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 times normal. an increase in lung air volume, which expands the sur- UNIT VIII 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. Genes associated with vascular endothelial growth The normal diffusing capacity for O2 through the pul- factor, which stimulates angiogenesis monary membrane is about 21 ml/mm Hg per minute, Erythropoietin genes that stimulate red blood cell and this diffusing capacity can increase as much as 3-fold production during exercise. A similar increase in diffusing capacity Mitochondrial genes involved with energy utiliza- 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, Glycolytic enzyme genes involved with anaerobic the work capacity of all muscles, cardiac as well as skel- metabolism etal muscle, is greatly decreased in a state of hypoxia. In Genes that increase availability of nitric oxide, which general, work capacity is reduced in direct proportion to causes pulmonary vasodilation the decrease in maximum rate of O2 uptake that the body In the presence of adequate oxygen, the subunits of can achieve. HIF required to activate various genes are downregulated To give an idea of the importance of acclimatization in and inactivated by specific HIF hydroxylases. In hypoxia, increasing work capacity, consider the large differences in the HIF hydroxylases are themselves inactive, allowing work capacities as a percentage of normal for unacclima- the formation of a transcriptionally active HIF complex. tized and acclimatized people at an altitude of 17,000 feet, Thus, the HIFs serve as a “master switch” that permits the shown in Table 44-2. 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 but the constriction is much greater in some parts UNIT VIII 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: of this force is said to be +1 G because it is equal to the 1. The red blood cell mass and hematocrit become ex- pull of gravity. If the force with which the person presses ceptionally high. against the seat becomes five times the normal weight 2. The pulmonary arterial pressure becomes elevated during pull-out from a dive, the force acting on the seat even more than the normal elevation that occurs is +5 G. during acclimatization. If the airplane goes through an outside loop so that the person is held down by the seat belt, negative G is applied 3. The right side of the heart becomes greatly enlarged. to the body. If the force with which the person is held down 4. The peripheral arterial pressure begins to fall. by the seat belt is equal to the weight of the body, the nega- 5. Congestive heart failure ensues. tive force is −1 G.␣ 6. Death often follows unless the person is moved to a lower altitude. Effects of Centrifugal Acceleratory Force on the There are probably three main causes of this sequence Body (Positive G) of events: Effects on the Circulatory System. The most important 1. The red blood cell mass becomes so great that the effect of centrifugal acceleration is on the circulatory sys- blood viscosity increases severalfold. This increased tem because blood is mobile and can be translocated by viscosity tends to decrease tissue blood flow so that centrifugal forces. O2 delivery also begins to decrease. When an aviator is subjected to positive G, blood is cen- 2. The pulmonary arterioles become vasoconstricted trifuged toward the lowermost part of the body. Thus, if the centrifugal acceleratory force is +5 G and the person is in an 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 +3.3 G is suddenly applied to a sitting person. Note that 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 50 Acceleration (G) 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 “anti-G” suits have been developed to prevent pooling of baroreceptor reflexes. blood in the lower abdomen and legs. The simplest of these Acceleration greater than 4 to 6 G causes “blackout” of applies positive pressure to the legs and abdomen by inflat- vision within a few seconds and unconsciousness shortly ing compression bags as the G force increases. thereafter. If this great degree of acceleration is continued, Theoretically, a pilot submerged in a tank or suit of wa- the person will die.