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The earth and its atmosphere provide environments that are compatible with an extraordinary number of diverse life forms, each adapted to its particular ecological niche. However, not all the earth's surface is equally friendly for human survival, let alone comfort and function. Mountain climbers and deep-sea divers know the profound effects of barometric pressure (P b ) on human physiology, and astronauts quickly learn how the physically equivalent forces of gravity and acceleration affect the body. Humans can adapt to changes in P b and gravity up to a point, but survival under extreme conditions requires special equipment; otherwise, our physiological limitations would restrict our occupancy of this planet to its lowland surfaces.
Much can be learned from exposure to extreme environmental conditions. Although most people do not seek out these extreme environments, the same physiological responses that occur under extreme environmental conditions may also occur, to a lesser extent, in everyday life. In this chapter, we first discuss general principles of environmental physiology and then focus on extreme environments encountered in three activities: deep-sea diving, mountain climbing, and space flight.
Claude Bernard introduced the concept of the milieu intérieur (basically the extracellular fluid in which cells of the organism live; see pp. 3–4 ) and the notion that fixité du milieu intérieur (the constancy of this extracellular fluid) is the condition of “free, independent life.” Most of this book focuses mainly on the interaction between cells and their extracellular fluid. In this chapter, we consider how the milieu extérieur, which physically surrounds the whole organism, affects our body functions and how we, in turn, modify our surroundings when it is necessary to improve our comfort or to extend the range of habitable environments.
The milieu extérieur, in fact, has several layers: the skin surface, the air that surrounds the skin, clothing that may surround that air, additional air that may surround the clothing, a structure (e.g., a house) that may surround that air, and finally a natural environment that surrounds that structure. As we interact with our multilayered environment, sensors monitor multiple aspects of the milieu extérieur and involuntary physiological feedback control mechanisms—operating at a subconscious level—make appropriate adjustments to systems that control a panoply of parameters, including blood pressure (see pp. 533–545 ), ventilation (see pp. 675–683 ), effective circulating volume (see pp. 554–555 ), gastric secretions (see pp. 865–872 ), blood glucose levels (see p. 1038 ), and temperature (see p. 1193 ).
The sensory input can also rise to a conscious level and, if perceived as discomfort, can motivate us to take voluntary actions that make the surroundings more comfortable. For example, if we sense that we are uncomfortably hot, we may move out of the sun or, if indoors, turn on the air conditioning. If we then sense that we are too cool, we may move into the sun or turn off the air conditioning. Such conscious actions are part of the effector limb in a complex negative-feedback system that includes sensors, afferent pathways, integration and conscious decision making in the brain, efferent pathways to our muscles, and perhaps inanimate objects such as air conditioners.
For a voluntary feedback system to operate properly, the person must be aware of a signal from the surroundings and must be able to determine the error by which this signal deviates from a desirable set-point condition. Moreover, the person must respond to this error signal by taking actions that reduce the error signal and thereby restore the milieu intérieur to within a normal range. Humans respond to discomfort with a wide variety of activities that may involve any layer of the environment. Thus, we may adjust our clothing, build housing, and eventually even make equipment that allows us to explore the ocean depths, mountain heights, and outer space.
Physiological control mechanisms—involuntary or voluntary—do not always work well. Physicians are acutely aware that factors such as medication, disease, or the extremes of age can interfere with involuntary feedback systems. These same factors can also interfere with voluntary feedback systems. For example, turning on the air conditioning is a difficult or even impossible task for an unconscious person, a bedridden patient, or a perfectly healthy baby. In these situations, a caregiver substitutes for the voluntary physiological control mechanisms. However, to perform this role effectively, the caregiver must understand how the environment would normally affect the care recipient and must anticipate how the involuntary and voluntary physiological control mechanisms would respond. N61-1
In the text, we pointed out that a person's involuntary or voluntary physiological control mechanisms sometimes may not function properly. Under these conditions, a caregiver must take control. In a systematic approach, the caregiver would (1) assess the environmental stresses to which the care recipient may be subjected, including their range of intensity; (2) predict the body's ideal involuntary and voluntary reactions to the stresses; (3) consider how the limitations of the care recipient interfere with the natural reactions; (4) determine how to supplement or replace control mechanisms that are not functioning adequately; and (5) express the essential empathy between the caregiver and the patient (i.e., the important words, “I care”).
