Autonomic cardiovascular regulation in subjects with acute mountain sickness

Abstract

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...

Normo or hypobaric hypoxic tests: propositions for the determination of the individual susceptibility to altitude illnesses

“…In NH and in HH, AMS mean scores are related to ventilatory variables (Df in NH, V T in HH) and to CpO 2 whereas in NH, AMS mean scores are also Eur J Appl Physiol (2007) 100:193-205 203 related to HCR (P = 0.04). An exaggerated chemoreflex activity could explain the relationships between these cardioventilatory variables and AMS means scores, as suggested by Lanfranchi et al (2005). Consequently, CpO 2 appears still to be an important variable to predict AMS mean scores in our experimental conditions.…”

“…More original is the characterization of AMS from a quantitative and not from a qualitative point of view. Indeed, today subjects are divided in AMS+ or AMS-subjects (Richalet et al 1988;Rathat et al 1992;Lanfranchi et al, 2005). This procedure is very interesting but, for medical considerations, it is also interesting for a subject found susceptible to AMS to know the potential AMS severity and the risk of mal-adaptation that he could have during an ascent.…”

“…Richalet et al (1988) and Rathat et al (1992) showed that, during a retrospective study, the most AMS-clinically subjects presented at least one abnormal response (ventilatory or cardiac response to hypoxia at F I O 2 = 0.115), especially during exercise. Recently, Lanfranchi et al (2005) reported that an abnormally high low-frequency component of systolic blood pressure response during 10 min of hypoxia, indicating an exaggerated chemoreflex vasoconstrictive response to hypoxia, may predict AMS. On contrast, Sutton et al (1976), Milledge et al (1988Milledge et al ( , 1991 and Savourey et al (1995a) did not find any correlation between AMS and HVR but these last authors showed that both sea level and altitude PetO 2 (4,500 m) were predictive for AMS.…”

Oximetry, heart rate variability, and the diagnosis of mild-to-moderate acute mountain sickness

“…Earlier research has shown contradictory findings when evaluating measures of heart rate variability in participants with AMS under hypoxic conditions. For instance, individuals with AMS had elevated LF/HF ratios when subjected to 8-12 h of simulated hypobaric hypoxia (4850 m) [6], whereas in a field study, Lanfranchi et al [7] showed that the LF/HF ratio tended to be lower in 17 participants with AMS than those without. Clearly, further research is warranted to determine the effects of AMS on measures of heart rate variability and the prognostic value of changes in these measures in establishing the risk for AMS.…”

Severe Acute Mountain Sickness and Suspected High Altitude Cerebral Edema Related to Nitroglycerin Use

“…The leading theory is that HACE is a vasogenic edema (Basnyat and Murdoch, 2003;Hackett and Roach, 2004;Van Osta et al, 2005), due to raised intracranial pressure concomitant to increased permeability of the blood-brain barrier. Experimental studies have demonstrated that stimulation of central noradrenergic output increases such permeability (Raichle et al, 1978); raised sympathetic activity has been documented in humans at high altitude (Reeves, 1993), in particular in individuals suffering from AMS (Lanfranchi et al, 2005). Moreover blood-brain barrier permeability may be increased by several chemical mediators, including iNOS-generated nitric oxide.…”