␣ ter might experience little effect of G forces on the circula- Effects on the Vertebrae. Extremely high acceleratory tion because the pressures developed in the water pressing forces for even a fraction of a second can fracture the ver- on the outside of the body during centrifugal acceleration tebrae. The degree of positive acceleration that the average would almost exactly balance the forces acting in the body. person can withstand in the sitting position before verte- However, the presence of air in the lungs still allows for dis- bral fracture occurs is about 20 G.␣ placement of the heart, lung tissues, and diaphragm into Negative G. The effects of negative G on the body are seriously abnormal positions despite submersion in water. less dramatic acutely but possibly more damaging perma- Therefore, even if this procedure were used, the limit of nently than the effects of positive G. An aviator can usually safety almost certainly would still be less than 10 G.␣ go through outside loops up to negative acceleratory forces Effects of Linear Acceleratory Forces on the Body of −4 to −5 G without causing permanent harm, although 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 Occasionally, negative G forces can be so great (e.g., spacecraft goes into abnormal gyrations. However, blast-off −20 G), and centrifugation of the blood into the head is so acceleration and landing deceleration can be tremendous; great, that the cerebral blood pressure reaches 300 to 400 both are types of linear acceleration, with one being posi- mm Hg, sometimes causing small vessels on the surface of tive and the other negative. the head and in the brain to rupture. However, the vessels Figure 44-4 shows an approximate profile of accelera- inside the cranium show less tendency for rupture than tion during blastoff in a three-stage spacecraft, demon- would be expected for the following reason. The cerebro- strating that the first-stage booster causes acceleration as spinal fluid is centrifuged toward the head at the same time high as 9 G and the second-stage booster as high as 8 G. that blood is centrifuged toward the cranial vessels, and the In the standing position, the human body could not with- greatly increased pressure of the cerebrospinal fluid acts as stand this much acceleration, but in a semireclining posi- a cushioning buffer on the outside of the brain to prevent tion transverse to the axis of acceleration, this amount of intracerebral vascular rupture. acceleration can be withstood easily, despite the fact that Because the eyes are not protected by the cranium, in- the acceleratory forces continue for as long as several min- tense hyperemia occurs in them during strong negative G. utes at a time. Therefore, the reason for the reclining seats As a result, the eyes often become temporarily blinded with used by astronauts can be understood. what is called redout.␣ Problems also occur during deceleration when the Protection of the Body Against Centrifugal Accelera- spacecraft re-enters the atmosphere. A person traveling at tory Forces. Specific procedures and apparatus have been Mach 1 (the speed of sound and of fast airplanes) can be developed to protect aviators against the circulatory col- safely decelerated in a distance of about 0.12 mile, whereas lapse that might occur during positive G. First, if the aviator 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- zero G force, sometimes called 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. short-arm centrifuges that create forces of up to 2 to 3 G. 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  CHAPTER 45 UNIT VIII Physiology of Deep-Sea Diving and Other Hyperbaric Conditions When people descend beneath the sea, the pressure NITROGEN NARCOSIS AT HIGH NITROGEN around them increases progressively as they go to greater PRESSURES depths. To keep the lungs from collapsing, air must be About four-fifths of the air is nitrogen. At sea level pressure, supplied at very high pressure to keep them inflated. This the nitrogen has no significant effect on bodily function, but maneuver exposes the blood in the lungs to extremely at high pressures, it can cause varying degrees of narcosis. high alveolar gas pressures, a condition called hyperba- When the diver remains beneath the sea for 1 hour or more rism. Beyond certain limits, these high pressures cause and is breathing compressed air, the depth at which the first major alterations in body physiology and can be lethal. symptoms of mild narcosis appear is about 120 feet. At this level, the diver begins to exhibit joviality and loss of many Relationship of Pressure to Sea Depth. A column of of his or her cares. At 150 to 