Hemodynamic effects of positive end-expiratory pressure applied as a ramp

Abstract

Hypotheses on the decrease in cardiac output due to positive end-expiratory pressure (PEEP) were tested during positive-pressure ventilation by application of PEEP from 0 to 15 cmH2O as a ramp input function, i.e., a continuous rise. Yorkshire pigs (n = 47, 5–7 wk old) were used under steady-state anesthesia (pentobarbital) and muscle relaxation. Cardiac output decreased nonlinearly in three distinct phases, I up to PEEP 3 cmH2O, II from 3 to 10 cmH2O, and III above 10 cmH2O, with the sharpest decline occurring in phase II. This three-phase cardiac output decrease was more pronounced when the individual responses were normalized to the inflection points between the phases. Heart rate did not change when related to PEEP, but when normalized to the inflection points a significant increase was observed in the phase I and III, whereas in phase II a decrease was evident. Based on a diversity of hemodynamic responses myocardial depression and right ventricular afterload were rejected as major causal mechanisms for the decrease of cardiac output. We hypothesized that the nonlinear response of cardiac output on PEEP is due to a combination of three types of mechanisms. First, the rise of central venous pressure with PEEP decreases cardiac output linearly. Second, the concomitant fall of arterial pressure elicits compensatory mechanisms, which flatten the slope of this venous return curve. Finally, above 3 cmH2O PEEP a lung stretch reflex is elicited, which performs an inhibitory effect on the circulation, causing the steeper fall in cardiac output as well as the decrease in heart rate in phase II.