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

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.

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).

The Use of a Fully Automated Automatic Adaptive Servoventilation Algorithm in the Acute and Long-term Treatment of Central Sleep Apnea

CHEST Journal ◽  
2015 ◽  
Vol 148 (6) ◽  
pp. 1454-1461 ◽  
Author(s):  
Shahrokh Javaheri ◽  
David Winslow ◽  
Pamela McCullough ◽  
Paul Wylie ◽  
Meir H. Kryger
Keyword(s):  
Sleep Apnea ◽  
Central Sleep Apnea ◽  
Term Treatment ◽  
Adaptive Servoventilation ◽  
Long Term Treatment

Adaptive Servoventilation in Central Sleep Apnea

2014 ◽  
Vol 9 (1) ◽  
pp. 69-85 ◽  
Author(s):  
Winfried J. Randerath ◽  
Shahrokh Javaheri
Keyword(s):  
Sleep Apnea ◽  
Central Sleep Apnea ◽  
Adaptive Servoventilation

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.

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