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High altitude medical problem
2,031m




    2,102 m




  2,195 m




2,285 m
Altitude          Height                   Effect
Intermediate    1520 - 2440 m      exercise performance
altitude        (5000 - 8000 ft)
                                   alveolar ventilation
                                   ↔arterial oxygen transport



High altitude   >2440 m (>8000
                ft)
                                   AMS

Very high       4270 - 5490 m
                (14,000 - 18,000
                                   AMS
altitude
                ft)
PATHOPHYSIOLOGY
ventilation

• PaO2   carotid body& respiratory center

               ventilation     PaCO2
                               Chronic hypoxia
                               Sedative agent
               Performance     During sleep
ventilatory acclimatization

                 ventilation




  pH return to
                                pH (respi alkalosis)
    normal




                   HCO3
                 excrete via                    Acetazolamide
                   kidney
• EPO w/in 2 hr
• Rbc mass w/in
  days to wks
• if excessive 
  chronic
  polycythemia
Fluid Balance
• Reset Osm stat:  plasma volume and
  hyperosmolality (s osm290 - 300)
• diuresis and hemoconcentration :healthy
  response
• Antidiuresis is a hallmark of AMS


   Peripheral venous    in central      ADH        diuresis
      constriction     blood volume   &aldosterone
Cardiovascular System
  CO =   SV      HR

Pulm.vasoconstriction    pulm.pressure



Cerebral blood volume   O2 to brain   ICP
Exercise capacity
• measured by VO2max, drops dramatically on
  ascent to altitude
• During acclimatization, submaximal
  endurance after 10 days
Sleep at High Altitude
• Sleep stages III and IV ↓ stage I   frequent
  arousals (improve with time at altitude)
• Cheyne-Stokes respiration in those sleeping at
  >2700 m (>8860 ft)
• the frequent awakenings & periodic breathing
  not related to AMS
• mechanism of the lighter sleep →cerebral
  hypoxia.
• Quality of sleep and arterial oxygenation during
  sleep improve with acclimatization and with
  acetazolamide
HIGH-ALTITUDE SYNDROMES
High altitude syndrome
•   Acute hypoxia
•   Acute mountain sickness
•   High-Altitude cerebral edema
•   High-Altitude pulmonary edema
•   Peripheral edema
•   High-altitude retinopathy
•   High-altitude pharyngitis and bronchitis
•   Chronic mountain polycythemia
•   UV keratoconjunctivitis
Acute hypoxia

• occurs in the setting of sudden and severe
• Unacclimatized persons become unconscious
  at SaO2 50 - 60%, PaO2 < 30 mm Hg, or a
  jugular venous PO2 of <15 mm Hg
• immediate administration of oxygen, rapid
  descent
Acute Mountain Sickness
• setting of more gradual and less severe
  hypoxic
• characterized by headache, GI disturbances,
  dizziness or light-headedness, and sleep
  disturbance
What’re factors determine individual
          susceptibility to AMS ?
•   Age
•   Sex
•   Body weight
•   physical fitness
Pathophysiology
• renin-angiotensin aldosterone ADH

 The cerebral edema, interstitial pulmonary
 edema, peripheral edema, and antidiuresis
Clinical feature
• mild : alcohol hangover
• Headaches : bifrontal and worsen with
  bending over or performing a Valsalva
  maneuver
• GI symptoms : anorexia, N/V
• irritable & wants to be left alone
• Sleepiness
• deep inner chill also are common
Clinical feature
• rapid ascent of an unacclimatized person to
  ≥2000 m
• Symptoms develop between 1 -6 hours later,
  but sometimes are delayed for 1 - 2 days

   Severe                           Ataxia
             vomiting   oliguria             HACE
  headache                         and AOC
Physical examination
• percent SaO2 overall correlates poorly with
  the diagnosis of AMS
• postural hypotension may be present
• Localized rales ≥ 20%
• Funduscopy :tortuosity and dilatation, and
  retinal hemorrhages (at altitudes >5000 m)
• facial and peripheral edema is a hallmark
The goals of treatment are to

      prevent progression


      abort the illness


      improve acclimatization
3 principles of Rx
(1) do not proceed to a higher sleeping altitude
  in the presence of symptoms
(2) descend if symptoms do not abate or
  become worse despite treatment
(3) descend and treat immediately in the
  presence of a change in
  consciousness, ataxia, or pulmonary edema
Treatment
• Oxygen effectively relieves symptoms, but it is
  generally unavailable in the field or reserved
  for those with moderate to severe AMS
Medication

