Pre-existing cardiovascular conditions and high altitude travel

Donegani, E; Hillebrandt, David; Windsor, Jeremy S.; Gieseler, Ulf; Rodway, George W.; Schöffl, Volker; Küpper, Thomas

doi:10.1016/j.tmaid.2014.02.004

Cited by 34 publications

(14 citation statements)

References 48 publications

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“…Its efficacy depends on the duration of individual’s exposure to altitude, age, sea level partial pressure of oxygen in arterial blood (PaO 2 ) and minute ventilation. 2 , 3 , 4S,5S These crucial processes include increase in ventilation, cardiac output, red cell mass and blood O 2 carrying capacity, and other metabolic modifications at the microvascular and cellular levels ( Take home figure ). Some of these mechanisms are activated almost immediately, whereas others need hours to days to attain full expression.…”

Section: Physics and Cardiovascular Physiology At High Altitudementioning

confidence: 99%

Clinical recommendations for high altitude exposure of individuals with pre-existing cardiovascular conditions

Parati

Agostoni

Basnyat

et al. 2018

European Heart Journal

151

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Take home figureAdapted from Bärtsch and Gibbs2 Physiological response to hypoxia. Life-sustaining oxygen delivery, in spite of a reduction in the partial pressure of inhaled oxygen between 25% and 60% (respectively at 2500 m and 8000 m), is ensured by an increase in pulmonary ventilation, an increase in cardiac output by increasing heart rate, changes in vascular tone, as well as an increase in haemoglobin concentration. BP, blood pressure; HR, heart rate; PaCO2, partial pressure of arterial carbon dioxide.

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Section: Physics and Cardiovascular Physiology At High Altitudementioning

confidence: 99%

Clinical recommendations for high altitude exposure of individuals with pre-existing cardiovascular conditions

Parati

Agostoni

Basnyat

et al. 2018

European Heart Journal

151

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“…Inconsistencies in the current literature may reflect marked inter-individual variability in the hypertensive response to altitude—a point highlighted recently in the Consensus statement of the Medical Commission of the Union Internationale des Associations d’Alpinisme [ 25 ]. Furthermore, it is difficult to separate the effect of altitude on blood pressure from the multitude of other potentially confounding factors including ascent rate, altitude sickness, dehydration, temperature and stress associated with an environmental change [ 4 , 25 , 26 ]. Consequently, a large prospective dataset of both normotensive and hypertensive individuals with a controlled ascent profile (hypoxic exposure) is required to clarify the altitude threshold, incidence, severity, duration and reversibility of any hypertensive effect.…”

Section: Discussionmentioning

confidence: 99%

High altitude-related hypertensive crisis and acute kidney injury in an asymptomatic healthy individual

et al. 2016

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BackgroundHigh-altitude exposure causes a mild to moderate rise in systolic and diastolic blood pressure. This case report describes the first documented case of a hypertensive crisis at altitude, as well as the first report of the occurrence of acute kidney injury in the context of altitude-related hypertension.Case presentationA healthy, previously normotensive 30-year old, embarked on a trek to Everest Base Camp (5300 m). During his 11-day ascent the subject developed increasingly worsening hypertension. In the absence of symptoms, the individual initially elected to remain at altitude as had previously been the plan. However, an increase in the severity of his hypertension to a peak of 223/119 mmHg resulted in a decision to descend. On descent he was found to have an acute kidney injury that subsequently resolved spontaneously. His blood pressure reverted to normal at sea level and subsequent investigations including a transthoracic echocardiogram, cardiac magnetic resonance imaging, renal ultrasound, and urinary catecholamines were normal.ConclusionThis report challenges the view that transient rises in blood pressure at altitude are without immediate risk. We review the evidence that altitude induces hypertension and discuss the implications for the management of hypertension at altitude.

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“…When treating heart failure in the plateau region (area at an altitude of 2,500 metres above sea level), the increase in pulmonary artery pressure caused by the application of β-AR antagonists can also decrease tolerance, which can then increase the risk of adverse cardiovascular events associated with exposure to high-altitude hypoxia (Agostoni et al, 2011(Agostoni et al, , 2013Bärtsch & Gibbs, 2007;Donegani et al, 2014).…”

Section: Controlmentioning

confidence: 99%

Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats

Zhang

Cao

et al. 2020

Experimental Physiology

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New Findings What is the central question of this study?The acute hypoxic compensatory reaction is based on haemodynamic changes, and β‐adrenoceptors are involved in haemodynamic regulation. What is the role of β‐adrenoceptors in haemodynamics during hypoxic exposure? What is the main finding and its importance?Activation of β2‐adrenoceptors attenuates the increase in pulmonary artery pressure during hypoxic exposure. This compensatory reaction activated by β2‐adrenoceptors during hypoxic stress is very important to maintain the activities of normal life. Abstract The acute hypoxic compensatory reaction is accompanied by haemodynamic changes. We monitored the haemodynamic changes in rats undergoing acute hypoxic stress and applied antagonists of β‐adrenoceptor (β‐ARs) subtypes to reveal the regulatory role of β‐ARs on haemodynamics. Sprague–Dawley rats were randomly divided into control, atenolol (β1‐AR antagonist), ICI 118,551 (β2‐AR antagonist) and propranolol (non‐selective β‐AR antagonist) groups. Rats were continuously recorded for changes in haemodynamic indexes for 10 min after administration. Then, a hypoxic ventilation experiment [15% O2, 2200 m a.sl., 582 mmHg (0.765 Pa), PnormalO2 87.3 mmHg; Xining, China] was conducted, and the indexes were monitored for 5 min after induction of hypoxia. Plasma catecholamine concentrations were also measured. We found that, during normoxia, the mean arterial pressure, heart rate, ascending aortic blood flow and pulmonary artery pressure were reduced in the propranolol and atenolol groups. Catecholamine concentrations were increased significantly in the atenolol group compared with the control group. During hypoxia, mean arterial pressure and total peripheral resistance were decreased in the control, propranolol and ICI 118,551 groups. Pulmonary arterial pressure and pulmonary vascular resistance were increased in the propranolol and ICI 118,551 groups. During hypoxia, catecholamine concentrations were increased significantly in the control group, but decreased in β‐AR antagonist groups. In conclusion, the β2‐AR is involved in regulation of pulmonary haemodynamics in the acute hypoxic compensatory reaction, and the activation of β2‐ARs attenuates the increase in pulmonary arterial pressure during hypoxic stress. This compensatory reaction activated by β2‐ARs during hypoxic stress is very important to maintain activities of normal life.

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Pre-existing cardiovascular conditions and high altitude travel

Cited by 34 publications

References 48 publications

Clinical recommendations for high altitude exposure of individuals with pre-existing cardiovascular conditions

Clinical recommendations for high altitude exposure of individuals with pre-existing cardiovascular conditions

High altitude-related hypertensive crisis and acute kidney injury in an asymptomatic healthy individual

Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats

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