Involuntary control mechanisms (see pp. 1198–1201 ) can only go so far in stabilizing body core temperature in the face of extreme environmental temperatures. Thus, voluntary control mechanisms can become extremely important.
The usual range of body core temperature is 36°C to 38°C (see Table 59-1 ). At an environmental temperature of 26°C to 27°C and a relative humidity of 50%, a naked person is in a neutral thermal environment (see p. 1196 )—feeling comfortable and being within the zone of vasomotor regulation of body temperature. At 28°C to 29°C, the person feels warm, and ~25% of the skin surface becomes wetted with perspiration. At 30°C to 32°C, the person becomes slightly uncomfortable. At 35°C to 37°C, the person becomes hot and uncomfortable, ~50% of the skin area is wet, and heat stroke (see Box 59-1 ) may become a hazard. The environmental temperature range of 39°C to 43°C is very hot and uncomfortable, and the body may fail to regulate core temperature. At 46°C, the heat is unbearable and heat stroke is imminent—the body heats rapidly, and the loss of extracellular fluid to sweat (see pp. 1215–1219 ) may lead to circulatory collapse and death (see p. 1215 ).
At the other extreme, we regard environmental temperatures of 24°C to 25°C as cool, and 21°C to 22°C as slightly uncomfortable. N61-2 At temperatures of 19°C to 20°C, we feel cold, vasoconstriction occurs in the hands and feet, and muscles may be painful. N61-3
Thermal sensations reported by sedentary people wearing a summer shirt and trousers correspond closely to those predicted by computer models that simulate the changes in circulation between the core and surface of the body at either warm or cool environmental temperatures. Skin and clothing temperatures can be measured at a distance using an inexpensive infrared detector available at auto supply stores and used for measuring engine temperatures.
Performance of physically demanding labor in the heat or cold requires assessment of environmental temperature, wind speed, humidity, the clothing worn, and whether the work is light (standing at a bench), moderate (walking with a 3-kg load), or heavy (e.g., working with a pick and shovel). From these considerations one may predict the permissible duty cycle—for instance, 75% work and 25% recovery, where recovery is a rest period with warming up from a cold environment or cooling off from a hot environment. For a period of up to 3 weeks, acclimatization to heat improves tolerance for working in a hot environment.
Ventilation of a room ( ) must be sufficient to supply enough O 2 and to remove enough CO 2 to keep the partial pressures of these gases within acceptable limits. In addition, it may be necessary to increase even more to lower relative humidity and to reduce odors. Dry air in the natural environment at sea level (see Table 26-1 ) has a of ~159 mm Hg (20.95%) and a of ~0.2 mm Hg (0.03%).
In the United States, the Occupational Safety and Health Administration (OSHA) has adopted an acceptable lower limit for O 2 of 19.5% of dry air at sea level (i.e., 148 mm Hg).
According to OSHA, the acceptable upper limit for in working environments at sea level is 3.8 mm Hg, or 0.5% of dry air. This would increase total ventilation ( ) by ~7% (see p. 716), a hardly noticeable rise. Exposures to 3% CO 2 in the ambient air—which initially would cause more substantial respiratory acidosis (see p. 633 )—could be tolerated for at least 15 minutes, by the end of which time would be nearly double. With longer exposures to 3% CO 2 , the metabolic compensation to respiratory acidosis (see p. 641 ) would have already begun to increase plasma [ ] noticeably. N61-4
How do subjects respond to increasing levels of CO 2 in the surrounding air? An example follows. A normal person who breathed 3% CO 2 for 5 or 6 minutes had a total ventilation ( or minute volume of ventilation) of 8 L/min; then after a rest, the person breathed 5% CO 2 , which produced a of 27 L/min, and after another rest breathed 7.5% CO 2 , which produced a of 48 L/min.
We then repeated the experiment with a person with chronic obstructive pulmonary disease (COPD). For the same three CO 2 levels, this COPD patient had values of 12, 19, and 27 L/min instead of 8, 27, and 48 L/min. The reason why—at 3% CO 2 —the COPD patient had a higher (12 L/min) than the normal person (8 L/min) was that the COPD patient had a pathologically broad distribution of ratios and thus arterial hypoxemia. But the incremental values in response to 5% and 7.5% CO 2 were clearly depressed in the COPD patient, compared to the control, owing to a combination of mechanical obstruction and diminished responsiveness to CO 2 (due to metabolic compensation for respiratory acidosis).
