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Key Points:

  • Acute mountain sickness (AMS) affects up to 40% of travelers at moderate altitudes (up to 10,000 feet) and >50% of trekkers on popular high-altitude routes.

  • Ascending to moderate altitudes entails little risk for people with stable coronary artery disease.

  • An exercise or treadmill stress test can be a useful screening test in climbers with known coronary artery disease (CAD); in climbers with a low risk of CAD, the accuracy of the test is low, and the results can be misleading.

  • Headache is the most common symptom of AMS.

  • Climbers should never continue ascending if they have any symptoms of altitude illness.

  • Descent is the most reliable treatment for any type of altitude illness.

  • Dexamethasone is effective treatment for AMS and HACE. It also lowers pulmonary artery pressure in HAPE

  • Acute pulmonary edema (HAPE) is the most common cause of death from altitude illness.

  • The prophylactic administration of nifedipine prevents the exaggerated pulmonary hypertension of HAPE-susceptible subjects upon rapid ascent to high altitudes and thus prevents HAPE in most cases.

  • Nifedipine is effective against HAPE but has no effect against AMS.

What's New

  • Viagra (sildenafil) and Cialis (tadalafil ) are also now recommended for treating/preventing HAPE, but nifedipine remains the gold standard.

  • Phosphodiesterase (PDE-5) inhibitors, such as Viagra and Cialis, increase NO (nitric oxide) levels in the pulmonary vasculature, causing smooth muscle relaxation and drop in pulmonary artery pressure. This reduces formation of pulmonary edema fluid.

  • Severe or potentially fatal interaction can occur when PDE-5 inhibitors are taken concurrently with nitrates.

  • Acetazolamide appears to help prevent HAPE.

  • Salmeterol is more commonly used as an asthma medication, but it also can hasten the body's ability to re-absorb pulmonary edema fluid.

Altitude Illness

The term "altitude illness" describes disorders affecting the brain and the lung that can occur after a climber ascends to altitudes over 8,000 feet (2,500 meters). There are four categories of altitude-induced illness:

  • Acute Mountain Sickness (AMS)

  • High Altitude Pulmonary Edema (HAPE)

  • High Altitude Cerebral Edema (HACE)

  • High Altitude Pharyngitis/Bronchitis

The most common altitude-related disorder is acute mountain sickness (AMS), which affects the brain. The hallmark of AMS is headache and the AMS syndrome has been defined as the presence of headache in an unacclimatized person who has recently arrived at an altitude above 2,500 meters plus the presence of one or more of the following symptoms: loss of appetite, nausea, vomiting, fatigue, dizziness, or insomnia. The headache is dull and throbbing, worse during the night and in the morning, and increased by straining or bending over. AMS symptoms typically develop within 6 to 10 hours (but sometimes as soon as 1 hour); attain maximum severity within 1 to 2 days, and begin to decrease about the third day-provided additional ascent does not occur. AMS represents one end of the spectrum of altitude illness affecting the brain: it can progress to high-altitude cerebral edema (HACE), a life-threatening form of altitude illness.

High-altitude pulmonary edema (HAPE) affects the lung. It is less common than AMS, but accounts for most deaths from high-altitude illness. HAPE often occurs in someone already suffering from AMS. In fact, 50% of climbers with high-altitude pulmonary edema also have acute mountain sickness and 14% have high-altitude cerebral edema.

Incidence of AMS

The incidence of altitude illness depends on the altitude reached, the rate of ascent, and individual susceptibility. Studies reporting the incidence of AMS, however, show variable results. In some studies, the data is obtained from questionnaires of climbers or high altitude tourists; in other studies climbers were interviewed and also examined.* Another factor: climbers today know more about altitude illness and its prevention, which may contribute to a decreased incidence. For example, in 1976 Himalyan trekkers ascending to 14,000 feet had a 53% incidence of AMS; A study in 2001 reported an incidence of 28% amongst a similar group.

Data from an Austrian study in 1992 showed an incidence of AMS of 3.1% at 6600 feet altitude increasing to 9.5% at 10,000 feet altitude. Hackett states that there is 10-40% incidence of AMS at moderate altitudes (6500-11500 feet) and a 25-50% incidence of AMS in those climbing to altitudes above 13,000 feet.

A special cohort of potential victims are climbers ascending to, and often staying at, very high (12,000 to 18,000 feet) and extremely high altitudes (18,000+ feet). About 8% of the climbers who develop AMS at higher than 15,000 feet go on to develop cerebral and/or pulmonary edema.

*NOTE: Studies that use the Lake Louise AMS scoring system may report a higher incidence of AMS than those using the Hackett AMS scoring system.

