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Abnormal Pulmonary Artery and Wedge Pressure Waveforms

PAC monitoring is subject to the same technical artifacts inherent in all invasive pressure monitoring techniques,

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Figure 32-36 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). (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 5-6.)

as well as some additional problems unique to this method.[403] [450] [451] [452] 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 artifact observed in a PAC trace is a sharp pressure spike seen immediately after the ECG R wave at onset of systole ( Fig. 32-36 ).[450] [453] At this point in the cardiac cycle, tricuspid valve closure, right ventricular contraction, and ejection set the PAC in motion and inscribe a motion artifact in the pressure waveform. Note that this pressure artifact appears at the same time as the CVP c wave and may produce a factitiously low pressure or a pressure peak. If the bedside monitor detects this artifactual pressure nadir inappropriately, it may be erroneously designated as the pulmonary artery diastolic pressure (see Fig. 32-36 ). Repositioning the PAC by advancing or withdrawing it a few centimeters often ameliorates the problem.

Another common artifact in PAC pressure 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 is usually caused by distal catheter migration and eccentric balloon inflation that forces the catheter tip against the wall of the pulmonary artery. Rather


Figure 32-37 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). Before the third attempt at balloon inflation, the PA pressure lumen is flushed. Flushing restores the appropriate pulsatile pressure detailed to the PA and wedge pressure waveforms on the right side of the trace. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 5-7.)

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. 32-37 ). Note that over-wedged pressure is devoid of pulsatile detail, is much higher than pulmonary diastolic pressure, and continuously rises toward the flush pressure level. These observations all suggest that this cannot be an accurate measurement of PAWP.

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. When a wedge pressure tracing appears during partial balloon inflation, it 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 problem 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 pulmonary artery and wedge pressure waveforms ( Table 32-11 ). [454] One of the most widely recognized abnormalities is the tall v wave of mitral regurgitation ( Fig. 32-38 ). 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

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TABLE 32-11 -- Pulmonary artery wedge pressure waveform abnormalities
Condition Characteristics
Mitral regurgitation Tall regurgitant c-v wave

Obliteration of x descent
Ventricular septal defect Tall antegrade v wave
Mitral stenosis Tall a wave

Attenuation of y descent
Myocardial ischemia Tall a waves

Tall v waves

early systole and might be more precisely designated a regurgitant c-v wave. Mitral regurgitation causes fusion of the c and v waves and obliteration of the systolic x descent because the isovolumic phase of left ventricular systole is eliminated as a result of the retrograde ejection of blood into the left atrium.[312] Because the prominent v wave of mitral regurgitation is generated during ventricular systole, mean wedge pressure overestimates left ventricular filling pressure, just as measurement of mean CVP in patients with severe tricuspid regurgitation overestimates right ventricular filling pressure (see Fig. 32-26 ). In patients with severe mitral regurgitation, left ventricular end-diastolic pressure is estimated best by measuring wedge pressure before onset of the regurgitant v wave ( Fig. 32-38 and Fig. 32-39 ). Although mean wedge pressure exceeds left ventricular end-diastolic pressure in patients with severe mitral regurgitation, mean wedge pressure remains a good approximation of mean left atrial pressure. Consequently, the regurgitant v wave contributes to left atrial hypertension and the subsequent risk of hydrostatic pulmonary edema.

When large v waves are present in the wedge pressure trace, it is critically important to recognize them and be able to distinguish the wedge pressure 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


Figure 32-38 Mitral regurgitation. A tall regurgitant v wave (v) is seen in the pulmonary artery wedge pressure (PAWP) trace and may also be noted in the unwedged pulmonary artery pressure (PAP) waveform (arrow). (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 17-5.)


Figure 32-39 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, thus giving it a bifid appearance. The electrocardiogram (ECG) is abnormal because of ventricular pacing. Left ventricular end-diastolic pressure is estimated best by measuring PAWP at the time of the electrocardiographic R wave, before onset of the regurgitant v wave. Note that mean PAWP exceeds left ventricular end-diastolic pressure in this condition. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 17-11.)

steeper and slightly precedes the systemic arterial pressure upstroke, whereas a wedge tracing 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 Fig. 32-38 and Fig 32-39 ). [312] [429] 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 pulmonary artery and wedge pressure traces in patients with severe mitral regurgitation is the unusual morphology of the pulmonary artery waveform itself. The prominent regurgitant v wave distorts the pulmonary artery waveform by giving it a bifid appearance in systole and obscuring the normal end-systolic dicrotic notch (see Fig. 32-38 and Fig. 32-39 ). This is most evident in patients with the tallest wedge pressure v waves.[431] [455] 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 can avoid the disastrous situation in which a PAC migrates distally and becomes wedged unintentionally without balloon inflation and the clinician, not recognizing the wedge tracing, attempts to inflate the balloon and ruptures the pulmonary artery.

