Wilderness Cardiology

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Chapter 32 Wilderness Cardiology

The wilderness environment places great demands on the cardiovascular system. Certain wilderness activities, such as diving and high-altitude mountaineering, pose specific challenges to the cardiovascular system by imposing additional environmental stressors, such as water immersion and hypoxia, respectively, on top of the physical demands of the specific activity. In addition, many wilderness endeavors involve prolonged exposure to high or low ambient temperatures, posing challenges to thermoregulation. As the popularity of wilderness adventure continues to grow, the number of people with established cardiovascular disease who partake in wilderness adventure activities will also increase.

Probably the most important consideration related to wilderness activities for persons with known cardiovascular disease is remoteness of the environment, making modern medical technology and “usual” advanced care partly or completely inaccessible. Any person with cardiovascular disease who wishes to participate in wilderness activities needs to accept the risk that a cardiovascular event occurring in a remote environment may have a more adverse outcome compared with a similar event that transpires in the city.

This chapter reviews basic cardiovascular physiologic adaptations to the wilderness environment. Although basic cardiovascular responses to exercise are central to all wilderness activities, a detailed discussion of exercise physiology is beyond the scope of this chapter; the reader is referred elsewhere, including Chapter 98, for this information.30 In addition, we review cardiovascular conditions of relevance to wilderness travelers and physicians, with emphasis on basic management of common cardiovascular emergencies in the wilderness setting.

Cardiovascular System Responses to Specific Wilderness Environments

Hyperbaria (Underwater Diving)

Diving places a unique combination of physical stressors on the cardiovascular system. The physiologic stress of diving arises from the combination of immersion underwater and sustained moderate-intensity exercise. Immersion significantly reduces the effect of gravity on the diver’s body and therefore on the lower extremity venous blood pool when the diver is upright.19 This results in central redistribution of blood, with increases in intrathoracic blood volume and right atrial and ventricular filling pressures.20 The direction and magnitude of the fluid shift induced by water immersion depend on the position of the diver in the water. If the diver is upright, then the extensively researched physiology of upright water immersion applies. However, if the diver is horizontal or head down, entirely different hydrostatic gradients are induced, and these may be dynamic as the diver changes position in the water. For upright divers, as dictated by the Frank-Starling phenomenon, the increase in cardiac preload leads to immediate increases in stroke volume, cardiac output, and myocardial work. Patients with cardiomyopathy with or without prior congestive heart failure may be especially sensitive to cardiac volume overload and may become acutely symptomatic with these sudden shifts in volume status.

Physical exertion is also an important contributor to the overall cardiovascular stress of underwater exercise. Divers typically use large muscle groups at low intensity to propel themselves through the water, although this depends on the experience of the diver and the nature of the dive. This action may be continuous for the entire duration of the dive. The cardiovascular system facilitates this activity by increasing heart rate, stroke volume, and cardiac output. This translates into mildly increased myocardial oxygen demand and may cause myocardial ischemia in patients with underlying coronary artery disease (CAD) who are not well compensated. Fear, excitement, and emotional stressors may compound the physical stresses of diving, especially for inexperienced divers. It should be noted that the underwater environment is particularly remote. In particular, if underwater decompression stops are indicated, emergency ascent and access to medications (such as nitroglycerin) or medical care can be quite complicated. As with many other wilderness activities, it is not only the stress of the activity that is problematic, but also the risk for a cardiovascular event occurring in a remote setting.

The diving reflex is a unique autonomic reflex response to water immersion that has direct relevance to the safety of this popular sport. It was first described in 1870 by the French physiologist Paul Bert, when he observed that heart rate slowed dramatically during forced water submersion. The full diving reflex response involves transient slowing of the heart rate (typically by 20 to 30 beats/min) with subsequent reduction in cardiac output and peripheral vasoconstriction to maintain systemic blood pressure.6 The reflex is mediated by increased vagal nerve activity. Heart rates lower than 10 beats/min have been measured in accomplished breath-hold divers.18 Although typically well tolerated, such intense bradycardia may result in supraventricular and ventricular escape arrhythmias in susceptible individuals.40

