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

Hyperthermia

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

Hypothermia

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.

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.

FIGURE 32-2 Representative example of 12-lead electrocardiogram at rest (A) and peak exercise (B) in a 56-year-old man with cardiac risk factors of diabetes and dyslipidemia who underwent screening before high-altitude travel. B demonstrates ST-segment depression of greater than 1 mm in numerous contiguous ECG leads. This patient was found to have multivessel coronary artery disease with high-risk features necessitating coronary artery bypass grafting surgery.

It should be emphasized, however, that no laboratory-based exercise test is a perfect simulator of the wilderness environment. The combination of intense physical exercise and environmental extremes may precipitate myocardial ischemia that could not be triggered during stress testing. As such, we emphasize several principles to our ACAD patients who choose to engage in wilderness activity. First, we encourage all ACAD patients to be knowledgeable about the typical symptoms of this disease (e.g., exertional chest pain/pressure/tightness, inappropriate exertional dyspnea). Development of any of these symptoms during wilderness activity should prompt the patient to abort the activity and to seek immediate medical attention. Second, we encourage all ACAD patients to prepare as fully as possible for the physical demands of wilderness activity. This is best accomplished by using a progressive exercise-training program designed to mimic the specific challenges of the planned wilderness activity. Third, we emphasize the value of allowing ample time for wilderness environment acclimatization. Acclimatization techniques vary by activity and environment and may include gradual or staged high-altitude ascent or prolonged, low-intensity exercise under hot conditions.

Cardiomyopathy/Congestive Heart Failure

Cardiomyopathy refers to abnormal function of the heart muscle. Cardiomyopathy may be inherited/congenital (e.g., hypertrophic cardiomyopathy, familial dilated cardiomyopathy) or acquired (e.g., ischemic cardiomyopathy, cardiomyopathy secondary to a pathologic valvular condition) and thus can affect individuals of all ages. Risk associated with wilderness activity among patients with cardiomyopathy is determined by etiology and severity. Certain forms of cardiomyopathy (e.g., hypertrophic cardiomyopathy) are associated with increased risk for SCD in the context of vigorous physical activity. Patients with these forms of cardiomyopathy should either be excluded from wilderness activity or counseled extensively about the inherent risks associated with physical activity and wilderness isolation.

In addition to sudden death risk, cardiomyopathy may lead to development of heart failure (HF). HF is a syndrome defined as inability of the circulatory system to provide adequate circulation of blood to meet the demands of the body and to fill adequately at a low enough pressure to avoid congestion. HF severity can be assessed based on symptom severity and the results of an assessment of cardiac structure and function. Recently updated practice guidelines present an HF severity classification scheme that incorporates symptom severity and cardiac structural/functional parameters (Table 32-1).²⁵ Cardinal symptoms of HF include dyspnea, fatigue, exercise intolerance, and systemic venous congestion manifesting most commonly as peripheral edema. Noninvasive imaging such as echocardiography can provide important information such as left ventricular size and ejection fraction.

TABLE 32-1 ACC/AHA Classification of the Stages of Heart Failure

ACC, American College of Cardiology; AHA, American Heart Association.

Individuals with Class D HF are typically not capable of wilderness activity, and exposure to hypoxia, hyperbaria, or thermal extremes should be avoided. Individuals at risk for HF with (Class B) or without (Class A) documented structural or function cardiac abnormalities should undergo assessment of functional capacity by exercise testing before participating in wilderness activity. Class A and B patients that demonstrate normal, age-appropriate exercise capacity during formal testing can be expected to tolerate wilderness activity without complications and thus do not require restriction. The most difficult clinical decisions arise when clinician advisors are confronted with individuals with Class C disease. Class C individuals, particularly those with stable disease, can tolerate moderate-intensity exercise in controlled environments, such as cardiac rehabilitation programs, and may express interest in wilderness activity. It must be emphasized that these patients are at considerable risk for decompensation if activity intensity exceeds a certain threshold. Because this threshold differs markedly among Class C patients and may change rapidly in any given individual, we advise conservative recommendations in this patient population. In our opinion, the majority of Class C HF patients should be restricted from aggressive or extreme wilderness activities that significantly increase stress on the cardiovascular system. Clearance to perform low-intensity wilderness activity in this patient population must be considered carefully on a case-by-case basis.

