The hemodynamic impact of positive end-expiratory pressure in acute respiratory distress syndrome and the underlying mechanisms have not been extensively investigated during low stretch ventilation. Our aim was to evaluate the hemodynamic effect of increasing positive end-expiratory pressure when tidal volume and the plateau pressure are limited and to explore the underlying mechanisms.
Medical intensive care unit.
Twenty-one acute respiratory distress syndrome patients ventilated with a tidal volume of 6.0 ± 0.5 mL/kg of predicted body weight.
Positive end-expiratory pressure was significantly increased from 5 ± 1 cm H2O to 13 ± 4 cm H2O for reaching a plateau pressure of 30 ± 1 cm H2O. At high positive end-expiratory pressure, passive leg raising was performed for increasing the central blood volume.
We performed echocardiography and pulmonary artery catheterization during positive end-expiratory pressure increase and during passive leg raising at high positive end-expiratory pressure.
With positive end-expiratory pressure elevation, the cardiac index decreased by 13% ± 9%. The right ventricular end-diastolic area, right atrial pressure, and pulmonary vascular resistance increased by 13% ± 20%, 34% ± 24% and 32% ± 31%, respectively (p < .01; p = .04; and p < .01 vs. baseline, respectively). The transpulmonary pressure difference (mean pulmonary artery pressure – pulmonary artery occlusion pressure) increased (p < .05). Both at low and high positive end-expiratory pressure, an acute cor pulmonale was observed in the same three (14%) patients. At high positive end-expiratory pressure, the passive leg raising significantly increased the right and left ventricular end-diastolic areas and right atrial pressure. Passive leg raising also decreased the transpulmonary pressure difference (p < .05), increased the cardiac index by 14% ± 10%, and decreased the pulmonary vascular resistance by 21% ± 20% (both p < .01 vs. baseline).
In acute respiratory distress syndrome patients, a positive end-expiratory pressure increase with limited tidal volume and plateau pressure reduced cardiac output by increasing the right ventricular afterload. Passive leg raising restored cardiac output by reducing the transpulmonary pressure difference and the pulmonary vascular resistance. This suggests that some pulmonary microvessels were collapsed by positive end-expiratory pressure elevation and were recruited by increasing the central blood volume.