Factors That Increase Your Chance of Getting AMS

Previous ability to ascend to high altitudes without getting AMS is no guarantee you won't become afflicted in the future, but if you have been to a certain altitude before with no problems, you probably can return to that altitude without developing symptoms as long as you acclimatize properly and your level of exertion is not significantly different. Risk factors for AMS include the following:

  • Fast ascent (more than 3,000 feet/day)

  • Altitude reached, especially a sleeping altitude over 10,000 feet

  • Strenuous exertion at high altitudes

  • Time spent at high altitudes

  • History of high-altitude illness (the most important risk factor)

  • Living at sea level before your ascent

  • Obesity (Higher incidence of sleep apnea)

Factors Not Associated with-or Not Protective Against-AMS

  • Previous high-altitude experience
  • Smoking

  • Gender: Men and women (and children) are at equal risk

  • Pre-ascent training and increased physical fitness

It may seem surprising that good physical condition does not prevent AMS, but younger, fit persons often go higher and faster than others and may also engage in more strenuous activity at high altitudes. Conditions such as hypertension, coronary artery disease, mild chronic obstructive pulmonary disease, diabetes, and pregnancy do not appear to affect susceptibility to high-altitude illness.

Normal Symptoms at High Altitude

Shortness of Breath on Exertion Shortness of breath (dyspnea) on exertion is normal for anyone exercising at high altitudes. If dyspnea occurs at rest, however, high altitude pulmonary edema should be considered.

Frequent Nocturnal Awakening This often occurs because of periodic breathing (see later) or the need to urinate.

Edema of Altitude Swelling of the extremities and face because of fluid retention can occur as an isolated finding without symptoms of AMS. It responds to diuretics, dexamethasone, and descent.

Periodic Breathing It is now known that periodic breathing generally occurs during sleep and that it occurs in healthy persons. It is characterized by periods of rapid, deep breathing followed by slowing of respiration, then complete cessation of respiration (apnea). The period of apnea may last 10 to 15 seconds before breathing resumes and the cycle starts over. This can be quite startling to observe because the person really does (briefly) stop breathing. A large inspiratory breath may occur at the end of the period of apnea cause the person to awake, resulting in fragmented sleep and fatigue. If periodic breathing symptoms are troublesome, the drug acetazolamide (Diamox-see below) may be helpful. NOTE: Periodic breathing can also be associated with obstructive or mixed (central followed by obstructive) apnea. Ref: NEJM. September 23, 1999; pp. 985-987.

Hypoxic Ventilatory Response (HVR)

What is HVR? Simply put, it is the increase in breathing that occurs when you're not getting enough oxygen. A person with a lower hypoxic ventilatory response is more likely to suffer AMS, HACE, and HAPE than those with a high HVR. The HVR is controlled by a receptor (the carotid body) located in the carotid artery in your neck, and it signals the respiratory center in your brain to increase ventilation when it detects hypoxia. The increased rate and depth of respiration blow off carbon dioxide from your blood, allowing for a corresponding increase in arterial oxygen. Persons who have a sluggish HVR and who under-ventilate remain more hypoxic, especially during sleep. Adverse effects of hypoxia include increased cerebral blood flow triggering cerebral edema, pulmonary vasoconstriction and increased pulmonary artery pressure, and increased water retention by the kidney.

Causes of AMS

The physiologic changes that occur during ascent to high altitudes are complex, and there is considerable variation in how each individual responds. Perhaps the most important change that occurs is the increase in blood flow to the brain. The resulting rise in cerebral artery capillary pressure, in association with hypoxia, results in fluid leakage across the blood-brain barrier, and the resulting increase in brain water is termed vasogenic cerebral edema. This process appears to be the critical step in the genesis of AMS and the syndrome of HACE.

Facts About AMS

  • Of all the organs, the brain seems to be most vulnerable to the hypoxia of high altitudes, particularly extreme altitudes.

  • The dilation of the cerebral arteries caused by hypoxia is lessened by the constricting effect on the arteries caused by hypocapnea (low arterial carbon dioxide). Overall oxygen delivery to the brain is a result of the balance between vasodilation and vasoconstriction. In general, vasodilation overrides vasoconstriction.

  • The combination of increased cerebral blood flow and hypoxia can lead to vasogenic cerebral edema (as described).

  • Increased cerebral blood flow can also cause brain swelling from engorgement of the brain with blood.

  • All brains swell on ascent to high altitudes-either as a result of cerebral edema and/or engorgement with blood, but not all climbers develop AMS.

  • According to the "tight fit" hypothesis, cranial anatomy determines who might develop AMS. In climbers who remain relatively asymptomatic, the brain volume increase and corresponding rise in intracranial pressure are "buffered" by decreased intracranial blood flow (from vasoconstriction) as well as increased displacement of cerebral spinal fluid out of the skull.

  • If buffering is unsuccessful, cerebral edema and intracranial pressure continue to rise, resulting in the symptoms of AMS.

  • AMS can evolve into high HACE. HACE strikes only a minority of climbers, usually those at extreme altitudes.

  • Cases of mild AMS are probably caused by early cerebral edema.

  • There is a hazy line between moderate-to-severe AMS and HACE. Symptoms of more severe AMS include unrelieved headache, decreased urine output, vomiting, and lethargy-but not the loss of balance (ataxia) and the mental confusion or coma that define HACE.

