Guyton and Hall Physiology Chapter 44 - Aviation, High Altitude, and Space Physiology PDF

CHAPTER 44 UNIT VIII Aviation, High Altitude, and Space Physiology As h...

CHAPTER 44 UNIT VIII Aviation, High Altitude, and Space Physiology As humans have ascended to higher and higher altitudes 760 to 253 mm Hg, which is the usual measured value in aviation, mountain climbing, and space exploration, it at the top of 29,028-foot Mount Everest. Of this, 47 mm has become progressively more important to understand Hg must be water vapor, leaving only 206 mm Hg for all the effects of altitude and low gas pressures on the human the other gases. In the acclimatized person, 7 mm Hg of body. This chapter deals with these problems and accelera- the 206 mm Hg must be CO2, leaving only 199 mm Hg. tory forces, weightlessness, and other challenges to body If there were no use of O2 by the body, one-fifth of this homeostasis that occur at high altitudes and in space flight. 199 mm Hg would be O2 and four-fifths would be nitro- gen—that is, the Po2 in the alveoli would be 40 mm Hg. EFFECTS OF LOW OXYGEN PRESSURE However, some of this remaining alveolar O2 is continu- ON THE BODY ally being absorbed into the blood, leaving about 35 mm Hg O2 pressure in the alveoli. At the summit of Mount Barometric Pressures at Different Altitudes. Table Everest, only the best acclimatized people can barely sur- 44-1 lists the approximate barometric and oxygen pres- vive when breathing air. However, the effect is very differ- sures at different altitudes, showing that at sea level, the ent when the person is breathing pure O2, as we see in the barometric pressure is 760 mm Hg; at 10,000 feet, it is following discussions. only 523 mm Hg; and at 50,000 feet, it is 87 mm Hg. This decrease in barometric pressure is the basic cause of all Alveolar Po2 at Different Altitudes. The fifth column the hypoxia problems in high-altitude physiology, because of Table 44-1 shows the approximate Po2 values in the as the barometric pressure decreases, the atmospheric alveoli at different altitudes when one is breathing air for oxygen partial pressure (Po2) decreases proportionately, both the unacclimatized and the acclimatized person. At remaining at all times slightly less than 21% of the total sea level, the alveolar Po2 is 104 mm Hg. At 20,000 feet barometric pressure; at sea level, Po2 is about 159 mm Hg, altitude, it falls to about 40 mm Hg in the unacclimatized but at 50,000 feet, Po2 is only 18 mm Hg. person but only to 53 mm Hg in the acclimatized per- son. The reason for the difference between these two is that alveolar ventilation increases much more in the ac- ALVEOLAR PO2 AT DIFFERENT ELEVATIONS climatized person than in the unacclimatized person, as Carbon Dioxide and Water Vapor Decrease the Alveo- we discuss later. lar Oxygen. Even at high altitudes, carbon dioxide (CO2) is continually excreted from the pulmonary blood into the al- Saturation of Hemoglobin With Oxygen at Different veoli. In addition, water vaporizes into the inspired air from Altitudes. Figure 44-1 shows arterial blood O2 satura- the respiratory surfaces. These two gases dilute the O2 in tion at different altitudes while a person is breathing air the alveoli, thus reducing the O2 concentration. Water va- and while breathing O2. Up to an altitude of about 10,000 por pressure in the alveoli remains at 47 mm Hg as long as feet, even when air is breathed, the arterial O2 saturation the body temperature is normal, regardless of altitude. remains at least as high as 90%. Above 10,000 feet, the In the case of CO2, during exposure to very high alti- arterial O2 saturation falls rapidly, as shown by the blue tudes, the alveolar partial pressure of CO2 (Pco2) falls curve of the figure, until it is slightly less than 70% at from the sea level value of 40 mm Hg to lower values. 