Cardiovascular effects of positive end-expiratory pressure during acute left ventricular failure in dogs

Haemodynamic and metabolic effects of ventilation with positive end-expiratory pressure (PEEP) were studied in closed-chest dogs anaesthetized with sodium pentobarbital during normal cardiac function and during acute left ventricular (LV) failure. LV failure was induced by embolizing the left coronary bed with 50 micron plastic microspheres causing a marked depression of LV function. End-expiratory pressure was set to 0, 5, 10 and 15 cm H2O both before and after coronary embolization. During normal cardiac function PEEP above 5 cm H2O depressed cardiac output (CO) significantly. However, following coronary embolization after which LV function was seriously impaired, CO was maintained as PEEP was applied. This is attributed to reduced sensitivity to the LV pre-load reductions induced by PEEP during LV failure. PEEP reduced MBF both during normal and impaired LV function. This did not result in ischaemic myocardial metabolism assessed by lactate extraction either in normal hearts or following coronary embolization. The reduced MBF was, however, associated with reduced MVO2 both during normal cardiac function and during LV failure. It is suggested that the reduced MBF is mainly due to reduced myocardial oxygen demand probably caused by reduced LV wall tension during PEEP ventilation.