Dauterman and colleagues [1] described the effect on the left ventricular pressure-volume relation of a sudden interruption in inferior vena caval inflow to the right heart during the first 10 to 15 seconds. Although the authors' observations are interesting from a physiologic standpoint, I fail to appreciate their claim regarding the clinical significance or relevance of these observations. First, the reduction in right ventricular filling in the clinical setting is rarely, if ever, as sudden and dramatic as was dictated by the experimental design of the study. Second, the subsequent resumption of flow to the right side of the heart is rarely that abrupt. Third, observations recorded under experimental conditions (which last only for several seconds) cannot be expanded to the clinical continuum. The authors showed that immediately after the interruption of inferior vena caval inflow, left ventricular diastolic pressures decreased. End-diastolic volume (preload), however, did not change, presumably because of the preservation of left ventricular inflow by right ventricular and pulmonary circulation reservoirs. Within a few additional seconds of inferior vena caval obstruction, however, the left ventricular pressure-volume relation deteriorated, and stroke volume decreased. It is inappropriate to discuss practical implications and provide general therapeutic guidelines on the basis of results of such abrupt, short-lived, and artificial experimental conditions. The authors' concluding remarks stating that "... by careful volume reduction ... a considerable portion of the resting left ventricular diastolic pressure can be lowered without necessarily compromising cardiac output" are true (cardiac output is indeed increased by lowering excessive preload); however, these observations have little to do with the results of the study: There was nothing "careful" about volume reduction in the experimental design, and cardiac output was uncompromised for only a few seconds.

When low-output states are being addressed, it is a well-established bedside practice to manipulate various determinants of cardiac output (preload, afterload, contractility, and heart rate), depending on which factors are responsible, and to gauge the response by measuring changes in cardiac output. On the basis of the results, strategies to optimize cardiac output can then be designed. Results of experiments based on a sudden interruption of right ventricular filling and its consequences during the first several seconds, although interesting from physiologic and experimental standpoints, are not relevant to clinical situations.