20,000 feet and much less at still higher altitudes. In the acclimatized person, who increases ventilation about fivefold, the Pco2 falls to about 7 mm Hg because EFFECT OF BREATHING PURE OXYGEN ON of increased respiration. ALVEOLAR PO2 AT DIFFERENT ALTITUDES Now let us see how the pressures of these two gases affect the alveolar O2. For example, assume that the baro- When a person breathes pure O2 instead of air, most of the metric pressure falls from the normal sea level value of space in the alveoli formerly occupied by nitrogen becomes 553 UNIT VIII Aviation, Space, and Deep-Sea Diving Physiology Table 44-1 Effects of Acute Exposure to Low Atmospheric Pressures on Alveolar Gas Concentrations and Arterial Oxygen Saturationa Breathing Air Breathing Pure Oxygen Barometric PCO2 in PO2 in Arterial PCO2 in PO2 in Arterial Altitude Pressure PO2 in Air Alveoli Alveoli Oxygen Alveoli Alveoli Oxygen (ft/m) (mm Hg) (mm Hg) (mm Hg) (mm Hg) Saturation (%) (mm Hg) (mm Hg) Saturation (%) 0 760 159 40 (40) 104 (104) 97 (97) 40 673 100 10,000/3048 523 110 36 (23) 67 (77) 90 (92) 40 436 100 20,000/6096 349 73 24 (10) 40 (53) 73 (85) 40 262 100 30,000/9144 226 47 24 (7) 18 (30) 24 (38) 40 139 99 40,000/12,192 141 29 36 58 84 50,000/15,240 87 18 24 16 15 aNumbers in parentheses are acclimatized values. when breathing pure O2, is about 47,000 feet, provided Arterial oxygen saturation (percent) that the equipment supplying the O2 operates perfectly. 100 Breathing pure oxygen ACUTE EFFECTS OF HYPOXIA 90 Some of the important acute effects of hypoxia in the unacclimatized person breathing air, beginning at an 80 altitude of about 12,000 feet, are drowsiness, lassitude, Breathing air mental and muscle fatigue, sometimes headache, occa- 70 sionally nausea, and sometimes euphoria. These effects progress to a stage of twitchings or seizures above 18,000 60 feet and, above 23,000 feet in the unacclimatized person, end in coma, followed shortly thereafter by death. 50 0 10 20 30 40 50 One of the most important effects of hypoxia is Altitude (thousands of feet) decreased mental proficiency, which decreases judgment, memory, and performance of discrete motor movements. Figure 44-1. Effect of high altitude on arterial oxygen saturation when breathing air or pure oxygen. For example, if an unacclimatized aviator stays at 15,000 feet for 1 hour, mental proficiency ordinarily falls to about 50% of normal and, after 18 hours at this level, it falls to occupied by O2. At 30,000 feet, an aviator could have an about 20% of normal. alveolar Po2 as high as 139 mm Hg instead of 18 mm Hg when breathing air (see Table 44-1). ACCLIMATIZATION TO LOW PO2 The red curve of Figure 44-1 shows arterial blood hemoglobin O2 saturation at different altitudes when A person remaining at high altitudes for days, weeks, or a person is breathing pure O2. Note that the saturation years becomes more and more acclimatized to the low remains above 90% until the aviator ascends to about Po2, so it causes fewer deleterious effects on the body. 39,000 feet; then it falls rapidly to about 50% at about After acclimatization, it becomes possible for the person 47,000 feet. to work harder without hypoxic effects or to ascend to still higher altitudes. The “Ceiling” When Breathing Air and When Breath- The principal means whereby acclimatization comes ing Oxygen in an Unpressurized Airplane. When about are as follows: (1) a great increase in pulmonary comparing the two arterial blood O2 saturation curves ventilation; (2) increased numbers of red blood cells; (3) in Figure 44-1, one notes that an aviator breathing pure increased diffusing capacity of the lungs; (4) increased O2 in an unpressurized airplane can ascend to far higher vascularity of the peripheral tissues; and (5) increased altitudes than one breathing air. For example, the arte- ability of the tissue cells to use O2, despite low Po2. rial saturation at 47,000 feet when one is breathing O2 is about 50% and is equivalent to the arterial O2 saturation at Increased Pulmonary Ventilation—Role of Arterial 23,000 feet when one is breathing air. In addition, because Chemoreceptors. Immediate exposure to low Po2 stim- an unacclimatized person usually can remain conscious ulates the arterial chemoreceptors, and this stimulation until the arterial O2 saturation falls to 50%, the ceiling increases alveolar ventilation to a maximum of about 1.65 for an aviator for short exposure times in an unpressur- times normal. Therefore, compensation occurs within ized airplane when breathing air is about 23,000 