It is what we think we know already that often prevents us from learning.
Claude Bernard

Monitoring central venous pressure (CVP) and pulmonary artery occlusion (wedge) pressure are routine practices in critical care (1-3). Like all familiar practices, these measurements are not often scrutinized. As a result, they are often misinterpreted (4,5). Attention to the material in this chapter will help reduce errors in interpretation of these two measurements.



The zero reference point for venous pressures in the thorax is a point on the external thorax where the fourth intercostal space intersects the midaxillary line (i.e., the line midway between the anterior and posterior axillary folds). This point (called the phlebostatic axis) corresponds to the position of the right and left atrium when the patient is in the supine position. It is not a valid reference point in the lateral position, so CVP and wedge pressure should not be recorded when patients are placed in lateral positions (6).


The vascular pressure recorded at the bedside is an intravascular pressure; i.e., the pressure in the vessel lumen relative to atmospheric (zero) pressure. However, the vascular pressure that determines ventricular preload (stretch on the ventricular muscle) and the rate of edema formation is transmural pressure; i.e., the difference between the intravascular and extravascular pressures. Changes in thoracic pressures can cause a discrepancy between intravascular and transmural pressures. This discrepancy is illustrated by the respiratory variations in the CVP tracing shown in Figure 11.1. The intravascular pressure changes in this tracing are caused by respiratory variations in intrathoracic pressure that are transmitted into the lumen of the superior vena cava. If the changes in intrathoracic pressure are completely transmitted across the wall of the vessel, the transmural pressure remains constant throughout the respiratory cycle. (Because it is not possible to determine how much of the change in thoracic pressure is transmitted into the blood vessel in any individual patient, it is not possible to determine whether transmural pressure is absolutely constant.) Thus, changes in intravascular pressures in the thorax may not reflect physiologically important (transmural) pressure changes (7).


Intravascular pressures should be equivalent to transmural pressures when the extravascular pressure is zero. In the thorax, the extravascular pressure should be close to zero (i.e., atmospheric pressure) at the end of expiration. Therefore, intravascular pressures in the thorax should be measured at the end of expiration (1-3,7). The intrathoracic pressure at the end of expiration is positive relative to atmospheric pressure in patients who are actively exhaling (e.g., by grunting) and in the presence of positive end-expiratory pressure (PEEP) (8). In the latter situation, the vascular pressures should be measured while the patient is briefly removed from PEEP, or the level of PEEP should be subtracted from the pressures measured at end-expiration. The influence of active exhalation on end-expiratory pressures cannot be determined in individual patients without inducing muscle paralysis.

Pressure Monitors

If the oscilloscope display screens in the ICU are equipped with horizontal grids, the CVP and wedge pressures should be measured directly from the pressure tracings on the screen. The measurements obtained with this method are more accurate than digitally displayed pressures (9). If only digital pressure readings are available, the systolic pressure should be used in patients who are breathing spontaneously and the diastolic pressure should be used in patients receiving positive-pressure mechanical ventilators. The reason is that the digital display on most pressure monitors represents the pressure measured over specific time intervals (usually 4 seconds, or the time for one sweep across the oscilloscope screen). The systolic pressure is the highest pressure, the diastolic pressure is the lowest pressure, and the mean pressure is the integrated area under the pressure wave in each time period (Fig. 11.1). During spontaneous breathing, the pressure at the end of expiration is the highest pressure (i.e., systolic pressure), and during positive-pressure mechanical ventilation, the end-expiratory pressure is the lowest pressure (i.e., diastolic pressure). Therefore, systolic pressure should be used as the end-expiratory vascular pressure in patients who are breathing spontaneously, whereas diastolic pressure should be used in patients receiving mechanical ventilation. The mean pressure should never be used as a reflection of transmural pressure when there are respiratory variations in intravascular pressure (1-3,7).


