Mt. Naughton et al., EFFECT OF CONTINUOUS POSITIVE AIRWAY PRESSURE ON INTRATHORACIC AND LEFT-VENTRICULAR TRANSMURAL PRESSURES IN PATIENTS WITH CONGESTIVE-HEART-FAILURE, Circulation, 91(6), 1995, pp. 1725-1731
Background Continuous positive airway pressure (CPAP) can improve card
iac function in patients with congestive heart failure (CHF). We hypot
hesized that this effect might be related to CPAP-induced increases in
intrathoracic pressure, which would reduce left ventricular transmura
l pressure (LVP(tm)) during systole, thereby decreasing left ventricul
ar 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 peri
od and compared with a 75-minute time control period without CPAP in t
wo groups of subjects: 15 patients with CHF and 9 healthy subjects. In
trathoracic pressure was estimated from esophageal pressure (P-es), an
d systolic LVP(tm), a determinant of left ventricular afterload, was a
ssessed by subtracting P-es during systole from systolic blood pressur
e. Cardiac index (CI) was assessed by Doppler echocardiography. At bas
eline, inspiratory P-es amplitude, which reflects inspiratory muscle f
orce generation, was greater in the patients with CHF than in the heal
thy group (9.9+/-0.8 versus 5.5+/-0.4 mm Hg, P<.001). In addition, sys
tolic P-es, which represents the relative contribution of intrathoraci
c 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). Wh
ile on CPAP of 10 cm H2O, inspiratory P-es amplitude decreased and sys
tolic 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 t
he 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 p
er minute, P<.005) and the healthy group (from 82+/-8 to 60+/-6 mm HgX
breaths per minute, P<.05). Compared with time control, systolic LVP(t
m) 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 he
althy group. Moreover, systolic LVP(tm)Xheart rate decreased significa
ntly in the group with CHF (from 80.55+/-5.27 to 71.83+/-4.73 mm HgXbe
ats 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 i
nspiratory muscles generate greater force per breath and systolic P-es
contributes more to LVP(tm) than in healthy subjects. By increasing i
ntrathoracic pressure in patients with CHF, CPAP unloaded inspiratory
muscles and reduced left ventricular afterload without compromising CI
.