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High-Altitude Medicine

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Title: High-Altitude Medicine


1
High-Altitude Medicine
  • Alicia Bond MD

2
High altitude
  • Moderate altitude
  • 5,000 10,000 feet above sea level
  • Highest U.S. ski resorts
  • High altitude
  • 10,000 18,000 feet above sea level
  • High peaks in the lower 48, Europe
  • Extreme altitude
  • Greater that 18,000 feet above sea level
  • Denali, Himalaya, Karakoram, Andes

3
Epidemiology
  • 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
  • 30 million Western states visitors
  • 12,000 Mt. Everest trekkers
  • 1,200 Denali climbers
  • 1 million visitors to extreme high ranges
    worldwide

4
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

5
Factors affecting risk
  • Rate of ascent
  • Recent high-altitude exposure
  • Genetic variability
  • Sleeping altitude
  • Maximum altitude reached

6
Acclimatization
  • 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

7
Hypoxic ventilatory response
  • Most important component of acclimatization
  • Affected by genetics, ethanol, sleep medications,
    caffeine, cocoa, progesterone
  • PaO2 PiO2 (PaCO2/R)
  • 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

8
Cardiovascular
  • Initial increase in resting HR, which normalizes
    with acclimatization
  • Decrease in maximal heart rate
  • Decrease in plasma volume -gt lower stroke volume,
    increase in hematocrit
  • Shift to extracellular space
  • Diuresis from bicarbonate excretion
  • Decrease in max HR and SV are cardioprotective
    myocardial ischemia is rare

9
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

10
Oxygen-hemoglobin curve
  • Above 10,000 feet (PO2 60), small changes in
    PO2 cause large changes in SaO2
  • Initial increase in 2,3-diphosphoglycerate (DPG)
    promotes O2 release to tissues
  • Opposed by respiratory alkalosis, which shifts
    curve left, favoring oxygen uptake in the lung
    and higher SaO2

11
Sleep and periodic breathing
  • Disturbed sleep with less deep sleep and
    significant arousals common
  • Periodic breathing common
  • 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

12
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

13
Prevention of high-altitude illness
  • Avoid ascent to greater than 8,000 feet in one
    day
  • Spend 2-3 nights at 8,000-9,000 feet before
    further ascent
  • Dont 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

14
Acute mountain sickness
  • 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
  • Gastrointestinal discomfort
  • Sleep disturbance
  • Generalized weakness or fatigue
  • Dizziness or lightheadedness
  • Headache is usually throbbing, bitemporal, worse
    at night and with Valsalva

15
AMS Pathophysiology
  • 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)

16
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

17
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

18
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

19
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!

20
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

21
HACE Management
  • 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

22
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

23
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

24
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

25
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

26
HAPE Management
  • Symptoms resolve quickly upon descent of
    1500-3000 feet
  • Mild cases may be treated with bedrest and O2 to
    maintain SaO2 gt 90
  • Descent for severe symptoms, minimizing exertion
  • High-flow oxygen
  • Continuous positive airway pressure if available
  • Air drops of O2 may be lifesaving if descent not
    possible
  • Hyperbarics may help conserve O2 supply

27
Hyperbarics
  • Portable, lightweight,manually-pressurizedhyperb
    aric bags
  • Raise atmospheric pressure 2 psi (103 mmHg)
  • 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

Photo Rosens Emergency Medicine, Courtesy of
Thomas Dietz, MD
28
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!

29
Key References
  • Marx, JA, ed. Rosens Emergency Medicine, 7th Ed.
    Philadelphia Mosby Elsevier, 2010
  • Auerbach, PS, ed. Wilderness Medicine, 6th Ed.
    Philadelphia Mosby Elsevier, 2012
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