Finally, we repeated the experiment with a person having a depressed respiratory center. For the same three CO 2 levels, this patient had values of 11, 11, and 12 L/min. In other words, this patient exhibited virtually no increase in in response to inhaling CO 2 .
In some cases, particularly if the person is anesthetized, it becomes necessary to take over the mechanical work of breathing by using a ventilation pump that is set to provide sufficient ventilation in liters per minute to keep the arterial CO 2 level at ~40 mm Hg (equal to an end-tidal alveolar CO 2 level of ~5.6% of dry gas in healthy lungs). A spring-loaded safety valve is used to prevent the pump from delivering too much pressure, which could burst the lungs, and an alarm system alerts an attendant in case the pump fails to deliver the necessary amount of ventilation.
Two approaches are available for determining . The first is a steady-state method that requires knowing (1) the rate of CO 2 production ( ) by the occupants of the room and (2) the fraction of the room air that is CO 2 . The equation is analogous to the one we introduced for determining alveolar ventilation, beginning with Equation 31-9 :
We could use a similar equation based on the O 2 mole fraction and the rate of O 2 extraction (
) by the occupants.
N61-5
Suppose the occupant of a room has a resting metabolic rate that produces 200 mL/min (standard temperature and pressure/dry [STPD]) of CO 2 and removes 250 mL/min (STPD) of O 2 . STPD means mL at 760 mm Hg (or torr), 0°C, dry gas. However, if the ambient temperature is 24°C and the relative humidity is 50%, then the resting metabolic rate would have to increase by ~10%, so that the would be ~220 mL/min (0.220 L/min) and the would be ~275 mL/min (0.275 L/min).
In addition, suppose that air (ambient temperature 24°C and relative humidity 50%) enters and leaves this room at a rate of 100 L/min—the room ventilation ( ). Fresh air has almost zero CO 2 and 20.9% O 2 . The pulmonary ventilation of the occupant would raise the CO 2 of the air inside and leaving the room by (0.220 L/min)/(100 L/min) = 0.22%, and would lower the O 2 by (0.275 L/min)/(100 L/min) = 0.275%. Thus, the inspired O 2 would be reduced from 20.9% to (20.9% − 0.27%) = 20.63%, and this concentration of O 2 (and also the correspondingly elevated concentration of CO 2 ) would be easily tolerated by the occupant. Suppose, however, that the person were exercising, with 10 times the metabolic rate, or that 10 people were in the room in a resting condition. The CO 2 level would increase to 10 persons × 0.22%/person = 2.2%, and the O 2 would fall to 20.9% − (10 persons × 0.275%/person) = 20.9 − 2.75 = 18.15%. Given a minimal standard for O 2 of 19.5%, we would clearly need to increase room ventilation.
In the exponential decay method, the second approach for determining , the washout of a gas from the room is monitored. The approach is to add a test gas (e.g., CO 2 ) to the room and then measure the concentrations of the gas at time zero (C initial ) and—as washes out the gas over some time interval (Δt)—at some later time (C final ). The equation for exponential decay is as follows: N61-6
The equation that describes the washout of a volume (V) by a flow ( ) is:
Here τ is the time constant. For example, imagine that we have stirred a 1-L beaker filled with water containing some dye. If we flow clear water into this beaker at a rate of 1 L/min and simultaneously remove 1 L/min of the newly mixed solution, the dye concentration will decrease exponentially with a time constant of ( ) = (1 L)/(1 L/min) = 1 min. One minute after the start of the flow (i.e., after 1 time constant), the dye concentration will have fallen to 1/ e of its initial value. We could compute the time constant by comparing dye concentrations obtained at any two convenient times. For example, if C initial is the initial dye concentration and C final is the dye concentration after some time Δt, then
Substituting Equation NE 61-2 into Equation NE 61-1 , we have
The above is analogous to Equation 61-2 in the text.
In Equation 61-3 , we saw that the ventilation of the hypothetical room ( ) is 1871 L/min. This amount of ventilation would be adequate for a person exercising at 10 met (i.e., a metabolic rate that is 10-fold higher than resting metabolism) because the CO 2 production of 2.20 L/min N61-5 would be diluted by 1871 L/min of ventilation to raise the room CO 2 concentration to 0.12%. Similarly, the O 2 uptake of 2.75 L/min N61-5 —diluted by 1871 L/min—would lower the incoming level from 20.9% to (20.9% − 0.15%) = 20.75%. Both the computed CO 2 level and the computed O 2 level are easily tolerated. Note that the room ventilation of 1871 L/min in this example is 18 times as much as the room ventilation in the example in N61-5 , where the occupant had to work with a room ventilation of only 100 L/min.
