+ Acute mountain sickness is associated with sleep desaturation at high altitude
Respirology 2004 9 (4) 485-492
Keith R. BURGESS,1,2 Pamela JOHNSON,1 Natalie EDWARDS, 2 Jackie COOPER,1. 1 Peninsula Private Sleep Laboratory, Sydney, Australia. 2 University of Sydney, Sydney, Australia
Abstract
Study Objectives: This study was intended to demonstrate a biologically important association between acute mountain sickness (AMS) and sleep disordered breathing.
Methods: A total of 14 subjects (eight males, six females aged 36 ± 10 years) were studied at six different altitudes from sea level to 5050 m over 12 days on a trekking route in the Nepal Himalaya. AMS was quantified by Lake Louise (LL) score. At each altitude, sleep was studied by 13 channel polysomnography (PSG). Resting arterial blood gases (ABG) and exercise SaO2 were measured. Ventilatory responses (VR) were measured at sea level. Individual data were analysed for association at several altitudes and mean data were analysed for association over all altitudes.
Results: ABG showed partial acclimatization. For the mean data, there were strong positive correlations between LL score and altitude, and periodic breathing, as expected. Strong negative correlations existed between LL score and PaO2, PaCO2, sleep SaO2 and exercise SaO2, but there was no correlation with sea level VR. There were equally tight correlations between LLs/PaO2 and LL score/ sleep SaO2. The individual data showed no significant correlations with LL score at any altitude, probably reflecting the non-steady state nature of the experiment. In addition, mean SaO2 during sleep was similar to minimum exercise SaO2 at each altitude and minimum sleep SaO2 was lower, suggesting that the hypoxic insult during sleep was equivalent to or greater than walking at high altitude.
Conclusion: It is concluded that desaturation during sleep has a biologically important association
with AMS, and it is speculated that under similar conditions (trekking) it is an important cause of AMS.
+ Central and obstructive sleep apnoea during ascent to high altitude
Respirology 2004 9 (2) 222-229
Keith R. BURGESS,1,2 Pamela L. JOHNSON, 1 Natalie EDWARDS 2
1 Peninsula Private Sleep Laboratory, Sydney, Australia. 2 University of Sydney, Sydney, Australia
Abstract
Study Objectives: The aim of the study was to investigate the relationship between central sleep apnoea (CSA) at high altitude and arterial blood gas tensions, and by inference, ventilatory responsiveness.
Methods: Fourteen normal adult volunteers were studied by polysomnography during sleep,
and analysis of awake blood gases during ascent over 12 days from sea level to 5050 m in the Nepal Himalayas.
Results: Thirteen subjects developed CSA. Linear regression analysis showed tight negative correlations between mean CSA index and mean values for sleep SaO2, PaCO2 and PaO2 over the six altitudes (r2 = 0.74 for all, P < 0.03). Paradoxically there was poor correlation between the individual data for CSA index and those parameters at the highest altitude (5050-m) where CSA was worst (r2 < 0.12 for all, NS), possibly due to variation in degree of acclimatization between subjects. In addition, CSA replaced mild obstructive sleep apnoea during ascent. Obstructive sleep apnoea index fell from 5.5 ± 6.9/h in rapid eye movement sleep at sealevel to 0.1 ± 0.3/h at 5050 m (P < 0.001, analysis of variance), while CSA index rose from 0.1 ± 0.3/h to 55.7 ± 54.4/h (P < 0.001).
Conclusion: There was a general relationship between decreasing PaCO2 and CSA, but there were significant effects from variations in acclimatization that would make hypoxic ventilatory response an unreliable predictor of CSA in individuals.
+ No Evidence of Sleep Apnea in Children with Attention Deficit Hyperactivity Disorder
Clinical Pediatrics 2004 43 (7) 609-614
Jacky COOPER, 1 Louise TYLER, 1 I. WALLACE, 3 Keith R. BURGESS, 1,2,4
1 Peninsula Private Sleep Laboratory, Sydney, Australia, 2 Department of Critical Care, Manly Hospital, 3 Forestway Psychology Centre, Sydney, Australia, 4 University of Sydney, Sydney, Australia.
Abstract
Study Objectives: Children with attention deficit hyperactivity disorder (ADHD) may have a component of sleep apnea causing arousal and contributing to ADHD behavior during the day.
Methods: Twenty non-ADHD children between 4 and 16 years of age were compared with 18 children with ADHD with use of nocturnal polysomnography (PSG) and psychometric tests.
Results: The psychometric testing confirmed that the control group were normal and that the ADHD children fulfilled the diagnostic criteria for ADHD. The PSG showed normal arousal indexes for the ADHD group (9.8 ± 3.9/hr) and controls (10.2 ± 3.1/hr), and normal apnea/hypnea indexes for the ADHD group (1.0 ± 2.4/hr) and controls (0.6 ± 0.9/hr). The sleep architecture was not significantly different between groups.
