This document discusses various medical problems that can occur at high altitudes. It begins by outlining different altitude ranges and their associated effects on the human body. It then covers the pathophysiology of altitude illness, including how the body acclimatizes to low oxygen levels over time. Various high altitude syndromes are defined such as acute mountain sickness (AMS), high altitude cerebral edema (HACE), and high altitude pulmonary edema (HAPE). Treatment strategies focus on descent, supplemental oxygen, medications, and prevention through gradual ascent.
6. ventilation
• PaO2 carotid body& respiratory center
ventilation PaCO2
Chronic hypoxia
Sedative agent
Performance During sleep
7. ventilatory acclimatization
ventilation
pH return to
pH (respi alkalosis)
normal
HCO3
excrete via Acetazolamide
kidney
8.
9. • EPO w/in 2 hr
• Rbc mass w/in
days to wks
• if excessive
chronic
polycythemia
10. Fluid Balance
• Reset Osm stat: plasma volume and
hyperosmolality (s osm290 - 300)
• diuresis and hemoconcentration :healthy
response
• Antidiuresis is a hallmark of AMS
Peripheral venous in central ADH diuresis
constriction blood volume &aldosterone
11. Cardiovascular System
CO = SV HR
Pulm.vasoconstriction pulm.pressure
Cerebral blood volume O2 to brain ICP
12. Exercise capacity
• measured by VO2max, drops dramatically on
ascent to altitude
• During acclimatization, submaximal
endurance after 10 days
13. Sleep at High Altitude
• Sleep stages III and IV ↓ stage I frequent
arousals (improve with time at altitude)
• Cheyne-Stokes respiration in those sleeping at
>2700 m (>8860 ft)
• the frequent awakenings & periodic breathing
not related to AMS
• mechanism of the lighter sleep →cerebral
hypoxia.
• Quality of sleep and arterial oxygenation during
sleep improve with acclimatization and with
acetazolamide
16. Acute hypoxia
• occurs in the setting of sudden and severe
• Unacclimatized persons become unconscious
at SaO2 50 - 60%, PaO2 < 30 mm Hg, or a
jugular venous PO2 of <15 mm Hg
• immediate administration of oxygen, rapid
descent
17. Acute Mountain Sickness
• setting of more gradual and less severe
hypoxic
• characterized by headache, GI disturbances,
dizziness or light-headedness, and sleep
disturbance
18.
19. What’re factors determine individual
susceptibility to AMS ?
• Age
• Sex
• Body weight
• physical fitness
21. Clinical feature
• mild : alcohol hangover
• Headaches : bifrontal and worsen with
bending over or performing a Valsalva
maneuver
• GI symptoms : anorexia, N/V
• irritable & wants to be left alone
• Sleepiness
• deep inner chill also are common
22. Clinical feature
• rapid ascent of an unacclimatized person to
≥2000 m
• Symptoms develop between 1 -6 hours later,
but sometimes are delayed for 1 - 2 days
Severe Ataxia
vomiting oliguria HACE
headache and AOC
23. Physical examination
• percent SaO2 overall correlates poorly with
the diagnosis of AMS
• postural hypotension may be present
• Localized rales ≥ 20%
• Funduscopy :tortuosity and dilatation, and
retinal hemorrhages (at altitudes >5000 m)
• facial and peripheral edema is a hallmark
24. The goals of treatment are to
prevent progression
abort the illness
improve acclimatization
25. 3 principles of Rx
(1) do not proceed to a higher sleeping altitude
in the presence of symptoms
(2) descend if symptoms do not abate or
become worse despite treatment
(3) descend and treat immediately in the
presence of a change in
consciousness, ataxia, or pulmonary edema
26. Treatment
• Oxygen effectively relieves symptoms, but it is
generally unavailable in the field or reserved
for those with moderate to severe AMS
27. Medication
Indications for acetazolamide
(1) a history of altitude illness
(2) abrupt ascent to >3000 m (>9840 ft)
(3) AMS requiring treatment
(4) bothersome periodic breathing during sleep
28. Symptomatic treatment of AMS
• Headache :aspirin, acetaminophen or
ibuprofen
• N/V: ondansetron
• f/q wakening: zolpidem,diphenhydramine
29. Prevention
• Graded ascent with adequate time for
acclimatization is the best prevention
• Prophylactic acetazolamide
– started 24 hr before the ascent
– continued for the first 2 days at altitude
– restarted if illness develops
30. HACE
• HACE : progressive neurologic deterioration in
someone with AMS or HAPE
• altered mental status, ataxia, stupor, and
progression to coma if untreated
• severe, diffuse cerebral edema with multiple
small hemorrhages and sometimes
thrombosis
31. Treatment of HACE
• oxygen supplementation
• descent(the highest priority)
• steroid therapy
• acetazolamide may be used as an adjunct
33. HAPE
• most lethal of the altitude illnesses
• easily reversible with descent and oxygen
administration
• Risk factors:heavy exertion, rapid ascent, cold,
excessive salt ingestion, use of a sleeping
medication
34. Pathophysiology
• HAPE is a noncardiogenic, hydrostatic edema
• The culprit in HAPE is high microvascular
pressure Pulmonary hypertension
35. Clinical
• Early diagnosis is critical, exercise
performance & dry cough are enough to raise
the suspicion of early HAPE
• The condition typically worsens at night
• Low-grade fever is common, and tachycardia
and tachypnea
• SO2 low for altitude
37. Treatment
• The key to successful Rx : early recognition,
early stage is easily reversible
• Immediate descent is the Rx of choice, but this
is not always possible
• The optimal therapy depends on
– the environmental setting,
– evacuation options
– availability of oxygen or hyperbaric units
– ease of descent
39. medication
• Because oxygen and descent are so effective,
experience with drugs has been limited
• nifedipine, phosphodiesterase 5
inhibitors:sildenafil and tadalafil
40.
41.
42. Other high altitude medical problem
• Peripheral edema
• High-altitude retinopathy
• High-altitude pharyngitis and bronchitis
• UV keratoconjunctivitis
43. Special population
• Patients who have hypoxic cardiovascular and
pulmonary diseases such as COPD or CHF ,
CAD, pregnant