Cardiac Preload Assessment beyond the Pulmonary Artery Catheter: Systolic Pressure Variation and Other Dynamic Indicators

The starting point for resuscitation of a patient with circulatory failure is intravascular volume expansion to optimize cardiac preload. Goal-directed resuscitation is predicated on the availability of monitored information that accurately indicates whether specific hemodynamic goals are being achieved, including a measure of cardiac preload such as CVP or PAWP. As noted in the earlier discussion of CVP and PAC monitoring, use of these filling pressure surrogates for ventricular preload is subject to a number of confounding variables that complicate their interpretation. Moreover, these cardiac filling pressures are static indicators of preload: they may be in the low, normal, or high range, but not necessarily "optimal" for a given patient in a particular clinical setting.

Figure 32-52 Systolic pressure variation. When compared with systolic blood pressure recorded at end-expiration (1), a small increase occurs during positive-pressure inspiration (2, Δ Up), followed by a decrease (3, Δ Down). Normally, the total variation in systolic pressure does not exceed 10 mm Hg. In this instance, the large Δ Down indicates hypovolemia even though systolic arterial pressure and the heart rate are relatively normal. (Redrawn from Mark JB: Atlas of Cardiovascular Monitoring. New York, Churchill Livingstone, 1998, Fig. 16-16.)

Rather than these traditional static markers of cardiac filling, newer dynamic markers of volume responsiveness have been described that may provide more useful information for determining the appropriate end points for fluid resuscitation. ^[600] The variations in arterial blood pressure observed during positive-pressure mechanical ventilation are the most widely studied of these dynamic indicators of cardiac preload. These changes in blood pressure are readily observed on the bedside monitor in patients who are undergoing direct arterial blood pressure monitoring, and they result from changes in intrathoracic pressure and lung volume that occur during the respiratory cycle.^{[601] [602] [603] [604]}

During positive-pressure inspiration, increasing lung volume compresses and displaces the pulmonary venous reservoir and propels it into the left heart chambers, thereby increasing left ventricular preload. Simultaneously, the increase in intrathoracic pressure reduces left ventricular afterload. The increase in left ventricular preload and decrease in afterload produce an increase in left ventricular stroke volume and an increase in systemic arterial pressure. In most patients, the preload effects are more important, but in patients with severe left ventricular systolic failure, the reduction in afterload plays an important role in increasing left ventricular ejection. At the same time that left heart filling is increasing during early inspiration, the rising intrathoracic pressure causes a decrease in systemic venous return and right ventricular preload. The increased lung volume may also increase PVR slightly and thereby increase right ventricular afterload. These effects combine to reduce right ventricular ejection during inspiration.

Toward the end of inspiration or during early expiration, the reduced right ventricular stroke volume that occurred during inspiration crosses the pulmonary vascular bed and leads to reduced left ventricular filling. As a result, left ventricular stroke volume falls, and systemic arterial blood pressure decreases. This cyclic variation in systemic arterial pressure may be measured and quantified as the systolic pressure variation (SPV).^[303]

SPV is often subdivided into inspiratory and expiratory components by measuring the increase (Δ Up) and decrease (Δ Down) in systolic pressure in relation to the end-expiratory, apneic baseline pressure ( Fig. 32-52 ). In a mechanically ventilated patient, the normal SPV is 7 to 10 mm Hg, with Δ Up being 2 to 4 mm Hg and Δ Down

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In a heterogeneous group of intensive care patients, Marik demonstrated that a large SPV (>15 mm Hg) was highly predictive of a low PAWP (<10 mm Hg). ^[610] Using echocardiography to measure the left ventricular cross-sectional area as a surrogate for preload, Coriat and colleagues found Δ Down to be a better predictor of preload than wedge pressure was.^[606]

Other uses of SVP focus on changes in the Δ Up portion of the arterial pressure trace. Just as Δ Down may reveal changes in cardiac preload, the Δ Up portion of the arterial pressure trace may provide clues to the afterload dependence of the left ventricle. Preliminary evidence suggests that a marked increase in Δ Up during positive-pressure inspiration occurs when the increased pleural pressure reduces transmural left ventricular pressure sufficiently that left ventricular stroke output increases in the failing, afterload-dependent left ventricle.^{[602] [603] [604] [611]}

As a dynamic indicator of cardiac preload, SPV and Δ Down provide valuable clinical information beyond that provide by static preload indicators such as CVP or wedge pressure. It appears that the magnitude of blood pressure variation accurately predicts patients who will subsequently respond to a volume challenge by increasing stroke volume and cardiac output. Using receiver-operator curve analysis, Tavernier and coworkers showed that the magnitude of Δ Down was a far better indicator of volume responsiveness than PAWP or echocardiographically derived left ventricular end-diastolic area was.^[612]

Although most monitoring trials to date have examined SPV and Δ Down as indicators of preload, other closely related variables have also been found to be useful clinical measures of volume responsiveness. Some authors have suggested that rather than measure absolute SPV, focusing on Δ Down as a percentage of the systolic pressure during apnea will provide a more accurate measure of volume status, particularly in patients with large changes in blood pressure or significant arterial hypotension.^[613] Another dynamic marker of preload based on arterial waveform analysis has been the pulse pressure variation (PPV), defined as the maximal difference in arterial pulse pressure measured over the course of the positive-pressure respiratory cycle divided by the average of the maximal and minimal pulse pressures.^{[609] [614] [615]} Normal PPV should not exceed 13%.^[609] Finally, new pulse contour methods for measurement of cardiac output (see later) allow on-line measurement of variations in left ventricular stroke volume, so-called stroke volume variation (SVV).^{[609] [616]} Like the other related dynamic indicators of cardiac preload, the normal SVV is approximately 10%, and greater variability accurately predicts a positive response to a fluid challenge.^{[609] [616]}

Despite rapidly accumulating evidence for the value of SPV and its related measures as accurate predictors of cardiac preload, these measures have not found widespread clinical adoption for a number of reasons. The original description of this method required transient interruption of mechanical ventilation to identify an apneic baseline for measurement of Δ Down and Δ Up.^[605] More recently, Schwid and Rooke have shown that use of the end-expiratory value for systolic blood pressure serves as an alternative suitable baseline that does not require a change in the pattern of ventilation.^[617] Although an automated method for continual computation and display of SPV by the bedside monitor is not widely available, computer-derived measurements appear to be accurate and could be incorporated into newer monitoring devices.^{[618] [619]}

Finally, a large number of clinical factors preclude wider application of this technique. Although cyclic changes in systemic arterial pressure are often observed during spontaneous ventilation, using SPV to predict hypovolemia has been well validated only in patients receiving positive-pressure mechanical ventilation. Among other things, the tidal volume and changes in intrathoracic pressure during spontaneous ventilation are too variable from breath to breath for accurate interpretation of these respiratory-circulatory interactions.^[605] The magnitude of the SPV observed in any patient will be influenced by positive-pressure ventilatory parameters, including tidal volume and peak inspiratory pressure. Values will be further confounded by the presence of arrhythmias, changes in chest wall and lung compliance, the addition of PEEP, and other pulmonary pathology.^[619] As a final point, the physiologic basis for SPV is not entirely related to the changes in left ventricular preload described earlier,^[620] and some studies have suggested that SPV is not as accurate as other more traditional measures (left ventricular area or wedge pressure) during severe hemorrhagic hypovolemia. ^[621]