INTRODUCTION — The number of individuals exposed to high altitude through air travel and recreational activities continues to increase, with tens of millions of people traveling to high altitude destinations each year [1]. Changes in physiological functions during high altitude exposure vary given an individual’s physical fitness, rate of ascent, severity and/or duration of exposure, cultural habits, geographical locations, and genetic variation [2]. While high altitude is well tolerated by most individuals, patients with cardiovascular disease are at risk of complications caused by tissue hypoxia and reduced oxygen delivery, sympathetic stimulation, increased myocardial demand, paradoxical vasoconstriction, and alterations in hemodynamics that occur with exposure to high altitude [3-5]. The duration of travel, ascent profile, degree of exertion, and any prior cardiovascular history can each impact the health of a patient with cardiovascular disease who is considering traveling to high altitude.
High altitude provides a unique physiologic challenge to the cardiovascular system. The cardiovascular response to high altitude in both healthy individuals and in patients with cardiovascular disease will be reviewed here. A general overview of high altitude disease will also be included to provide a comprehensive understanding. (See "High-altitude illness: Physiology, risk factors, and general prevention".)
Most importantly, this topic will discuss the impact of high altitude on the heart and the hemodynamic changes. Altitude exposure can also lead to a variety of well-described clinical syndromes including some not directly involving the cardiovascular system, such as acute mountain sickness (AMS), high altitude pulmonary edema, high altitude cerebral edema, and high altitude retinal hemorrhage. These maladies are discussed in detail within this report. (See "High-altitude pulmonary edema" and "Acute mountain sickness and high-altitude cerebral edema" and "High-altitude illness: Physiology, risk factors, and general prevention", section on 'Other altitude-related illnesses'.)
BAROMETRIC PRESSURE AND PIO2 — When moving from sea level to high altitude, there are reductions in atmospheric pressure, oxygen pressure, humidity, and temperature [4]. It is noteworthy to point out that significant changes occur beyond the critical height of 2500 meters (8200 feet) above sea level [6]. Factors such as degree of change in elevation, degree of hypoxia, rate of ascent, level of acclimatization, exercise intensity, previous history of high altitude illness, genetics, and age significantly affect the physiological change that the human body will experience during ascents [7]. One study involving Chinese men aged 18 to 35 years noted that increasing age (from 26 to 35 years old) was an independent risk factor for acute mountain sickness (AMS) upon rapid ascent to high altitude (from 500 to 3700 meters) and that the prevalence of AMS was more predominant with increasing age [8]. Hypoxia induces peripheral vasodilation and a pulmonary vasoconstriction, leading to changes in systemic blood pressure and an increase in pulmonary blood pressure that can also contribute to high altitude pulmonary edema [9].
Although altitude is the most obvious determinant of barometric pressure and its resulting physiologic stress, other factors can contribute to a reduction in barometric pressure including a decrease in temperature, deteriorating weather, such as blizzards, hail, or extreme winds, or distance from the equator.
An understanding of barometric pressure, the primary determinant of the partial pressure of oxygen in inspired air (PiO2, in mmHg), is essential to understanding the cardiovascular stress of high altitude. The relationship between the PiO2, the fraction of oxygen in inspired air (FiO2), and barometric pressure (in mmHg) is described by the following equation:
PiO2 = FiO2 x barometric pressure
FiO2 is the same at all altitudes. As the barometric pressure changes, the FiO2 remains constant while the partial pressure of oxygen is altered with the change in barometric pressure. Specifically, the partial pressure of arterial oxygen decreases with altitude (hypobaric environments) and increases with depth (hyperbaric environments). In addition, oxygen within inspired air is reduced by the presence of water vapor obtained during transport into the lungs (typically 47 mmHg). As a result, the above equation can be written as:
PiO2 = 0.21 x (barometric pressure - 47)
The approximate pressures of oxygen in the atmosphere, inspired air, alveoli, and arterial blood at a variety of altitudes are shown in the following table (table 1). At 2439 meters (8000 feet), which is the maximal allowable cabin pressure (altitude equivalent) in commercial airliners, the barometric pressure is decreased to 564 mmHg (compared with 760 mmHg at sea level). The net effect is a PiO2 of 108 mmHg, with associated partial pressures of oxygen in the alveoli and arterial blood of normal individuals of 69 and 60 mmHg, respectively. At sea level, the oxygen saturation is 99 to 100 percent. The oxygen saturation at 2439 meters (8000 feet) should be higher than 85 percent (approximately 90 percent) for a partial pressure of oxygen in arterial blood (PaO2) of 60 mmHg based on the oxygen saturation curve. The partial pressure of oxygen in inspired air (PiO2) is greater than the alveolar and arterial pO2 at any altitude. This is caused by anatomical dead space in the respiratory system in which all inspired oxygen (air in the mouth and trachea) does not take part in gas exchange.
NORMAL CARDIOVASCULAR RESPONSE TO HIGH ALTITUDE — Information on the physiologic cardiovascular consequences of altitude exposure comes from both "at altitude" studies and those in which altitude is simulated in a hypobaric chamber.
Short-term altitude exposure — Several circulatory changes occur within minutes of exposure to high altitude. Maximal aerobic exercise capacity is decreased at high altitudes due to a decrease in arterial oxygen content from decreased inspired partial pressure of oxygen [10]. This results in tissue hypoxia (hypobaric hypoxia) from inspiring oxygen-poor air, which causes compensatory physiological changes at high altitude both at rest and during exercise [11].
The initial response to hypoxia is an attempt to increase more oxygen delivery. The minute ventilate rate and tidal volume are increased to allow for optimal systemic arterial tension [12]. Furthermore, the pulmonary arteries constrict in response to tissue hypoxia, a condition known as hypoxic pulmonary vasoconstriction. This physiologic phenomenon occurs to redirect blood flow to alveoli located within areas containing the highest oxygen content. The hypoxic vasoconstriction ultimately leads to pulmonary hypertension and furthermore, an increase in the alveolar-arterial oxygen (A-a) gradient (the difference between the alveolar and arterial concentration of oxygen that is used in diagnosing the source of hypoxemia) [13]. The increased A-a gradient is caused by an unequal perfusion to the lungs from hypoxic vasoconstriction and is important in the development of high altitude pulmonary edema [14]. For instance, after 24 hours, 15 percent of subjects develop pulmonary edema without symptoms, while 75 percent have an increase in pulmonary extravascular fluid [15]. Sustained exposure to high altitude for ≥24 hours results in the development of pulmonary edema. (See "High-altitude pulmonary edema".)
