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High Altitude Illness

High Altitude Illness. David Gonzales, MD. Medicine You Will Probably Never Use in Texas. Guadalupe Peak, 8,749 feet Might as well be in New Mexico. Outline. Challenges of High Altitude Physiologic Response to Hypobaric Hypoxia High Altitude Syndromes

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High Altitude Illness

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  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

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

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

  14. 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

  15. 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

  16. 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.

  17. 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

  18. 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

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

  20. 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

  21. Gamow Bag

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

  23. 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

  24. 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)

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

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

  27. 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

  28. 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

  29. 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

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