feet and, seconds for the high altitude, and this alone allows the 554  Chapter 44 Aviation, High Altitude, and Space Physiology person to rise several thousand feet higher than would be Part of the increase results from increased pulmonary possible without the increased ventilation. If the person capillary blood volume, which expands the capillaries and remains at a very high altitude for several days, the chem- increases the surface area through which O2 can diffuse oreceptors increase ventilation still more, up to about five into the blood. Another part of this increase results from UNIT VIII times normal. an increase in lung air volume, which expands the sur- The immediate increase in pulmonary ventilation on face area of the alveolar-capillary interface still more. A rising to a high altitude blows off large quantities of CO2, final part results from an increase in pulmonary arterial reducing the Pco2 and increasing the pH of the body blood pressure, which forces blood into greater numbers fluids. These changes inhibit the brain stem respiratory of alveolar capillaries than normal, especially in the upper center and thereby oppose the effect of low Po2 to stimu- parts of the lungs, which are poorly perfused under usual late respiration via the peripheral arterial chemoreceptors conditions. in the carotid and aortic bodies. However, this inhibition fades away during the ensuing 2 to 5 days, allowing the Peripheral Circulatory System Changes During Accli- respiratory center to respond with full force to the periph- matization—Increased Tissue Capillarity. The cardiac eral chemoreceptor stimulus from hypoxia, and ventila- output often increases as much as 30% immediately af- tion increases to about five times normal. ter a person ascends to a high altitude but then decreases The cause of this fading inhibition is believed to be back toward normal over a period of weeks as the blood mainly a reduction of bicarbonate ion concentration in hematocrit increases, so the amount of O2 transported to the cerebrospinal fluid, as well as in the brain tissues. This the peripheral body tissues remains about normal. reduction, in turn, decreases the pH in the fluids sur- Another circulatory adaptation is growth of increased rounding the chemosensitive neurons of the respiratory numbers of systemic circulatory capillaries in the non- center, thus increasing the respiratory stimulatory activity pulmonary tissues, called angiogenesis. This adaptation of the center. occurs especially in animals born and bred at high alti- An important mechanism for the gradual decrease in tudes but less so in animals that become exposed to high bicarbonate concentration is compensation by the kid- altitudes later in life. neys for the respiratory alkalosis, as discussed in Chapter In active tissues exposed to chronic hypoxia, the 31. The kidneys respond to decreased Pco2 by reduc- increase in capillarity is especially marked. For example, ing hydrogen ion secretion and increasing bicarbonate capillary density in right ventricular muscle increases excretion. This metabolic compensation for the respira- markedly because of the combined effects of hypoxia and tory alkalosis gradually reduces plasma and cerebrospinal excess workload on the right ventricle caused by pulmo- fluid bicarbonate concentrations and pH toward normal nary hypertension at high altitude. and removes part of the inhibitory effect on respiration of a low hydrogen ion concentration. Thus, the respira- Cellular Acclimatization. In animals native to altitudes tory centers are much more responsive to the peripheral of 13,000 to 17,000 feet, cell mitochondria and cellular chemoreceptor stimulus caused by the hypoxia after the oxidative enzyme systems are slightly more plentiful than kidneys compensate for the alkalosis. in sea level inhabitants. Therefore, it is presumed that the tissue cells of high altitude–acclimatized human beings Increase in Red Blood Cells and Hemoglobin Con- also can use O2 more effectively than can their sea level centration During Acclimatization. As discussed in counterparts. Chapter 33, hypoxia is a major stimulus for increasing red HYPOXIA-INDUCIBLE FACTORS—A blood cell