Hyperventilation leads to a decrease in carbon dioxide and causes respiratory alkalosis. This leads to a shift of the oxygen-hemoglobin dissociation curve to the left, resulting in an increased binding of oxygen to hemoglobin and thus less oxygen delivery to the tissues. Subsequently, after a few hours, there is an increase in 2,3-diphosphoglycerate that shifts the curve back to the right to improve oxygen delivery by facilitating the unloading of oxygen to the tissues. However, this makes it more difficult for oxygen to bind to hemoglobin in the lungs during gas exchange [16].
Oxygen delivery is the product of cardiac output and oxygen content. Given the reduction in oxygen content with increased altitude, cardiac output must increase to maintain the same oxygen delivery to the tissues. This can be achieved by increasing heart rate or stroke volume. Initially, at high altitudes, the cardiac output is augmented due to an increased heart rate and stroke volume [11]. Despite this effort, there is ultimately a lower peak cardiac output at high altitudes as opposed to at sea level. Such limitations are autonomic responses to limit myocardial oxygen demand and consumption during times of reduced oxygen availability. Over one to two weeks, the stroke volume is decreased from reduced preload and a lowered plasma volume from respiratory (hyperventilation), urinary (hypoxic diuresis), and cutaneous losses. Increased urine output is a response to high altitude hypoxia. Diuresis serves to increase bicarbonate losses in the urine to stimulate increased breathing. The increased urine output also serves to increase the hematocrit by 1 to 2 g/dL to increase the oxygen-carrying capacity of the blood per unit volume [17]. Within hours of exposure to altitude, the red blood cell count begins to increase in response to an increase in erythropoietin. However, the overall buildup process of the red blood cell count is slow, taking months to reach equilibrium. As expected, the degree of polycythemia is related to the level of altitude.
The increase in the rate-pressure product (heart rate x systolic blood pressure), reduction in arterial oxygen saturation, and elevation in lactate concentration illustrate the potential oxygen supply/demand mismatch observed with exercise at altitude [4]. Even though the cardiac output and rate-pressure product at a given activity level tend to be higher as altitude increases, paradoxically, the maximum attainable cardiac output, heart rate, and maximum attainable workload fall with increased altitude as discussed above [18].
In addition, after rapid ascent to a high altitude, the sympathetic nervous system is activated, which stimulates the release of epinephrine [19]. This shift towards sympathetic predominance during acute exposure to hypoxia has also been manifested by reduced heart rate variability [20] (see "Evaluation of heart rate variability"). The higher the altitude, the higher the arterial epinephrine concentration rises to enhance cardiac output, increasing bronchodilation in the lungs, and furthering vasodilation in the skeletal muscles [21]. This vasodilation counterbalances the escalation in cardiac output such that blood pressure changes do not markedly occur [22,23].
Several changes are observed in the resting electrocardiogram (ECG) and echocardiographic-Doppler imaging for normal individuals exposed to high altitude. During ECG recordings taken from members of an expedition who climbed Mount Everest and achieved altitudes of 5335, 6250, and 7988 meters (17,500, 20,500 and 26,200 feet, respectively), the following ECG changes were noted [24]:
●Increase in resting heart rate (HR)
●Prolongation of the QT interval
●ST-T wave flattening
●Rightward shift in the frontal QRS axis
●Increase in P-wave amplitude in lead II
The last two changes are thought to reflect evidence of right ventricular and right atrial "strain" arising from hypoxia-induced pulmonary hypertension. At the most extreme altitude, 3 of the 12 patients developed a new right bundle branch block and three others showed changes consistent with right ventricular hypertrophy. Some of the ECG changes, primarily the increased HR, QT lengthening, and ST-T wave abnormalities, can be blunted with beta-blocker administration [25], suggesting a role for catecholamines in their development. Since virtually all ECG abnormalities abate upon descent, they are not thought to be clinically significant.
Another study of 456 subjects who performed a 20-minute hypoxia exercise test with continuous recording of ECG noted a dose-dependent, hypoxia-induced decrease in the amplitude of the P, QRS, and T waves [26].
Echocardiographic-Doppler imaging studies of healthy adults at rest after rapid ascent to high altitudes have noted [10]:
●Threefold increase in mean pulmonary artery pressure
●Altered right and left ventricular diastolic function
●Prolonged isovolumic relaxation time
●Maintained right ventricular systolic function
●Improved left ventricular systolic function
Long-term altitude exposure — After three to four days, the initial sympathetic nervous system manifestations of altitude exposure resolve as early acclimatization begins. Longer-term exposure to altitude is associated with a number of other adaptive physiologic responses. These include:
●Resetting of the "hypoxic ventilatory response" to allow increased ventilation at a given hypoxic stimulus.
●Increase in red blood cell mass mediated by erythropoietin.
●Increased tissue capillary density, predominantly in highly engaged muscular tissue.
●Reduction in the alveolar-arterial oxygen gradient.
●Reduced parasympathetic nervous activity as a key mechanism for the elevated heart rate in chronic hypoxia [27].
●Right-ward shift of the oxygen-hemoglobin dissociation curve, facilitating oxygen unloading to tissues. The sequence of events is as follows: at high altitude, the initial hypoxia and decreased dissolved oxygen in the blood stimulate peripheral chemoreceptors, which in turn send signals to respiratory drives, leading to hyperventilation, leading to respiratory alkalosis, leading to shifts of the oxygen-hemoglobin dissociation curve to the left so that hemoglobin can pick up oxygen easier. Next, the kidney responds to alkalosis by generating hydrogen ions to correct the pH; after two to three days, the red blood cell 2,3-diphosphoglycerate level increases, shifting the oxygen-hemoglobin dissociation curve to the right and making oxygen delivery easier to the tissues.
ALTITUDE STRESS IN HEART DISEASE — The effects of high altitude exposure may have important implications for patients with various types of heart disease. (See "High-altitude illness: Physiology, risk factors, and general prevention".)
In addition to the baseline changes to the cardiovascular system, the possible development of high altitude diseases (mountain sickness or pulmonary or cerebral edema) can add further stress to the cardiovascular system. As a result, cardiac patients engaged in recreational activities at higher altitudes should be warned about the signs of altitude illness and, in certain circumstances, carry the appropriate prophylactic medicines such as acetazolamide [28] and dexamethasone [29]. Lastly, these patients should follow basic advice about altitude illness prevention, most notably acclimatization (ideally for five days) with gradual ascent and proper hydration [30]. In addition, patient compliance for the prescribed dosing of their current antianginal medications and treatment of their cardiovascular disease should be emphasized. Importantly, they should be advised that the quickest and most effective treatment of altitude-related illness is descent. Supplementary oxygen may also be beneficial in some individuals [31]. (See "High-altitude illness: Physiology, risk factors, and general prevention".)
