The association of lung distention, PEEP and biventricular failure.

Although positive and expiratory pressure (PEEP) is known to depress the cardiac output, the mechanism remains debated. Two series of experiments were designed to explore this mechanism. In the first study, the application of 15 cm H(2)O of PEEP to nine anesthetized, ventilated dogs led to a reduction of cardiac index from (mean +/- one standard error of the mean) 2.71 L/min .m (2) +/- 0.35 to 2.19 L/min m(2) +/- 0.22 (p < .05) and a drop in mean arterial pressure (MAP) from 117 mm Hg +/- 8 to 91 mm Hg +/- 11 (p < .01). The mean net (vascular minus pleural pressure) pulmonary artery pressure (MPAP) rose from 15.3 mm Hg +/- 1.2 to 20.6 mm Hg +/- 1.8 (p < .02). The mean net central venous pressure (CVP) rose from 5.2 mm Hg +/- 0.9 to 8.4 mm Hg +/- 0.9 (p < .05) and the net pulmonary arterial wedge pressure (PAWP) rose from 6.7 mm Hg +/- 0.7 to 9.5 mm Hg +/- 0.9 (p < .01). There was a nonsignificant rise in the mean net left atrial pressure (LAP). As PEEP was raised in increments from 0 to 20 cm H(2)O, both LAP and PAWP increased. The rise in PAWP was always greater than the increase in LAP. The difference between PAWP and LAP was strongly correlated with the increase in MPAP (r = 0.98). This relationship was useful in correcting the PAWP during PEEP. The problem of cardiac depression was evaluated in a second series of eight dogs. These animals underwent complete chest wall excision to eliminate any possible direct effects of increased pleural pressure on the heart and great vessels. The absence of the chest wall permitted hyperexpansion of the lungs, particularly with positive end expiratory pressure. At 15 cm H(2)O of PEEP, the mean cardiac index fell in these animals from 2.36 L/min. m(2) +/- 0.26 to 1.47 L/min.m(2) +/- 0.18 (p < .01) and the MAP fell from 105 mm Hg +/- 16.2 to 68 mm Hg +/- 4.8 (p < .001). The CVP rose from a mean of 5.5 mm Hg +/- 0.4 to 8.3 mm Hg +/- 0.6 (p < .01) and the LAP rose from 6.3 mm Hg +/- 0.8 to 8.0 mm Hg +/- 1.1 (p < .05). The MPAP rose from 18.0 mm Hg +/- 0.6 to 23.3 mm Hg +/- 1.6 (p < .01). Comparison of Group I and II showed a significantly greater depression of the cardiac output and MAP in the open-chested animals. At the same time LAP was significantly higher. These data strongly suggest that PEEP and particularly pulmonary hyperinflation induce biventricular failure.