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Hyperbaric Conditions

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Abstract

Exposure to elevated ambient pressure (hyperbaric conditions) occurs most commonly in underwater diving, during which respired gas density and partial pressures, work of breathing, and physiological dead space are all increased. There is a tendency toward hypercapnia during diving, with several potential causes. Most importantly, there may be reduced responsiveness of the respiratory controller to rising arterial CO2, leading to hypoventilation and CO2 retention. Contributory factors may include elevated arterial PO2, inert gas narcosis and an innate (but variable) tendency of the respiratory controller to sacrifice tight control of arterial CO2 when work of breathing increases. Oxygen is usually breathed at elevated partial pressure under hyperbaric conditions. Oxygen breathing at modest hyperbaric pressure is used therapeutically in hyperbaric chambers to increase arterial carriage of oxygen and diffusion into tissues. However, to avoid cerebral and pulmonary oxygen toxicity during underwater diving, both the magnitude and duration of oxygen exposure must be managed. Therefore, most underwater diving is conducted breathing mixtures of oxygen and inert gases such as nitrogen or helium, often simply air. At hyperbaric pressure, tissues equilibrate over time with high inspired inert gas partial pressure. Subsequent decompression may reduce ambient pressure below the sum of tissue gas partial pressures (supersaturation) which can result in tissue gas bubble formation and potential injury (decompression sickness). Risk of decompression sickness is minimized by scheduling time at depth and decompression rate to limit tissue supersaturation or size and profusion of bubbles in accord with models of tissue gas kinetics and bubble formation and growth. © 2011 American Physiological Society. Compr Physiol 1:163‐201, 2011.

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Figure 1. Figure 1.

Recreational “scuba” (self‐contained underwater breathing apparatus) diver using a standard single‐cylinder and open‐circuit demand valve regulator configuration.

Figure 2. Figure 2.

Diver using a closed‐circuit rebreather. U.S. Navy Experimental Diving Unit photograph.

Figure 3. Figure 3.

Divers in surface supply diving equipment. Each diver has an umbilical supplying gas from the surface and an emergency “bailout” cylinder of gas. Note the oronasal mask visible behind the helmet faceplate of the diver facing the camera. U.S. Navy photograph by Chief Petty Officer Andrew McKaskle.

Figure 4. Figure 4.

Monoplace hyperbaric chamber. The patient is the only occupant. The chamber may be pressurized with air and 100% oxygen delivered via a demand valve and oronasal mask, or the chamber may simply be pressurized with oxygen.

Figure 5. Figure 5.

Multiplace hyperbaric chamber. The chamber is pressurized with air, and delivery of 100% oxygen may be achieved either by the use of a hood sealed around the neck through which oxygen free flows or by a demand valve and oronasal mask.

Figure 6. Figure 6.

Pooled data demonstrating the fall in maximum breathing capacity as ambient pressure increases. The studies were conducted using nonimmersed subjects breathing air.

Reproduced with permission from Camporesi and Bosco
Figure 7. Figure 7.

Maximum expiratory flow‐volume curves and isovolume pressure‐flow curves at 75% vital capacity (VC) for a single subject breathing air at 1 and 10 atm abs. In the 1 atm abs condition, a small increase in pleural pressure results in a substantial increase in flow. At 10 atm abs, a small increase in flow requires a much greater increase in pleural pressure, and further increases are limited by the plateau of the isovolume pressure‐flow curve at relatively low flow rates. TLC, total lung capacity.

Reproduced with permission from Wood and Bryan
Figure 8. Figure 8.

Schematics to represent static lung loading (or transrespiratory pressure) during immersion. Panel A depicts upright head‐out immersion in which there is a negative static lung load of approximately −20 cmH2O. Panel B depicts an upright scuba diver breathing from a regulator in which there is a similar negative static lung load of approximately −20 cmH2O irrespective of depth. Panel C depicts a closed‐circuit rebreather diver with a back‐mounted counterlung. All of the scenarios depicted in panels (A), (B), and (C) produce a negative static lung load because the airway is in continuity with a gas supply at lower pressure than the hydrostatic pressure acting at the lung centroid. In contrast, Panel D depicts a scuba diver in the head‐down position where there is a positive static lung load because gas supply pressure (measured at the depth of the regulator mouthpiece) is now greater than the hydrostatic pressure acting at the lung centroid. SLL, static lung load.