High-Altitude Cerebral Edema

This is the most severe form of AMS. At this stage, significant brain edema and increased intracranial pressure have developed. In general, 24-36 hours elapse between the onset of AMS and HACE, but HACE can also occur abruptly, with few antecedent sypmtoms. These symptoms include nausea and vomiting. irrational behavior, confusion, lethargy, ataxia (loss of balance), and finally, coma. The progression from initial symptoms to coma may take as little as 12 hours. Death follows if early treatment is not administered.

High-Altitude Pulmonary Edema

The second organ of the body most affected by hypoxia is the lung, but the cause of high-altitude pulmonary edema is completely different from AMS and HACE. Basically, in HAPE, a high-pressure fluid leak occurs in the lung. Here's the mechanism: Hypoxia causes pulmonary artery vasoconstriction and an elevation of pulmonary artery pressure. The vasoconstriction, however, is unevenly distributed throughout the lung, and those regions of lung tissue less constricted become overperfused with blood, resulting in regional elevations of pulmonary capillary pressure. The increased capillary pressure disrupes the basement membrane and forces water and proteins through the capillary walls into the pulmonary air spaces, resulting in pulmonary edema (high-pressure overperfusion edema). The flooding of these patchy areas of lung tissue further reduces oxygen delivery to the blood, further increasing hypoxia.

Persons who have a low hypoxic ventilatory response (HVR) have more pulmonary hypertension and are more susceptible to HAPE. More importantly, a low HVR may permit extreme hypoxemia during sleep, explaining why HAPE often strikes in the middle of the night. In addition, persons susceptible to HAPE have other genetic differences; for example, their production of nitric oxide (a chemical that dilates arteries) in the lung is diminished.

The early symptoms of HAPE are breathlessness on exertion and reduced exercise tolerance, greater than expected for the altitude. Untreated, there is progression to breathlessness at rest, especially at night, and persistent cough. The cough can be dry or progress to produce white, watery, or frothy fluid. Severe fatigue or exercise intolerance is nearly universal and may be the most reliable hallmark of HAPE. The most reliable combination of diagnostic signs and symptoms is dry cough and fatigue plus lung crackles and oxygen desaturation (measured with a pulse oximeter and more pronounced than calculated for the altitude) or tachycardia and increased oxygen desaturation.

HAPE strikes 2%-4% of those who travel above 12,000 feet. (Fatal cases, however, have occurred as low as 8,000 feet.) At increased risk are those who have previously experienced HAPE; they have a 60% chance of recurrence during another ascent to high altitudes.

HAPE kills more travelers each year than any other altitude-related condition but is reversible if recognized early and treated properly.

Reducing the Risks of AMS and HAPE

Reduce Activity If you travel rapidly to an elevation higher than 8,000 feet (2,500 meters), you can reduce your chance of illness by not engaging in strenuous activity for the first 2 days.

Acclimatize The major cause of altitude sickness is going too high too fast. You can avoid or lessen AMS by making a slow, gradual ascent. Slow ascent means not increasing your sleeping altitude by over 2,000 to 3,000 feet (600 to 900 meters) on successive nights, especially when climbing above 10,000 feet. An alternate strategy, called staging, is to spend 2 to 3 days at an intermediate altitude (e.g., 8,000 to 10,000 feet) before resuming ascent. A stop at around 12,000 feet is especially advised, In addition, no matter how high you are climbing during the day, try to sleep at a lower altitude, if this is an option.

Unfortunately, cautious guidelines on the rate of ascent are impractical for most climbers. For example, if you were to climb Mt. Kilimanjaro on a guided tour, you would find yourself ascending on a schedule that forces you to sleep at much higher altitudes each successive night. You begin the climb at 5,000 feet. The huts where you sleep are at 9,000, 12,000, and 14,500 feet. Only a single rest day is spent (sometimes) at the highest hut before the final ascent to the 19,000-foot summit the following morning. Needless to say, AMS is a frequent occurrence among those climbing Mt. Kilimanjaro.

Take a Prophylactic Drug In situations where you are going rapidly to altitudes above 8,000 feet, or arriving by airplane at a high destination (Table 15.1), there are two drugs that can help: (1) acetazolamide, which accelerates acclimatization; and (2) dexamethasone, which reduces symptoms, but has no effect on acclimatization itself. Prophylaxis is especially important if you have previously experienced altitude sickness, but drug prophylaxis isn't uniformly recommended by some experts for those who plan a reasonably slow ascent schedule to moderate altitudes. The problem here is: How many people actually practice slow ascent?

Copyright Thomas E. Dietz, M.D. Used with permission.