production. Ordinarily, when a person remains “MASTER SWITCH” FOR THE BODY’S exposed to low O2 for weeks at a time, the hematocrit RESPONSE TO HYPOXIA rises slowly from a normal value of 40% to 45% to an aver- age of about 60%, with an average increase in whole blood Hypoxia-inducible factors (HIFs) are DNA-binding hemoglobin concentration from a normal value of 15 g/dl transcription factors that respond to decreased oxygen to about 20 g/dl. availability and activate several genes that encode pro- In addition, the blood volume also increases, often by teins needed for adequate oxygen delivery to tissues and 20% to 30%, and this increase, multiplied by the increased energy metabolism. HIFs are found in virtually all oxygen- blood hemoglobin concentration, gives an increase in breathing species, ranging from primitive worms to total body hemoglobin of 50% or more. humans. Some of the genes controlled by HIFs, especially HIF-1, include the following: Increased Diffusing Capacity After Acclimatization.
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VUJMJ[B- occurs at high altitudes. tion 555 UNIT VIII Aviation, Space, and Deep-Sea Diving Physiology 28 Mountain dwellers Table 44-2 Differences in Work Capacities Quantity of oxygen in blood (vol %) 26 (15,000 ft) Work Capacity 24 (% of Normal) (Arterial values) 22 X Unacclimatized 50 20 X 18 Acclimatized for 2 months 68 X Sea-level dwellers 16 X 14 Native living at 13,200 feet but 87 (Venous values) working at 17,000 feet 12 10 8 6 at a high altitude is only 40 mm Hg but, because of the 4 greater quantity of hemoglobin, the quantity of O2 in 2 their arterial blood is greater than that in the blood of the 0 natives at the lower altitude. Note also that the venous 0 20 40 60 80 100 120 140 Po2 in the high-altitude natives is only 15 mm Hg less Pressure of oxygen in blood (PO2) (mm Hg) than the venous Po2 for the lowlanders, despite the very Figure 44-2. Oxygen-hemoglobin dissociation curves for blood of low arterial Po2, indicating that O2 transport to the tis- high-altitude residents (red curve) and sea level residents (blue curve) sues is exceedingly effective in the naturally acclimatized showing the respective arterial and venous PO2 levels and oxygen high-altitude natives. contents as recorded in their native surroundings. (Data from Pan American Health Organization. Oxygen-dissociation curves for bloods REDUCED WORK CAPACITY AT HIGH of high-altitude and sea-level residents. Life at high altitudes. Wash- ington, DC: Pan American Health Organization Scientific Publication ALTITUDES AND POSITIVE EFFECT OF No. 140, 1966.) ACCLIMATIZATION In addition to the mental depression caused by hypoxia,
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Thus, naturally acclimatized native body to respond appropriately to hypoxia. persons can achieve a daily work output even at a high altitude almost equal to that of a lowlander at sea level, NATURAL ACCLIMATIZATION OF NATIVE but even well-acclimatized lowlanders can almost never PEOPLE LIVING AT HIGH ALTITUDES achieve this result. Many native people in the Andes and in the Himalayas ACUTE MOUNTAIN SICKNESS AND HIGH- live at altitudes above 13,000 feet. One group in the Peru- ALTITUDE PULMONARY EDEMA vian Andes lives at an altitude of 17,500 feet and works in a mine at an altitude of 19,000 feet. Many of these natives A small percentage of people who ascend rapidly to high are born at these high altitudes and live there all their altitudes become acutely sick and can die if not given O2 lives. They are superior to even the best-acclimatized or rapidly moved to a low altitude. The sickness begins lowlanders in all aspects of acclimatization, even though from a few hours up to about 2 days after ascent. Two the lowlanders might have lived at high altitudes for 10 events frequently occur: or more years. Acclimatization of the natives begins in 1. Acute cerebral edema. This edema is believed to infancy. The chest size, especially, is greatly increased, result from local vasodilation of the cerebral blood whereas the body size is somewhat decreased, giving a vessels, which is caused by the hypoxia. Dilation of high ratio of ventilatory capacity to body mass. The