Reproduced with permission from Lundgren
Figure 9. Figure 9.

(A) Dead space (Vd) as a function of tidal volume (Vt) in nonimmersed subjects breathing air at 1 atm abs (“surface”) and during experimental hyperbaric chamber exposures (“depth”) to between 47 and 66 atm abs (inspired gas densities between 12.3 and 17.1 g/liter). (B) The Vd/Vt ratio during increasing levels of exercise at the “surface” and at “depth.” At the surface during exercise at 360 kpm, the ratio decreases by 43% of the resting value in comparison with a 10% decrease at depth.

Reproduced with permission from Salzano et al.
Figure 10. Figure 10.

Pooled data from human studies (closed circles) illustrating the effect of gas density (ρ in the formula) on the Vd/Vt ratio as respired gas density increases. The extremely high‐density datapoint (open circle) comes from a liquid‐breathing experiment in dogs.

Reproduced with permission from Moon et al.
Figure 11. Figure 11.

Rates of development of pulmonary symptoms and decrements in slow vital capacity in human subjects continuously breathing oxygen at increasing inspired pressures (ATA = atm abs).

Reproduced with permission from Clark et al.
Figure 12. Figure 12.

Blood oxygen content for oxygen partial pressures extending into hyperbaric conditions. The right‐angle arrows illustrate oxygen extraction of 5 vol% for air breathing at sea level (left arrow) and for oxygen breathing at 3 atm abs.

Figure 13. Figure 13.

Intercapillary diffusion distances for oxygen depicted using the Krogh cylinder model under conditions of air breathing at 1 atm abs (top left); oxygen breathing at 3 atm abs (top right); and oxygen breathing at 3 atm abs assuming countercurrent flow in adjacent capillaries (bottom). Cylinder boundaries are defined by the calculated distance from capillary to the point where tissue Po2 falls to 12 mmHg. The advantage of a high Pao2, particularly at the arterial end of the capillary is clearly apparent, as is the potential advantage of a countercurrent flow pattern during hyperbaric oxygen breathing.

Reproduced with permission from Saltzman
Figure 14. Figure 14.

Ambient pressure (solid line) versus time and the corresponding total gas pressures (ΣPtisj) in two compartments (half‐times of 1 and 5 min) for an air‐breathing dive. Classical decompression is scheduled to keep dissolved gas pressure in k modeled compartments less than or equal to a maximum permissible value, Ptisk ≤ akPamb + bk. For simplicity, the above figure shows only two compartments and sets a = 1 and b = 0 so that the “safe ascent depth”, Pamb = max[(Ptiskb)/a], is equal to max(Ptisk). By convention, decompression stops are taken at increments of 10 fsw (0.3 atm abs) deeper than sea level.

Figure 15. Figure 15.

Simulation of the equilibration of blood with inspired nitrogen with compression breathing air. Simulation is based on the standard, resting 70‐kg man with inspired gas, alveolar gas, pulmonary blood, and the body in series, the latter composed of four parallel compartments representing vessel rich, muscle, fat, and vessel poor tissue groups . The simulation uses nitrogen tissue solubility coefficients (α) of 0.015 (blood), 0.015 (lean), and 0.075 (fat) and an estimated lung nitrogen diffusing capacity of 0.15 liters/min/kPa . A ramp in inspired Pn2 occurs with compression from 101 kPa (sea level) to 404 kPa (4 atm abs) ambient pressure (dashed line). Ninety‐nine percent equilibration of arterial blood with inspired Pn2 (solid line) occurs 2.5 min after reaching depth. Throughout the time course of this simulation, there less than 0.3% difference between arterial blood and alveolar Pn2.

Figure 16. Figure 16.

(A) Washout of nitrogen (sum of dissolved and free gas) from tissue for the cases of all gas remaining dissolved (dotted line) according to Eq. , for phase equilibrium between bubble and dissolved gas partial pressures (thin line) according to Eq. , and for a single, spherical bubble in a small tissue volume (equivalent to a very high bubble density of 10−6 bubbles/ml, thick line) by using a three‐region model diffusion‐limited bubble growth . (B) Dissolved tissue Pn2 (thin line, left axis) and bubble volume (thick line, right axis) for the spherical bubble case illustrated in panel (A).

