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Sleep-Disordered Breathing and Cardiac Disease
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Sleep-disordered breathing (SDB) is prevalent in patients with cardiac diseases, contributing to a reduced quality of life, a reduced functional capacity, and poor health. SDB causes acute and chronic physiologic stressors that can exacerbate cardiac ischemia, reduce systolic and diastolic function, cause cardiac structural and electrical remodeling, and increase the risk of cardiac arrhythmias and sudden death. Despite strong evidence linking SDB to cardiovascular disease (CVD), and the vulnerability of the cardiac patient to SDB-related stressors, SDB often goes unrecognized in cardiology practice, so there is potential for improved recognition and initiation of interventions. This chapter reviews aspects of SDB recognition, pathophysiology, and health outcomes relevant to cardiac disease.
Definitions
SDB refers to a spectrum of sleep-related breathing disorders that includes obstructive sleep apnea (OSA), central sleep apnea (CSA), Cheyne-Stokes respiration, and sleep-related hypoventilation. The mechanisms and risk factors for these disorders have overlapping as well as unique characteristics. Each is associated with impaired ventilation during sleep and sleep disruption, but differ with regard to degree of abnormalities in neuromuscular respiratory drive and airway collapsibility. The constellation of symptoms, the diagnostic criteria, and their associations with CVD are summarized in Table 89.1 .
TABLE 89.1
Key Features of Obstructive Sleep Apnea and Central Sleep Apnea
| Obstructive Sleep Apnea | Central Sleep Apnea | |
|---|---|---|
| Common presenting symptoms | Snoring, observed apneas, gasping or snorting during sleep, daytime sleepiness | Observed apneas, gasping or snorting during sleep, frequent awakenings, unrefreshed sleep, fatigue |
| Diagnosis | Home sleep apnea test or polysomnography showing AHI >5 with a predominance of obstructive apneas or hypopneas (>50%) | Polysomnography showing a predominance of central apneas or hypopneas (>50%) with a central apnea hypopnea index >5 Cheyne-Stokes respiration: ≥3 consecutive central apneas/central hypopneas separated by crescendo and decrescendo change in breathing amplitude with a cycle length ≥40 sec associated with central AHI >5 |
| Associated risk factors | Obesity, male, middle-older age | Male, older age |
| Associated cardiovascular disease ∗ | Resistant hypertension, stroke, heart failure (preserved and reduced ejection fraction), atrial fibrillation, coronary artery disease | Atrial fibrillation, heart failure (reduced or preserved ejection fraction), stroke, pulmonary hypertension, coronary artery disease |
∗ Order shown indicating approximate relative strength of association.
Typical symptoms of OSA include loud or disruptive snoring, snorting or gasping during sleep, poor sleep quality, unrefreshed sleep, and excessive daytime sleepiness. Diagnosis requires objective sleep testing using an in-laboratory polysomnograph or a home sleep apnea test, with demonstration of recurrent episodes of apneas and/or hypopneas. An apnea indicates a near absence of airflow during the period of upper airway obstruction for at least 10 seconds, while a hypopnea signifies a reduction in airflow relative to baseline accompanied by drop in oxygen saturation or a cortical arousal ( Fig. 89.1 ). Apneas and hypopneas are further classified as “obstructive” based on the occurrence of concurrent respiratory effort during periods of reduced or absent airflow, and otherwise as “central”. Diagnostic criteria for OSA are: (1) symptoms of breathing disturbances during sleep (snoring, snorting, gasping, or breathing pauses) or daytime sleepiness or fatigue, despite sufficient opportunities to sleep and unexplained by other medical problems; and (2) five or more apneas or hypopneas per hour of sleep (apnea-hypopnea index [AHI]). OSA may be diagnosed in the absence of symptoms if the AHI is greater than 15). OSA severity is judged based on the frequency of breathing disturbances (AHI level), degree of hypoxemia and sleep disruption, and associated symptoms. Excessive daytime sleepiness, in particular, marks severe disease that is associated with an increased risk of adverse CVD outcomes, as well as better adherence with OSA treatment.
CSA often overlaps with OSA and is identified when more than 50% of respiratory disturbances are unaccompanied by respiratory effort.
