A 44-year-old man was hospitalized for the management of recently diagnosed and refractory congestive cardiac failure, deep venous thrombosis of the left lower extremity, atrial fibrillation, mild hypothyroidism, and morbid obesity (weight, 450 pounds). When questioned, the patient admitted to severe excessive daytime somnolence.

Blood gas analysis showed the following results: pH, 7.31; PaO₂, 51.3 mm Hg; PCO₂, 71.3 mm Hg; and HCO₃, 41.4 mEq/L. The ejection fraction was estimated to be 30% by echocardiography and radionuclide ventriculography. Polysomnography established severe obstructive sleep apnea with an apnea-hypopnea index of 95. The response to nasal continuous positive airways pressure at 12.5 cm of H₂O during the next 10 days was dramatic, with a vigorous diuresis and 15-pound weight loss associated with progressive reduction in daytime sleepiness and clinical and radiologic evidence showing resolution of congestive cardiac failure. A repeat assessment of contractile cardiac function showed an ejection fraction of at least 55%. Blood gas analysis at discharge showed the following results: pH, 7.43; PaO₂, 66.8 mm Hg; PCO₂, 53.6 mm Hg; and HCO₃, 30.3 mEq/L.

The association of reversible and severe left ventricular dysfunction with obstructive sleep apnea was recently recognized [1, 2]. An increase in right and left ventricular afterload during obstructive apnea, hypoxia, episodic nocturnal systolic hypertension with peaks just after apnea termination, and excessive sympathetic activation are important mechanisms. Cardiac output decreases progressively during episodes of apnea; the magnitude of this effect varies and can reduce the cardiac index by 35% during prolonged (35- to 40-second) apneas [3]. The hemodynamics of the Muller maneuver and episodes of obstruction are similar—during diastole, right ventricular filling increases initially, increasing pericardial pressure and displacing the septum to the left, resulting in impaired left ventricular filling [4]. In systole, left ventricular afterload increases, due in part to retention of blood in the thoracic aorta. The decrease in ventricular stroke volume at apnea termination occurs independently of oxygen desaturation [5].

Recognition of this association is important. I have seen four similar male patients during the past 4 years; their characteristics are described in Table 1.