Positive Pressure Therapy
Nasal continuous positive airway pressure (CPAP) therapy is the first-line therapy for obstructive sleep apnea (see also Chapter 6). CSA occurring in combination with episodes of obstructive or mixed apnea may respond to nasal CPAP therapy. In addition, there is evidence that some patients with pure CSA may respond to nasal CPAP therapy (58), especially if central apnea is worse in the supine position. One possible explanation is that nasal CPAP increases lung volume and oxygen stores and alleviates hypoxia. Alternatively, nasal CPAP prevents the occurrence of upper airway narrowing or occlusion during central apnea (59). The net effect is to mitigate the ensuing ventilatory overshoot and perpetuation of ventilatory instability.
Nasal CPAP has been used to treat CSA in patients with CHF. It may be beneficial in these patients because of its direct effect as an upper airway pneumatic splint and the indirect effects on respiratory muscles and cardiac function. One study demonstrated increased left-ventricular ejection fraction and a reduction of combined mortality-cardiac transplantation risk by 81%. This effect did not manifest in patients without CSA (60).
Despite the promising early studies, a more recent randomized, controlled trial failed to demonstrate a survival benefit in patients with central apnea and heart failure receiving nasal CPAP. The Canadian Continuous Positive Airway Pressure (CANPAP) for patients with CSA and heart failure trial tested the hypothesis that CPAP would improve the survival rate of patients who have CSA and heart failure (61). The trial enrolled 258 patients who had heart failure and central apnea; these patients were randomly assigned to receive CPAP or no CPAP and were followed for a mean of two years. The CPAP group had greater reductions in the frequency of episodes of apnea and hypopnea and in norepinephrine levels and greater increase in the mean nocturnal oxygen saturation, ejection fraction and the distance walked in six minutes. However, there was no difference in the number of hospitalizations, quality of life, or atrial natriuretic peptide levels. More importantly, there was no difference in survival rate. The results of this study do not support the routine use of CPAP to extend life in patients who have CSA and heart failure.
Pharmacological therapy for central apnea is of limited benefit. There are only two medications that have demonstrated promise in small clinical studies: acetazolamide and theophylline. Neither drug has been studied in large-scale clinical trials nor has been adopted widely (62).
Acetazolamide is a carbonic anhydrase inhibitor that causes mild metabolic acidosis; it is also a weak diuretic. Acetazolamide ameliorates CSA when administered as a single dose of 250 mg before bedtime in patients with idiopathic CSA and in patients with central apnea associated with heart failure (63,64). Nevertheless, the long-term effects of acetazolamide in patients with CSA are unknown. Likewise, theophylline ameliorates CSR in patients with CHF (65) without adversely affecting sleep quality or inducing cardiac arrhythmias. Nevertheless, the available findings are based on a small number of studies.
Several studies have demonstrated a salutary effect of supplemental O2 in patients with idiopathic CSA and patients with CHF-CSR (30,66). The postulated mechanism of benefit is ameliorating hypoxemia and minimizing the subsequent ventilatory overshoot. It is plausible that nocturnal oxygen therapy may improve outcome in patients with CHF and central apnea; however, long-term studies have yet to be conducted. Despite this limitation, it is prudent to evaluate the effect of supplemental O2 in alleviating central apnea. Finally, elevation of PaCO2 above the apneic threshold is effective in eliminating central apnea. This can be accomplished by inhalation of supplemental CO2 or added dead space (67-70). However, availability and a myriad of practical issues preclude widespread utilization of this therapy.
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