What Is The Nonpharmacologic Treatment For Sleep-Related Breathing Disorders In Heart Failure?

Sleep-related breathing disorders, notably obstructive and central sleep apnea associated with Cheyne-Stokes respiration, are present in 40% to 50% of heart failure patients. Central sleep apnea is the most frequent breathing disorder in heart failure and is characterized by repetitive cycles of apnea, blood oxygen desaturation, sympathetic excitation, and waking with a surge in blood pressure. The increase in adrenergic and mechanical (after)load does not respond to conventional pharmacologic therapy and calls instead for an optimized management strategy offering a choice between two main interventions.

Nocturnal oxygen supplementation.

In their double-blind crossover study, Staniforth et al reported that nocturnal oxygen produced a modest, but significant, increase in minimum oxyhemoglobin saturation, a slight but significant reduction in the frequency of central apnea and hypopnea, and, perhaps most remarkably, a significant 50% reduction in the nocturnal urinary excretion of norepinephrine but not epinephrine.

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It had no effect on daytime plasma norepinephrine levels, sleep quality, daytime symptoms, cognitive function, or natriuretic peptide levels in plasma or urine. These results suggest that nocturnal oxygen therapy has only a limited, albeit beneficial, role in the management of central sleep apnea in heart failure.

Continuous positive airway pressure.

The most tested and effective treatment for central sleep apnea in heart failure is continuous positive airway pressure (CPAP). In randomized controlled trials, long-term CPAP at 10 to 12. 5 cm H20 for 1 to 3 months not only increased nocturnal oxygenation, and decreased nocturnal norepinephrine excretion, waking frequency, and the frequency of central apnea and hypopnea by increasing PaC02 above the apneic threshold, it also lowered daytime heart rate and plasma norepinephrine and atrial natriuretic peptide levels. Most importantly, CPAP significantly increased the left ventricular ejection fraction and decreased mitral regurgitation, while improving symptoms and decreasing hospitalization frequency. Thus, its benefits extend beyond those of nocturnal oxygen and include beneficial reverse remodeling of the ventricular architecture, thanks to its ability to decrease preload and afterload by raising intrathoracic pressure.

Despite its benefits, some patients cannot tolerate the device, in which case they should be offered nocturnal oxygen supplementation. Although objective measures of heart failure severity, including mortality, have not shown improvement in response to CPAP or nocturnal oxygen, the above effects are strong evidence for the independent benefit of specific treatment for central sleep apnea in heart failure. Large-scale outcome trials are required to confirm its efficacy in decreasing mortality.

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