Section 3: Anesthesia Management
Part B: Monitoring
Chapter 30: Cardiovascular Monitoring

Pulmonary Artery Pressure and Pulmonary Artery Wedge Pressure Waveforms

Normal Waveforms

As the flow-directed, balloon-tipped PAC is floated from a central vein to its proper position in the pulmonary artery, characteristic pressure waveforms are recorded (see Fig. 30–34). When the catheter tip reaches the superior vena cava or right atrium, a CVP waveform should be observed, with its a, c, and v waves and low mean pressure value (see Table 30–1). At this point, the PAC balloon is inflated, and the catheter is advanced until it crosses the tricuspid valve to record right ventricular pressure. This waveform is recognized by the sudden increase in systolic pressure, the wide pulse pressure, and the low diastolic pressure that approximates CVP. The PAC next enters the right ventricular outflow tract and floats across the pulmonic valve into the main pulmonary artery. Often, this passage is heralded by arrhythmias, especially premature ventricular beats, as the balloon-tipped catheter strikes the right ventricular infundibulum. Pulmonary artery pressure is characterized by the step-up in diastolic pressure recorded as the catheter crosses the pulmonic valve. In the absence of pulmonic valve stenosis, systolic PAP closely approximates right ventricular systolic pressure, but PADP generally exceeds right ventricular dia-stolic pressure. On occasion, it may be difficult to distinguish right ventricular pressure from PAP, particularly if only digital values for these pressures are reported. However, by examining the diastolic pressure contours, the distinction between right ventricular pressure and PAP becomes clear. PAP decreases steadily during diastole, as blood flows from the pulmonary artery toward the left atrium. In contrast, right ventricular pressure increases steadily during diastole as blood flows into the right ventricle through the open tricuspid valve (see Fig. 30–34). 325 

TABLE 30–1. Normal Cardiovascular Pressures

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FIGURE 30–34 Characteristic waveforms recorded during passage of the pulmonary artery catheter. The right atrial pressure resembles a central venous pressure waveform and displays a, c, and v waves. Right ventricular pressure shows a higher systolic pressure than seen in the right atrium, although the end-diastolic pressures are equal in these two chambers. Pulmonary artery pressure shows a diastolic step-up compared with RVP. Note also that RVP increases during diastole, whereas pulmonary artery pressure decreases during diastole (shaded boxes). Pulmonary artery wedge pressure has a similar morphology to right atrial pressure, although the a-c and v waves appear later in the cardiac cycle relative to the electrocardiogram. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 3–1.)

Under normal conditions, the PAP upstroke slightly precedes the radial artery pressure upstroke (Fig. 30–35). This reflects the longer duration of left ventricular isovolumic contraction, as well as the transmission time of the central aortic pressure upstroke to the downstream radial artery recording site. 145  Although the PAP upstroke precedes the radial artery pressure upstroke by 50 milliseconds, peak PAP precedes peak radial artery pressure by only 10 milliseconds. 398  As a practical matter, PAP and systemic arterial pressure contours appear to overlap on the bedside monitor, with these pressures rising, peaking, and falling at approximately the same points in time (see Fig. 30–35). 325  Understanding these temporal relations is critically important if one is to properly interpret abnormal PAP and PAWP waveforms, particularly when tall v waves are present in these traces (see later discussion).

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FIGURE 30–35 Temporal relations between normal systemic arterial pressure (ART), pulmonary artery pressure (PAP), central venous pressure (CVP), and pulmonary artery wedge pressure (PAWP). Note that the PAWP a-c and v waves appear to occur later in the cardiac cycle compared with their counterparts on the right side of the heart seen in the CVP trace. ART pressure scale on the left; PAP, CVP, and PAWP pressure scales on the right. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 3–3.)

The PAC, with balloon inflated, finally reaches the wedge position. As noted above, the PAWP is an indirect measurement of pulmonary venous pressure and LAP and should therefore resemble these pressure waveforms. Consequently, the PAWP waveform may be identified as a venous pressure trace that displays characteristic a and v waves and x and y descents. However, owing to the pulmonary vascular bed interposed between the PAC tip and left atrium, PAWP is a delayed representation of LAP. 313, 399  On average, 160 milliseconds are required for the LAP pulse to traverse the pulmonary veins, capillaries, arterioles, and arteries. As a consequence of this delay, the wedge-pressure a wave appears to follow the ECG R wave in early ventricular systole (see Fig. 30–35). However, the a wave is an end-diastolic pressure event, produced by left atrial contraction. This time delay in phasic wedge pressure waves must be appreciated for proper waveform interpretation.

