Anesthesia Management |
|Chapter 30:||Cardiovascular Monitoring|
Central Venous Pressure Waveforms
Strictly speaking, CVP is the pressure at the junction of the vena cavae and the right atrium and reflects the driving force for filling the right atrium and ventricle. Because the large veins of the thorax, abdomen, and proximal extremities form a compliant reservoir for a sizable percentage of the total blood volume, CVP is highly dependent on intravascular blood volume and intrinsic vascular tone of these capacitance vessels. In other words, the CVP or right atrial pressure reflects the appropriateness of the blood volume to the capacity of the venous system. 282 In addition to providing a measure of the circulating blood volume, CVP reflects the functional capacity of the right ventricle. Based on the Frank-Starling mechanism, higher right heart filling pressures are required to maintain the ventricular stroke output when right ventricular contractility is impaired. Thus, in clinical practice, CVP monitoring is used for assessment of blood volume and right heart function.
CVP monitoring is performed using the same fluid-filled pressure tubingtransducer setup described earlier for direct arterial pressure monitoring (see the earlier section Technical Aspects of Direct Blood Pressure Measurement). Although a simple fluid-filled mechanical manometer may be used to estimate CVP, this method is not preferred for routine monitoring. First, manometric measurements are not as accurate as electronically transduced pressures and can only be measured intermittently, not displayed continuously. 283, 284, 285 Second, the use of an open manometer system may expose the patient to unnecessary risk of infection and venous air embolism. Finally, a wealth of information exists in the CVP waveform, which can be observed only by electronic transduction and display on a bedside monitor. 80
The normal mechanical events of the cardiac cycle are responsible for the sequence of waves seen in a typical CVP trace. The CVP waveform consists of five phasic events, three peaks (a, c, v) and two descents (x, y) (Table 30–5, Fig. 3027). 286, 287, 288 The most prominent wave is the a wave of atrial contraction, which occurs at end-diastole following the ECG P wave. The a wave increases atrial pressure and provides the atrial kick to fill the right ventricle through the open tricuspid valve. Atrial pressure decreases following the a wave, as the atrium relaxes. This smooth decline in pressure is interrupted by the c wave. This wave is a transient increase in atrial pressure produced by isovolumic ventricular contraction, which closes the tricuspid valve and displaces it toward the atrium. The c wave always follows the ECG R wave, because it is generated by the beginning of ventricular systole.
TABLE 30–5. Central Venous Pressure Waveform Components
|FIGURE 3027 Normal central venous pressure (CVP) waveform. The diastolic components (y descent, end-diastolic a wave) and the systolic components (c wave, x descent, end-systolic v wave) are all clearly delineated. A mid-diastolic plateau wave, the h wave, is also seen because heart rate is slow. Waveform identification is aided by timing the relation between individual waveform components and the electrocardiographic R wave, which is highlighted. Waveform timing using the arterial (ART) pressure trace is more confusing, owing to the relative delay in the systolic arterial pressure upstroke. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Fig. 25.)|
Atrial pressure continues its decline during ventricular systole, owing to continued atrial relaxation and changes in atrial geometry produced by ventricular contraction and ejection. This is the x descent or systolic collapse in atrial pressure. The x descent can be divided into two portions, x and x′, corresponding to the segments before and after the c wave. The last atrial pressure peak is the v wave, caused by venous filling of the atrium during late systole, while the tricuspid valve remains closed. The v wave usually peaks just after the ECG T wave. Atrial pressure then decreases, inscribing the y descent or diastolic collapse, as the tricuspid valve opens and blood flows from atrium to ventricle. (A final component of the CVP waveform, the h wave, occasionally appears as a pressure plateau in mid- to late diastole. The h wave is not normally seen unless the heart rate is slow and venous pressure is elevated. 289, 290 ) In summary, the normal venous waveform components may be remembered as follows: the a wave results from atrial contraction; the c wave from tricuspid valve closure and isovolumic right ventricular contraction; and the v wave from ventricular ejection, which drives venous filling of the atrium.