Coronary heart disease — Exercise at real or simulated altitude in patients with stable coronary heart disease (CHD) appears to be relatively safe, provided patients take the same precautions as they would at sea level [32-36]. However, the acute hemodynamic changes associated with altitude/hypoxemia result in an earlier onset of angina symptoms or ischemic electrocardiogram (ECG) changes (essentially, a shorter time to notable symptoms) [34,37].
In a study that compared 23 patients (mean age 51 years) with stable CHD and a mean left ventricular ejection fraction (LVEF) of 39 percent with control subjects during maximal bicycle ergometer stress testing at both 1000 and 2500 meters [32]:
●Patients with CHD, who were more often receiving therapy with a beta blocker and angiotensin-converting enzyme (ACE) inhibitor, had a lower peak rate-pressure product (beta-blocker effect) than controls at both altitudes.
●In both patients and controls, exercise capacity was lower at high altitude compared with baseline, while the maximal heart rate was the same at both altitudes.
●Both groups maintained percent oxygen saturations in the low to mid 90s at rest and with exercise at both baseline and altitude. There were no complications such as high-grade arrhythmias or provocation of significant ischemia.
In another report that demonstrates both the effect and safety of exercise at altitude, nine patients with stable CHD were evaluated during maximal treadmill stress testing both at baseline (1750 meters [5740 feet]) and at altitude (3390 meters [11,120 feet]) [33]. Exercise at altitude was associated with the expected increase in minute ventilation and reductions in both maximal exercise duration and maximal oxygen uptake. Although the rate-pressure product at which angina or significant ST-segment depression occurred was similar at both altitudes, this occurred at a lower level of exercise when at the higher altitude. Exercise was not associated with an increase in the extent or complexity of ventricular arrhythmias.
A third study of the response to and safety of exercise at altitude evaluated 22 patients with a prior myocardial infarction (MI) following revascularization with stress tests, both at rest and within one to three hours following rapid ascent to 3454 meters (11,330 feet) [35]. Patients were required to have a LVEF above 45 percent, no evidence of ischemia on a baseline stress test, and controlled blood pressure. Beta blockers were withheld from patients for five days prior to the study protocol. All patients tolerated the rapid ascent, none of the cardiopulmonary stress tests needed to be stopped prematurely, and neither evidence of ischemia nor significant arrhythmias were observed in any patients during stress testing at high altitude.
Of interest, lower mortality rates from CHD and higher levels of serum high-density lipoprotein cholesterol have been observed in populations residing at high altitude [38].
Patients without diagnosed CHD — An intriguing finding is the frequency with which ischemia is provoked in subjects with no history of CHD when exercising at high altitude. This was addressed in a Holter monitor evaluation study that was performed in 149 selected skiers beginning at an altitude of 3430 meters (11,250 feet) [39]. Only 5.6 percent of the skiers over age 40 showed ECG evidence of ischemia [39]. This is similar to the 5 percent incidence of ischemia noted in screening stress tests in asymptomatic individuals at sea level [40].
It is important to note that multiple cardiovascular risk factors are affected by the combination of high altitude and increasingly cold temperatures, with an increased incidence of MI occurring [41].
These studies suggest that both ascending and exercising to higher altitudes can be safe in patients with stable CHD or a remote acute coronary event. We suggest that when advising a patient with CHD who is planning a trip to a high altitude destination, the health care provider needs to consider the patient's functional level, clinical status, ischemic threshold, and anticipated stress workload. A graded exercise test at sea level may be prudent for assessment of exercise tolerance and provocable ischemia for clinical assessment [30]. In addition, specific recommendations include:
●In patients with recent acute coronary syndromes who have not had revascularization, there should be no ascent to high altitudes until maximal stress testing has been performed and an absence of overt ischemia is confirmed. Patients who have had an MI within two weeks should only undergo air travel, a potential stress itself, if there is no angina, dyspnea, or hypoxemia at rest and there is no fear of flying. In addition, they should fly with a companion, carry nitroglycerin, and be able to cope with the emotional and physical demands of travel.
●Patients should be warned that anginal symptoms will probably occur more easily at lower workloads, and so strenuous activities should be approached with a higher degree of caution, particularly during the first three or four days at higher altitudes [32,35]. Therefore, acclimatization for at least five days is advised [30]. Access to appropriate medicines and medical care should also be confirmed prior to high altitude travel.
●Optimization of CHD medications and discussions regarding compliance of medications should be performed prior to high altitude exposure.
Heart failure — Patients with heart failure (HF) are especially susceptible to the physiologic changes from high altitude exposure [42]. The increased sympathetic activity elevates systemic vascular resistance, blood pressure, and heart rate, which results in reduced exercise capacity [43]. (See "High-altitude illness: Physiology, risk factors, and general prevention", section on 'High altitude physiology'.)
The pulmonary vasoconstriction and hypertension that result from high altitude (hypoxemia) impair right ventricle loading and output [44]. In addition to the hypoxic pulmonary vasoconstriction, increased erythropoiesis places an increased pressure load on the right ventricle [5]. Together, these factors reduce cardiovascular performance in patients with HF [45-47].
Additional factors that may predispose patients with chronic heart failure to exacerbations at high altitude include [47]:
●Chronically elevated catecholamine levels (see "Pathophysiology of heart failure: Neurohumoral adaptations", section on 'Neurohumoral adaptations')
●Increased transcapillary permeability in the lung
●Poor skeletal muscle metabolism (see "Skeletal muscle dysfunction and exercise intolerance in heart failure")
●High oxygen extraction in the periphery (see "Exercise capacity and VO2 in heart failure")
●Poor pulmonary function
●Concurrent CHD
The response to various simulated altitudes (from 92 to 3000 meters [302 to 9840 feet]) during bicycle ergometry was studied in 14 control patients and 38 patients with stable HF who were categorized on the basis of mild, moderate, or severe impairment in baseline functional capacity (peak VO2) [48]. Findings included:
●All patients and controls showed the expected decreases in maximum workload attained and peak oxygen consumption with increasing altitude, but the percentage decrease was greater in the patients with HF, particularly those with the lowest baseline functional capacity (peak VO2 <15 mL/min per kg) (figure 1).
●None of the patients, including 12 with the lowest functional capacity, were limited at altitude by arrhythmia, angina, or ECG evidence of ischemia.
●In patients with HF, maximum work rate decreased in parallel with increased simulated altitude, with a greater reduction in maximum physical activity in proportion to their exercise capacity at sea level.
Similar considerations also apply to patients with left ventricular dysfunction. As described above, patients with stable CHD and a mean ejection fraction of at least 39 percent showed no complications with exercise during brief exposure to 2500 meters (8200 feet) [32]. (See 'Coronary heart disease' above.)
