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Anesthesia at High Altitude
Overview
In the course of common anesthetic practice, it is unusual to worry about alterations in total environmental pressure, because the majority of anesthetic procedures are conducted within a limited pressure range. In fact, most organized hospital settings have developed in a narrow span of altitudes not far from sea level, although a significant portion of the world’s population continues to live at high altitude (HA). Traditional surgical and anesthetic techniques have been expanded to countries in development, such as Nepal in Asia, the Andean Highlands of South America, and elevated African regions such as Zimbabwe. Utilization of gas-based anesthesia has increased at altitudes where total barometric pressure is reduced.
It is interesting to explore the effects of low barometric pressures with attention to the physiologic changes commonly associated with anesthesia; the results provide principles and insights applicable to daily practice at “normal” environmental pressure. The first part of this chapter provides a description of the principal physiologic challenges introduced by low pressure. The second part summarizes anesthetic considerations at low barometric pressures.
Gases Around the Body
The pressure exerted by gas molecules on all surfaces of the body constitutes the environmental pressure. This pressure is the result of both the atmospheric gases prevailing at any one site and the composition of the gases in the column of air above the location. Total environmental pressure at sea level amounts to 760 mm Hg (14.7 lb/in 2 absolute [psia]). This value undergoes frequent, often daily changes; at most, it ranges by ±10–15 mm Hg as a consequence of weather fluctuations. The composition of atmospheric air, on the other hand, is singularly constant in its original constituents and is summarized in Table 21.1 .
Table 21.1
Composition of Atmospheric Gas (Dry, Sea Level)
| Gas | mm Hg | % of Total |
|---|---|---|
| Nitrogen | 594 | 78.09 |
| Oxygen | 159 | 20.95 |
| Carbon dioxide | 0.2 | 0.03 |
| Other inert gases | 7 | 0.93 |
| Water vapor | 0 | 0.00 |
| Total | 760.2 | 100.00 |
Only water vapor content varies significantly as a function of total humidity, and the partial pressure of the water molecules may contribute various amounts to the total pressure. Water vapor pressure ( PH2O
The addition of water vapor to atmospheric gases and the usual heating of the inspired gas to body temperature both induce substantial changes in the partial pressure of all gases and, in particular, to the partial pressure of oxygen (PO 2 ) ( Table 21.2 ). Nitrogen and oxygen are the only gases present in substantial concentration in dry air. Moist, warm tracheal air contains significant amounts of water vapor.
Table 21.2
Approximate Composition of Inspired Gases at Atmospheric Pressure at Sea Level
| Gas | Dry Air (mm Hg) | Moist Tracheal Air (mm Hg) | Alveolar Gas (mm Hg) |
|---|---|---|---|
| Nitrogen | 601 | 564 | 568 |
| Oxygen | 159 | 149 | 105 |
| Carbon dioxide | 0.2 | 0.2 | 40 |
| Water vapor | 0 | 47 | 47 |
| Total | 760 | 760 | 760 |
Because the total barometric pressure is unchanged in the trachea, water vapor displaces each of the other gases, thereby decreasing their partial pressures. Alveolar gas contains approximately 100–105 mm Hg of oxygen. Commonly, oxygen is taken up by the blood in the lungs, and carbon dioxide is released into the alveoli. During respiratory processes, the gases are primarily moved by convection from the atmosphere to the alveolar space and back to the exhaled gas outside the body. In the alveolar compartment, diffusion is the primary mechanism for oxygen and carbon dioxide exchange. Therefore, changes in oxygen partial pressure in the inspired gas lead to proportional changes in the alveolar PO 2 .
High-altitude environments are characterized by a decreased barometric pressure and thus a reduced partial pressure of inspired oxygen compared with sea level values. While breathing air, there is a large range of total atmospheric pressure changes still compatible with adequate gas exchange, from pressures on the highest mountains (about 300 mm Hg total pressure) to those at several hundred feet underwater (about six to seven times 760 mm Hg). The limits can be extended, especially at altitude, by slow adaptive phenomena that require several days to weeks to unfold fully; these phenomena are in part under genetic control.