Thus, in relation to the cardiac cycle and ventricular mechanical actions, the CVP waveform can be considered to have three systolic components (c wave, x descent, v wave) and two diastolic components (y descent, a wave). By recalling the mechanical actions that generate the pressure peaks and troughs, it is easy to identify these waveform components properly by aligning the CVP waveform and the ECG trace and using the ECG R wave to mark end-diastole and the onset of systole. When the radial artery pressure trace is used for CVP waveform timing instead of the ECG, confusion may arise because the arterial pressure upstroke occurs nearly 200 milliseconds after the ECG R wave (see Fig. 3027). This normal physiologic delay reflects the times required for the spread of the electrical depolarization through the ventricle (»60 milliseconds), isovolumic left ventricular contraction (»60 milliseconds), transmission of aortic pressure rise to the radial artery (»50 milliseconds), and transmission of the radial artery pressure rise through fluid-filled tubing to the transducer (»10 milliseconds). 126, 145
The normal CVP peaks have been designated systolic (c, v) or diastolic (a) according to the phase of the cardiac cycle in which the wave begins. However, one generally identifies these waves not by their onset or upstroke, but rather by the location of their peaks. For instance, the a wave generally begins and peaks in end-diastole, but the peak may appear delayed to coincide with the ECG R wave, especially in a patient with a short PR interval. In this instance, a and c waves merge, and this composite wave is termed an a-c wave. Designation of the CVP v wave as a systolic event may be even more confusing. Although the ascent of the v wave begins during late systole, the peak of the v wave occurs during isovolumic ventricular relaxation, immediately prior to atrio-ventricular valve opening and the y descent. Consequently, the most precise description would be that the v wave begins in late systole, but peaks during isovolumic ventricular relaxation, the earliest portion of diastole. For clinical purposes, it is simplest to consider the v wave to be a systolic wave, and most authors have adopted this approach. 286, 289
Although three distinct CVP peaks (a, c, v) and two troughs (x, y) are discernible in the normal venous pressure trace, heart rate changes and conduction abnormalities alter this pattern. A short ECG PR interval causes fusion of a and c waves, and tachycardia reduces the length of diastole and the duration of the y descent, causing v and a waves to merge. In contrast, bradycardia causes each wave to become more distinct, with separate x and x′ descents visible and a more prominent h wave. Although there are circumstances in which other pathologic waves may be evident in the CVP trace, one should resist the temptation to assign physiologic significance to each small pressure peak, as many will arise as artifacts of fluid-filled tubing-transducer monitoring systems. Instead, search for the expected waveform components, including those waveforms that are characteristic of the pathologic conditions suspected.
Various pathophysiologic conditions may be diagnosed or confirmed by examination of the CVP waveform. One of the most common applications is the rapid diagnosis of cardiac arrhythmias. 291 In atrial fibrillation (Fig. 3028A), the a wave disappears and the c wave becomes more prominent, because atrial volume is greater at end-diastole and onset of systole, owing to the absence of effective atrial contraction. Occasionally, atrial fibrillation or flutter waves may be seen in the CVP trace, when the ventricular rate is slow. Isorhythmic atrioventricular dissociation or junctional (nodal) rhythm (Fig. 3028B) alters the normal sequence of atrial contraction prior to ventricular contraction. Instead, atrial contraction now occurs during ventricular systole, when the tricuspid valve is closed, thereby inscribing a tall cannon a wave in the CVP waveform. Absence of normal atrioventricular synchrony during ventricular pacing (Fig. 3028C) can be identified in a similar fashion by searching for cannon waves in the venous pressure trace. In these instances, the CVP helps diagnosis the cause of arterial hypotension; loss of the normal end-diastolic atrial kick may not be as evident in the ECG trace as it is in the CVP waveform.