Not only is PAWP a delayed representation of LAP, but it is also a damped reflection of phasic atrial pressure waves. The amount of damping is variable, but when LAP waves are prominent, the pressure peaks may be significantly underestimated and the pressure nadirs significantly overestimated by the wedge trace (Fig. 30–36). Even though the PAWP waveform will always appear to be a damped, delayed version of LAP, the mean pressure recorded from these two sites should be similar under most circumstances. 287 

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FIGURE 30–36 Pulmonary artery wedge pressure (PAWP) is a damped, delayed reflection of left atrial pressure (LAP). The tall regurgitant v waves (v) caused by severe mitral regurgitation are seen clearly in the LAP trace but appear delayed and smaller in magnitude in the PAWP trace. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 4–4.)

To recognize prominent a or v waves in the PAWP trace, it is not always necessary to inflate the PAC balloon and obtain wedge position (Fig. 30–37). Because the wedge pressure records LAP waves transmitted in retrograde fashion from the left atrium, these waves will normally sum with the antegrade PAP waves produced by right ventricular ejection. The PAP trace thus becomes a composite wave, reflecting both retrograde and antegrade components. Consequently, tall left atrial a and v waves distort the normal PAP contour, with the a wave inscribed at the onset of the systolic upstroke and the v wave distorting the dicrotic notch (see Fig. 30–37). 313, 400  Once these waves are identified by observing the wedge pressure and comparing it with the PAP trace, it is convenient, and perhaps more prudent, to follow the wedge-pressure a and v waves in the PAP trace, without repeatedly inflating the balloon to measure wedge pressure. However, marked changes in PAP values or wave morphology should initiate balloon inflation and wedge-pressure measurement, because artifacts occasionally mimic these observations (see later discussion).

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FIGURE 30–37 Tall left atrial pressure (LAP) a and v waves transmitted in a retrograde direction through the pulmonary vasculature distort the antegrade pulmonary artery pressure (PAP) waveform. The LAP a wave distorts the systolic upstroke, and the v wave distorts the dicrotic notch. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 4–10.)

In summary, PAWP measured with a balloon-tipped PAC provides a delayed, damped estimate of LAP, by measuring the pressure where flow resumes at a pulmonary venous junction point near the left atrium. Mean PAWP will always be lower than mean PAP; otherwise, blood would not flow in an antegrade direction. The PAWP waveform should display small a and v waves just as the LAP waveform, and these phasic components should be identifiable if the pressure trace is displayed with sufficient gain and resolution on the monitor screen.

Left Atrial Pressure, Pulmonary Artery Wedge Pressure, and Pulmonary Capillary Pressure

Because of its method of placement, direct left arterial pressure ( LAP) monitoring is usually restricted to patients undergoing cardiac surgery. The most common technique for monitoring LAP involves catheterization of the left atrium with a thin catheter introduced through the right superior pulmonary vein and secured with a purse-string suture. The catheter is brought out through the skin beneath the xiphoid process and attached to a closed pressure monitoring tubing–transducer system. Because LAP monitoring is discontinued in the postoperative period simply by withdrawing the left atrial catheter through the skin, transseptal methods for LAP monitoring during surgery have been proposed to reduce the risk of bleeding following catheter removal. 213, 401, 402  LAP measurement has also been performed for diagnostic cardiac catheterization by a retrograde arterial approach, transseptal venous catheterization, and even percutaneous direct left atrial puncture from a right paravertebral insertion site. 403 

LAP monitoring is less widely practiced today than in the past, largely because it has been supplanted by PAC monitoring. This has occurred, no doubt, because the PAC simultaneously provides an estimation of left ventricular filling pressure as well as additional useful monitoring information, including CVP and cardiac output. Although some authors have shown modest discrepancies between the LAP and PAWP in the period immediately following cardiopulmonary bypass, 404  the PAWP generally provides an excellent estimate of LAP for cardiac surgical patients in the postoperative period. 316, 404, 405  Furthermore, the pathophysiologic conditions that alter the relationships among the PADP, PAWP, and LAP have been well described and should be recognized by the physician to avoid misinterpretation of the data provided by these monitors (see later discussion).

Direct LAP monitoring continues to be particularly useful in pediatric patients undergoing complex congenital heart surgery, because of the difficulties using some of the standard percutaneous techniques in this patient population. Gold et al 406  reported use of more than 6,000 transthoracic left atrial and right atrial pressure monitoring catheters, with complications from LAP monitoring occurring in only 0.68 percent of 2,393 left atrial catheters. 407  However, the physician must recognize that direct access to the left heart chambers always carries the risk of air and particulate embolization to the systemic circulation. LAP monitoring therefore requires close attention to proper management by the entire team of caregivers to ensure that line patency is maintained and flushing is performed with care. The most common complications of LAP monitoring actually result from catheter removal. Because of the risk of bleeding from the cardiac site of catheter entry, the left atrial catheter must be removed before mediastinal chest drains. When the catheter cannot be withdrawn through the skin, surgical reexploration is needed to remove the retained catheter. Other rare complications of LAP monitoring include entrapment of the catheter in mechanical aortic or mitral valve prostheses, 406, 408  fistula formation between the right superior pulmonary vein and the right mainstem bronchus, 406  and unrecognized retained catheter fragments that serve as a source of systemic embolization. 409 