Reduced Environmental Pressure
Acute awareness of the adverse effects of the low barometric pressure of HA is recorded in literature regarding the Spanish invasion of South America; these effects were commonly attributed to the “thinness of the air.” Acute mountain sickness (AMS) at an elevation of about 10,000 feet was first described in 1671 by the physiologist Borelli.
Acute exposure to altitude can be achieved in a decompression chamber, by rapid ascent in an airplane, or by a brisk climb on a mountain. The decrease in total barometric pressure with altitude and the attendant reduction in inspired PO 2 are shown in Fig. 21.1 . Fig. 21.2 illustrates the approximate values for PO 2 in inspired air, moist tracheal air, alveolar gas, and arterial and mixed venous blood. High altitude significantly affects the human body because of a decrease in PO 2 in an environment of low ambient barometric pressure. A whole spectrum of disturbances and diseases was described for sojourners into HA. On one hand, the lack of oxygen generally triggers physiologic mechanisms and may result in a well-compensated state called acclimatization . The extent to which a person adapts to this depends on the rate and extent of the ascent and the baseline physiologic status of the individual. On the other hand, high-altitude illness (HAI) refers to the set of symptoms that range from mild to severe, sometimes even life-threatening consequences, such as cerebral and pulmonary edema.
Acclimatization
Acclimatization is a physiologic state that tends to improve oxygen transport and utilization at HA. An essential adaptation to acute HA hypoxia is hyperventilation. In the range of altitude from 10,000 to 15,000 feet, the increase in altitude causes an increase in ventilation proportional to the decrease in density of the air. Thus, the increase in ventilation approximates the amount required to produce equivalent delivery of oxygen to the alveolar spaces. This is achieved by an increase in respiratory rate and tidal volume. The arterial hypoxemia results in stimulation of peripheral chemoreceptors, which causes an increase in alveolar ventilation. Carbon dioxide is washed out of the alveoli at an increased rate, and the arterial partial pressure of carbon dioxide (PaCO 2 ) is decreased. The reduction of PaCO 2 leads to a respiratory alkalosis with an associated increase of arterial pH, and these changes stimulate the excretion of bicarbonate from the blood and the kidneys. This increase in ventilation is generally sustained for several days, and it may not reach a plateau until several days at altitude. Consequently, during the following days, the blood bicarbonate is reduced, and a new level appropriate for the level of hyperventilation is established, with a near normal pH. Thus, the respiratory alkalosis is compensated.
The respiratory adaptations and the bicarbonate excretion affect the electrolyte status of spinal fluid and alter subsequent ventilatory responses. As the bicarbonate is excreted from the blood, bicarbonate is also lost from cerebrospinal fluid (CSF). In view of this decreased buffer capacity, changes in carbon dioxide in the CSF result in faster changes in hydrogen ion concentration and lead to an increased sensitivity to carbon dioxide. At this point in adaptation, ventilatory sensitivity to carbon dioxide is enhanced. Gradually, the respiratory system adapts (respiratory acclimatization) to hypoxia, resulting in an increase in the hypoxic ventilatory response. A resetting of the arterial PaCO 2 set point also occurs. These processes result in restoration of normoxia with persistent hyperventilation and hypocapnia. Overall, the hypocapnia is beneficial for oxygen transport, because it shifts the dissociation curve to the left with increased affinity of hemoglobin (Hb) for oxygen; this enhances the oxygenation of blood at the lung. Extreme altitude results in an arterial PO 2 of about 20 mm Hg, resulting in a profound depression of the central nervous system (CNS) and ventilatory drive.
Other Effects
Additional effects on lung function have been demonstrated with exposure to altitude, including an increase in pulmonary diffusing capacity, an increase in pulmonary blood flow to the apical lung regions, larger lung volumes with increased vital and total lung capacity, hypoxic pulmonary vasoconstriction, and an increase in pulmonary vascular pressures. Hypoxic pulmonary vasoconstriction is a vasomotor response of small, muscular pulmonary arteries that tends to increase resistance to flow in areas of alveolar hypoxia, thereby improving ventilation/perfusion (V/Q) match and reducing the shunt fraction. As a result, prolonged arterial hypoxemia increases right-ventricular pressure for extended periods of time and induces right ventricular hypertrophy, with predictable electrocardiographic (ECG) changes of right-axis deviation and right ventricular strain.
