CSA is defined by an absence of at least 10 s duration of both airflow and respiratory effort in sleep, and central hypopnea indicates a reduction of these parameters causing reduced tidal volume. CSA comprises a heterogeneous group of congenital and acquired disorders, and in the latter grouping neurological conditions affecting the brainstem include the stroke syndromes of cerebrovascular disease. CSA is also seen in a striking proportion of males with left ventricular cardiac failure (33-40 %) [137,138], and OSA may coexist in some of these patients . CSA is also seen in high-altitude exposure and uncommonly in miscellaneous other medical conditions.
In the CSA of cardiac failure, recumbent pulmonary venous congestion stimulates vagal pulmonary afferents causing hyperventilation and hypocarbia, and arousals further stimulate ventilation and drive hypocarbia below the apnea threshold. The apneas and hypoxia of CSA promote sympathetic nervous system activation and negative cardiovascular consequences for the cardiac patient. There is currently no consensus for the optimal treatment of CSA in cardiac failure . Optimizing cardiac failure drug therapy with diuretics, ACE inhibitors and ^-blockers and other specific cardiac medications should be pursued. Supplementary nocturnal oxygen therapy has been shown to have salutary effects in short-term trials of therapy of CSA in cardiac failure [140, 141]. Various forms of noninvasive positive airway pressure support during sleep have been tried in CSA of cardiac failure but to date only CPAP has been shown to have beneficial short-term functional and symptomatic effects [142-144] and, in a small study, long-term improvement in mortality or progression to cardiac transplantation . However, results of the larger (n = 258) CANPAP study of CPAP use in heart failure patients with CSA, showed no difference in primary endpoints (mortality or heart transplantation) between the nocturnal CPAP-treated group and the non-CPAP group after a mean follow-up of 2 years .
Acetazolamide is a carbonic anhydrase inhibitor that produces a metabolic acidosis, thereby stimulating ventilation, and a consequent shift in the arterial carbon dioxide tension that defines the apnea threshold. It has been used successfully to treat the CSA of high altitude, but there is not an extensive literature on its more general use in CSA. Side effects including paresthesia are common and may preclude continuation of therapy. Interestingly, acetazolamide has also undergone trials in OSA patients with objective benefit, but again tolerability of the drug was a problem .
Although theophylline has been shown to reduce CSA events in a small number of compensated cardiac failure patients , the drugs arrhythmogenic potential in advanced cardiac failure patients probably precludes its long-term use.
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