Probing the limits of arterial pulse contour analysis to predict preload responsiveness.

T he management of hemodynamically unstable patients presents one of the most challenging experiences for the acute care physician, and incorrect treatment or delay in appropriate treatment results in markedly increased morbidity and mortality. Nowhere is this more obvious than in the perioperative care of the critically ill cardiac patient. Anesthesia-induced changes in arterial tone, myocardial stunning, impaired graph performance, altered peripheral vascular reactivity, rapid changes in core temperature, and varying blood rheology summate make the moment-to-moment assessment of cardiovascular status difficult. In this arena, assessment of preload responsiveness is highly useful. Numerous studies have documented the usefulness of direct measures of positive-pressure ventilation-induced variations on left ventricular output as a robust marker of preload responsiveness. For a fixed tidal volume (8–12 mL/kg), if stroke volume variation (SVV), directly measured using transesophageal echocardiographic techniques (1), or arterial pulsepressure variation (PPV) (2,3), as a surrogate of SVV, exceeds some minimal value, then cardiac output will increase if intravascular blood volume is increased by volume loading. Although highly predictive of preload responsiveness, transesophageal echocardiographic is not practical for the longitudinal management of cardiac patients because it requires a more chronic use of a complex device, echocardiography, the presence of an experienced operator, and significant patient discomfort. Although PPV is an accurate and validated method for defining preload responsiveness, it is still a surrogate of SVV. Thus, measures of SVV should be more accurate and potentially less influenced by changes in arterial vasomotor tone. Presently, two alternative bedside techniques are available to the clinician that may potentially measure SVV. They are the esophageal pulsed Doppler and arterial pulsed contour techniques. Of the two techniques, arterial pulse contour is presently receiving the most interest, primarily because SVV estimates are incorporated into existing vascular monitoring device display. Specifically, the Pulsion PiCCO thermodilution catheter system (Pulsion Medical, Inc, Cornelius, NC) displays a SVV number that it calculates from the variations in calculated left ventricular stroke volume over a short time interval. Excitingly, arterial pulse contour analysis may allow for the use of arterial pressure waveforms to calculate stroke volume and its change during ventilation. Thus, is would allow one to use this technique to define both PPV and SVV. Such an approach would be very attractive for several reasons: First, it would allow calculation of cardiac output changes and thus be a guide to assess global cardiovascular responsiveness to vasoactive therapies, such as fluid resuscitation and inotrope infusions. Second, because the ratio of PPV to SVV reflects central capacitor tone, and because the ratio of mean arterial blood pressure changes to SVV reflects arterial tone, this ratio could be used to continuously monitor arterial tone, a major determinant of cardiovascular performance. Finally, by noting the product of maximal pressure-to-stroke volume ranges over a breath, one would also know the operative cardiac power range, a primary output measure of ventricular pump function (4). Arterial pulse contour analysis is not a new technology but one described in the early 1940s. The calculation of stroke volume from the arterial pressure profile is based on the principle that the magnitude of the arterial pulse pressure and pressure decay profile describe a unique stroke volume for a given arterial input impedance. However, how the pressure profile is analyzed compared with the strength given to spectral power analysis, the weight given to resistive versus compliant elements, and mean arterial blood pressure vary among published algorithms. Numerous modifications of the original construct are continuously being proposed to address the fundamental Accepted for publication December 26, 2002. Address correspondence and reprint requests to Michael R. Pinsky, MD, Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, PA 15260. Address e-mail to pinskymr@ccm.upmc. edu.