The most common forms of SDB in heart failure patients are obstructive sleep apnea and central sleep apnea with Cheyne-Stokes breathing.
SDB is important to recognize because it is associated with adverse cardiovascular outcomes and mortality, and because accumulating evidence suggests that treatment of SDB can improve heart failure-related outcomes and quality of life.
Two types of sleep-disordered breathing (SDB) are common among patients with heart failure: obstructive sleep apnea (OSA) and central sleep apnea with Cheyne-Stokes breathing (CSA-CSB)
CSB is characterized by cyclic crescendo-decrescendo respiratory effort and airflow during wakefulness or sleep, without upper airway obstruction. When the decrescendo effort is accompanied by apnea during sleep, it is considered a type of central sleep apnea syndrome.
The pathogenesis of CSA-CSB is uncertain, but the favored hypothesis is based on the observation that patients who have heart failure and CSA-CSB tend to have lower arterial carbon dioxide tensions (PaCO2) than patients who have heart failure without CSA-CSB [3,4]. It is best conceptualized as a sequence of events: ●In an effort to correct the hypocapnia, a hypersensitive respiratory control center initiates an apnea. This occurs when the PaCO2 is below the "apneic threshold." The PaCO2 then begins to rise. ●The duration from the beginning of the apnea until the respiratory control center detects the increasing PaCO2 is prolonged due to the increased circulatory time caused by the heart failure. Although some circulatory delay is required for CSA-CSB to occur, its importance as a contributor to CSA-CSB is debated . ●Hypercapnia exists by the time the respiratory control center terminates the apnea. ●The hypercapnia then stimulates robust hyperpnea, which yields marked hypocapnia and allows the cycle of events to repeat.
Elimination of the hypocapnia with inhaled CO2, continuous positive airway pressure (CPAP), or oxygen can markedly attenuate CSA-CSB
Both OSA and CSA-CSB can impair systolic and diastolic cardiac function by a variety of mechanisms. First, intermittent hypoxemia and arousals induce adrenergic surges that may lead to heart disease progression. Second, the extremely negative intrapleural pressures increase ventricular transmural wall stress and afterload . More specifically, transmural pressure of the left ventricle is the pressure inside the left ventricle minus the pressure outside the left ventricle (ie, approximately the intrathoracic or pleural pressure). During spontaneous inspiration, the intrathoracic pressure becomes more negative, which increases the transmural pressure. The increase in transmural pressure contributes to left ventricular wall stress during left ventricular ejection (ie, afterload). This effect is greater in patients with heart failure who must generate more negative intrathoracic pressures to overcome low lung compliance caused by pulmonary congestion .
While obstructive sleep apnea (OSA) is more common than central sleep apnea with Cheyne-Stokes breathing (CSA-CSB) in the general population, CSA-CSB may be more common than OSA in patients with heart failure, particularly among patients with reduced ejection fraction [1,12,13].
Single-center observational studies estimate that the prevalence of SDB may be as high as 50 percent among all patients with heart failure and as high as 70 percent among patients with heart failure who are referred to a sleep laboratory [12-15]. The prevalence may be even higher among patients with acute decompensated heart failure , as suggested by a study that detected an apnea-hypopnea index ≥10 events per hour of sleep in 22 out of 29 such patients (76 percent) . Such prevalence estimates are limited by referral bias, variable definitions of SDB, variable severities of heart failure, and variable optimization of the medical management of the heart failure.
SDB appears to be common even among patients whose heart failure is optimally managed. A prospective cohort study followed 108 patients who visited a heart failure clinic with stable heart failure, which was defined as clinical stability without hospitalizations or medication changes within the past 30 days . SDB was detected in 61 percent of patients and was independently associated with the presence of atrial fibrillation and a worse New York Heart Association (NYHA) functional class.
Risk factors for OSA include advanced age and an increasing body mass index (BMI). Risk factors for CSA-CSB in patients with heart failure include male sex, advanced age, atrial fibrillation, and hypocapnia (ie, transcutaneous carbon dioxide ≤38 mmHg)
Sleep-disordered breathing (SDB) in patients with heart failure is under-recognized but important because it may independently predict mortality due to heart failure and may contribute to disease progression.
Multiple observational studies have found that heart failure accompanied by SDB is associated with a worse prognosis than heart failure in the absence of SDB
With respect to obstructive sleep apnea (OSA), a prospective cohort study followed 164 patients who had heart failure and a left ventricular ejection fraction of 45 percent or less . At a mean of three years, patients who had OSA (defined as an apnea-hypopnea index (AHI) of at least 15 events per hour) had a higher cardiac mortality than patients who did not have OSA (8.7 versus 4.2 deaths per 100 patient-years).
With respect to central sleep apnea with Cheyne-Stokes breathing (CSA-CSB), a prospective cohort study followed 62 patients with NYHA class II to III heart failure . At a mean of 28 months, cardiac mortality was associated with an AHI greater than 30 events per hour. The AHI was a better predictor of cardiac mortality than demographic variables, Holter monitoring, exercise studies, echocardiography, or autonomic testing. CSB was found to predict mortality in numerous other studies of patients with heart failure [13,22-25].
When obstructive sleep apnea (OSA) is the predominant type of SDB, poor sleep quality and snoring are common. As a result, sleep disruption and easy fatigability often exist and may be out of proportion to the severity of the heart failure. However, sleepiness is relatively uncommon in patients with heart failure for reasons that remain unclear . While not specific to OSA, additional signs and symptoms may include awakening with a sensation of gasping or choking, morning headaches, and poor concentration or memory impairment.
When central sleep apnea with Cheyne-Stokes breathing (CSA-CSB) is the predominant type of SDB, symptoms due to CSA-CSB may be indistinguishable from those due to the heart failure . Symptoms of poor sleep quality (eg, excessive daytime sleepiness) are subtle and generally unreliable. Occasionally, patients with CSA-CSB report paroxysmal nocturnal dyspnea (due to the hyperpnea that follows an apnea) . A bed partner may report episodic hyperpnea, hypopnea, and apneic periods.
SDB may contribute to nocturnal angina in patients with heart failure, presumably due to hypoxemia and catecholamine release
recurrent arrhythmias, such as atrial fibrillation or ventricular tachycardia, may be triggered or perpetuated by SDB [15,30-33]. SDB has also been identified as a risk factor for appropriate cardioverter-defibrillator therapies in heart failure patients with ICDs. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy", section on 'Clinical manifestations'.) These arrhythmias often occur in the absence of any symptoms or signs of SDB. Thus, a high index of suspicion should be maintained and evaluation for SDB should be considered in heart failure patients with recurrent arrhythmias.
Patients with heart failure who report snoring, excessive daytime somnolence, and poor sleep quality should have their sleep patterns assessed formally by polysomnography in a sleep laboratory or out-of-center sleep testing. We also consider diagnostic testing for sleep-disordered breathing (SDB) in heart failure patients with the following symptoms and signs, since they have been associated with SDB in observational studies: ●Nocturnal angina ●Recurrent arrhythmias ●Refractory heart failure symptoms ●Witnessed abnormal respiratory pattern or apneas ●Repetitive oxygen desaturations during sleep 
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