Human Skeletal Muscle and Subcutaneous Tissue Carbon Dioxide, Nitrogen, and Oxygen Gas Tension Measurements Under Ambient and Hyperbaric Conditions

George B. Hart, MD, FACS*†

Charles H. Wells, PhD*

Michael B. Strauss, MD, FACS, AAOS*†

 

*Baromedical Department, Long Beach Memorial Medical Center, Long Beach, California

†University of California Irvine, Irvine, California

 

Supported by the Memorial Foundation, Long Beach Memorial Medical Center, Long Beach, California.

 

KEY WORDS: hyperbaric oxygen, tissue gas analysis, tissue oxygen, tissue carbon dioxide, tissue nitrogen, monoplace chamber, multiplace chamber

ABSTRACT

Objectives: (1) To measure tissue O₂, CO₂, and N₂ tensions in subcutaneous (SQ) and muscle (MM) tissues of the thigh in room air and at two atmospheres absolute (ATA) pressure. (2) To compare the differences in continuous O₂ exposures with O₂ breathing with air breaks under hyperbaric conditions on O₂ and N₂ in MM and SQ tissues. (3) To observe the effect of these exposures on MM and SQ tissue CO₂s.

Method: Gas tensions in resting MM and SQ tissues were recorded at 4-minute intervals during a 3-hour period. Two protocols were compared: protocol A-continuous O₂ breathing in 2 ATA O₂, which represented a monoplace chamber treatment schedule; and protocol B-analogous to a multiplace hyperbaric oxygen treatment with intermittent air breaks between O₂ breathing.

Results: Mean room air MM O₂ is 33% less (P < .001) than adjacent SQ O₂, mean MM CO₂ exceeds SQ CO₂ by 13% (P < .001) of the adjacent SQ. Mean MM N₂ tensions are 20% less than the adjacent SQ N₂ tensions (P < .001). Protocol A is superior for reducing MM N₂ (P < .001) compared with protocol B. Muscle O₂ increases more rapidly and to higher levels than the SQ O₂ in protocol B, In protocol A SQ O₂ increases above MM O₂ tensions. Protocol A’s SQ O₂ tensions increased 12% more than protocol B. Muscle and SQ CO₂ decrease significantly (P < .001) in 2 ATA O₂ in both protocols.

Conclusions: (1) Resting ambient MM N₂ is significantly lower than subcutaneous tissue N₂. (2) Protocol A is superior for muscle N₂ washout. (3) There are differences in SQ and MM O₂ uptake at 2 ATA as well as differences in uptake between protocols A and B for these tissue compartments. (4) Carbon dioxide decreases in the lower extremity under hyperbaric oxygen conditions.

INTRODUCTION

Tissue gas measurements aid in the diagnosis and management of disorders that impair tissue perfusion or gas exchange. Hyperbaric oxygen (HBO) therapy is an intervention that increases oxygen (O₂) and lowers inert gas tissue pressures, but few resting tissue gas tension measurements are reported under hyperbaric conditions. Campbell,1 Lambertsen et al,2 and Van Liew et al3 measured gas tensions from gas pockets and proposed that their technique be considered for measuring extravascular tissue gas tensions. Niinikoski and Hunt4 and Kivisari and Niinikoski5 measured wound O₂ and carbon dioxide (CO₂) tensions of gas samples from implanted silastic tubes. This technique was used to document changes in gas tension in tissues proximal to wounds from necrotizing infections.6 Sheffield7 and Sheffield and Workman8 measured tissue O₂ tensions with miniature polarographic electrodes. Woldring et al,9,10 using implanted tissue gas collection probes fitted with silastic diffusion membranes, made serial mass spectroscopy measurements of O₂ and CO₂ tensions in the aorta and vena cava.  Brantigan et al.11 reported that this technique did not create thrombi or emboli.

Brantigan et al12 used low permeability Teflon probes to prevent depletion of gases at the sampling site for the measurement of gases in extra vascular tissues. Hart et al,13 Wells et al,14 and Horrigan et al15 reported measurements of muscle (MM) and subcutaneous (SQ) gas tensions in eight male subjects, also using low-permeability Teflon probes. In contrast to intracellular myoglobin,16 near infra-red spectroscopy (NIRS),17 and magnetic resonance imaging (MRI) studies,18 tissue Argon, CO₂, N₂ gas tensions as well as O₂ measurements are made.

We report our findings in a study of over 30 men and women using low-permeability Teflon probes and the mass spectrometer. From this study we have established normal values for tissue O₂, CO₂, and N₂ tensions in healthy men and women volunteers, and compared the effects of two hyperbaric treatment protocols on augmenting tissue O₂ enhancement, N₂ loading, and N₂ washout.

