Title: Altitude and the Heart: Is Going High Safe for Your Cardiac Patient?
Topic: General Cardiology
Date Posted: 2/8/2010
Author(s): Higgins JP, Tuttle T, Higgins JA.
Citation: Am Heart J 2010;159:25-32.
Clinical Trial: No
Perspective: Ease of travel and an interest in high altitude recreation exposes patients to the acute physiologic effects of high altitude and lower oxygen availability. Acute exposure to high altitude is associated with significant alterations to the cardiovascular system, with acute hypoxia, increased myocardial work, increased epinephrine release, and increased pulmonary artery pressures. This review summarized the physiology and clinical evidence regarding acute altitude exposure on the cardiopulmonary system, and made practical recommendations for patients with cardiovascular disease. Points to remember are:
1. Environmental changes when moving from sea level to high altitude include reductions in atmospheric pressure, oxygen pressure, humidity, and temperature. Significant changes typically begin at about 2500 m (8200 ft). The effect on patients depends on the degree of hypoxia, change in elevation, rate of ascent, level of acclimatization, exercise intensity at altitude, age, and genetics.
2. Moderate altitude is defined as 1500-2500 m (4950-8250 ft). High altitude is defined as >2500 m (8250 ft).
3. The acute cardiopulmonary effects of altitude include:
Tissue hypoxia, as a result of the significant decrease in oxygen availability in inspired air. Pulmonary vascular resistance increases 50-300%.
Initial hyperventilation leads to respiratory alkalosis that transiently shifts leftward the oxygen-hemoglobin dissociation curve. (After a few hours, increased red cell production of 2,3-diphosphoglycerate shifts the curve back to the right.)
Heart rate increased at rest. There is only a minimal reduction in resting stroke volume, but a decrease in maximal heart rate response lowers peak cardiac output.
A reduction in plasma volume caused by increased respiratory, urinary, and cutaneous losses. The resulting increased hematocrit is responsible for higher oxygen-carrying capacity per unit blood volume, helping maintain resting stroke volume.
Parasympathetic nervous system deactivation, with predomination of sympathetic nervous responses.
Glycogenolysis stimulated by the increase in epinephrine, causing increased use of glucose at rest and with exercise, and increased blood lactate levels.
4. Coronary artery disease. The acute physiological changes associated with high altitude result in earlier onset of ischemia and symptomatic angina in patients with coronary artery disease, and at a lower pressure-rate product.
5. Heart failure. Increased sympathetic activity results in vasoconstriction and tachycardia, as well as release of inflammatory mediators. Increased sympathetic activity results in increased heart rate and systemic vascular resistance. Pulmonary vasoconstriction leads to pulmonary hypertension (exacerbated with exercise), probably the most significant factor in reducing cardiopulmonary performance at altitude in patients with heart failure.
6. High altitude pulmonary edema. High-altitude (noncardiogenic) pulmonary edema affects unacclimatized people with a genetic predisposition, typically within 4 days of arriving at altitude. Causes are probably multifactorial, including pulmonary vascoconstriction leading to increased intravascular pressure.
Slow ascent serves as a preventative measure. (For ascent >3050 m [10,000 ft], ascent should be ≤305 m [1000 ft] daily with a rest every 1000 m [3300 ft].)
If suspected, immediate descent and administration of supplemental oxygen is the treatment of choice.
Nifedipine (sustained release 20-30 mg orally q 6 to 12 h) can both prevent and treat high-altitude pulmonary edema.
Tadalafil 10 mg bid or sildenafil 50 mg q 8h can be used to prevent high-altitude pulmonary edema, but treatment doses have not been established.
7. Arrhythmia. Increased sympathetic activity associated with high altitude can increase the frequency and duration of supraventricular and ventricular arrhythmias with or without underlying heart disease.
8. Congenital heart disease. In simple uncomplicated congenital heart disease (including atrial septal defect, restrictive ventricular septal defects, and patent ductus arteriosus), arterial oxygen desaturation can occur at high altitude when the usual left-to-right shunting of blood reverses, owing to increased right-sided pressures.
9. Recommendations for all people. The following recommendations apply to all individuals who plan to ascend to high altitude and/or exercise at elevation:
Limit activity to a lower maximal level than at sea level.
Raise sleeping altitude gradually.
At least moderate physical conditioning at sea level is encouraged before exercise at altitude.
Alcohol consumption should be minimized, and hydration should be maintained.
If cardiac status is unknown, exercise testing can be considered prior to travel.
10. Recommendations for patients with cardiovascular disease. The following recommendations apply to individuals with known cardiovascular disease who plan to ascend to high altitude and/or exercise at elevation:
Patients with unstable cardiac disease (unstable angina, uncontrolled ventricular arrhythmias, decompensated heart failure) should not exercise at high altitude.
Patients with severe cardiac diseases (including severe angina, heart failure, or valve disease) should not ascend to high altitude. Patients should avoid traveling to high altitude for 14 days after an acute coronary event. Patients with stable heart disease should limit physical activity for the first few days after ascent. Patients should be advised that they could become symptomatic at lower workloads when at altitude. Patients with prior high-altitude pulmonary edema and known intracardiac shunt should be advised to avoid travel to high altitude. Patients with pacemakers can safely travel to high altitude with no impact on ventricular stimulation thresholds.
David S. Bach, M.D., F.A.C.C.
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