Respiratory sinus arrhythmia during obstructive sleep apnoeas in humans.

Respiratory sinus arrhythmia (RSA) reflects parasympathetic modulation of heart rate (HR) during the respiratory cycle. Since the time-course of RSA during obstructive sleep apnoea (OSA) is not known, an analysis was made of ECG in samples of consecutive OSA recorded in 5 patients during NREM sleep while breathing room air (OSA-AIR, mean lowest SaO2 83.0 +/- 6.5%) or supplemental oxygen (OSA +/- O2, mean lowest SaO2 91.7 +/- 2.2%), respectively. For each breath, HR at the transition from expiration to inspiration (HRei), and HR at maximal inspiration (HRie) were calculated, and the inspiratory increase in HR estimated as the ratio: HRie/subsequent HRie. Similarly, the expiratory decrease in HR was estimated as: HRie/subsequent HRei. RSA was identified by an inspiratory increase in HR (HRei/HRie < 1), and an expiratory decrease in HR (HRie/HRei > 1). OSA-AIR and OSA + O2 did not differ for duration or oesophageal pressure nadir. During OSA-AIR, the inspiratory increase in HR became progressively more marked from the first occluded to the first open breath, whereas during OSA + O2 it remained stable throughout the apnoeic cycle. The expiratory decrease in HR remained constant during the apnoeic phase, but was blunted in the first open breaths irrespective of O2 administration. In summary, hypoxia appeared to affect inspiratory, but not expiratory HR. Instead, the expiratory slowing of HR transiently disappeared in the immediate post-apnoeic phase, suggesting a possible effect of arousal or pulmonary inflation. These data suggest that the parasympathetic system may contribute to cardiovascular regulation during OSA.