Severity of Central Sleep Apnea Does Not Improve Sleeping Oxygen Saturation During Ascent to High Altitude

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Jordan Bird ◽  
A. Kalker ◽  
J. Chan ◽  
A. Rimke ◽  
G. Chan ◽  
...  
Author(s):  
Jordan D. Bird ◽  
Anne Kalker ◽  
Alexander N Rimke ◽  
Jason S Chan ◽  
Garrick Chan ◽  
...  

Central sleep apnea (CSA) is characterized by periodic breathing (PB) during sleep, defined as intermittent periods of apnea/hypopnea and hyperventilation, with associated acute fluctuations in oxyhemoglobin saturation (SO2). CSA has an incidence of ~50% in heart failure patients but is universal at high-altitude (HA; ≥2,500 m), increasing in severity with further ascent and/or time at altitude. However, whether PB is adaptive, maladaptive, or neutral with respect to sleeping SO2 at altitude is unclear. We hypothesized that PB severity would improve mean sleeping SO2 during acclimatization to HA due to relative, intermittent hyperventilation subsequent to each apnea. We utilized portable sleep monitors to assess the incidence and severity of CSA via apnea-hypopnea index (AHI) and oxygen desaturation index (ODI), and peripheral oxygen saturation (SpO2) during sleep during two ascent profiles to HA in native lowlanders: (I) rapid ascent to and residence at 3,800 m for 9 days/nights (n=21) and (II) incremental ascent to 5,160 m over 10 days/nights (n=21). In both ascent models, severity of AHI and ODI increased and mean sleeping SpO2 decreased, as expected. However, during sleep on the last night/highest altitude of both ascent profiles, neither AHI nor ODI were correlated with mean sleeping SpO2. In addition, mean sleeping SpO2 was not significantly different between high and low CSA. These data suggest that CSA is neither adaptive nor maladaptive with regard to mean oxygen saturation during sleep, owing to the relative hyperventilation between apneas, likely correcting transient apnea-mediated oxygen desaturation and maintaining mean oxygenation.


2018 ◽  
Vol 124 (5) ◽  
pp. 1341-1348 ◽  
Author(s):  
Keith R. Burgess ◽  
Samuel J. E. Lucas ◽  
Katie M. E. Burgess ◽  
Kate E. Sprecher ◽  
Joseph Donnelly ◽  
...  

Earlier studies have indicated an important role for cerebral blood flow in the pathophysiology of central sleep apnea (CSA) at high altitude, but were not decisive. To test the hypothesis that pharmacologically altering cerebral blood flow (CBF) without altering arterial blood gas (ABGs) values would alter the severity of CSA at high altitude, we studied 11 healthy volunteers (8M, 3F; 31 ± 7 yr) in a randomized placebo-controlled single-blind study at 5,050 m in Nepal. CBF was increased by intravenous (iv) acetazolamide (Az; 10 mg/kg) plus intravenous dobutamine (Dob) infusion (2–5 μg·kg−1·min−1) and reduced by oral indomethacin (Indo; 100 mg). ABG samples were collected and ventilatory responses to hypercapnia (HCVR) and hypoxia (HVR) were measured by rebreathing and steady-state techniques before and after drug/placebo. Duplex ultrasound of blood flow in the internal carotid and vertebral arteries was used to measure global CBF. The initial 3–4 h of sleep were recorded by full polysomnography. Intravenous Az + Dob increased global CBF by 37 ± 15% compared with placebo ( P < 0.001), whereas it was reduced by 21 ± 8% by oral Indo ( P < 0.001). ABGs and HVR were unchanged in both interventions. HCVR was reduced by 28% ± 43% ( P = 0.1) during intravenous Az ± Dob administration and was elevated by 23% ± 30% ( P = 0.05) by Indo. During intravenous Az + Dob, the CSA index fell from 140 ± 45 (control night) to 48 ± 37 events/h of sleep ( P < 0.001). Oral Indo had no significant effect on CSA. We conclude that increasing cerebral blood flow reduced the severity of CSA at high altitude; the likely mechanism is via a reduction in the background stimulation of central chemoreceptors.NEW & NOTEWORTHY This work is significant because it shows convincingly for the first time in healthy volunteers that increasing cerebral blood flow will reduce the severity of central sleep apnea in a high-altitude model, without the potentially confounding effects of altering partial pressure of arterial carbon dioxide or the ventilatory response to hypoxia. The proposed mechanism of action is that of increasing the removal of locally produced CO2from the central chemoreceptors, causing the reduction in hypercapnic ventilatory response, hence reducing loop gain.


