Magnitude and time course of hemodynamic responses to Mueller maneuvers in patients with congestive heart failure

Abstract

To simulate the immediate hemodynamic effect of negative intrathoracic pressure during obstructive apneas in congestive heart failure (CHF), without inducing confounding factors such as hypoxia and arousals from sleep, eight awake patients performed, at random, 15-s Mueller maneuvers (MM) at target intrathoracic pressures of −20 (MM −20) and −40 cmH2O (MM −40), confirmed by esophageal pressure, and 15-s breath holds, as apneic time controls. Compared with quiet breathing, at baseline, before these interventions, the immediate effects [first 5 cardiac cycles (SD), P values refer to MM −40 compared with breath holds] of apnea, MM −20, and MM −40 were, for left ventricular (LV) systolic transmural pressure (Ptm), 1.0 ± 1.9, 7.2 ± 3.5, and 11.3 ± 6.8 mmHg ( P < 0.01); for systolic blood pressure (SBP), 2.9 ± 2.6, −5.5 ± 3.4, and −12.1 ± 6.8 mmHg ( P < 0.01); and for stroke volume (SV) index, 0.4 ± 2.8, −4.1 ± 2.8, and −6.9 ± 2.3 ml/m2( P < 0.001), respectively. Corresponding values over the last five cardiac cycles were for LVPtm 6.4 ± 4.4, 5.4 ± 6.6, and −4.5 ± 9.1 mmHg ( P < 0.01); for SBP 6.9 ± 4.2, −8.2 ± 7.7, and −24.2 ± 6.9 mmHg ( P < 0.01); and for SV index −0.4 ± 2.1, −5.2 ± 2.8, and −9.2 ± 4.8 ml/m2( P < 0.001), respectively. Thus, in CHF patients, the initial hemodynamic response to the generation of negative intrathoracic pressure includes an immediate increase in LV afterload and an abrupt fall in SV. The magnitude of response is proportional to the intensity of the MM stimulus. By the end of a 15-s MM −40, LVPtm falls below baseline values, yet SV and SBP do not recover. Thus, when −40 cmH2O intrathoracic pressure is sustained, additional mechanisms, such as a drop in LV preload due to ventricular interaction, are engaged, further reducing SV. The net effect of MM −40 was a 33% reduction in SV index (from 27 to 18 ml/min2), and a 21% reduction in SBP (from 121 to 96 mmHg). Obstructive apneas can have adverse effects on systemic and, possibly, coronary perfusion in CHF through dynamic mechanisms that are both stimulus and time dependent.