Acetazolamide (Diamox)-Acetazolamide has been shown to reduce susceptibility to AMS and the incidences of HAPE and HACE. This is the drug of choice for preventing AMS and is about 75% effective. Acetazolamide works through several mechanisms: (1) It forces the kidneys to excrete bicarbonate, acidifying the blood. The resulting metabolic acidosis acts as a respiratory stimulant, increasing ventilation and improving arterial oxygenation. The drug is especially effective in preventing extreme hypoxia during sleep-a situation that can also trigger HAPE, especially in persons with a history of this disorder; (2) It reduces cerebrospinal fluid (CSF) formation and possibly CSF pressure; and (3) It causes a diuresis, counteracting the fluid retention that occurs in AMS.

Standard dosage: 125 to 250 mg every 12 hours, or 500 mg daily of the slow-release preparation (Diamox-SR). Start acetazolamide 24 hours before starting your ascent and continue it for 3 days at the higher altitude. Side effects include frequent urination (polyuria) and a tingling sensation of the face and lips (paresthesia).

Dexamethasone (Decadron)-Dexamethasone is not routinely recommended as a prophylactic agent for AMS or HAPE, but it may be the ideal prophylactic agent to reduce the risk of HAPE and AMS in HAPE-susceptible persons, or those who must ascend rapidly (for example, those going on a mountain rescue mission), as it has now been shown to reduce the incidence of both conditions in this population. *

Prophylaxis dosage: 8 mg orally twice a day, begun the day of ascent. Side effects: taking dexamethasone on an extended trekcould lead to hyperglycemia, immunosuppresion, and steroid psychosis.

*In a study reported in 2006, the incidence of HAPE was reduced from 78% to 0% in climbers taking prophylactic dexamethasone)* Maggiorini M, et al. Both tadalafil (Cialis) and dexamethasone may reduce the incidence of high-altitude pulmonary edema. Ann Int Med. 2006;145:497-506.

Nifedipine-A climber with a history of HAPE could also use the 20-mg slow-release capsule (available in Europe and Asia under various brand names) every 8 hours, or the 30-mg slow-release (available as Adalat-CC or Procardia-XL in North America) every 12 hours. All climbers above 10,000 feet should also carry standby treatment doses of the rapid-acting 10-mg capsules. Nifedipine reduces the incidence of HAPE from 60% to 10% in susceptinble individuals. Cialis (tadalafil), in a dose of 10 mg twice daily, has also been shown to be effective.

Aspirin-Pretreatment with aspirin before travel to high altitudes appears to decrease the incidence and severity of headaches, the main symptom of mild AMS. Take one aspirin tablet every 4 hours for three doses before arrival. After arrival, take two tablets three times daily for 3 days. (Ibuprofen also works.)

Ginkgo biloba-This herb has shown mixed results in preventing AMS.

Diagnosing Altitude Sickness

When diagnosing and treating AMS, HACE, or HAPE keep in mind other diagnoses that can mimic altitude sickness. Consider:

  • Dehydration (can cause nausea, weakness, headache)

  • Hypothermia (can cause loss of balance, staggering gait)

  • Exhaustion (can cause lethargy, loss of balance, staggering gait)

  • Respiratory infection (symptoms include coughing, shortness of breath)

  • Carbon monoxide poisoning (can result from cooking in enclosed spaces such as tents, snow caves; causes rapid breathing, headache, mental changes, coma.)

  • Hyperventilation (rapid breathing from anxiety; may simulate pulmonary edema)

  • Psychiatric problems with psychosis can cause irrational behavior mimicking some aspects of HACE.

  • The combination of high altitudes, hypoxia, and dehydration can predispose to venous thrombosis-cerebral, retinal, and pulmonary. Women on birth control pills who smoke may be at higher risk for a pulmonary embolus.

  • Altitude-unrelated illness, e.g., diabetes (hypoglycekia, ketoacidosis), a seizure disorder, symptoms of an undiagnosed brain tumor, viral or bacterial infection

Although the valuable aphorism "any illness at altitude should be considered AMS until proved otherwise" is usually true, it is sometimes impossible, perhaps even unnecessary, to make an immediate diagnosis. Symptomatic treatment, such as oxygen, quickly followed by descent, should be the first priority. An exact diagnosis can often wait until after the climber has descended.


Mild AMS by itself is a benign illness but you must watch for progression to more severe AMS, HACE, or HAPE. In general, management depends on the acuity and severity of symptoms. The principles of treatment are as follows:

  • Stop further ascent and rest. Administer adjunctive treatment, as indicated.

  • Descend if there is no improvement or if symptoms worsen.

  • Descend immediately if there are symptoms or signs of cerebral or pulmonary edema.

Mild AMS

The first rule applies: Stop your ascent and rest. Symptoms should improve in 8 to 12 hours; if not, descend. To help the headache, take aspirin, acetaminophen, or ibuprofen. Acetazolamide (Diamox), 125 mg to 250 mg twice daily may reduce symptoms within 12 hours. Dexamethasone (4 mg orally or intramuscularly every 6 hours) works within 6 hours and is possibly more effective than acetazolamide. Combining dexamethasone and acetazolamide may be even more effective but no studies have yet proved this. No further ascent should be attempted until symptoms have cleared. Continue to take acetazolamide for several days as prophylaxis. Drinking extra fluids doesn't help AMS but if you are dehydrated you will feel better.