2007 ◽  
Vol 102 (2) ◽  
pp. 658-664 ◽  
Author(s):  
Philip N. Ainslie ◽  
Katie Burgess ◽  
Prajan Subedi ◽  
Keith R. Burgess

We tested the hypothesis that, following exposure to high altitude, cerebrovascular reactivity to CO2 and cerebral autoregulation would be attenuated. Such alterations may predispose to central sleep apnea at high altitude by promoting changes in brain Pco2 and thus breathing stability. We measured middle cerebral artery blood flow velocity (MCAv; transcranial Doppler ultrasound) and arterial blood pressure during wakefulness in conditions of eucapnia (room air), hypocapnia (voluntary hyperventilation), and hypercapnia (isooxic rebeathing), and also during non-rapid eye movement (stage 2) sleep at low altitude (1,400 m) and at high altitude (3,840 m) in five individuals. At each altitude, sleep was studied using full polysomnography, and resting arterial blood gases were obtained. During wakefulness and polysomnographic-monitored sleep, dynamic cerebral autoregulation and steady-state changes in MCAv in relation to changes in blood pressure were evaluated using transfer function analysis. High altitude was associated with an increase in central sleep apnea index (0.2 ± 0.4 to 20.7 ± 23.2 per hour) and an increase in mean blood pressure and cerebrovascular resistance during wakefulness and sleep. MCAv was unchanged during wakefulness, whereas there was a greater decrease during sleep at high altitude compared with low altitude (−9.1 ± 1.7 vs. −4.8 ± 0.7 cm/s; P < 0.05). At high altitude, compared with low altitude, the cerebrovascular reactivity to CO2 in the hypercapnic range was unchanged (5.5 ± 0.7 vs. 5.3 ± 0.7%/mmHg; P = 0.06), while it was lowered in the hypocapnic range (3.1 ± 0.7 vs. 1.9 ± 0.6%/mmHg; P < 0.05). Dynamic cerebral autoregulation was further reduced during sleep ( P < 0.05 vs. low altitude). Lowered cerebrovascular reactivity to CO2 and reduction in both dynamic cerebral autoregulation and MCAv during sleep at high altitude may be factors in the pathogenesis of breathing instability.


2018 ◽  
Vol 19 (2) ◽  
pp. 178-184 ◽  
Author(s):  
Jeremy E. Orr ◽  
Erica C. Heinrich ◽  
Matea Djokic ◽  
Dillon Gilbertson ◽  
Pamela N. Deyoung ◽  
...  

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A25-A25
Author(s):  
Jordan Bird ◽  
Jason Chan ◽  
Alexander Rimke ◽  
Anne Kalker ◽  
Garrick Chan ◽  
...  

Abstract Introduction Sleep disordered breathing comes in two forms: obstructive and central sleep apnea (SA). Obstructive sleep apnea (OSA) is caused by upper airway collapse during sleep, and is associated with increases in morbidity and mortality. Conversely, central sleep apnea (CSA) results from increases in respiratory chemosensitivity to blood gas challenges in the context of high-altitude ascent. CSA increases in severity and apneas shorten in duration with higher ascent and/or time spent at altitude. Although both types of SA are characterized by intermittent periods of apnea and hyperventilation, the underlying mechanisms and phenotypes between OSA and CSA are different. A universal scoring system for the two types of context-dependent SA may lead to errors in quantification. The American Association of Sleep Medicine (AASM) developed assessment criteria for SA, which are universally-utilized for all types of SA to quantify an apnea-hypopnea index (AHI; events/hour), where apneas are scored as cessation of breathing ≥10-sec. We aimed to assess the effect of reducing the apnea-detection threshold (ADT) to &lt;10-sec to quantitatively assess the extent that a shorter ADT affects the scoring of AHI in the context of high-altitude ascent, where CSA is universal. Methods We assessed CSA using portable polysomnography (ApneaLink, ResMed) during ascent to 5160m in the Nepal Himalaya over 10 days in 15 healthy participants. Files were archived digitally for later analysis using automated scoring software (ApneaLink Reporting Software, ResMed). We quantified and compared AHI using AASM criteria (i.e., 10-sec ADT) and a shorter 5-sec ADT. Results AHI was 3.9±4.1 events/hour at 1045m prior to ascent, with AHI increasing to 37.5±32.8 events/hour (P&lt;0.0001) at 5160m after 10 days of incremental ascent using AASM criteria (i.e., 10-sec ADT). When the ADT was reduced to 5-sec at 5160m, AHI was increased to 61.6±38.1 (+61%; P=0.0002). Conclusion This preliminary report suggests that the AASM criterion for scoring apneas, which is broadly applied to OSA at low altitude, may underestimate the assessment and quantification of CSA with ascent to and prolonged stays at high altitude. Development of distinct assessment criteria for OSA and CSA may be warranted. Support (if any) Natural Science sand Engineering Research Council of Canada


2015 ◽  
Vol 16 (3) ◽  
pp. 313-314 ◽  
Author(s):  
Tomasz J. Kuźniar

2017 ◽  
Vol 89 (1) ◽  
pp. 103-106
Author(s):  
A K Myrzaakhmatova

Obstructive sleep apnea (OSA) is an important and socially relevant problem of modern medicine, which is referred to as a most common pathological condition. The problem of OSA is especially urgent for inhabitants of high mountainous regions, as a combination of climatic, social, and cultural factors can significantly affect the course of the disease in both indigenous highlanders and people temporarily residing at high altitude. The paper reviews the current literature covering the problem of OSA at high altitude. It gives the data of Russian and foreign literature on the pathogenesis and clinical presentation of OSA. The author also analyzes an update on the impact of high altitude on the course of OSA in indigenous highlanders and people temporarily living at high altitude. She emphasizes the role of hypobaric hypocapnia as the most important factor for the development of central sleep apnea in the presence of conditions that are obstructive and aggravating the course of the disease.


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