Normal LAP waveforms resemble CVP or right atrial pressure waveforms, although there are few subtle morphologic distinctions. Because atrial depolarization originates in the sinoatrial node located at the junction of the superior vena cava and the right atrium, the right-sided a wave appears slightly earlier than the left-sided a wave (Fig. 30–38). Although the a wave is the most prominent pressure peak in a normal CVP trace, the v wave is often taller than the a wave in a normal LAP waveform. These observations suggest that right atrial contraction is generally more forceful than left atrial contraction, and that the left atrium is less distensible than the right atrium during passive systolic filling. 145  Finally, the interval between right atrial contraction and right ventricular contraction is longer by approximately 40 milliseconds than the interval between left atrial contraction and left ventricular contraction. 145  Consequently, a and c waves are seen more often as separate waves in a right atrial pressure trace than in a LAP trace. In normal LAP waveforms, the a and c waves merge into a composite a-c wave, although most clinicians simply describe this pressure peak as the a wave. Similarly, the PAWP waveform generally displays only a and v waves, because the PAWP c wave is obscured further by the transpulmonary damping effect of the lung vasculature.

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FIGURE 30–38 Normal temporal relations between the electrocardiographic, central venous pressure (CVP), and left atrial pressure (LAP) traces. The LAP and CVP waveforms have nearly identical morphologies, although the CVP a wave slightly precedes the LAP a wave. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 2–9.)

The terms PAWP and pulmonary artery occlusion pressure (PAOP) are used interchangeably and refer to the same measurement obtained from the tip of a PAC following balloon inflation and flotation to the wedged position. As already discussed, PAWP and PAOP are used as indirect estimates of mean LAP. In contrast, the hydrostatic pressure in the pulmonary capillaries is a different pressure that must exceed LAP to maintain antegrade blood flow through the lungs. This pulmonary capillary pressure must not be confused with PAWP or LAP, nor should these terms be used interchangeably. 410  Continued use of the phrase “pulmonary capillary wedge pressure” to mean PAWP or PAOP has perpetuated misconceptions about these measurements. Although the magnitude of the difference between pulmonary capillary pressure and PAWP is generally small, it can increase markedly when resistance to flow in the pulmonary veins is elevated. In most situations, the major component of pulmonary vascular resistance occurs at the precapillary, pulmonary arteriolar level. However, rare conditions like pulmonary veno-occlusive disease may cause a marked increase in postcapillary resistance to flow within the pulmonary veins. A similar situation arises in other conditions that disproportionately increase pulmonary venous resistance, such as central nervous system injury, acute lung injury, hypovolemic shock, endotoxemia, and norepinephrine infusion. 410, 411  Under these conditions, measurement of PAWP will underestimate pulmonary capillary pressure substantially and thereby underestimate the risk of hydrostatic pulmonary edema. Although pulmonary capillary pressure may be measured at the bedside by analyzing the decay in PAP following PAC balloon inflation, these techniques have not been adopted widely in clinical practice. 412, 413, 414, 415, 416, 417  To avoid confusion, the phrase “pulmonary capillary wedge pressure” should be abandoned because it is imprecise and misleading. 410 

Abnormal Waveforms

PAC catheter monitoring is subject to the same technical artifacts inherent in all invasive pressure monitoring techniques, as well as some additional problems unique to this method. 385, 418, 419, 420  Because the PAC is longer than other intravascular catheters, greater attention must be paid to ensure that the lumens are free from clot or air bubbles that will distort the pressure waveforms. In addition, the PAC passes through the heart and is subject to pressure recording artifacts resulting from cardiac-induced catheter motion. These artifactual pressure spikes may be distinguished from the underlying physiologic pressure waveform by their unique morphology and timing.

The most common prominent pressure spike artifact observed in a PAC trace is seen immediately following the ECG R wave at the onset of systole (Fig. 30–39). 418, 421  At this point in the cardiac cycle, tricuspid valve closure and right ventricular contraction and ejection set the PAC in motion and inscribe a spurious, nonphysiologic pressure wave. Note that this artifactual PAP wave occurs at the same time as the CVP c wave and may appear as an artifactual pressure trough, as well as artifactual pressure peak. If this artifactual trough pressure is detected inappropriately by the bedside monitor, it may be reported as a spuriously low value for PADP. Repositioning the PAC by advancing or withdrawing it a few centimeters often helps it assume a slightly different position in the heart and ameliorates this problem. 418 

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FIGURE 30–39 Artifactual pressure peaks and troughs in the pulmonary artery pressure (PAP) waveform caused by catheter motion. The correct value for pulmonary artery end-diastolic pressure is 8 mm Hg (A) although the monitor digital display erroneously reports the PAP as 28/0 mm Hg (B). See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 5–6.)

