Cardiovascular Consequences of Sleep Apnea

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Cardiovascular modulation in normal sleep and in obstructive sleep apnea

Studies in healthy humans using microneurography (which allows for direct recording of peripheral sympathetic nerve traffic) suggest that the cardiovascular influence of sleep is more complex than a generalized inhibition of the sympathetic nervous system.12 In non–rapid eye movement (NREM) sleep, parasympathetic tone increases and sympathetic tone decreases resulting in a decrease of heart rate, blood pressure, systemic vascular resistance, and cardiac output. This sleep phase, which

Pathophysiologic influence of obstructive sleep apnea in cardiovascular disease

Patients with sleep apnea have recurrent “cycles” of sleep, airway obstruction, arousal, and resumption of ventilation (Fig. 1). Several physiologic stresses arise from this intermittent airway occlusion during sleep including cyclical hypoxemia of varying duration and severity, strenuous respiratory efforts against an occluded airway resulting in the generation of severely negative intrathoracic pressures, sympathetic activation, parasympathetic withdrawal, and reduced total sleep time. These

Epidemiologic observations

In addition to acute blood pressure swings at night, evidence supports that sustained diurnal hypertension can arise from obstructive apnea. This hypertension appears to be in part related to a “carryover” phenomenon of heightened sympathetic activity29 Two large observational longitudinal-based studies have measured the relation of baseline OSA severity and the risk of development of hypertension in a community-based cohort free of hypertension over a 2- to 5-year follow-up period. In the

Prevalence of Cardiac Arrhythmias in Obstructive Sleep Apnea

In healthy subjects, physiologic nocturnal changes in autonomic activity result in various types of benign, stable cardiac rhythms such as sinus bradycardia, sinus pause, first-degree atrioventricular (AV) block, and Mobitz type I second-degree AV block.

In patients with OSA, typical nocturnal cardiac rhythm disturbances, such as bradycardia with or without alternating tachycardia, have been well described.139, 140 However, the extension of the association between OSA and pathologic cardiac

Prevalence of Pulmonary Hypertension in Obstructive Sleep Apnea

PH is common in patients with OSA, with reported estimates ranging between 16% and 42%.160, 161 Discrepancies in prevalence estimates result from differences in study methodology. For example, most studies include only a small number of patients often unselected for comorbidities, and use varying definitions of pulmonary hypertension as well as modalities to measure pulmonary arterial pressure (Table 1). Most experts, however, estimate the prevalence of PH in uncomplicated OSA patients to be

Summary/public health implications

Multiple prospective observational cohort studies have demonstrated that OSA significantly increases the risk of cardiovascular disease independent of potential confounding risk factors. This finding implies that there are mechanisms mediated by sleep apnea that confer vascular risk. The current literature suggests that such mechanisms include: intermittent hypoxia, systemic inflammation, and atherosclerosis; nocturnal sympathetic activation; diurnal hypertension; metabolic dysregulation;

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