For example, imagine that we wish to measure the ventilation of a room that is 3 × 3 × 3 m—a volume of 27 m 3 or 27,000 L. Into this room, we place a tank of 100% CO 2 and a fan to mix the air. We then open the valve on the tank until an infrared CO 2 meter reads 3% CO 2 (C initial = 3%), at which point we shut off the valve on the tank. Ten minutes later (Δt = 10 minutes), the meter reads 1.5% (C final = 1.5%). Substituting these measured values into Equation 61-2 yields N61-6
This approach requires that the incoming air contain virtually no CO 2 and that the room contain no CO 2 sources (e.g., people). Diffusion, thermal convection, and turbulence produce proper mixing of the gases.
More insidious than hypoxia, and less noticeable, is the symptomless encroachment of carbon monoxide (CO) gas on the oxyhemoglobin dissociation curve (see pp. 649–652 ). CO—which can come from incomplete combustion of fuel in furnaces, in charcoal burners, or during house fires—suffocates people without their being aware of its presence. Detectors for this gas are thus essential for providing an early warning. CO can be lethal when it occupies approximately half of the binding sites on hemoglobin (Hb), which occurs at a P CO of ~0.13 mm Hg or 0.13/760 ≅ 170 parts per million (ppm). N61-7 However, the half-time for washing CO into or out of the body is ~4 hours. Thus, if the ambient CO level were high enough to achieve a 50% saturation of Hb at equilibrium, then after a 2-hour exposure (i.e., one half of the half-time) the CO saturation would be × × 50% = 12.5%. The symptoms N29-5 at this point would be mild and nonspecific and would include headache, nausea, vomiting, drowsiness, and interference with night vision. Victims with limited coronary blood flow could experience angina. N61-8 After a 4-hour exposure (i.e., one half-time), the CO saturation would be × 50% = 25%. The symptoms would be more severe and would include impaired mental function and perhaps unconsciousness.
To calculate the carboxyhemoglobin (HbCO) concentration, remember that when the Hb is exposed to CO the HbCO concentration will equal the HbO 2 concentration when the Hb is exposed to oxygen at 210 times the CO concentration. For example, at equilibrium, Hb is 50% saturated with O 2 when the is 28 mm Hg. Similarly, the Hb is 50% saturated with CO at a P CO of 28/210 mm Hg, which would be 0.13 mm Hg of CO. Because an atmosphere of pressure is 760 mm Hg, 0.13 mm Hg of CO is 0.13/760 of an atmosphere of CO, that is, 0.000,170 of an atmosphere or 170 ppm of CO.
The heart muscle extracts most of the oxygen from the blood supplied to it in the coronary circulation. With exercise, autoregulation of coronary blood flow normally supplies more oxygen to the myocardium by increasing coronary blood flow. However, in stable angina, the fixed rate of coronary blood flow prevents autoregulation. Thus, when carboxyhemoglobin (HbCO) reduces the ability of arterial blood to release O 2 due to the leftward shift of the Hb-O 2 dissociation curve (see pp. 654–655 ), the heart muscle is deprived of oxygen and anginal pain develops even upon mild exercise.
Threshold limit values (TLVs) are reasonable environmental levels of toxic substances or physical agents (e.g., heat or noise) to which industrial workers can be exposed—over a lifetime of working days—without causing predictable harm. Rather than depending on concentrations measured in air or food, we can use biological exposure indices (BEIs) to limit exposure to toxic substances by detecting changes in the body— biomarkers of exposure (e.g., carboxyhemoglobin levels in blood)—that correlate with the intensity and duration of exposure to toxic substances (e.g., CO). N61-9
A list of threshold limit values and biological exposure indices applicable to industrial exposure can be obtained from the American Conference of Governmental Industrial Hygienists (ACGIH) in Cincinnati, Ohio ( http://www.acgih.org/home , accessed February 2015).
Standing motionless on the earth's surface at sea level, we experience a gravitational force (ℱ) N61-10 —our weight—that is the product of our mass (m) and the acceleration due to gravity ( g = 9.8 m · s –2 ):
Newton's first law of motion establishes the concept of inertia: an object at rest remains at rest, and a body in motion remains in motion—at the same velocity—unless acted upon by an external force.
