (±30%) of 1.9 to 3.5 l/min/m².²⁰ However, a cardiac output of 2.2 l/min/m² is widely used as a lower acceptable limit because values below this have been associated with increased mortality rates following myocardial infarction.²¹ Whether this lower limit applies in ventilated postoperative cardiac surgery patients is unknown.

The clinical assessment of cardiac output in the early period following cardiac surgery is unreliable. In one small study of uncomplicated cardiac surgery patients, physicians and nurses were asked to estimate whether cardiac output was normal, low, or high, based on clinical assessment.²² In patients whose cardiac outputs were outside the normal range, clinical assessment was usually wrong (13/20 patients). Furthermore, cardiac output was below the lower limit of normal (<1.9 l/min/m²) in 12 of 50 cases. This latter finding raises an important issue: what should be done in response to a low cardiac output in a patient who is otherwise stable? It is possible that inappropriate interventions to increase oxygen delivery, such as the administration of inotropic drugs, fluid, or blood, could actually increase morbidity and mortality rates. This may be part of the explanation for the adverse outcome associated with the use of the PAC identified in some studies. We do not recommend the measurement of cardiac output in all cardiac surgery patients. However, because cardiac output cannot be reliably assessed clinically, formal measurement should be undertaken in patients with hemodynamic instability or signs of inadequate oxygen delivery (acidosis, elevated lactate, oliguria, low superior vena cava oxygen saturation). Also, treatment should not be instituted on the basis of moderately low cardiac output (i.e., 1.8 to 2.2 l/min/m²) in patients who are otherwise stable, particularly in patients who are sedated and mechanically ventilated and are therefore likely to have low oxygen consumption.

CAPNOGRAPHY

Capnography involves the continuous measurement of the concentration of carbon dioxide in a patient’s airway during the respiratory cycle. Although capnography has been in widespread use as a monitoring device during anesthesia for many years, it has only recently begun to be used routinely in the ICU environment. Various methods of carbon dioxide sampling and analysis are available, but the most widely used technique involves sampling respiratory gas (at a rate of 150 to 500 ml/min) via a small-bore plastic tube connected to the airway. This gas is then drawn into a remote infrared carbon dioxide analyzer, which is typically integrated into the patient monitor.

Normal capnograph traces during mechanical ventilation and spontaneous breathing are shown in Fig. 8-13A and C. The peak carbon dioxide concentration at end-expiration is known as the end-tidal carbon dioxide concentration (P_ETco₂) and is normally 1 to 2 mmHg less than the arterial carbon dioxide concentration (P_aco₂). Thus, P_ETco₂ can be used as a surrogate for P_aCO₂ and interpreted accordingly. Capnography is useful in a range of circumstances encountered in the ICU. In mechanically ventilated patients, loss of the capnograph trace may indicate a circuit disconnection or inadvertent extubation. P_ETCO₂ can be used to titrate minute ventilation and facilitate weaning.³⁰ Identification of exhaled carbon dioxide is the gold standard for confirming successful placement of an endotracheal tube. During percutaneous tracheostomy or bronchoscopy, capnography is also useful to confirm the adequacy of ventilation. In extubated patients, the tip of the carbon dioxide sampling tube can be placed inside an oxygen face mask to provide a measure of respiratory rate. Failure of the endinspiratory carbon dioxide concentration to return to zero indicates rebreathing within the ventilator circuit (see Fig. 8-13 D). A carbon dioxide concentration that continues to rise throughout expiration (see Figure 8-13 B) is typical of airway obstruction.

Figure 8.13 Normal and abnormal capnograph traces. A, a normal capnograph trace during mechanical ventilation. The phases of expiration are shown: phase I represents dead space gas; phase II represents a mixture of dead space and alveolar gas; phase III represents alveolar gas. Phase III normally has a slight upward slope due to uneven emptying of lung units with variable ventilation-perfusion (V/Q) ratios (see Chapter 1). Lung units with low V/Q ratios (i.e., underventilated lung units with high carbon dioxide concentration) and a long time constant (i.e., emptying slowly) release a high concentration of carbon dioxide during late expiration. The end-expiratory value is known as the end-tidal carbon dioxide concentration (ETCO₂). B, Phase III may have a very steep upslope in the presence of marked airflow obstruction that could be caused by, for example, emphysema. C, a normal capnograph trace during spontaneous ventilation. D, the effect of carbon dioxide rebreathing in the same patient.

(Redrawn from Moon RE, Camporesi EM: Respiratory monitoring. In Miller RD, ed. Anesthesia, ed. 4. Fig. 36.14, p. 1271; Fig. 36.15, p. 1272. Philadelphia, Churchill Livingstone, 1994.)

