In one breath
When adaptation fails, altitude makes people ill in four overlapping ways: acute mountain sickness within 4–8 hours of arrival; chronic mountain sickness (Monge’s disease) after long residence; high altitude pulmonary hypertension with edema; and high altitude cerebral edema. Hypoxic pulmonary vasoconstriction and thickened pulmonary arteries drive the chest picture, and leaky cerebral capillaries drive the brain picture. Treatment begins with descent, and adds acetazolamide, glucocorticoids, hyperbaric O₂ and nifedipine for what descent does not settle.
Builds on: Acclimatization to high altitude · Pulmonary circulation · Leads to: Pulmonary edema and drowning · Hypoxia
Types of illness
High altitude illness covers four conditions:
| Illness | When |
|---|---|
| Acute mountain sickness | Hours after sudden ascent |
| Chronic mountain sickness (Monge’s disease) | Long-term residence |
| High altitude pulmonary hypertension and edema | Prolonged hypoxia; also in severe acute hypoxia |
| High altitude cerebral edema | Severe hypoxia |
Acute mountain sickness
Sudden exposure to high altitude produces a cluster of signs and symptoms called acute mountain sickness (AMS).
- Timing: they begin 4 to 8 hours after you get there, and can run on for several days.
- Usual symptoms: fatigue, dyspnea, nausea, vomiting, diarrhea, headache, insomnia, palpitations.
- Not uncommon: loss of coordination, memory and judgment.
- Also seen: euphoria and other emotional changes.
- In severe hypoxia, or in susceptible people, pulmonary and cerebral edema develop.
Don't stop at fatigue and headache
Examiners want the neurological and emotional features too: loss of coordination, memory and judgment, euphoria, emotional change — and the fact that severe hypoxia or a susceptible person can go on to pulmonary and cerebral edema. Worth knowing, though not in your pages: ataxia and altered judgment are treated clinically as warning signs of cerebral edema, because the climber loses the ability to decide to descend.
Chronic mountain sickness (Monge’s disease)
Years of residence bring this one on, not arrival. Its features are gathered under the single name chronic mountain sickness:
- malaise and fatigue
- hypervolemia
- exercise intolerance
- polycythemia
- pulmonary hypertension
- right ventricular hypertrophy
- heart failure
Hyper-, not hypo-
Monge’s disease carries hypervolemia with polycythemia — blood volume and red cell mass are both up, and it is the resulting viscosity and pulmonary hypertension that fail the right heart. A “which is NOT a feature” question usually plants hypovolemia or anemia.
Pulmonary hypertension and edema
The chain runs:
- Prolonged hypoxia at altitude.
- Alveolar hypoxia → pulmonary vasoconstriction (the hypoxic pulmonary vasoconstriction of Pulmonary circulation).
- In chronic hypoxia the smooth muscle of the pulmonary arteries hypertrophies and undergoes hyperplasia, so the lumen narrows — a fixed, structural rise in resistance.
- In severe hypoxia the pulmonary veins constrict as well.
- Alveolar capillary pressure rises → pulmonary edema.
- The raised pulmonary pressure also loads the right heart → right ventricular hypertrophy; when it is severe, the right side of the heart fails.
Draw it: high altitude pulmonary hypertension
Draw a flow chart down the page in single boxes: low PIO₂ → alveolar hypoxia → pulmonary vasoconstriction. From that box branch two arrows. Left arrow: medial smooth muscle hypertrophy and hyperplasia → narrowed lumen → sustained pulmonary hypertension → right ventricular hypertrophy → right heart failure. Right arrow: venous constriction in severe hypoxia → raised alveolar capillary pressure → pulmonary edema. Mark the vasoconstriction box “reversible on descent” and the hypertrophy box “structural”.
Cerebral edema
- Increased capillary permeability lets fluid into the brain, producing cerebral edema.
- It may be accompanied by disorientation and ataxia.
- In severe cases, coma follows herniation of the brain through the tentorium.
Two different leaks
The lung edema is a pressure problem — hypoxic vasoconstriction raising alveolar capillary pressure. The brain edema is a permeability problem. Say which mechanism you mean; examiners ask for both separately.
Treatment of high altitude illness
First and most important: bring the person down to low altitude as early as possible. The condition improves immediately with descent. Add drug treatment only if features persist, especially continuing cerebral or pulmonary edema.
| Treatment | Physiological basis |
|---|---|
| Diuretics — acetazolamide preferred | Carbonic anhydrase inhibited → more HCO₃⁻ excreted, alkali load falls, less CSF formed |
| Steroids (glucocorticoid) | Reduces cerebral edema |
| Oxygen therapy — hyperbaric O₂ | Very useful when pulmonary edema is present |
| Nifedipine (calcium channel blocker) | Lowers pulmonary arterial pressure |
| Other drugs | To improve the general condition |
Applied: why acetazolamide and not any diuretic
Acetazolamide is chosen for what it does to acid–base balance, not just for the water it removes. By dumping bicarbonate it undoes the alkalosis that blunts the hypoxic ventilatory drive (see Acclimatization to high altitude), so ventilation can rise; and by cutting CSF formation it works directly against the raised pressure inside the skull. Both of those are the reason the book names this diuretic and not another.
Worth knowing, though not in your pages: acetazolamide is also given before ascent, as prophylaxis, because it pre-empts the same alkalosis; and dexamethasone is the glucocorticoid usually named for high altitude cerebral edema.
Exam-answer skeleton: "Mountain sickness: types, features and physiological basis of treatment" (short note)
- Define high altitude illness and name its four forms.
- Acute mountain sickness: sudden ascent, symptoms within 4–8 hours, lasting days; list the symptoms, including loss of coordination, memory and judgment.
- Chronic mountain sickness (Monge’s disease): long residence; malaise, fatigue, hypervolemia, exercise intolerance, polycythemia, pulmonary hypertension, right ventricular hypertrophy, heart failure.
- Mechanism of pulmonary hypertension and edema: alveolar hypoxia → vasoconstriction → medial hypertrophy and hyperplasia → narrowed lumen; venoconstriction in severe hypoxia → raised capillary pressure → edema; right ventricular hypertrophy and failure.
- Mechanism of cerebral edema: increased capillary permeability; disorientation, ataxia; coma from tentorial herniation.
- Treatment: immediate descent first.
- Then acetazolamide (carbonic anhydrase inhibition, bicarbonate loss, less CSF), glucocorticoid for cerebral edema, hyperbaric O₂ for pulmonary edema, nifedipine to lower pulmonary arterial pressure.
Asked in exams
- Mountain sickness: May 2022, 5 marks