Gas Exchange and Hemodynamics During Sleep

Abstract

Sleep in normal individuals is associated with mild alveolar hypoventilation, which results in 2 to 8 mm Hg increases in PaCO2 and 3 to 11 mm Hg reductions in PaO2, which decreases mean arterial oxyhemoglobin saturation by less than 2 per cent. Arterial blood pressure and heart rate consistently decrease during sleep, and cardiac output either decreases or remains unchanged. Greater variability in these hemodynamic variables occurs during REM than during NREM sleep. Cyclical fluctuations in ventilation, blood pressure, and heart rate have been observed in normal subjects, and fewer than five apneas per hour sleep is considered to be normal. In patients with obstructive sleep apnea, reductions in SaO2 that occur with apneas and hypopneas are highly variable within and between individuals. Multiple variables interact to determine the severity of the episodes of oxyhemoglobin desaturation that are associated with cyclical changes in heart rate and systemic blood pressure. The magnitude of the increase in systemic pressure is related to the severity of the oxyhemoglobin desaturation, with mean elevations in systolic and diastolic pressures being on the order of 25 per cent. However, the magnitude of the systemic pressor response to oxygen desaturation varies widely between individuals. Pulmonary artery pressure often increases with sequential apneas to substantially elevated values, and this increase in combination with the large negative intrathoracic pressures generated during obstructive apneas increases ventricular afterload. Alterations in stroke volume and cardiac output in response to the dynamic events that occur with apneas have not been adequately investigated. Reductions in heart rate that occur during apneas are related to the severity of the oxyhemoglobin desaturation and the arterial chemoreceptor-mediated increase in vagal efferent activity. Marked sinus bradycardia, sinus pauses of 2 to 13 seconds' duration, second-degree heart block, and ventricular tachyarrhythmias have all been associated with severe arterial hypoxemia. Sudden death during sleep in obstructive sleep apnea presumably results from a lethal cardiac arrhythmia, but the relative contributions of severe bradyarrhythmias and ventricular tachyarrhythmias are unknown.