Abstract
Central sleep apnea is prevalent in patients with heart failure, healthy individuals at high altitudes, and chronic opiate users and in the initiation of “mixed” (that is, central plus obstructive apneas). This brief review focuses on (a) the causes of repetitive, cyclical central apneas as mediated primarily through enhanced sensitivities in the respiratory control system and (b) treatment of central sleep apnea through modification of key components of neurochemical control as opposed to the current universal use of positive airway pressure.
Highlights
Central sleep apneas (CSAs) occur when there is a transient reduction by the ponto-medullary respiratory rhythm generator
The periodic waxing and waning of tidal volume (Vt) followed by apneas of at least 10 seconds’ duration accompanied by intermittent hypoxemia and transient cortical electroencephalography arousal are typical of non-rapid eye movement (NREM) sleep in congestive heart failure (CHF) with periodic cycles of at least 50 seconds
CSA and “cluster type” periodic breathing with short periodic cycles (10–25 seconds) are common in healthy sojourners during NREM sleep at high altitudes (>3000 m, oxygen saturation [SaO ] of about 90%) and even at more moderate high altitudes in susceptible people, especially with prolonged residencies[3,4]. This cluster-type periodic breathing with relatively short cycles is common at sea level in over half of chronic opioid users, and the severity of CSA is proportional to opiate dose[5]
Summary
Central sleep apneas (CSAs) occur when there is a transient reduction by the ponto-medullary respiratory rhythm generator. One possibility here is an increased plant gain secondary to opioid-induced steady-state hypoventilation and CO2 retention during sleep with subsequent displacement of ventilation and PaCO2 down the isometabolic hyperbola (Figure 2, top panel) This means that the apneic threshold will be reached with extremely small transient increases in alveolar ventilation[45]. Non-positive airway pressure treatments of central sleep apnea aimed at ameliorating one or more components of high loop gain Congestive heart failure The use of nocturnal supplemental O2 in the mildly hyperoxic range addresses the primary problem of excessive chemoreceptor sensitivity and has successfully reduced AHI and eliminated CIH in several descriptive studies using relatively small numbers of patients with CHF2,62,63. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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