Individuals with underlying heart disease may tolerate diving poorly, as evidenced by data that document a significant percentage of diving fatalities attributable to cardiac causes. Depending on the age of the population, sudden cardiac death (SCD) and myocardial infarction account for 12% to 27% of diving fatalities.15 It is important to emphasize that this statistic does not mean that diving “caused” the fatality but rather that acute coronary events occur in middle-age divers who may not have access to usual emergency care if an event occurs during diving. Adequate screening for underlying cardiovascular disease is essential at a reasonable interval before any diving excursion, especially in patients with known disease. Individuals with significant cardiovascular disease, including incompletely revascularized CAD and cardiomyopathy/congestive heart failure, are typically at high risk for complications during diving and should be given restrictive recommendations. In addition, patients who have undergone coronary artery bypass grafting and have had chest tubes placed occasionally have scarring and air trapping that could place such individuals at risk for pneumothorax during compressed-air diving. At the very least, a chest radiograph should document no evidence for scarring before allowing such patients to dive; occasionally other tests for air trapping, such as chest computed tomography, could be indicated. Recommendations used to advise patients with cardiac disease who want to participate in competitive sports may be useful for diving and other wilderness activities as well.36 If patients have normal left ventricular function, are well revascularized, and have no provocable ischemia or arrhythmias, consideration could be given to individual patients to be allowed to dive. It must be emphasized that divers, should they become incapacitated during a dive, put not only themselves at risk, but also their diving partners. Therefore some recommendations may be more restrictive than just for individual assumption of risk.

Hypoxia (High-Altitude Activity)

The cardiovascular system’s response to hypoxia is a dynamic process that begins immediately on exposure and evolves over days, weeks, and years of prolonged exposure. Although the temporal nature of this response has inherent interindividual variability, it is useful to consider the response in two distinct phases: acute hypoxia and sustained hypoxia. Important changes in cardiovascular function during acute and sustained hypoxia are summarized in Figure 32-1.


FIGURE 32-1 Changes in cardiovascular parameters during acute and sustained exposure to hypoxia.

(Modified from Baggish AL, Levine BD: The cardiovascular system at high altitude. In Horbein TF, Schoene RB: High altitude: An exploration of human adaptation, New York, [in press], Marcel Dekker, Inc.)

Acute hypoxia decreases alveolar and arterial oxygen content, leading to sympathetic nervous system activation.26,37 This activation is the key element of the acute hypoxic response of the cardiovascular system. Increased sympathetic activity (with or without vagal withdrawal) leads to increased heart rate and thus increased cardiac output. However, peripheral vasoconstriction, the expected vascular response to increased sympathetic tone, appears to be blunted by the release of local vasodilatory substances, constituting a phenomenon equivalent to the “functional sympatholysis” that occurs during sustained endurance exercise.23 Cardiac output increases while systemic vascular resistance and blood pressure decrease transiently. Acute hypoxia also causes dilation of the coronary arteries, although in patients with CAD who may have endothelial dysfunction, appropriate coronary dilation may not occur and may even be associated with paradoxical vasoconstriction.5

As hypoxia becomes sustained, arterial oxygen concentration (CaO2) increases secondary to hemoconcentration, ventilatory acclimatization, and increases in red cell mass. These changes lead to some abatement of the hyperdynamic state of the circulatory system. Ventricular contractile function remains normal, but reductions in plasma volume and ventricular filling lead to decreased stoke volume as predicted by the Frank-Starling mechanism.24 Persistent sympathetic hyperactivity leads to downregulation of cardiac β-receptors45 and increased vagal activity,10 which combine to promote a reduction in resting heart rate. However, resting heart rate remains elevated during sustained hypoxia when compared with sea-level conditions. These heart rate and stroke volume reductions lead to an overall fall in cardiac output, especially at maximal exercise. In the systemic circulation, blood pressure gradually rises as the peripheral mechanisms responsible for local vasodilation diminish. For patients with hypertension, this sympathetic activation may result in substantial increases in blood pressure during high-altitude excursions.

