Human beings, being the most intelligent animal on this planet, keep on exploring the surroundings. Their habitat is not only limited to suitable physiological environments but also high mountains. The delivery of anesthesia care in such locations is challenging because of various factors like:
Difficulty in reaching the location.
The barometric pressure and temperature are different from that at sea level.
The calibrated anesthesia equipment may not function optimally at locations other than sea levels.
The anesthetic challenges at high altitudes and those in hyperbaric chambers are overviewed in this chapter.
Anesthesia at High Altitude
More than 140 million members of the human race have permanent settlement at altitudes greater than 2,500 m, and many of them may require medical care. Anesthesia practitioners must understand the unique challenges at high altitude. The noteworthy physiological changes are as follows:
The partial pressure of oxygen at high altitudes decreases with a decrease in atmospheric pressure.
Increased 2,3-diphosphoglycerate in red blood cells shifts the oxygen dissociation curve to the right, leading to increased oxygen delivery and unloading in tissues.
Respiratory alkalosis (secondary to hyperventilation) shifts the oxygen dissociation curve to the left. This increases oxygen’s affinity to red blood cells and favors uptake through the alveolar circulation.
The mixed venous blood of a person at high altitude has the same PO2 because of the following compensatory mechanisms:
Hyperventilation (primary mechanism), which may increase alveolar oxygen tension by 25 to 30%.
Lowered tissue metabolism due to decreased availability of oxygen.
Adjustment of oxygen transport characterized by:
Increase in pulmonary oxygen diffusion capacity by three- to fourfold.
Increase in pulmonary capillary blood flow.
Increase in lung volume and surface area of the alveolar membrane.
Increase in blood supply to the upper lobes of the lung.
Hypothermia: It leads to platelet dysfunction, cold injuries, and cardiac arrest in the worst scenario.
Immune suppression: It results in ineffective healing and increased risk of infection.
Physiologic adaptations to high altitudes start around 2 to 3 weeks, and it may take months to complete. The decrease in the partial pressure of oxygen stimulates the kidney to produce more erythropoietin, which leads to a rise in hemoglobin (15 to 22 g/dL). The hematocrit increases from 45 to 65% as plasma volume drops by 10 to 20%, secondary to intravascular fluid shifts into the interstitial compartment.
Hypoxia leads to an increase in sympathetic output, which contributes to the rise in cardiac output, mostly due to the rise in heart rate. Stroke volume decreases due to a decrease in preload. Systemic blood pressure rises as a result of peripheral vasoconstriction.
The short-term and long-term stay at high altitude exposes the individuals to lower oxygen tension. This exposure can lead to a multiple forms of sickness, affecting the mainly respiratory and central nervous system. The common high altitude illnesses are:
a. High-altitude pulmonary edema (HAPE)
It is noncardiogenic pulmonary edema seen at high altitudes in the setting of an elevation in pulmonary artery pressures. The underlying mechanisms are:
Decreased barometric pressure and partial pressure of O2, leading to pulmonary vasoconstriction and elevated pulmonary artery pressure (PAP).
Patchy pulmonary vasoconstriction with some parts of the lungs receiving over perfusion cause fluid leakage, plus elevated PAP and increased blood viscosity, leading to capillary endothelial damage and fluid leakage.
Fibrin thrombin formation in the lungs due to an increase in plasma fibrinogen levels.
Increased production of oxygen-free radicals, causing oxidation of alveolar intracellular lipids and mitochondrial cell membranes.
Common symptoms are dyspnea at rest, decreased exercise performance; chest congestion, and cough (frothy pink sputum).
Signs of HAPE include lung crackles, tachycardia, tachypnea, and cyanosis.
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