The second law of motion deals with changes in momentum, which is the product of mass and velocity. Because velocity has both magnitude and direction, so does momentum. When an external force (which also has magnitude and direction) acts on a body, the change in the body's momentum is in the direction of the force. Furthermore, momentum changes at a rate that is proportional to the magnitude of the force. Thus, the change in the momentum (i.e., velocity) of a spacecraft depends on the magnitude, direction, and duration of the force (i.e., thrust) exerted by the engine.
The third law of motion states that application of an external force generates an equivalent, but opposing, inertial force (“for every action, there is an equal and opposite reaction”).
Under a particular condition, we may experience a different acceleration (a) from that due to gravity. The G force is a dimensionless number that describes force ( m · a ) that we experience under a particular condition relative to the gravitational force ( m · g ):
Thus, we normally experience a force of +1G that would cause us to fall with an acceleration of 9.8 m · s –2 if we were not supported in some way.
Accelerations besides that due to gravity also affect physiology. An accelerometer, placed on a belt, would show that we can jump upward with an acceleration of ~3G. It would also show that, on landing, we would strike the ground with a force of +3G—a force that our bones and other tissues can tolerate if we flex the joints. We discuss G forces from the perspective of air and space flight on pages 1232–1233.
At +1G, each square centimeter of the cross section of a vertebral body, for example, can withstand the compressive force generated by a mass of ~20 kg before the trabeculae begin to be crushed. N61-11 Thus, at +1G a vertebral body with a surface area of 10 cm 2 could support the compressive force generated by a mass of ~200 kg, far more than enough to support 35 kg, the mass of the upper half of the body of a 70-kg person. In fact, this strength would be adequate to withstand a G force of a (200 kg)/(35 kg) = +5.7G—provided the backbone is straight. However, if the backbone is not straight, the tolerance could be +3G, or approximately the acceleration achieved by jumping upward and landing on the feet with the back curved. When a pilot ejects from an aircraft, the thrust of the explosive cartridges accelerates the seat upward, and this can crush a vertebral body unless the pilot keeps the back straight.
In the text, we analyzed the body mass that a vertebral body could withstand at +1G. Another way to approach the problem is to determine the maximal pressure that a vertebral body can withstand.
At +1G, each square centimeter of a vertebral body, for example, can withstand the compressive force generated by a mass of ~20 kg before the trabeculae begin to be crushed. In other words, a vertebral body can withstand a compressive pressure of
Thus, a vertebral body with a cross-sectional area of 10 cm 2 could support a maximal force (ℱ Max ) of
This ℱ Max is more than enough to support the upper half of the body of a 70-kg person (i.e., 35 kg). Because a vertebral body with a cross-sectional area of 10 cm 2 could support a mass of 20 kg/cm 2 × 10 cm 2 = 200 kg at 1 × G, it could withstand a headward acceleration of (200 kg/35 kg) = +5.7G—provided the backbone were straight.
With increasing age, bones tend to demineralize (see p. 1243 ), which weakens them. Stepping off a curb, an elderly person with demineralized bones may fracture the neck of the femur or crush a vertebra. Demineralization of the vertebrae also reduces stature. Other causes of demineralization are immobilization and space flight. In one study a 6- to 7-week period of immobilization from bed rest led to losses of 14 g of calcium from bones, 1.7 kg of muscle, 21% in the strength of the gastrocnemius muscle, and 6% in average blood volume. The subjects became faint when suddenly tilted on a board, head above feet. After resuming ambulation, the subjects required 4 weeks for muscle strength to return to normal.
As discussed in the next two subchapters, extremely high or extremely low values of P b create special challenges for the physiology of the body, particularly the physiology of gases. N26-8 Dalton's law (see Box 26-2 ) states that P b is the sum of the partial pressures of the individual gases in the air mixture. Thus, in the case of ordinary dry air (see Table 26-1 ), most of the sea-level P b of 760 mm Hg is due to N 2 (~593 mm Hg) and O 2 (~159 mm Hg), with smaller contributions from trace gases such as argon (~7 mm Hg) and CO 2 (~0.2 mm Hg). As P b increases during diving beneath the water, or as P b decreases during ascent to high altitude, the partial pressure of each constituent gas in dry ambient air changes in proportion to the change in P b . At high values of P b , this relationship is especially important for ambient and , which can rise to toxic levels. At low values of P b , this relationship is important for ambient , which can fall to levels low enough to compromise the O 2 saturation of Hb (see pp. 649–652 ) and thus the delivery of O 2 to the tissues.
