Probing the Limits of Arterial Pulse Contour Analysis to Predict Preload Responsiveness (2003)

The 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 pulse-pressure 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 weakness of this computational approach (5). Not surprisingly, the algorithms used to calculate stroke volume by industry are proprietary, thus making any direct analysis of their ability to track actual stroke volume as arterial circuit conditions very difficult if not impossible. This is not a minor point of scientific interest but lies at the center of the Achilles’ heel of the technique. If changes in arterial tone occur, then the primary assumptions about the interaction between stroke volume and pressure also change, and the validity of a specific algorithm may be either retained or degraded. The determinants of arterial input impedance are complex because they reflect a lumped variable of the entire circulation, whereas actual vascular conductance among different arterial beds may vary significantly and rapidly in disease states (6). Accordingly, if either global arterial tone or blood flow distribution among vascular beds were to vary, then the relation between the arterial pressure profile and stroke volume may also vary. Because the weight to which specific aspects of the vascular conductivity used in constructing each algorithm is different, knowing that one method of pulse contour analysis is accurate under a given set of conditions does not mean that another method will also be accurate. Furthermore, arterial contour analyses have only been validated under steady-state conditions against indirect measures of cardiac output, such as the thermodilution or dye dilution techniques (7). Accordingly, the arterial pulse contour technique has not been validated to monitor rapid changes in stroke volume, as may occur over a single breath. It is these estimates of stroke volume change over a breath that are used to calculate SVV by the pulse contour technique. Potentially, rapid changes in stroke volume could induce non-steady-state changes in arterial vascular loading. However, the extent to which ventilation may alter the determinants of arterial input impedance used to calculate stroke volume is not known. As previously suggested, if this derived variable actually reflects true SVV, then it should closely parallel changes in PPV because the two are coupled. Regrettably, although several clinical studies using the PiCCO-derived SVV have appeared in the literature over the past 3 yr, none either simultaneously measured PPV or directly measured SVV using echocardiographic techniques (8–10). The lack of scientific rigor is unfortunate. Hopefully, some clinical trial will actually use a “gold standard” measure to define the validity of arterial pulse contour-derived SVV so that its usefulness and limitations in a specific clinical setting can be defined. Until such a study or studies are performed, various clinical trials using each specific arterial pulse contour device separately need to be compared to each other under the specific sets of clinical conditions studied and not to extrapolate too widely as to their application under conditions wherein arterial tone may change rapidly and unexpectedly. In that regard, the study by Wiesenack et al. (11) in this issue of the journal is very interesting. They examined the ability of the PiCCO-derived SVV to predict preload responsiveness (change in cardiac output in response to 7 mL/kg of 6% hydroxyethyl starch) in 20 cardiac surgery patients after the induction of anesthesia. Although fluid resuscitation induced a decrease in SVV, SVV did not predict the subsequent increase in either stroke volume or cardiac output. They conclude that PiCCO-derived SVV cannot be used in this patient population to predict preload responsiveness. In fact, other estimates of preload, known to be inaccurate, fared better than pulse contour-derived SVV in predicting preload responsiveness. These findings are in contrast to the studies of Reuter et al. (10), who showed that the PiCCO-derived SVV predicted preload responsiveness in cardiac surgery patients. One must ask why these two groups of investigators got divergent results. Importantly, the two studies are not completely similar, and these apparently minor differences may be at the center of the differences in SVV validity. First, and perhaps most important, Reuter et al. (10) used a large nonphysiological tidal volume (15 mL/kg) to induce SVV, whereas the Wiesenack et al. (11) study used a smaller tidal volume (10 mL/kg) that is still larger than that recommended for the long-term management of subjects with acute respiratory failure. The larger the tidal volume, the more often both true SVV and changes in non-steady-state arterial capacitance will occur, tending to make any pulse contour technique more accurate. Second, the cardiovascular states of the patients in the two studies were different. In the Reuter et al. (10) study, the subjects were stable, whereas in the Wiesenack et al. (11) study, they were relatively hypovolemic. Fluid resuscitation in a functionally hypovolemic patient would be expected to result in a greater reduction in arterial tone than that seen in a stable subject. Such changes in arterial tone may alter the relation between stroke volume and pulse contour-derived stroke volume. Third, in functionally hypovolemic patients, actual SVV will be less than PPV because arterial elastance will be increased (increased vasomotor tone). Thus, an accurate SVV signal may be less than expected for the same degree of PPV. But no matter what the reasons are for the inconsistencies among studies, the lack of any definitive studies comparing pulse contour-derived SVV with actual measures of SVV or PPV during positive-pressure ventilation should make the clinician wary of using this system for clinical decision making. Positive-pressure ventilation alters the arterial pressure power spectrum in the time domain, inducing phase-dependent changes in arterial impedance (12). Furthermore, Denault et al. (13) demonstrated that in cardiac surgery patients, this power variation might exceed that actual change in left ventricular stroke volume. As previously noted (14), the hemodynamic monitoring literature is in need of well designed validation studies that can address this fundamental issue for each specific patient group. Because the use of SVV assumes both the accurate measure of mean stroke volume and its degree of variation over a breath, both of which are important for the assessment of hemodynamic instability, until more accurate validation studies document its accuracy under specific clinical conditions, as exemplified by the data from the Wiesenack et al. (11) study, the use of arterial pulse contour-derived SVV for clinical decision making cannot be recommended.