An observational study on heart transplant patients found that those living at 610 to 1220 meters (2000 to 4000 feet) had an improved survival duration compared with those living at lower levels, suggesting that chronic exposure to higher altitude may benefit this group [49].
Lastly, a study of 23 healthy subjects reported that those with significantly elevated brain natriuretic peptide levels while exercising at 5150 meters (16,896 feet) were more likely to suffer acute mountain sickness (AMS) compared with those at sea level [50].
Our approach — Only limited information and guidance from clinical studies are available concerning altitude exposure in patients with chronic HF. Prior to approving exposure to altitude, the following should be assessed for this class of patients:
●Baseline functional capacity
●Expected altitude that will be encountered
●Anticipated activity level and expected duration of time spent at high altitude
If a patient exhibits symptoms at rest or during minimal activity, or requires oxygen therapy at rest (New York Heart Association class IV), even the stress of air flight may be significant and should therefore be approached with caution. In such patients, oxygen therapy should be considered; for patients already receiving oxygen, increased flow rates can be used to alleviate symptoms.
By comparison, patients with only mild functional issues at sea level will probably tolerate moderate altitudes, but they should be warned that they will become symptomatic at lesser degrees of exercise.
Patients with HF are likely to notice a reduced functional capacity at moderate to high altitude when compared with sea level [4]. It is essential that altitude be considered in the etiology of any symptoms and that the patient be advised to arrange immediate descent if decompensation occurs. Symptoms that would herald decompensation include chest pain, palpitations, shortness of breath, dyspnea, and fatigue. Furthermore, medication dose and frequency adjustments may be needed.
This report concurs with the British Cardiovascular Society’s “Fitness to fly for passenger with cardiovascular disease” report, which suggested no flying or exposure to altitude for six weeks after an acute left ventricular failure episode [51].
Valvular heart disease — Travel to high altitude can aggravate symptoms in patients with underlying valvular heart disease. For those with severe valvular heart disease or those with symptoms, altitude exposure should be avoided. In those with mild to moderate valvular heart disease, echocardiography to document their current valvular and ventricular function and an exercise stress test to evaluate their hemodynamic changes and functional capacity at sea level is recommended. The patient should be warned to reduce their activity levels below their baseline activity level (particularly during the first five days at altitude), to be cautious with or avoid alcohol, and to be aware of possible hemodynamic alterations such as hypertension. Moreover, they should be given additional instructions on adjusting their medications as needed.
In patients with preexisting valvular disease, the acute hemodynamic changes induced by the additional hypoxic stress of altitude may result in decompensation of their condition. Acutely, exposure to hypoxia results in the increase of a number of factors, including heart rate, cardiac contractility, cardiac output, and both systemic and pulmonary artery resistance and pressures [10,52-54]. These changes have the potential to decrease pressure and create volume overload in patients, affecting their heart in the following ways:
●The increased myocardial workload and oxygen demand will mean valvular symptoms may acutely worsen (dyspnea, near-syncope).
●The increased systemic afterload may increase the regurgitant fraction in both aortic and mitral regurgitation, worsening symptoms.
●The increased pulmonary afterload from increased pulmonary vascular resistance may exacerbate pulmonary and tricuspid regurgitation.
●Dehydration may result in reduced preload and may worsen symptoms of valvular stenosis. Elevated heart rates may increase gradients across stenotic valves and increase symptoms.
For those with prosthetic mechanical heart valves, the hypercoagulable state induced by acute high altitude exposure may the increase risk of valvular thrombosis, especially if the anticoagulation level is not in the desired range [55].
In addition, patients should be cautious about consuming alcohol. The combined vasodilatory and dehydrating effects of a commercial flight, alcohol, and the approximate 2730 meters (9000 feet) of altitude may result in hemodynamic effects that could exacerbate their valvular condition.
It is important to remember that there is a great deal of variability between individuals with the same valvular condition with regards to their responses to high altitude; additionally, cold temperature, humidity, exercise, stress, and their functional reserve can also compound the effect [52]. One protocol used to gain significant insight into how a patient will respond to air travel is the hypoxia altitude simulation test. This procedure involves a patient breathing a gas mixture with an oxygen saturation of 15.1 percent, which simulates a cabin pressure of an airplane at 2440 meters (8000 feet) and allows the clinician to screen for hypoxia, significant symptoms, and arrhythmias. Repeating the test with supplemental oxygen will ensure that the patient will receive an acceptable benefit for its use when flying [56].
Given all of the variables that can affect a patient with valvular heart disease, patients should be treated in a highly personalized, individual manner by their clinicians. Prior to ascent to high altitude or air travel, the following should be considered:
●For those who are asymptomatic with mild to moderate valvular disease, exercise testing and transthoracic echocardiography at rest/stress is recommended for evaluating their current status and response to exercise [52,57].
●For those with symptomatic and/or severe valvular disease, exposure to altitude is contraindicated [52,57].
●Hypoxic challenge tests such as the hypoxia altitude simulation test may be helpful to obtain more practical information about possible hemodynamic effects and symptoms during high altitude exposure [58].
●Education about blood pressure self-monitoring and treatment titration is needed if uncontrolled hypertension or hypotension can potentially develop [52].
●For those on anticoagulation, instructions for self-monitoring and dose adjustment should be given [52,55].
●Alcohol consumption should be avoided or consumed with caution.
Arrhythmias — It appears that altitude can aggravate arrhythmias, particularly during acute exposure and with exercise. This is especially noteworthy in older adults and those with known arrhythmias or CHD. Air travel alone is probably of low risk, except in those with baseline (resting) ventricular and supraventricular arrhythmias in whom the added stress of mild hypoxemia might lead to decompensation. Such patients should be cautioned about air travel and/or have supplemental oxygen recommended.
Similar guidance applies to those contemplating vacationing at high altitude, and patients should be warned to reduce their activity level to below their sea level baseline capacity, particularly during the first five days at altitude. Patients with arrhythmias should also be aware of and immediately treat both cardiac and noncardiac manifestations of altitude exposure.
Caution is clearly needed in patients with poorly controlled rhythm disorders. Deaths at high altitude are often sudden and, while ascertainment of the cause of death is often difficult, the possibility that rhythm-related causes are being underestimated needs to be kept in mind.
The incidence of arrhythmias at high altitudes is variable and depends upon the patient group under study. Heightened sympathetic activity associated with high altitude may increase the frequency and duration of supraventricular and ventricular arrhythmias in patients with underlying heart disease [59,60].
