© 2004 American Thoracic Society
More Respect for Respiratory Variation in Arterial PressureTo the Editor:We read with interest Dr. Magder's Clinical Commentary on the respiratory variations in arterial pressure (1). We would like to address the following comments. Prior studies have clearly demonstrated that respiration has complex effects on the filling and emptying of the right and left ventricles. Thus, it is somewhat surprising that Dr. Magder did not mention the effects of respiration on pulmonary circulation, ventricular interdependence, cardiac compliance, and pulmonary transit time. As a result, Dr. Magder ignored numerous prior contributions constructively addressing the physiologic basis of arterial pressure variation. We believe that only the rational analysis of the subtle heart–lung interactions helps to understand why stroke volume variation and hence arterial pressure variation give a reliable prediction of fluid responsiveness (2, 3). We also have great reticence to rely on the superposition of venous return and cardiac function curves (see Figures E2–E4, E6–E8, E10, and E13 in the online supplement to the Clinical Commentary) in explaining the physiologic determinants of the respiratory variation in arterial pressure. This framework may be useful to describe cardiac physiology under steady state conditions. However, we do not believe that this framework can be used to explain the transient effects of mechanical insufflation for at least two reasons: (1) the pulmonary circulation appears as a rigid tube interposed between the right atrium and the left ventricle, and this is not a tenable view, especially when respiratory changes in stroke volume are discussed; and (2) the transmural central venous pressure (the x axis of the cardiac function curve) and the intramural central venous pressure (the x axis of the venous return curve) do not vary in the same direction during mechanical insufflation: the transmural pressure decreases, whereas the intramural pressure increases. Dr. Magder raised doubts about the rationale for using the pulse pressure instead of the systolic pressure variation to predict fluid responsiveness (1). The pulse pressure depends on stroke volume and on arterial compliance (4); the systolic pressure depends on stroke volume, arterial compliance, and diastolic pressure (systolic pressure = pulse pressure + diastolic pressure). Therefore, from a physiologic point of view, pulse pressure is more closely related to stroke volume than systolic pressure. Furthermore, from a clinical point of view, pulse pressure variation works better than systolic pressure variation to predict fluid responsiveness (2, 5). Finally, the respiratory variation in arterial pressure has been validated as a predictor of fluid responsiveness only in mechanically ventilated and deeply sedated patients. No need to say that this may limit the clinical usefulness of pulse pressure variation in intensive care units (ICUs), as clearly indicated in previous studies (2, 3). Importantly, this limitation does not apply to most operating room patients, by far the largest field of application of this clinical tool. Predicting fluid responsiveness is a relevant question in patients with acute circulatory failure in whom we believe that increasing cardiac output could be beneficial. Fortunately, "most of ICU patients with acute circulatory failure are sedated and receiving mechanical ventilation" as stated a few years ago by Dr. Magder (6) when discussing the limitations of the inspiratory decrease in central venous pressure as a tool to predict fluid responsiveness. Although there is a trend in using a lower level of sedation during mechanical ventilation, the accurate assessment of respiratory mechanics (e.g., the measurement of airway plateau pressure or total positive end-expiratory pressure) frequently requires sedation, at least transiently. In this regard, Morelot-Panzini and colleagues (7) proposed to combine the analysis of arterial pressure variation with the evaluation of respiratory mechanics. This approach should extend the clinical usefulness of the respiratory variation in arterial pressure to most mechanically ventilated patients.
a Massachusetts General Hospital-Harvard Medical School Boston, Massachusetts FOOTNOTES Conflict of Interest Statement: F.M., D.C., and J.-L.T. do not have a financial relationship with a commercial entity that has an interest in the subject of this letter. REFERENCES
From the Author: I thank Dr. Michard and coworkers for their comments on my article (1). I fully agree that respiration has "complex effects" on the filling and emptying of the ventricles; however, my task was not to give a comprehensive analysis of this complex interaction, but rather to explain the phenomenon of arterial pulse variation and how it is affected by volume status. Too often authors describe all possible factors that impact on a phenomenon, many of which have only minimal quantitative effects, and truly important factors are not made clear. This confuses the audience and fails to give meaningful mechanisms. In their articles, Dr. Michard and coworkers described many aspects of heart–lung interaction but never actually explained how these processes produce the respiratory variations in arterial pressure or why the phenomena is volume responsive. My explanation does so very satisfactorily. Dr. Michard and coworkers raise two problems with the venous return–right heart interaction analysis. The first is that it does not account for pulmonary compliance and effect of changes in lung volume. In a classic article, which is not often quoted, Scharf and colleagues (2) showed that the increase in pleural pressure rather than the increase in transpulmonary pressure is the primary determinant of the decrease in cardiac output with positive-pressure ventilation (2). Furthermore, Denault and colleagues (3) showed that opening the chest removes respiratory variation in left ventricular volume and arterial pressure without a change in tidal volume. Thus, I based my analysis on the assumption that the change in pleural pressure is the dominant factor. The second criticism was that the venous return–cardiac function analysis does account for changes in transmural pressure. It certainly does. The movement of the cardiac function curve relative to the atmospheric reference point accounts for this. I agree with Dr. Michard and colleagues that pulse pressure was a better indicator in one study than the systolic pressure variation, but dDown (fall in pressure relative to end-expiratory value) really should be most representative of the fluid-responsive component, and this is likely better reflected in the pulse pressure change. Before writing my clinical perspective, it was not obvious to me that the proposed tests are only valid in patients with no respiratory effort, and I suspect that it was not obvious to others. The intensive care unit at my institution rarely has patients with no respiratory effort. Furthermore, even when studying patients in the operating room, which Dr. Michard has not done, differences in tidal volume, aortic compliance, peripheral resistance, and even abdominal pressure have important effects on quantitative predictions on the basis of respiratory variations in arterial pressure. I believe that Michard and coworkers need to have more respect for the limitations of these tests.
McGill University Health Centre Montreal, Quebec, Canada FOOTNOTES Conflict of Interest Statement: S.M. does not have a financial relationship with a commercial entity that has an interest in the subject of this letter. REFERENCES
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