More Severe AMS

Treatment of more severe AMS (which is essentially a pre-HACE condition) is directed at stopping the formation of vasogenic cerebral edema. A descent of 1,500 to 3,000 feet is the best initial treatment. Adjunctive measures include oxygen, steroids, acetazolamide, rest, and staying warm.

  • Start oxygen, if available, at a flow rate of 2 to 4 liters/minute
  • Administer dexamethasone, 8 mg immediately, then 4 mg every 6 hours, plus acetazolamide, 250 mg every 12 hours.
  • Plan for descent as soon as possible.

High-Altitude Cerebral Edema (HACE)

The hallmarks of HACE are confusion and ataxia (staggering gait). To test for ataxia, have the climber attempt to walk a straight line, one foot in front of the other, heel to toe. A climber who struggles to stay on the line, falls off to one side, or falls down should be considered to have HACE. At the first sign of ataxia, if not before, descent should be started. Adjunctive treatments are listed in the preceding paragraph. A portable hyperbaric chamber, such as the Gamow bag (see below), will improve oxygenation, give temporary relief, and will facilitate descent; but use of the Gamow bag should not unduly delay descent. NOTE: HACE and high-altitude pulmonary edema (HAPE) often occur simultaneously, but HACE can also occur as a single entity without pulmonary symptoms.

High-Altitude Pulmonary Edema (HAPE)

Treatment depends on the severity of the illness and the environment. If oxygen and medical expertise are not available, immediate descent is indicated. If diagnosed early, a descent of 1,500 to 3,000 feet usually gives rapid improvement. Two or 3 days of rest at the lower elevation usually adequate for complete recovery. Once the symptoms have resolved, cautious re-ascent may be attempted. NOTE: Some authorities state, however, that once a diagnosis of HAPE is made, the individual should be evacuated to a medical facility for proper follow-up treatment. This is probably indicated only in more severe cases. Re-ascent can be attempted cautiously, but only if prophylactic acetazolamide and nifedipine or a PDE-5 inhibitor is available.

Treatment Options for HAPE

  • Oxygen, at an initial flow rate of 2 to 4 liters/minute, can be lifesaving. Reduce flow to 1 to 2 liters to keep SaO2>90%.

  • Administer nifedipine, Viagra, or Cialis (see below). Although oxygen and descent are the best treatments for HAPE, nifedipine and PDE-5 inhibitors are effective adjuncts, especially when oxygen is not available.

  • If conscious, have the patient swallow the first dose. If lethargic or comatose, pierce the capsule (if using nifedipine) and squirt it under the tongue. Continue treatment with the slow-release form, 20 to 30 mg every 12 hours.

  • Nifedipine rapidly reduces pulmonary vasoconstriction, thus reducing pulmonary hypertension and over-perfusion edema. The reduction in vasoconstriction also makes pulmonary blood flow more homogeneous, which improves oxygenation. Sublingual administration of nifedipine results in a 10% rise in arterial oxygen saturation within 10 to 15 minutes. Nifedipine and PDE-5 inhibitors can sometimes be used alone with strict bed rest in a person with only very mild HAPE, otherwise they is used only in combination with the other treatments: descent, oxygen, and hyperbaric therapy.

  • Administering hyperbaric treatment in the Gamow bag (see next) for a total of 2 to 4 hours usually results in dramatic improvement, facilitating descent.

  • Keep the patient warm. Not only will the patient be more comfortable, cold stress increases pulmonary artery pressure.

Nifedipine (Procardia®, Adalat®)

Nifedipine comes in 10 mg and 20 mg capsules. Also available in extended release forms (Procardia XL, Adalat CC) in 30, 60, and 90 mg capsules.

  • First-line for prevention/treatment of High Altitude Pulmonary Edema (HAPE).
  • Calcium channel blocker. Reduces systemic as well as pulmonary artery pressure.
  • Prevention dose: 20 mg orally three times daily or 30 mg-60 mg of sustained release for prevention of HAPE when started on the day of ascent and continued for 72 hrs at higher altitudes. Especially indicated when ascending to altitudes >12,000 feet.
  • Treatment dose: 10 mg orally once then 20 mg sustained release four times daily.
  • Side effects: Hypotension and reflex tachycardia, dizziness, nausea may occur, but cardiovascular effects are usually not a problem in treating or preventing HAPE.

Sildenafil/Tadalafil (Viagra®, Cialis®)

Sildenafil (Viagra) comes in 25, 50, and 100 mg tablets and is a popular drug prescribed for erectile dysfunction. It is also effective for treating High Altitude Pulmonary Edema (HAPE) through the mechanism of lowering pulmonary artery pressure.

Tadalafil (Cialis ) comes in 5, 10, and 20 mg and is also commonly prescribed for the treatment of erectile dysfunction. It is used off-label for treating or preventing HAPE. Viagra and Cialis are in a class of drugs called phosphodiesterase (PDE-5) inhibitors.

