Normal Central Venous Pressure Waveforms

Strictly speaking, CVP is the pressure at the junction of the venae cavae and right atrium and reflects the driving force for filling the right atrium and ventricle. Because the large

TABLE 32-7 -- Normal cardiovascular pressures

Pressure	Average (mm Hg)	Range (mm Hg)
Right Atrium
a wave	6	2–7
v wave	5	2–7
Mean	3	1–5
Right Ventricle
Peak systolic	25	15–30
End-diastolic	6	1–7
Pulmonary Artery
Peak systolic	25	15–30
End-diastolic	9	4–12
Mean	15	9–19
Pulmonary Artery Wedge
Mean	9	4–12
Left Atrium
a wave	10	4–16
v wave	12	6–21
Mean	8	2–12
Left Ventricle
Peak systolic	130	90–140
End-diastolic	8	5–12
Central Aorta
Peak systolic	130	90–140
End-diastolic	70	60–90
Mean	90	70–105

veins of the thorax, abdomen, and proximal ends of the extremities form a compliant reservoir for a sizable percentage of the total blood volume, CVP is highly dependent on the intravascular blood volume and intrinsic vascular tone of these capacitance vessels. In other words, CVP or right atrial pressure reflects the appropriateness of the blood volume to the capacity of the venous system.^[304] 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 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.^[305] Normal CVP in an awake, spontaneously breathing patient ranges between 1 and 7 mm Hg.

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 32-8 , Fig. 32-24 ). ^{[306] [307] [308]} The most prominent wave is the a wave of atrial contraction, which occurs at end-diastole after 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 after 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 during the onset of ventricular systole. (Note that the c wave observed in a jugular venous pressure trace might 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.^[309] Because jugular venous pressure also reflects right atrial pressure, however, this c wave probably represents both arterial [carotid impact] and venous [tricuspid motion] origins.)

Atrial pressure continues its decline during ventricular systole because of continued atrial relaxation and

TABLE 32-8 -- Central venous pressure waveform components

Waveform Component	Phase of Cardiac Cycle	Mechanical Event
a wave	End-diastole	Atrial contraction
c wave	Early systole	Isovolumic ventricular contraction, tricuspid motion toward the right atrium
v wave	Late systole	Systolic filling of the atrium
h wave	Mid to late diastole	Diastolic plateau
x descent	Midsystole	Atrial relaxation, descent of the base, systolic collapse
y descent	Early diastole	Early ventricular filling, diastolic collapse

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Figure 32-24 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 the heart rate is slow. Identification of the waveform is aided by timing the relationship between individual waveform components and the electrocardiographic R wave. Timing of the waveform with the arterial pressure (ART) trace is more confusing because of the relative delay in systolic arterial pressure upstroke. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 2-5.)

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. 32-24 ). This normal physiologic delay reflects the times required for the spread of electrical depolarization through the ventricle (≅60 milliseconds), isovolumic left ventricular contraction (≅60 milliseconds), transmission of the increase in aortic pressure to the radial artery (≅50 milliseconds), and transmission of the increase in radial artery pressure through fluid-filled tubing to the transducer (≅10 milliseconds).^{[113] [136]}

The normal CVP peaks are 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, the 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 ascent of the v wave begins during late systole, the peak of the v wave occurs during isovolumic ventricular relaxation, immediately before opening of the atrioventricular valve 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.

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 the a and c waves, and tachycardia reduces the length of diastole and the duration of the y descent, which causes the 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 in some circumstances other pathologic waves may be evident in the CVP trace, one should resist the temptation to assign physiologic significance to each small pressure peak because many will arise as artifacts of fluid-filled tubing-transducer monitoring systems. Instead, search for the expected waveform components, including the waveforms that are characteristic of the pathologic conditions suspected.