Hemoglobin (Hb) concentration increases rapidly at altitude, within hours; this is because of rapidly rising hemoconcentration. Eventually, however, a real increase in erythropoiesis and a true increase in red cell mass ensues that may not be fully realized for several weeks. As the red cell mass and Hb concentration increase, the erythropoietin level decreases. Because of the sigmoid shape of the oxygen-hemoglobin dissociation curve, up to 3000 m (9843 feet) of elevation, Hb saturation with oxygen is maintained; beyond 3000 m (9843 feet), the arterial PO 2 falls steeply, resulting in lower hemoglobin-oxygen saturation. Soon after the development of the hypoxic state, production of 2,3-diphosphoglycerate (2,3-DPG) increases, which shifts the Hb dissociation curve to the right and allows for more effective oxygen unloading in the capillaries.
Cardiac output is characteristically increased as a result of an increase in the heart rate in response to hypoxia. This response adapts during continuing exposure as cardiac output decreases as a result of diuresis and a lower plasma volume. Tissue blood flow tends to increase as a result of increased nitric oxide (NO) concentration in the plasma, which causes vasodilation. A corresponding increase in organ blood flow occurs that includes pulmonary, cardiac, and cerebral blood flow. Increased pulmonary blood flow leads to failure of red blood corpuscles to fully equilibrate with the alveolar gas, which augments any existing hypoxia. High altitude may induce a hypercoagulable state as a result of polycythemia and platelet activation, which increases the risk of thromboembolic events.
In acclimatization, a state of improved oxygen transport and utilization combats the HA hypoxia; molecular responses involved include activation of gene coding for proteins involved in oxygen transport (hypoxia inducible factor 1 [HIF-1]) and proliferation of blood vessels (vascular endothelial growth factor [VEGF]) in the heart.
Despite these adaptive responses to altitude, no significant change occurs in either resting oxygen consumption or in the ability to perform high levels of exercise at moderate altitude. At altitudes in excess of 10,000 feet, exercise tolerance is limited with acute exposure, and other symptoms of acute hypoxia manifest themselves by interference with several organ systems.
High-Altitude Illness
High Altitude Illness (HAI) is composed of a group of syndromes that develop as a result of continuous exposure to hypoxia, and it is generally divided into four categories: (1) AMS, (2) high-altitude cerebral edema (HACE), (3) high-altitude pulmonary edema (HAPE), and (4) chronic mountain sickness. The risk of HAI is directly proportional to the rate of ascent and the altitude reached; therefore, a gradual ascent to promote acclimatization may be the best strategy to prevent HAI. Guidelines suggest that above an altitude of 2500 m (8200 feet), the altitude at which a person sleeps should not be increased by more than 600 m (1970 feet) per day ( Table 21.3 ). , Treatment may include steroids and/or diuretics, but the only real alternative to acclimatization is descent to a lower altitude.
Table 21.3
High-Altitude Illness and Various Clinical Syndromes
Modified from Leissner KB, Mahmood FU: Physiology and pathophysiology at high altitude: considerations for the anesthesiologist, J Anesth 23(4):543–553, 2009; and Moon R, Camporesi EM: Clinical care in extreme environments: at high and low pressure and in space. In Miller R, Eriksson L, Fleischer LA, Wiener-Kronish J, editors: Miller’s anesthesia , ed 7, Philadelphia, 2010, Churchill Livingstone.
