Effect of Continuous Positive Airway Pressure on Intrathoracic and Left Ventricular Transmural Pressures in Patients With Congestive Heart Failure

Abstract

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 (LVP tm ) during systole, thereby decreasing left ventricular afterload. Methods and Results The effect of graduated CPAP from 0 to 10 cm H 2 O 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 (P es ), and systolic LVP tm , a determinant of left ventricular afterload, was assessed by subtracting P es during systole from systolic blood pressure. Cardiac index (CI) was assessed by Doppler echocardiography. At baseline, inspiratory P es 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 P es , which represents the relative contribution of intrathoracic pressure to LVP tm , 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 H 2 O, inspiratory P es amplitude decreased and systolic P es 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, P es amplitude×respiratory rate decreased significantly while on CPAP in both the group with CHF (from 188±22 to 112±17 mm Hg×breaths per minute, P <.005) and the healthy group (from 82±8 to 60±6 mm Hg×breaths per minute, P <.05). Compared with time control, systolic LVP tm 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 LVP tm ×heart rate decreased significantly in the group with CHF (from 80.55±5.27 to 71.83±4.73 mm Hg×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 P es contributes more to LVP tm than in healthy subjects. By increasing intrathoracic pressure in patients with CHF, CPAP unloaded inspiratory muscles and reduced left ventricular afterload without compromising CI.