Chest
Volume 96, Issue 3, September 1989, Pages 480-488
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Clinical Investigations
Respiration and Abnormal Sleep in Patients with Congestive Heart Failure

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We investigated the interaction between respiration and sleep in ten male outpatients with severe, stable, maximally treated congestive heart failure (CHF). Cheyne-Stokes respiration (CSR), defined as periodic breathing with apnea or hypopnea, was found in all patients with a mean duration of 120±87 minutes [50.2±34.4 percent total sleep time (TST)]. The CSR was found predominantly during stage 1 (20.6±6.7 percent TST) and stage 2 (25.8±6 percent TST) NREM sleep and occurred rarely during slow wave sleep (SWS) (1.6±1 percent TST) and REM sleep (1.6±0.5 percent TST). All apneas and hypopneas were central. Despite normal awake arterial oxygenation (SaO2) (96.1±1.6 percent), significant, severe hypoxemia was found during sleep in seven patients with SaO2 less than 90 percent for 9 to 59 percent TST (mean ± SD, 23 ± 23 percent TST), and this was significantly related to the duration of CSR (r = 0.66, p<0.05). The mean minimum SaO2 for sleep stage was lowest during stage 1 (82.1 percent ±2.6 percent) and stage 2 (78.9 percent ±2.8 percent) NREM sleep, intermediate during REM sleep (84.5 percent ±1.8 percent) and highest during SWS (87.6 percent ±2.7 percent). Sleep was disrupted to a variable extent in all patients with a short mean TST (287±106 minutes), a high proportion of stage 1 sleep (26±19 percent TST), virtual absence of SWS (5±7 percent TST) which was found in only four patients, and a high number of sleep stage changes (30±27/hour) and arousals (28±25/hour). Arousals occurred predominantly during stage 1 (17±20/hour) and stage 2 (10±7/hour) NREM sleep and the majority immediately followed the hyperpneic phase of CSR. The amount of CSR (percent TST) was inversely related to the length of TST (r = –0.73, p<0.05), and directly related to the number of sleep stage changes (r = 0.79, p<0.01) and the number of arousals (r = 0.66, p<0.05). We conclude that in severe, stable CHF, CSR occurs predominantly during light sleep, that despite normal awake arterial oxygen saturation, significant hypoxemia may develop during sleep due to CSR, and that sleep is unstable and disrupted due to frequent arousals caused by the hyperpneic phase of CSR. These sequelae of CSR may be important determinants of the clinical status and outcome of patients with severe CHF.

Section snippets

METHODS

Ten male patients were investigated from March 1987 to April 1988. All patients were referred by the cardiology service which had been informed of our study protocol. Inclusion criteria for participation in the study were as follow: (1) male patients less than 70 years old with a clinical diagnosis of significant, stable congestive heart failure (New York Heart Association class 3 or 4); (2) left ventricular ejection fraction <35 percent; (3) no evidence of neurologic disease, significant

RESULTS

Ten patients aged 40 to 66 years were studied (Table 1). None was morbidly obese. All had congestive heart failure which was due to ischemic cardiomyopathy in nine patients and alcoholic cardiomyopathy in one. Two patients had chronic atrial fibrillation and two had a permanent pacemaker in situ. Although their congestive cardiac failure was clinically stable (all were ambulatory outpatients), it was nevertheless severe as evidenced by New York Heart Association classification 3 to 4 and the

DISCUSSION

We found that sleep structure was grossly abnormal in heart failure. This study describes the role of sleep and arousal state in congestive heart failure with particular regard to the distribution of CSR during sleep and the interaction between CSR, arterial oxygen saturation and sleep architecture. Cheyne-Stokes respiration was found in all patients and occurred predominantly during stage 1 and 2 NREM sleep. Arterial oxygenation was normal during wakefulness, although awake breathing pattern

ACKNOWLEDGMENTS:

We are grateful to Ms Zoe Pouliot for typing the manuscript.

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  • Cited by (0)

    Supported by Canadian Heart Association and St. Boniface General Hospital Research Foundation.

    Manuscript received December 2; revision accepted February 1.

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