Is Syncope Related to Moderate Altitude Exposure?

Nicholas, Richard

doi:10.1001/jama.1992.03490070086048

Cited by 35 publications

(25 citation statements)

References 15 publications

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“…The observed decrease in baroreXex sensitivity in hypoxia sheds some light on why acute exposure to hypoxia can result in syncope (Nicholas et al 1992;Westendorp et al 1997). Furthermore, in contrast to the potentially beneWcial higher autonomic cardiac modulation, which was observed in hypoxia after carbohydrate loading , the results of the present study suggest that oral carbohydrate loading, although it evidently causes sympathoexcitation, exerts no beneWcial eVect on the baroreXex blood pressure regulation, as evident from a signiWcantly lower baroreXex sensitivity in the CHO, as compared to the control experiment, in both normoxic and hypoxic phases of the present study.…”

Section: Discussionmentioning

confidence: 93%

“…However, assessing BRS will nevertheless provide indirect information about the eYciency of baroreXex system to maintain optimal blood pressure in a variety of conditions (Jordan et al 2002). Second, syncope at high altitude is most often induced within the Wrst 24 h of arrival at high altitude (Nicholas et al 1992), thus over a time period which is usually longer than the majority of experimental acute hypoxic exposures. Thus, in real life, a longer interplay between local, respiratory, cardiovascular, and cerebrovascular control systems takes place than in experimental conditions, but mid-term measurements of parameters, such as, for example, muscle sympathetic nerve activity that may signiWcantly add to the conclusions of the present study, may well not be feasible over such time period.…”

Section: Discussionmentioning

confidence: 99%

“…It has been proposed that hypoxia decreases BRS (Sagawa et al 1997;Roche et al 2002), that susceptibility to syncope may be increased at high altitude (Nicholas et al 1992), and that exposure to acute severe hypoxia can be a suYcient cause for syncope in healthy individuals (Westendorp et al 1997). To a certain extent, however, these negative eVects of hypoxia may be attenuated by carbohydrate loading.…”

Section: Introductionmentioning

confidence: 99%

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Baroreflex sensitivity in acute hypoxia and carbohydrate loading

Klemenc¹,

Golja

2011

Eur J Appl Physiol

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Hypoxia decreases baroreflex sensitivity (BRS) and can be a sufficient cause for syncope in healthy individuals. Carbohydrate loading enhances efferent sympathetic activity, which affects cardiac contractility, heart rate and vascular resistance, the main determinants of blood pressure. Thus, in both normoxia and hypoxia, carbohydrate loading may be more than simply metabolically beneficial, as it may affect blood pressure regulation. We hypothesised that carbohydrate loading will, in both normoxia and hypoxia, alter the regulation of blood pressure, as reflected in a change in baroreflex sensitivity. Fourteen subjects participated in two experiments, composed of a 15-min normoxic period, after which the subjects ingested water or an equal amount of water with carbohydrates. A 30-min rest period was then followed by a 10-min second normoxic and a 30-min hypoxic period. Blood pressure and heart rate were monitored continuously during the experiment to determine BRS. Despite an increased sympathetic activation, reflected in increased heart rate (P < 0.001) BRS was lower (P < 0.01) after carbohydrate loading, as compared to the water experiment, in both normoxic [23.7 (12.4) versus 28.8 (13.8) ms/mmHg] and hypoxic [16.8 (11.0) versus 24.3 (12.3) ms/mmHg] phases of the present study. As BRS was decreased in acute hypoxic exposure, the results confirm that hypoxia interferes with blood pressure regulation. However, although oral carbohydrate loading induced sympathoexcitation, it did not improve blood pressure regulation in hypoxia, as evident from the BRS data. Baroreflex effects of other forms of carbohydrate loading, not causing postprandial blood shifts to digestive system, should therefore be investigated.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Baroreflex sensitivity in acute hypoxia and carbohydrate loading

Klemenc¹,

Golja

2011

Eur J Appl Physiol

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“…However, medical emergencies among passengers during flight seem to be rare [19±21]. This disparity may depend on several factors [22]. Hypoxaemia-related symptoms may be rare because the cabin pressure during most flights corresponds to an altitude lower than 2,438 m, as described by COTTRELL et al [5].…”

Section: Discussionmentioning

confidence: 99%

Development of severe hypoxaemia in chronic obstructive pulmonary disease patients at 2,438 m (8,000 ft) altitude