We used two protocols. Protocol A follows a typical monoplace HBO treatment schedule and protocol B follows a treatment schedule commonly used in the multiplace chamber. Subjects in protocol A were pressurized in a pure O₂ environment, breathing O₂ directly from within the chamber at 2 ATA during the exposures. In protocol B, the subjects were pressurized in 2 ATA air and breathed O₂ via a regulator for each HBO exposure. Protocol A differed from protocol B in two other ways: (1) the total HBO exposure time of protocol B exceed that of protocol A and (2) protocol B’s HBO exposures were interrupted with short intervals of hyperbaric air breathing; also known as “air breaks.”

METHODS

Study Population

We enrolled 36 healthy volunteers from the staff and their families at Long Beach Memorial Medical Center, Long Beach, California, for the study (Table 1). All 36 participated in protocol A and 33 (92%) participated in protocol B. Three men (8%) did not participate in protocol B. No subject participated in protocol B less than 30 days after completing protocol A. All subjects were appropriately informed of the risks and objectives of the study and the study protocol in accordance with our institution’s standards for use of human subjects and the Helsinki Accords,

Study Protocol

Oxygen, CO₂, and N₂ tensions of MM and adjacent SQ sites from the lateral mid-thigh were determined while the subjects were exposed to air at 1 ATA, hyperbaric air at 2 ATA, and HBO at 2 atmospheres. Mass spectrometer catheters, inserted into the thigh before the subject’s entered the hyperbaric chamber, were used to sample the tissue gases. Recordings were made with a mass spectrometer. Resting tissue gas readings were recorded at 1 ATA air before pressurization in the monoplace chamber  (Sechrist Model 2500B Monoplace Chamber, Sechrist Industries, Anaheim, CA; used for all exposures) using one of the 2 protocols (Table 2).

Mass Spectroscopy

Tissue gas analysis was performed with a Perkin-Elmer 1100 Mass Spectrometer® (Perkin-Elmer Inc, Foster City, CA) with four fixed detectors to record argon, CO₂, N₂, and O₂ ion tensions in mm Hg surrounding the instrument’s two sampling catheters. One was used to measure gases in the SQ space and the other in the MM compartment. Measurements were made at 2-minute intervals alternating the compartments. Thus, gas tensions for each sampling site were obtained every 4 minutes for the SQ space and every 4 minutes for the MM compartment. Tissue gases were obtained by continuous vacuum evacuation of minute gas samples from indwelling tubular catheters fitted with low-permeability Teflon (Medspec Catheters, Allied Health Care Products, St. Louis, MO) membranes. The 45.72 cm (18 in) long catheters had malleable, tubular stainless steel cores with an outside diameter of 0.139 cm (0.055 in). The exterior of the catheter was covered with a low-permeability Teflon sheath.

A small area, approximately 1 cm2, near the membrane tip was in communication with perforations into the catheter lumen. This served as the catheter’s gas sampling surface. Gases entered the catheter lumen by diffusion through the Teflon sheath. The gases were vacuum evacuated into the mass spectrometer for analysis. Each catheter was connected to the sampling port of the spectrometer with a 6-foot malleable stainless steel extension catheter and passed through gas tight fittings in the cephalic bulkhead of the hyperbaric chamber.

Calibration

The mass spectrometer was calibrated with catheters in dry 37˚C (98˚F) reference gases before probe insertion. Each gas was adjusted to zero while immersed in a reference gas free of N₂, O₂, or CO₂. The catheters were then immersed in a 37˚C, one ATA reference gas at the following partial pressures: (1) O_2, 152 mm Hg; (2) CO_2, 38 mm Hg; (3) N₂ at 380 mm Hg; and (4) argon at 190 mm Hg. Mass spectrometer readouts were calibrated to the preceding values. Calibration stability was assessed by repeating the above testing at the completion of each day’s trial. Dry gas calibration was used for expedience. Differences between dry and wet calibration are relatively minor, are predictable, and are amenable to simple mathematical correction. (This is discussed subsequently in this report.)

Catheter Insertion

After calibration, the catheters were inserted into skeletal MM and adjacent SQ tissues of each volunteer’s mid-lateral thigh at the onset of each trial. The vastus lateralis of the quadriceps group was used as the MM site, and the overlying SQ served as the representative SQ gas-sampling site.

The catheters were inserted into these sites through angiocaths. A 0.5-cm Lidocaine wheal provided local epidermal anesthesia. No additional anesthesia was used. The angiocaths, 20 cm (8 in) long, were inserted through the wheals and advanced 12.7 cm (5 in) distally into the chosen site. The angiocath trochars were removed and discarded. Then the 22-gauge thermistor-tipped probes were introduced into the catheters and positioned so the thermistor was at the tip of the angiocath sheath at the future gas sampling sites. The angiocath sheaths were left undisturbed for 20 minutes to facilitate hemostasis along the track of angiocath insertion and to provide time for thermal equilibration of the thermistor. The sampling site temperatures were recorded and the probes removed.