The proportionality between P b and the partial pressure of constituent gases breaks down in the presence of liquid water. When a gas is in equilibrium with liquid water—as it is for inspired air by the time it reaches the trachea (see p. 600 )—the partial pressure of water vapor ( ) depends not on P b but on temperature. Thus, becomes a negligible fraction of P b at the very high pressures associated with deep-sea diving, whereas becomes an increasingly dominant factor as we ascend to altitude.
The average P b at sea level is 760 mm Hg. In other words, if you stand at sea level, the column of air extending from your feet upward for several tens of kilometers through the atmosphere exerts a pressure of 1 atmosphere (atm). In a deep mine shaft, over which the column of air is even taller, P b is higher still. However, it is only when diving underwater that humans can experience extreme increases in P b . A column of fresh water extending from the earth's surface upward 10.3 m exerts an additional pressure of 760 mm Hg—as much as a column of air extending from sea level to tens of kilometers skyward. The same is true for a column of water extending from the surface of a lake to a depth of 10.3 m. For seawater, which has a density ~2.5% greater than that of fresh water, the column must be only 10 m to exert 1 atm of pressure. Because liquid water is virtually incompressible, P b increases linearly with the height (weight) of the column of water ( Fig. 61-1 ). Ten meters below the surface of the sea, P b is 2 atm, 1 atm for the atmospheric pressure plus 1 atm for the column of water. As the depth increases to 20 m and then to 30 m, P b increases to 3 atm, then 4 atm, and so on.
Increased external water pressure does not noticeably compress the body's fluid and solid components until a depth of ~1.5 km. However, external pressure compresses each of the body's air compartments to an extent that depends on the compliance of the compartment. In compliant cavities such as the intestines, external pressure readily compresses internal gases. In relatively stiff cavities, or those that cannot equilibrate readily with external pressure, increases of external pressure can distort the cavity wall and result in pain or damage. For example, if the eustachian tube is blocked, the middle-ear pressure cannot equilibrate with external pressure, and blood fills the space in the middle ear or the tympanic membrane ruptures.
According to Boyle's law, N26-8 pressure and volume vary inversely with each other. Thus, if the chest wall were perfectly compliant, a breath-holding dive to 10 m below the surface would double the pressure and compress the air in the lungs to half its original volume. Aquatic mammals can dive to extreme depths because rib flexibility allows the lungs to empty. Whales, for example, can extend a breath-hold dive for up to 2 hours, descending to depths as great as 900 m (91 atm) without suffering any ill effects. The human chest wall does not allow complete emptying of the lungs—except in a few trained individuals, and indeed the human record for a breath-hold dive is in excess of 200 m below the surface. N61-12
Imagine that a person at sea level makes a maximal inspiration, achieving a total lung capacity ( TLC; see p. 602 ) of 6 L. What happens if this individual then dives into seawater to a depth of 10 m? The P b as well as the pressure of the air in the lungs doubles to 2 atm at this depth. If the chest wall is perfectly compliant, this increase in P b would reduce the original lung volume to (6 L)/2, or 3 L. This new lung volume is only about twice the lung's normal residual volume (RV), which is normally 1.5 to 1.9 L (see p. 602 ).
If the person descends an additional 10 m to a total depth of 20 m, P b will now increase to 3 atm. Under these conditions, lung volume will fall to one third of its original value, or to 2 L.
A total descent to 30 m (P b = 4 atm) will reduce lung volume to one quarter of its initial value, or to about the normal RV.
Competitive freediving is organized by two international bodies: the International Association for the Development of Apnea (AIDA) and the World Underwater Federation (CMAS). These organizations recognize different disciplines, based on the permissible methods of descent and ascent. In the No-Limits Apnea category, Herbert Nitsch reached a depth of 214 m in 2007.
If the person is using a SCUBA system (see p. 1226 ) to breathe compressed air, then the lungs will re-expand to normal volume. If the individual at depth were to make a maximal inspiration to TLC, remove the SCUBA mouthpiece, and then rapidly ascend toward the surface, the air in the lungs would expand to a greater-than-physiological volume. Therefore, the individual would have to exhale during the ascent to prevent the lungs from overexpanding.
