Am. J. Respir. Crit. Care Med., Volume 156, Number 5, November 1997, 1549-1555

Left Ventricular Volume in Patients with Heart Failure and Cheyne-Stokes Respiration during Sleep

RUZENA TKACOVA, MICHAEL J. HALL, PETER P. LIU, FABIA S. FITZGERALD, and T. DOUGLAS BRADLEY

Queen Elizabeth Hospital Sleep Research Laboratory, the Nuclear Cardiology Laboratory of the Toronto Hospital; and Centre for Cardiovascular Research, the Department of Medicine of the University of Toronto, Toronto, Ontario, Canada

In patients with congestive heart failure (CHF), elevated, left ventricular (LV) volume might lead to pulmonary congestion and hypocapnia, which would create a predisposition to the development of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). In addition, because LV volume affects cardiac output, it should influence the lengths of hyperpneas. We therefore evaluated LV volumes and transcutaneous PCO₂ (PtcCO₂) during wakefulness and stage 2 sleep in 16 patients with CHF due to nonischemic dilated cardiomyopathy (NIDC). Data were then compared between those with (n = 7) and those without CSR-CSA (n = 9). LV end-diastolic volume (LVEDV) was significantly higher in patients with than those without CSR-CSA (585 ± 118 versus 312 ± 41 ml, p < 0.05). Compared with patients without CSR-CSA, those with CSR-CSA had lower mean stage 2 sleep PtcCO₂ (36.3 ± 2.2 versus 41.2 ± 1.2 mm Hg, p < 0.05) and a lesser change in PtcCO₂ from wakefulness to stage 2 sleep (0.4 ± 0.3 versus 2.0 ± 0.4 mm Hg, p < 0.001). Among patients with CSR-CSA, hyperpnea length was inversely related to LVEDV (R = 0.769, p = 0.043) owing to the direct relationship of cardiac output to LVEDV (R = 0.791, p = 0.034). We conclude that CSR-CSA in patients with CHF due to NIDC is associated with increased LV volumes possibly through the direct or indirect influence of LV volume on Pa_CO2 and cardiac output.

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