Hemodynamic consequences of obstructive sleep apnea.

Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden 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 altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.

Patients with obstructive sleep apnea have an abnormal peripheral vascular response to hypoxia.

Patients with obstructive sleep apnea (OSA) have been reported to have an augmented pressor response to hypoxic rebreathing. To assess the contribution of the peripheral vasculature to this hemodynamic response, we measured heart rate, mean arterial pressure (MAP), and forearm blood flow by venous occlusion plethysmography in 13 patients with OSA and in 6 nonapneic control subjects at arterial oxygen saturations (Sa(O(2))) of 90, 85, and 80% during progressive isocapnic hypoxia. Measurements were also performed during recovery from 5 min of forearm ischemia induced with cuff occlusion. MAP increased similarly in both groups during hypoxia (mean increase at 80% Sa(O(2)): OSA patients, 9 +/- 11 mmHg; controls, 12 +/- 7 mmHg). Forearm vascular resistance, calculated from forearm blood flow and MAP, decreased in controls (mean change -37 +/- 19% at Sa(O(2)) 80%) but not in patients (mean change -4 +/- 16% at 80% Sa(O(2))). Both groups decreased forearm vascular resistance similarly after forearm ischemia (maximum change from baseline -85%). We conclude that OSA patients have an abnormal peripheral vascular response to isocapnic hypoxia.

Relationship between velopharyngeal dimensions and palatal EMG during progressive hypercapnia.

To examine the contribution of specific palatal muscles to velopharyngeal dimensions, we recorded electromyographic (EMG) activity in the levator veli palatini, the tensor veli palatini, and the palatoglossus while examining the velopharynx (VP) with videoendoscopy in eight awake normal adults. Simultaneous display of VP images and airflow provided precise timing of events. Video images and EMG signals were recorded during progressive hypercapnia. Every tenth breath was analyzed. For each selected breath, VP area, anteroposterior and lateral diameters, and EMG activity were determined at five points: beginning, middle, and end of inspiration and middle and end of expiration. VP measurements changed significantly during the respiratory cycle. Although maximum area was measured at end inspiration or middle expiration and minimum area at the beginning or end of the breath, respiratory-related changes in VP measurements and EMG activity were characterized by substantial inter- and intrasubject variability. This variability is similar to velopharyngeal behavior during nonrespiratory tasks and suggests that upper airway patency is determined by multiple factors.

Sleep stage influences the hemodynamic response to obstructive apneas.

Blood pressure (BP) rises at the termination of obstructive episodes in patients with sleep apnea. Although the relationship of these BP elevations to oxygen saturation (SaO2) and arousal has been explored, the influence of sleep stage is undefined. To examine the effects of sleep stage on the postapnea BP elevation, we enrolled 12 patients with obstructive sleep apnea (OSA), and successfully collected data from seven of these (all male). Subjects slept overnight in the sleep laboratory, with full sleep and respiratory monitoring. Arterial pressure was assessed continuously with a radial artery catheter (six patients) or with digital photoplethysmography (one patient). Apneas occurring in both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep were matched for duration and degree of desaturation. When mean arterial pressure (MAP) at termination of apneas during NREM sleep associated with SaO2 nadirs 78 to 82% (NREM 80%) was compared with MAP following apneas in REM with the same SaO2 nadir (REM 80%), there was a significant difference (NREM 80% 122 +/- 15.3 mm Hg, REM 80% 132 +/- 11.0; p = 0.0109). We also analyzed the effect of oxygen desaturation on MAP during REM sleep, by comparing events with SaO2 nadirs of 78 to 82% with events with nadirs of < 75% (REM < 75%). In REM, further desaturation was associated with significant lengthening of the obstructive episodes and significantly higher postapnea BP increases (REM 75% 143 +/- 19.9 mm Hg, p = 0.0392). We conclude that sleep stage alters the hemodynamic response to obstructive apneas during sleep.