In a breath-hold dive that is deep enough to double P b , alveolar will also double to 80 mm Hg (see p. 1225 ). Because this value is substantially higher than the of mixed-venous blood at sea level (46 mm Hg), the direction of CO 2 diffusion across the blood-gas barrier reverses, alveolar CO 2 enters pulmonary-capillary blood, and thus arterial increases. In time, metabolically generated CO 2 accumulates in the blood and eventually raises mixed-venous to values higher than alveolar , so CO 2 diffusion again reverses direction and CO 2 diffuses into the alveoli. The increase in arterial can reduce the duration of the dive by increasing ventilatory drive (see p. 716 ). During a rapid ascent phase of a breath-hold dive, the fall in P b leads to a fall in alveolar and , which promotes the exit of both gases from the blood and thus a rapid fall in both arterial (a) and . The fall in reduces the drive to breathe. The fall in —and thus cerebral —can lead to deep-water blackout. N61-13
Imagine that a person excessively hyperventilates before taking a deep breath and attempting to swim a long distance underwater. During the underwater exercise, arterial will fall, and the person may become hypoxic before the arterial rises sufficiently to increase the drive to ventilate and cause the swimmer to surface. The result can be shallow-water blackout and—if help is not close at hand—drowning.
Although it may be intuitive to overbreathe in preparation for a long underwater swim, beware of too much of a good thing: two deep breaths are acceptable, but prolonged hyperventilation can be fatal.
Technical advances have made it possible for divers to remain beneath the water surface for periods longer than permitted by a single breath-hold. One of the earliest devices was a diving bell that surrounded the diver on all sides except the bottom. Such a bell was reportedly used by Alexander the Great in 330 bc and then improved by Sir Edmund Halley in 1716 ( Fig. 61-2 ). N61-14 By the early 19th century, pumping compressed air from above the water surface through a hose to the space underneath the bell kept water out of the bell. In all of these cases, the diver breathed air at the same pressure as the surrounding water. Although the pressures both surrounding the diver's chest and inside the airways were far higher than at sea level, the pressure gradient across the chest wall was normal. Thus, the lungs were normally expanded.
The following is a translation of a passage from a book (written in German) titled Diseases of Air Pressure with Special Considerations of So-called Caisson Disease by Dr. Richard Heller, Dr. Wilhelm Mager, and Hermann von Schroetter, PhD, MD.
“There are several reports that Aristotle had the idea to provide air to divers underwater by using an air tube. One also hears from Figuier that a diver apparatus was used in Venice in the beginning of the 17th century. This apparatus was called ‘Cornemuse’ or ‘Capuchon’ and used a bellow to provide air. *
* This apparatus was supposed to contain a pipe with an enlargement at the lower end that could go over the head of the diver. This pipe provided air driven by bellows, while another pipe returned exhaled air to the surface.
Nevertheless, the first certain information we have is that Denys Papin had the idea to renew air in diver bells by way of bellows and valves to prolong the time to remain underwater.
“Therefore, a new period of diving begins with Papin and Halley, who actually put the idea into practice in 1716. The new period brings about the most important progress in this area.
“The invention of the Cornemuse, as well as the inventions of Papin and Halley, constitute the beginning of the diving apparatus in use today.
“Papin dealt already in 1672, in a theoretical publication with Huygens, with the influence of changes in air pressure and gave an explanation why animals die under a vacuum chamber venting valve.
“Edm. Halley, the famous Astronomer and Secretary of the English Society of Sciences, wrote up his experiences in 1716 in the ‘Transactions anglic’ under the title of ‘The art of living under water.’
“For low depths, the air delivery into the diving bell was achieved by two leather tubes, whereby one was used to pump in air with a bellows and the other allowed the air to escape. This arrangement with bellows did not work for greater depths of over 3 fathoms [i.e., 18 feet or ~5.5 m]. For these depths, barrels with air would be lowered into the water, while the used air was released into the water through a valve. Halley lowered himself together with 4 other persons to a depth of 9–10 fathoms, about 17 m, in 1721, whereby 7-8 barrels of air had to be used.
“His diving bell was made of wood, 8 feet high, in the form of a cut-off cone, with 3 feet diameter at the apex and 5 feet at the base [see Fig. 61-2 ]. The diving bell had a cap of lead. Additional lead weights were fastened at the lower edge so that the bell could sink to the bottom of the sea…. Glass in the ceiling served as window. There was a valve in the dome, through which the used-up, warm air could escape. A type of platform was attached to the free edge of the bell with ropes and fixed in place through weights. Divers would use this platform.