Although some clinicians use the height of the wedge pressure v wave as an indicator of the severity of mitral regurgitation, this practice is fraught with problems and has some fundamental physiologic limitations.[456] [457] [458] [459] [460] Because wedge pressure is a damped reflection of left

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atrial pressure, there may be some instances in which a prominent left atrial pressure v wave is not transmitted to the wedge pressure trace.[461] More important, the wedge pressure v wave is a pressure surrogate for a volume event, namely, regurgitant systolic filling across the incompetent mitral valve.

A closer look at the left atrial pressure-volume relationships helps explain the apparently paradoxical coexistence of severe mitral regurgitation and a normal PAWP trace.[457] [462] 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 regurgitant volume ( Fig. 32-40 ). Given that the left atrial pressure-volume relationship is curvilinear, the same volume of regurgitation will result in a variable increment in systolic pressure, depending on the preexisting atrial volume at the onset of systole. Similarly, the shape of the left atrial pressure-volume curve, which reflects atrial stiffness or compliance, will determine the height of the pressure wave for any given regurgitant volume. Accordingly, patients with acute mitral regurgitation tend to have tall wedge pressure v waves because they have smaller, stiffer left atria than do patients with chronic valvular regurgitation. Although the total regurgitant volume of blood entering the left atrium will influence the height of the v wave, this is clearly 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 the severity of mitral regurgitation.[457] [458] [459] [460] Prominent wedge pressure v waves may exist in the absence of mitral regurgitation when left atrial pressure is high, as might occur when the left atrium is compressed.[463] Tall v waves are also seen commonly in patients with hypervolemia, congestive heart failure, and ventricular septal defects.[457] Note that the giant v waves observed in patients with ventricular septal defects are not caused by retrograde flow, but rather by excessive antegrade systolic flow into the left atrium from the left-to-right shunt, which increases pulmonary blood flow and systolic atrial filling through the pulmonary veins.[456]


Figure 32-40 Height of the v wave as an indicator of the severity of mitral regurgitation. Left atrial pressure-volume curves describe the three factors that determine the height of the v wave. 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). (Redrawn 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 wedge pressure 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 wedge pressure, 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 wedge pressure 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 of the absence of obstruction to flow across the mitral valve during diastole. Because patients with advanced mitral stenosis often have coexisting atrial fibrillation, the a wave will not be present in many of these cases, although the other hemodynamic features persist ( Fig. 32-41 ).[312]

Myocardial ischemia is accompanied by a number of physiologic abnormalities that are detectable with the PAC. Ischemia impairs left ventricular relaxation and thereby results in diastolic dysfunction. This pattern of ischemia is particularly characteristic of the demand ischemia associated with tachycardia or induced by rapid atrial pacing.[295] [464] [465] [466] [467] [468] [469] Impaired ventricular relaxation results in a stiffer, less compliant left ventricle in diastole, which leads to increased left ventricular end-diastolic pressure. Not only does this, in turn, increase left atrial and wedge pressure, 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.[467] [470] [471] [472] [473] [474] [475] [476] Although myocardial ischemia will often be detectable as a rise in pulmonary artery diastolic, mean, or systolic pressure, these changes are generally less striking than the accompanying change in wedge pressure and the new appearance of tall a and v waves ( Fig. 32-42 ). In patients with left ventricular ischemia, the tall wedge pressure a wave is produced by

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Figure 32-41 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 Fig. 32-38 and Fig. 32-39 ). Because of atrial fibrillation, a waves are not seen in the PAWP or CVP traces. ART, arterial blood pressure. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 17-19.)


Figure 32-42 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. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 12-4.)

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end-diastolic 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.[425] [474] [477] Although the diastolic dysfunction accompanying myocardial ischemia leads to an increase in left ventricular end-diastolic pressure, this pressure elevation often coexists with decreased left ventricular end-diastolic volume or preload.[295] The dissociation between filling pressure and filling volume in this condition must be appreciated to avoid diagnostic and therapeutic errors.