Like any physiologic variable, vascular pressures in the thorax can vary spontaneously, without a change in the clinical condition of the patient. The spontaneous variation in wedge pressure is 4 mm Hg or less in 60% of patients, but it can be as high as 7 mm Hg in any individual patient (10). In general, a change in CVP or wedge pressure of less than 4 mm Hg should not be considered a clinically significant change.


Most vascular pressures are measured with electronic pressure transducers that record the pressure in millimeters of mercury (mm Hg). An alternative method of measuring pressure (usually reserved for CVP) is water manometry, where pressure is recorded in cm H2O (11). Because mercury is 13.6 times more dense than water (see Table A1.1), pressures measured in cm H2O are divided by 1.36 to convert the units to mm Hg:

CVP (in cm H2O)/1.36 = CVP (in mmHg)

The pressure correlations in cm H2O and mm Hg are shown in Table 11.1.


Few pressures in the ICU are misinterpreted as frequently, and as consistently, as pulmonary capillary wedge pressure (4,5,12). Probably the most important feature of the wedge pressure is what it is not:

Wedge pressure is not left-ventricular preload.

Wedge pressure is not pulmonary capillary hydrostatic pressure.

Wedge pressure is not a reliable measure for differentiating cardiogenic from noncardiogenic pulmonary edema.

These limitations are explained in the description of wedge pressure that follows.


When the pulmonary artery catheter is properly positioned, inflation of the balloon at the tip of the catheter causes the pulsatile pressure to disappear. This is demonstrated in Figure 11.2. As mentioned, the nonpulsatile pressure created by balloon inflation is considered to be the pressure in the pulmonary microcirculation; hence it is called pulmonary capillary wedge pressure (PCWP). The wedge pressure shown in Figure 11.2 is lower than the pulmonary artery diastolic pressure because the pressure tracing is from a patient with pulmonary hypertension. In the absence of pulmonary artery hypertension, the wedge pressure is usually within a few mm Hg of the pulmonary artery diastolic pressure (13). (The inflection point in Figure 11.2, indicated as the possible hydrostatic pressure, is explained later.)


The rationale for the wedge pressure measurement is illustrated in Figure 11.3 (13). Inflation of the balloon at the tip of pulmonary artery catheter obstructs blood flow and creates a static column of blood between the catheter tip and the left atrium. In this situation, the pressure at the tip of the pulmonary artery catheter should be the same as the pressure in the left atrium.

This condition is expressed by the hydraulic equation below (where Pc is capillary pressure, PLA is left-atrial pressure, Q is pulmonary blood flow, and Rv is pulmonary venous resistance).
Pc – PLA = Q x Rv
if Q = O,     Pc – PLA = O, and
Pc = PLA

Thus, balloon inflation allows the pulmonary artery catheter to measure the pressure in the left atrium. Because left-atrial pressure is normally the equivalent of left-ventricular end-diastolic pressure (LVEDP), the pulmonary capillary wedge pressure can be used as a measure of left-ventricular filling pressure. What the wedge pressure actually measures is the focus of the remainder of this chapter.


The wedge pressure is often used as a reflection of left-ventricular filling during diastole (i.e., ventricular preload). In Chapter 1, preload was defined as the force that stretched a muscle at rest, and the preload for the intact ventricle was identified as end-diastolic volume (EDV). However, wedge pressure is a measure of end-diastolic pressure, and end-diastolic pressure may not be an accurate reflection of preload (EDV) when the compliance (distensibility) of the ventricle is abnormal (see Fig. 1.1). Therefore, wedge pressure is a reflection of left-ventricular preload only when compliance of the ventricle is normal or constant (13,14).

Several conditions can alter ventricular compliance in patients in the ICU, such as ventricular hypertrophy, positive pressure ventilation, myocardial ischemia, and myocardial edema (e.g., after cardiopulmonary bypass surgery). Therefore, wedge pressure may not be a reliable index of left-ventricular preload in a large number of patients in the ICU.


