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Duration at High Altitude Influences the Onset of Arrhythmogenesis During Apnea
Author(s) -
Berthelsen Lindsey,
Van Diepen Sean,
Steele Andrew,
Vanden Berg Emily,
Bird Jordan,
Thrall Scott,
Wilson Richard,
Jendzjowsky Nicholas,
Day Trevor,
Steinback Craig
Publication year - 2021
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.2021.35.s1.01952
Subject(s) - medicine , apnea , effects of high altitude on humans , heart rate , bradycardia , cardiology , anesthesia , hypoxia (environmental) , altitude (triangle) , ventilation (architecture) , pulse oximetry , blood pressure , oxygen , mechanical engineering , chemistry , geometry , mathematics , organic chemistry , engineering , anatomy
Excitation of both sympathetic and parasympathetic systems occur concurrently at high‐altitude (chronic hypoxia), via the carotid chemoreflex. We have demonstrated this autonomic conflict manifests as cardiac arrhythmias during voluntary apnea. We sought to determine the duration of hypoxic exposure at high‐altitude necessary to unmask cardiac arrhythmias during instances of voluntary apnea. We hypothesized that the occurrence of cardiac arrhythmias during apnea would be increased following 24 hours of high‐altitude exposure. Measurements of oxygen saturation (SpO 2 ; pulse oximetry) and continuous electrocardiogram (ECG; lead II) were collected in 22 participants (8 females) at low altitude (1045m) and over 8 consecutive days at high‐altitude (3800m). Following a 2 minute baseline participants performed an end‐expiratory apnea to volitional breakpoint. ECG rate and rhythm were evaluated at baseline and during apnea. The nadir heart rate was used to quantify bradycardia and abnormal ECG rhythm was classified based on origin (e.g., sinus node) and type (e.g., sinus arrest). Differences in resting ventilation, SpO 2 , and the heart rate response to apnea on each day at high‐altitude (Day 1‐8) were compared to that at low altitude (Day 0) using a repeated‐measures ANOVA design, with a Holm‐Sidak post‐hoc analysis where main effect of time was significant. Baseline SpO 2 was lower for all days at high‐altitude (average of all days, 89±3) compared to low altitude (98 ± 2) (p<0.01). At high‐altitude (all days), baseline heart rate was higher compared to low altitude (p<0.01). A main effect of time (p<0.01) was identified for the delta change in heart rate during apnea. At low altitude, the average apnea induced decrease in heart rate was ‐9±15bpm, whereas the average decrease in heart rate at high altitude (all days) was ‐24±16bpm. Bradycardia became more pronounced with acclimatization, with the greatest drop in heart rate (‐31±16bpm) occurring on Day 5. At low altitude 14% (3/22) of participants developed arrhythmias during apnea. At high‐altitude, cardiac arrhythmias during apnea became most prevalent (>50%) following Day 5. Changes in saturation during apnea and apnea duration were not associated with the magnitude of bradycardia during apnea (saturation, r= ‐0.007 p=0.92; apnea duration, r=0.005 p=0.94). Interestingly, the magnitude of bradycardia was correlated with the incidence (percentage) of arrhythmia per day (r=0.8; p=0.004), suggesting a similar underlying mechanism. Our data indicate chronic hypoxia is associated with a progressive increase in vagal tone, as indicated by augmented bradycardia during apnea and progressively increased incidence of arrhythmia at high‐altitude. Additionally, the increased incidence of arrhythmia with acclimatization suggests that chemoreflex sensitization may play a role in this phenomenon. This study provides insight into cardiac electrophysiology at high‐altitude and has implications as a future functional model for exploring the effects of heightened chemoreflex stress on autonomic control of heart.