Congenital Heart Disease

Congenital heart disease (CHD) is a term that includes a wide array of cardiac abnormalities that are present at birth. CHD can include abnormalities of the heart muscle, cardiac valves, coronary arteries, and electrical conduction system and may be confined to the heart or a component of a systemic disorder. From a functional perspective, CHD can be categorized as either cyanotic or acyanotic. Cyanotic CHD is characterized by reduced arterial oxygen saturation due to right-to-left intracardiac shunting with direct venous to arterial transit of blood. Cyanotic CHD is relatively rare and involves complex and severe structural cardiac malformations, such as tetralogy of Fallot. Most individuals with cyanotic CHD present early in life because of failure to thrive or markedly reduced exercise capacity and are treated with surgical reconstruction. Individuals with complex cyanotic CHD are at high risk for decompensation during wilderness activity and should be restricted from wilderness activity for this reason. Among patients with successful surgical correction of cyanotic CHD, the risk associated with wilderness activity is highly variable. For example, patients who have undergone a surgical Fontan procedure and who do not have right-to-left shunting tolerate acute exposure to high altitude surprisingly well.²¹ Nevertheless, the impact of chronic exposure to high altitude in such patients has not been well defined. The decision to prohibit or restrict activity in this patient population should be made on a case-by-case basis in consultation with a cardiovascular specialist with expertise in CHD.

Acyanotic CHD, defined by the presence of an abnormality associated with normal arterial oxygen saturation, is more common than is cyanotic disease. Common causes of acyanotic CHD include atrial and ventricular septal defects. In these conditions, intracardiac shunting of blood travels in a left-to-right direction and does not produce arterial hypoxemia. Many individuals have their acyanotic CHD go undetected through childhood and adulthood and can be expected to have normal exercise capacity and life expectancy. However, normal development and previous clinical stability in a patient with acyanotic heart disease do not necessarily indicate an acceptable risk for wilderness activity. This is particularly true of wilderness activity that involves exposure to hypoxia, such as that which occurs during high-altitude travel. Hypoxia facilitates pulmonary vasoconstriction, leading to increased pulmonary vascular resistance. The increased pulmonary vascular resistance and resultant increase in right ventricular and atrial pressures may lead to right-to-left intracardiac shunting and conversion to cyanotic CHD physiology. The risk associated with wilderness travel among patients with common acyanotic CHD is variable and largely determined by the specific form and severity of the intracardiac lesion. Before wilderness activity, individuals with acyanotic CHD should consult with a cardiovascular specialist with expertise in CHD.

Two other conditions deserve specific comment. One rare condition, consisting of congenital absence of the right pulmonary artery, places patients at grave risk for high-altitude pulmonary edema, even at relatively low altitudes. It is crucial for practitioners of wilderness medicine to be aware of this condition and counsel such patients to avoid high-altitude exposure.

The second is patent foramen ovale. This condition is quite common, present in perhaps 5% of the adult population, and has been associated with acute mountain sickness and high-altitude pulmonary edema.^1,31 However, there is no evidence that closing a patent foramen ovale has any effect on exercise performance at altitude or the risk for high-altitude illness, and such a procedure should be avoided unless there are other strong clinical conditions. For individuals with a known patent foramen ovale wishing to go to high altitude, consideration should be given for high-altitude pulmonary edema prophylaxis with a pulmonary vasodilator such as nifedipine³⁹ or tadalafil.³⁴

Arrhythmias

Disturbance of cardiac rhythm, arrhythmia, is a common form of cardiac disease. Arrhythmias are commonly categorized by their site of anatomic origin. Supraventricular arrhythmias arise from foci above the atrioventricular node, typically in the atria or adjacent vessels, such as the pulmonary veins. In contrast, ventricular arrhythmias originate below the atrioventricular node within the ventricular myocardium or His-Purkinje conduction fibers. The clinical implications of cardiac arrhythmia are highly variable and constitute a full spectrum of severity.