High-altitude activities, such as hiking, trekking, and mountaineering, also generally include sustained, low-intensity exercise for prolonged periods of time. The combination of reduced arterial oxygen content and perhaps paradoxical vasoconstriction during exercise (increased myocardial oxygen demand) results in provocation of myocardial ischemia with acute altitude exposure at work rates somewhat less than that provoked at sea level.32 However, with at least 5 days of acclimatization, responses near those noted at sea level can be restored. Mountain walking, even at the relatively moderate altitudes seen in the Alps, is associated with a slightly increased risk for SCD,11 although this risk seems greatest in persons who are least fit. Overall, there is one SCD per 780,000 hiking hours and one SCD per 1,630,000 skiing hours in the Alps,11 and one “cardiac event” per 957,000 hours of mountain activities,41 which increases substantially in individuals over the age of 50 to 60 years. This risk seems somewhat higher than the one death per 3,000,000 jogging hours reported by Thompson and colleagues.43 For patients with known CAD, if they are adequately revascularized, exercise at high altitude appears reasonably safe.17,42


The healthy human body is capable of tolerating and even successfully performing vigorous physical exercise during exposure to high ambient temperature. The hypothalamic thermoregulatory center prevents elevation of core body temperature during ambient heat exposure by causing peripheral vasodilation and increased sweat production. Humans thermoregulate predominantly by sending blood to the skin; during an acute heat stress, up to 8 to 10 L/min of cardiac output may be directed to the skin (and therefore unavailable to other organs) to maintain body temperature. Especially for persons with compromised circulation, such as with heart failure (HF),4,13 heat exposure may be poorly tolerated. With ample oral hydration and electrolyte repletion, moderate physical exercise can be performed in the face of significant thermal exposure for extended periods, although safe performance requires adequate heat acclimatization. The absolute intensity and duration of work that can be performed in the heat by a given individual are dictated by numerous factors, including prior heat acclimatization, physical fitness, and ambient temperature and relative humidity.

Heatstroke occurs when the cooling system fails and core body temperature rises. Heatstroke is defined clinically as a core body temperature that rises above 42° C (107.6° F), with signs and symptoms including hot, dry skin and central nervous system abnormalities such as delirium, convulsions, or coma.9 Cardiovascular complications of heatstroke include atrial fibrillation, various electrocardiographic abnormalities (T-wave changes and prolongation of the QT interval), pulmonary edema, pericardial effusion, right ventricular dysfunction, hypotension, and ventricular arrhythmias.46


Classically hypothermia is defined as a core body temperature of less than 35° C (95° F). Hypothermia may develop in numerous wilderness scenarios, including but not limited to cold-water immersion, snow burial, and exercise in cool to cold ambient temperatures. Unlike heat exposure, humans do not acclimatize to an appreciable degree to cold exposure, so survival in the cold depends on behavior (e.g., clothing, shelter). The initial response to cold exposure is increased sympathetic nervous system activity leading to peripheral vasoconstriction and tachycardia.28 This causes a rise in systemic arterial blood pressure and a tendency toward central redistribution of blood volume. Acute exercise in the cold, especially in patients with CAD, is associated with increased risk for acute coronary events.

With sustained mild hypothermia (core body temperature of 33° to 35° C [91.4° to 95° F]), this central volume shift promotes diuresis, which can lead to dehydration. As hypothermia becomes more pronounced (moderate hypothermia is 30° to 33° C [86° to 91.4° F]), heart rate and cardiac output fall and the electrocardiogram may show characteristic findings of prolonged QT interval or Osborn waves. Bradycardia, caused by direct slowing of sinoatrial function and concomitant changes in tissue pH, oxygen concentration, and electrolyte concentrations, becomes more marked as core temperature continues to drop.33 The drops in core temperature and pulse rate typically observe a linear relationship; deviations from this relationship, particularly tachycardia in the moderately hypothermic patient, should raise suspicion of a secondary process, such as toxin ingestion or hypovolemia. Premature atrial and/or ventricular beats and atrial fibrillation commonly occur in the moderately hypothermic person.

In severe hypothermia (<30° C [86° F]), there are significant reductions in stroke volume, heart rate, and blood pressure. All types of atrial and ventricular tachyarrhythmias can occur during severe hypothermia.14 It should be noted that rough handling or jostling of the severely hypothermic patient could trigger arrhythmias, so care should be taken to avoid unnecessary physical manipulation of the hypothermic patient.28 At temperatures below 25° C (77° F), spontaneous ventricular fibrillation and/or asystole may occur. As discussed in further detail below, victims of hypothermia may tolerate periods of cardiac arrest longer than do victims under normothermic conditions. Thus the appropriate window for initiating and continuing resuscitation for a hypothermic patient may exceed that in other cardiac arrest situations.

