High Altitude illness, including
Acute Mountain Sickness, High Altitude
Cerebral Edema (
HACE) and
High Altitude Pulmonary Edema (
HAPE), pathophysiology and management of each condition in handwritten tutorial lecture format for medical students preparing for
USMLE.
High Altitude Illness are syndromes that occur during or following an ascent.
PATHOPHYSIOLOGY OF HIGH ALTITUDE SICKNESS
Hypobaric hypoxemia -
Pressure of inspired oxygen is equal to
Fraction of inspired oxygen is multiplied by the barometric pressure - 47 mmHg. At sea level the barometric pressure is 760 mmHg and so there is
150 mmhg of partial pressure of oxygen. During ascent the barometric pressure decreases causing a decreased in pressure of oxygen inspired.
Aclimitization - induction of hypoxemia inducible factor (
HIF-1) increases transcription factors that activate over
100 genes that increase oxygen levels. Aortic
Bodies and
Carotid body detect oxygen levels and when the oxygen levels are low then they will trigger increase ventilation known as the hypoxic ventilation response (
HVR). But as you hyperventilate the amount of
CO2 begins to decrease, while there is an increase ventilation. This means the acidity will also decrease leading to alkalosis. Hyperventilation does allow maintenance of oxygen, but it is hindered by alkalosis.
Central chemoreceptors respond to this carbon dioxide, or actually the acidity produced by the carbon dioxide. As alkalosis develops then there will be a decrease in ventilation reversing oxygen and then causing carbon dioxide to go back up.
Renal correction for high altitude illness can help by decreases the bicarbonate level and allowing the carbon dioxide to increase and prevent the negative respiration effect and then increase the oxygen level again. In other words the bicarbonate can stop inhibitory effect of central chemoreceptors. Therefore acclimitization can take up to 2-4 days.
Circulatory changes will also occur do to sympathetic activation causing increase cardiac output, blood pressure, heart rate, and venous tone. However, there will also be loss of intravascular volume to offset some of the circulatory changes. Increase in erythropoeitin take 10-14 days and therefore increase
RBC. This leads to hemoconcentration that increases the oxygen carrying capacity.
Oxygen dissociation curve in high altitude has a left shift due to alkalosis and therefore there will be less oxygen available to tissue. Therefore, the body will produce
2,3-DPG will be produced. This will not help above 4,000meters.
HIF-1 also causes angiogenesis causing more BF and oxygen delivery.
EPIDEMIOLOGY OF HIGH ALTITUDE ILLNESS
Affects all ages and fitness levels, however, there is some genetic factors. The rate of ascent is the largest risk factors.
Drugs such as sedative and hypnotics.
COPS, Restrictive,
Cystic Fibrosis,
Pneumonia,
Pulmonary Hypertension. However, Asthma and Anemia may improve during ascent and is not a risk factor.
ACUTE MOUNTAIN SICKNESS
Unadapted individual ascends quickly up a mountain.
Symptoms will be similar to alcohol hangover (headache, fatigue, nausea and vomiting). Lab will all be normal (vitals,
CBC) therefore it is fairly mild.
Treatment consist of conservative such as no further ascent, decrease physical activity. Usually acclimitization occurs within 2-4 days.
Symptomatic releif with aspirin and acetominophen.
Descent should be done if they are not improving. If there are any neurological or pulmonary edema then must ascend until they feel better.
Supplemental oxygen 2-4L/minute for 15-20 minutes especially at night and may be seen as alternative to descent.
Hyperbaric oxygen portable and inflatable are also avialable.
HIGH ALTITUDE CEREBRAL EDEMA (HACE)
Onset on cerebral dysfunction (2000-2500 meter after
AMS). Symptoms of ataxis gait, decrease consciousness. LP will have a high opening pressure and hypoxemia. CT will show cerebral edema. Treatment is to descent as soon as possible.
Comatose patients you should secure airway.
HIGH ALTITUDE PULMONARY EDEMA (HAPE)
Generally occurs 2-4 days later and may accompany AMS/HACE.
Present with subtle non productive cough 2-4 days at new altitude and more severe at night and exertion.
Eventually there will be frothy, frank blood, exercise intolerance, hypoxemia. Tachycardia, tachypnea and inspiratory crackles middle lobe and become more diffuse.
Pulse oximetry will show oxygen that will be 10points lower than expected. On
Chest X-ray there will be patchy infiltrate.
Ultrasound will show extrasvascular lung water. Treatment is to decrease pulmonary artery pressure, decrease physical activity and cold. Supplemental oxygen can cause vasodilation, rest and warm.
Finally descent 500-1000m, hyperbaric chamber and
CPAP. Pharmacological such as nifedipine sildanefel and beta agonist.
- published: 27 May 2015
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