In general, supraventricular arrhythmias are better tolerated than are ventricular arrhythmias. Many individuals experience completely asymptomatic supraventricular arrhythmias. Individuals with a history of asymptomatic supraventricular arrhythmias who are free of other forms of cardiac disease may participate fully in wilderness activity. Patients with a history of symptomatic supraventricular arrhythmias, including those taking medications for maintenance of sinus rhythm and/or heart rate control, should undergo exercise testing to assess for rhythm stability and circulatory sufficiency during high-intensity exercise. Carrying an extra “pill in the pocket,” such as a short-acting β-blocker like propranolol, may be a useful precaution for such patients. Some patients with paroxysmal or chronic supraventricular arrhythmias are managed with anticoagulation (e.g., aspirin, warfarin). These patients may be susceptible to bleeding complications of trauma and should be advised to take appropriate precautions in the wilderness environment. Patients with a history of ventricular arrhythmia, fibrillation, or tachycardia should be considered at risk for recurrence unless the underlying cause of the rhythm has been identified and corrected. We typically recommend restriction from high-intensity exercise, including competitive sports and wilderness activity, in such patients.

Implantable Cardioverter-Defibrillators and Pacemakers

Implantable cardioverter-defibrillators (ICDs) are placed for the primary and secondary prevention of SCD in patients susceptible to malignant ventricular arrhythmias. Recent expansion of ICD appropriateness criteria has lead to continually increasing numbers of patients with these devices.¹⁶ By definition, individuals with ICDs are at high risk for arrhythmia and subsequent device discharge during strenuous activity and therefore should avoid all high-intensity exercise. Device discharge may be painful and may render the recipient temporarily incapacitated. Accordingly, all wilderness activities during which transient compromises in cognitive or motor function may have grave consequences to the patient or partners are contraindicated in patients with ICDs. Examples include underwater diving, rock climbing, and hang gliding. Low- to moderate-intensity exercise may be appropriate for patients with ICDs. We encourage careful assessment of heart rate and rhythm response during formal exercise testing in ICD patients who choose to pursue such activities.

Cardiac pacemakers are used in patients with native conduction system disease and associated symptoms. Although individuals with pacemakers have no specific exercise limitations as a result of the presence of their devices, early-generation pacemakers were not designed to accommodate the physiologic demands of exercise and left recipients with reduced exercise capacity. Recent advances in pacemaker technology have been substantial. With respect to exercise capacity and wilderness activity, the most important advances involve the ability of newer devices to augment heart rate and cardiac output during volitional exercise. Devices now sense the need for heart rate/cardiac output augmentation by tracking some combination of patient body motion, respiratory rate, and properties of the intact native conduction system. The presence of a pacemaker should not constitute grounds for restriction from wilderness activity. However, patients should undergo device interrogation for battery life and sensing/pacing thresholds before participation.

Hypertension

Because blood pressure rises with chronic altitude exposure, hypertension that is well controlled at sea level may become uncontrolled at high altitude. Patients with hypertension, especially those with other comorbidities, are advised to carry a small, wrist type of blood pressure cuff to check their blood pressure and to discuss with their physicians strategies to increase the dose of current medications or add a new drug if necessary. Drugs with combined α/β-blocking effects, such as carvedilol or labetalol, may be especially effective at high altitude.

Chest Pain

Myocardial ischemia most commonly manifests with chest discomfort. The quality of this discomfort varies among individuals and may be reported as heaviness, tightness, or a dull ache. The chest discomfort attributable to myocardial ischemia is often accompanied by other symptoms, including diaphoresis, nausea, dyspnea, or pain in adjacent anatomic structures, including the neck, jaw, or left arm. Among wilderness adventurers, new-onset chest discomfort without a clear musculoskeletal cause should be considered an ominous sign. It should be assumed that nontraumatic chest discomfort is indicative of an active coronary artery process until proved otherwise. Definitive and effective therapy for active myocardial ischemia requires access to hospital-based resources.^2,3 As such, wilderness travelers who experience chest discomfort suspected to be of myocardial ischemic origin should place emphasis on gaining access to a capable medical facility with minimal delay. In some cases, assistance from search and rescue programs with the capability to provide rapid transport may be appropriate. In the field, acetylsalicylic acid (aspirin), preferably in a chewable, rapidly absorbed form, should be given immediately once myocardial ischemia is suspected. Nitroglycerin-based agents, additional anticoagulants, including low-molecular-weight heparin, and analgesic medications may be appropriate if administered in the field by a clinician trained in their use.