| Syndrome | Special Features | Prevention | Clinical Features | Management |
|---|---|---|---|---|
| Mild acute mountain sickness (AMS); includes high-altitude headache | Most recover | Slow ascent or staging; a acetazolamide b | Headache, reduced appetite, nausea, vomiting, edema, insomnia, dizziness, fatigue | Stop ascent, rest, and acclimatize for at least a day; if symptoms do not improve, descend ≥500 m Acetazolamide, 125–250 mg bid Symptomatic treatment as necessary with analgesics (aspirin, ibuprofen) and antiemetics |
| Moderate to severe AMS | Similar to AMS but increased in severity | Slow ascent or staging; a acetazolamide b | Headache, reduced appetite, nausea, vomiting, edema, insomnia, dizziness, fatigue | As for AMS, plus: Oxygen supplementation (if available) Dexamethasone 4 mg PO, IM, or IV q6h Hyperbaric therapy |
| High-altitude cerebral edema | A medical emergency (vasogenic cerebral edema) | Slow ascent or staging; a acetazolamide b | Ataxia, altered consciousness, papilledema, focal deficits | As for AMS, plus : Immediate descent or evacuation Minimize exertion and keep warm Consider tracheal intubation to protect airway or if respiration is inadequate |
| High-altitude pulmonary edema | Occurs within first few days; increased pulmonary capillary pressure and exudate in alveoli because of inhomogeneous HPV | Slow ascent; for susceptible persons, nifedipine, tadalafil, or dexamethasone are prophylactic | Fatigue, dyspnea, cough, cyanosis | As for AMS, plus : Nifedipine, 10 mg PO q4h titrated to response, or 10 mg PO once, followed by ER q12–24h Nitric oxide therapy and/or: Tadalafil 10 mg bid or sildenafil 50 mg q8h; various other modalities to lower pulmonary arterial pressure |
| Chronic mountain sickness | Known as Monge syndrome; the result of excessive erythrocytosis, pulmonary hypertension leading to cor pulmonale leading to CHF | A public health problem in the Andean plateau; abatement includes modifying risk factors (e.g., smoking, obesity, pollution, lung disease) | Headache, dizziness, dyspnea, palpitations, localized cyanosis, burning sensation in the palms and soles, venous dilation, joint and muscle pain, lack of mental concentration, memory changes | Phlebotomy for transient relief Descent to lower altitude ACEIs, domperidone, acetazolamide, and respiratory stimulants (medroxyprogesterone and almitrine) Nifedipine and sildenafil to reduce pulmonary artery pressure |
ACEI, Angiotensin-converting enzyme inhibitor; bid, twice per day; CHF, congestive heart failure; ER, extended-release; HPV, hypoxic pulmonary vasoconstriction; IM, intramuscular; IV, intravenous; PO, by mouth.
a Several days are spent at an intermediate altitude of 2000 m.
b Produces a state of bicarbonate diuresis and thereby augments the ventilatory response to hypoxia; may also produce tissue respiratory acidosis and diuresis and inhibits carotid body response to carbon dioxide.
Gamow Bag
The Gamow bag is a rescue product for high-altitude climbers and trekkers that can be used for the treatment of moderate to extreme altitude sickness. A Gamow bag is an inflatable pressure bag large enough to fit a person inside. By inflating the bag with a foot pump, ambient pressure experienced by the patient can be increased. This allows the “effective altitude” to be decreased by as much as 7000 feet, thus relieving the symptoms of AMS. The Gamow bag is used for treatment of life-threatening HAPE and HACE. Gamow bags are constructed of durable nylon and are reinforced with circular nylon straps. A lengthwise zipper allows patients access into the bag, and the four clear windows allow visual contact during treatment. The bag is pressurized with ambient air to 2 psig (100 mm Hg above outside ambient pressure) by use of a foot pump powered by partners standing outside the bag ( Fig. 21.3 ). Gamow bag treatments for altitude sicknesses are used to provide temporary relief in the hope that it will give the patient enough time and strength to descend to a lower altitude, alleviating the need for a full-blown lifesaving rescue effort by everyone on the mountain. Expeditious descent to a lower altitude is the only definitive therapy.
Pregnancy and Altitude
Because the fetus in utero does not derive oxygen directly from the low barometric pressure at HA, it seems to be little affected by acute exposure to altitudes up to 2500–3000 m and suffers no adverse effects. Adaptation to chronic exposure to HA includes a decrease in villous membrane thickness and an increase in placental capillary volume. Infants born at HA are suddenly exposed to the hypoxic environment, causing the transition to adult circulation to occur more gradually, with a higher incidence of patent foramen ovale (PFO) and patent ductus arteriosus. An increased incidence of acute respiratory distress syndrome (ARDS) and pulmonary arterial hypertension that requires oxygen and/or mechanical ventilation are also seen.
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