Conclusion: There were no sleep abnormalities in the ADHD children that could be responsible for, or contributing to, the disorder.
This study was supported by Dalwood Ladies Auxiliary and Peninsula Private Sleep Laboratory.
+ Spirometry values in Himalayan high altitude residents (Sherpas)
Respiratory Physiology & Neurobiology 2002 132 223-232
Adrian P. HAVRYK, 1,2 Mark GILBERT, 1, Keith R. BURGESS 1,2
1 Department of Critical Care, Manly Hospital. 2 University of Sydney, Sydney, Australia. 3 Royal Australasian College of General Practitioners, Melbourne, Australia
Abstract
Methods: We compared the spirometric values of the isolated racial group of Himalayan Sherpas with those predicted for the European Coal and Steel Community (EC&S). 146 normal adult Sherpas (64 males, 82 females) and 103 adolescents (37 females and 66 males, age 10–18 years) resident at an altitude of 3840 m were studied. Predicted values for each adult individual were calculated using the EC&S reference equations and separate Caucasian values for children were used, and new predictive equations for the Sherpa population derived.
Results: The FEV1 of boys, adult male and female Sherpas are all significantly greater than predicted (% Predicted (PP) (95% Confidence Interval (CI)), 113% (110–116), 110% (107–114) and 116% (112–121), Pı0.0001 for all groups) as is forced vital capacity (FVC) (112% (111–119), 113% (109–117) and 121% (117–125) respectively, Pı0.0001 for all groups). Sherpa girls displayed a smaller difference in FEV1 and FVC (PP(CI), 104% (99–109) Pı0.1 and 108% (103–114) P=0.005, respectively).
Conclusions: We conclude that the Sherpa race has significantly larger spirometric values than Caucasians. We speculate that this is an adaptation in response to chronic hypoxia and high levels of habitual exercise.
+ The effect of partial acclimatization to high altitude on loop gain and central sleep apnoea severity
Respirology 2012 17 (5) 835-840
Gareth ANDREWS, 1,2 Philip N AINSLIE, 3 Kelly SHEPHERD, 2 Andrew DAWSON, 2 Marianne SWART , 2 Samuel LUCAS, 3 Keith R BURGESS 1
1 Department of Medicine, University of Sydney, Sydney, Australia, 2 Peninsula Respiratory Group, Sydney, Australia, 3 Department of Physiology, University of Otago, Dunedin, New Zealand
Abstract
Background and Objectives: Loop gain is an engineering term that predicts the stability of a feedback control system, such as the control of breathing. Based on earlier studies at lower altitudes, it was hypothesized that acclimatization to high altitude would lead to a reduction in loop gain and thus central sleep apnoea (CSA) severity.
Methods: This study used exposure to very high altitude to induce CSA in healthy subjects to investigate the effect of partial acclimatization on loop gain and CSA severity. Measurements were made on 12 subjects (age 30 ± 10 years, body mass index 22.8 ± 1.9, eight males, four females) at an altitude of 5050 m over a 2-week period upon initial arrival (days 2–4) and following partial acclimatization (days 12–14). Sleep was studied by full polysomnography, and resting arterial blood gases were measured. Loop gain was measured by the ‘duty cycle’ method (duration of hyperpnoea/ cycle length).
Results: Partial acclimatization to high-altitude exposure was associated with both an increase in loop gain (duty cycle fell from 0.60 ± 0.05 to 0.55 ± 0.06 (P = 0.03)) and severity of CSA (apnoea-hypopnoea index increased from 76.8 ± 48.8 to 115.9 ± 20.2 (P = 0.01)), while partial arterial carbon dioxide concentration fell from 29 ± 3 to 26 ± 2 (P = 0.01).
Conclusions: Contrary to the results at lower altitudes, at high-altitude loop gain and severity of CSA increased.
+ Worsening of central sleep apnea at high altitude – a role for cerebrovascular function
Journal of Applied Physiology 2013 114 8 1021-1028.
Keith R BURGESS, 1,2 Samuel JE LUCAS, 3 Kelly SHEPHERD, 1 Andrew DAWSON, 1 Marianne SWART, 1 Kate N THOMAS, 3 Rebekah AI LUCAS, 3 Joseph DONNELLY, 3 Karen C PEEBLES, 3 Rishi BASNYAT, 4,5 Philip N. AINSLIE, 6
1 Peninsula Sleep Laboratory, Sydney, Australia. 2 University of Sydney, Sydney, Australia. 3 University of Otago, Dunedin, New Zealand. 4 Nepal International Clinic, Kathmandu, Nepal. 5 Banner Good Samaritan Medical Center, Phoenix, USA. 6 Centre for Heart, University of British Columbia, Canada
Abstract
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.
