Augmented Sympathetic Activation During Short-Term Hypoxia and High-Altitude Exposure in Subjects Susceptible to High-Altitude Pulmonary Edema

Duplain, Hervé; Vollenweider, L; Delabays, Alain; Nicod, Pascal; Bärtsch, Peter; Scherrer, Urs

doi:10.1161/01.cir.99.13.1713

Cited by 195 publications

(136 citation statements)

References 28 publications

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“…A loss of sensitivity of the sinus node secondary to excessive sympathetic neurohumoral activity has been proposed to be one of the factors at the origin of reduced LF in heart failure (5). Increased neural and humoral sympathetic activities have been reported as features of established AMS (4,11,21). We may speculate that, as in heart failure, a loss of sensitivity of the sinus node secondary to excessive and more sustained sympathetic neurohumoral activity could explain the blunted LF RR NU we observed in subjects with AMS.…”

Section: Cardiovascular Variability and Amsmentioning

confidence: 53%

“…At low altitude, subjects underwent physical examination, ECG, and autonomic function assessment as described above. The autonomic assessment was performed at rest (baseline) and during short-term hypocapnic hypoxia with a 12% O 2-in-N2 gas mixture (4), which the subjects breathed by mouth from a 120-liter reservoir bag. At 20 min after instrumentation, the subjects were exposed to 15 min of hypoxic gas, the first 5 min serving to reach a steady state.…”

Section: Data Collectionmentioning

confidence: 99%

“…A marked increase in peripheral sympathetic activity is a common feature of mountain sickness (4,11) and has also been suggested to contribute to the genesis of high-altitude pulmonary edema (4). Whether autonomic hyperactivation may play a role in the genesis of AMS is not known.…”

mentioning

confidence: 99%

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Autonomic cardiovascular regulation in subjects with acute mountain sickness

Lanfranchi¹,

Colombo²,

Cremona³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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The aims of this study were 1) to evaluate whether subjects suffering from acute mountain sickness (AMS) during exposure to high altitude have signs of autonomic dysfunction and 2) to verify whether autonomic variables at low altitude may identify subjects who are prone to develop AMS. Forty-one mountaineers were studied at 4,559-m altitude. AMS was diagnosed using the Lake Louise score, and autonomic cardiovascular function was explored using spectral analysis of R-R interval and blood pressure (BP) variability on 10-min resting recordings. Seventeen subjects (41%) had AMS. Subjects with AMS were older than those without AMS (P Ͻ 0.01). At high altitude, the lowfrequency (LF) component of systolic BP variability (LFSBP) was higher (P ϭ 0.02) and the LF component of R-R variability in normalized units (LFRRNU) was lower (P ϭ 0.001) in subjects with AMS. After 3 mo, 21 subjects (43% with AMS) repeated the evaluation at low altitude at rest and in response to a hypoxic gas mixture. LFRRNU was similar in the two groups at baseline and during hypoxia at low altitude but increased only in subjects without AMS at high altitude (P Ͻ 0.001) and did not change between low and high altitude in subjects with AMS. Conversely, LFSBP increased significantly during short-term hypoxia only in subjects with AMS, who also had higher resting BP (P Ͻ 0.05) than those without AMS. Autonomic cardiovascular dysfunction accompanies AMS. Marked LFSBP response to short-term hypoxia identifies AMS-prone subjects, supporting the potential role of an exaggerated individual chemoreflex vasoconstrictive response to hypoxia in the genesis of AMS.hypoxia; autonomic nervous system; heart rate; blood pressure ACUTE MOUNTAIN SICKNESS (AMS) is a complex syndrome characterized by headache, gastrointestinal symptoms, weakness, insomnia, and certain neurological signs, including ataxia and changes in mental status (1). It may occur in subjects ascending to Ͼ2,500 m and is reported in 53% of those at Ͼ4,000-m altitude (6,22).AMS is generally harmless and transient but may occasionally progress to the more serious life-threatening cerebral and pulmonary forms of mountain sickness, i.e., high-altitude cerebral and pulmonary edema (1, 6).The exact mechanism causing AMS is unknown, although the prevailing hypothesis points to a process within the central nervous system (1), possibly an altered adaptation to the neurohumoral and hemodynamic adjustments during hypoxia (8). A marked increase in peripheral sympathetic activity is a common feature of mountain sickness (4, 11) and has also been suggested to contribute to the genesis of high-altitude pulmonary edema (4). Whether autonomic hyperactivation may play a role in the genesis of AMS is not known.The autonomic nervous system plays a role in the modulation of the oscillatory behavior of the cardiovascular system (23, 32a). Spectral analysis of variability in the R-R interval is a recognized tool that allows quantification of the oscillatory components, which in short-term recordings appear mainly organized...