The AHI and other indices of sleep are measured with multichannel overnight recordings. Polysomnography performed in the sleep laboratory records airflow, breathing effort and oxygen saturation, as well as data from the electroencephalogram, electrocardiogram, and leg muscles; providing the ability to identify apneas and hypopneas as well as stage sleep, quantify sleep fragmentation, and identify other sleep-related phenomena such as arrhythmias and periodic leg movements. Home-based sleep apnea tests collect data on breathing parameters, but do not typically record additional information. Although home sleep apnea tests are increasingly used due to their lower cost, in-laboratory polysomnography still serves to evaluate patients with complex comorbidities, such as heart failure (HF). When interpreting the results of home sleep apnea tests, it is important to note that they can underestimate the AHI by approximately 12%, and larger misclassifications are likely in patients with poor sleep quality, such as those with HF, and in women, who typically have shorter respiratory events with less desaturation than men.
Pathophysiology
Pathophysiology of Obstructive Sleep Apnea
The pharyngeal airway has no bony or cartilaginous support, and its size and shape change dynamically with each expiration and inspiration (when negative intraluminal pressure causes the airway to be “sucked” inward). Its patency therefore depends on the activation of pharyngeal dilator muscles, which decreases with sleep onset. Whether an apnea occurs depends on whether the level of neuromuscular activation of the upper airway muscles is adequate to overcome forces that promote airway collapse during sleep. The presence of an anatomically small airway (e.g., micrognathia, fat deposition in the lateral pharyngeal walls) and lying in the supine position (when gravitational and positional factors alter the position of the tongue and other soft tissues) increase the level of neuromuscular drive needed to maintain airway patency. Therefore, patients with small oropharyngeal airways due to craniofacial factors or excessive airway soft tissue have an increased risk for OSA. When a person is in the recumbent position, there can be a rostral redistribution of peripheral fluid from the lower extremities to the neck area, contributing to airway narrowing during sleep, and this factor can predispose patients with HF and even mild peripheral edema or venous stasis to OSA. Lung volume influences pharyngeal wall stiffness through tractional forces; therefore, reduced lung volumes, as may occur in obesity or with pulmonary congestion, can exacerbate propensity for OSA. Conversely, high lung volumes, as in chronic obstructive lung disease, may modestly protect against OSA. Increased nasal resistance (e.g., due to nasal septal deviation, polyps) promotes airway collapse by increasing the negative intraluminal suction pressure and is a risk factor for OSA in conditions such as pregnancy or allergy associated with nasal swelling.
Pharyngeal muscle activation depends both on the sensitivity of central and peripheral respiratory chemoreceptors and on neuromuscular responsiveness to CO 2 ( Fig. 89.2 ). During sleep, the blood CO 2 typically increases mildly, and this helps to activate respiratory muscles and stiffen airway dilators, protecting the upper airway (i.e., increasing critical closing pressure, P crit ). Depressed chemosensitivity and arousal response may prevent appropriate termination of apneas, prolonging the duration of the apnea and the severity of oxyhemoglobin desaturation. This ventilatory control problem can cause pathologic CO 2 retention and acidosis during sleep, a phenomenon common in obesity-hypoventilation and sleep-hypoventilation syndromes. Conversely, an overly sensitive response to CO 2 (i.e., reflecting high loop gain) can cause wide fluctuations in the ventilatory drive, resulting in central nervous system arousal and sleep fragmentation. Episodic hyperventilation can drive CO 2 levels to below the apneic threshold, precipitating cycles of apneas. This mechanism also occurs in CSA, and in its most extreme form is manifested as Cheyne-Stokes respiration.
The severity of OSA can vary by sleep stage and position. During rapid eye movement (REM) sleep, the neuromuscular drive is low and fluctuating, sympathetic tone is high, and apneic events tend to be longest and associated with the most severe oxyhemoglobin desaturation. “REM-dependent” OSA, characterized by a predominance of respiratory events in REM as compared to non-REM sleep, better predicts incident hypertension and mortality compared to the overall AHI level. OSA also can worsen following acute ingestion of alcohol, which reduces neuromuscular activation, and when a person is in the supine position.
Pathophysiology of Central Sleep Apnea
In adults, CSA often occurs in association with cardiac or cerebrovascular disease. Its pathogenesis relates to a heightened sensitivity to CO 2 and a prolonged circulation delay between the pulmonary capillaries and carotid chemoreceptors, causing instability in breathing. Periods of hyperventilation cause CO 2 levels to fall below the apneic threshold, precipitating apneas and hypopneas. The occurrence of cycles of crescendo-decrescendo breathing is recognized as Cheyne-Stokes respiration; cycle lengths of 60 seconds are characteristic of patients with HF.
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