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

Abstract

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...

Children at high altitude have less nocturnal periodic breathing than adults

“…The shorter cycle length of periodic breathing additionally contributed to a much lower fraction of the night-time spent with periodic breathing, i.e. ,10%, compared with 22-34% in adults, which is similar to the corresponding value of 25% previously observed in adults at 3,650 m [8]. To evaluate potential mechanisms responsible for the greater stability of ventilation in children, the current authors applied the concepts described by DEMPSEY [30], NAKAYAMA et al [14] and XIE et al [33], as illustrated in figure 4.…”

“…Acute exposure to hypobaric hypoxia at 3,450 m resulted in a similar degree of hypoxaemia in children and adults with a mean arterial O 2 saturation of 84-86% (table 1), which is comparable to the mean nocturnal O 2 saturation of 86% previously observed in healthy adults at 3,605 m [8], but lower than the value of 91% recorded at 3,109 m in children aged 3-36 months [31]. According to the expected ventilatory stimulation at altitude [2], V9E and mean inspiratory flow, which reflect respiratory centre drive [32], were proportionally increased by 22% to 42% in children and adults, while PET,CO 2 , the study surrogate of Pa,CO 2 , was decreased to 33 mmHg, indicating a similar degree of hypoxic-induced hyperventilation in children and adults (table 1).…”

“…Periodic breathing was defined as a pattern of waxing and waning of ventilation with periods of hyperventilation alternating with central apnoeas/hypopnoeas for at least three successive cycles, with hypopnoeas showing a .50% amplitude reduction of the inductive plethysmographic VT signal compared with the preceding 2-min baseline of stable breathing for .5 s ( fig. 1) [5,8,25]. The number of periodic breathing cycles, their length (the cycle time), and the fraction of TIB spent with periodic breathing were determined.…”

“…Validation of the calibration in the morning after sleep studies revealed a deviation of tidal volume (VT) by inductance plethysmography from corresponding flow meter values of f20% in all instances. Wrist actigraphy was performed as an indirect measure of sleep and wakefulness (Actiwatch; Cambridge Neurotechnology, Cambridge, UK) [8,24].…”

“…Periodic breathing characterised by crescendodecrescendo ventilation with hyperpnoea alternating with hypopnoea/apnoea is typically observed in adults at high altitude. Periodic breathing causes frequent arousals from sleep [6,7] resulting in poor sleep quality, one of the manifestations of acute mountain sickness [8,9]. There is a considerable inter-subject variability in periodic breathing due to individual differences in autonomic control of ventilation [10].…”