hearts the arterioles increases blood flow into the capillar- of natives, which from birth onward pump extra amounts ies, thus increasing capillary pressure, which in turn of cardiac output, are also considerably larger than the causes fluid to leak into the cerebral tissues. Chemi- hearts of lowlanders. cal factors such as vascular endothelial growth fac- Delivery of O2 by the blood to the tissues is also highly tor and inflammatory cytokines may also contribute facilitated in these natives. For example, Figure 44-2 to edema by increasing endothelial cell permeabil- shows O2-hemoglobin dissociation curves for natives ity. The cerebral edema can then lead to severe diso- who live at sea level and for their counterparts who live rientation and other effects related to cerebral dys- at 15,000 feet. Note that the arterial Po2 in the natives function. 556  Chapter 44 Aviation, High Altitude, and Space Physiology 2. Acute pulmonary edema. The cause of acute pul- Effects of Acceleratory Forces on the Body in monary edema is still uncertain, but may be ex- Aviation and Space Physiology plained by the following. The severe hypoxia caus- Because of rapid changes in velocity and direction of mo- es the pulmonary arterioles to constrict powerfully, tion in airplanes or spacecraft, several types of acceleratory UNIT VIII but the constriction is much greater in some parts forces affect the body during flight. At the beginning of of the lungs than in other parts, so more and more flight, simple linear acceleration occurs, at the end of flight, of the pulmonary blood flow is forced through few- deceleration occurs, and every time the vehicle turns, cen- er and fewer still unconstricted pulmonary vessels. trifugal acceleration occurs. The postulated result is that the capillary pressure Centrifugal Acceleratory Forces in these areas of the lungs becomes especially high, When an airplane makes a turn, the force of centrifugal ac- and local edema occurs. Extension of the process celeration is determined by the following relationship: to progressively more areas of the lungs leads to spreading pulmonary edema and severe pulmo- mv2 f= nary dysfunction that can be lethal. Allowing the r person to breathe O2 usually reverses the process in which f is centrifugal acceleratory force, m is the mass within hours. The same chemical factors that have of the object, v is velocity of travel, and r is the radius of been suggested to increase capillary permeability curvature of the turn. From this formula, it is obvious that in the brain may also contribute to increased pul- as the velocity increases, the force of centrifugal accelera- tion increases in proportion to the square of the velocity. It monary capillary permeability and edema in the is also obvious that the force of acceleration is directly pro- lungs. portional to the sharpness of the turn (the less the radius). CHRONIC MOUNTAIN SICKNESS Measurement of Acceleratory Force—“G.” When an aviator is simply sitting in his seat, the force with which he Occasionally, a person who remains at a high altitude too or she is pressing against the seat results from the pull of long experiences chronic mountain sickness, in which the gravity and is equal to the person’s weight. The intensity following effects occur: PG
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because of the lung hypoxia. This vasoconstriction immobilized standing position, the pressure in the veins of results from the hypoxic vascular constrictor effect the feet becomes greatly increased (to ≈450 mm Hg). In the that normally operates to divert blood flow from sitting position, the pressure becomes nearly 300 mm Hg. In low-O2 to high-O2 alveoli, as explained in Chapter addition, as pressure in the vessels of the lower body increas- 39. However, because all the alveoli are now in the es, these vessels passively dilate so that a major portion of low-O2 state, all the arterioles become constricted, the blood from the upper body is translocated into the lower the pulmonary arterial pressure rises excessively, vessels. Because the heart cannot pump unless blood returns and the right side of the heart fails. to it, the greater the quantity of blood “pooled” in this way 3. The alveolar arteriolar spasm diverts much of the in the lower body, the less is available for the cardiac output. blood flow through nonalveolar pulmonary vessels, Figure 44-3 shows the changes in systolic and diastolic thus causing an excess of pulmonary shunt blood arterial pressures (top and bottom curves, respectively) in the upper body when a centrifugal acceleratory force of flow where the blood is poorly oxygenated, which 