Another common artifact in PAP measurement occurs when attempts to inflate the balloon cause the catheter tip to become obstructed and thus fail to measure intravascular pressure. This phenomenon is generally termed overwedging and usually is caused by distal catheter migration, with subsequent eccentric balloon inflation that forces the catheter tip against the pulmonary artery wall. Rather than recording intravascular pressure, the catheter now records the gradually rising pressure produced by the continuous flush system as it builds up pressure against the obstructed distal opening. (Fig. 30–40) Note that the overwedged pressure is devoid of pulsatile detail, much higher than PADP, and is continuously rising toward the flush pressure level. These observations all suggest that this cannot be an accurate measurement of PAWP.

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FIGURE 30–40 Overwedging of the pulmonary artery (PA) catheter causes artifactual waveform recordings. The first two attempts to inflate the PA catheter balloon (first two arrows) produce a nonpulsatile increasing pressure caused by an occluded catheter tip. After the catheter is withdrawn slightly, balloon inflation allows proper wedge-pressure measurement (third arrow). Prior to the third attempt at balloon inflation, the PA pressure lumen is flushed. This restores the appropriate pulsatile detailed to the PA and wedge-pressure waveforms on the right side of the trace. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 5–7.)

As emphasized earlier, each PAC balloon inflation allows the catheter tip to migrate distally several centimeters to reach the wedge position. This flotation process generally occurs over several cardiac cycles. “Instant wedge pressure” occurring before full balloon inflation suggests that the PAC is located inappropriately in a smaller, distal branch of the pulmonary artery. The catheter should be withdrawn before overwedging results in vascular injury or pulmonary infarction. A distally positioned catheter may overwedge itself without balloon inflation. This must be recognized immediately by observing the waveform, and the PAC must be withdrawn until a normal PAP tracing is restored.

Pathophysiologic conditions involving the left-sided cardiac chambers or valves produce characteristic changes in the PAP or PAWP waveforms. 422  One of the most widely recognized abnormalities is the tall v wave of mitral regurgitation (Fig. 30–41). Unlike a normal wedge pressure v wave produced by late systolic pulmonary venous inflow, which fills the left atrium while the mitral valve is closed, the prominent v wave of mitral regurgitation begins in early systole and might be more precisely designated a regurgitant c-v wave. Mitral regurgitation causes fusion of c and v waves and obliteration of the systolic x descent, as the isovolumic phase of left ventricular systole is eliminated owing to the retrograde ejection of blood into the left atrium. 292  Because the prominent v wave of mitral regurgitation is generated during ventricular systole, measurement of mean PAWP will result in overestimation of left ventricular filling pressure, just as measurement of mean CVP in patients with severe tricuspid regurgitation will result in overestimation of right ventricular filling pressure (see Fig. 30–29). In patients with severe mitral regurgitation, left ventricular end-diastolic pressure (LVEDP) is estimated best by measuring PAWP prior to onset of the regurgitant v wave ( Fig. 30–42; see Fig. 30–41). Although mean wedge pressure exceeds LVEDP in patients with mitral regurgitation, it remains a good approximation of mean LAP. Consequently, the regurgitant v wave contributes to left atrial hypertension and the subsequent risk of hydrostatic pulmonary edema.

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FIGURE 30–41 Mitral regurgitation. A tall regurgitant v wave (v) is seen in the pulmonary artery wedge pressure (PAWP) trace and also may be noted in the unwedged pulmonary artery pressure (PAP) waveform (arrow). See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 17–5.)

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FIGURE 30–29 Central venous pressure (CVP) changes in tricuspid valve disease. (A) Tricuspid regurgitation increases CVP and the waveform displays a tall systolic c-v wave that obliterates the x descent. In this example, the a wave is not seen because of atrial fibrillation. Right ventricular enddiastolic pressure is estimated best at the time of the electrocardiographic R wave (arrows) and is lower than mean CVP. See text for greater detail. (B) Tricuspid stenosis also increases mean CVP, but the characteristic venous waveform is different from the one seen in tricuspid regurgitation. The diastolic y descent is attenuated and the end-diastolic a wave is prominent. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Figs. 17–3 and 17–15.)

