High Altitude Illness

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High Altitude Illness

• David Gonzales, MD

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Medicine You Will Probably Never Use in Texas

• Guadalupe Peak, 8,749 feet
• Might as well be in New Mexico

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Outline

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

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Oxygen Good

• Amount of oxygen available to breathe is a
  function of the percentage of oxygen in the air
  and barometric pressure.
• Earths atmosphere is 21 oxygen
• Barometric pressure at sea level 760 mm Hg
• Pressure of inspired oxygen 149 mm Hg

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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)

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

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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

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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

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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)

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

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Pathologic Syndromes

• Acute Mountain Sickness (AMS)
• A headache (any of the following)
• Nausea/vomiting
• Fatigue
• Dizziness
• Sleep disturbance

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Diagnosis

• Suspect in non-acclimatized persons above 8,200
  feet
• Rapid ascent

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AMS Pathophysiology

• Not so much hypoxia, rather your bodys response
  to it
• Lag time between onset of symptoms
  acclimatization cures

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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

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Treatment of AMS

• Prevention is best treatment
• Avoid abrupt ascent to sleeping altitudes gt10,000
  feet
• Dont 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

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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.

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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

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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

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Treatment of HACE

• Early recognition is key
• Oxygen 2-4 liters
• Dexamethasone
• Immediate Descent

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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

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Gamow Bag
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Portable Altitude Chamber

• Zipper placement makes it easier to use than
  Gamow
• Low, low price of 1,200

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High Altitude Pulmonary Edema (HAPE)

• Most common cause of high-altitude related death
• Easily treated/prevented with prompt recognition
• lt1 in 10,000 in Colorado skiers
• 1 in 50 in climbers on Mt. McKinley
• Risk factors include individual susceptibility,
  rapid ascent, exertion, altitude reached

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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)

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Manifestations of HAPE

• Temperature gt38.5
• Ulcers on tongue
• Sinus tachycardia
• Other signs of acute pulmonary hypertension
• RBBB
• RAD
• RVH voltage

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Manifestations of HAPE

• Respiratory Alkalosis
• Severe hypoxemia
• Fluffy infiltrates
• Autopsy consistent with noncardiogenic pulmonary
  edema

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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

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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

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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