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Effect of Prolonged High‐Altitude Exposure on Heart Rate Response to Central Sleep Apnea
Author(s) -
Berthelsen Lindsey,
Steele Andrew,
Vanden Berg Emily,
Bird Jordan,
Thrall Scott,
Wilson Richard,
Jendzjowsky Nicholas,
Day Trevor,
Steinback Craig
Publication year - 2022
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.2022.36.s1.r4193
Subject(s) - bradycardia , apnea , medicine , heart rate , anesthesia , sleep apnea , effects of high altitude on humans , hyperventilation , central sleep apnea , cardiology , polysomnography , blood pressure , anatomy
Central sleep apnea (CSA) is common at high‐altitude (>2500m) and is characterized by a cyclical pattern of hyperventilation and transient arterial hypocapnia, triggering apnea. We have demonstrated that voluntary wakeful apnea at altitude promotes a greater degree of bradycardia and cardiac arrhythmias than at sea level. However, whether bradyarrhythmias are observed during CSA at altitude has not been investigated. We investigated the duration dependent effect of altitude on heart rate changes during periods of apnea overnight. We hypothesized that overnight apnea would result in a greater magnitude of bradycardia with prolonged hypoxic exposure. Central sleep apnea (Apnea‐hypopnea index; AHI) was assessed overnight at low altitude (1045m), early (Night 2‐3) and late (Night 9‐10) at high altitude (N=14; 6 female). Heart rate (HR) and rhythm (electrocardiogram; ECG lead II) was collected alongside sleep data (RESMED Apnealink) to quantify sleep apnea events and desaturations. HR data were averaged over 10s prior to and 10s following apneas. Delta HR during apnea (BL HR – Nadir HR apnea) was determined to characterize bradycardia. Differences in heart rate prior to, during, and post apnea were compared using a repeated‐measures ANOVA design, with a Holm‐Sidak post‐hoc analysis where main effect of condition was significant. The magnitude of bradycardia during apneas between early and late time points were compared using a paired t‐test. Additional analyses of sex differences were performed using a two‐way mixed model ANOVA. AHI was augmented at high altitude (main effect p=0.012) but not different between early and late time points (p=0.193). The incidence of central apneic events was greater late at high‐altitude compared to low altitude (p=0.0045). Overnight oxygen saturation was decreased at high altitude (main effect of time, p<0.01) but was elevated late (84 ± 3%) compared to early (82 ± 4%) at altitude (p=0.038). Average HR overnight was similar between early (74 ± 11bpm) and late (69 ± 10bpm) time points (p=0.134). HR dropped during apneas at early (‐6.2±4.6 bpm; p=0.018) and late (‐6.4±2.8 bpm; p<0.001) timepoints. Female participants had a lower AHI at high altitude (p=0.006) but tended to have a greater bradycardia (‐7.7± 5.6bpm early, ‐7.6±2.9bpm late) compared to men (‐3.9±0.68bpm early; ‐4.5±1.4bpm late; main effect of sex, p=0.052). We demonstrate that CSA at altitude is associated with bradycardia that does not appear to become greater with prolonged exposure. It appears females may be less susceptible to CSA but have a greater bradycardic response during apneas compared to males.