Mechanisms of hypoxia‐induced periodic breathing during sleep in humans.

Abstract

SUMMARY1. Ventilation was studied during wakefulness and sleep in six healthy humans in normoxia (mean barometric pressure (PB) = 740 torr), and in hypobaric hypoxia (AB = 455 torr).2. Hypoxia caused hyperventilation and hypocapnic alkalosis (APpao2 =c-7 torr)during wakefulness and in all sleep states. 3. Periodic breathing was the predominant pattern of breathing in all stages of non-rapid eye movement (non-r.e.m.) sleep in hypoxia, but was rarely observed during wakefulness or r.e.m. sleep.4. Periodic breathing was composed of repetitive oscillations of reproducible cycle length characterized by clusters of breaths with augmented inspiratory effort (VT/TI) and highly variable distribution of breath-to-breath minute ventilation (VE) and tidal volume (VT), which alternated regularly with prolongations of the expiratory pause of the last breath of each cluster (apnea duration = 5-18 see). 5. Hypoxia-induced periodic breathing was eliminated by: (a) acute restoration of normoxia coincident with a 3-6 torr increase in PaIc2; and (b) augmented F1,c2(at constant arterial oxygen saturation) which rapidly and reversibly eliminated apneas and stabilized breathing pattern with a < 2 torr increase in Paco2. If hypocapnia was prevented (by augmented F1,co,) during acute induction of hypoxia in non-r.e.m. sleep, periodic breathing was also prevented. 6. We propose that the genesis of hypoxia-induced periodic breathing requires the combination of hypoxia and hypocapnia. Periodicity results from oscillations in CO2 about a C02-apnea threshold whose functional expression is critically linked to sleep state.

Ventilatory control in patients with sleep apnoea and left ventricular dysfunction: comparison of obstructive and central sleep apnoea

“…Eucapnic hypoxia is not associated with periodic respiration. This primary role for hypoxia is confirmed by the elimination of unstable respiration with supplemental oxygen [29]. In contrast, oxygen is reported to reduce (by approximately 50%), but not abolish, central apnoeas in heart failure, suggesting that, while hypoxia amplifies unstable respiratory control in heart failure [30], it is not the main factor responsible for central apnoea.…”

Impact of changes in inspired oxygen and carbon dioxide on respiratory instability in the lamb

“…A further important difference is that the human controller apparently has a relatively fixed apneic threshold for CO 2 (19,30), whereas the lamb and several other species do not (12,28). It seems likely that these fundamental differences are the reason hypoxia normally precipitates PB in sleeping humans (6,27), whereas it has never been reported to do so in the lamb.…”

Acute mountain sickness is related to nocturnal hypoxemia but not to hypoventilation

“…However, direct measurements of respiratory drive would have been required to corroborate this point. A potentially confounding influence on nocturnal ventilation derives from the sleep/wakefulness-state dependence of ventilatory drive [24]. Since actigraphic recordings indicate reduced sleep efficiency in AMS subjects, their higher ventilation might in part be related to a shorter nocturnal sleep period (table 3).…”

“…Transient reductions in breathing amplitude to v50% baseline over 5-10 s were also scored as apnoeas/hypopnoeas if they occurred as part of a periodic breathing pattern with waxing and waning of ventilation with periods of hyperventilation alternating with central apnoeas/ hypopnoeas over at least three successive cycles ( fig. 1) [24,25]. Central apnoeas/hypopnoeas were identified by absence of rib cage-abdominal asynchrony [14].…”