200 feet, the diver becomes seawater 33 feet (10.1 meters) deep exerts the same pres- drowsy. At 200 to 250 feet, the person’s strength wanes con- sure at its bottom as the pressure of the atmosphere above siderably, and the diver often becomes too clumsy to per- the sea. Therefore, a person 33 feet beneath the ocean sur- form the work required. Beyond 250 feet (8.5 atm pressure), face is exposed to 2 atmospheres (2 atm) pressure, with 1 the diver usually becomes almost useless as a result of nitro- atm of pressure caused by the weight of the air above the gen narcosis if he or she remains at these depths too long. water and the second atmosphere caused by the weight of Nitrogen narcosis has characteristics similar to those of the water. At 66 feet, the pressure is 3 atm, and so forth, in alcohol intoxication, and for this reason it has frequently accord with the table in Figure 45-1.␣ been called “raptures of the depths.” The mechanism of this narcotic effect is believed to be the same as that of most other Effect of Sea Depth on the Volume of Gases—Boyle’s gas anesthetics. That is, it dissolves in the fatty substances Law. Another important effect of depth is the compres- in neuronal membranes and, because of its physical effect sion of gases to smaller and smaller volumes. The illustra- on altering ionic conductance through the membranes, it tion in Figure 45-1 shows a bell jar at sea level containing reduces neuronal excitability. Ascent to a shallower depth 1 liter of air. At 33 feet beneath the sea, where the pressure reverses the narcosis within a few minutes, with no known is 2 atm, the volume has been compressed to only a half- long-term effects if the ascent is not too rapid. ␣ liter, and at 8 atm (233 feet) it has been compressed to one- eighth liter. Thus, the volume to which a given quantity of gas is compressed is inversely proportional to the pressure. OXYGEN TOXICITY AT HIGH PRESSURES This principle of physics is called Boyle’s law, and it is ex- Effect of Very High Po2 on Blood Oxygen Transport. tremely important in diving physiology because increased When the PO2 in the blood rises above 100 mm Hg, the pressure can collapse the air chambers of the diver’s body, amount of O2 dissolved in the water of the blood increases especially the lungs, and may cause serious damage. markedly. This effect is shown in Figure 45-2, which de- Often in this chapter it is necessary to refer to actual vol- picts the same O2-hemoglobin dissociation curve as that ume versus sea level volume. For example, we might speak shown in Chapter 41 but with the alveolar PO2 extended of an actual volume of 1 liter at a depth of 300 feet; this is to more than 3000 mm Hg. Also depicted by the lowest the same quantity of air as a sea level volume of 10 liters.␣ curve in the figure is the volume of O2 dissolved in the fluid of the blood at each PO2 level. Note that in the normal EFFECT OF HIGH PARTIAL PRESSURES range of alveolar PO2 ( ≈2 atm PO2), the 0 hemoglobin-O2 buffering mechanism fails, and the tissue 0 760 1560 2280 3040 PO2 can then rise to hundreds or thousands of mm Hg. At Oxygen partial pressure in lungs (mm Hg) these high levels, the amounts of oxidizing free radicals Figure 45-2. Quantity of O2 dissolved in the fluid of the blood and in literally swamp the enzyme systems designed to remove combination with hemoglobin at very high PO2 values. them, and now they can have serious destructive and even 562  Chapter 45 Physiology of Deep-Sea Diving and Other Hyperbaric Conditions lethal effects on the cells. One of the principal effects is same high pressure as that in the alveolar breathing mixture, to oxidize the polyunsaturated fatty acids that are essen- and over several more hours, enough nitrogen is carried to tial components of many of the cell membranes. Another all the tissues of the body to raise their tissue nitrogen partial effect is to oxidize some of the cellular enzymes, thus dam- pressure to equal the nitrogen pressure in the breathing air. aging the cellular metabolic systems severely. The nervous Because nitrogen is not metabolized by the body, it UNIT VIII tissues are especially susceptible because of their high remains dissolved in all the body tissues until the nitro- lipid content. Therefore, most of the acute lethal effects of gen pressure in the lungs is decreased back to some lower acute O2 toxicity are caused by brain dysfunction.