Figure 17. Figure 17.

The oxygen window. (A) Increasing dissolved oxygen and CO2 concentrations for a liquid at equilibrium with increasing partial pressures of these gases for Ostwald solubility coefficients of 0.024 for oxygen and 0.528 for CO2. (B) Relationship similar to panel A, but with axes reversed. Upper arrow indicates extraction of 2.5 vol% oxygen from the liquid, and lower arrow indicates replacement with 2.5 vol% CO2; the dotted line indicates the resulting oxygen window that is the net difference for the sum of all gas partial pressures in the liquid. Note that extraction of more oxygen, similarly replaced with CO2, would result in a larger oxygen window.

Figure 18. Figure 18.

Change in the sum of all dissolved tissue gas partial pressures (heavy solid line) in response to a compression (dot‐dash) and subsequent change in inspired oxygen fraction (thin solid line, arbitrary scale). The inherent unsaturation (oxygen window) is equal to the vertical distance between the dashed line and the tissue gas partial pressure. Prior to compression, the tissue is inherently unsaturated. For a period following the compression, the total unsaturation (ambient – tissue) exceeds the inherent unsaturation until the alveolar and tissue Pn2 reequilibrate. Increasing the inspired oxygen fraction causes washout of tissue nitrogen and a corresponding increase in the inherent unsaturation. Inher. Unsat., inherent unsaturation.

Figure 19. Figure 19.

The oxygen window increases with increase inspired Po2 because of the nonlinear relationship between blood oxygen content and Po2 due to oxygen‐hemoglobin dissociation (x‐ and y‐axes reversed from the familiar presentation, such as in Figure ). The two right‐angle arrows indicate the arterial‐venous Po2 differences resulting from 5 vol% oxygen extraction for inspired Po2 of 1.3 or 0.2 atm abs. Since the corresponding increase in Pco2 will be approximately equal in both cases, and assuming equilibrium between tissue and venous blood gases, the difference between the vertical segments of the arrows illustrates the difference in magnitude of the oxygen window for the two cases.

Figure 20. Figure 20.

Whole‐body washout of helium and nitrogen. Y‐axis is the fraction of total expired gas collected. Drawn from data of Behnke and colleagues .

Figure 21. Figure 21.

Isobaric exchange of helium and nitrogen in a compartment with fivefold difference in time constants (τHe = 7.2, = 36). Panel A is a simulation of a compartment at equilibrium with 90% N2‐10% O2 inspired gas at 10 atm abs ambient pressure and a switch to 90% He‐10% O2 inspired gas at time zero. Dashed and thin lines indicate partial pressures of helium and nitrogen. The thick line indicates the sum of both inert gases and metabolic gases. The compartment is transiently supersaturated, while the sum of gases is above ambient pressure (dotted line). Panel B shows the reverse gas switch.



Figure 1.

Recreational “scuba” (self‐contained underwater breathing apparatus) diver using a standard single‐cylinder and open‐circuit demand valve regulator configuration.



Figure 2.

Diver using a closed‐circuit rebreather. U.S. Navy Experimental Diving Unit photograph.



Figure 3.

Divers in surface supply diving equipment. Each diver has an umbilical supplying gas from the surface and an emergency “bailout” cylinder of gas. Note the oronasal mask visible behind the helmet faceplate of the diver facing the camera. U.S. Navy photograph by Chief Petty Officer Andrew McKaskle.



Figure 4.

Monoplace hyperbaric chamber. The patient is the only occupant. The chamber may be pressurized with air and 100% oxygen delivered via a demand valve and oronasal mask, or the chamber may simply be pressurized with oxygen.



Figure 5.

Multiplace hyperbaric chamber. The chamber is pressurized with air, and delivery of 100% oxygen may be achieved either by the use of a hood sealed around the neck through which oxygen free flows or by a demand valve and oronasal mask.



Figure 6.

Pooled data demonstrating the fall in maximum breathing capacity as ambient pressure increases. The studies were conducted using nonimmersed subjects breathing air.