  • Phosphodiesterase (PDE-5) inhibitors increase NO (nitric oxide) levels in the pulmonary vasculature, causing smooth muscle relaxation and drop in pulmonary artery pressure. This reduces formation of pulmonary edema fluid.
  • Prevention Dose: Tadalafil (Cialis) 10 mg orally twice daily for prevention of HAPE.
  • Treatment Dose: Sildenafil (Viagra) 50 mg orally three times daily or tadalafil 10 mg orally twice daily for treatment of HAPE.
  • Severe or potentially fatal interaction can occur when PDE-5 inhibitors are taken concurrently with nitrates.

Salmeterol (Serevent®)

Available as a metered dose inhaler. Salmeterol is more commonly used as an asthma medication, but it also can hasten the body's ability to re-absorb pulmonary edema fluid.

  • Dose: 120 mcg (2 puffs) inhaled twice daily for HAPE prevention and possibly treatment, starting the day prior to ascent and continued for 2 days at maximum altitude.
  • Mechanism: Upregulates pulmonary sodium transport across alveolar membranes to increase clearance of alveolar fluid.
  • Side effects: Mild tachycardia.

The Portable Hyperbaric Chamber (Gamow Bag)

This device is an airtight, 7-foot cylindrical bag made of coated nylon weighing about 18 lbs. with a pump and/or rebreathing unit. It is used for the treatment of more severe AMS or HACE, especially when a person is too ill to descend immediately. The stricken climber is placed inside the bag, which is then pressurized with a foot or hand pump. This pressurization simulates a decrease of 1,500 to 2,500 meters in altitude and, depending on the starting altitude, is usually sufficient to raise arterial oxygen saturation to more than 90%. A 1-hour treatment provides rapid relief from most symptoms of AMS, but the effect is temporary, lasting only 10 to 11 hours. This may buy enough time to walk the stricken climber to a lower altitude. By contrast, climbers receiving dexamethasone will improve more slowly but with sustained, longer-lasting effects. Although the administration of dexamethasone is simple, the same can't be said for the mobile hyperbaric chamber. Maintaining therapeutic pressure and air flow in often extreme weather can be a daunting task. In addition, access to the victim is restricted.

The main advantages of the Gamow-type bag are its rapid action and independence from consumable oxygen. The device is best suited for alpine expeditions and search and rescue teams that don't carry bottled oxygen. Gamow bags can be purchased or rented form Chinook Medical Gear, Inc., 120 Rock Point Drive, Unit C, Durango, CO 81301; 970-375-1241; 800-766-1365.


This is usually supplied by "E" type cylinders that weigh about 18 lbs. One full tank will last about 4 hours at a flow rate of 2 liters/minute. Supplemental oxygen is slightly more effective than the Gamow bag in raising arterial oxygen saturation and its use does not restrict access to the victim.

Sleeping Pills

It is usually recommended that high-altitude travelers not take sleeping pills because they might depress respiration, increase oxygen desaturation and hypoxia, and increase the incidence or severity of AMS. However, a recent study (conducted at an elevation of 5,300 meters) among members of the British Mount Everest Expedition found that small doses (10 mg) of the short-acting benzodiazepine, temazepam (Restoril), improved the subjective quality of sleep without adversely affecting respiration. Better sleep, defined as longer periods without arousal, resulted in less daytime drowsiness and improved endurance. In 1996, French researchers found that a 10-mg dose of zolpidem (Ambien) taken at a simulated altitude of 4,000 meters was associated with fewer sleep arousals and no increase in period breathing. From these studies, it appears that the short-acting hypnotics may actually be safe adjuncts for improving comfort and rest as well as high-altitude performance.

Acute Altitude Sickness in Children

The incidence of AMS in children is about the same as in adults, but diagnosing the condition can be problematic because the symptoms-cough, headache, irritability, and loss of appetite-are often mistaken for a viral illness. If a child does become sick at altitude, the parents should assume that AMS is a possibility, descend, and seek prompt medical consultation. Drug prophylaxis/treatment for AMS could be considered as for adults, but with appropriate pediatric doses. These medications have not been specifically studied for treating children with AMS.

The Heart at High Altitudes

Ascent to moderate altitude appears to entail little risk for travelers with coronary artery disease who are ordinarily asymptomatic or who have moderate exercise tolerance. They may develop angina at a lower level of exertion, but generally have no impairment of their ability to acclimatize. They should rest for a few days after arrival at altitude, and ascend slowly thereafter. If the traveler is on treatment for angina, atrial fibrillation, hypertension, or mild compensated congestive heart failure their medications should be carefully adjusted, especially to keep the blood pressure and pulse well controlled.

However, the question that many people (and their doctors) ask about high-altitude travel is "will it trigger a heart attack?" or "Is there a risk of sudden death?" Younger people need not worry about this, but what if you're a 50-year-old man in relatively poor physical condition, perhaps with several cardiovascular risk factors? Is trekking a good idea? Reports in the medical literature demonstrate an increased incidence of sudden cardiac death associated with abrupt exercise in sedentary people, but there are little data about the risk during participation in mountain sports.

