High-Altitude Medicine by A. Bond

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High-Altitude Medicine
Alicia Bond MD
High altitude
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Moderate altitude
5,000 – 10,000 feet above sea level
 Highest U.S. ski resorts
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High altitude
10,000 – 18,000 feet above sea level
 High peaks in the lower 48, Europe
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Extreme altitude
Greater that 18,000 feet above sea level
 Denali, Himalaya, Karakoram, Andes
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Epidemiology
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Most cases of high-altitude illness take place in
people rapidly ascending to altitudes between
8,000 and 12,000 feet
Can affect people who live at low altitude as well
as people who live at high altitude and return
from travel to lower altitude (re-entry)
Millions at risk each year – roughly 20-40%
affected by some type of altitude illness
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30 million Western states visitors
12,000 Mt. Everest trekkers
1,200 Denali climbers
1 million visitors to extreme high ranges worldwide
High-altitude environments
Decreased barometric pressure =
logarithmically lower partial pressure of
oxygen (PO2) in inspired air
 Higher latitudes have lower barometric
pressure at equivalent altitudes
 Weather systems can significantly lower
barometric pressure transiently
 Cold, dry conditions may be contribute to
high-altitude illness
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Factors affecting risk
Rate of ascent
 Recent high-altitude exposure
 Genetic variability
 Sleeping altitude
 Maximum altitude reached
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Acclimatization
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Series of physiologic adaptations to maintain
tissue oxygenation
Ability to acclimatize varies genetically
Hours: Hypoxic ventilatory response (HVR), fluid
shift to increase hematocrit, increase in cardiac
output
Days: Increased erythropoiesis, return of cardiac
function to baseline, increase in 2,3-DPG
Weeks: Increased plasma volume and red blood
cell mass
Hypoxic ventilatory response
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Most important component of acclimatization
Affected by genetics, ethanol, sleep
medications, caffeine, cocoa, progesterone
PaO2 = PiO2 (PaCO2/R)
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Hyperventilation decreases the partial pressure of CO2 in the alveoli,
thereby increasing the partial pressure of oxygen in the alveoli to
facilitate oxygenation
Resulting metabolic alkalosis slows HVR, and
ventilation slowly increases over several days as
kidneys excrete bicarb
Can be facilitated by acetazolamide
People with low HVR at higher risk for illness
Cardiovascular
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Initial increase in resting HR, which normalizes
with acclimatization
Decrease in maximal heart rate
Decrease in plasma volume -> lower stroke
volume, increase in hematocrit
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Shift to extracellular space
Diuresis from bicarbonate excretion
Decrease in max HR and SV are
cardioprotective – myocardial ischemia is rare
Hematopoietic response
Initial increase in hematocrit due to fluid
shift and diuresis
 Erythropoietin stimulated early, resulting in
new RBCs within 4-5 days
 Over weeks to months, red cell and total
circulating volume expand to meet
demand
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Oxygen-hemoglobin curve
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Above 10,000 feet
(PO2 ~ 60), small
changes in PO2 cause
large changes in SaO2
Initial increase in 2,3diphosphoglycerate
(DPG) promotes O2
release to tissues
Opposed by respiratory
alkalosis, which shifts
curve left, favoring
oxygen uptake in the
lung and higher SaO2
Sleep and periodic breathing
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Disturbed sleep with less deep sleep and
significant arousals common
Periodic breathing common
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Hyperpnea and respiratory alkalosis cause apnea
CO2 builds during apnea, causing hyperpnea
Not usually associated with significant hypoxemia or
high-altitude illness
Decreases with acclimatization
People with low HVR may have overall regular
breathing pattern with periods of more significant
apnea and hypoxemia, which are associated
with high-altitude illness
Acute high-altitude illness
Spectrum of disease with intertwining
pathophysiology
 Acute mountain sickness (AMS)
 High altitude cerebral edema (HACE)
 High altitude pulmonary edema (HAPE)
 All correct rapidly with descent
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Prevention of high-altitude illness
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Avoid ascent to greater than 8,000 feet in one
day
Spend 2-3 nights at 8,000-9,000 feet before
further ascent
Don’t ascend sleeping altitude more than 1500
feet per day
Limit exertion, alcohol, and sedative-hypnotics
during first days at altitude
Day trips to higher altitude while maintaining
sleeping altitude can speed acclimatization
Acetazolamide 125-250 mg BID
Acute mountain sickness
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Most common with rapid ascent from below
3,000 feet to above 8,000 feet
Develops within hours of ascent
Headache plus at least one of:
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Gastrointestinal discomfort
