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 normally, 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. In recent years, 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 low barometric pressure at high altitudes with attention to the physiologic changes commonly associated with anesthesia, and the results provide principles and insights applicable to daily practice at “normal” environmental pressure. The first part of the 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 atmospheric [psia]). This value undergoes frequent, often daily changes; at most, it ranges up and down by 10 to 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 28-1 .
| 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 ( <SPAN role=presentation tabIndex=0 id=MathJax-Element-1-Frame class=MathJax style="POSITION: relative" data-mathml='PH2O’>PH2OPH2O
P H 2 O
) depends on available water molecules in the atmosphere at a certain temperature. At 0° C, air that is fully saturated has a water vapor pressure of approximately 5 mm Hg, whereas at body temperature (37° C), the water vapor pressure is increased to 47 mm Hg. Whatever humidity and temperature prevail in the gas outside the body, as soon as air is inspired and equilibrated with moist tracheal gas, it is rapidly fully saturated and is heated or cooled to body temperature. Water vapor is added to gases in the airways by the moist linings of the respiratory tract.
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 (PaO 2 ) ( Table 28-2 ). Nitrogen and oxygen are the only gases present in substantial concentration in dry air. Moist, warm tracheal air contains significant amounts of water vapor.
| 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 to 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 PaO 2 .
High-altitude environments are characterized by a decreased barometric pressure and 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 6 to 7 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 hereditary control.
Reduced Environmental Pressure
Acute awareness of the adverse effects of the low barometric pressure of high altitude 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 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 PaO 2 are shown in Figure 28-1 ; Figure 28-2 illustrates the approximate values for PaO 2 in inspired air, moist tracheal air, alveolar gas, and arterial and mixed venous blood. High altitude (HA) significantly affects the human body because of a decrease in the PaO 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 hypoxia 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. As a consequence, 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 PaO 2 in the range of 20 mm Hg, a profound depression of the central nervous system (CNS) is unmasked, and ventilatory drive is depressed.
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 hypoxia 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 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 hemoglobin concentration rise, the erythropoietin level decreases. Because of the sigmoid shape of the oxygen dissociation curve, up to 3000 m (9843 feet) of elevation, oxygen saturation is maintained; beyond 3000 m (9843 feet), the arterial PaO 2 falls steeply, resulting in lower oxygen saturation. Soon after the development of the hypoxic state, production of 2,3 diphosphoglycerate (2,3-DPG) increases, which shifts the hemoglobin dissociation curve to the right and allows for more effective extraction 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. HA 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 growth of blood vessels (vascular endothelial growth factor [VEGFA]) 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
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) acute mountain sickness, 2) high-altitude cerebral edema, 3) high-altitude pulmonary edema, 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 meters (1970 feet) per day ( Table 28-3 ).
| Syndrome | Special Features | Prevention | Clinical Features | Management |
|---|---|---|---|---|
| Mild acute mountain sickness (AMS); includes high-altitude headache | Most recover | Slow ascent or staging ∗ ; acetazolamide † | 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 ∗ ; acetazolamide † | 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 ∗ ; acetazolamide † | 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 by titration to response, or 10 mg PO once, followed by 30-mg 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 |
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
