PubMed · 5780706
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K N Sullivan. 1969. Hippus.. https://pubmed.ncbi.nlm.nih.gov/5780706/
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Nocturnal periodic breathing (PB) is often observed in patients with congestive heart failure (CHF). We investigated the sleep architecture polysomnographically in a 54-year-old man with CHF due to mitral regurgitation before and after surgical treatment. We found that the overnight frequency of central dominant sleep apnea decreased from 154 to 56, and the lowest nocturnal oxygen saturation increased from 66% to 85% postoperatively. These improvements in the manifestations of PB might be attributed to the improved hemodynamics after successful valve replacement.
Many of the factors that appear to cause Cheyne-Stokes Breathing (CSB) in sleeping patients with congestive heart failure (CHF) are present during wakefulness. We studied the stability of ventilatory pattern in nine awake CHF patients (left ventricular ejection fraction 9-48%) who demonstrated CSB only while asleep and compared results with 13 age-matched normals. The test involved brief (30-50-second) exposure to hypoxia (end-tidal PO2 = 55 Torr) followed by breathing pure oxygen. During hypoxia, ventilation increased about 40% above air breathing control in both groups, whereas end-tidal CO2 declined to 92% of control in both groups. During hyperoxia, however, breathing pattern differed between groups. In the normals, ventilation gradually declined to air-breathing levels and did not significantly undershoot. In the patients, ventilation dropped more rapidly to baseline and an overshoot was present with ventilation being 72% and air-breathing control at 45 seconds of hyperoxia. Circulatory delay was calculated from the time interval between alveolar hypoxia and in increase in ventilation, and when corrections for circulatory delay were applied to ventilation during hyperoxia the differences between groups increased in that the patients' ventilation was less than baseline immediately after the delay. In the normals, the gradual decline in hyperoxic ventilation probably represents the decay of short-term potentiation (STP) activated by hypoxic hyperventilation. Results in the patients were compatible with absence of such STP decay, but could also have been due to a reduction in ventilatory drive early in hyperoxia related to prolonged circulation times.(ABSTRACT TRUNCATED AT 250 WORDS)
We investigated the prevalence of sleep-disordered breathing in 20 outpatients on a heart transplant waiting list. All were younger than 60 years and had severe stable cardiac failure with a cardiac index below 2.5 L/min/m2 and a left ventricular ejection fraction below 25%. Nine patients (45%) exhibited ten or more apneas and hypopneas per hour of sleep (apneic group). In all patients but one, apneas and hypopneas were predominantly of the central type and occurred during Cheyne-Stokes respiration. There were no statistically significant differences between the apneic and nonapneic groups of patients in terms of age (51 +/- 5 years vs 49 +/- 11), body mass index (24 +/- 4 kg/m2 vs 22 +/- 3), cardiac index (1.87 +/- 0.35 L/min/m2 vs 1.84 +/- 0.40), isotopic left ventricular ejection fraction (13 +/- 5 vs 12 +/- 3%), arterial blood gas, or pulmonary function tests. Hypnogram characteristics showed poorer sleep quality in the apneic group than in the nonapneic group, with a larger number of arousals; this difference was found both for arousals lasting more than 30 s (8 +/- 5/h vs 4 +/- 2) and for arousals lasting less than 30 s (18 +/- 16/h vs 5 +/- 6) and was associated with increased wakefulness after sleep onset in the apneic group (138 +/- 82 min vs 84 +/- 45). Arousals were strongly associated with hyperpneic phases of Cheyne-Stokes respiration. We conclude that sleep-disordered breathing is common in patients with end-stage heart disease and adversely affects the quality of sleep.