“The entire apparatus was fastened to the main spreader of a ship used to move the bell to its destination. To renew air when the bell was underwater, Halley used two small barrels of 160 L each and lowered the barrels with the aid of weights. The barrels were connected to the bell via a leather tube that was puttied with wax and oil into the cover of the barrel. A hole in the bottom of the barrel allowed water to enter it thus generating pressure to move the air into the bell.
“The barrels were moved to the surface, refilled with air and re-lowered on a signal. The diver serviced the tubes, brought them into the bell, and regulated the airflow through valves at the end of the tubes.
“Nevertheless, the divers suffered, as described by Halley, from the significant increase in temperature within the bell due to compression of the air so that any stay in the bell was difficult. Moreover, he describes that the workers had pain in their ears, and nosebleeds once they were back at the surface.
“During this time, there was also remarkable progress in efforts to get air travel going. On August 8, 1709, the Portuguese Pater Bartholomeo Laurenco de Gussmann lifted himself up in the air with an airship constructed by him in the Indian House in Lisbon and in front of King John V and the entire court. Unfortunately, he got stuck at the roof of the palace and crashed. His device consisted of stiffened paper and the uplifting was caused by heated air. … As often seen in the history, this great invention was snagged by an unfortunate, small obstruction so that the inventor got forgotten.”
The conditions are essentially the same in a modern-day caisson, a massive, hollow, pressurized structure that functions like a large diving bell. Once again, the pressure inside the caisson (3 to 4 atm) has to be high enough to prevent water at the bottom of the caisson from entering. Several workers (“sand hogs”) at the bottom of the caisson may excavate material from the bottom of a river for constructing tunnels or foundations of bridges.
Technical advances also extended to individual divers, who first wore diving suits with spherical helmets over their heads ( Fig. 61-3 A ). The air inside these helmets was pressurized to match exactly the pressure of the water in which they were diving. In 1943, Jacques Cousteau perfected the self-contained underwater breathing apparatus, or SCUBA, that replaced cumbersome gear and increased the mobility and convenience of an underwater dive (see Fig. 61-3 B ). N61-15
In the diving helmet shown in Figure 61-3 A , a nonreturn valve was placed at the point where the air hose met the helmet. This device prevented air from escaping from the helmet in case the hose were to rupture.
The SCUBA system devised by Jacques Cousteau (see Fig. 61-3 B ) consists of five major elements:
A tank of gas compressed to a pressure that exceeds the highest pressures that the diver will encounter during the dive.
A reducing valve that delivers gas from the tank to the diver's hose at a pressure of 6 to 7 atm.
A “demand” breathing valve for inspiration, triggered to open by the slight decrease in pressure caused by the diver's inspiration. This valve delivers the air mixture to the diver at the ambient pressure.
An exhaust valve that allows expired air to be released at a pressure that is slightly higher than the ambient pressure.
A face mask or mouthpiece with a gas-delivery system that has a small ventilatory dead space (see p. 675 ).
Deep dives for extended periods of time require training and carry the risk of drowning secondary to muscle fatigue and hypothermia. Air flotation and thermal insulation of the diving suit lessen these hazards. For reasons that will become apparent, use of any of these techniques while breathing room air carries additional hazards, including nitrogen narcosis, O 2 toxicity, and problems with decompression.
Descending beneath the water causes the inspired —nearly 600 mm Hg at sea level (see Table 26-1 )—to increase as P b increases. According to Henry's law (see Box 26-2 ), the increased will cause more N 2 to dissolve in pulmonary-capillary blood and, eventually, the body's tissues. The dissolved [N 2 ] in various compartments begins to increase immediately but may take many hours to reach the values predicted by Henry's law. Because of its high lipid solubility, N 2 dissolves readily in adipocytes and in membrane lipids. A high reduces the ion conductance of membranes, and therefore neuronal excitability, by mechanisms that are similar to those of gas anesthetics. Diving to increased depths (e.g., 4 to 5 atm) while breathing compressed air causes nitrogen narcosis. Mild nitrogen narcosis resembles alcohol intoxication (e.g., loss of psychosocial inhibitions). According to “Martini's law,” each 15 m of depth has the effects of drinking an additional martini. Progressive narcosis occurs with increasing depth or time of the dive and is accompanied by lethargy and drowsiness, rapid onset of fatigue, and, eventually, a loss of consciousness. Because it develops insidiously, nitrogen narcosis poses a potentially fatal threat to divers who are not aware of the risks.
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