• S M Scharf, L Chen, D Slamowitz, and P S Rao.
• Division of Pulmonary and Critical Care, Long Island Jewish Medical Center, Albert Einstein College of Medicine, New Hyde Park, NY 11042, USA.
• J Crit Care. 1996 Jun 1; 11 (2): 57-64.

AbstractContinuous positive airway pressure (CPAP) increases cardiac output (CO) in congestive heart failure (CHF). In six sedated pigs that were normovolemic (NV) and hypervolemic (HV), and seven previously instrumented pigs with pacing-induced CHF, we tested the hypothesis that this is associated with decreased total body sympathetic nerve activity (SNA). Hemodynamic variables and plasma norepinephrine level measurements were measured at baseline, CPAP 5 and 10 cm H2O, and recovery. Arterial O2 saturation was maintained at greater than or equal to 90% and PCO2 did not change. For NV baseline plasma norepinephrine level (PNE) was 97 +/- 61 pg/mL, CO 2.4 +/- .5 L/min, and pulmonary wedge pressure (Pw) 10.1 +/- 2.4 mmHg and did not change with CPAP. HV and CHF were associated with increased baseline Pw (18-21 mmHg). Baseline CO was increased with HV and unchanged with CHF. Baseline PNE was increased 4 to 5-fold with both HV and CHF. CO increased at CPAP 5 compared with baseline with both HV and CHF. However, PNE decreased with CPAP in HV, and increased with CPAP in CHF. Increased CO was always associated with decreased systemic vascular resistance. We conclude the following: (1) increased CO with CPAP can be associated with either increasing or decreasing SNA; (2) CPAP can produce increases in CO when the heart is distended whether baseline LV function is relatively normal (HV) or depressed (CHF); and (3) there are probably a number of different mechanism increasing CO with CPAP and these may vary from condition to condition.

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