Does continuous positive airway pressure (CPAP) reduce left ventricular transmural pressure and afterload in patients with congestive heart failure?
In patients with congestive heart failure, CPAP unloads inspiratory muscles and reduces left ventricular afterload without compromising cardiac index.
BACKGROUND: Continuous positive airway pressure (CPAP) can improve cardiac function in patients with congestive heart failure (CHF). We hypothesized that this effect might be related to CPAP-induced increases in intrathoracic pressure, which would reduce left ventricular transmural pressure (LVPtm) during systole, thereby decreasing left ventricular afterload. METHODS AND RESULTS: The effect of graduated CPAP from 0 to 10 cm H2O on the above variables was examined over a 75-minute period and compared with a 75-minute time control period without CPAP in two groups of subjects: 15 patients with CHF and 9 healthy subjects. Intrathoracic pressure was estimated from esophageal pressure (Pes), and systolic LVPtm, a determinant of left ventricular afterload, was assessed by subtracting Pes during systole from systolic blood pressure. Cardiac index (CI) was assessed by Doppler echocardiography. At baseline, inspiratory Pes amplitude, which reflects inspiratory muscle force generation, was greater in the patients with CHF than in the healthy group (9.9 +/- 0.8 versus 5.5 +/- 0.4 mm Hg, P < .001). In addition, systolic Pes, which represents the relative contribution of intrathoracic pressure to LVPtm, was more negative in the patients with CHF than in the healthy group (-4.1 +/- 0.3 versus -2.2 +/- 0.1 mm Hg, P < .001). While on CPAP of 10 cm H2O, inspiratory Pes amplitude decreased and systolic Pes increased significantly in the group with CHF (from 11.1 +/- 1.1 to 7.5 +/- 1.1 mm Hg, P < .025 and from -4.7 +/- 0.6 to 0.6 +/- 0.6 mm Hg, P < .001, respectively), but CPAP had no effect on these variables in the healthy subjects. Compared with the equivalent time control period, Pes amplitude x respiratory rate decreased significantly while on CPAP in both the group with CHF (from 188 +/- 22 to 112 +/- 17 mm Hg x breaths per minute, P < .005) and the healthy group (from 82 +/- 8 to 60 +/- 6 mm Hg x breaths per minute, P < .05). Compared with time control, systolic LVPtm decreased significantly while on CPAP, from 116.0 +/- 5.3 to 110.3 +/- 4.5 mm Hg (P < .025) in the group with CHF, but did not change in the healthy group. Moreover, systolic LVPtm x heart rate decreased significantly in the group with CHF (from 80.55 +/- 5.27 to 71.83 +/- 4.73 mm Hg x beats per minute/100, P < .005) but not in the healthy group. CI decreased significantly while on CPAP in the healthy group (P < .025) but did not change in the group with CHF. CONCLUSIONS: In patients with CHF, the inspiratory muscles generate greater force per breath and systolic Pes contributes more to LVPtm than in healthy subjects. By increasing intrathoracic pressure in patients with CHF, CPAP unloaded inspiratory muscles and reduced left ventricular afterload without compromising CI.
Naughton et al. (1995) studied this question.