High Altitude Medicine
Definition
Pathophysiology
High altitude: >1500m (4900ft)
Mod high altitude: 2000 – 3500m (6600-11500ft)
Very high altitude: 3500-5500m (11500-18000ft)
Extreme altitude: >5500m
Sea level: ppO2 760, piO2 150
1000m: ppO2 670, piO2 140
2000m: ppO2 600, piO2 120
5500m: ppO2 380, piO2 70
8848m (Mt Everest): ppO2 240, piO2 40
Acute mountain sickness (AMS): occurs at >2500m; usually self limited
High altitude cerebral oedema (HACE(: a continuum of AMS; progression of neurological symptoms in
setting of AMS; can be fatal
High altitude pulmonary oedema (HAPE): a continuum of AMS; can be fatal (cause of most deaths); begins
>3500m
Chronic mountain sickness (CMS): after prolonged exposure; headaches, insomnia, lethargy, Hct >60%, Hb
>20
Others: snow blindness, retinal haemorrhage, thromboembolism, retinopathy, immunosuppression,
hypothermia, epistaxis
Acclimitisation: physiological adaptation to hypoxia which improves systemic O2 delivery;  risk
AMS/HACE; most people can acclimitise up to 5500m, but differing capability between individuals
Respiratory (primary response): periodic breathing >3000m (max at 1/52), tachypnoea  respiratory
alkalosis  HCO3 diuresis  continued  RR (acetazolamide helps with this);  lung volume, 
pulmonary capillary blood volume (  diffusing capacity); pulmonary HTN; Typical ABG at 8848m = pO2
28, pCO2 7
CV:  max HR,  pulmonary artery pressure, SV,  BP,  central blood volume due to peripheral
vasoconstriction ( diuresis   plasma volume, hyperosmolality, haemoconcentration);  CO
Haematological: RBC (over days – wks; has no effect on initial climitisation),  erythropoietin (within
2hrs)
Other: vascularity of tissues,  tissues ability to use O2,  cerebral blood flow,  2,3,DPG  shift curve
to R (but respiratory alkalosis shifts curve to L)
High altitude illness: Hypoxia occurs with rapid ascent;  exercise tolerance 9% for each 1000m; relative
hypoventilation, impaired gas exchange, fluid retention and redistribution,  sympathetic drive
AMS: cytotoxic and vasogenic cerebral oedema, neurotransmitter dysfunction  cerebral oedema and 
ICP
HACE
HAPE: due to exaggerated pressor response to altitude and hypoxia  non-cardiogenic pulmonary oedema
(hydrostatic; possible due to impaired Na-driven clearance of alveolar fluid), high pulmonary artery
pressure
Epidemiology
High altitude illness: occurs in 25% sea level dwellers to ascent rapidly to >2400m
AMS: 30% incidence at >3500m; 50-60% incidence at >4000m
HACE: occurs in 1-2% AMS at >4500m; fatal in 1-2/7 if not treated
HAPE: preceded by AMS in 50%, by HACE in 14%; 15% at 4000m, 0.1% at 2500-3000m
Risk Factors
AMS: PMH same, individual susceptibility, obesity, CV/RS disease. NOT related to age / physical fitness
rate of ascent (especially >300m/day), altitude, time at altitude, degree of physical exertion, previous
recent exposure, sleeping altitude
HAPE: as above; also cold temp, pre-existing respiratory infection
Assessment
AMS: onset within 24 hours of arrival at altitude (usually 1-6 hours); headache, fatigue out of proportion,
insomnia, anorexia, N+V, SOB, oliguira; no physical findings (except maybe evidence of fluid retention)
HACE: progresses over 1-3/7; consider if >3000m and altered LOC, impaired mental capacity ( visual
acuity / attention span / short term memory / decision making), marked truncal ataxia, 3rd + 6th nerve
palsy; can progress to coma within 24 hours of onset of ataxia
HAPE: consider alternate diagnosis; onset 2-4/7 after arrival at altitude; non-productive cough ( pink,
frothy sputum), SOB; tachycardia, tachypnoea, cyanosis, crepitations (RML 1st, exercise induced), patchy
opacities on CXR (often more in RML); ECG (RVH, RAD, RBBB); severe hypoxia  HACE, coma, death
Do not go higher in presence of symptoms; avoid ETOH and sedatives; carbohydrates may help arterial
oxygenation ( resp quotient, alveolar pO2;  risk of AMS by 30%); rest
Mild/mod AMS: halt ascent; rest; O2 and consider drugs as below; hydration, analgesia; usually settles over
2-3/7 as acclimitisation occurs; or consider descent by up to 300m/day with rest day every 2-3/7
Management
Prevention
Prognosis
Severe / HACE / HAPE:
O2: (1-2L/min until symptoms resolve; aim SaO2 >90%; in HAPE, if SOB improves with this, can observe at
altitude until recovery)
Descent (immediately if change in LOC / ataxia / pulmonary oedema; otherwise descend if O2 not helping;
by >300m in AMS, by >500-1000m / evacuate in HAPE, ASAP >1000m / until improvement / evacuate in
HACE)
Hyperbaric Oxygen: if unable to descend / temporising measure; Gamow bag simulates 600m descent,
requires scavenger etc…
Dexamethasone: in AMS / HACE; 8mg STAT  4mg Q6h PO/IM/IV ASAP; onset 4hrs, max effect 12-24hrs;
?duration of treatment; as effective as acetazolamide
Acetazolamide: consider if not already used as prophylaxis in AMS / HACE; 250mg BD PO;  symptoms
within 24hrs in 75%; stop once symptoms resolve (or continue if plan to re-ascend); contra-indicated in
sulphur drug allergy; use as prophylaxis for HAPE, but not treat; cause HCO3 diuresis so allow more
hyperventilation
Nifedipine: in HAPE; 10mg SL STAT  20-30mg SR BD/TDS; drug of choice if O2 / descent not available; 
pulmonary artery pressure; used as prophylaxis and treatment of HAPE
Symptomatic treatment: analgesia, antiemetics, beta-agonists; CPAP in HAPE
Diuretics (eg. Frusemide, mannitol): only if generalised oedema present; avoid loop diuretics in HAPE as
most are dehydrated
Avoid flying directly to high altitude; limit activity for 24 hours after arrival; graded, slow ascent; when
>3000m, ascent <300m/day; rest day every 1000m / every 2-3/7; avoid ETOH; eat carbohydrates; avoid
over-exertion; avoid night sedation
Acetazolamide: drug of choice; CA inhibitor (causes HCO3 diuresis and metabolic acidosis,  CSF formation,
 ventilatory drive, maintains O2 during sleep; 125-250mg BD, commence at least 1/7 prior to ascent,
continue until descent begun
Dexamethasone: not as effective as acetazolamide; 4mg PO BD, but more side effects; use if acetazolamide
contra-indicated or if rapid effect needed (eg. Rescue workers)
Nifedipine: for prevention HAPE; 20mg SR BD/TDS
Salmeterol: for prevention HAPE
AMS: Most respond rapidly to treatment, with complete recovery
HACE: recovery may be prolonged
HAPE: most recover in 2-3/7