Worsening of central sleep apnea at high altitude—a role for cerebrovascular function

2013 ◽  
Vol 114 (8) ◽  
pp. 1021-1028 ◽  
Author(s):  
Keith R. Burgess ◽  
Samuel J. E. Lucas ◽  
Kelly Shepherd ◽  
Andrew Dawson ◽  
Marianne Swart ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
High Altitude ◽  
Repeated Measures ◽  
Sleep Onset ◽  
Central Sleep Apnea ◽  
Blood Gases ◽  
Periodic Breathing ◽  
Apnea Hypopnea Index ◽  
Arterial Blood ◽  
Cerebrovascular Function

Although periodic breathing during sleep at high altitude occurs almost universally, the likely mechanisms and independent effects of altitude and acclimatization have not been clearly reported. Data from 2005 demonstrated a significant relationship between decline in cerebral blood flow (CBF) at sleep onset and subsequent severity of central sleep apnea that night. We suspected that CBF would decline during partial acclimatization. We hypothesized therefore that reductions in CBF and its reactivity would worsen periodic breathing during sleep following partial acclimatization. Repeated measures of awake ventilatory and CBF responsiveness, arterial blood gases during wakefulness. and overnight polysomnography at sea level, upon arrival (days 2–4), and following partial acclimatization (days 12–15) to 5,050 m were made on 12 subjects. The apnea-hypopnea index (AHI) increased from to 77 ± 49 on days 2–4 to 116 ± 21 on days 12–15 ( P = 0.01). The AHI upon initial arrival was associated with marked elevations in CBF (+28%, 68 ± 11 to 87 ± 17 cm/s; P < 0.05) and its reactivity to changes in PaCO2 [>90%, 2.0 ± 0.6 to 3.8 ± 1.5 cm·s−1·mmHg−1 hypercapnia and 1.9 ± 0.4 to 4.1 ± 0.9 cm·s−1·mmHg−1 for hypocapnia ( P < 0.05)]. Over 10 days, the increases resolved and AHI worsened. During sleep at high altitude large oscillations in mean CBF velocity (CBFv) occurred, which were 35% higher initially (peak CBFv = 96 cm/s vs. peak CBFv = 71 cm/s) than at days 12–15. Our novel findings suggest that elevations in CBF and its reactivity to CO2 upon initial ascent to high altitude may provide a protective effect on the development of periodic breathing during sleep (likely via moderating changes in central Pco2).

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

2021 ◽  
Author(s):  
Jordan D. Bird ◽  
Anne Kalker ◽  
Alexander N Rimke ◽  
Jason S Chan ◽  
Garrick Chan ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
Oxygen Saturation ◽  
High Altitude ◽  
Central Sleep Apnea ◽  
Periodic Breathing ◽  
Oxygen Desaturation ◽  
Apnea Hypopnea Index ◽  
Peripheral Oxygen Saturation ◽  
Oxyhemoglobin Saturation ◽  
Rapid Ascent

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.

scholarly journals The Contribution of Arterial Blood Gases in Cerebral Blood Flow Regulation and Fuel Utilization in Man at High Altitude

2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Altitude ◽  
Cerebral Metabolism ◽  
Venous Blood ◽  
Blood Gases ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood Gases ◽  
Arterial Blood ◽  
Cerebrovascular Function

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.

scholarly journals Increasing cerebral blood flow reduces the severity of central sleep apnea at high altitude

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 ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Sleep Apnea ◽  
Healthy Volunteers ◽  
High Altitude ◽  
Ventilatory Response ◽  
Central Sleep Apnea ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Central Chemoreceptors

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.

Alterations in cerebral dynamics at high altitude following partial acclimatization in humans: wakefulness and sleep

2007 ◽  
Vol 102 (2) ◽  
pp. 658-664 ◽  
Author(s):  
Philip N. Ainslie ◽  
Katie Burgess ◽  
Prajan Subedi ◽  
Keith R. Burgess
Keyword(s):  
Blood Pressure ◽  
Sleep Apnea ◽  
High Altitude ◽  
Cerebral Autoregulation ◽  
Central Sleep Apnea ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Low Altitude ◽  
Dynamic Cerebral Autoregulation

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.

scholarly journals Adaptive Servoventilation as Treatment for Central Sleep Apnea Due to High-Altitude Periodic Breathing in Nonacclimatized Healthy Individuals

2018 ◽  
Vol 19 (2) ◽  
pp. 178-184 ◽  
Author(s):  
Jeremy E. Orr ◽  
Erica C. Heinrich ◽  
Matea Djokic ◽  
Dillon Gilbertson ◽  
Pamela N. Deyoung ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
High Altitude ◽  
Central Sleep Apnea ◽  
Periodic Breathing ◽  
Healthy Individuals ◽  
Adaptive Servoventilation

