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CHAPTER SUMMARY AND CENTRAL ILLUSTRATION
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Chapter Summary
This chapter explores the pathophysiology of obstructive and central sleep apnea, as well as the purported causal relationship between these and hypertension, atherosclerosis, cardiac rhythm disorders, and cardiac failure. Obstructive sleep apnea (OSA)—involving cyclic asphyxia, microarousals from sleep, and negative swings in intrathoracic pressure—induces adverse systemic effects that disrupt normal cardiovascular physiology and function (see Fuster and Hurst’s Central Illustration). Notably, however, central sleep apnea of the Hunter-Cheyne-Stokes type is a consequence of cardiac failure rather than a cause. Treatment of sleep-disordered breathing with positive airway pressure devices and other therapeutic regimens has been shown to improve cardiovascular outcomes in patients with OSA. Randomized controlled trials have failed to show any mortality benefit, but this is likely related to methodological issues with the trials. Treatment of central sleep apnea remains difficult. Two randomized, controlled trials are ongoing: one with low-flow nocturnal oxygen and another with improved adaptive servo-ventilation. Phrenic nerve stimulation has shown benefits in a randomized, controlled trial. Finally, cardiac transplant recipients have been of particular interest because it was anticipated that preexisting central sleep apnea might be cured; however, OSA is prevalent in this patient population due to weight gain, potentially contributing to hypertension, poor quality of life, and even cardiac rejection.
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Normal sleep is associated with favorable autonomic nervous system activity, and a reduced blood pressure (BP), heart rate, and metabolic rate1 (Fig. 60–1). However, in the presence of sleep-disordered breathing (SDB), sleep is disrupted with adverse consequences. SDB encompasses apneas, hypopneas, and hypoventilation syndromes. Hypoventilation syndromes have been reviewed elsewhere2,3 and are beyond the scope of this chapter.
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There are two main types of respiratory events, namely apneas and hypopneas (apnea implying complete cessation of ventilation and hypopnea diminished ventilation). For each of these events the pathophysiological mechanism can be either obstructive, central or mixed central/obstructive. Obstructive sleep apnea/hypopnea (hitherto referred to as OSA) is quite common in the general population and in subjects with cardiovascular disease (CVD), and is rising in prevalence, primarily linked to the obesity epidemic. Central sleep apnea/hypopnea (hitherto referred to as CSA) is rare in the general population but is common in patients with left ventricular (LV) systolic dysfunction with or without overt clinical heart failure (HF), and is also observed in subjects with atrial fibrillation (AF) and stroke.3 Another main cause of CSA is opioid use.4
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The most common symptom of OSA for which subjects are referred to a sleep physician is ...