High altitude medicine: Difference between revisions

Latest revision as of 21:32, 1 May 2024

Background

Relationship between total atmospheric pressure and altitude above sea level.

Altitude Stages

Stage	Altitude	Physiology
Intermediate Altitude	5,000 - 8,000 ft (1,524 - 2,438 meters)	Decreased exercise performance without major impairment in SaO2
High Altitude	8,000 - 12,000 ft (2,438 - 3,658 meters)	Decreased SaO2 with marked impairment during exercise and sleep
Very High Altitude	12,000-18,000 ft (3,658 - 5,487 meters)	Abrupt ascent can be dangerous; acclimatization is required to prevent illness
Extreme Altitude	>18,000 ft (>5,500 meters)	Only experienced by mountain climbers; accompanied by severe hypoxemia and hypocapnia Sustained human habitation is impossible RV strain, intestinal malabsorption, impaired renal function, polycythemia

Height of Mount Everest (tallest in world): 29,035 feet (8,850 meters)

Height of Mount Whitney (tallest in contiguous US): 14,505 feet (4,421 meters)

Conversion: 1 meter = ~3.28 feet (calculator)

Physiology of Acclimatization

Ventilation

Increased elevation → decreased partial pressure of O2 → decreased PaO2
- Hypoxic ventilatory response results in ↑ ventilation to maintain PaO2
- Vigor of this inborn response relates to successful acclimatization
Initial hyperventilation is attenuated by respiratory alkalosis
- As renal excretion of bicarb compensates for respiratory alkalosis, pH returns toward normal
Process of maximizing ventilation culminates within 4-7 days at a given altitude
- With continuing ascent the central chemoreceptors reset to ever lower values of PaCO2
- Completeness of acclimatization can be gauged by partial pressure of arterial CO2
- Acetazolamide, which results in bicarb diuresis, can facilitate this process

Blood

Erythropoietin level begins to rise within 2 days of ascent to altitude
Takes days to weeks to significantly increase red cell mass
- This adaptation is not important for the initial acclimatization process

Fluid Balance

Peripheral venoconstriction on ascent to altitude causes increase in central blood volume
- This leads to decreased ADH → diuresis
- This diuresis, along with bicarb diuresis, is considered a healthy response to altitude
  - One of the hallmarks of AMS is antidiuresis

Cardiovascular System

SV decreases initially while HR increases to maintain CO
Cardiac muscle in healthy patients can withstand extreme hypoxemia without ischemic events
Pulmonary circulation constricts with exposure to hypoxia
- Degree of pulmonary hypertension varies; a hyper-reactive response is associated with HAPE

Differential Diagnosis

High Altitude Illnesses

High Altitude Syndromes

High altitude management algorithm.

All caused by hypoxia
All are seen in rapid ascent in unacclimatized patients
- Hypoxemia is maximal during sleep; the altitude in which you sleep is most important
- Above 10,000ft rule of thumb is to sleep no higher than 1,000 additional ft/day
All respond to O2/descent

Expected SpO₂ and PaO₂ levels at altitude^[1]

Altitude	SpO₂	PaO₂ (mm Hg)
1,500 to 3,500 m (4,900 to 11,500 ft)	about 90%	55-75
3,500 to 5,500 m (11,500 to 18,000 ft)	75-85%	40-60
5,500 to 8,850 m (18,000 to 29,000 ft)	58-75%	28-40

References

↑ Gallagher, MD, Scott A.; Hackett, MD, Peter (August 28, 2018). "High altitude pulmonary edema". UpToDate. Retrieved May 2, 2019.

Authors:

[1] Gallagher, MD, Scott A.; Hackett, MD, Peter (August 28, 2018). "High altitude pulmonary edema". UpToDate. Retrieved May 2, 2019.

[1]