The following conditions can influence the accuracy of the wedge pressure as a measure of left-atrial pressure.

Lung Zones

If the pressure in the surrounding alveoli exceeds capillary (venous) pressure, the pressure at the tip of the pulmonary artery (PA) catheter may reflect the alveolar pressure more than the pressure in the left atrium. This is illustrated in Figure 11.3. The lung in this figure is divided into three zones based on the relationship between alveolar pressure and the pressures in the pulmonary circulation (1-3,13). The most dependent lung zone (zone 3) is the only region where capillary (venous) pressure exceeds alveolar pressure. Therefore, wedge pressure is a reflection of left-atrial pressure only when the tip of the pulmonary artery catheter is located in zone 3 of the lung.

Catheter Tip Position

Although the lung zones shown in Figure 11.3 are based on physiologic rather than anatomic criteria, the lung regions below the left atrium are considered to be in lung zone 3 (1-3). Therefore, the tip of the pulmonary artery catheter should be positioned below the level of the left atrium to ensure that the wedge pressure is measuring left-atrial pressure. Most PA catheters are advanced into lung regions below the level of the left atrium (because of the higher blood flow in dependent lung regions). However, as many as 30% of PA catheters are positioned with their tips above the level of the left atrium (13). When patients are supine, routine portable (anteroposterior) chest x rays cannot be used to identify the catheter tip position relative to the left atrium. Rather, a lateral view of the chest is needed. However, lateral films have not gained favor for this use in most ICUs, probably because they are too time-consuming for the small percentage of improperly located catheter tips that will be revealed. Instead, catheter tips can be assumed to be positioned in zone 3 of the lung in all but the following conditions: when there are marked respiratory variations in the wedge pressure, and when PEEP is applied and wedge pressure increases by 50% or more of the applied PEEP (13).

Positive End-Expiratory Pressure

The presence of PEEP can reduce the area of zone 3 in the lung. In fact, when PEEP is combined with a low wedge pressure, there may be no zone 3 conditions in the lung, even in the most dependent lung regions. When this occurs, the wedge pressure is not an accurate reflection of left-atrial pressure, even when the catheter tip is below the level of the left atrium (13). Therefore, when PEEP is being applied, the wedge pressure should be measured while PEEP is temporarily discontinued (if this can be done without causing dangerous decreases in arterial oxygenation). PEEP can also be generated internally by patients who have inadequate emptying of the lungs during expiration (see Chapter 28). This type of intrinsic or auto-PEEP is common in patients with obstructive lung disease, particularly when they are breathing rapidly or receiving large inflation volumes during mechanical ventilation. A bedside maneuver that can help detect auto-PEEP is presented in Chapter 28.

Wedged Blood Gases

As many as 50% of the nonpulsatile pressures produced by balloon inflation represent damped PA pressures rather than pulmonary capillary pressures (15). Aspiration of blood from the catheter tip during balloon inflation can be used to identify a true wedge (capillary) pressure using the three criteria shown in Table 11.2. Although this is a cumbersome practice that is not used routinely, it seems justified when making important diagnostic and therapeutic decisions based on the wedge pressure measurement.


Even when wedge pressure is an accurate reflection of left-atrial pressure, there may be a discrepancy between wedge (left-atrial) pressure and LVEDP. This can occur under the following conditions (13).

Aortic insufficiency: LVEDP can be higher than PCWP because the mitral valve closes prematurely while retrograde flow continues to fill the ventricle.

Noncompliant ventricle: Atrial contraction against a stiff ventricle produces a rapid rise in end-diastolic pressure that closes the mitral valve prematurely. The result is a PCWP that is lower than LVEDP.

Respiratory failure: PCWP can exceed LVEDP in patients with pulmonary disease. The presumed mechanism is constriction of small veins in lung regions that are hypoxic (17).