Several caveats concerning the use of capnography must be considered. Unless the sampling tube is placed close to the patient’s airway, usually on the ventilator side of the endotracheal tube filter, P_ETCO₂ may not reflect P_aCO₂. This is particularly true for spontaneously breathing and extubated patients. Also, the sampling tube can become blocked or kinked, resulting in loss of or alteration in the shape of the capnograph trace. Finally, in the setting of increased alveolar dead space (see Chapter 1), the P_ETCO₂-P_aCO₂ difference may greatly exceed 1 to 2 mmHg. This circumstance is most obviously apparent when end-tidal and arterial carbon dioxide concentrations are compared in patients receiving cardiac massage during a cardiac arrest. An abrupt fall in P_ETCO₂ should always alert the clinician to the possibility of a precipitous fall in cardiac output.

TEMPERATURE MONITORING

Temperature management is an essential component of intensive care practice. Hypothermia is associated with impaired cardiac performance, coagulopathy, shivering, and myocardial ischemia. Hyperthermia leads to increased oxygen consumption, is associated with adverse neurologic outcome in cardiac surgery patients, and may portend the development of infection. Following cardiac surgery, patients are usually actively rewarmed. Under certain circumstances, notably in cases of suspected hypoxic ischemic encephalopathy following a cardiac arrest, patients are actively cooled. Certain therapies such as hemofiltration and extracorporeal circulation predispose a patient to hypothermia. For all of these reasons, accurate measurement of temperature in the ICU is essential.

Methods of measurement of temperature include mercury thermometers, electronic thermometers (containing a thermistor or thermocouple), infrared tympanic thermometers, and thermistors located on devices such as urinary catheters, PACs, and nasopharyngeal probes. Blood temperature measured by a thermistor located on a PAC is considered the gold standard for temperature measurement in the ICU. Compared to pulmonary artery blood, reasonable levels of agreement are obtained in temperature measured in the esophagus, rectum, bladder, and axilla.³¹ In one study, the mean differences (±95% confidence interval) in blood temperature were −0.21 ± 0.2°C and 0.27 ± 0.45°C for the bladder and axilla, respectively.³¹ The narrow confidence interval, ease of measurement (a thermistor attached to a urinary catheter), and ability to record temperature continuously make the urinary bladder an attractive site for routine temperature measurement during the early postoperative period. Temperatures obtained from the tympanic membrane appear to be less reliable than those obtained from other sites^32,33 but have the advantages of being rapid, noninvasive, and easy to obtain.

TONOMETRY

Gastric tonometry is a technique of measuring gastric mucosal carbon dioxide tension, from which intracellular pH (pH_i) and other variables can be derived. The clinical rationale for gastric tonometry is its use as a measure of gastric mucosal hypoxia and, by inference, the hypoxia of other tissues. The technique involves the equilibrium of carbon dioxide between gastric mucosal cells and a saline or air-filled balloon placed in the stomach. If the carbon dioxide tension in the balloon is assumed to be the same as that in the adjacent tissues, and the mucosal bicarbonate concentration is assumed to be the same as the arterial bicarbonate concentration, then pH_i can be calculated from the Henderson-Hasselbalch equation (see Chapter 31):

8-2

The normal value for pH_i is 7.35 and mucosal hypoperfusion is considered to exist when the pH_i is less than 7.32. pH_i has been widely investigated as a marker of tissue hypoperfusion and as a predictor of adverse patient outcome in critically unwell patients.³⁴ Patients with normal or high pH_i show improved survival rates compared to those with low pH_i.^35,36 However, it has not been clearly established that, in patients with a low pH_i, therapy to improve tissue perfusion (fluid, inotropes, blood) improves outcome. Thus, a normal pH_i may simply identify patients who are less sick. Furthermore, there are technical and methodologic problems that limit the applicability of the technique. As an alternative to pH_i, the PCO₂ gap (the difference between the tonometric and either the arterial or the end-tidal PCO₂) has been proposed, and it may be a more sensitive marker of tissue hypoperfusion than pH_i.³⁷ In automated gas tonometers, tonometric carbon dioxide tension is referenced to P_ETCO₂; a value higher than 1.5 to 2 kPa (10 to 14 mmHg) is considered abnormal.³⁴ Recently, there has been interest in sublingual tonometry, which also provides evidence of tissue hypoperfusion but appears to be associated with fewer technical problems than are associated with gastric tonometry.³⁸

Despite initial enthusiasm, gastric tonometry has not been widely adopted, mainly because of technical difficulties and methodologic concerns. It remains to be seen whether sublingual tonometry has a role as a routine clinical tool in the management of critically unwell patients.