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The Effect of Inspired Hypoxia and Hyperoxia on Respiratory Sinus Arrhythmia Reactivity
Author(s) -
Lazar Brendan,
Nguyen Stephanie,
Betton Matthew,
Olar Evan,
Day Trevor A.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.09895
Subject(s) - hyperoxia , vagal tone , hypoxia (environmental) , expiration , cardiology , anesthesia , ventilation (architecture) , respiratory system , medicine , oxygenation , heart rate , lung volumes , chemistry , heart rate variability , lung , oxygen , blood pressure , physics , thermodynamics , organic chemistry
Respiratory sinus arrhythmia (RSA) is the normal fluctuation in heart rate (HR) in phase with the respiratory cycle, whereby HR increases during inspiration and decreases during expiration. The underlying mechanisms and potential utility remain elusive. RSA magnitude is thought to be affected by autonomic balance, whereby a dominant parasympathetic nervous system (NS) at rest facilitates RSA, and sympathetic NS activation attenuates its magnitude. Carotid body stimulation via acute hypoxia elicits sympathetic activation, whereas hyperoxia facilitates sympathetic withdrawal. In addition, RSA has been hypothesized to facilitate improvements in ventilation/perfusion (V/Q) matching, improving oxygenation when hypoxic. We hypothesized that (a) acute hypoxia and hyperoxia would increase and decrease the magnitude of RSA reactivity, respectively and (b) when hypoxic, those with larger RSA magnitude during deep breathing would have larger improvements in oxygen saturation (SpO 2 ). Healthy participants (n=13) were instrumented with a pneumotachometer and coached to breathe at three percentages (30, 40 and 50%) of their forced vital capacity (FVC) using visual cues while inspiring room air (21% F I O 2 ), hypoxia (13.5% F I O 2 ), hyperoxia (100% F I O 2 ). RSA was quantified via the peak‐valley approach, and RSA reactivity (RSA R ) was quantified via linear regression to calculate the slope of changes in RSA magnitude across all three FVC levels. RSA magnitude increased linearly with increases in inspired tidal volume in all three gases (R 2 >0.98). No significant differences were found in RSA R slopes between room air (0.32±0.2 ΔBPM/%FVC), hypoxia (0.33±0.26 ΔBPM/%FVC), and hyperoxia (0.34±0.26 ΔBPM/%FVC; P=0.97). There was also no correlation between RSA magnitude during deep breathing (50%FVC) and the associated improvements in SpO 2 in hypoxia (r=−0.11, P=0.72). Given that RSA R is not affected by oxygen availability, our data provides evidence that hypoxic stimulation of the carotid bodies elicits activation of both arms of the autonomic nervous system, maintaining autonomic balance and normal heart rate variability. In addition, RSA magnitude does not appear to bestow advantages on V/Q matching in the context of acute hypoxia. Support or Funding Information MRU Faculty of Science and Technology