Low acute hypoxic ventilatory response and hypoxic depression in acute altitude sickness

Moore, Lorna G.; Harrison, G. L.; McCullough, R. E.; McCullough, R. G.; Micco, A. J.; Tucker, Adam; Weil, John V.; Reeves, J. T.

doi:10.1152/jappl.1986.60.4.1407

Cited by 130 publications

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“…In a study by BARTSCH et al [8], subjects with AMS revealed a transient decrease in isocapnic hypoxic ventilatory response (but neither in poikilocapnic hypoxic nor hypercapnic ventilatory response) within 4 h after arrival at 4,559 m, whereas this was not observed in controls. No differences in isocapnic and poikilocapnic hypoxic, and in hypercapnic ventilatory responses were present among AMS and control subjects at low altitude, and after they had spent a night at 4,559 m. A low ventilatory response to hypoxia has also been observed in subjects experiencing symptoms of AMS during short-term exposure to 4,800 m in a hypobaric chamber over up to 7 h [10]. Thus, subjects prone to AMS may have an initial relative hypoventilation within hours after rapid ascent to high altitude.…”

Section: Discussionmentioning

confidence: 76%

“…Hypoxia seems to play an important role [3,6,7]. A reduced ventilatory response to hypoxia, and impaired pulmonary gas exchange related to pulmonary fluid accumulation, and water and salt retention have been implicated in development of exaggerated hypoxemia in subjects with AMS [8][9][10]. As AMS often develops or worsens over the night, when periodic breathing and repetitive oxygen desaturation are also prevalent, a causal relationship or a common pathophysiological pathway have been evaluated [11,12].…”

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confidence: 99%

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Acute mountain sickness is related to nocturnal hypoxemia but not to hypoventilation

Pa¹,

Anastasi²,

Senn³

et al. 2004

Eur Respir J

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Acute mountain sickness is related to nocturnal hypoxemia but not to hypoventilation. P. Erba, S. Anastasi, O. Senn, M. Maggiorini, K.E. Bloch. #ERS Journals Ltd 2004. ABSTRACT: The purpose of the study was to investigate determinants of acute mountain sickness after rapid ascent to high altitude.A total of 21 climbers were studied ascending from v1,200 m to Capanna Regina Margherita, a hut in the Alps at 4,559 m, within v24 h. During their overnight stay at 4,559 m, breathing patterns and ventilation were recorded by calibrated respiratory inductive plethysmography along with pulse oximetry. In the following morning, acute mountain sickness was assessed.Altogether, 11 mountaineers developed pronounced symptoms of acute mountain sickness (Lake Louise score o5) and 10 did not (controls). Compared to controls, subjects with acute mountain sickness had lower nocturnal oxygen saturation (mean¡SD 59¡13% versus 73¡6%), higher minute ventilation (7.94¡2.35 versus 6.06¡ 1.34 L?min -1 ), and greater mean inspiratory flow, a measure of respiratory centre drive (0.29¡0.09 versus 0.22¡0.05 L?s -1 ). Periodic respiration was prevalent but not significantly different among the two groups (apnoea/hypopnea index 60.1¡34.6 versus 47.1¡42.6 events per h).The data suggest that pronounced nocturnal hypoxemia, which was not related to hypoventilation, may have promoted acute mountain sickness. Periodic breathing seems not to play a predominant role in the pathogenesis of acute mountain sickness. Otherwise healthy subjects ascending rapidly to altitudes w2,500 m often develop acute mountain sickness (AMS), a condition characterised by insomnia, headache, dizziness, loss of appetite, nausea and vomiting [1]. In the Alps, symptoms and signs of AMS sufficiently severe to force a reduction in activity were found in 6-8% of climbers examined at altitudes between 2,850 and 3,650 m, and in 30% of climbers at 4,559 m [2]. AMS is promoted by a rapid ascent rate, depends on the altitude reached, and on acclimatisation [3]. It occurs in both sexes, at all ages, and athletic fitness does not protect against it [1,4,5].Despite its high prevalence, the pathophysiology of AMS is incompletely understood. Hypoxia seems to play an important role [3,6,7]. A reduced ventilatory response to hypoxia, and impaired pulmonary gas exchange related to pulmonary fluid accumulation, and water and salt retention have been implicated in development of exaggerated hypoxemia in subjects with AMS [8][9][10]. As AMS often develops or worsens over the night, when periodic breathing and repetitive oxygen desaturation are also prevalent, a causal relationship or a common pathophysiological pathway have been evaluated [11,12]. However, the results of these earlier studies were inconclusive due to the small number of subjects with AMS enrolled, and the lack of quantitative estimation of ventilation during sleep.Therefore, the purpose of the current study was to further explore the potential role of periodic respiration, and other characteristics of breathing patterns, in p...