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FIGURE 30–42 Severe mitral regurgitation. A tall systolic v wave (v) is inscribed in the pulmonary artery wedge pressure (PAWP) trace and also distorts the pulmonary artery pressure (PAP) trace, giving it a bifid appearance. The electrocardiogram (ECG) is abnormal owing to ventricular pacing. Left ventricular end-diastolic pressure is estimated best by measuring PAWP at the time of the electrocardiographic R wave, prior to onset of the regurgitant v wave. Note that mean PAWP exceeds left ventricular enddiastolic pressure in this condition. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 17–11.)

When large v waves are present in the PAWP trace, it is critically important to recognize them and be able to distinguish the PAWP waveform from the unwedged PAP waveform. At first glance, a wedge trace with a tall systolic v wave resembles a typical unwedged PAP trace, but closer observation reveals a number of discriminating morphologic details. The PAP upstroke is steeper and slightly precedes the systemic arterial pressure upstroke, whereas a PAWP with a prominent v wave has a more gradual upstroke that begins after the radial artery pressure upstroke. Although the PAP peak occurs at about the same time as the systemic arterial pressure peak and the ECG T wave, the wedge pressure v wave reaches its peak later in the cardiac cycle, after the ECG T wave (see Figs. 30–41 and 30–42). 292, 398  This so-called “rightward shift” in the PAP waveform should be recognized by careful scrutiny and comparison of the ECG, systemic arterial, pulmonary artery, and wedge pressure traces. Another feature that distinguishes PAP and PAWP traces in patients with severe mitral regurgitation is the unusual morphology of the PAP waveform itself. The prominent regurgitant v wave distorts the PAP waveform, giving it a bifid appearance in systole and obscuring the normal end-systolic dicrotic notch (see Figs. 30–41 and 30–42). This is most evident in patients with the tallest wedge pressure v waves. 400, 423  By recognizing these subtle but important diagnostic details, a clinician may monitor the wedge pressure v wave by observing the unwedged PAP trace and obviate the need for repeated balloon inflation. Of greater importance, one should hope to avoid the disastrous situation in which a PAC migrates distally, becomes wedged unintentionally without balloon inflation, and the clinician, not recognizing the wedge tracing, attempts to inflate the balloon and thus causes pulmonary artery rupture.

Although some clinicians use the height of the PAWP v wave as an indicator of mitral regurgitation severity, this practice is fraught with problems and has some fundamental physiologic limitations. 292, 424, 425, 426, 427, 428  Because wedge pressure is a damped reflection of LAP, there may be some instances in which a prominent v wave is present in the LAP trace but is obscured in the wedge pressure trace. 429  More important, the PAWP v wave is a pressure surrogate for a volume event, namely regurgitant systolic flow, across the mitral valve. A closer look at left atrial pressure-volume relations helps to elucidate the apparently paradoxic coexistence of severe mitral regurgitation and a normal PAWP trace. 425, 430  Three factors determine whether mitral regurgitation produces a prominent v wave in the left atrial or wedge pressure traces: left atrial volume (often termed the patient‘s volume status), left atrial compliance, and volume of regurgitation (Fig. 30–43). Given that the left atrial pressure-volume relation is curvilinear, the same volume of regurgitation will result in a small increment in systolic pressure or a large increment in pressure, depending on the preexisting atrial volume at onset of systole. Similarly, the shape of the left atrial pressurevolume curve, which reflects atrial stiffness or compliance, will determine the height of the pressure wave for any given regurgitant volume. This may explain why patients with acute mitral regurgitation tend to have prominent PAWP v waves, in that they have smaller, stiffer left atria than patients with chronic valvular regurgitation. 426, 430  Although the total regurgitant volume of blood entering the left atrium will influence the height of v wave, this clearly is not the only determinant of v wave magnitude. Therefore, it is not surprising that wedge-pressure v waves are neither sensitive nor specific indicators of mitral regurgitation severity. 425, 426, 427, 428  Prominent PAWP v waves may exist in the absence of mitral regurgitation when LAP is elevated, which might occur when the left atrium is compressed, 431  and they also are seen commonly in patients with hypervolemia, congestive heart failure, and ventricular septal defect. 425  Note that the giant v waves seen in patients with ventricular septal defect have a different cause. They result from exaggerated antegrade systolic flow into the left atrium, caused by the left-to-right shunt, which increases pulmonary blood flow and systolic atrial filling through the pulmonary veins. 424 

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FIGURE 30–43 V wave height as an indicator of mitral regurgitation severity. Left atrial pressure–volume curves describe the three factors that determine v wave height. (A) Influence of left atrial volume. For the same regurgitant volume (x), the left atrial v wave will be taller if baseline atrial volume is greater (point B versus point A) (B) Influence of left atrial compliance. For the same regurgitant volume (x), the left atrial v wave will be taller if baseline atrial compliance is reduced (point B versus point A). (C) Influence of regurgitant volume. Beginning at the same baseline left atrial volume (points A and B), if regurgitant volume increases (X versus x), the left atrial pressure v wave will increase (V versus v). See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 17–13.)

