Sleep disordered breathing in patients with heart failure: pathophysiology and management

Abstract

Sleep disordered breathing (SDB) is common in heart failure patients across the range of ejection fractions and is associated with adverse prognosis. Although effective pharmacologic and device-based treatment of heart failure may reduce the frequency or severity of SDB, heart failure treatment alone may not be adequate to restore normal breathing during sleep. Continuous positive airway pressure (CPAP) is the major treatment for SDB in heart failure, especially if obstructive rather than central sleep apnea (CSA) predominates. Adequate suppression of CSA by PAP is associated with a heart transplant-free survival benefit, although randomized trials are ongoing. Bilevel PAP (BPAP) may be as effective as CPAP in treating SDB and may be preferable over CPAP in patients who experience expiratory pressure discomfort. Adaptive (or auto) servo-ventilation (ASV), which adjusts the PAP depending on the patient's airflow or tidal volume, may be useful in congestive heart failure patients if CPAP is ineffective. Other therapies that have been proposed for SDB in congestive heart failure include nocturnal oxygen, CO(2) administration (by adding dead space), theophylline, and acetazolamide; most of which have not been systematically studied in outcome-based prospective randomized trials.

Figure 1

Polysomnogram showing crescendo–decrescendo pattern of breathing (as shown by the rib cage and abdomen movements), known as Cheyne Stokes breathing. Note the central apneas in which cessation of airflow (shown in nasal pressure channel) occurs without respiratory effort (in the rib cage and abdomen belt channels). In addition, desaturations are observed with each apnea, but somewhat delayed in time due to slowed circulation. Arousals from sleep commonly occur during periods of hyperpnea, yielding paroxysmal nocturnal dyspnea.

Figure 2

Polysomnogram showing obstructive apnea. Note the cessation of airflow for more than 10 s (detected by nasal thermistor, CFLOW channel) associated with continued respiratory effort as shown by thoracic and abdominal movements (detected in the thoracic and abdominal belt channels). There is also associated snoring. The top 6 channels (F4-M1 to O1-M2) show the electroencephalogram with stage 2 sleep.