Reproduced with permission from Camporesi and Bosco


Figure 7.

Maximum expiratory flow‐volume curves and isovolume pressure‐flow curves at 75% vital capacity (VC) for a single subject breathing air at 1 and 10 atm abs. In the 1 atm abs condition, a small increase in pleural pressure results in a substantial increase in flow. At 10 atm abs, a small increase in flow requires a much greater increase in pleural pressure, and further increases are limited by the plateau of the isovolume pressure‐flow curve at relatively low flow rates. TLC, total lung capacity.

Reproduced with permission from Wood and Bryan


Figure 8.

Schematics to represent static lung loading (or transrespiratory pressure) during immersion. Panel A depicts upright head‐out immersion in which there is a negative static lung load of approximately −20 cmH2O. Panel B depicts an upright scuba diver breathing from a regulator in which there is a similar negative static lung load of approximately −20 cmH2O irrespective of depth. Panel C depicts a closed‐circuit rebreather diver with a back‐mounted counterlung. All of the scenarios depicted in panels (A), (B), and (C) produce a negative static lung load because the airway is in continuity with a gas supply at lower pressure than the hydrostatic pressure acting at the lung centroid. In contrast, Panel D depicts a scuba diver in the head‐down position where there is a positive static lung load because gas supply pressure (measured at the depth of the regulator mouthpiece) is now greater than the hydrostatic pressure acting at the lung centroid. SLL, static lung load.

Reproduced with permission from Lundgren


Figure 9.

(A) Dead space (Vd) as a function of tidal volume (Vt) in nonimmersed subjects breathing air at 1 atm abs (“surface”) and during experimental hyperbaric chamber exposures (“depth”) to between 47 and 66 atm abs (inspired gas densities between 12.3 and 17.1 g/liter). (B) The Vd/Vt ratio during increasing levels of exercise at the “surface” and at “depth.” At the surface during exercise at 360 kpm, the ratio decreases by 43% of the resting value in comparison with a 10% decrease at depth.

Reproduced with permission from Salzano et al.


Figure 10.

Pooled data from human studies (closed circles) illustrating the effect of gas density (ρ in the formula) on the Vd/Vt ratio as respired gas density increases. The extremely high‐density datapoint (open circle) comes from a liquid‐breathing experiment in dogs.

Reproduced with permission from Moon et al.


Figure 11.

Rates of development of pulmonary symptoms and decrements in slow vital capacity in human subjects continuously breathing oxygen at increasing inspired pressures (ATA = atm abs).

Reproduced with permission from Clark et al.


Figure 12.

Blood oxygen content for oxygen partial pressures extending into hyperbaric conditions. The right‐angle arrows illustrate oxygen extraction of 5 vol% for air breathing at sea level (left arrow) and for oxygen breathing at 3 atm abs.



Figure 13.

Intercapillary diffusion distances for oxygen depicted using the Krogh cylinder model under conditions of air breathing at 1 atm abs (top left); oxygen breathing at 3 atm abs (top right); and oxygen breathing at 3 atm abs assuming countercurrent flow in adjacent capillaries (bottom). Cylinder boundaries are defined by the calculated distance from capillary to the point where tissue Po2 falls to 12 mmHg. The advantage of a high Pao2, particularly at the arterial end of the capillary is clearly apparent, as is the potential advantage of a countercurrent flow pattern during hyperbaric oxygen breathing.

Reproduced with permission from Saltzman


Figure 14.

Ambient pressure (solid line) versus time and the corresponding total gas pressures (ΣPtisj) in two compartments (half‐times of 1 and 5 min) for an air‐breathing dive. Classical decompression is scheduled to keep dissolved gas pressure in k modeled compartments less than or equal to a maximum permissible value, Ptisk ≤ akPamb + bk. For simplicity, the above figure shows only two compartments and sets a = 1 and b = 0 so that the “safe ascent depth”, Pamb = max[(Ptiskb)/a], is equal to max(Ptisk). By convention, decompression stops are taken at increments of 10 fsw (0.3 atm abs) deeper than sea level.



Figure 15.