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Section: Discussionmentioning

confidence: 76%

mentioning

confidence: 99%

Acute mountain sickness is related to nocturnal hypoxemia but not to hypoventilation

Pa¹,

Anastasi²,

Senn³

et al. 2004

Eur Respir J

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“…First, there is a variable degree of susceptibility to acute mountain sickness in the current subjects. Others have shown that individuals not susceptible to acute mountain sickness have a higher HVR than those who are susceptible to acute mountain sickness [28] or to HAPE [8]. If only subjects without a history of severe acute mountain sickness from the control group were compared with HAPE-susceptible subjects, HVR was almost significantly lower (p50.07) in HAPE-susceptible subjects.…”

Section: Pulmonary Vascular Responsementioning

confidence: 94%

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

Dehnert

Grünig²,

Mereles³

et al. 2005

European Respiratory Journal

105

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Individuals susceptible to high-altitude pulmonary oedema (HAPE) are characterised by an abnormal increase of pulmonary artery systolic pressure (PASP) in hypoxia and during normoxic exercise, reduced hypoxic ventilatory response, and smaller lung volume.In 37 mountaineers with well-documented altitude tolerance, it was investigated whether any combination of these noninvasive measurements, including exercise in hypoxia, could improve the identification of HAPE-susceptible subjects at low altitude.HAPE-susceptible subjects showed a significant higher increase of PASP during hypoxia at rest (48¡10 mmHg) compared with controls (38¡3 mmHg), as well as during normoxic exercise (57¡14 versus 38¡7 mmHg) and hypoxic exercise (69¡13 versus 49¡8 mmHg). PASP could not be assessed in three and eight subjects during normoxic or hypoxic exercise, respectively, due to insufficient Doppler profiles or systemic arterial hypertension. Sensitivity (77-94%) and specificity (76-93%) were not significantly different between the various testing conditions. Additional assessment of hypoxic ventilatory response and lung function parameters did not improve identification of HAPE-susceptible subjects in a multivariate analysis.Due to the greater number of missing values in pulmonary artery systolic pressure measurements during hypoxic exercise, it was concluded that pulmonary artery systolic pressure measurements at rest during hypoxia or exercise in normoxia are most feasible for the identification of high-altitude pulmonary oedema-susceptible subjects.KEYWORDS: Doppler echocardiography, exercise, hypoxia, hypoxic ventilatory response, lung volumes, pulmonary artery pressure H igh-altitude pulmonary oedema (HAPE) is a noncardiogenic pulmonary oedema that occurs at an altitude of 4,559 m in up to 6% of otherwise healthy unselected subjects [1]. Altitude, speed of ascent, pre-acclimatisation and, above all, individual susceptibility are determinants for its occurrence. The combination of fast ascent and susceptibility to HAPE increases the incidence of HAPE at 4,559 m to ,60% [1]. Since HAPE is a life-threatening condition, it would be helpful to identify HAPE-susceptible subjects at low altitude, particularly in those with no previous altitude exposure.It has been widely demonstrated that increased hypoxic pulmonary vasoconstriction leading to abnormally high pulmonary artery pressure is the major contributor in the development of HAPE. The crucial role of high pulmonary artery pressure is confirmed by elevated pulmonary artery pressures in patients with HAPE [2-4], enhanced pulmonary vasoconstrictive response in HAPE-susceptible subjects to acute hypoxia [5][6][7][8] or exercise in normoxia [6,7,9]. It is also confirmed by the fact that interventions decreasing pulmonary artery pressure are effective in the treatment [10, 11] and prevention [4] of HAPE. A previous study suggested that pulmonary artery systolic pressure (PASP) does not exceed 40 mmHg in healthy subjects during acute hypoxic exposure (inspiratory oxygen fractio...

