Arterial Pressure Waveform Analysis During Hypovolemia

To the Editor: I read with great interest the work of Rooke et al. [1] describing the effect of graded hemorrhage on the systolic pressure variation (SPV) in humans. The authors have confirmed the results of our previous experimental and clinical papers, namely, that SPV and dDown (delta down) are reliable indicators of intravascular volume status [2-5]. They have also found, as expected, that the systolic pressure variation is very difficult to quantify in spontaneously breathing patients, since their tidal volume and inspiratory effort vary constantly. Their study, however, raises two questions. The first one concerns the dUp (delta up), which is the difference between the maximum and the end-expiratory (baseline) systolic pressures during one respiratory cycle. The authors found that the dUp increased during hemorrhage and decreased during volume replacement. These findings are in contradistinction to our previous studies, in which the dUp was nearly absent during hypovolemia, but was prominent during hypervolemia and/or congestive heart failure [2-4]. The dUp is the early increase in the systolic pressure during a mechanical breath and reflects a transient augmentation of left ventricular stroke output. Its main cause is an increase in the preload to the left ventricle due to squeezing of pulmonary blood. Brower et al. [6] have shown that such positive inspiratory pulmonary venous flow occurs only when the lung is in Zone III conditions and is absent during hypovolemia (when the lung is oligemic), which explains our dUp being absent during hypovolemia. A less common cause for a prominent dUp is the reduction in afterload that is associated with the increased intrathoracic pressure during inspiration. This mechanism may be operational in patients in congestive heart failure and was actually used to augment cardiac output by increasing airway pressure [7]. Thus, there is no logical explanation to Rooke et al.'s finding of an increased dUp during hypovolemia and a decreased dUp during retransfusion. The problem may be due to the difficulty of determining the end-expiratory systolic pressures that were used as the reference values for the measurement of dUp and dDown. The original method uses a short apnea of 5 s to accurately determine this reference pressure, and such apnea was not used in this study. Nevertheless, since the SPV is the difference between the maximum and minimum blood pressure values, it is unaffected by this reference pressure, and the SPV values reported in this study are correct and reliable. On the other hand, the values of the dDown may have been underestimated during hypovolemia and overestimated during volume replacement. The other problem relates to the determination of the dUp and dDown during spontaneous ventilation. As expected, Rooke et al. have found that one cannot use uneven spontaneous ventilation as a meaningful challenge of the cardiovascular system. They did, however, define the late increase in the systolic pressure during spontaneous exhalation as dUp, a fact that may throw unnecessary confusion into pressure waveform analysis. The expiratory increase in the systolic pressure during spontaneous ventilation may be due in part to an active expiratory effort (squeezing), which is different from the physiological nature of the dUp during mechanical ventilation. I therefore suggest that, as originally described, pressure waveform analysis should be limited to patients under controlled mechanical ventilation, and that the term dUp should be restricted to the early increase in systolic pressure during a mechanical breath.