High-Altitude Syncope: History Repeats Itself

Perrill, Charles V.

doi:10.1001/jama.1993.03500050065015

Cited by 4 publications

(1 citation statement)

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“…Hypoxia‐related syncope is a risk for mountain sojourners, aircraft passengers, and unfit individuals traveling to mountainous locations. 22 Syncope is common, even at moderate altitudes (2700 m), typically occurs <24 hours after ascent, and is likely related to peripheral vasodilatation from acute hypoxic exposure, compounded by cerebral vasoconstriction from hyperventilation‐induced hypocapnia. 23 Among healthy individuals at a simulated altitude of 3660 m, presyncope resulted from ineffective peripheral vasoconstriction refractory to increased sympathetic nerve activity (functional sympatholysis) and insufficient cerebral perfusion because of cerebral vasoconstriction as the result of hypoxic hyperventilation‐induced hypocapnia.…”

Section: Syncope At High Altitudementioning

confidence: 99%

Clinical Implications for Exercise at Altitude Among Individuals With Cardiovascular Disease

Cornwell¹,

Baggish²,

Bhatta³

et al. 2021

JAHA

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An increasing number of individuals travel to mountainous environments for work and pleasure. However, oxygen availability declines at altitude, and hypoxic environments place unique stressors on the cardiovascular system. These stressors may be exacerbated by exercise at altitude, because exercise increases oxygen demand in an environment that is already relatively oxygen deplete compared with sea‐level conditions. Furthermore, the prevalence of cardiovascular disease, as well as diseases such as hypertension, heart failure, and lung disease, is high among individuals living in the United States. As such, patients who are at risk of or who have established cardiovascular disease may be at an increased risk of adverse events when sojourning to these mountainous locations. However, these risks may be minimized by appropriate pretravel assessments and planning through shared decision‐making between patients and their managing clinicians. This American Heart Association scientific statement provides a concise, yet comprehensive overview of the physiologic responses to exercise in hypoxic locations, as well as important considerations for minimizing the risk of adverse cardiovascular events during mountainous excursions.

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Section: Syncope At High Altitudementioning

confidence: 99%

Clinical Implications for Exercise at Altitude Among Individuals With Cardiovascular Disease

Cornwell¹,

Baggish²,

Bhatta³

et al. 2021

JAHA

View full text Add to dashboard Cite

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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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Acute mountain sickness: Do different time courses point to different pathophysiological mechanisms?

Berger

Sareban

Bärtsch

2020

Journal of Applied Physiology

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Acute mountain sickness (AMS) is a syndrome of nonspecific symptoms (i.e., headache, anorexia, nausea, vomiting, dizziness, and fatigue) that may develop in nonacclimatized individuals after rapid exposure to altitudes ≥2,500 m. In field studies, mean AMS scores usually peak after the first night at a new altitude. Analyses of the individual time courses of AMS in four studies performed at 3,450 m and 4,559 m revealed that three different patterns are hidden in the above-described overall picture. In 41% of those who developed AMS (i.e., AMS-C score >0.70), symptoms peaked on day 1, in 39%, symptoms were most prominent on day 2, and in 20%, symptoms were most prominent on day 3. We suggest to name the different time courses of AMS type I, type II, and type III, respectively. Here, we hypothesize that the variation of time courses of AMS are caused by different pathophysiological mechanisms. This assumption could explain why no consistent correlations between an overall assessment of AMS and single pathophysiological factors have been found in a large number of studies over the past 50 yr. In this paper, we will briefly review the fundamental mechanisms implicated in the pathophysiology of AMS and discuss how they might contribute to the three different AMS time courses.

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High-Altitude Syncope: History Repeats Itself

Cited by 4 publications

References 0 publications

Clinical Implications for Exercise at Altitude Among Individuals With Cardiovascular Disease

Clinical Implications for Exercise at Altitude Among Individuals With Cardiovascular Disease

Initial Orthostatic Hypotension at High Altitude

Acute mountain sickness: Do different time courses point to different pathophysiological mechanisms?

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