Christensen¹,

Ryg²,

Refvem³

et al. 2000

Eur Respir J

103

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Development of severe hypoxaemia in chronic obstructive pulmonary disease patients at 2,438m (8,000 ft) altitude. C.C. Christensen, M. Ryg, O.K. Refvem, O.H. Skjùnsberg. #ERS Journals Ltd 2000. ABSTRACT: The arterial oxygen tensions (Pa,O 2 ) in chronic obstructive pulmonary disease (COPD) patients travelling by air, should, according to two different guidelines, not be lower than 7.3 kPa (55 mmHg) and 6.7 kPa (50 mmHg), respectively, at a cabin pressure altitude of 2,438 m (8,000 ft). These minimum in-flight Pa,O 2 values are claimed to correspond to a minimum Pa,O 2 of 9.3 kPa (70 mmHg) at sea-level. The authors have tested whether this limit is a safe criterion for predicting severe in-flight hypoxaemia.The authors measured arterial blood gases at sea-level, at 2,438 m and at 3,048 m (10,000 ft) in an altitude chamber at rest and during light exercise in 15 COPD patients with forced expiratory volume in one second (FEV1) <50% of predicted, and with sea-level Pa,O 2 >9.3 kPa.Resting Pa,O 2 decreased below 7.3 kPa and 6.7 kPa in 53% and 33% of the patients, respectively, at 2,438 m, and in 86% and 66% of the patients at 3,048 m. During light exercise, Pa,O 2 dropped below 6.7 kPa in 86% of the patients at 2,438 m, and in 100% of the patients at 3,048 m. There was no correlation between Pa,O 2 at 2,438 m and preflight values of Pa,O 2 , FEV1 or transfer factor of the lung for carbon monoxide.In contrast to current medical guidelines, it has been found that resting arterial oxygen tension >9.3 kPa at sea-level does not exclude development of severe hypoxaemia in chronic obstructive pulmonary disease patients travelling by air. Light exercise, equivalent to slow walking along the aisle, may provoke a pronounced aggravation of the hypoxaemia. Eur Respir J 2000; 15: 635±639.

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“…Orthostatic tolerance appears to be reduced after acute exposure to high altitude (HA, hypobaric chamber at 3660 m; <24 hours) (Blaber et al, 2003) and there have been reports of syncope upon standing at HA in otherwise healthy young individuals (Nicholas et al, 1992;Perrill, 1993;Freitas et al, 1996;Basnyat et al, 2004). It has been established that a common cause of syncope is initial orthostatic hypotension (IOH) (Wieling et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Initial Orthostatic Hypotension at High Altitude

Thomas

Burgess

Basnyat

et al. 2010

High Altitude Medicine & Biology

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There are several reports on syncope occurring following standing at high altitude (HA), yet description of the detailed physiological responses to standing at HA are lacking. We examined the hypothesis that appropriate physiological adjustments to upright posture would be compromised at HA (5050 m). Ten healthy volunteers stood up rapidly from supine rest, for 3 min, at sea level and at 5050 m. Beat-to-beat mean arterial blood pressure (MAP, Finometer), middle cerebral artery blood velocity (MCAv, Transcranial Doppler), end-tidal PCO(2) and PO(2), and heart rate (ECG) were recorded continuously. After 14 days at HA, baseline MAP and MCAv were not different to sea level, although HR was elevated. Neither the magnitude of initial (<15 s) responses to standing, nor the time course of initial recovery differed at HA compared with sea level (p > 0.05). By 3 min of standing, MAP was restored to supine values both at sea level (-3 +/- 12 mmHg) and HA (4 +/- 10 mmHg), although there was more complete recovery of HR at sea level (+13 +/- 10 b.min(-1), p = 0.02 vs. + 23 +/- 10 b.min(-1), p = 0.01). Reduced MCAv at 3 min was comparable at sea level and altitude (both -16%). These data indicate that initial cardiovascular and cerebrovascular responses to standing are unaltered when partially acclimatized to HA.

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Is Syncope Related to Moderate Altitude Exposure?

Abstract: Short-term exposure to moderate altitude may be related to otherwise unexplained syncope in healthy young adults. We suggest the name high-altitude syncope for this entity and encourage further research in this area.

Cited by 35 publications

References 15 publications

Baroreflex sensitivity in acute hypoxia and carbohydrate loading

Baroreflex sensitivity in acute hypoxia and carbohydrate loading

Development of severe hypoxaemia in chronic obstructive pulmonary disease patients at 2,438 m (8,000 ft) altitude

Initial Orthostatic Hypotension at High Altitude

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