A study among young, healthy individuals without arrhythmias was conducted in a hypobaric chamber study of eight healthy men aged 21 to 31 years who were observed during exercise at simulated altitudes up to the equivalent of the summit of Mount Everest (8850 meters [29,020 feet]) [61]. No arrhythmias or conduction defects were seen [61].
Examining a more advanced age group, a Holter monitor study of healthy middle-aged men found the incidence of both supraventricular and ventricular premature beats nearly doubled at an altitude of 1350 meters (4430 feet) as compared with 200 meters (660 feet) [62]. At a still-higher altitude (2630 meters [8630 feet]), the frequency of ectopy was increased six- to sevenfold [63]. It was hypothesized that the increase in premature beats was due to beta adrenergic stimulation at the higher altitude brought on by the early release of catecholamines.
Patients with stable CHD have also been evaluated. In a previously described study, 10 older adult patients with exercise-induced ischemic changes at sea level were studied at 2500 meters (8200 feet), both acutely and after five days of acclimatization [34]. Ventricular premature beats were significantly increased with acute exposure but returned to sea level values after acclimatization. This suggests early sympathetic stimulation on acute exposure to altitude is driving these changes.
Pacemaker function — The issue of pacemaker safety at altitude and the possibility of alterations in stimulation thresholds are uncertain since data sources cite conflicting findings:
●In one study simulating altitude with inhalation of 10 percent oxygen, a significant but reversible increase in stimulation thresholds was noted [64]. In another phase of threshold testing, hypocapnia (low level of CO2 in the blood), induced by mechanic hyperventilation, led to a reduction in pacing stimulation thresholds.
●In another report, stepwise simulated hypobaric chamber ascent from 450 to 4000 meters (1480 to 13120 feet) produced no change in stimulation threshold, in spite of a significant fall in partial pressure of oxygen in arterial blood (PaO2) [65].
It seems likely that the competing effects of hypoxia and hypocapnia, each pushing the pacing stimulation threshold in a different direction, may balance each other out in some cases and prevent any net change during the physiologic stress of high altitude exposure.
Based on the limited data, it appears that pacing thresholds can be expected to remain unchanged at the moderate altitudes seen with air travel and recreational skiing. The safety of pacemakers at the extreme altitudes, as with trekking and mountaineering, is not known. However, the development of advanced pacing algorithms and the active fixation of placement leads are innovations that have improved pacemaker function/reliability.
Airport security gates may detect pacemakers and defibrillators but do not appear to interfere with device function [35]. By contrast, there is a theoretical risk that handheld metal detectors may interfere with personal electronic devices and, hence, pacemakers and defibrillators.
Congenital heart disease — When advising a child or adult with congenital heart disease who is contemplating high altitude exposure, the guidelines must be individualized and based upon the nature of the congenital defect and expected stresses. Patients most at risk are those with intracardiac communication defects and the propensity to worsen right-to-left shunting in the presence of elevated right-sided pressure. Consultation with a pediatric or adult cardiologist specializing in congenital defects should precede high altitude exposure.
Congenital heart disease associated with intracardiac or extracardiac shunts may be associated with a net shunting of blood from the left, high-pressure side of the heart to the right, low-pressure side. However, with exposure to high altitude and hypobaric hypoxia, pulmonary vascular resistance and right-sided pressures are increased [14]. This results in an increase in right-to-left shunting, leading to arterial oxygen desaturation [66-68]. The extent to which arterial oxygen desaturation occurs will depend upon many factors, including the size of the communication, baseline right-sided pressures, and the extent of altitude-induced pulmonary hypertension.
It is important to appreciate that there may be an increased prevalence of congenital heart disease (ie, atrial septal defect/patent foramen ovale [PFO], or patent ductus arteriosus [PDA]) at high altitudes. This is likely due to a persistence of the fetal pattern of the pulmonary vasculature (thick, smooth muscle cells, narrow lumens, small pulmonary vessels, increased pulmonary, and right ventricular pressures) [69-71]. In a prospective study of 1116 school children, there was a high prevalence of PDA and atrial septal defect at three high altitude sites, as well as a graded effect as altitude increased [72]. One explanation is that lower oxygen tension fails to constrict the ductus and thus closure of both the ductus and the foramen ovale is inhibited.
A large cross-sectional study examined children aged 4 to 18 years in the Qinghai province of China, where 1633 cases of congenital heart disease were discovered. Of those, the prevalence of congenital heart disease was found to increase in a gradient-like fashion as the altitude increased by 4.9 per thousand at 2535 meters (8320 feet), 5.7 per thousand at 3600 meters (11,810 feet), and 8.7 per thousand at 4200 meters (13,780 feet) [73].
Another study demonstrated higher pulmonary artery pressures in children with atrial septal defects born at higher altitudes compared with both those without such defects at the higher altitudes and those with similar defects born at sea level [74]. Similar findings were noted in another report in which children with ventricular septal defects born in Denver (1609 meters [5280 feet]) had twice the pulmonary vascular resistance of children born with such defects at sea level [75].
Exaggerated pulmonary hypertension and right ventricular dysfunction has also been found in patients with PFO living at high altitude. The presence of PFO was associated with right ventricular enlargement at rest and an exaggerated increase in right ventricular pressure gradient and dysfunction (25 ± 7 mmHg versus 15 ± 9 mmHg, p <.001) and a blunted increase in fractional area change of the right ventricle (3 [-1, 5] versus 7 percent [3, 16], p = .008) during mild exercise [76]. Persons who undergo successful closure of their PFO are able to travel or live at high altitude without difficulty [77].
Moreover, in a small study of adults with cyanotic congenital defects, it was reported that exposure to moderate altitude (1500 to 2500 meters [4920 to 8200 feet]) is safe [78]. The upper range of the altitude in this study is relevant in that commercial airplanes are pressurized to this altitude when flying.
Lastly, data from a limited study suggest that it is safe for Eisenmenger patients to travel in commercial airlines as long as the airplanes are adequately pressurized [79]. Supplemental oxygen should be available, although its efficacy in this specific population is unproven. The approach to patients with Eisenmenger syndrome who wish to either travel in commercial airlines or visit geographies at altitude is discussed in detail elsewhere within this report [79]. (See "Evaluation of patients for supplemental oxygen during air travel" and "Pulmonary hypertension in adults with congenital heart disease: General management and prognosis", section on 'High altitude'.)
Blood pressure patterns — There is a subsegment of patients with hypertension who do not exhibit the normal nocturnal fall in blood pressure, (sometimes referred to as “nondippers”) compared with other hypertensive patients with a normal circadian (sometimes referred to as “dippers”) [80]. One study examined the effects of high altitude on these two groups, finding that those who did not have a nocturnal fall in blood pressure showed poor cardiac compensatory and inadequate adaptation abilities to acute high altitude [81].