In contrast to mitral regurgitation, which distorts the systolic portion of the PAWP waveform, mitral stenosis alters the morphology of the diastolic portions of this waveform. In this condition, the holodiastolic pressure gradient across the mitral valve results in an increased mean PAWP, a slurred early diastolic y descent, and a tall end-diastolic a wave. Similar hemodynamic abnormalities are seen in patients with left atrial myxoma or whenever there is obstruction to mitral flow. Diseases that increase left ventricular stiffness (e.g., left ventricular infarction, pericardial constriction, aortic stenosis, and systemic hypertension) produce changes in PAWP that resemble in part those seen in mitral stenosis. In these conditions, mean wedge pressure is increased and the trace displays a prominent a wave, but the y descent remains steep, because there is no obstruction to flow across the mitral valve during diastole. Because patients with advanced mitral stenosis often have coexisting atrial fibrillation, the prominent PAWP a wave will not be present in many of these cases, although the other hemodynamic features persist (Fig. 30–44). 292 

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FIGURE 30–44 Mitral stenosis. Mean pulmonary artery wedge pressure (PAWP) is increased (35 mm Hg), and the diastolic y descent is markedly attenuated. Compare the slope of the y descent in the PAWP trace with the y descent in the central venous pressure (CVP) trace. In addition, compare this PAWP y descent with the PAWP y descent in mitral regurgitation (see Figs. 30–41 and 30–42). A waves are not seen in the PAWP or CVP traces owing to atrial fibrillation. Arterial blood pressure (ART). See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 17–19.)

Myocardial ischemia is accompanied by a number of physiologic abnormalities that are detectable with the PAC. Ischemia impairs or delays left ventricular relaxation and produces diastolic dysfunction. This pattern of ischemia is particularly characteristic of demand ischemia associated with tachycardia or induced by rapid atrial pacing. 183, 432, 433, 434, 435, 436, 437  Impaired ventricular relaxation results in a stiffer, less compliant left ventricle in diastole, causing LVEDP to rise. Not only does this, in turn, increase LAP and PAWP, but the morphology of these waveforms changes as well, with the phasic a and v wave components becoming more prominent as diastolic filling pressure increases. 435, 438, 439, 440, 441, 442, 443, 444  Although myocardial ischemia will often be detectable as a rise in PAP, (diastolic, mean, or even systolic pressure), these changes are generally less striking than the accompanying change in wedge pressure and the appearance of tall a and v waves in the PAWP trace (Fig. 30–45). In patients with left ventricular ischemia, the tall PAWP a wave is produced by end-dia-stolic atrial contraction into a stiff, incompletely relaxed left ventricle, and underscores the fact that the atrial kick provides a greater than normal contribution to ventricular filling under these conditions. 315, 442, 445  Although the hallmark of left ventricular diastolic dysfunction is an elevated LVEDP, this pressure elevation often coexists with a reduced left ventricular end-diastolic volume. 183, 433  The astute clinician must recognize that an elevated diastolic PAP or wedge pressure in patients with myocardial ischemia may not indicate increased left ventricular preload.

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FIGURE 30–45 Myocardial ischemia. Pulmonary artery pressure (PAP) is relatively normal and mean pulmonary artery wedge pressure (PAWP) is only slightly elevated (15 mm Hg). However, PAWP morphology is markedly abnormal with tall a waves (21 mm Hg) resulting from the diastolic dysfunction seen in this condition. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 12–4.)

Myocardial ischemia produces a characteristic pattern of left ventricular systolic dysfunction in addition to the dia-stolic abnormalities noted earlier. Systolic dysfunction is the hallmark of supply ischemia, caused by a sudden reduction or cessation of coronary blood flow to a region of the myo-cardium. 434, 446  With severe systolic dysfunction, changes in global left ventricular pump performance may be detected with hemodynamic monitoring. As ejection fraction falls and left ventricular end-diastolic volume and LVEDP rise, hemodynamic monitoring will show systemic arterial hypotension and elevated diastolic PAP and wedge pressures. This hemodynamic pattern is uncommon during anesthesia and surgery and suggests severe systolic myocardial dysfunction. 447, 448, 449  A more common hemodynamic manifestation of myocardial ischemia occurs when left ventricular geometry is distorted or when the region of ischemic myocardium overlies a papillary muscle. 450  Acute mitral valve regurgitation may result, not because of any inherent abnormality of the mitral valve leaflets, but rather because of critical alterations in the supporting structures of the mitral valve, including the mitral annulus, chordae tendineae, papillary muscles, and underlying left ventricular myocardium. 450, 451  This form of mitral regurgitation is often termed “papillary muscle ischemia” or “functional mitral regurgitation.” As noted earlier, PAC monitoring is particularly well suited to detect this event by revealing the onset of new regurgitant v waves in the PAWP or PAP traces (see Figs. 30–41 and 30–42).

