HEMODYNAMIC CONSEQUENCES OF OBSTRUCTIVE SLEEP-APNEA

Patients with obstructive sleep apnea demonstrate both acute and chron ic hemodynamic changes attributable to their disease. Acutely, these p atients experience repetitive nocturnal hemodynamic oscillations. Sudd en increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of al tered cardiovascular control. Patients with sleep apnea, even when sle eping without obstructions, fail to display the normal nocturnal decli ne in arterial pressure of 10-15% from the waking value. The absence o f a nocturnal decline may have chronic consequences, such as developme nt of left ventricular hypertrophy. Another chronic hemodynamic conseq uence of sleep apnea may be sustained diurnal hypertension. Epidemiolo gic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for othe r risk factors. Although sleep apnea may contribute to pulmonary, as w ell as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of th e hemodynamic consequences of sleep apnea has grown in recent years, m uch remains to be learned.