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further compounds the problem. Most people with both these pressures fall below 22 mm Hg for the first few this condition recover within days or weeks when seconds after the acceleration begins but then return to a they are moved to a lower altitude. 557 UNIT VIII Aviation, Space, and Deep-Sea Diving Physiology 10 Arterial pressure (mm Hg) 100 8 Acceleration (G) 50 6 0 0 5 10 15 20 25 30 Time from start of G to symptoms 4 (sec) Figure 44-3. Changes in systolic (top of curve) and diastolic (bottom 2 of curve) arterial pressures after abrupt and continuing exposure of a sitting person to an acceleratory force from top to bottom of 3.3 G. First Second Space (Data from Martin EE, Henry JP: Effects of time and temperature upon booster booster ship 0 tolerance to positive acceleration. J Aviation Med 22:382, 1951.) 0 1 2 3 4 5 Minutes systolic pressure of about 55 mm Hg and a diastolic pres- Figure 44-4. Acceleratory forces during takeoff of a spacecraft. sure of 20 mm Hg within another 10 to 15 seconds. This secondary recovery is caused mainly by activation of the iBOUJ
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causing intense momentary hyperemia of the head. Occa- Acceleratory Forces in Space Travel. Unlike an airplane, sionally, psychotic disturbances lasting for 15 to 20 minutes a spacecraft cannot make rapid turns, and therefore cen- occur as a result of brain edema. trifugal acceleration is of little importance except when the 0DDBTJPOBMMZ
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a person traveling at a speed of Mach 100 (a speed possi- tightens his or her abdominal muscles to an extreme degree ble in interplanetary space travel) would require a distance and leans forward to compress the abdomen, some of the of about 10,000 miles for safe deceleration. The principal pooling of blood in the large vessels of the abdomen can reason for this difference is that the total amount of energy be prevented, delaying the onset of blackout. Also, special that must be dispelled during deceleration is proportional 558  Chapter 44 Aviation, High Altitude, and Space Physiology to the square of the velocity, which alone increases the re- Weightlessness (Microgravity) in Space quired distance for decelerations between Mach 1 versus A person in an orbiting satellite or a nonpropelled Mach 100 by about 10,000-fold. Therefore, deceleration spacecraft experiences weightlessness, or a state of near- must be accomplished much more slowly from a high ve- [FSP
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microgravity. That is, locity than from a lower velocity. UNIT VIII the person is not drawn toward the bottom, sides, or Deceleratory Forces Associated With Parachute Jumps. top of the spacecraft but simply floats inside its cham- When the parachuting aviator leaves the airplane, the ve- bers. The cause of this weightlessness is not failure of locity of fall is at first exactly 0 feet/sec. However, because gravity to pull on the body because gravity from any of the acceleratory force of gravity, within 1 second the ve- nearby heavenly body is still active. However, the grav- locity of fall is 32 feet/sec (if there is no air resistance), in ity acts on the spacecraft and the person at the same 2 seconds it is 64 feet/sec, and so on. As the velocity of fall time so that both are pulled with exactly the same ac- increases, the air resistance tending to slow the fall also in- celeratory forces and in the same direction. For this creases. Finally, the deceleratory force of the air resistance reason, the person simply is not attracted toward any exactly balances the acceleratory force of gravity, so after specific wall of the