Screening and Preparation for Wilderness Travel

Asymptomatic Wilderness Adventurers

Participation in wilderness activities can place considerable stress on the cardiovascular system. Before wilderness activity, healthy individuals without known preexisting cardiovascular disease should seek medical consultation with a clinician familiar with the demands of the wilderness environment. This recommendation is similar to that for individuals considering starting an intensive exercise program or participation in competitive sports. Assessment of the asymptomatic individual should focus on determining risk for underlying, previously unrecognized cardiovascular conditions. A detailed medical history focused on prior exercise experience, wilderness adventure experience, medications, allergies, a detailed family history of cardiovascular disease or premature sudden/unexplained death should be obtained. Individuals should be specifically questioned about established cardiovascular risk factors, including tobacco use, hypertension, diabetes, family history of premature coronary disease, and dyslipidemia.

A comprehensive physical examination should be performed, beginning with a basic assessment of vital signs to exclude systemic hypertension and arrhythmia. Auscultation of the heart and lungs should be performed to exclude congenital or acquired valvular heart lesions and pulmonary vascular congestion. Peripheral pulse examination should be performed to detect the presence of atherosclerotic peripheral vascular disease and aortic coarctation. Although not specifically designed for wilderness travelers, the American College of Cardiology/American Heart Association’s athletic pre-participation medical history and physical examination template may prove to be a useful guide for clinicians in this setting.35

Asymptomatic wilderness travelers with a normal medical history and physical examination typically tolerate wilderness activity without cardiovascular complications and should not be restricted from any specific activities based on cardiac risk. Individuals with abnormalities detected during the medical history or physical examination may require further testing. Some combination of 12-lead electrocardiography, transthoracic echocardiography, exercise stress testing, and ambulatory rhythm monitoring may be useful in such individuals. The decision to perform one or more of these diagnostic tests must be individualized based on characteristics of the patient.

Established Coronary Artery Disease

Atherosclerotic coronary artery disease (ACAD) is the leading cause of death in middle-age and older individuals in the developed world. Atherosclerosis is the process of arterial lumen narrowing caused by accumulation of lipids, inflammatory cells, and calcium within the walls of an artery. ACAD leads to clinically relevant myocardial ischemia in one of two principal fashions. ACAD may progress steadily and often slowly over a period of months to years to the point at which arterial lumen narrowing is sufficient to cause myocardial demand–related ischemia. In this setting, ACAD manifests as exertional chest discomfort, referred to as angina pectoris. Patients with angina pectoris are managed clinically with medications to reduce myocardial oxygen demand (e.g., β-blockers, nitrates), prescribed exercise therapy, aggressive risk factor modification, and symptom-driven revascularization.

Alternatively, ACAD may manifest with sudden and complete occlusion of a coronary artery. This phenomenon is triggered by ulceration or rupture of an atherosclerotic plaque with subsequent development of a platelet-rich clot. This dramatic and often catastrophic ACAD presentation leads to myocardial infarction and/or a malignant ventricular arrhythmia. Effective management of plaque rupture and complete coronary arterial occlusion requires pharmacologic (systemic thrombolytics) or mechanical reperfusion (percutaneous coronary angioplasty and stenting), which are typically not feasible in the wilderness environment.

Individuals with coronary artery disease should not necessarily be restricted from wilderness activity. Patients with clinically stable ACAD (i.e., patients fully revascularized or incompletely revascularized but without recent change in anginal threshold) who are on a well-tolerated medical regimen should not universally be excluded from wilderness activity. We recommend that all individuals with established ACAD undergo some form of exercise stress testing before wilderness activity, because exercise stress testing provides an accurate assessment of both exercise capacity and the efficacy of medical therapy. Stress testing using continuous 12-lead electrocardiographic monitoring can be done using a number of exercise modalities, including treadmill running/walking and upright or supine cycle ergometry. Typical electrocardiographic findings of myocardial ischemia are illustrated in Figure 32-2. The choice of exercise modality can be made based on patient and clinician preferences. Concomitant myocardial imaging may be necessary to achieve adequate diagnostic accuracy in patients with certain pretest features (Box 32-1). Imaging can be performed using nuclear perfusion tracers or echocardiography as dictated by available expertise. Individuals with clinically stable ACAD who have normal left ventricular function and no myocardial ischemia during exercise testing performed at least to a workload commensurate with the demands of the expected activity should not be restricted from wilderness activity based on cardiovascular disease.

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