• P C van den Berg, C A Grimbergen, J A Spaan, and M R Pinsky.
• Department of Anesthesiology and Critical Care Medicine, University Hospital of Leiden, The Netherlands.
• J Crit Care. 1997 Jun 1; 12 (2): 56-65.

PurposeThe purpose of this study was to determine the dynamic changes in right ventricular (RV) and left ventricular (LV) output during positive airway pressure inspiratory hold maneuvers so as to characterize the interaction of processes in creating steady-state cardiac output during positive pressure ventilation.Materials And MethodsWe examined the disparity of RV and LV outputs at 5 seconds (early) and 20 seconds (late) into a 24-second inspiratory hold maneuver in 14 subjects in the intensive care unit immediately following coronary artery bypass surgery. RV output was measured by the thermodilution technique, whereas LV output was measured by the arterial pulse contour method. RV and LV volumes were also measured by thermal and radionuclide ejection fraction techniques, respectively.ResultsAs P(aw) was progressively increased from 0 to 20 cm H2O in sequential inspiratory hold maneuvers, both RV and LV outputs changed differently both at 5 seconds and 20 seconds into the inspiratory hold maneuvers. When expressed as change in cardiac output (L/min) for every cm H2O P(aw) increase relative to end-expiratory values, RV output increased at 5 seconds (0.05 +/- 0.15 L/min) then decreased at 20 seconds (-0.08 +/- 0.21, P < .05). LV output decreased slightly at 5 seconds (-0.14 +/- 0.22) and did not change from this minimal depressed level at 20 seconds (P < .05). Changes in RV and LV output were paralleled by changes in RV and LV end-diastolic volumes, respectively.ConclusionPositive pressure inspiration induces time-dependent changes in central hemodynamics, which are dissimilar between RV and LV function. Initially, inspiration increases RV output but decreases LV output, such that intrathoracic blood volume increases. However, sustained inspiratory pressures induce proportionally similar decreases in both RV and LV outputs. Thus, the hemodynamic effects of positive pressure ventilation will depend on the degree of lung inflation, the inspiratory time, and when measurements are made within the ventilatory cycle. These data also suggest that positive pressure ventilation with up to 20 cm H2) P(aw) does not significantly impair ventricular performance in humans.

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