In a report of sudden deaths among high mountain hikers and skiers in Austria, hikers were more than twice as likely to die as skiers. Among the hikers, the risk of death was highly associated with an age of more than 40 years and lack of prior physical activity. In contrast, a study of medical evacuations of climbers and trekkers in Nepal showed that cardiac disease accounted for only 5% of the evacuations, and none of the deaths. One reason for this difference could be that the climbers that went to Nepal were in much better physical condition.

The possibility of an acute cardiac event has prompted efforts to screen asymptomatic travelers in an effort to identify the presence of coronary disease before the occurrence of a serious problem. A stress test is often recommended. Unfortunately, exercise stress tests have limited effectiveness because they don't show the anatomy of the coronary arteries. They miss plaques that are not large enough to obstruct blood flow, but that have the potential to destabilize and rupture, causing new-onset angina, heart attack, or cardiac arrest. More sensitive tests are needed to detect these asymptomatic plaques, and if found, to stabilize them.

  • Coronary artery disease (CAD) is a disease where there is build-up of atherosclerotic "plaques" within the arterial wall.

  • Plaques consist of a lipid-rich core, inflammatory cells, calcium, and a fibrous cap.

  • Your risk of heart attack is related not only to the existence and extent of coronary artery plaques, but to their biochemical stability.

  • Unstable plaques can fissure or rupture, triggering thrombosis and blockage of the coronary artery.

  • Larger plaques are more likely to rupture than small plaques, but smaller plaques are more numerous, and present the greater risk for a heart attack.

  • Stabilizing plaque is a key goal in reducing risk.

  • Statin drugs can stabilize plaques. Regular exercise reduces the risk of plaque rupture.

  • Reducing cardiac risk factors reduces plaque formation.

Exercise stress tests are probably most useful for evaluating the functional capacity of the hearts of people who already have diagnosed coronary artery disease. The results can also help their physician adjust their medication for maximum benefit

If you are planning a trip to moderate-to-high altitudes, here are some guidelines:

  • If you are younger than age 50, without symptoms of heart disease, and in good physical condition, and you have no cardiac risk factors, especially no family history of early heart disease, you don't need a cardiac evaluation before your trip. Standard pre-travel counseling (Chapter 2) is sufficient. Follow the guidelines in this chapter for preventing altitude illness.

  • If you have one or more risk factors (including male older than age 50), but have no cardiac symptoms, consult your physician. Depending on the nature of your planned excursion, the number of risk factors, your overall medical and physical condition, plus whatever anxiety you might have about your heart, pre-ascent treadmill exercise testing may be recommended. However, there can be drawbacks to testing people who are considered low risk for having coronary artery disease (CAD). Low pretest probability results in a high rate of false positive tests. For example, if you have a low (say 5%) pretest probability of CAD, the positive predictive value (post-test probability) of a positive test is only 21% (assuming a test sensitivity of 50% and a specificity of 90%). That means that if 1000 people with risk factors like your's are tested, 120 will have a positive result-but 95 of them will not have significant CAD. If the your test shows only minor or nonspecidic ECG abnormalities, it could open a diagnostic Pandora's box. Your doctor may advise further imaging studies-perhaps even a coronary angiogram. Although coronary angiograms are considered the gold standard, they are invasive and not without risk of serious, immediate complications. A newer, noninvasive technology, 64-slice CT coronary angiography, has a high chance of showing your coronary arteries in enough detail to diagnose coronary artery disease, but entails significant radiation, as well as expense. The test, however, does not involve arterial catheterization and takes only 15 minutes. The CT angiogram is about 85% sensitive in its ability to diagnose CAD whereas a negative CT angiogram is 90% reliable in excluding significant coronary artery disease. Read more . . .

  • The bottom line: In most circumstances, stress testing for diagnosis of CAD is warranted only if you have at least an intermediate (25%-75%) pretest probability of disease.

Exercise ECG Testing Without Imaging - Basic Facts

The exercise test plays an important role in the diagnosis of CAD because it is readily available, inexpensive, and easily performed. It does not require injections or involve exposure to radiation. Since it does not accurately localize the site or extent of myocardial ischemia, it is less useful in patients who have undergone CABG or PCI, in whom other forms of stress testing are recommended.

Exercise places major demands on the cardiopulmonary system; thus, it can be considered the most practical test of cardiac perfusion and function. Myocardial oxygen consumption can be reasonably estimated by the product of the heart rate and systolic blood pressure. This is valuable information, since exercise-induced angina often occurs at the same cardiac workload.

Symptom-limited treadmill or bicycle exercise is the preferred form of stress because it provides information concerning patient symptoms, cardiovascular function, and hemodynamic response during activity. Cardiac ischemia and angina at a low workload indicates a greater likelihood of severe disease than at a high workload.