Myocardial ischemia produces a characteristic pattern of left ventricular systolic dysfunction in addition to the diastolic 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 myocardium.[466] [478] With severe systolic dysfunction, changes in global left ventricular contractile performance may be detected with hemodynamic monitoring. As the ejection fraction falls and left ventricular end-diastolic volume and pressure rise, hemodynamic monitoring will show systemic arterial hypotension and elevated pulmonary diastolic and wedge pressure. This hemodynamic pattern is uncommon during anesthesia and surgery and suggests severe systolic myocardial dysfunction. [479] [480] [481] A more common hemodynamic manifestation of myocardial ischemia occurs when left ventricular geometry is distorted or when the region of ischemic myocardium underlies a papillary muscle.[482] 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.[482] [483] 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 pulmonary artery or wedge pressure trace (see Fig. 32-38 and Fig. 32-39 ).

Whether the PAC should be used in high-risk patients as a supplemental monitor for detection of myocardial ischemia remains uncertain.[484] [485] [486] [487] However, if physicians choose this form of monitoring, they should have a clear understanding of the mechanism by which ischemia alters pulmonary artery and wedge pressure and an appreciation for the anticipated pressure waveform changes. None of the current methods of detecting perioperative myocardial ischemia is perfectly sensitive or specific. Although patients with left ventricular ischemia are likely to have higher mean wedge pressure than those without ischemia, these differences are small and may be difficult to detect clinically.[476] Furthermore, clear quantitative threshold values for mean wedge pressure or a and v wave peak pressures that are diagnostic of ischemia have not been identified, perhaps because of the wide variation in the normal range of these pressures. Consequently, when a PAC is used to diagnose myocardial ischemia, the best approach is to integrate the PAC data with other monitored values and use changes in pulmonary artery or wedge pressure as parts of the diagnostic puzzle.[467] [488]

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 this is one of the few situations in which CVP may be higher than wedge pressure. 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.[11] [306] [467] [489] [490] The CVP waveform in this condition is described as having an M or W configuration, which refers to the tall a and v waves and steep x and y descents. Severe pulmonary artery hypertension may also result in secondary right ventricular ischemia and dysfunction and increased CVP, but this condition is distinguished from primary right ventricular dysfunction in that PAP and the calculated PVR are not increased 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.[489] [491] 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. 32-43 ). 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.[167] [492] [493] [494]

Another hemodynamic hallmark of pericardial constriction is observed in the right and left ventricular pressure traces. These traces demonstrate rapid, but short-lived early diastolic ventricular filling, which produces a diastolic "dip-and-plateau" pattern or "square root sign" ( Fig. 32-44 ).[166] [495] In some cases, particularly when the 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 the atrium to the ventricle, followed by a mid-diastolic h wave (the plateau) from the interruption in flow imposed by the restrictive pericardial shell (see Fig. 32-43 and Fig. 32-44 ).

Like pericardial constriction, cardiac tamponade impairs cardiac filling, but in the case of tamponade, a compressive pericardial fluid collection produces this effect. This filling defect results in a marked increase in CVP and reduced cardiac diastolic volume, stroke volume, and cardiac output. Despite many similar hemodynamic features, tamponade and constriction may be distinguished by the

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Figure 32-43 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 (asterisk) or h wave. ART, arterial blood pressure. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 18-1.)

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 the right atrium to the right ventricle is impaired by the surrounding compressive pericardial fluid collection ( Fig. 32-45 ).[166] [167] [489] [492] [496] [497] [498] 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. 32-19 ).[499] 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. 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. In some instances, patients may show features of more than one condition, such as seen in patients with effusive-constrictive


Figure 32-44 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. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 18-3.)

pericarditis who have constriction of the heart by the visceral pericardium in addition to a pericardial effusion that compresses the heart.[500]

Probably the single most important waveform abnormality or interpretive problem in PAC monitoring is discerning the correct pressure measurement in patients receiving positive-pressure mechanical ventilation or those who have labored spontaneous respiration. When any pulmonary artery or wedge pressure 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 the earlier section "Physiologic Considerations for Central Venous Pressure Monitoring: Diastolic Pressure-Volume Relationships and Transmural Pressure"). During positive-pressure mechanical ventilation,

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Figure 32-45 Cardiac tamponade. The central venous pressure waveform shows an increased mean pressure (16 mm Hg) and attenuation of the y descent. Compare with Figure 32-43 and Figure 32-44 . (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 18-5.)

inspiration increases pulmonary artery and wedge pressure. By measuring these pressures at end-expiration, the confounding effect of this inspiratory increase in intrathoracic pressure is obviated ( Fig. 32-46 ). [303] Forceful inspiration during spontaneous ventilation has the opposite effect, but again, measurement of these pressures at end-expiration eliminates this confounding factor (see Fig. 32-27 ). Bedside monitors are designed with algorithms that aim to identify and report the numeric values for end-expiratory pressures.[501] [502] [503] [504] Unfortunately, these algorithms 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.[504] [505]

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