11c. High-Altitude Disorders.pdf

HIGH-ALTITUDE DISORDERS TAMAR SARIA INTRODUCTION High altitude (>2440 m [>8000 ft]) is a hypoxic environment. Concentration of oxygen in the troposphere remains constant at 21%, Partial pressure of oxygen (PO2) decreases as a function of the barometric pressure. HYPOXIA! So, the main pr...

HIGH-ALTITUDE DISORDERS TAMAR SARIA INTRODUCTION High altitude (>2440 m [>8000 ft]) is a hypoxic environment. Concentration of oxygen in the troposphere remains constant at 21%, Partial pressure of oxygen (PO2) decreases as a function of the barometric pressure. HYPOXIA! So, the main problem will be to treat and deal with Hypoxia ALTITUDE STAGING Intermediate altitude, 1520 to 2440 m (5000 to 8000 ft) - decreased exercise performance and increased alveolar ventilation without major impairment in arterial oxygen transport – or AMS HIGH ALTITUDE 2440 to 4270 m - (8000 to 14,000 ft) is associated with decreased arterial oxygen saturation (SaO2); marked hypoxemia may occur during exercise and sleep. VERY HIGH ALTITUDE 4270 to 5490 m (14,000 to 18,000 ft), Abrupt ascent can be dangerous, and a period of acclimatization is required to prevent illness. S02 – 86-84% EXTREME ALTITUDE, >5490 M (>18,000 FT), Is experienced only by mountain climbers and is accompanied by severe hypoxemia and hypocapnia. Progressive physiologic deterioration eventually outstrips acclimatization, and sustained human habitation is impossible. Because hypoxemia is maximal during sleep, the sleeping altitude is the critical altitude to consider. ADAPTATION MECHANISMS Hyperventilation - The hypoxic ventilatory response is modulated by the carotid body, which senses a decrease in arterial oxygenation and signals the central respiratory center in the medulla to increase ventilation Blood - Within 2 hours of ascent to altitude, serum erythropoietin level increases and results in increased red cell mass over days to weeks FLUID BALANCE Peripheral venous constriction on ascent to altitude causes an increase in central blood volume that triggers baroreceptors to suppress secretion of antidiuretic hormone and aldosterone and induces a diuresis CARDIOVASCULAR SYSTEM HIGH-ALTITUDE SYNDROMES Although the different hypoxic clinical syndromes overlap, all share a fundamental mechanism, all are seen in the same setting of rapid ascent in unacclimatized persons, and all respond to the same essential therapy: descent and oxygen. ACUTE MOUNTAIN SICKNESS AMS is a syndrome characterized by headache along with some combination of GI disturbance, dizziness, fatigue, or sleep disturbance AMS is due to hypobaric hypoxia, but the exact sequence of events leading to illness is unclear Treatment - Acetazolamide, 250 milligrams PO twice a day, and/or dexamethasone, 4 milligrams PO every 6 h Hyperbaric therapy THE THREE PRINCIPLES OF TREATMENT ARE (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, and (3) descend and treat immediately in the presence of a change in consciousness, ataxia, or pulmonary edema. HIGH-ALTITUDE CEREBRAL EDEMA High-altitude cerebral edema is defined as progressive neurologic deterioration in someone with AMS or high-altitude pulmonary edema. It is characterized by altered mental status, ataxia, stupor, and progression to coma if untreated. Treatment of high-altitude cerebral edema is oxygen supplementation, descent, and steroid therapy Descent is the highest priority. HIGH-ALTITUDE PULMONARY EDEMA High-altitude pulmonary edema is the most lethal of the altitude illnesses. Risk factors include heavy exertion, rapid ascent, cold, excessive salt ingestion, use of a respiratory depressant, a previous history indicating inherent individual susceptibility, and pulmonary hypertension. High-altitude pulmonary edema is a noncardiogenic, hydrostatic edema factors that play a role include pulmonary venous constriction and uneven arterial vasoconstriction, HAPE Early diagnosis is critical, and decreased exercise performance and dry cough are enough to raise the suspicion of early high-altitude pulmonary edema Immediate descent is the treatment of choice, but this is not always possible ULTRAVIOLET KERATITIS (SNOW BLINDNESS) Ultraviolet A and ultraviolet B light penetrate the atmosphere to a greater degree at high altitude because there is less cloud cover, less water vapor, and less particulate matter in the air. Radiation increases roughly 5% for every 300 m (980 ft) gained Ultraviolet keratitis generally is self-limited and heals within 24 hours, but the condition is sufficiently painful to warrant administration of systemic analgesics. Application of cold compresses also may provide some relief. Prevention cannot be overemphasized, because this condition can be disabling, especially in hazardous terrain. Sunglasses should transmit