High-Altitude-Related Illnesses
Pulmonary and Critical Care Medicine · High-Altitude-Related Illnesses 🎯 Practice these cards
The strongest risk factor for altitude illness is a ____. Rapid ascent is defined as more than ____ m in less than 2 days, or more than ____ m per day above 3000 m. ____ is a risk factor, but lack of ____ is NOT.
Key risk factors for altitude illness include a prior episode of high-altitude illness (recurrence is common and it is the strongest risk factor), rapid ascent (more than 3500 m in less than 2 days, or more than 500 m per day above 3000 m), exertion, and medical comorbidities that impair oxygenation (ILD, COPD, pulmonary hypertension). Susceptibility is individualized: altitude illness occurs at all ages regardless of fitness level — exertion is a risk factor, but lack of physical fitness is NOT.
AMS typically develops ____ to ____ hours after ascent. Symptoms are ____ and resolve within ____ to ____ hours if there is no further ascent. Mild AMS is treated with ____ plus an ____, and even a minor descent of ____ to ____ m may relieve symptoms.
AMS is the most common high-altitude illness, typically developing 6 to 12 hours after ascent. Symptoms are nonspecific — headache, malaise, anorexia, nausea, vomiting, fatigue, dizziness — with a paucity of physical findings. Provided there is no further ascent, symptoms typically resolve within 24 to 48 hours. For mild AMS, rest alone with an analgesic (aspirin or an NSAID for headache) may be adequate; even a minor descent of 400 to 500 m may relieve symptoms.
The drug of choice for AMS prevention is ____, at a dose of ____ mg twice daily starting ____ day(s) before ascent. It works by inhibiting renal ____, causing bicarbonate diuresis and metabolic ____ that stimulates ventilation. In patients with sulfa anaphylaxis, use ____ instead.
Acetazolamide is the drug of choice for AMS prevention. It inhibits renal carbonic anhydrase, causing prompt bicarbonate diuresis and metabolic acidosis that stimulates ventilation and accelerates acclimatization. Dose: 125 mg twice daily, starting 1 day before ascent and continued for about 3 days at the same altitude; meta-analysis shows a relative risk reduction of about 48%. It is a nonantibiotic sulfonamide — use dexamethasone instead in patients with a history of sulfa anaphylaxis.
Per WMS 2024, acetazolamide remains first-line AMS/HACE prophylaxis and is still effective when started on the ____ if the day-before start was missed. Dexamethasone used for more than ____ to ____ days should be ____ rather than stopped abruptly, and dexamethasone is not recommended for AMS prophylaxis in ____.
Per the WMS 2024 guideline update, acetazolamide 125 mg twice daily remains first-line prophylaxis for AMS and HACE and is still effective when started on the day of ascent if the day-before start was missed. Dexamethasone used for more than 5 to 7 days should be tapered over a week rather than stopped abruptly, and dexamethasone is not recommended for AMS prophylaxis in children. Ibuprofen 600 mg three times daily also reduces AMS incidence; ginkgo biloba is ineffective.
The hallmarks of HACE are ____ and ____; any ____ at altitude should be treated as HACE until proven otherwise. MRI classically shows increased signal in the ____ of the corpus callosum. Definitive treatment is immediate ____, with adjunctive ____ (____ mg loading, then ____ mg every 6 hours).
HACE is an encephalopathy occurring at higher elevations (3000–4000 m) whose hallmarks are ataxia and altered consciousness with diffuse cerebral involvement but generally without focal neurologic deficits; progression to coma and death can be rapid. MRI shows vasogenic edema with increased signal in the white matter, particularly the splenium of the corpus callosum. Any ataxia or altered consciousness at altitude should be treated as HACE until proven otherwise. Definitive treatment is immediate descent; adjuncts include supplemental oxygen and dexamethasone (8 mg PO/IM/IV, then 4 mg every 6 hours). A portable hyperbaric bag simulates descent but does not replace it.
HAPE typically develops ____ to ____ days after arrival at a new altitude and rarely occurs after ____ to ____ days at the same altitude. It is ____ necessarily preceded by AMS. Early clues include ____ greater than expected at the altitude and a dry, persistent ____; pink frothy sputum heralds ____.