060 Challenging the current assessment criteria for scoring central sleep apnea at altitude

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A25-A25
Author(s):  
Jordan Bird ◽  
Jason Chan ◽  
Alexander Rimke ◽  
Anne Kalker ◽  
Garrick Chan ◽  
...  
Keyword(s):  
Sleep Apnea ◽  
High Altitude ◽  
Detection Threshold ◽  
Central Sleep Apnea ◽  
Upper Airway ◽  
Assessment Criteria ◽  
Apnea Hypopnea Index ◽  
Engineering Research ◽  
Obstructive Sleep ◽  
Underlying Mechanisms

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

scholarly journals The effect of acetazolamide on sleep apnea at high altitude: a systematic review and meta-analysis

2016 ◽  
Vol 11 (1) ◽  
pp. 20-29 ◽  
Author(s):  
Hsin-Ming Liu ◽  
I-Jen Chiang ◽  
Ken N. Kuo ◽  
Cher-Ming Liou ◽  
Chiehfeng Chen
Keyword(s):  
Sleep Apnea ◽  
High Altitude ◽  
Meta Analysis ◽  
Periodic Breathing ◽  
Effect Sizes ◽  
Cochrane Library ◽  
Apnea Hypopnea Index ◽  
Obstructive Sleep ◽  
Daily Dose ◽  
Healthy Participants

Background: Acetazolamide has been investigated for treating sleep apnea in newcomers ascending to high altitude. This study aimed to assess the effect of acetazolamide on sleep apnea at high altitude, determine the optimal therapeutic dose, and compare its effectiveness in healthy trekkers and obstructive sleep apnea (OSA) patients. Methods: PubMed, Embase, Scopus, Cochrane Library, and Airiti Library databases were searched up to July 2015 for randomized controlled trials (RCTs) performed above 2500 m in lowlanders and that used acetazolamide as intervention in sleep studies. Studies including participants with medical conditions other than OSA were excluded. Results: Eight studies of 190 adults were included. In healthy participants, the pooled mean effect sizes of acetazolamide on Apnea–Hypopnea Index (AHI), percentage of periodic breathing time, and nocturnal oxygenation were 34.66 [95% confidence interval (CI) 25.01–44.30] with low heterogeneity ( p = 0.7, I2 = 0%), 38.56% (95% CI 18.92–58.19%) with low heterogeneity ( p = 0.24, I2 = 28%), and 4.75% (95% CI 1.35–8.15%) with high heterogeneity ( p < 0.01, I2 = 87%), respectively. In OSA patients, the pooled mean effect sizes of acetazolamide on AHI and nocturnal oxygenation were 13.18 (95% CI 9.25–17.1) with low heterogeneity ( p = 0.33, I2 = 0%) and 1.85% (95% CI 1.08–2.62%) with low heterogeneity ( P = 0.56, I2 = 0%). Conclusions: Acetazolamide improves sleep apnea at high altitude by decreasing AHI and percentage of periodic breathing time and increasing nocturnal oxygenation. Acetazolamide is more beneficial in healthy participants than in OSA patients, and a 250 mg daily dose may be as effective as higher daily doses for healthy trekkers.

scholarly journals Randomized controlled trial of an integrated approach to treating insomnia and improving the use of positive airway pressure therapy in veterans with comorbid insomnia disorder and obstructive sleep apnea

SLEEP ◽  
2020 ◽  
Author(s):  
Cathy A Alessi ◽  
Constance H Fung ◽  
Joseph M Dzierzewski ◽  
Lavinia Fiorentino ◽  
Carl Stepnowsky ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Sleep Onset ◽  
Apnea Hypopnea Index ◽  
Sleep Onset Latency ◽  
Pressure Therapy ◽  
Comorbid Insomnia ◽  
Obstructive Sleep