Whether the PAC should be used in all high-risk patients as a supplemental monitor for detection of myocardial ischemia remains debatable. 299, 452, 453, 454, 455  However, if physicians choose this form of monitoring, they should have a clear understanding of the mechanism by which ischemia alters PAP and PAWP, as well as an appreciation for the characteristic pressure waveform changes that will be produced. None of the current methods for detecting perioperative myocardial ischemia is perfectly sensitive or specific. Although patients with left ventricular ischemia are likely to have a higher mean PAWP than those without ischemia, these differences are small and may be difficult to detect clinically. 444  Furthermore, clear quantitative threshold values for mean wedge pressure or a and v wave peak pressures that are diagnostic of ischemic have not been identified, perhaps owing to the wide variation in these pressures in healthy individuals. 438, 439, 440, 441, 444  Consequently, the best approach is to integrate the PAC data with other monitored values and use changes in the PAWP or PAP as valuable parts of the diagnostic puzzle. 435, 456 

Right ventricular ischemia produces characteristic hemodynamic patterns that may be recognized with PAC monitoring. Just as left ventricular ischemia increases PAWP, right ventricular ischemia increases CVP and is one of the situations in which CVP may be higher than PAWP. In addition, CVP waveform morphology changes in a characteristic manner and displays a prominent a wave, resulting from right ventricular diastolic dysfunction, and a prominent v wave, resulting from ischemia-induced tricuspid regurgitation. 10, 287, 435, 457, 458  The CVP waveform in this condition is described as having an M or W configuration, referring to the tall a and v waves and steep x and y descents. 435  Severe pulmonary artery hypertension also may result in secondary right ventricular ischemia and dysfunction and increase CVP, but this condition is distinguished from primary right ventricular dysfunction because the PAP and pulmonary vascular resistance will be normal in the latter condition.

The CVP waveform in right ventricular infarction shares many morphologic features with that recorded from patients with restrictive cardiomyopathy or pericardial constriction, including elevated mean pressure, prominent a and v waves, and steep x and y descents. 458, 459  The pathophysiologic feature common to these conditions is impaired right ventricular diastolic compliance and is often termed “restrictive physiology.” In pericardial constriction, this arises from the restraining effect of the diseased pericardium, whereas in restrictive cardiomyopathy and right ventricular infarction, diastolic dysfunction impairs ventricular relaxation and increases intrinsic ventricular stiffness. Pericardial constriction, also termed constrictive pericarditis or pericardial restriction, limits cardiac filling because of the rigid, often calcified pericardial shell. Impaired venous return decreases end-diastolic volume, stroke volume, and cardiac output. Despite reduced cardiac volumes, cardiac filling pressures are markedly elevated and equal in all four chambers of the heart at end-diastole (Fig. 30–46). Although PAC monitoring reveals this pressure equalization, the characteristic M or W configuration is more apparent in the CVP trace than in the PAWP trace, most likely because of the damping effect of the pulmonary vasculature on the left-sided filling pressure as recorded by the PAC. 156, 158, 287, 460, 461, 462

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FIGURE 30–46 Pericardial constriction. This condition causes elevation and equalization of diastolic filling pressures in the pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP) traces. The CVP waveform reveals tall a and v waves with steep x and y descents and a mid-diastolic plateau wave (*) or h wave. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 18–1.)

Another hemodynamic hallmark of pericardial constriction is observed in the right and left ventricular pressure traces. These demonstrate rapid but short-lived early dia-stolic ventricular filling, which produces a diastolic “dip-and-plateau” pattern or “square root sign” (Fig. 30–47). 158, 463  In some cases, particularly when heart rate is slow, a similar waveform pattern may be noted in the CVP trace: a steep y descent (the diastolic dip) produced by rapid early diastolic flow from atrium to ventricle, followed by a mid-diastolic h wave (the plateau) from the interruption in flow imposed by the restrictive pericardial shell (see Figs. 30–46 and 30–47).

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FIGURE 30–47 Pericardial constriction. The diastolic filling abnormality in this condition inscribes a “dip-and-plateau pattern” or “square root sign” in both the right ventricular (RV) and right atrial (RA) pressure traces. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 18–3.)

