Basic overview of high altitude illnesses

1. High Altitude Illness
David Gonzales, MD

2. Medicine You Will Probably
Never Use in Texas
Guadalupe Peak,
8,749 feet
Might as well be in
New Mexico

3. Outline
Challenges of High Altitude
Physiologic Response to Hypobaric
Hypoxia
High Altitude Syndromes
Acute Mountain Sickness/ High Altitude
Cerebral Edema
High Altitude Pulmonary Edema

4. Oxygen = Good
Amount of oxygen available to breathe
is a function of the percentage of
oxygen in the air and barometric
pressure.
Earth’s atmosphere is 21% oxygen
Barometric pressure at sea level = 760 mm
Hg
Pressure of inspired oxygen =149 mm Hg

5. Less oxygen = bad
Denver = 5000 feet
PiO2 = 124 mm Hg
Santa Fe = 7000 feet
PiO2 = 115 mm Hg
Highest human habitation = 18,000 ft.
PiO2 = 73 mm Hg
Mt. Everest = 29,528 ft
PiO2 = 42 mm Hg (about ¼ that of sea level)

6. Oxygen saturation
does not decrease
until PaO2 reaches
approximately 60
torr
Corresponds to an
altitude of 10,000 ft.

7. Physiologic Response to
Hypoxia
Acclimatization
A gradual process (days to weeks)
whereby individuals respond to hypoxia in
order to adapt and increase performance
Rate varies among individuals
Mediated through sympathetic nervous
system

8. Ventilatory Response
Carotid body senses decreased PaO2;
signals medulla to increase ventilation
Respiratory alkalosis ensues, decreasing
ventilation
Subsequent HCO3 diuresis occurs through
the kidney and ventilation subsequently
increases again
This process stabilizes after 4-7 days,
provided altitude does not change

9. Cardiovascular Response
Heart rate increases, leading to a
moderate rise in cardiac output
Pulmonary artery pressure increases
secondary to hypoxic vasoconstriction
Cerebral blood flow increases
These last 2 adaptations may become
pathologic (more on this later)

10. At moderate
altitude, curve does
not shift
Extreme altitude
leads to severe
alkalosis and a
leftward shift
PCO2 may decrease
to 10 torr

11. Pathologic Syndromes
Acute Mountain Sickness (AMS)
A headache + (any of the following)
Nausea/vomiting
Fatigue
Dizziness
Sleep disturbance

15. Diagnosis
Suspect in non-acclimatized persons
above 8,200 feet
Rapid ascent

16. AMS Pathophysiology
Not so much hypoxia, rather your
body’s response to it
Lag time between onset of symptoms;
acclimatization cures

17. Pathophysiology of AMS
Low ventilatory response increases risk
Fluid retention
Evidence suggests vasogenic cerebral
edema plays a central role, however
cellular mechanisms not yet elucidated
Big brain, small skull

18. Treatment of AMS
Prevention is best treatment
Avoid abrupt ascent to sleeping altitudes >10,000
feet
Don’t increase sleeping altitude by more than 2000 ft.
per night
Climb high, sleep low philosophy
Acetazolamide (Diamox)
125 to 250 mg po bid
Carbonic anhydrase inhibitor
Diuresis
Metabolic acidosis  increased breathing
Decreases CSF production

19. Treatment of AMS
Supportive analgesics, antiemetics
Diamox to hasten acclimatization
Minimize exertion
Low flow oxygen if available
Consider dexamethasone
Failure of symptoms to improve with
treatment or progression of symptoms
despite 24 hours of acclimatization is an
indication to descend.

20. High Altitude Cerebral Edema
(HACE)
A progression of AMS to a severe, life-
threatening condition
AMS +
Ataxia
Altered consciousness
Severe lassitude
Cerebral edema is cytotoxic rather than
vasogenic

21. High Altitude Cerebral Edema
(HACE)
Cellular swelling thought to be caused
in part by NMDA-receptor mediated
calcium influx.
Trial using magnesium infusion (an NMDA
blocker) were clinically unsuccessful in
treating AMS; prophylaxis with Mg citrate
only caused diarrhea

22. Treatment of HACE
Early recognition is key
Oxygen 2-4 liters
Dexamethasone
Immediate Descent

23. Gamow Bag
An impermeable bag that can be
inflated to simulate a lower altitude
Patient placed inside but reassessed
periodically
HAPE = 2 to 4 hours of treatment
HACE = 4 to 6 hours of treatment

24. Gamow Bag

25. Portable Altitude Chamber
Zipper placement
makes it easier to
use than Gamow
Low, low price of
$1,200

26. High Altitude Pulmonary
Edema (HAPE)
Most common cause of high-altitude
related death
Easily treated/prevented with prompt
recognition
<1 in 10,000 in Colorado skiers
1 in 50 in climbers on Mt. McKinley
Risk factors include individual
susceptibility, rapid ascent, exertion,
altitude reached

27. Manifestations of HAPE
Decreased exercise performance
Dyspnea at rest; often occurs during
sleep
AMS (50%)
Dry cough
Cyanosis
RLL crackles
Pink, frothy sputum (late sign)

28. Manifestations of HAPE
Temperature >38.5
Ulcers on tongue
Sinus tachycardia
Other signs of acute
pulmonary
hypertension
RBBB
RAD
RVH voltage

29. Manifestations of HAPE
Respiratory Alkalosis
Severe hypoxemia
Fluffy infiltrates
Autopsy consistent
with noncardiogenic
pulmonary edema

30. Pathophysiology of HAPE
Pulmonary Hypertension-A fact of life at
high altitude
Global hypoxic pulmonary vasoconstrictor
response
When is it pathologic?
Increased Capillary Permeability
Shear forces vs. endothelial dysfunction
Decreased HVR
Role in nighttime hypoxia

31. Treatment of HAPE
Early recognition should lead to
evacuation/descent
This will limit severity and hasten recovery
O2 if available; Gamow bag
Vasodilators as adjuncts
Nifedipine
Salmeterol
Ounce of prevention

32. Summary
Altitude acclimatization is a highly
individualized process
Mild AMS is best treated supportively
HACE and HAPE require more
aggressive treatment
Common sense and adequate
preparation go a long way