Abstract Study Objectives Cognitive behavioral therapy for insomnia (CBTI) for comorbid insomnia and obstructive sleep apnea (OSA) has had mixed results. We integrated CBTI with a positive airway pressure (PAP) adherence program and tested effects on sleep and PAP use. Methods 125 veterans (mean age 63.2, 96% men, 39% non-Hispanic white, 26% black/African American, 18% Hispanic/Latino) with comorbid insomnia and newly-diagnosed OSA (apnea-hypopnea index ≥ 15) were randomized to 5-weekly sessions integrating CBTI with a PAP adherence program provided by a “sleep coach” (with behavioral sleep medicine supervision), or 5-weekly sleep education control sessions. Participants and assessment staff were blinded to group assignment. Outcomes (baseline, 3 and 6 months) included Pittsburgh Sleep Quality Index (PSQI), 7-day sleep diary (sleep onset latency [SOL-D], wake after sleep onset [WASO-D], sleep efficiency [SE-D]), 7-day actigraphy (SE-A), and objective PAP use (hours/night and nights ≥ 4 h). Insomnia Severity Index (ISI), Epworth Sleepiness Scale (ESS), and Functional Outcomes of Sleep Questionnaire-10 (FOSQ-10) were also collected. Results Compared to controls, intervention participants showed greater improvement (baseline to 3 and 6 months, respectively) in PSQI (−3.2 and −1.7), SOL-D (−16.2 and −15.5 minutes), SE-D (10.5% and 8.5%), SE-A (4.4% and 2.6%) and more 90-day PAP use (1.3 and 0.9 more hours/night, 17.4 and 11.3 more nights PAP ≥ 4 h). 90-day PAP use at 3 months was 3.2 and 1.9 h/night in intervention versus controls. Intervention participants also had greater improvements in ISI, ESS, and FOSQ-10 (all p &lt; 0.05). Conclusions An intervention integrating CBTI with a PAP adherence program delivered by a supervised sleep coach improved sleep and PAP use in adults with comorbid insomnia and OSA. Trial Registration ClinicalTrials.gov Study name: Novel Treatment of Comorbid Insomnia and Sleep Apnea in Older Veterans URL: https://clinicaltrials.gov/ct2/results?cond=&term=NCT02027558&cntry=&state=&city=&dist= Registration: NCT02027558

393 Comparison of Oxygenation Abnormalities Between Obstructive Sleep Apnea and Central Sleep Apnea

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A156-A157
Author(s):  
Sikawat Thanaviratananich ◽  
Hao Cheng ◽  
Maria Pino ◽  
Krishna Sundar
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Demographic Data ◽  
Central Sleep Apnea ◽  
Nrem Sleep ◽  
Rate Of Change ◽  
Apnea Hypopnea Index ◽  
P Value ◽  
Obstructive Sleep ◽  
Cheyne Stokes Breathing

Abstract Introduction The apnea-hypopnea index (AHI) is used as a generic index to quantify both central sleep apnea (CSA) and obstructive sleep apnea (OSA) syndromes. Patterns of oxygenation abnormalities seen in CSA and OSA may be key to understanding differing clinical impacts of these disorders. Oxygen desaturation and resaturation slopes and durations in OSA and CSA were compared between OSA and CSA patients. Methods Polysomnographic data of patients aged 18 years or older with diagnosis of OSA and CSA, at University of Iowa Hospitals and Clinics, were analyzed and demographic data were collected. Oximetric changes during hypopneas and apneas were studied for desaturation/resaturation durations and desaturation/resaturation slopes. Desaturation and resaturation slopes were calculated as rate of change in oxygen saturation (ΔSpO2/Δtime). Comparison of hypoxemia-based parameters between patients with OSA and CSA was performed using unpaired t-test. Results 32 patients with OSA with median AHI of 15.4 (IQR 5.1 to 30.55) and median ODI of 15.47 (IQR 9.50 to 29.33) were compared to 15 patients with CSA with a median AHI of 20.4 (IQR 12.6 to 47.8) and median ODI of 27.56 (IQR 17.99 to 29.57). The mean number of desaturation and resaturation events was not significantly different between patients with OSA and CSA (OSA - 106.81±87.93; CSA - 130.67±76.88 with a p-value 0.1472). 4/15 CSA patients had Cheyne-Stokes breathing, 2/15 had treatment emergent central sleep apnea, 1/15 had methadone-associated CSA and for 8/15, no etiologies for CSA were found. Mean desaturation durations was significantly longer in OSA (20.84 s ± 5.67) compared to CSA (15.94 s ± 4.54) (p=0.0053) and consequently the desaturation slopes were steeper in CSA than OSA (-0.35%/sec ±0.180 vs. -0.243 ± 0.073; p=0.0064). The resaturation duration was not significantly longer in OSA (9.76 s ± 2.02) than CSA (9.057 s ± 2.17) (p=0.2857). Differences between desaturation duration and slopes between CSA and OSA persisted during REM and NREM sleep, and in supine sleep. Conclusion As compared to OSA, patients with CSA have different patterns of desaturations and resaturations with lesser hypoxic burden with CSA. This may have implications on the clinical outcomes seen between these two disorders. Support (if any):

Sign in / Sign up

Export Citation Format

Share Document