High altitude medicine: Difference between revisions
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=== [[Acute Mountain Sickness (AMS)]] === | === [[Acute Mountain Sickness (AMS)]] === | ||
=== High Altitude Cerebral Edema (HACE) === | === [[High Altitude Cerebral Edema (HACE)]] === | ||
=== High Altitude Pulmonary Edema (HAPE) === | === High Altitude Pulmonary Edema (HAPE) === | ||
Revision as of 00:44, 13 June 2012
Physiology of Acclimatization
Ventilation
- Increased elevation -> decreased partial pressure of O2 -> decreased PaO2
- Hypoxic ventilatory response results in incr 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 resp alkalosis, pH returns toward normal
- At this point ventilation continues to increase
- Process of maximizing ventilation culminates 4-7d 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
- As renal excretion of bicarb compensates for resp alkalosis, pH returns toward normal
Blood
- Erythropoietin level begins to rise within 2d of ascent to altitude
- Takes days to weeks to significantly increase red cell mass
- This adaptation is not important for the initial 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 pts can withstand extreme hypoxemia w/o ischemic events
- Pulmonary circulation constricts w/ exposure to hypoxia
- Degree of pulm HTN varies; a hyperreactive response is associated with HAPE
Altitude Stages
- Intermediate Altitude (5000-8000ft)
- Decreased exercise performance without major impairment in SaO2
- High Altitude (8000-12,000ft)
- Decreased SaO2 with marked impairment during exercise and sleep
- Very High Altitude (12,000-18,000ft)
- Abrupt ascent can be dangerous; acclimatization is required to prevent illness
- Extreme Altitude (>18,000ft)
- Only experienced by mountain climbers; accompanied by severe hypoxemia and hypocapnia
- Sustained human habitation is impossible
- RV strain, intestinal malabsorption, impaired renal function, polycythemia
High Altitude Syndromes
- All caused by hypoxia
- All are seen in rapid ascent in unacclimatized pts
- 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 1000 additional ft/day
- All respond to O2/descent
Acute Mountain Sickness (AMS)
High Altitude Cerebral Edema (HACE)
High Altitude Pulmonary Edema (HAPE)
Background
- Noncardiogenic pulm edema d/t increased microvascular pressure in the pulm circulation
- Most lethal of the altitude illnesses
- Occurs in <1/10,000 skiers in Colorado; 2-3% of Mt. McKinley climbers
- Typical pt is strong and fit; may not have symptoms of AMS before onset of HAPE
- Most commonly noticed on the second night at a new altitude
- Risk Factors:
- Heavy exertion
- Rapid ascent
- Cold
- Excessive salt ingestion
- Use of a sleeping medication
- Preexisting pulmonary HTN
- Preexisting respiratory infection (children)
- Previous history of HAPE
Clinical Features
- Early
- Dry cough, decreased exercise performance, dyspnea on exertion, localized rales
- Resting SaO2 is low for the altitude and drops markedly w/ exertion (aids in the dx)
- Late
- Dyspnea at rest, marked weakness, productive cough, cyanosis, generalized rales
- Tachycardia and tachypnea correlate with the severity of illness
- Altered mental status and coma (from severe hypoxemia)
- ECG
- Right strain pattern
- CXR
- Progresses from interstitial to localized-alveolar to generalized-alveolar infiltrates
Treatment
- Immediate descent is treatment of choice
- While pt is descending attempt to limit exertion as much as possible
- If cannot descend use combination of:
- Supplemental O2
- Can completely resolve the pulmonary edema within 36-72hr
- Hyperbaric bag
- Keep pt warm (cold stress elevates pulm artery pressure)
- Use expiratory positive airway pressure mask
- Consider the medications listed below that are usually used for prevention
- Supplemental O2
Disposition
- Admission
- Warranted for severe illness that does not respond immediately to descent
- Discharge
- Progressive clinical and X-ray improvement and a PaO2 of 60mmHg or SaO2>90%
Prevention
- Nifedipine 20mg q8hr while ascending is effective prophylaxis in pts who had HAPE before
- Tadalafil 10mg BID 24hr prior to ascent
- Salmeterol inhaled BID
High Altitude Peripheral Edema
- Swelling of face and distal extremities is common (20% of trekkers at 14,000ft)
- Often associated with AMS but not in all cases
- Resolves spontaneously with descent
High Altitude Retinopathy
- Retinal hemorrhages are common at sleeping altitudes >16,000ft
- Not considered an indication for descent unless vision changes are present
High Altitude Pharyngitis and Bronchitis
- Dry, hacking cough is common at >8000ft
- Purulent bronchitis/painful pharyngitis common w/ prolonged periods at extreme altitude
- Severe coughing spasms can result in cough fx of ribs
- Treatment
- Alubterol
- Breathing steam, sucking on hard candies, forcing hydration
- Abx are not helpful
Chronic Mountain Sickness
- Excessive polycythemia for a given altitude (Hb >20
- Occurs in pts living at high-altitude who have COPD, sleep apnea or impaired resp drive
- Head ache, difficulty thinking, impaired peripheral circulation, drowsiness
- Treatment
- Phlebotomy
- Relocation to lower altitude
- Home O2 use
Ultraviolet Keratitis (Snow Blindness)
- High UV exposure can lead to corneal burns w/in 1hr
- May also see with arc welders, tanning beds
- Symptoms develop after delay of up to 6-12hr
- Ocular pain, foreign-body sensation, photophobia, tearing, conj erythema, chemosis
- Generally is self-limited and heals within 24-36hr
Source
Tintinalli
