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Sleep-disordered breathing (SDB), or sleep apnea, is common in patients with cardiovascular disease (CVD), and its presence is associated with a poorer prognosis and high health-care costs.1,2 Increasingly, international guidelines suggest it is worthwhile to screen for this condition and that appropriate treatment may not only improve the patient's quality of life, but may also reduce the risk of cardiovascular events. However, recent evidence suggests that the relationship between SDB and the underlying cardiovascular condition may be complex, particularly in heart failure (HF), and further research is required to clarify the most appropriate treatment pathway for the individual patient.


SDB includes obstructive sleep apnea (OSA), central sleep apnea (CSA), or a combination of both. In OSA (the most common form of SDB in the general population), there is collapse of the pharynx during sleep with consequent upper airway obstruction, often with snoring (Fig. 77–1).3 Predisposing factors include obesity, a short neck, and retrognathism. In HF, rostral fluid shift during sleep can lead to pharyngeal edema, which may exacerbate the tendency to obstruction.4

FIGURE 77–1.

Normal airflow during respiration (A) and common points of obstruction in a patient with obstructive sleep apnea (B). Modified with permission from Levitsky MG. Using the pathophysiology of obstructive sleep apnea to teach cardiopulmonary integration. Adv Physiol Educ. 2008 Sep;32(3):196-202.3

CSA is usually associated with HF, although it has also been observed in patients with stroke, especially in the acute phase, and in those with renal failure.5 In CSA, the underlying abnormality is in the regulation of breathing in the respiratory centers of the brainstem. In normal physiology, minute ventilation during sleep is primarily regulated by chemoreceptors in the brainstem and carotid bodies, which trigger an increase in respiratory drive in response to a rise in partial pressure of arterial carbon dioxide (PaCO2), thus maintaining PaCO2 within a narrow range. Patients with HF and CSA tend to have an exaggerated respiratory response to carbon dioxide (CO2), associated with excess sympathetic nervous activity, so that modest rises in PaCO2 that may occur during sleep result in inappropriate hyperventilation.5,6,7 This drives the PaCO2 below the “apneic threshold,” at which point the neural drive to respire is too low to stimulate effective inspiration and an apnea (complete pause in breathing) or hypopnea (partial reduction in airflow) ensues. PaCO2 subsequently rises, and the cycle is repeated. This overshoot of the homeostatic feedback loop is exacerbated by the prolonged circulation time between the alveoli and the brainstem seen in more severe HF, so that the PaCO2 sensed in the brainstem may not accurately reflect the PaCO2 at the lung. CSA is associated with lower resting ...

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