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Respiratory sinus arrhythmia during obstructive sleep apnoeas in humans
Author(s) -
BONSIGNORE MARIA R.,
ROMANO S.,
MARRONE O.,
INSALACO G.
Publication year - 1995
Publication title -
journal of sleep research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.297
H-Index - 117
eISSN - 1365-2869
pISSN - 0962-1105
DOI - 10.1111/j.1365-2869.1995.tb00190.x
Subject(s) - medicine , cardiology , anesthesia , ventilation (architecture) , vagal tone , respiratory system , obstructive sleep apnea , heart rate , expiration , apnea , non rapid eye movement sleep , heart rate variability , blood pressure , mechanical engineering , eye movement , engineering , ophthalmology
SUMMARY 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 SaO 2 83.0 ±6.5%) or supplemental oxygen (OSA + O 2 , mean lowest SaO 2 91.7 ± 2.2%), respectively. For each breath, HR at the transition from expiration to inspiration (HR ei ), and HR at maximal inspiration (HR ie ) were calculated, and the inspiratory increase in HR estimated as the ratio: HR ei /subsequent HR ie . Similarly, the expiratory decrease in HR was estimated as: HR ie /subsequent HR ei . RSA was identified by an inspiratory increase in HR (HR ei /HR ie <1), and an expiratory decrease in HR (HR ie /HR ei > 1). OSA‐AIR and OSA + O 2 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 + O 2 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 O 2 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.