Effects of continuous positive airway pressure on cardiac output in experimental heart failure

Abstract

Continuous positive airway pressure (CPAP) is used to treat congestive heart failure (CHF) Mechanisms for improved cardiac output (CO) include increased left ventricular (LV) surface pressure, changes in sympathoadrenal tone, nonadrenergic vasodilation, or shifting blood volume from intra- to extrathoracic compartments. At CPAP = 0 and CPAP = 5 cm H2O we measured CO, LV surface pressure, plasma norepinephrine (PNE), and systemic vascular resistance (SVR) in normal and hypervolemic pigs and pigs with CHF (rapid ventricular pacing). In normovolemia CPAP led to no change in CO. With both hypervolemia and CHF, CPAP led to increased CO (10-20%). With CPAP, LV surface pressure increased slightly in normovolemia, but did not increase, or even decreased, in hypervolemia. With CPAP, PNE did not change in normovolemia, increased in hypervolemia, and decreased in CHF SVR always decreased when cardiac output increased with CPAP. We conclude that changes in cardiac surface pressure and overall sympathoadrenal tone cannot explain changes in CO with CPAP. Non-adrenergic mediated vasodilation could lead to unloading the LV. Alternatively, volume shift from intra- to extrathoracic compartments could lead to greater decreases in systolic than diastolic volume, thus increasing stroke volume. CPAP increases CO in the presence of cardiac distension whether or not myocardial function is impaired.