Indications for acetazolamide
(1) a history of altitude illness
(2) abrupt ascent to >3000 m (>9840 ft)
(3) AMS requiring treatment
(4) bothersome periodic breathing during sleep
Symptomatic treatment of AMS

• Headache :aspirin, acetaminophen or
  ibuprofen
• N/V: ondansetron
• f/q wakening: zolpidem,diphenhydramine
Prevention
• Graded ascent with adequate time for
  acclimatization is the best prevention
• Prophylactic acetazolamide
  – started 24 hr before the ascent
  – continued for the first 2 days at altitude
  – restarted if illness develops
HACE
• HACE : progressive neurologic deterioration in
  someone with AMS or HAPE
• altered mental status, ataxia, stupor, and
  progression to coma if untreated
• severe, diffuse cerebral edema with multiple
  small hemorrhages and sometimes
  thrombosis
Treatment of HACE
•   oxygen supplementation
•   descent(the highest priority)
•   steroid therapy
•   acetazolamide may be used as an adjunct
MRI findings
reversible white matter edema evidenced byT2 signal, esp.in the splenium
   of the corpus callosum
HAPE
• most lethal of the altitude illnesses
• easily reversible with descent and oxygen
  administration
• Risk factors:heavy exertion, rapid ascent, cold,
  excessive salt ingestion, use of a sleeping
  medication
Pathophysiology

• HAPE is a noncardiogenic, hydrostatic edema
• The culprit in HAPE is high microvascular
  pressure  Pulmonary hypertension
Clinical
• Early diagnosis is critical, exercise
  performance & dry cough are enough to raise
  the suspicion of early HAPE
• The condition typically worsens at night
• Low-grade fever is common, and tachycardia
  and tachypnea
• SO2 low for altitude
Chest radiographic




progress from interstitial  localized alveolar  generalized alveolar infiltrates
Treatment
• The key to successful Rx : early recognition,
  early stage is easily reversible
• Immediate descent is the Rx of choice, but this
  is not always possible
• The optimal therapy depends on
  – the environmental setting,
  – evacuation options
  – availability of oxygen or hyperbaric units
  – ease of descent
Portable hyperbaric bag
medication
• Because oxygen and descent are so effective,
  experience with drugs has been limited
• nifedipine, phosphodiesterase 5
  inhibitors:sildenafil and tadalafil
Other high altitude medical problem
•   Peripheral edema
•   High-altitude retinopathy
•   High-altitude pharyngitis and bronchitis
•   UV keratoconjunctivitis
Special population
• Patients who have hypoxic cardiovascular and
  pulmonary diseases such as COPD or CHF ,
  CAD, pregnant

