No abstract

Continuous positive airway pressure (CPAP) has been used to increase cardiac index (CI) in patients with congestive cardiomyopathy in the presence of elevated pulmonary wedge pressure. We hypothesized that with normovolemia, CPAP would decrease CI because of decreased left ventricular (LV) preload, whereas in hypervolemia CPAP would increase CI because of a decrease in afterload. We tested this hypothesis on nine sedated, unanesthetized pigs instrumented 5 to 10 d before study. We measured CI, heart rate, stroke volume, LV end-diastolic and end-systolic pressures, and LV dimensions at CPAP levels 0, 5, 10, 15, and 20 cm H2O before and after volume expansion with hetastarch (35 ml/kg). From LV dimensions, LV end-diastolic (LVEDV) and LV end-systolic volumes (LVESV) and LV ejection fraction (LVEF) were calculated. With normovolemia, CI and LVEDV decreased with increased CPAP. Volume infusion produced mild cardiac dysfunction as evidenced by increased LV volumes, decreased LVEF, and decreased contractility. With hypervolemia, CPAP produced an increase in CI, decrease in LVEDV and LVESV, and an increase in LVEF. At higher values of CPAP, we observed decreased CI and LVEDV as with normovolemia. We conclude that with normovolemia, CPAP's effects are mainly related to changes in preload. Hypervolemia produced mild cardiac dysfunction. The improvement in CI with CPAP appears predominantly to be secondary to decrease in LV afterload, but a mild preload effect, which parallels the effect seen with normovolemia, was superimposed on afterload changes at higher CPAP values.

Continuous positive airway pressure (CPAP) may improve left ventricular (LV) function in patients with congestive heart failure (CHF). To understand mechanisms involved, in nine sedated, unanesthetized pigs with pacing-induced CHF we measured cardiac index (CI), heart rate (HR), LV pressures and volumes, ejection fraction (LVEF), and maximal rate of LV pressure rise (dp/dtmax). LV end-systolic transmural pressure (afterload) was estimated as LV end-systolic pressure (LVESP)-CPAP. Measurements were taken at CPAP 0, 5, 10, and 15 cm H2O and during recovery. At CPAP 5 cm H2O, CI increased from 4.23 +/- 1.00 to 4.99 +/- 0.88 L/min/m2 (p < 0.005), LV end-systolic volume decreased from 82.3 +/- 32.1 to 72.7 +/- 30.3 ml (p < 0.04) and LVEF increased from 0.30 +/- 0.09 to 0.36 +/- 0.12 (p < 0.02), and dp/dtmax increased. LVESP-CPAP was unchanged. After CPAP was discontinued, there was a rise in CI (p < 0.03), HR (p < 0.03), LVESP (p < 0.02), dp/dtmax (p < 0.02) and a decrease in total peripheral resistance (p < 0.03). We conclude that in CHF, low levels of CPAP improved CI, at least partly by improving contractility. Increased CI after discontinuing CPAP may be due to sympathoadrenal stimulation or withdrawal of alpha-adrenergic tone.

It has been postulated that increased cardiac surface pressure with continuous positive airway pressure (CPAP) results in decreased left-ventricular (LV) transmural pressure. We tested this hypothesis in seven sedated, unanesthetized, and previously instrumented pigs. We measured pericardial (Pperi), LV, airway (P(aw)), and esophageal (Pes) pressures at CPAP values of 0, 4, 8, and 12 cm H2O before and after blood-volume expansion. With normovolemia, CPAP resulted in an increase in Pperi (from -2.0 +/- 7.6 mm Hg at CPAP 0 to 2.3 +/- 5.6 mmHg at CPAP 12, p < 0.05). Baseline end-diastolic Pperi rose with volume expansion from -2.0 +/- 7.6 mm Hg to 5.4 +/- 5.4 mm Hg, p < 0.05. With hypervolemia, CPAP was associated with a decrease in Pperi (from 5.42 +/- 5.4 mm Hg to 2.3 +/- 5.6 mm Hg, p < 0.05). By contrast, Pes rose equally under both conditions with CPAP. LV transmural end-diastolic pressure (TMEDP) fell significantly under normovolemic conditions (from 16.5 +/- 7.4 mm Hg at CPAP 0 to 13.6 +/- 9.0 mm Hg at CPAP 12). The changes in FRC (pneumotachometry) with CPAP were similar under both conditions. We conclude that the CPAP-induced decrease in LV volume under hypervolemic conditions cannot be explained by an increase in cardiac surface pressure. We present a model to explain the decrease in cardiac surface pressure with CPAP.