Source: Emergency Medicine Reports. September 1, 2008

  • Stress tests vary by features. Exercise tests may be assessed by 1) changes in the ECG alone, 2) by perfusion (blood flow) defects on myocardial perfusion imaging, or 3) by heart wall motion abnormalities on stress echocardiography.

  • If you complete a high-intensity stress test without any problems, essentially no limits should be imposed on your physical activity. If your stress test, however, is significantly abnormal (e.g., chest pain at a low workload, diagnostic ECG abnormalities, drop in blood pressure), you may be a candidate for coronary angiography and revascularization with coronary artery bypass grafting surgery (CABG) or angioplasty with stenting (PCI - percutaneous coronary intervention).

  • Caution: Unless you are found to have severe disease of the left main coronary artery or severe, crippling, or unstabe angina, bypass surgery is no more effective than conservative medical treatment* that lowers blood pressure and cholesterol. Angioplasty and stenting may be even less helpful, and can actually raise the risk of heart attack in patients with blocked arteries who are otherwise stable.

  • If you have had previous CABG surgery or a stent, climbing or travel to high altitudes is certainly possible, but the indications for ascent should be examined carefully. The American Heart Association/American College of Cardiology guidelines recommend exercise stress testing with myocardial perfusion imaging or echocardiography in patients who have undergone PCI or CABG.

* The foundation of medical management includes the antiplatelet drugs aspirin and/or clopidogrel (Plavix) and high-dose lipid-lowering statins (e.g., Lipitor, Zocor - which also promote plaque stabilization). Medications may also include beta blockers (e.g., Toprol), ACE inhibitors, calcium channel blockers, and nitrates. Blood pressure should be normalized, with additional drugs if necessary. Non-pharmacological management includes smoking cessation, moderation of alcohol, and a diet high in fruit, vegetables, fish and poultry. A weight reducing diet, customized exercise program and a stress reduction program may also be indicated.

The Heart and High Altitudes

  • Judicious exercise at altitude usually causes few problems in the traveler with stable cardiac disease.

  • High altitude increases cardiac work during the first 3 or 4 days at altitude. Overly strenuous activity should be avoided during this time. Activity should be limited to that tolerated at lower altitudes.

  • At least a moderate degree of physical conditioning is desirable before commencing any strenuous activity in the mountains. Physical conditioning is especially important for those ages 40 and older.

  • Heart attack (myocardial infarction) can be triggered by heavy physical exertion in habitually sedentary people. Regular exercise protects against it.

  • Gradual, rather than abrupt ascent is always better.

  • Blood pressure should be kept under good control.

  • Travelers with a history of congestive heart failure often decompensate at high altitudes because of fluid retention.

  • When angina drugs are prescribed, calcium channel blockers may be preferable to beta blockers.

  • Cardiac arrhythmia, such as atrial fibrillation, may worsen after rapid ascent to altitude, even without underlying coronary artery disease.

  • Trekkers who have had cardiac bypass surgery (CABG) have climbed as high as 19,000 feet without problems, but the risks for them from mountaineering and trekking at extreme altitudes are simply not known. Every traveler must be evaluated individually.

  • Your maximal physical exertion at high altitudes is usually limited more by your lung function than by your heart.

  • The guidelines for travel to higher altitudes by people with heart disease are somewhat elusive and not well standardized.

  • Taking a cholesterol-lowering statin drug, such as atorvastatin (Lipitor), may reduce the risk of a cardiac event. Atorvastatin, in higher doses, stabilizes coronary artery plaques, reducing the risk of plaque rupture and acute coronary syndrome (new-onset angina, heart attack).

  • Aspirin and clopidogrel (Plavix) reduce the risks of heart attack and stroke, but bleeding can be a side effect.

The decision to travel should be based on your physician's advice, plus your own desire to go. Bear in mind that if problems occur, you could be far away from a hospital. However, many intelligent, well-informed people, knowing the risks, as well as their own capabilities and limitations, want to live life to the fullest. This is a human desire that should not unnecessarily be restricted.

How Two Physicians Advise Their Patients Who Climb

Dr. Drummond Rennie, an internist and experienced trekker/climber advises, "My own practice is to take a careful history from people who ask if they can go trekking at high altitudes. I explain that if they are able to carry out strenuous, long, continued exercise at sea level, they can probably expect to do so at high altitude. I suggest also that, if possible, they should give themselves a trial at moderate altitude, say 8,000 feet. If they have any symptoms, say angina, they should ascend even more slowly than usual so that they can acclimatize." And Dr. Charles Houston, who is a world-renowned expert on altitude sickness, says, "Coronary artery disease, per se, is not an absolute contraindication to trekking at higher altitudes. If reserve circulation is sufficient, if the patient is wise in recognizing symptoms and accepting limits, if the anticipated stresses of hiking and climbing do not produce signs and symptoms at sea level, then a person may go ahead, properly warned and prepared, because the emotional and psychological benefits are large.