Key result
Acute exposure to normobaric hypoxia significantly increased RMSSD (33.49 vs. 20.76 ms; p<0.01) compared to ambient air in patients with pulmonary vascular disease.
Why the study?
Patients with pulmonary vascular disease have autonomic cardiovascular dysregulation and may be particularly vulnerable to hypoxia-induced autonomic dysregulation.
Does acute exposure to normobaric hypoxia alter resting heart rate variability in stable patients with pulmonary vascular disease?
Population
17 stable patients with pulmonary vascular disease and resting PaO2 ≥ 7.3 kPa
Comparison
Normobaric hypoxia (FiO2 = 15%) vs ambient air (FiO2 = 21%)
Design
Randomised crossover trial
Authors
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Hypoxia effects on autonomic markers warrant clinical caution in pulmonary vascular disease; leaves open relevance for future autonomic modulation research.
RCT (n=17)
Random order
Does acute exposure to normobaric hypoxia alter resting heart rate variability in stable patients with pulmonary vascular disease?
Absolute Event Rate: 33.49% vs 20.76%
p-value: p=< 0.01
Acute exposure to normobaric hypoxia in patients with pulmonary vascular disease increases heart rate variability, suggesting parasympathetic dominance rather than the expected sympathetic overactivation.
Mészáros et al. (2023) conducted an RCT in Pulmonary vascular disease (n=17). Normobaric hypoxia vs. Ambient air (FiO2 = 21%) was evaluated on Root mean squared sum difference of RR intervals (RMSSD) (p=< 0.01). Acute exposure to normobaric hypoxia significantly increased RMSSD (33.49 vs. 20.76 ms; p<0.01) compared to ambient air in patients with pulmonary vascular disease.
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