␣ level, at which time the nitrogen can be removed by the reverse respiratory process. However, this removal often Chronic Oxygen Poisoning Causes Pulmonary Disa- takes hours to occur and is the source of multiple prob- bility. A person can be exposed to only 1 atm pressure of lems, collectively called decompression sickness. O2 almost indefinitely without developing the acute oxy- gen toxicity of the nervous system just described. How- Volume of Nitrogen Dissolved in the Body Fluids at ever, after only about 12 hours of 1 atm O2 exposure, lung Different Depths. At sea level, almost exactly 1 liter of passageway congestion, pulmonary edema, and atelectasis nitrogen is dissolved in the entire body. Slightly less than caused by damage to the linings of the bronchi and al- one-half of this nitrogen is dissolved in the water of the veoli begin to develop. The reason for this effect in the body, and a little more than one-half is dissolved in the fat lungs but not in other tissues is that the air spaces of the of the body, because nitrogen is five times as soluble in fat lungs are directly exposed to the high O2 pressure, but O2 as in water. is delivered to the other body tissues at almost normal Po2 After the diver has become saturated with nitrogen, because of the hemoglobin-O2 buffer system.␣ the sea level volume of nitrogen dissolved in the body at different depths is as follows: CARBON DIOXIDE TOXICITY AT GREAT DEPTHS IN THE SEA Feet Liters 0 1 If the diving gear is properly designed and functions 33 2 properly, the diver has no problem due to toxicity because depth alone does not increase the CO2 partial 100 4 pressure in the alveoli. This is true because depth does 200 7 not increase the rate of CO2 production in the body, and 300 10 as long as the diver continues to breathe a normal tidal volume and expires the CO2 as it is formed, alveolar CO2 Several hours are required for the gas pressures of pressure will be maintained at a normal value. nitrogen in all the body tissues to come nearly to equilib- In certain types of diving gear, however, such as the rium with the gas pressure of nitrogen in the alveoli. The diving helmet and some types of rebreathing appara- reason for this requirement is that the blood does not flow tuses, CO2 can build up in the dead space air of the appa- rapidly enough, and the nitrogen does not diffuse rapidly ratus and be rebreathed by the diver. Up to an alveolar enough, to cause instantaneous equilibrium. The nitrogen CO2 pressure (PCO2) of about 80 mm Hg, twice that in dissolved in the water of the body comes to almost com- normal alveoli, the diver usually tolerates this buildup by plete equilibrium in less than 1 hour, but the fat tissue, increasing the minute respiratory volume a maximum which requires five times as much transport of nitrogen of 8- to 11-fold to compensate for the increased CO2. and has a relatively poor blood supply, reaches equilib- Beyond 80 mm Hg alveolar PCO2, however, the situation rium only after several hours. Thus, if a person remains becomes intolerable, and eventually the respiratory cen- under water at a deep level for only a few minutes, not ter begins to be depressed, rather than excited, because much nitrogen dissolves in the body fluids and tissues, of the negative tissue metabolic effects of high PCO2. The whereas if the person remains at a deep level for several diver’s respiration then begins to fail rather than com- hours, both the body water and body fat become satu- pensate. In addition, the diver experiences severe respi- rated with nitrogen.␣ ratory acidosis and varying degrees of lethargy, narcosis, and finally even anesthesia, as discussed in Chapter 43.␣ Decompression Sickness (Also Known as Bends, Com- pressed Air Sickness, Caisson Disease, Diver’s Paraly- sis, Dysbarism). If a diver has been beneath the sea long DECOMPRESSION OF THE DIVER AFTER enough that large amounts of nitrogen have dissolved in EXCESS EXPOSURE TO HIGH PRESSURE the body, and the diver then suddenly comes back to the When a person breathes air under high pressure for a long surface of the sea, significant quantities of nitrogen bub- time, the amount of nitrogen dissolved in the body fluids bles can develop in the body fluids, either intracellularly increases. This is because blood flowing through the pul- or extracellularly, and can cause minor or serious damage monary capillaries becomes saturated with nitrogen to the in almost any area of the body, depending on the