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High altitude syndrome

  • 2. 2,031m 2,102 m 2,195 m 2,285 m
  • 3.
  • 4. Altitude Height Effect Intermediate 1520 - 2440 m exercise performance altitude (5000 - 8000 ft) alveolar ventilation ↔arterial oxygen transport High altitude >2440 m (>8000 ft) AMS Very high 4270 - 5490 m (14,000 - 18,000 AMS altitude ft)
  • 6. ventilation • PaO2 carotid body& respiratory center ventilation PaCO2 Chronic hypoxia Sedative agent Performance During sleep
  • 7. ventilatory acclimatization ventilation pH return to pH (respi alkalosis) normal HCO3 excrete via Acetazolamide kidney
  • 8.
  • 9. • EPO w/in 2 hr • Rbc mass w/in days to wks • if excessive  chronic polycythemia
  • 10. Fluid Balance • Reset Osm stat:  plasma volume and hyperosmolality (s osm290 - 300) • diuresis and hemoconcentration :healthy response • Antidiuresis is a hallmark of AMS Peripheral venous in central ADH diuresis constriction blood volume &aldosterone
  • 11. Cardiovascular System CO = SV HR Pulm.vasoconstriction pulm.pressure Cerebral blood volume O2 to brain ICP
  • 12. Exercise capacity • measured by VO2max, drops dramatically on ascent to altitude • During acclimatization, submaximal endurance after 10 days
  • 13. Sleep at High Altitude • Sleep stages III and IV ↓ stage I   frequent arousals (improve with time at altitude) • Cheyne-Stokes respiration in those sleeping at >2700 m (>8860 ft) • the frequent awakenings & periodic breathing not related to AMS • mechanism of the lighter sleep →cerebral hypoxia. • Quality of sleep and arterial oxygenation during sleep improve with acclimatization and with acetazolamide
  • 15. High altitude syndrome • Acute hypoxia • Acute mountain sickness • High-Altitude cerebral edema • High-Altitude pulmonary edema • Peripheral edema • High-altitude retinopathy • High-altitude pharyngitis and bronchitis • Chronic mountain polycythemia • UV keratoconjunctivitis
  • 16. Acute hypoxia • occurs in the setting of sudden and severe • Unacclimatized persons become unconscious at SaO2 50 - 60%, PaO2 < 30 mm Hg, or a jugular venous PO2 of <15 mm Hg • immediate administration of oxygen, rapid descent
  • 17. Acute Mountain Sickness • setting of more gradual and less severe hypoxic • characterized by headache, GI disturbances, dizziness or light-headedness, and sleep disturbance
  • 18.
  • 19. What’re factors determine individual susceptibility to AMS ? • Age • Sex • Body weight • physical fitness
  • 20. Pathophysiology • renin-angiotensin aldosterone ADH The cerebral edema, interstitial pulmonary edema, peripheral edema, and antidiuresis
  • 21. Clinical feature • mild : alcohol hangover • Headaches : bifrontal and worsen with bending over or performing a Valsalva maneuver • GI symptoms : anorexia, N/V • irritable & wants to be left alone • Sleepiness • deep inner chill also are common
  • 22. Clinical feature • rapid ascent of an unacclimatized person to ≥2000 m • Symptoms develop between 1 -6 hours later, but sometimes are delayed for 1 - 2 days Severe Ataxia vomiting oliguria HACE headache and AOC
  • 23. Physical examination • percent SaO2 overall correlates poorly with the diagnosis of AMS • postural hypotension may be present • Localized rales ≥ 20% • Funduscopy :tortuosity and dilatation, and retinal hemorrhages (at altitudes >5000 m) • facial and peripheral edema is a hallmark
  • 24. The goals of treatment are to prevent progression abort the illness improve acclimatization
  • 25. 3 principles of Rx (1) do not proceed to a higher sleeping altitude in the presence of symptoms (2) descend if symptoms do not abate or become worse despite treatment (3) descend and treat immediately in the presence of a change in consciousness, ataxia, or pulmonary edema
  • 26. Treatment • Oxygen effectively relieves symptoms, but it is generally unavailable in the field or reserved for those with moderate to severe AMS
  • 27. Medication Indications for acetazolamide (1) a history of altitude illness (2) abrupt ascent to >3000 m (>9840 ft) (3) AMS requiring treatment (4) bothersome periodic breathing during sleep
  • 28. Symptomatic treatment of AMS • Headache :aspirin, acetaminophen or ibuprofen • N/V: ondansetron • f/q wakening: zolpidem,diphenhydramine
  • 29. Prevention • Graded ascent with adequate time for acclimatization is the best prevention • Prophylactic acetazolamide – started 24 hr before the ascent – continued for the first 2 days at altitude – restarted if illness develops
  • 30. HACE • HACE : progressive neurologic deterioration in someone with AMS or HAPE • altered mental status, ataxia, stupor, and progression to coma if untreated • severe, diffuse cerebral edema with multiple small hemorrhages and sometimes thrombosis
  • 31. Treatment of HACE • oxygen supplementation • descent(the highest priority) • steroid therapy • acetazolamide may be used as an adjunct
  • 32. MRI findings reversible white matter edema evidenced byT2 signal, esp.in the splenium of the corpus callosum
  • 33. HAPE • most lethal of the altitude illnesses • easily reversible with descent and oxygen administration • Risk factors:heavy exertion, rapid ascent, cold, excessive salt ingestion, use of a sleeping medication
  • 34. Pathophysiology • HAPE is a noncardiogenic, hydrostatic edema • The culprit in HAPE is high microvascular pressure  Pulmonary hypertension
  • 35. Clinical • Early diagnosis is critical, exercise performance & dry cough are enough to raise the suspicion of early HAPE • The condition typically worsens at night • Low-grade fever is common, and tachycardia and tachypnea • SO2 low for altitude
  • 36. Chest radiographic progress from interstitial  localized alveolar  generalized alveolar infiltrates
  • 37. Treatment • The key to successful Rx : early recognition, early stage is easily reversible • Immediate descent is the Rx of choice, but this is not always possible • The optimal therapy depends on – the environmental setting, – evacuation options – availability of oxygen or hyperbaric units – ease of descent
  • 39. medication • Because oxygen and descent are so effective, experience with drugs has been limited • nifedipine, phosphodiesterase 5 inhibitors:sildenafil and tadalafil
  • 40.
  • 41.
  • 42. Other high altitude medical problem • Peripheral edema • High-altitude retinopathy • High-altitude pharyngitis and bronchitis • UV keratoconjunctivitis
  • 43. Special population • Patients who have hypoxic cardiovascular and pulmonary diseases such as COPD or CHF , CAD, pregnant