AIR TRAVEL — Most patients with well-compensated heart disease can travel without difficulty. The safety of air travel has been increased by a Federal Aviation Administration requirement, implemented in April 2004, that all aircraft carrying at least 30 passengers and having at least one flight attendant carry an emergency medical kit and an automated external defibrillator (AED) [82,83]. (See "Automated external defibrillators".)
A variety of practical guidelines for the cardiopulmonary patient traveling by air are presented in a table (table 2).
Potential risk — Although commercial airplanes typically travel at an altitude between 6700 and 13,400 meters (22,000 and 44,000 feet) to improve efficiency, the pressurization process maintains cabin pressure at an altitude equivalent to 2439 meters (8000 feet) or less, with typical cabin pressures ranging from 1524 to 2439 meters (5000 to 8000 feet) [84,85]. At that altitude, the barometric pressure is decreased to 564 mmHg, compared with 760 mmHg at sea level. The net effect is a partial pressure of oxygen in inspired air (PiO2) of 108 mmHg, with associated partial pressures of oxygen in the alveoli and arterial blood of normal individuals of 69 and 60 mmHg, respectively. (See 'Barometric pressure and PiO2' above.)
While an individual with a normal cardiopulmonary reserve can easily compensate for the reduced arterial PO2 at these altitudes and maintain adequate tissue oxygen delivery, those with little or no reserve are at risk for profound arterial desaturation and cardiopulmonary decompensation. Individuals with limited cardiopulmonary reserve exposed to high altitude may experience light headedness, chest pain, tingling in the extremities, palpitations, dyspnea, and hyperventilation. Further stress from air travel may result from associated immobility, jet lag, vibration, noise, and low humidity [86].
Incidence of problems — There is a paucity of information regarding the incidence of serious health problems occurring during flight and, in the absence of any central registries or reporting requirements by airlines, it is likely that incidences are underestimated. In a United States study, the most common reasons for a flight to be diverted were cardiac incidents (28 percent), neurologic problems (20 percent), and food poisoning (20 percent) [87-90]. It is likely that the majority of cardiac incidents are vasovagal syncope related to dehydration, alcohol, recumbency, and emotional stress. With regards to in-flight deaths, a range of one death per 1.5 to 4.7 billion passenger miles flown has been reported.
The incidence of in-flight problems in patients with known coronary artery disease has not been well studied in patients receiving contemporary medical and revascularization therapies. One study investigated the transporting of patients with a recent myocardial infarction (MI) using a medical repatriation (returning a person back to one's place of origin or citizenship) company. During the period from April of 2004 through November of 2005, a total of 213 patients were transported 6 to 38 days (mean 12.9 days) following presentation with ST elevation MI (STEMI) or non-ST elevation MI (NSTEMI) [91]. No serious complications occurred in any of these patients. Despite relatively frequent asymptomatic hypoxemia (defined as pulse oximetry <92 percent), none of the 56 patients with prior NSTEMI experienced in-flight angina, and only 3 of 157 patients with prior STEMI had angina. Among those experiencing angina, all were within 14 days of their MI. It is noteworthy that patients who made their flight ≥14 days after their MI experienced no angina.
Recommendations — Guidance provided by the British Cardiovascular Society “Fitness to fly for passengers with cardiovascular disease” also recommends:
●Arrive at the airport in sufficient time to avoid rushing
●Warn the carrier and/or airport authority well in advance of the date of departure of any requirements for assistance, including the requirement for in-flight oxygen
●Carry an appropriate supply of medication, as well as a clear list of all medications with the recommended doses
●Carry a letter from the appropriate caregiver(s) explaining the condition, drugs, allergies, and devices (such as a pacemaker or implantable cardioverter defibrillator [ICD])
Other recommendations are provided in the table (table 2).
Patients with poorly controlled heart disease should be advised against air travel. The key cardiac contraindications for air travel include [82]:
●Uncomplicated MI within two to three weeks.
●Complicated MI within six weeks.
●Uncontrolled hypertension.
●Coronary artery bypass graft surgery within 10 to 14 days (this time interval varies according to individual practice patterns).
●Cerebrovascular accident within two weeks.
●Unstable angina.
●High-grade ventricular premature beats or uncontrolled ventricular or supraventricular arrhythmias.
●Severe decompensated heart failure (HF) [82,92]. Patients with class III or IV New York Heart Association HF should be carefully assessed to determine whether they will need in-flight oxygen. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Evaluation of patients for supplemental oxygen during air travel".)
●Symptomatic valvular heart disease (relative contraindication).
●Eisenmenger’s syndrome and pulmonary hypertension.
Supplemental oxygen — Patients who require supplemental oxygen at sea level will require supplemental oxygen during air travel [82]. This is discussed in detail elsewhere. (See "Evaluation of patients for supplemental oxygen during air travel".)
Stable coronary artery disease — Evaluation of the patient with known coronary disease before flying should include a careful history and physical examination to identify signs or symptoms of recent angina, volume overload, or dysrhythmia [82]. A resting electrocardiogram (ECG) should be obtained and, if it is abnormal, a copy should be given to the patient to carry during all air travel. Among patients with chronic stable angina, routine stress testing prior to air travel is not necessary unless there has been a recent significant change in clinical status.
Myocardial infarction — The American College of Cardiology/American Heart Association (ACC/AHA) guidelines on air travel after STEMI [93] recommend that air travel within the first two weeks after an MI should only be undertaken if the patient has no angina, no dyspnea at rest, and no fear of flying [93-96]. The guidelines further suggest that early, low-level exercise testing after a STEMI may be reasonable to assess functional capacity and the ability to perform tasks at home and at work, evaluate the efficacy of medical therapy, and assess the risk of a subsequent cardiac event. Two low-level exercise testing protocols have been suggested if the following requirements are met: 1) Low-level exercise during in-hospital cardiac rehabilitation; 2) no symptoms of angina or HF; and 3) stable ECG 48 to 72 hours prior to testing. Submaximal stress testing (done at three to five days in patients without complications) or a symptom-limited exercise test (done at five days or later) is reasonable to “permit detection of profound ischemia or other indicators of high risk that could be associated with post-discharge cardiac events.” Taking all of this into account regarding flight preparations, the patient should have a companion, carry nitroglycerin, and request airport transportation to avoid rushing. Patients with an MI complicated by severely depressed cardiac function or another significant complication (eg, HF, sudden cardiac arrest, or cardiogenic shock) should not fly until two weeks after they are deemed medically stable.