Next, the calibrated mass spectrometer catheters were inserted through the angiocath sheaths and advanced the length of the sheath. The catheters were held in place, and the angiocath sheaths were withdrawn. The catheters were secured to the extremity with adhesive tape so the gas-sampling surface was positioned at the deepest point of penetration.

Sampling Site Temperature Effects

Mass spectrometer gas measurement systems used in this study were, as expected, sensitive to sampling site temperature (Figure 1). Tissue catheters were calibrated to reflect the sampling site temperatures of each subject at the onset of each trial. In vivo tissue gas tension readings were mathematically corrected for temperature in two fashions: First, corrections were made for measurement errors from catheter calibration at one temperature and tissue recordings made at another. Second, corrections were made for dry and for wet catheter calibrations.

Gender differences of the temperature recordings were substantial. Consequently, we used gender-specific temperature corrections (Table 3). Compensations for both errors are incorporated into the correction values. Correction constants are obtained by multiplying the mean temperature difference from 37° by the mass spectrometer reading of the measured versus calibrated gas ratio.

Mass Spectrometer Response Delays

Mass spectrometers using low-permeability catheters do not respond instantaneously to changes in gas tensions. Changes in calibration gases are not fully reflected in the mass spectrometer readouts for 6 minutes. This delay is a reflection of the time required for gas diffusion through the diffusion-limiting membranes, transport through the catheter tubing, and processing in the mass spectroscopy unit itself.

Chamber Operations

Both protocols use a clinical monoplace hyperbaric chamber. Chamber flush rates of 400 L/min were used throughout the study to minimize adiabatic temperature effects and exhaled gas build-up (Figure 2).

Adiabatic increases in chamber gas temperature occurred with pressurization occurred, as expected (the Charles Gas Law Effect), with both flow rates. Temperatures increased in the chamber secondary to radiant heat exchange from the subjects at the slower flow rate as the time in the chamber increased.

Statistical Assessments

Analysis of variance used the F-test while the t-test revealed the probability of differences between the variables. We assessed the differences between the SQ spaces and the MM compartments of O₂, N₂, and CO₂ tensions in each protocol at each time interval. Individual step analyses (ISA) distinguished the significance of the differences between the SQ and MM spaces at each 4-minute interval (Tables 4 through 10). Nonsignificant conclusions are noted as NS, and significant differences are described in the text as well as tabulated in their level of significance (Tables 4 and 5).

RESULTS

Room Air

The mean MM N₂ tension from recordings at 4-minute intervals for each protocol are 20% lower (P < .001) than the adjacent subcutaneous measurements (Figures 3 and 4). Also, the MM O₂ and CO₂ tensions in each protocol are significantly lower than their SQ tensions: O₂.

Compression in Air

With compression in air to 2 ATA, O₂ and N₂ tensions increased significantly with essentially no differences between the two protocols, because to this point the protocols were identical. The MM O₂ increased significantly (P < 0.001) in both protocols. The MM N₂ increased significantly over the SQ N₂ in both protocols (protocol A, P = .043 and protocol B, P < .001).

The pooled (i.e., summation of both protocols) tension CO₂ increased significantly (P < .001) from 38.7 to 39.6 mm Hg in the SQ tissue, and the MM CO₂ decreased significantly (P = .037) from 45.6 to 45.1 mm Hg.

Hyperbaric O₂ Protocols

The N₂ tensions decreased significantly (P < .001) in both protocols. The MM N₂ in protocol A declined more in 90 minutes than it did after 120 minutes in protocol B (P < .001).

The increase of inhaled O₂ after changing from 2 ATA air to 2 ATA O₂ produced a significant (P < .001) increase in MM and SQ O₂ tensions in both protocols. However, no significant differences were seen between the MM and SQ compartment O₂ tensions during the entire 90-min breathing period in protocol A at 2 ATA. The MM O₂ is significantly increased (P = .024 to P < .001) over the SQ O₂ after each 20-minute O₂ period, but returns to nonsignificant levels that are lower than the SQ values after each air break (Tables 6 and 7). The air breaks produce a sharp saw tooth plot for the MM N₂ washout and a blunt hill and valley plot for the O₂ uptake.

Muscle and SQ CO₂ tensions declined significantly (P < .001) in both protocols. This accounted for a 10% decrease in CO₂ tension by the end of the 90-min O₂ breathing period at 2 ATA (Figure 5). After each air break in protocol B barely perceptible elevations in mean CO₂ tensions were seen. The MM CO₂ tensions were approximately 10% higher than the SC CO₂ tensions for both protocols (P < .001).