spacecraft. falling for about 12 seconds, the person will be falling at a Physiological Challenges of Weightlessness (Micro- terminal velocity of 109 to 119 miles/ hour (175 feet/sec). gravity). The physiological challenges of weightlessness If the parachutist has already reached terminal velocity be- have not proved to be of much significance as long as the fore opening the parachute, an “opening shock load” of up period of weightlessness is not too long. Most of the prob- to 1200 pounds could occur on the parachute shrouds. lems that do occur are related to three effects of the weight- The usual-sized parachute slows the fall of the parachut- lessness: (1) motion sickness during the first few days of ist to about one ninth the terminal velocity. In other words, travel; (2) translocation of fluids within the body because the speed of landing is about 20 feet/sec, and the force of of failure of gravity to cause normal hydrostatic pressures; impact against the earth is 1/81, the impact force without a and (3) diminished physical activity because no strength parachute. Even so, the force of impact is still great enough of muscle contraction is required to oppose the force of to cause considerable damage to the body unless the par- gravity. achutist is properly trained in landing. Actually, the force Almost 50% of astronauts experience motion sickness, of impact with the earth is about the same as that which with nausea and sometimes vomiting, during the first 2 to would be experienced by jumping without a parachute from 5 days of space travel. This motion sickness probably results a height of about 6 feet. Unless forewarned, the parachutist from an unfamiliar pattern of motion signals arriving in the will be tricked by her or his senses into striking the earth equilibrium centers of the brain and, at the same time, lack with extended legs, and this position, on landing, will result of gravitational signals. in tremendous deceleratory forces along the skeletal axis of The observed effects of a prolonged stay in space the body, resulting in fracture of his pelvis, vertebrae, or leg. are the following: (1) decrease in blood volume; (2) de- Consequently, the trained parachutist strikes the earth with crease in red blood cell mass; (3) decrease in muscle knees bent but muscles taut to cushion the shock of landing. strength and work capacity; (4) decrease in maximum cardiac output; and (5) loss of calcium and phosphate “Artificial Climate” in the Sealed Spacecraft from the bones, as well as loss of bone mass. Most of Because there is no atmosphere in outer space, an artificial these same effects also occur in people who lie in bed atmosphere and climate must be produced in a spacecraft. for an extended period. For this reason, exercise pro- Most importantly, the O2 concentration must remain high grams are carried out by astronauts during prolonged enough and the CO2 concentration low enough to prevent space missions. suffocation. In some earlier space missions, a capsule at- In previous space laboratory expeditions, in which the mosphere containing pure O2 at about 260 mm Hg pressure exercise program was less vigorous, the astronauts had se- was used but, in modern space travel, gases about equal to verely decreased work capacities for the first few days after those in normal air are used, with four times as much nitro- returning to Earth. They also tended to faint (and still do, to gen as O2 and a total pressure of 760 mm Hg. The presence some extent) when they stood up during the first day or so of nitrogen in the mixture greatly diminishes the likelihood after return to gravity because of diminished blood volume of fire and explosion. It also protects against development and diminished responses of the arterial pressure control of local patches of lung atelectasis that often occur when mechanisms. Cardiovascular, Muscle, and Bone “Deconditioning” breathing pure O2 because O2 is absorbed rapidly when small bronchi are temporarily blocked by mucous plugs. During Prolonged Exposure to Weightlessness. Dur- For space travel lasting more than several months, it is ing very long space flights and prolonged exposure to impractical to carry along an adequate