Like pericardial constriction, cardiac tamponade impairs cardiac filling, but in the case of tamponade, a compressive pericardial fluid collection produces this effect. This results in a marked increase in CVP and a reduced cardiac diastolic volume, stroke volume, and cardiac output. Despite many similar hemodynamic features, tamponade and constriction may be distinguished by the different CVP waveforms seen in these two conditions. In tamponade, the venous pressure waveform appears more monophasic and is dominated by the systolic x pressure descent. The diastolic y pressure descent is attenuated or absent, because early diastolic flow from right atrium to right ventricle is impaired by the surrounding compressive pericardial fluid collection (Fig. 30–48). 156, 158, 287, 458, 460, 464, 465, 466  Clearly, other clinical and hemodynamic clues help distinguish these diagnoses, such as the presence of pulsus paradoxus, which is an almost invariable finding in cardiac tamponade (see Fig. 30–23). 467  CVP traces in pericardial constriction and cardiac tamponade thus have many similarities but also important distinguishing features. As a general rule, the CVP waveform in pericardial constriction has prominent x and y descents or a predominant y descent, whereas in cardiac tamponade, the venous pressure waveform shows attenuation or obliteration of the y descent. Coexisting abnormalities such as tachycardia, arrhythmias, and atrial contractile failure may complicate interpretation of these waveforms. 460, 461, 462, 464  On occasion, localized pericardial constriction may simulate valvular stenosis, and hypovolemia may lower cardiac filling pressures to within the normal range and confound the diagnosis. 158, 461, 462  In some instances, patients may show features of more than one condition, such as seen in patients with effusive-constrictive pericarditis who have constriction of the heart by the visceral pericardium in addition to a pericardial effusion that compresses the heart. 468 

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FIGURE 30–48 Cardiac tamponade. The central venous pressure waveform shows an increased mean pressure (16 mm Hg) and attenuation of the y descent. Compare with Figures 30–46 and 30–47. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 18–5.)

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FIGURE 30–23 Beat-to-beat variability in arterial pressure waveform morphologies. (A) Pulsus alternans. (B) Pulsus paradoxus. The marked decline in systolic arterial pressure and pulse pressure during spontaneous inspiration (arrows) is characteristic of this condition. (C) Systolic pressure variation. Compared with systolic blood pressure recorded at end expiration (1) a small increase occurs during positive pressure inspiration (2, D up) followed by a decrease (3, D down). Normally, total systolic pressure variation does not exceed 10 mm Hg. In this instance, the large D down indicates hypovolemia even though systolic arterial pressure and heart rate are relatively normal. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Figs. 18–10C, and 16–16.)

Probably the single most important waveform abnormality or interpretive problem in PAC monitoring is discerning the correct pressure measurement in patients receiving positive pressure ventilation. When any PAP or PAWP recording is used to estimate ventricular preload, the physician must consider the confounding effects of changes in intrathoracic pressure that occur during the respiratory cycle. Just as in the case of CVP monitoring, transmural cardiac filling pressures are estimated best when end-expiratory pressure values are recorded. (See previous sections discussing Cardiac Filling Pressure Monitoring; Physiologic Considerations: Diastolic Pressure-Volume Relations and Transmural Pressure, and Central Venous Pressure Waveforms.) During positive pressure mechanical ventilation, inspiration increases PAP and PAWP. By measuring these pressures at end-expiration, the confounding effect of this inspiratory increase in intrathoracic pressure is obviated (Fig. 30–49). 160  Forceful inspiration during spontaneous ventilation has the opposite impact on measured PAP and PAWP, but again, measurement of these pressures at end-expiration eliminates this confounding factor (see Fig. 30–30). Bedside monitors are designed with algorithms that aim to identify and report the numeric values for endexpiratory pressures. 469, 470, 471, 472  Unfortunately, these are notoriously inaccurate. The most reliable method for measuring central vascular pressures at end-expiration is examination of the waveforms on a calibrated monitor screen or paper recording. 472, 473 

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FIGURE 30–49 Influence of positive pressure mechanical ventilation on pulmonary artery pressure. Pulmonary artery pressure should be measured at end expiration (#1, 15 mm Hg) in order to obviate the artifact caused by positive pressure inspiration (#2, 22 mm Hg). Compare with Figure 30–30. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 16–3.)

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FIGURE 30–30 Respiratory influences on the measurement of central venous pressure (CVP). (A) During spontaneous ventilation, onset of inspiration (arrows) causes a reduction in intrathoracic pressure, which is transmitted to both the CVP and the pulmonary artery pressure (PAP) waveforms. CVP should be recorded at end-expiration (mean CVP 14 mmHg). (B) During positive pressure ventilation, onset of inspiration (arrows) causes an increase in intrathoracic pressure. CVP is still recorded at end-expiration (mean CVP 8 mmHg). See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Figs. 16–1 and 16–2.)