Arrhythmias

A rapid but regular heart rate with normal sinoatrial node origin (sinus tachycardia) may be caused by appropriate physiologic response to the intense physical or emotional stress of the wilderness environment. In contrast, pathologic tachyarrhythmias may develop suddenly and may originate in the atria, atrioventricular node, or ventricles. Sinus tachycardia is typically associated with a clear stimulus, develops gradually as the stimulus intensifies, and abates gradually once the stimulus is removed, although it may also be a sign of inadequate compensation to altitude or heat. Sinus tachycardia is generally not associated with additional symptoms unless an individual harbors significant occult or previously documented heart disease. In contrast, pathologic tachyarrhythmias may begin suddenly either at rest or during exertion and typically fail to resolve gradually with activity cessation. They are often accompanied by symptoms that include light-headedness, palpitations, or chest discomfort. Resolution of tachyarrhythmia is typically abrupt.

Differentiation between normal sinus tachycardia and a pathologic tachyarrhythmia can be difficult in the wilderness setting. A prior medical history of confirmed pathologic arrhythmia (e.g., Wolff-Parkinson-White syndrome, atrial fibrillation, or atrial flutter) or underlying structural heart disease can be helpful. Brief physical examination may provide additional clues. The patient’s pulse should be assessed for rate, regularity, and beat-to-beat variability. The jugular venous column should be inspected for the presence of atrioventricular dissociation or flutter waves. Direct auscultation of the heart using either a stethoscope or the simple placement of an ear on the patient’s bare chest can provide clues about rhythm origin. These clues include paradoxical splitting of the second heart sound (characteristic of the left bundle branch block that accompanies ventricular tachycardia, or supraventricular tachycardia with aberrancy) or the presence of Rytand’s murmur (a murmur of varying intensity that indicates advanced heart block).

Management of the symptomatic patient with suspected pathologic tachyarrhythmia should focus on rapid transportation to a medical facility with advanced cardiac life support capabilities.⁸ When transportation to professional medical attention is not an immediate option, several therapeutic maneuvers can be attempted. Carotid sinus massage can be used to terminate several forms of tachyarrhythmia. External pressure on the carotid sinus stimulates baroreceptors that trigger increased vagus nerve activity and decreased sympathetic nervous system activity, thereby potentially terminating the arrhythmia. The patient with tachyarrhythmia should be placed in a supine or lateral decubitus position with the neck fully extended and turned away from the care provider. The carotid pulse should be palpated close to the angle of the jaw to approximate the common carotid artery bifurcation. Firm pressure should then be applied with a gentle rotating motion for 5 seconds. If there is no response, the procedure should be attempted on the patient’s other side. The procedure should never be performed on both sides simultaneously. In patients who do not respond to carotid sinus massage, alternative vagus nerve stimulation maneuvers may be attempted. Prolonged breath holding, a Valsalva maneuver, putting the face in cold water (to induce the “diving reflex”), or a strong cough against a closed glottis may also cause a vagal response adequate to terminate a tachyarrhythmia.

Syncope

Syncope is defined as transient loss of consciousness accompanied by loss of postural tone. Syncope occurs because of rapid reduction in cerebral blood flow culminating in significant central nervous system hypoperfusion. There are numerous causes of syncope. Syncope may be attributable to an underlying cardiovascular pathologic condition, including structural, valvular, or electrical heart disease. Such underlying processes need to be considered when evaluating any patient with a prior syncopal event. Most commonly, syncope occurs in healthy individuals without explanatory heart disease and is attributable to autonomic mechanisms (vasovagal or neurally mediated syncope). The physiology of neurally mediated syncope is beyond the scope of this text; the interested reader is referred to several excellent reviews of this topic.^27,29,38

Neurally mediated syncope is common among physically fit individuals who may choose to engage in wilderness activity¹² and has been reported to occur during the early phases of altitude acclimatization as a result of plasma volume loss, hyperventilation, and perhaps hypoxia-mediated vasodilation. Individuals with a predisposition for neurally mediated syncope may be at increased risk for syncope during wilderness activity that produces dehydration (prolonged strenuous exercise) and/or significant peripheral vascular dilation (thermal exposure). The individual with neurally mediated syncope will typically report presyncopal feelings of warmth, diaphoresis, or light-headedness, which culminate in loss of consciousness ranging from several seconds to minutes.

