Sustained hyperoxia stabilizes breathing in healthy individuals during NREM sleep

Abstract

The present study was designed to determine whether hyperoxia would lower the hypocapnic apneic threshold (AT) during non-rapid eye movement (NREM) sleep. Nasal noninvasive mechanical ventilation was used to induce hypocapnia and subsequent central apnea in healthy subjects during stable NREM sleep. Mechanical ventilation trials were conducted under normoxic (room air) and hyperoxic conditions (inspired PO(2) > 250 Torr) in a random order. The CO(2) reserve was defined as the minimal change in end-tidal PCO(2) (PET(CO(2))) between eupnea and hypocapnic central apnea. The PET(CO(2)) of the apnea closest to eupnea was designated as the AT. The hypocapnic ventilatory response was calculated as the change in ventilation below eupnea for a given change in PET(CO(2)). In nine participants, compared with room air, exposure to hyperoxia was associated with a significant decrease in eupneic PET(CO(2)) (37.5 ± 0.6 vs. 41.1 ± 0.6 Torr, P = 0.001), widening of the CO(2) reserve (-3.8 ± 0.8 vs. -2.0 ± 0.3 Torr, P = 0.03), and a subsequent decline in AT (33.3 ± 1.2 vs. 39.0 ± 0.7 Torr; P = 001). The hypocapnic ventilatory response was also decreased with hyperoxia. In conclusion, 1) hyperoxia was associated with a decreased AT and an increase in the magnitude of hypocapnia required for the development of central apnea. 2) Thus hyperoxia may mitigate the effects of hypocapnia on ventilatory motor output by lowering the hypocapnic ventilatory response and lowering the resting eupneic PET(CO(2)), thereby decreasing plant gain.

Treatment of Central Sleep Apnea in US Veterans

“…Arousal index was calculated as the number of AASM-defined arousals per hour of sleep and included arousals related to all respiratory events-including RERAs (respiratory effort related arousals). 37 In order to clarify the effect of optimal therapy on sleep continuity, the arousal index was calculated during the baseline study period and, specifically, for the period of PAP or PAP+O 2 therapy that produced an optimal response (as described above).…”

“…Periodic breathing (or Cheyne-Stokes respiration pattern) has been defined as repetitive crescendo-decrescendo pattern of central apneas and hypopneas lasting ≥ 10 min. 37 To ascertain if periodic breathing produced an optimal response with PAP or PAP+O 2 therapy in each patient, a periodic breathing index was calculated. The highest peak in the sine-wave crescendodecrescendo oscillatory breathing pattern was first identified, then the number of peaks were summed and divided by the corresponding total sleep time to arrive at the index.…”

“…Third, the presence of REM sleep could have eliminated the central events during the latter portion of the PAP titration; however, the majority of sleep time was in NREM sleep with REM occupying only 8% to 14% of the TST. Fourth, we referred to the AASM scoring manual 37 for a qualitative definition of Cheyne-Stokes/periodic breathing pattern. However, proper quantification of periodic breathing cycles requires concomitant measurement of esophageal or supraglottic pressure for accurate classification of central and obstructive events, especially hypopnea.…”

“…The "alternate" scoring criterion provided by the 2007 AASM manual was used to score hypopneas: 50% reduction in flow associated with a 3% oxygen desaturation or an arousal. 37 Patients were diagnosed with OSA if the sum of the obstructive apneas and hypopneas per hour of sleep (the apnea-hypopnea index [AHI]), was ≥ 5/h. Patients were diagnosed with CSA if the number of CA per hour of sleep (central apnea index [CAI]) was > 5/h during a baseline PSG or the diagnostic portion of a split-night PSG.…”

Reduced respiratory neural activity elicits a long-lasting decrease in the CO2 threshold for apnea in anesthetized rats

“…Moreover, although modulation of the AT and RT is well recognized (Altose et al, 1986; Boden et al, 1998; Chowdhuri et al, 2010b; Duffin et al, 2005; Nakayama et al, 2002; Pleschka et al, 1965; Tanaka et al, 1993), the ability of these important respiratory parameters to undergo plasticity is relatively unknown. Here, we tested the hypothesis that patterns of neural apnea associated with iPMF elicit long-lasting changes in the CO 2 -dependent AT and RT for phrenic inspiratory activity.…”