number 563 UNIT VIII Aviation, Space, and Deep-Sea Diving Physiology Pressure Outside Body vessels are affected. Tissue ischemia and sometimes tissue Before After sudden death result. decompression decompression In most people with decompression sickness, the O2 = 1044 mm Hg O2 = 159 mm Hg symptoms are pain in the joints and muscles of the legs N2 = 3956 N2 = 601 and arms, affecting 85% to 90% of persons who experience Total = 5000 mm Hg Total = 760 mm Hg decompression sickness. The joint pain accounts for the term “bends” that is often applied to this condition. In 5% to 10% of people with decompression sickness, nervous system symptoms occur, ranging from dizziness in about 5% to paralysis or collapse and unconsciousness in as many as 3%. The paralysis may be temporary, but in some cases, damage is permanent. Finally, about 2% of people with decompression sick- Body Body ness experience “the chokes,” caused by massive numbers of Gaseous pressure Gaseous pressure microbubbles plugging the capillaries of the lungs. This con- in the body fluids in the body fluids dition is characterized by serious shortness of breath, often H2O = 47 mm Hg H2O = 47 mm Hg followed by severe pulmonary edema and, occasionally, death.␣ CO2 = 40 CO2 = 40 O2 = 60 O2 = 60 N2 = 3918 N2 = 3918 Nitrogen Elimination From the Body; Decompression Total = 4065 Total = 4065 Tables. If a diver is brought to the surface slowly, enough A B of the dissolved nitrogen can usually be eliminated by Figure 45-3. Gaseous pressures inside and outside the body show- expiration through the lungs to prevent decompression ing (A) saturation of the body to high gas pressures when breathing air at a total pressure of 5000 mm Hg and (B) the great excesses of sickness. About two-thirds of the total nitrogen is liber- intrabody pressures responsible for bubble formation in the tissues ated in 1 hour, and about 90% is liberated in 6 hours. when the lung intra-alveolar pressure body is suddenly returned from Tables that detail procedures for safe decompression 5000 mm Hg to the normal pressure of 760 mm Hg. have been prepared by the US Navy. To give the reader an idea of the decompression process, a diver who has and sizes of bubbles formed. This phenomenon is called been breathing air and has been on the sea bottom for 60 decompression sickness. minutes at a depth of 190 feet undergoes decompression The principles underlying bubble formation are shown according to the following schedule: in Figure 45-3. In Figure 45-3A, the diver’s tissues have 10 minutes at 50-feet depth become equilibrated to a high dissolved nitrogen pressure 17 minutes at 40-feet depth (PN2 = 3918 mm Hg), about 6.5 times the normal amount 19 minutes at 30-feet depth of nitrogen in the tissues. As long as the diver remains deep 50 minutes at 20-feet depth beneath the sea, the pressure against the outside of the 84 minutes at 10-feet depth body (5000 mm Hg) compresses all the body tissues suffi- Thus, for a work period on the sea bottom of only 1 ciently to keep the excess nitrogen gas dissolved. However, hour, the total time for decompression is about 3 hours.␣ when the diver suddenly rises to sea level (Figure 45-3B), the pressure on the outside of the body becomes only 1 Tank Decompression and Treatment of Decompres- atm (760 mm Hg), while the gas pressure inside the body sion Sickness. Another procedure widely used for de- fluids is the sum of the pressures of water vapor, CO2, O2, compression of professional divers is to put the diver into and nitrogen, or a total of 4065 mm Hg, 97% of which is a pressurized tank and then gradually lower the pressure caused by the nitrogen. Obviously, this total value of 4065 back to normal atmospheric pressure, using essentially mm Hg is far greater than the 760-mm Hg pressure on the the same time schedule as noted earlier. outside of the body. Therefore, the gases can escape from Tank decompression is even more important for treating the dissolved state and form bubbles, composed almost people in whom symptoms of decompression sickness develop entirely of nitrogen, both in the tissues and in the blood, minutes or even hours after they have returned to the surface. where they plug many small blood vessels. The bubbles In this case, the diver undergoes recompression immediately may not appear for many minutes to hours because some- to a deep level, and then decompression is carried out over a times the gases can remain dissolved in the “supersatu- period several times as long as the usual decompression period.