HAPE typically develops 2 to 4 days after arrival at a new altitude and rarely occurs after 4 to 5 days at the same altitude. It is not necessarily preceded by AMS. The initial manifestation may be a reduction in exercise tolerance greater than expected; a dry, persistent cough may presage HAPE, followed by blood-tinged sputum. As illness progresses, tachypnea and tachycardia occur even at rest, with crackles or wheezing; pink frothy sputum heralds respiratory failure. Risk factors include rapid ascent, history of HAPE, respiratory tract infections, cold temperatures, and male sex.
HAPE is a ____ pulmonary edema with ____ pulmonary artery wedge pressure. Patchy hypoxic vasoconstriction raises pulmonary capillary pressure above ____ mm Hg, causing capillary '____' failure. Unlike ____, lung architecture is usually well preserved, so abnormalities reverse rapidly — often within ____ days.
HAPE is a noncardiogenic pulmonary edema with normal pulmonary artery wedge pressure: patchy hypoxic vasoconstriction leads to overperfusion in some regions, raising pulmonary capillary pressure (above 18 mm Hg) and causing capillary 'stress' failure with leak into the alveoli. Contributing mechanisms include reduced nitric oxide bioavailability, elevated endothelin-1, and sympathetic pulmonary venoconstriction. Because lung architecture is usually well preserved (unlike ARDS), abnormalities reverse rapidly — often within 2 days of oxygen and descent.
The cornerstones of HAPE treatment are ____, rest, and ____, with oxygen ____ to ____ L/min aiming for SpO2 above ____%. Adjunctive vasodilators include ____ and ____ inhibitors. ____ and ____ are NOT recommended in HAPE.
Treatment of HAPE rests on oxygen, rest, and descent. Supplemental oxygen (4–6 L/min, aiming for SpO2 above 90%) acutely reduces pulmonary artery pressures. Oral sustained-release nifedipine 30 mg every 12 hours serves as adjunctive therapy, and PDE-5 inhibitors are used in clinical practice. Diuretics and nitrates are NOT recommended — HAPE is noncardiogenic with normal wedge pressure, so furosemide or nitrates do not address the mechanism and risk worsening dehydration and hypoperfusion. Intubation may be required in severe cases.
The preferred drug for HAPE prophylaxis is sustained-release ____ ____ mg twice daily. Per WMS 2024, pharmacologic HAPE prophylaxis is restricted to patients with ____, and there is no role for concurrent ____ plus ____. In one trial, ____ reduced HAPE risk by about 65% and ____ by about 78%.
Sustained-release nifedipine 30 mg twice daily prevents HAPE in people who must ascend rapidly or who have a history of HAPE; alternatives include tadalafil (10 mg twice daily), sildenafil (50 mg three times daily), and dexamethasone (8 mg twice daily) — in one trial, tadalafil reduced HAPE risk by about 65% and dexamethasone by about 78%. Per WMS 2024, pharmacologic HAPE prophylaxis is now restricted to patients with prior HAPE: nifedipine is preferred, tadalafil is reserved for when nifedipine is unsuitable, and there is no role for concurrent nifedipine plus tadalafil. Preventive therapy should continue about 3 days after arriving at target altitude.
The ____ guideline formally added ____ as adjunctive HAPE treatment. The HAPER CAPER trial (2025), the first ____ trial of this intervention, randomized ____ dyspneic adults at altitude with SpO2 below ____% to CPAP at ____ cm H2O plus high-flow oxygen versus sham. Fingertip pulse oximetry becomes unreliable once SpO2 falls below about ____%.
The WMS 2024 guideline formally added CPAP as adjunctive HAPE treatment, or when oxygen and vasodilators are unavailable. The HAPER CAPER trial (2025), the first randomized trial of CPAP for HAPE, was a multicenter, double-blind, sham-controlled study that randomized 64 dyspneic adults at altitude with SpO2 below 85% and radiographic noncardiogenic edema to CPAP (10 cm H2O) plus high-flow oxygen versus sham CPAP plus oxygen, measuring speed of resolution. Practical caveat: fingertip pulse oximetry becomes unreliable once SpO2 falls below about 80%.