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“…In two previous studies (King and Robinson 1972;Moore et al 1986), it was determined that individual differences in ventilatory sensitivities were related to differences in ventilation and AMS symptomatology during subsequent hypobaric exposures. The conclusions derived from these "successful" studies clearly disagree with our results.…”

Section: Discussionmentioning

confidence: 99%

“…However, studies that have directly related pre-altitude ventilatory sensitivities to AMS utilized small numbers of subjects whose data were either selected for analyses after their illness had occurred (King and Robinson 1972) or whose subjects were selected based on prior knowledge that they would or would not get sick (Moore et al 1986). It has not been determined if it is possible t-preselect a subgroup of individuals who are likely to get sick at moderate altitudes froln a larger group of individuals whose susceptibility to AMS is unknown using the results of ventilatory sensitivity tests conducted at low altitudes prior to deployment.…”

Section: Introductionmentioning

confidence: 99%

The Use of Hypoxic and Carbon Dioxide Sensitivity Tests of Predict the Incidence and Severity of Acute Mountain Sickness in Soldiers Exposed to an Elevation of 3800 Meters

Fulco¹,

Trad²,

Forte³

et al. 1991

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OCT 2 2 i9 . 'ii 91-13717UNITED STATES ARMY MEDICAL RESEARCH & DEVELOPMENT COMMANDThe findings in this report are not to be construed as an official Department of the Army positi'n, unless so designated by other authorized documents. DISPOSITION INSTRUCTIONSDestroy this report when no longer needed.Do not return to the originator. THE USE OF HYPOXIC AND CARBON DIOXIDE SENSITIVITY TESTS TO PREDICT THE INCIDENCE AND SEVERITY OF ACUTE MOUNTAIN SICKNESS IN SOLDIERS EXPOSED TO AN ELEVATION OF 3800 METERS.Charles Do., 'eso.:-se -.0,-C:"i t-e to, tf ,ew~nq mst C 'C 0 sea0 at p .-0 :f-g adt 'e.edc a' nc Approved for public release; distribution unlimited. N13x,rr_;-m200wor,iÃ clute mountain sickness (AMS) is characterized by headache, nausea, and dizzines with individual differences occurring susceptibility. At any altitude, there will'be individuals who will show little or no symptoms while others will be severely incapacitated. Previous studies have shown that individuals with no symptoms of AMS tend to ventilate more than those who develop severe symptomis. The main objective of this study was to determine if susceptibility to AM5 can be predlicted from ventilatory responses to breathing hypoxic and carbon dioxi de ĩ as mixtures for 7-10 minutes prior to an altitude exposure. Another obJqctive was to determine 1q there was a difference between cigarette smokers and nonsmokers in susceptibility. Fortyseven soldiers (25 smokers and 22 nonsmokers) performed an isocapnic hp oxic ventilator,' response (HVR) test and a hypercapnic ventilatory response IHCVR test at F Riley, KS (450 mgrnor to being deployed to the Santa Lucia Base Camp, Potosi Bolivia (3500 to 4050 in). AM symptoms were assessed in Bolivia by the self-administered Environmental Symptoms Questionnaire during the first two days of exposure. Eighteen of 47 soldiers (38%) developec AMS. There was no relationship between either of the ventilatory tests and4 the subsequenm development of AM S regardless of smoking history. The results suggest that the use of the HVR and HCVR tests to preselect individuals who will develop AMS at moderate altitudes is no: warranted. It was also found that there was no difference in the incidence rate (40% vs 36%) or sev~ity of AMS batween smokers and nonsmokers. FC-90) of approximately 450 U.S. soldiers and marines were exposed to altitudes ranging from 3500 to 4050 m for nearly rive months on the Andean altiplano, in the vicinity of Potosi, Bolivia, South America to participate in a large construction project. The Task Force consisted principally of engineers and road builders assembled from Ft. Riley, KS and represented the largest commitment of U.S. troops ever exposed to such high altitudes during peacetime or war. The troops conducted an operational scenario comparable to one usually conducted under sea-level conditions. Therefore, a unique opportunity existed to study the incidence and severity of altituderelated illnesses, decrements in physical and mental performance, and changes in dietary habits. The 450 army and m...

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Low acute hypoxic ventilatory response and hypoxic depression in acute altitude sickness

Cited by 130 publications

References 0 publications

Acute mountain sickness is related to nocturnal hypoxemia but not to hypoventilation

Acute mountain sickness is related to nocturnal hypoxemia but not to hypoventilation

Identification of individuals susceptible to high-altitude pulmonary oedema at low altitude

The Use of Hypoxic and Carbon Dioxide Sensitivity Tests of Predict the Incidence and Severity of Acute Mountain Sickness in Soldiers Exposed to an Elevation of 3800 Meters

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