EFFECT OF CONTINUOUS POSITIVE AIRWAY PRESSURE ON INTRATHORACIC AND LEFT-VENTRICULAR TRANSMURAL PRESSURES IN PATIENTS WITH CONGESTIVE-HEART-FAILURE

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 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 (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 H2O, 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 amplitudeXrespiratory rate decreased significantly while on CPAP in both the group with CHF (from 188+/-22 to 112+/-17 mm HgXbreaths per minute, P<.005) and the healthy group (from 82+/-8 to 60+/-6 mm HgXbreaths 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)Xheart rate decreased significantly in the group with CHF (from 80.55+/-5.27 to 71.83+/-4.73 mm HgXbeats 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.