Central Sleep Apnea in Congestive Heart Failure: Prevalence, Mechanisms, Impact, and Therapeutic Options

Shahrokh Javaheri, M.D.


Semin Respir Crit Care Med. 2005;26(1):44-55. 

In This Article

Abstract and Introduction

Heart failure due to left ventricular systolic dysfunction is a prevalent syndrome and associated with morbidity, mortality, and huge economic cost. According to reports from several laboratories, a large number of patients with heart failure have central sleep apnea. Central sleep apnea causes arousals and sleep disruption, alters blood gases, and increases sympathetic activity. The pathophysiological consequences of central sleep apnea could adversely affect left ventricular structure and functions and worsen prognosis of heart failure.

Several treatment options, including use of nocturnal supplemental oxygen, positive airway pressure devices, and theophylline have been systematically studied and have been shown to improve central sleep apnea. Long-term studies, however, are necessary to determine the impact of therapy on natural history of left ventricular systolic dysfunction.

Central apnea is due to temporary cessation of breathing rhythmogensis. Polygraphically, it is characterized by cessation of naso-oral air flow and absence of thoracoabdominal excursions. The latter is due to the cessation of inspiratory activity of the thoracic pump muscles.

There are many causes of central apnea. However, heart failure with systolic dysfunction is the most common cause of central sleep apnea in the population. This is because heart failure is a common disorder and central sleep apnea is common in the setting of the failing heart.[1]

Historically, periodic breathing and central apnea have been known for two centuries to occur in patients with heart failure.[2,3,4,5] Recognition of this disorder preceded that of obstructive sleep apnea. John Cheyne[4] and William Stokes[5] have been credited with description of periodic breathing in heart failure. However, 37 years before John Cheyne's description, John Hunter, a British surgeon, had observed this unique pattern of breathing. Describing the case history of Mr. Boyed, who apparently suffered from atrial fibrillation and congestive heart failure, Hunter wrote,[2,3] "The pulse was irregular, as usual, and quick; but his breathing was very particular: he would cease breathing for twenty or thirty seconds, and then begin to breathe softly, which increased until he breathed extremely strong, or rather with violent strength, which gradually died away till we could not observe that he breathed at all. He could not lie down without running the risk of being suffocated, therefore he was obliged to sit up in his Chair."


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