O2 supply. For this microgravity, gradual “deconditioning” effects occur on reason, recycling techniques have been proposed to use the the cardiovascular system, skeletal muscles, and bone, same O2 over and over again. Some recycling processes de- despite rigorous exercise during the flight. Studies of pend on purely physical procedures, such as electrolysis of astronauts on space flights lasting several months have water to release O2. Others depend on biological methods, shown that they may lose as much 1.0% of their bone such as use of algae with their large store of chlorophyll to mass each month, even though they continue to exer- release O2 from CO2 by the process of photosynthesis. A cise. Substantial atrophy of cardiac and skeletal muscles completely satisfactory system for recycling has yet to be also occurs during prolonged exposure to a microgravity achieved. environment. 559 UNIT VIII Aviation, Space, and Deep-Sea Diving Physiology One of the most serious effects is cardiovascular “de- Dunham-Snary KJ, Wu D, Sykes EA, et al: Hypoxic pulmonary va- conditioning,” which includes decreased work capacity, re- soconstriction: from molecular mechanisms to medicine. Chest duced blood volume, impaired baroreceptor reflexes, and 151:181, 2017. reduced orthostatic tolerance. These changes greatly limit Hackett PH, Roach RC: High-altitude illness. N Engl J Med 345:107, 2001. the astronaut’s ability to stand upright or perform normal Hargens AR, Bhattacharya R, Schneider SM. Space physiology VI: ex- daily activities after returning to the full gravitational force ercise, artificial gravity, and countermeasure development for pro- of Earth. longed space flight. Eur J Appl Physiol 113:2183, 2013. Astronauts returning from space flights lasting 4 to 6 Imray C, Wright A, Subudhi A, Roach R: Acute mountain sickness: months are also susceptible to bone fractures and may re- pathophysiology, prevention, and treatment. Prog Cardiovasc Dis quire several weeks before they return to preflight cardio- 52:467, 2010. vascular, bone, and muscle fitness. As space flights become Luks AM: Physiology in medicine: A physiologic approach to preven- longer in preparation for possible human exploration of tion and treatment of acute high-altitude illnesses. J Appl Physiol other planets, such as Mars, the effects of prolonged micro- 118:509, 2015. gravity could pose a very serious threat to astronauts after Moore LG: Measuring high-altitude adaptation. J Appl Physiol 123:1371, 2017. they land, especially in the event of an emergency landing. Penaloza D, Arias-Stella J: The heart and pulmonary circulation at Therefore, considerable research effort has been directed high altitudes: healthy highlanders and chronic mountain sickness. toward developing countermeasures, in addition to exer- Circulation 115:1132, 2007. cise, that can prevent or more effectively attenuate these Prabhakar NR, Semenza GL: Adaptive and maladaptive cardiorespira- changes. One such countermeasure that is being tested is tory responses to continuous and intermittent hypoxia mediated by the application of intermittent “artificial gravity” caused by hypoxia-inducible factors 1 and 2. Physiol Rev 92:967, 2012. short periods (e.g., 1 hour each day) of centrifugal accelera- Prabhakar NR, Semenza GL: Oxygen sensing and homeostasis. Physi- tion of the astronauts while they sit in specially designed ology (Bethesda) 30:340, 2015. TIPSU
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( Prisk GK: Pulmonary circulation in extreme environments. Compr Physiol 1:319, 2011. Swenson ER, Bärtsch P: High-altitude pulmonary edema. Compr Physiol 2:2753, 2012. Bibliography West JB: High-altitude medicine. Am J Respir Crit Care Med 186:1229, Bloomfield SA, Martinez DA, Boudreaux RD, Mantri AV: Microgravity 2012. stress: bone and connective tissue. Compr Physiol 6:645, 2016. West JB: physiological effects of chronic hypoxia. N Engl J Med Dekker MCJ, Wilson MH, Howlett WP: Mountain neurology. Pract 376:1965, 2017. Neurol 2019 Jun 8. pii: practneurol-2017-001783. https://www. Wilson MH, Imray CH: The cerebral venous system and hypoxia. J doi.org/10.1136/practneurol-2017-001783. Appl Physiol 120:244, 2016. 560