@@ Line 1: / Line 1: @@
-==Acute Mountain Sickness (AMS)==
+==Background==
+[[File:Altitude and air pressure & Everest.jpg|thumb|Relationship between total atmospheric pressure and altitude above sea level.]]
+===Altitude Stages===
+{| class="wikitable"
+| align="center" style="background:#f0f0f0;"|'''Stage'''
+| align="center" style="background:#f0f0f0;"|'''Altitude'''
+| align="center" style="background:#f0f0f0;"|'''Physiology'''
+|-
+| Intermediate Altitude ||5,000 - 8,000 ft
+:(1,524 - 2,438 meters)
+||
+*Decreased exercise performance without major impairment in SaO2
+|-
+| High Altitude||8,000 - 12,000 ft
+:(2,438 - 3,658 meters)
+||
+*Decreased SaO2 with marked impairment during exercise and sleep
+|-
+| Very High Altitude ||12,000-18,000 ft
+:(3,658 - 5,487 meters)
+||
+*Abrupt ascent can be dangerous; acclimatization is required to prevent illness
+|-
+| Extreme Altitude ||>18,000 ft
+:(>5,500 meters)
+||
+*Only experienced by mountain climbers; accompanied by severe hypoxemia and hypocapnia
+*Sustained human habitation is impossible
+*RV strain, intestinal malabsorption, impaired renal function, polycythemia
+|}
+Height of Mount Everest (tallest in world): 29,035 feet (8,850 meters)
-- acetazolamide- Start day before ascent 125- 150 mg BID or qhs for 2- 3 days while at altitude and then stop. Peds dose is 5mg/kg/day. Watch for sulfa allergy, paresthesias, diuresis.
+Height of Mount Whitney (tallest in contiguous US): 14,505 feet (4,421 meters)
-- Dexamethasone- prevents as well as treats cerebral edema. 4mg BID- QID, day of ascent and taper off over several days. Can combine with acetazolamide.
+Conversion: 1 meter = ~3.28 feet  [https://www.metric-conversions.org/length/meters-to-feet.htm (calculator)]
-- Treatment- rest, descend 500- 1000m, acetazolamide 250- 500mg, dex 4mg with taper, Gamow bag (portable hyperbaric chamber)
+==Physiology of Acclimatization==
+===Ventilation===
+*Increased elevation → decreased partial pressure of O2 → decreased PaO2
+**Hypoxic ventilatory response results in ↑ ventilation to maintain PaO2
+**Vigor of this inborn response relates to successful acclimatization
+*Initial hyperventilation is attenuated by respiratory alkalosis
+**As renal excretion of bicarb compensates for respiratory alkalosis, pH returns toward normal
+*Process of maximizing ventilation culminates within 4-7 days at a given altitude
+**With continuing ascent the central chemoreceptors reset to ever lower values of PaCO2
+**Completeness of acclimatization can be gauged by partial pressure of arterial CO2
+**[[Acetazolamide]], which results in bicarb diuresis, can facilitate this process
+===Blood===
+*Erythropoietin level begins to rise within 2 days of ascent to altitude
+*Takes days to weeks to significantly increase red cell mass
+**This adaptation is not important for the initial acclimatization process
-==High Altitude Pulmonary Edema (HAPE)==
+===Fluid Balance===
+*Peripheral venoconstriction on ascent to altitude causes increase in central blood volume
+**This leads to decreased ADH → diuresis
+**This diuresis, along with bicarb diuresis, is considered a healthy response to altitude
+***One of the hallmarks of AMS is antidiuresis
+===Cardiovascular System===
+*SV decreases initially while HR increases to maintain CO
+*Cardiac muscle in healthy patients can withstand extreme hypoxemia without ischemic events
+*Pulmonary circulation constricts with exposure to hypoxia
+**Degree of pulmonary hypertension varies; a hyper-reactive response is associated with [[High altitude pulmonary edema|HAPE]]
-- definition: two symptoms: dyspnea at rest, cough, weakness, chest tightness or congestion.
+==Differential Diagnosis==
+{{High altitude DDX}}
-And
+==High Altitude Syndromes==
+[[File:Altitude flow sheet.png|thumb|High altitude management algorithm.]]
+*All caused by hypoxia
+*All are seen in rapid ascent in unacclimatized patients
+**Hypoxemia is maximal during sleep; the altitude in which you sleep is most important
+**Above 10,000ft rule of thumb is to sleep no higher than 1,000 additional ft/day
+*All respond to O2/descent
-two signs: central cyanosis, crackles or wheezes, tachypnea, tachycardia.
+{{Expected SpO2 at altitude}}
-- most common medical cause of altitude related death.
+==See Also==
+*[[Commercial in-flight medical emergencies]]
-- >2500m, young males, usually second night of altitude or after 3- 4 days ascent.
+==References==
+<references/>
-- recent URI predisposes
+[[Category:Environmental]]
-- highest risk in mountain dweller who descends to sea level and then reascends- possibly due to pulm art muscle remodeling.
-- is noncardiogenic pulmonary edema with pulm hypertension and inflammation of capillaries and transepithelial water and sodium transport. Caused by combination of both pulm hypertension and increased cap permeability.
-- Nitric oxide (NO) inhalation decreases pulm art pressures and can improve oxygenation. Dz possibly due to NO deficiency?
-- Prevention
-- limit exercise for first 1- 2 days. Also limit ascent when over 2500m to 300- 350m/day.
-- Nifedipine 20mg TID or 30- 6- mg extended release qd- prevents HAPE but not pulm edema of exercise of AMS or HACE.
-- Treatment-
-- descend, oxygen, nifedipine 10 mg po, CPAP mask, diuretics, GAMOW bag.
-- Can reascend in 2- 3days in needed but at increased risk for reoccurence.
-==High Altitude Cerebral Edema (HACE)==
-- Acute Mountain Sickness plus altered mental status or ataxia. Of if mountain sickness not present, is ataxia with mental status changes.
-- occurs >4000m
-- due to increased brain water, not just volume. Get increased intracranial pressure.
-- initially get vasogenic edema- fluid and protein crosses BBB, Get reversible changes in white matter, especially corpus callosum.. Later get cytotoxic edema by toxins and ischemia. Mostly of gray matter and has poorer px.
-- Theories: angiogenesis model- hypoxemia causes macrophages to release cytokines and vascular endothelium growth factor. Basement membranes of capillaries are dissolved causing leaks and petechial hemorrhages. Inhibited by dexamethasone.
-- Other theory is due to unexpandable cranial vault. As brain volume increases buffering ability of CSF overcome and brain swells in closed nonexpanding space.
-- Prevent as with AMS
-Treatment- descend, oxygen, dex 4- 8mg IV, then 4mg q6hr. If GAMOW bag available- 4-8 hr recompression may allow pt to walk down mountain (big help).
-[[Category:Environ]]