By contrast, the Aerospace Medical Association recommends that no air travel be undertaken within two to three weeks of an uncomplicated MI and within six weeks of a complicated MI [92].
The British Cardiovascular Society, in their “Fitness to fly for passengers with cardiovascular disease” report, also performed a comprehensive review of the evidence (mostly observational) upon which recommendations for air flight after an acute coronary syndrome can be made [51]. They concluded that such passengers should be stratified into groups assigned as very low risk, medium risk, and high risk and that air travel is reasonable after 3 and 10 days for the low- and medium-risk groups. Those at high risk, or awaiting further investigation/treatment, should defer air travel until a more stable situation is achieved and delay altitude exposure for a minimum of six weeks. These three groups were defined as follows:
●Very low risk – <65 years of age, first event, successful reperfusion, left ventricular ejection fraction (LVEF) >45 percent, no complications, and no cardiac investigations or interventions pending.
●Low (or medium) risk – LVEF >40 percent, no symptoms of HF, no evidence of inducible ischemia or arrhythmia, and no further cardiac investigations or interventions pending.
●High risk – LVEF <40 percent with signs and symptoms of HF, pending further investigations for revascularization or device therapy.
We advise the approach proposed by the British Cardiovascular Society with regard to early exercise testing for symptom evaluation [51].
Percutaneous coronary intervention — Immediately after coronary stent placement, airline travel should be avoided due to the increased risk of acute stent thrombosis during this time [82]. Following this procedure, postponing travel arrangements for at least two days in uncomplicated cases or two weeks in complicated cases is recommended.
Coronary artery bypass graft surgery — Those who have undergone coronary artery bypass grafting should wait at least 10 days, as there is a potential risk of barotrauma caused by expanding gases artificially introduced to the chest during coronary bypass surgery [89]. However, it is recognized that some institutions, after careful patient evaluation, allow stable patients to fly a few days sooner than 10 days.
Implanted devices — Air travel has not been shown to interfere with the function of pacemakers or ICDs [97-99]. Patients should carry a card identifying the type of device [82].
When passing through airport security, patients are advised to request a non-detector hand search, if possible [82]. If a handheld detector must be used, the patient should request that it not be held over the implanted device for more than a few seconds and that at least 30 seconds should elapse between passes. Many newer-generation ICD devices and pacemakers have been designed to resist the rigors of metal detectors and magnetic resonance imaging (MRI). These are described separately. (See 'Pacemaker function' above and "Cardiac implantable electronic device interactions with electromagnetic fields in the nonhospital environment", section on 'Security systems' and "Patient evaluation for metallic or electrical implants, devices, or foreign bodies before magnetic resonance imaging", section on 'Cardiovascular implantable electronic device'.)
We agree with the report from the British Cardiovascular Society “Fitness to fly for passengers with cardiovascular disease,” which suggests that following placement of ICD or pacemaker and in the absence of pneumothorax or other complication (bleeding, electrode problem), patients can travel to altitude within two days of implantation [51]. They should be advised to restrict arm movements and/or to carry heavy loads on the contralateral side to minimize mechanical complications such as lead displacement.
The safety of another type of implantable device, the leadless pacemaker, is not well established in relation to travel and ascent to high altitude and should be considered with caution. While device dislodgements occurred early on in their development, the incidence of dislodgements has been dramatically reduced [100].
Patients traveling and utilizing wearable defibrillators should disclose their situation in advance to the airline so that necessary accommodations can be arranged in order to minimize risk for other passengers and crew in the rare event that the device delivers in-flight shocks.
Deep vein thrombosis and pulmonary embolism — Patients at risk of pulmonary embolism (PE) should be advised to exercise their limbs at regular intervals and, with especially long flights, take walks within the aisle every hour. The use of below-the-knee compression stockings should also be considered. For the patient at high risk of PE contemplating a prolonged flight, aspirin or anticoagulation therapy may be appropriate. A more detailed discussion of these issues is provided in this report. (See "Assessment of adult patients for air travel", section on 'Venous thromboembolism' and "Prevention of venous thromboembolic disease in adult nonorthopedic surgical patients".)
TREKKING AND MOUNTAINEERING — The allure of the high altitude environment is attracting increasing numbers of adventurers to travel to mountains all over the world. Although the most extreme ascents are still performed by young and middle-aged adults who appear to be at risk only from altitude-related illness and trauma (as opposed to exacerbation of cardiopulmonary disease), an increasing number of older individuals are venturing into the mountains as well. In one report of tourists seeking visas in Nepal (where about one-third come for trekking), 20 percent were 50 years or older [101].
Acute mountain sickness and high altitude illness — High altitude illness prevention and acute mountain sickness (AMS) prevention and treatment are described in detail elsewhere. (See "High-altitude illness: Physiology, risk factors, and general prevention" and "Acute mountain sickness and high-altitude cerebral edema".)
Risk of adverse cardiovascular events — The risk of adverse events is low. Among tourists trekking in Nepal, cardiac illness contributed to only about 5 percent of helicopter evacuations and none of the reported deaths [101]. Another review examined sudden deaths among participants engaging in high mountain hiking, skiing, or both in Austria between 1985 and 1991 [102]. A total of 416 deaths were deemed sudden, representing about 30 percent of all mountain sport-related deaths [102]. Most of the deaths occurred at altitudes between 1100 to 2100 meters (3600 to 6900 feet). Hikers were more than two times as likely as skiers to die. Among the hikers, the risk of death was highly influenced by age and lack of prior physical activity. The relatively low incidence of cardiac complications among trekkers and mountaineers most likely results from the low incidence of cardiovascular disease in this population. For instance, in a survey of ski mountaineers in the Austrian Alps, only 5.7 percent of women and 12.0 percent of men over the age of 40 reported any type of cardiovascular disease [60].
Prior myocardial infarction (MI) appears to be the greatest predictor of risk regarding sudden cardiac death (SCD) among those who snow ski. In a case-control study of 68 skiers who lost their lives to SCD, compared with 204 controls, those with a previous MI had a 93 times higher adjusted SCD risk, those with hypertension a ninefold higher risk, and those with known coronary heart disease (CHD) without prior MI a 4.8-fold increased risk [103].
Mitigating cardiovascular risk — Exercising at high altitudes should be approached carefully, and individuals should consider their own fitness level as they make their plans. Aerobic exercise intensifies the effects of altitude. We suggest not exercising the first day at altitude and planning out gradual increases in intensity as a trip moves forward. Paying attention to adequate hydration and avoiding alcohol are also important.