␣ rated” state for hours before bubbling.␣ “Saturation Diving” and Use of Helium-Oxygen Mix- Symptoms of Decompression Sickness (“Bends”). The tures in Deep Dives. When divers must work at very deep symptoms of decompression sickness are caused by gas levels—between 250 feet and nearly 1000 feet—they fre- bubbles blocking many blood vessels in different tissues. quently live in a large compression tank for days or weeks at a time, remaining compressed at a pressure level near At first, only the smallest vessels are blocked by minute that at which they will be working. This procedure keeps bubbles, but as the bubbles coalesce, progressively larger 564  Chapter 45 Physiology of Deep-Sea Diving and Other Hyperbaric Conditions the tissues and fluids of the body saturated with the gases to which they will be exposed while diving. Then, when they return to the same tank after working, there are no significant changes in pressure, so decompression bubbles Mask do not occur. UNIT VIII In very deep dives, especially during saturation diving, Hose helium is usually used in the gas mixture instead of nitro- gen for three reasons: (1) it has only about one-fifth the narcotic effect of nitrogen; (2) only about one-half as much Demand valve First-stage volume of helium dissolves in the body tissues as nitrogen, valve and the volume that does dissolve diffuses out of the tissues during decompression several times as rapidly as does ni- trogen, thus reducing the problem of decompression sick- ness; and (3) the low density of helium (one-seventh the density of nitrogen) keeps the airway resistance for breath- ing at a minimum, which is very important because highly compressed nitrogen is so dense that airway resistance can become extreme, sometimes making the work of breathing beyond endurance. Finally, in very deep dives, it is important to reduce the O2 concentration in the gaseous mixture because other- wise O2 toxicity would result. For example, at a depth of 700 feet (22 atm pressure), a 1% O2 mixture will provide all Air cylinders the O2 required by the diver, whereas a 21% mixture of O2 (the percentage in air) delivers a PO2 to the lungs of more than 4 atm, a level very likely to cause seizures in as little as 30 minutes.␣ Figure 45-4. Open-circuit demand type of SCUBA (self-contained underwater breathing apparatus). SELF-CONTAINED UNDERWATER BREATHING APPARATUS (SCUBA) the mask. Then, on expiration, the air cannot go back into DIVING the tank but, instead, is expired into the water. The most important problem with SCUBA is the lim- Before the 1940s, almost all diving was done using a diving ited amount of time a diver can remain beneath the water helmet connected to a hose through which air was pumped surface; For example, only a few minutes are possible at to the diver from the surface. Then, in 1943, the French a 200-foot depth. The reason for this limitation is that explorer Jacques Cousteau popularized a self-contained tremendous airflow from the tanks is required to wash underwater breathing apparatus, known as SCUBA. The CO2 out of the lungs—the greater the depth, the greater type of SCUBA used in more than 99% of all sports and the airflow in terms of quantity of air per minute required commercial diving is the open-circuit demand system because the volumes have been compressed to small sizes.␣ shown in Figure 45-4. This system consists of the follow- ing components: (1) one or more tanks of compressed air Special Physiological Problems in Submarines or some other breathing mixture; (2) a first-stage “reduc- ing” valve for reducing the very high pressure from the Escape From Submarines. Essentially the same prob- lems encountered in deep sea diving are often found in re- tanks to a low pressure level; (3) a combination inhala- lation to submarines, especially when it is necessary to es- tion “demand” valve and exhalation valve that allows air cape from a submerged submarine. Escape is possible from to be pulled into the lungs with slight negative pressure of as deep as 300 feet without use of any apparatus. However, breathing and then to be exhaled into the sea at a pressure proper use of rebreathing devices, especially when using level slightly positive to the surrounding water pressure; helium, can theoretically allow escape from as deep as 600 and (4) a mask and tube system with small “dead space.” feet or perhaps more. The demand system operates as follows. The first-stage One of the major problems of escape is prevention of reducing valve reduces the pressure from the tanks so air embolism. As the person ascends, the gases in the lungs that the air delivered to the mask has a pressure only a expand and sometimes rupture a pulmonary blood vessel, few mm Hg greater than the surrounding water pressure. forcing the gases to enter the vessel and cause air embolism The breathing mixture does not flow continually into the of the circulation. Therefore, as the person ascends, he or she must make a special effort to exhale continually.