Cardiopulmonary consequences of obstructive sleep apnea

Abstract

During sleep, oxygen consumption and systemic blood pressure decrease in normal subjects; during rapid eye movement sleep, irregular ventilation can be accompanied by brief periods of apnea. In patients with obstructive sleep apnea, alveolar ventilation during an apneic episode is immediately reduced to zero, and the metabolic demands for oxygen must be met from oxygen stores within the body. As the stores of oxygen within the lung are diminished, the rate of arterial oxyhemoglobin desaturation increases. The development of alveolar hypoventilation during wakefulness seems to be based on a balance between central ventilatory drives to breathe and mechanical loads placed on the respiratory system. Coexistent cardiopulmonary or neuromuscular disease in patients with obstructive sleep apnea contributes to the development of alveolar hypoventilation. During apneic episodes, the systemic blood pressure increases while the heart rate and cardiac output decrease. Both bradycardias and increased ventricular ectopic activity have been associated with these disordered breathing episodes. Because of the possibility of apnea-associated arrhythmias, patients with obstructive sleep apnea may be at increased risk for cardiovascular mortality. The influence of these recurrent nocturnal episodes of asphyxia on cardiovascular longevity needs further investigation.