Sleep apnea and the heart

The American Academy of Sleep Medicine Consensus statement recommends 7 or more hours of sleep regularly for optimal health including cardiovascular health. Sleeping 7 or less hours of sleep is associated with an increased risk for weight gain and obesity, diabetes, hypertension (HTN), heart disease, and stroke. Average sleep of less than 6 hours or more than 9 hours is associated with increased mortality risk. This risk is incremental with shorter durations of sleep.

Obstructive sleep apnea (OSA): Episodes of repetitive narrowing or complete collapse of the upper airway resulting in decreased airflow and associated with brief arousal on electroencephalogram and/or oxygen desaturation.

Central sleep apnea (CSA): Absence of respiratory effort resulting in lack of airflow and associated with arousal on electroencephalogram and/or oxygen desaturation. Cheyne-Stokes respiration is a form of CSA characterized by crescendo-decrescendo changes in respiratory effort with an associated central apnea event.

Complex sleep apnea: Emergent CSA or periodic breathing following treatment of OSA with positive airway pressure (PAP).

The symptoms associated with OSA include snoring and sudden arousals with choking/gasping, nocturia, excessive daytime sleepiness, and fatigue and are important clues to suspect the diagnosis. Some OSA symptoms may be difficult to distinguish from cardiac symptoms (sudden arousals with gasping vs. paroxysmal nocturnal dyspnea), and others overlap with cardiac symptoms like fatigue or nocturia. Importantly, these improve with treating OSA. Symptoms of OSA are summarized in Table 54.1 .

For OSA:

• Obesity (a 10% weight gain leads to a sixfold increase in the risk of OSA).

• Abnormal upper airway anatomy: Craniofacial abnormalities such as retrognathia, relative macroglossia, nasal obstruction, tonsillar hypertrophy, and increased pharyngeal adiposity.

• Chemical: Benzodiazepines, alcohol, opioid analgesics.

• Neck circumference greater than 17 inches in males and greater than 16 inches in females.

• Postmenopausal state.

For CSA:

• Congestive heart failure.

• Prior stroke.

• High altitude.

• Opioid analgesics.

• CSA can also be idiopathic.

The gold standard for diagnosis is polysomnography, an elaborate recording of multiple physiologic parameters during sleep. Polysomnography enables calculation of the apnea/hypopnea index (AHI), which reflects the average frequency of episodes of partial (hypopnea) or complete (apnea) airway narrowing per hour of sleep. A normal AHI is less than 5 per hour, and moderate to severe sleep apnea is present when AHI is greater than 15. Home sleep apnea testing is another option with limited physiologic parameter monitoring and is indicated for patients with high pretest probability for OSA who do not have significant cardiopulmonary or neuromuscular comorbidities. The technologies for home sleep testing include monitoring of nasal pressures and peripheral arterial tonometry.

OSA:

• PAP: Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BIPAP) remains the best treatment option that simultaneously delivers therapy and provides monitoring for adherence and treatment efficacy.

• Alternatives to PAP therapy:

• Surgical upper airway interventions.

• Mandibular advancing devices.

• Positional therapy (interventions to avoid supine sleep).

• Upper airway stimulation devices (hypoglossal nerve stimulation).

CSA:

• CPAP.

• BIPAP/BIPAP ST (ST = synchronized timed, adds backup respiratory rate).

• Adaptive servo-ventilation (ASV) should not be used in patients with heart failure with ejection fraction (EF) less than 45% due to increased mortality.

• Oxygen.

• Overdrive atrial pacing.

• Implantable phrenic nerve stimulator.

The hypoxemia and sleep fragmentation resulting from apnea/hypopnea episodes lead to a sympathetic surge and a rise in endothelin levels with significant elevation of blood pressure (BP) at the end of apneic episodes. Vagal tone is also blunted, further increasing the heart rate. There is also evidence that sleep deprivation and repetitive hypoxemia augment oxidative stress, activate proinflammatory mediators with elevations of C-reactive protein, induce inflammatory cytokines, and promote endothelial dysfunction. Furthermore, high negative intrathoracic pressure is generated during apnea/hypopnea episodes from vigorous inspiratory effort occurring against the collapsed airway. This leads to increased transmural pressure and wall stress in the cardiac chambers and great vessels, thus further increasing myocardial afterload ( Fig. 54.1 ).