␣ mask. Instead, with each inspiration, slight extra negative Health Problems in the Submarine Internal Environ- pressure in the demand valve of the mask pulls the dia- ment. Except for escape, submarine medicine generally phragm of the valve open, and this action automatically centers on several engineering problems to keep hazards releases air from the tank into the mask and lungs. In this out of the internal environment. First, in atomic subma- way, only the amount of air needed for inhalation enters 565 UNIT VIII Aviation, Space, and Deep-Sea Diving Physiology rines, there is the problem of radiation hazards, but with 70 mm Hg. Therefore, hyperbaric oxygenation of the tis- appropriate shielding, the amount of radiation received by sues can frequently stop the infectious process entirely and the crew submerged beneath the sea has been less than the thus convert a condition that formerly was almost 100% normal amount of radiation received above the surface of fatal into one that is cured in most cases by early treatment the sea from cosmic rays. with hyperbaric therapy. Second, poisonous gases, on occasion, escape into Other conditions in which hyperbaric O2 therapy has the atmosphere of the submarine and must be controlled been either valuable or possibly valuable include decom- rapidly. For example, during several weeks’ submergence, pression sickness, arterial gas embolism, carbon monoxide cigarette smoking by the crew can liberate enough carbon poisoning, osteomyelitis, and myocardial infarction. monoxide, if not removed rapidly, to cause carbon monox- ide poisoning. On occasion, even Freon gas has been found to diffuse out of refrigeration systems in sufficient quantity Bibliography to cause toxicity.␣ Brubakk AO, Ross JA, Thom SR: Saturation diving; physiology and pathophysiology. Compr Physiol 4:1229, 2014. Hyperbaric Oxygen Therapy Castellini M: Life under water: physiological adaptations to diving and living at sea. Compr Physiol 2:1889, 2012. The intense oxidizing properties of high-pressure O2 (hy- Doolette DJ, Mitchell SJ: Hyperbaric conditions. Compr Physiol 1:163, perbaric oxygen) can have valuable therapeutic effects in 2011. several important clinical conditions. Therefore, large pres- Fitz-Clarke JR: Breath-hold diving. Compr Physiol 8:585, 2018. sure tanks are now available in many medical centers into Leach RM, Rees PJ, Wilmshurst P: Hyperbaric oxygen therapy. BMJ which patients can be placed and treated with hyperbaric 317:1140, 1998. O2. The O2 is usually administered at PO2 values of 2 to 3 Pendergast DR, Lundgren CE: The underwater environment: car- atm pressure through a mask or intratracheal tube, whereas diopulmonary, thermal, and energetic demands. J Appl Physiol the gas around the body is normal air compressed to the 106:276, 2009. same high-pressure level. Pendergast DR, Moon RE, Krasney JJ, et al: Human physiology in an aquatic environment. Compr Physiol 5:1705, 2015. The same oxidizing free radicals responsible for O2 toxicity Poff AM, Kernagis D, D’Agostino DP: Hyperbaric environment: oxy- are also believed to be responsible for at least some of the ther- gen and cellular damage versus protection. Compr Physiol 7:213, apeutic benefits. Some of the conditions in which hyperbaric 2016. O2 therapy has been especially beneficial are described next. Rostain JC, Lavoute C: Neurochemistry of pressure-induced nitrogen One successful use of hyperbaric O2 has been for treat- and metabolically inert gas narcosis in the central nervous system. ment of gas gangrene. The bacteria that cause this condi- Compr Physiol 6:1579, 2016. tion, clostridial organisms, grow best under anaerobic con- Vann RD, Butler FkK, Mitchell SJ, Moon RE: Decompression illness. ditions and stop growing at O2 pressures greater than about Lancet 377:153, 2011. 566