Simulation of the equilibration of blood with inspired nitrogen with compression breathing air. Simulation is based on the standard, resting 70‐kg man with inspired gas, alveolar gas, pulmonary blood, and the body in series, the latter composed of four parallel compartments representing vessel rich, muscle, fat, and vessel poor tissue groups . The simulation uses nitrogen tissue solubility coefficients (α) of 0.015 (blood), 0.015 (lean), and 0.075 (fat) and an estimated lung nitrogen diffusing capacity of 0.15 liters/min/kPa . A ramp in inspired Pn2 occurs with compression from 101 kPa (sea level) to 404 kPa (4 atm abs) ambient pressure (dashed line). Ninety‐nine percent equilibration of arterial blood with inspired Pn2 (solid line) occurs 2.5 min after reaching depth. Throughout the time course of this simulation, there less than 0.3% difference between arterial blood and alveolar Pn2.



Figure 16.

(A) Washout of nitrogen (sum of dissolved and free gas) from tissue for the cases of all gas remaining dissolved (dotted line) according to Eq. , for phase equilibrium between bubble and dissolved gas partial pressures (thin line) according to Eq. , and for a single, spherical bubble in a small tissue volume (equivalent to a very high bubble density of 10−6 bubbles/ml, thick line) by using a three‐region model diffusion‐limited bubble growth . (B) Dissolved tissue Pn2 (thin line, left axis) and bubble volume (thick line, right axis) for the spherical bubble case illustrated in panel (A).



Figure 17.

The oxygen window. (A) Increasing dissolved oxygen and CO2 concentrations for a liquid at equilibrium with increasing partial pressures of these gases for Ostwald solubility coefficients of 0.024 for oxygen and 0.528 for CO2. (B) Relationship similar to panel A, but with axes reversed. Upper arrow indicates extraction of 2.5 vol% oxygen from the liquid, and lower arrow indicates replacement with 2.5 vol% CO2; the dotted line indicates the resulting oxygen window that is the net difference for the sum of all gas partial pressures in the liquid. Note that extraction of more oxygen, similarly replaced with CO2, would result in a larger oxygen window.



Figure 18.

Change in the sum of all dissolved tissue gas partial pressures (heavy solid line) in response to a compression (dot‐dash) and subsequent change in inspired oxygen fraction (thin solid line, arbitrary scale). The inherent unsaturation (oxygen window) is equal to the vertical distance between the dashed line and the tissue gas partial pressure. Prior to compression, the tissue is inherently unsaturated. For a period following the compression, the total unsaturation (ambient – tissue) exceeds the inherent unsaturation until the alveolar and tissue Pn2 reequilibrate. Increasing the inspired oxygen fraction causes washout of tissue nitrogen and a corresponding increase in the inherent unsaturation. Inher. Unsat., inherent unsaturation.



Figure 19.

The oxygen window increases with increase inspired Po2 because of the nonlinear relationship between blood oxygen content and Po2 due to oxygen‐hemoglobin dissociation (x‐ and y‐axes reversed from the familiar presentation, such as in Figure ). The two right‐angle arrows indicate the arterial‐venous Po2 differences resulting from 5 vol% oxygen extraction for inspired Po2 of 1.3 or 0.2 atm abs. Since the corresponding increase in Pco2 will be approximately equal in both cases, and assuming equilibrium between tissue and venous blood gases, the difference between the vertical segments of the arrows illustrates the difference in magnitude of the oxygen window for the two cases.



Figure 20.

Whole‐body washout of helium and nitrogen. Y‐axis is the fraction of total expired gas collected. Drawn from data of Behnke and colleagues .



Figure 21.

Isobaric exchange of helium and nitrogen in a compartment with fivefold difference in time constants (τHe = 7.2, = 36). Panel A is a simulation of a compartment at equilibrium with 90% N2‐10% O2 inspired gas at 10 atm abs ambient pressure and a switch to 90% He‐10% O2 inspired gas at time zero. Dashed and thin lines indicate partial pressures of helium and nitrogen. The thick line indicates the sum of both inert gases and metabolic gases. The compartment is transiently supersaturated, while the sum of gases is above ambient pressure (dotted line). Panel B shows the reverse gas switch.

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David J. Doolette, Simon J. Mitchell. Hyperbaric Conditions. Compr Physiol 2010, 1: 163-201. doi: 10.1002/cphy.c091004