|FIGURE 3028 Central venous pressure (CVP) changes caused by cardiac arrhythmias. (A) Atrial fibrillation obliterates the a wave, increases the c wave and preserves the v wave and y descent. This arrhythmia also causes variation in the electrocardiographic (ECG) R-R interval and left ventricular stroke volume, which can be seen in the ECG and arterial (ART) pressure traces. (B) Isorhythmic atrioventricular dissociation. In contrast to the normal end-diastolic a wave in the CVP trace (left panel), an early systolic cannon wave is inscribed (*, right panel). Reduced ventricular filling accompanying this arrhythmia causes a decreased arterial blood pressure. (C) Ventricular pacing. Systolic cannon waves are evident in the CVP trace during ventricular pacing (left panel). Atrioventricular sequential pacing restores the normal venous waveform and increases arterial blood pressure (right panel). ART scale left, CVP scale right. See text for greater detail. (From Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998: Figs. 141, 145, and 1416.)|
Right-sided valvular heart diseases alter the CVP waveform in different ways. 292 Tricuspid regurgitation (Fig. 3029A) produces abnormal systolic filling of the right atrium through the incompetent valve. A broad, tall systolic c-v wave is inscribed, which begins in early systole and obliterates the systolic x descent in atrial pressure. The CVP trace is said to be ventricularized, resembling right ventricular pressure. Note that this regurgitant wave differs in onset, duration, and magnitude from a normal CVP v wave caused by end-systolic atrial filling from the vena cavae. In patients with tricuspid regurgitation, right ventricular end-diastolic pressure is overestimated by the numeric display on the bedside monitor, which reports a single mean value for CVP. Instead, right ventricular end-diastolic pressure is estimated best by measuring the CVP value at the time of the ECG R wave, prior to the regurgitant systolic wave (see Fig. 3029A). Unlike tricuspid regurgitation, tricuspid stenosis (Fig. 3029B) is a diastolic defect in atrial emptying and ventricular filling. Mean CVP is elevated, and a pressure gradient exists throughout diastole between right atrium and ventricle. The a wave is unusually prominent and the y descent is slurred, owing to the impaired diastolic egress of blood from the atrium. Other conditions that reduce right ventricular compliance, such as right ventricular ischemia, pulmonary hypertension, or pulmonic valve stenosis, may produce a prominent end-diastolic a wave in the CVP trace but do not attenuate the early diastolic y descent. CVP waveform morphology changes in other characteristic ways in the presence of pericardial diseases and right ventricular infarction. These patterns are interpreted best in conjunction with PAP monitoring, which is discussed later.
|FIGURE 3029 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. 173 and 1715.)|
Perhaps the most important application of CVP monitoring is to provide an estimate of the adequacy of the circulating blood volume and right ventricular preload. As noted earlier, for this purpose, transmural CVP is always the pressure of physiologic interest. In clinical practice, however, we measure and record pressures referenced to ambient atmospheric pressure. Consequently, accurate interpretation of CVP requires the physician to consider alterations in intrathoracic or juxtacardiac pressure that occur during the respiratory cycle. 160, 178 During spontaneous breathing (Fig. 3030A), inspiration causes a decrease in pleural and juxta-cardiac pressures, which is transmitted, in part, to the right atrium and lowers CVP. This same decrease in pleural pressure will influence other measured central vascular pressures in a similar fashion (see Fig. 3030A). Note a subtle but critically important observation about the measurement of central vascular pressures. Although CVP measured relative to atmospheric pressure decreases during the inspiratory phase of spontaneous ventilation, transmural CVP, the difference between right atrial pressure and juxtacardiac pressure may actually increase slightly as more blood is drawn into the right atrium. The opposite pattern is observed during positive-pressure ventilation, in which inspiration increases intrathoracic pressure, raises the measured CVP, but decreases transmural CVP, because venous return is reduced by the elevated intrathoracic pressure. In clinical practice, transmural pressures are rarely measured, owing to difficulties in assessing juxtacardiac or intrathoracic pressure. Instead, end-expiratory values for cardiac filling pressures should be recorded in all patients, to provide the best estimate of transmural pressure. At the end of expiration, intrathoracic and juxtacardiac pressures approach atmospheric pressure, whether the patient is breathing spontaneously or receiving positive-pressure mechanical ventilation (Fig. 3030B). Proper pressure values can be determined by visual inspection of the CVP waveform on a calibrated monitor screen or paper recording. Under most circumstances, the transmural CVP and the end-expiratory value for CVP will be close to one another. This facilitates comparison of CVP values (and other cardiac filling pressures) obtained from the same patient under varying patterns of ventilation, a common situation in anesthesia and critical care.
|FIGURE 3030 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. 161 and 162.)|
Not only can individual CVP waveforms provide unique diagnostic clues about the circulation, but trends in CVP during anesthesia and surgery also are useful in estimating fluid or blood loss and guiding replacement therapy. It is important to remember that there is a significant range for normal values and that small changes in CVP may reflect significant changes in the circulating blood volume and right ventricular preload. Additional useful information may be derived from examining how a fluid bolus simultaneously alters CVP and other variables of clinical interest, such as the blood pressure, urine output, and so forth.
* The c wave observed in a jugular venous pressure trace may have a slightly more complex origin. This wave has been attributed to early systolic pressure transmission from the adjacent carotid artery and may be termed a carotid impact wave.289 Because the jugular venous pressure also reflects right atrial pressure, however, this c wave likely represents both arterial (carotid impact) and venous (tricuspid motion) origins.
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