Physiologic studies show that physiologic demands of aerobic exercise (especially high-intensity interval training [HIIT]) are beyond the demands of standard climbing and trekking mechanics [104-106]. If a person regularly exercises at sea level altitudes, they will be more likely to be able to properly handle the added stressors experienced at higher altitudes [79]. Other individuals should avoid extreme aerobic exercise at altitude because previously asymptomatic heart conditions are likely to be more severe in such conditions.
Available automated external defibrillators (AED) can be life-saving. A 36-year-old man exposed to high altitude while climbing Mount Fuji had chest pain and lost consciousness. He was saved after receiving electroshocks from an AED [107]. Medical personnel charged with caring for persons at high altitude should review the application of AEDs and cardiopulmonary resuscitation (CPR) in special circumstances [108], especially in the case of high altitude climbing where core body temperature will have a significant impact on the effectiveness of CPR.
Portable technology can provide real-time biofeedback, alerts about worsening medical conditions, and life-saving treatment. High altitude trekking has the potential to benefit from these technological advances, with heart rate variability (HRV) and cognitive monitoring available via portable technology [109,110]. HRV, the variation in the time intervals between heartbeats, can be measured in normoxic and simulated hypoxic environments prior to ascending to altitude, as well as during a climb. Studies suggest that monitoring HRV may have promise to determine the likelihood of AMS incidence and/or severity [109,111,112].
As medicine advances, the opportunities to evaluate the success of major transplants are presenting themselves. Medical advances are allowing people with significant medical conditions to adventure at high altitudes. For example, a high altitude expedition was coordinated that only included lung transplant patients and their accompanying medical personnel [113]. With 8 of the 10 transplant patients and all 24 escorting personnel reaching the peak, this 94 percent success rate was significantly higher than the reported 85 percent for that route.
With regards to tracking peripheral oxygen saturation (SpO2) and heart rate, the use of a simple pulse oximeter can be valuable in assessing the body’s response to high altitude. As expected, tracking how SpO2 decreases during ascent, how heart rate increases, and then how the opposite occurs during periodic pauses/acclimatation breaks can be informative and provide important feedback. Additionally, the development of AMS has been shown to be consistently associated with lower SpO2 values [114].
Advice for patients — There are few studies and no randomized trials upon which recommendations can be made for people with heart disease who want to travel to or exercise at high altitude [115]. Every patient must be assessed on an individual basis. Nevertheless, reasonable recommendations can be made when accounting for the following:
●Baseline functional capacity
●Expected altitude that will be encountered
●Anticipated activity level and expected duration of time to be spent at high altitude
An exercise stress test can be performed to evaluate heart disease before planning any activity at altitude if there are concerns about cardiovascular status or any changes in status [116]. However, exercise stress testing is not routinely recommended without cause.
Potential trekkers should be evaluated on the basis of known heart disease, as discussed above, and should be reminded of the importance of adequate training and conditioning before entering this extreme environment. Acute altitude-related illness remains a frequent cause of morbidity and mortality for trekkers either with or without cardiac disease.
For patients with heart disease who seek medical attention prior to such a trip, advice should include [4]:
●Maintain adequate control of blood pressure, arrhythmias, and other cardiac issues prior to ascent.
●Pay strict attention to taking usual medications and dealing with cardiac symptoms should they arise.
●Plan a slow ascent to allow time for acclimatization. A rule of thumb during mountaineering is to ascend no more than 305 meters (1000 feet) per day and to allow a day of rest (no ascent) after every third day [21].
●Pay close attention to the unusual physical exertion that occurs on the first day at altitude, daily during late morning hours, and under conditions of prolonged abstinence from food and fluid intake [117].
●Plan load weight in a conditioned climber not to exceed 32 percent of body weight. This percentage should be lower in a deconditioned climber [118].
●Be aware and plan for compromised sleep efficacy due to hypoxia-induced cardiovascular responses [119].
●Adhere to the usual prophylactic measures to prevent altitude sickness. (See "High-altitude illness: Physiology, risk factors, and general prevention".)
●Remember that descent is the safest and quickest path to resolution of altitude-related symptoms.
●Consider a personal AED or ensure that they know a device is within treatment distance when traveling or to high altitude.
●Wear a pulse oximeter to track SpO2 changes and adjust your ascent accordingly.
●Limit activity at moderate (1500 to 2500 meters [5000 to 8200 feet]) or high (>2500 meters [>5000 feet]) altitudes to a lower maximal level than typically performed at sea level (80 to 90 percent). This is especially true during the first few days.
●As an individual treks higher, ascend gradually and purposefully each day (<305 meters [1000 feet]), and include a “no ascent day” every third day.
●Achieve a moderate degree of physical conditioning at sea level before exercising at high altitude [82].
●Patients with coronary artery disease, arrhythmia, or congestive HF may become symptomatic at lower exercise workloads at high altitudes (>2500 meters [8200 feet]) [32,35]. Patients with poorly controlled hypertension should not travel to high altitude, and those with controlled hypertension should consider taking their own blood pressure during travel and adjust medications as needed.
●Patients who have undergone revascularization with either percutaneous coronary intervention or coronary artery bypass graft surgery within three weeks should not exercise above low altitude (<1500 meters [5000 feet]).
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Management of inflight medical events".)
SUMMARY
●Most patients with well-compensated heart disease can travel without difficulty. A variety of practical guidelines for the cardiopulmonary patient traveling by air are presented in a table (table 2). (See 'Air travel' above and 'Stable coronary artery disease' above.)
●Patients with poorly controlled heart disease should be advised against air travel. Patients within two weeks of an acute myocardial infarction (MI) should consider air travel only if there is no angina, dyspnea, or hypoxemia at rest. Moreover, patients should have no fear of flying; if the patient flies with a companion, make sure nitroglycerin is available and every effort should be made to avoid both the emotional and physical demands of travel. (See 'Recommendations' above and 'Myocardial infarction' above.)
●Patients with unstable angina, uncontrolled ventricular or supraventricular arrhythmias, symptomatic valvular heart disease, or decompensated heart failure (HF) should travel only in an emergency. (See 'Recommendations' above.)
●The ascent to high altitude without acclimatization can put patients with heart disease at risk for further cardiac events. This is especially true in patients who have marginal cardiopulmonary function at sea level or those with active or recent unstable acute coronary syndromes . (See 'Altitude stress in heart disease' above and 'Risk of adverse cardiovascular events' above.)
●Patients with recent, unstable cardiovascular conditions should be directed to refrain from any altitude exposure. By contrast, stable patients who exercise at sea level without symptoms can generally exercise at altitude as long as they are vigilant in monitoring their heart rate and blood pressure and plan to decrease the total intensity and duration of their exercise. (See 'Risk of adverse cardiovascular events' above and 'Mitigating cardiovascular risk' above and 'Advice for patients' above.)