MKSAP recommends limiting altitude gain to less than ____ m per day; a conservative itinerary limits increases in sleeping altitude above 3000 m to ____ m or less per day and takes every ____ day of gain as an extra acclimatization day. One prior week at 2000 m or higher reduces AMS at 4300 m by about ____%.
Gradual ascent with adequate time for acclimatization is the best prevention of altitude illness. MKSAP recommends limiting gain at high altitude to less than 500 m per day; a conservative itinerary additionally limits increases in sleeping altitude above 3000 m to 300 m or less per day, takes every third day of gain as an extra acclimatization day, and may include a night at an intermediate altitude. Recent high-altitude exposure is protective: one week at 2000 m or higher reduces the incidence and severity of AMS at 4300 m by about 50% compared with ascent from sea level.
Airline cabins are pressurized to a 'cabin altitude' equivalent of ____ to ____ m (roughly 5000–8000 ft), giving an inspired oxygen tension of ____ to ____ mm Hg — about ____% of sea-level values — and an arterial PO2 of approximately ____ mm Hg.
Commercial flight exposes every passenger to the equivalent of 1500 to 2500 m (roughly 5000–8000 ft) of altitude: airline cabins are pressurized to this 'cabin altitude,' resulting in an inspired oxygen tension between 110 and 120 mm Hg — about 70% of sea-level values. The resultant arterial PO2 of approximately 60 mm Hg is adequate for healthy individuals, but passengers with underlying pulmonary disease are at risk for significant hypoxemia during flight.
Preflight screening: sea-level SpO2 below ____% → prescribe in-flight oxygen (typically ____ to ____ L/min); SpO2 ____% to ____% → perform a ____ test; patients already on long-term oxygen should ____ their flow rate during flight. The BTS 2022 statement reframes the test as a tool to prescribe in-flight oxygen, not a ____ test.
For patients with chronic lung disease, pulse oximetry at sea level guides preflight oxygen planning: SpO2 below 92% indicates a likely need for in-flight supplemental oxygen (typically 2–3 L/min); saturations of 92% to 95% warrant hypoxia altitude simulation testing; patients already receiving long-term supplemental oxygen should double their flow rate during flight. Per the BTS 2022 statement, the hypoxic challenge test is reframed as a 'preflight oxygen test' — a tool to prescribe in-flight oxygen, not a fitness-to-fly test — reserved for those with SpO2 92–95%, prior or existing hypercapnia, or use of respiratory depressants.
The overall risk of pneumothorax during air travel is ____ because airline cabins are pressurized. In-flight symptoms of pneumothorax should prompt supplemental ____, which promotes ____ of pleural air. After cardiothoracic surgery, a delay of ____ to ____ weeks before air travel is reasonable.
Because airline cabins are pressurized, the overall risk of pneumothorax during air travel is low. In patients with chronic lung disease, in-flight symptoms suggestive of pneumothorax (acute chest pain, dyspnea) should prompt supplemental oxygen, which promotes resorption of pleural air. An existing pneumothorax has traditionally been a contraindication to flight because of expansion and tension risk, but travel may be safe with a small postoperative pneumothorax that is radiographically stable. After cardiothoracic surgery, a delay of 3 to 4 weeks before air travel is reasonable.
In a recently arrived traveler, hypoxemia with patchy infiltrates that clear within days of ____ and ____ is ____, not pneumonia. Inflammation in HAPE is a(n) ____ rather than the primary cause. HAPE chest radiographs lack ____ lines and the ____ pattern.
HAPE produces patchy radiographic opacities and can be accompanied by fever, peripheral leukocytosis, and an elevated ESR, so it was historically mistaken for pneumonia or heart failure. Strong evidence indicates that inflammation in HAPE is an epiphenomenon rather than the primary cause — although respiratory tract infections do predispose to HAPE. In a recently arrived traveler, hypoxemia with patchy infiltrates that clear within days of descent and oxygen is HAPE, not pneumonia. Chest radiography may show patchy or localized opacities or streaky interstitial edema — but not Kerley B lines or a bat-wing pattern.
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