Study Objectives: We hypothesized therefore that reductions in CBF and its reactivity would worsen periodic breathing during sleep following partial acclimatization.
Methods: 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.
Results: 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.
Conclusions: Our novel findings suggest that elevations in CBF and its reactivity to CO(2) 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).
+ Targeted Case Finding for OSA within the Primary Care Setting.
Journal of Clinical Sleep Medicine.
Keith R. Burgess, Ph.D.,1 Adrian Havryk, Ph.D.,1 Stephen Newton, M.B.A.,2 Willis H. Tsai, M.D., F.A.A.S.M.,3 and William A. Whitelaw, M.D., Ph.D.4
1 Peninsula Respiratory Group, Frenchs Forest, NSW, Australia 2 Healthy Sleep Solutions Pty Ltd, Sydney, NSW, Australia 3 Department of Community Health Sciences, University of Calgary, Calgary, Alberta, Canada 4 Department of Medicine, University of Calgary, Calgary, Alberta, Canada
Abstract
Study Objectives:The aim was to determine the feasibility of using an unattended 2-channel device to screen for obstructive sleep apnea in a population of high-risk patients using a targeted, case-finding strategy. The case finding was based on the presence of risk factors not symptoms in the studied population.
Methods: The study took place from June 2007 to May 2008 in rural and metropolitan Queensland and New South Wales. Family doctors were asked to identify patients with any of the following: BMI > 30, type 2 diabetes, treated hypertension, ischemic heart disease. Participants applied the ApneaLink+O2 at home for a single night. The device recorded nasal flow and pulse oximetry. Data were analyzed by proprietary software, then checked and reported by either of two sleep physicians.
Results: 1,157 patients were recruited; mean age 53 +/- 14.6, M/F% = 62/38, mean BMI = 31.8, obesity = 35%, diabetes = 16%, hypertension = 39%, IHD = 5%, Mean Epworth Sleepiness Scale score (ESS) = 8.3. The prevalence of unrecognized OSA was very high: 71% had an AHI > 5/h, 33% had an AHI > 15/h, and 16% had an AHI > 30/h. The ApneaLink+O2 device yielded technically adequate studies in 93% of cases.
Conclusions: The study shows that a "real world" simple low cost case finding and management program, based on unattended home monitoring for OSA, can work well in a population with risk factors and comorbidities associated with OSA, independent of the presence of symptoms. The prevalence of unrecognized OSA was very high.
Access the full article here.
+ Breathing and sleep at high altitude.
Journal of Respiratory Physiology and Neurobiology.
Ainslie PN1, Lucas SJ2, Burgess KR 3,4.
1 Centre of Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Okanagan Campus, British Columbia, Canada. 2 School of Sport, Exercise and Rehabilitation Sciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham, UK. 3 Peninsula Sleep Clinic, Sydney, New South Wales, Australia. 4 Department of Medicine, University of Sydney, Sydney, New South Wales, Australia.
Highlights
• Ventilatory acclimatization to altitude involves cellular and neurochemical re-organization in the peripheral chemoreceptors and CNS.
• Sleep at high altitude is disturbed by various factors, but principally by periodic breathing (PB).
• The extent of PB during sleep at altitude intensifies with duration and severity of exposure and is explained in part by elevations in loop gain.
• Because PB may elevate rather than reduce mean SaO2 during sleep this may represent an adaptive rather than maladaptive response.
• Although new mechanical and pharmacological means are emerging, oral acetazolamide remains the most effective and practical means to reduce PB.
Abstract: We provide an updated review on the current understanding of breathing and sleep at high altitude in humans. We conclude that: (1) progressive changes in pH initiated by the respiratory alkalosis do not underlie early (<48 h) ventilatory acclimatization to hypoxia (VAH) because this still proceeds in the absence of such alkalosis; (2) for VAH of longer duration (>48 h), complex cellular and neurochemical re-organization occurs both in the peripheral chemoreceptors as well as within the central nervous system. The latter is likely influenced by central acid-base changes secondary to the extent of the initial respiratory responses to initial exposure to high altitude; (3) sleep at high altitude is disturbed by various factors, but principally by periodic breathing; (4) the extent of periodic breathing during sleep at altitude intensifies with duration and severity of exposure; (5) complex interactions between hypoxic-induced enhancement in peripheral and central chemoreflexes and cerebral blood flow – leading to higher loop gain and breathing instability – underpin this development of periodic breathing during sleep; (6) because periodic breathing may elevate rather than reduce mean SaO2 during sleep, this may represent an adaptive rather than maladaptive response; (7) although oral acetazolamide is an effective means to reduce periodic breathing by 50–80%, recent studies using positive airway pressure devices to increase dead space, hyponotics and theophylline are emerging but appear less practical and effective compared to acetazolamide. Finally, we suggest avenues for future research, and discuss implications for understanding sleep pathology.
Access the full article here.
|