Management of wilderness syncope begins with removal of the patient from dangerous conditions. Individuals who succumb to syncope should be removed immediately from locations (e.g., partial water submersion, precarious heights) in which transient loss of consciousness could lead to trauma or further complications. Patients should be assessed for spontaneous ventilation and the presence of a regular pulse in a central artery. If spontaneous cardiorespiratory function is confirmed, it is best to observe the unconscious individual for several minutes to allow for spontaneous resumption of normal cognition and motor function. Once revived, efforts to correct or minimize the potential syncopal trigger, such as rehydration, active cooling, or activity cessation, are warranted. A physician should assess all individuals who have syncope during wilderness activity in a full-service medical facility as soon as possible to exclude an underlying cardiac pathologic condition. This assessment should include a detailed history, physical examination, and 12-lead electrocardiogram with further diagnostic evaluation on a case-by-case basis, unless typical “vasovagal” circumstances and symptoms are present.

Cardiac Arrest

The initial approach to the patient in the wilderness with presumed cardiac arrest, typically individuals with sudden collapse or those who suffer prolonged and severe hypoxia (e.g., avalanche burial, drowning) should be to confirm the absence of spontaneous circulatory activity. This is performed by manual palpation of a large central artery such as the carotid or femoral artery and simultaneous inspection of skin tone, motor activity, and chest wall motion. In patients with a palpable pulse but evidence of primary respiratory collapse, maneuvers to clear the upper and lower airways can be initiated.

Once the absence of spontaneous circulatory activity is confirmed, resuscitation in the form of basic life support measures should be initiated immediately. Historically, basic life support has been dictated by the ABC acronym that referred to the resuscitation sequence of airway, breathing, and circulation. The approach to basic resuscitation has recently undergone important modifications.

The most recent American Heart Association/American College of Cardiology consensus guidelines advocate a CAB or circulation–airway–breathing approach to basic life support.⁷ This strategy involves immediate initiation of chest compressions for unconscious patients without spontaneous or normal cardiorespiratory function. The logic for this paradigm shift is that there is ample oxygen present in the lungs and arterial system for several minutes following cardiac arrest to avoid ischemia if blood can reach the target organs. Thus immediate circulation of blood via chest compressions will facilitate optimal oxygenation of the brain and other key organs sooner than the conventional airway-first approach. The currently recommended sequence of adult basic life support can be summarized as follows:

Giving compressions and rescue breaths in a 30 : 2 ratio is recommended during resuscitation. Rescuers are advised to switch roles frequently to minimize the fatigue that is inherent in the delivery of effective chest compressions. A brief resuscitation pause to assess for the presence of spontaneous pulses should be performed every 2 minutes.

The success of cardiac arrest resuscitation typically requires access to advanced cardiac life support equipment and trained personnel. This may not be a reality when cardiac arrest occurs in wilderness environments. Cardiac arrest patients who do not respond to resuscitation efforts during the first 15 to 30 minutes of basic life support are very unlikely to recover any significant degree of brain function, even if spontaneous cardiopulmonary function is restored. The decision of when to terminate resuscitation in a wilderness setting is challenging. Recommendations for this task have been developed.²² In general, it is reasonable to terminate resuscitation efforts after 30 minutes if a spontaneous pulse has not been restored. An extension beyond this time limit should be considered for the hypothermic patient because hypothermia may extend the window of potential central nervous system survival. Current resuscitation guidelines provide recommendations for specific wilderness situations (Table 32-2).⁴⁴

TABLE 32-2 Considerations for Resuscitation of Cardiac Arrest Victims in Specific Wilderness Situations