Wedge pressure is often assumed to be a measure of hydrostatic pressure in the pulmonary capillaries. The problem with this assumption is that the wedge pressure is measured in the absence of blood flow. When the balloon is deflated and blood flow resumes, the pressure in the pulmonary capillaries is equivalent to the left-atrial (wedge) pressure only when hydraulic resistance in the pulmonary veins is negligible.This is expressed below, where Pc is capillary hydrostatic pressure, Rv is the hydraulic resistance in the pulmonary veins, Q is blood flow, and wedge pressure (PCWP) is substituted for left-atrial pressure.
Pc – PCWP = Q x Rv
if Rv = O,       Pc – PCWP = O

Pulmonary Venous Resistance

Unlike the systemic veins, the pulmonary veins contribute a significant fraction to the total vascular resistance across the lungs. (This is a reflection more of a low resistance in the pulmonary arteries than of a high resistance in the pulmonary veins.) As shown in Figure 11.4, 40% of the pressure drop across the pulmonary circulation occurs on the venous side of the circulation, which means that the pulmonary veins contribute 40% of the total resistance in the pulmonary circulation (16). Although this is derived from animal studies, the contribution in humans is probably similar in magnitude.

The contribution of the hydraulic resistance in the pulmonary veins may be even greater in critically ill patients because several conditions that are common in patients in the ICU can promote pulmonary venoconstriction. These conditions include hypoxemia, endotoxemia, and the acute respiratory distress syndrome (17,18). These conditions further magnify differences between wedge pressure and capillary hydrostatic pressure, as demonstrated below.

Wedge-Hydrostatic Pressure Conversion

Equation 11.4 can be used to convert wedge pressure (PCWP) to pulmonary capillary hydrostatic pressure (Pc). This conversion is based on the assumption that the pressure drop from the pulmonary capillaries to the left atrium (Pc – PLA) represents 40% of the pressure drop from the pulmonary arteries to the left atrium (Pa – PLA). Substituting wedge pressure for left-atrial pressure (i.e., PLA = PCWP) yields the following relationship:

Pc – PCWP = 0.4 (Pa – PCWP)
Pc = PCWP + 0.4 (Pa – PCWP)

For a normal (mean) pulmonary artery pressure of 15 mm Hg and a wedge pressure of 10 mm Hg, this relationship predicts the following:

Normal lung: Pc = 10 + 0.4 x (15 – 10)
Pc = 12 mmHg
Pc – PCWP = 2 mmHG

Thus, in the normal lung, wedge pressure is equivalent to capillary hydrostatic pressure. However, in the presence of pulmonary venoconstriction and pulmonary hypertension (e.g., in acute respiratory distress syndrome, ARDS), there can be a considerable difference between wedge pressure and capillary hydrostatic pressure. The example below is based on a mean PA pressure of 30 mm Hg and a venous resistance that is 60% of the total pulmonary vascular resistance.

ARDS:     Pc = 10 + 0.6 (30 – 10)
Pc = 22 mmHg
Pc – PCWP = 12 mmHg

Unfortunately, pulmonary venous resistance cannot be measured in critically ill patients, and this limits the accuracy of the wedge pressure as a measure of capillary hydrostatic pressure.


The transition from pulsatile pulmonary artery pressure to nonpulsatile wedge pressure in Figure 11.2 shows an initial rapid phase followed by a slower, more gradual pressure change. The initial rapid phase may represent the pressure drop across the pulmonary arteries, whereas the slower phase represents the pressure drop across the pulmonary veins. If this is the case, the inflection point marking the transition from the rapid to the slow phase represents the capillary hydrostatic pressure. Although this method can provide a more definitive determination of the capillary hydrostatic pressure than the equations used above, an inflection point is not often recognizable (19,20).


There are numerous sources of error in the interpretation of CVP and wedge pressure. Fortunately, with the ability to monitor cardiac output (Chapter 12) and systemic oxygen transport (Chapter 13), these pressures have become less important in the evaluation of hemodynamic status.


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