Sleep disturbance
Generalized weakness or fatigue
Dizziness or lightheadedness
Headache is usually throbbing, bitemporal,
worse at night and with Valsalva
AMS: Pathophysiology
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Pathophysiology incompletely understood
Vasodilatory response to hypoxemia, fluid shift,
inflammatory mediators, and alterations in
cerebrospinal fluid buffering capacity are all
implicated
No evidence of cerebral edema in AMS, but
some studies suggest transient ICP elevations
with exertion and Valsalva
At risk may be people with low HVR and people
with smaller CSF capacity (“tight fit”)
Hyperbaria contributes, but role unclear (AMS
does not develop with hypoxia alone)
AMS: Management
Usually resolves within 1-3 days if no
additional ascent
 Mild: Stop ascent, symptomatic treatment,
may consider acetazolamide
 Moderate to severe: Low-flow oxygen,
acetazolamide +/- dexamethasone 4 mg q
6 hours, hyperbarics, or descend
 Immediate descent if s/sx HAPE or HACE
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Acetazolamide
Carbonic anhydrase inhibitor
 Promotes bicarbonate diuresis and
metabolic acidosis, speeding
acclimatization
 Decreases CSF production
 Maintains oxygenation during sleep
 Side effects: polyuria and paresthesias
 125-250 mg BID for treatment and
prevention of AMS
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High-altitude cerebral edema
Least common but most severe form of
high-altitude illness
 Incidence 1-2% of ascents
 Usually develops above 12,000 feet
 Usually preceded by AMS and associated
with HAPE
 Most commonly develops days 1-3 after
ascent, but can develop later
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HACE: Presentation
Ataxia and altered mentation are
hallmarks – ataxia usually first symptom
 Focal neuro deficits may be present
 Seizures uncommon but reported
 Usually preceded by AMS symptoms
 Any ataxia or change in consciousness in
a person at altitude should elicit immediate
action!
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HACE: Pathophysiology
Vasogenic cerebral edema caused by
same group of mechanisms as AMS
(vasodilation, leakage of fluid from
vessels) – reversible
 Increased ICP causes decreased cerebral
blood flow, resulting in cell death
 At advanced stages, cytotoxic edema and
necrosis are present - not reversible
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HACE: Management
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Immediate descent is key
High-flow oxygen and dexamethasone 8 mg (IV,
IM, PO) followed by 4 mg q 6 hours if available
Hyperbarics may result in temporary
improvement but may delay descent
Intubation, hyperventilation if severely altered
Can try mannitol or furosemide but caution due
to dehydration common at altitude
HACE: Prognosis
If descent initiated early, may be
completely reversible over days to weeks
without sequelae
 Reports of ataxia and other neuro deficits
persisting months to years
 Mortality rate greater than 60% if
progresses to coma
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High-altitude pulmonary edema
Most common cause of altitude-related
death
 Incidence up to 15% of ascents
 Usually greater than 10,000 feet, or
greater than 8,000 feet with heavy exertion
 Develops within 2-4 days of ascent,
classically on the second night
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HAPE: Presentation
Early signs are severe dyspnea on
exertion, fatigue with minimal activity, and
dry cough
 Dyspnea at rest and clear, watery sputum
develop as illness progresses
 Dyspnea at rest is red flag for HAPE and
should prompt immediate action!
 Patchy infiltrates on CXR, worst right
middle lobe
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HAPE: Pathophysiology
Hypoxic vasoconstriction causes
pulmonary hypertension
 Uneven vasoconstriction (areas of
extreme hypoxia or anatomic difference)
causes hyperperfusion of some areas,
leading to vascular leak and patchy edema
 Both hypoxia and pulmonary hypertension
are exacerbated by exertion
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HAPE: Management
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Symptoms resolve quickly upon descent of
1500-3000 feet
Mild cases may be treated with bedrest and O2
to maintain SaO2 > 90
Descent for severe symptoms, minimizing
exertion
High-flow oxygen
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Continuous positive airway pressure if available
Air drops of O2 may be lifesaving if descent not
possible
Hyperbarics may help conserve O2 supply
Hyperbarics
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Portable, lightweight,
manually-pressurized
hyperbaric bags
Raise atmospheric
pressure 2 psi (103 mmHg)
Photo: Rosen’s Emergency Medicine,
Courtesy of Thomas Dietz, MD
Simulates descent of
4,000-5,000 feet at moderate
altitudes, more at higher altitudes
Can be lifesaving in HAPE and HACE, relieving
symptoms so that patients can descend without
evacuation
Take-home
Slow ascent and acetazolamide are
effective in preventing illness
 Ataxia, altered mentation, and dyspnea at
rest are red flags for serious illness
 Early recognition of HAPE and HACE with
descent prevents morbidity and mortality
 Have fun up there!
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Key References
Marx, JA, ed. Rosen’s Emergency
Medicine, 7th Ed. Philadelphia: Mosby
Elsevier, 2010
 Auerbach, PS, ed. Wilderness Medicine,
6th Ed. Philadelphia: Mosby Elsevier, 2012
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