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Section: Cardiovascular Variability and Amsmentioning

confidence: 53%

Section: Data Collectionmentioning

confidence: 99%

See 1 more Smart Citation

Autonomic cardiovascular regulation in subjects with acute mountain sickness

Lanfranchi¹,

Colombo²,

Cremona³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…They have lower HVR [12,67] and stronger sympathetic tone [68]. HVR is set largely by the peripheral chemoreceptors, which results in a lower alveolar oxygen tension and higher carbon dioxide tension at the same altitude as HAPE-resistant subjects, and thus leads to a stronger stimulus for HPV [69].…”

Section: Haemodynamicsmentioning

confidence: 99%

Acute high-altitude sickness

2017

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At any point 1-5 days following ascent to altitudes ⩾2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

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“…An inverse relationship between sympathetic nerve activity and arterial SpO 2 in subjects with and without history of high altitude pulmonary oedema has been observed. 42 Sympathetic nerve activity was also directly related to pulmonary artery pressure. Even though this study was conducted under different conditions (after 24---36 h of staying at 4559 m above sea level), the relationship between sympathetic activity and SpO 2 remains important.…”

Section: Correlation Between Hrv Measurements In Normoxia and Spo 2 Imentioning

confidence: 99%

Cardiorespiratory parameters during submaximal exercise under acute exposure to normobaric and hypobaric hypoxia

Basualto-Alarcón

Rodas

Galilea

et al. 2012

Apunts. Medicina de l'Esport

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Seven healthy young men were submitted twice to a hypoxia tolerance test at a simulated altitude (3000 m). Their first acute exposure was in a hypobaric chamber; and the second, in a hypoxic tent. Cardiorespiratory parameters and heart rate variability measurements were obtained under each hypoxic condition. A significant decrease of 6% to 8% compared to normal oxygen conditions was observed in arterial oxygen saturation (SpO 2 ) in both hypoxic conditions at rest; whereas exercise led to decreases of 10% in SpO 2 despite an increase of 27% in respiratory minute volume. The low frequency (LF) and high frequency (HF) components of heart rate variability significantly changed from normoxia (LF: 37.1, HF: 62.9, LF/HF: 1.27) to hypobaric hypoxia (HH) (LF: 49.1, HF: 50.6, LF/HF: 1.96). However, these changes were not observed under normobaric hypoxia. Thus, heart rate variability behaved differently in the two hypoxic conditions, supporting the hypothesis that normobaric hypoxia and hypobaric hypoxia are not equal stimuli to the cardiovascular and respiratory systems. A correlation was found between sympathetic and vagal modulations in normoxia and SpO 2 at exercise under hypobaric hypoxia (HH). Individuals with higher sympathetic modulation (LF%) in normoxia had higher SpO 2 at exercise under HH (r = 0.808, P < 0.05) and individuals with higher vagal modulation (HF%) in normoxia showed a trend to lower SpO 2 in exercise under HH (r = −0.636, P = 0.125). This opens up the possibility of using this correlation as a tool for predicting the individual capacity to altitude acclimatization. © 2011 Consell Català de l'Esport. Generalitat de Catalunya. Published by Elsevier España, S.L. All rights reserved. * Corresponding author. E-mail address: gviscor@ub.edu (G. Viscor). PALABRAS CLAVEVariabilidad de la frecuencia cardiaca; Prueba de tolerancia a hipoxia; Tienda hipóxica; Cámara hipobárica; Saturación arterial de oxígeno Parámetros cardiorrespiratorios durante ejercicio submáximo en hipoxia aguda hipobárica y normobáricaResumen Siete jóvenes sanos y en buena condición física realizaron dos pruebas de tolerancia a hipoxia a una altitud simulada de 3.000 m. La primera fue en cámara hipobárica, mientras que la segunda se efectuó en una tienda hipóxica. Se registraron varios parámetros cardiorrespiratorios y la variabilidad de la frecuencia cardiaca. En comparación con las condiciones de normoxia, se observó un decremento significativo del 6% al 8% en la saturación de oxígeno arterial (SpO 2 ) en reposo en ambas condiciones de hipoxia. El ejercicio desencadenó descensos de un 10% en SpO 2 pese a un incremento del 27% del volumen minuto ventilatorio. Tanto los componentes de baja (LF) como alta frecuencia (HF) de la variabilidad del ritmo cardiaco cambiaron significativamente en hipoxia hipobárica (LF: 49,1, HF: 50,6, LF/HF: 1,96) respecto a normoxia (LF: 37,1, HF: 62,9, LF/HF: 1,27). Estos cambios no se apreciaron en condiciones de hipoxia normobárica, lo cual apoya la hipótesis de que la hipoxia hipobárica y norm...

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Augmented Sympathetic Activation During Short-Term Hypoxia and High-Altitude Exposure in Subjects Susceptible to High-Altitude Pulmonary Edema

Cited by 195 publications

References 28 publications

Autonomic cardiovascular regulation in subjects with acute mountain sickness

Autonomic cardiovascular regulation in subjects with acute mountain sickness

Acute high-altitude sickness

Cardiorespiratory parameters during submaximal exercise under acute exposure to normobaric and hypobaric hypoxia

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