One Atmosphere Air Recovery Period

After decompression and a 30-minute observation period breathing ambient air (approximately 1 ATA), the MM and SQ O₂ tensions remained elevated above their precompression levels. The MM and SQ N₂ tensions increased gradually but remained less than precompression tensions during this 30-min observation period (Table 8 and 9).

COMPLICATIONS

One subject developed a hematoma at the probe site which resolved spontaneously; data from this subject were not included. We suspected a hematoma or arterial cannulation when the recorded O₂ level exceeded 1000 mm Hg on exposure to 2 ATA O₂. One week later, a nodule was noted in the muscle near the probe insertion site in this subject. We avoided this complication subsequently by not inserting the mass spectrometer catheter until the angiocath sheath remained in the tissue site for 30 minutes. Although minor complaints of middle ear barotraumas were noted such as “ear popping” and “clicking sounds” with middle ear pressure equilibration, feelings of fullness behind the ear drum and muting of sound after the exposures; no subject needed medical interventions for these complaints. No seizures occurred in our subjects during the study and no study was interrupted due to what could be considered prodromal seizure symptoms such as anxiety, tunnel vision, tinnitus, tremors, or hyperventilation.

DISCUSSION

We report the largest collection of human volunteer tissue gas measurements: over 16,000 measurements. Our study is the first to compare tissue gas measurements for two commonly used monoplace and multiplace HBO treatment protocols. From this information, it is apparent that there are differences in O₂ loading and N₂ washout using HBO with and without air breaks. Whether or not these differences have clinical significance will need to be ascertained with further studies. Although our subjects were healthy volunteers, we assume that similar or magnified effects would be observed in patients in whom HBO is being used for appropriate clinical indications.

Our measurements were consistent with previous reports that used a variety of measurement techniques including gas pocket, implanted silastic tube, polarographic, and mass spectrometry technologies.1,5,13,14 In room air, MM O₂ tensions were about one third (approximately 30 mm Hg) of normal arterial gas O₂ tension (approximately 100 mm Hg). Remarkably, the resting SQ O₂ tensions were much higher (approximately 45 mm Hg). This is almost 50% of the arterial gas O₂ tension, but approximately one third of the ambient air O₂ tension (approximately 152 mm Hg). Our conclusion from these observations is that O₂ from the ambient air diffuses through the skin into SQ tissues.

Muscle and SQ CO₂ tensions were essentially the same for each compartment regardless of the protocol used and are consistent with a prior mass spectroscopy study.15 The CO₂ data as in the O₂ observations support our hypotheses that the skin is also an organ of gas exchange for CO₂, consistent with a previous report.19 Mean resting SQ N₂ tensions in both protocols approximated the computed theoretical values15 and expected values. (NOTE: N₂ may reasonably be assumed to be metabolically inert. Therefore, the N₂ tension of normal internal human tissue under steady state conditions should approximate that of blood and alveolar gases. Alveolar gas tension at 1 ATA is 760 mm Hg. Only N₂, O₂, CO₂, H₂O, and argon are present in the typical alveolar gas mixtures in greater than trace amounts. H₂O vapor’s pressure, at a nominal 37°C core temperature, is 47 mm Hg. CO₂’s partial pressure in alveolar gas may be taken to be approximately 40 mm Hg, O₂’s 100 mm Hg, and argon’s to be 7mm Hg. The remainder should be almost entirely N₂ [760–47–40–100 – 7 = 566 mm Hg].)

However, the mean MM N₂ tension of 425 mm Hg was more than 20% below this expected value even though we expect MM N₂ to be in equilibrium with capillary alveolar N₂ tensions. We are unable to explain this discrepancy, but the consistency of our recordings suggests that there is an underlying physiologic explanation.

Tissue Gas Tensions in Hyperbaric Air

To this point in our study, protocols A and B were identical. As expected, increasing the ambient pressure to 2 ATA air increased the N₂ and O₂ tensions in both the MM and the SQ during the 30 minute exposure. However, the increases in O₂ MM and SQ tensions, which ranged from 20% to 26.7%, were more than the 12.5% increments predicted from Dalton’s (partial pressure} and Charles’ (gas solubility) laws. Possible explanations include:

(1) The elevation of O₂ tensions induced vasoconstriction, which in turn reduce perfusion,20–23 decreasing flow so less O₂ extraction occurred.

(2) Because 2.5% of the O₂ carrying capacity of the blood is by physically dissolved O₂ in the plasma, the doubling of the inspired O₂ partial pressure would only double the physically dissolved portion of the O₂ carrying capacity of the blood. This would theoretically account for 10.25% increase in the O₂ carrying capacity of blood rather than the 20 % we observed. (NOTE: “Doubling” the physical dissolved oxygen increases the arterial blood O₂ content from 20 volumes (vol) percent to 20.5%. This should be reflected in a 10.25% increase in tissue oxygenation.)   

(3) Elevations in tissue O₂ tensions interfere with oxyhemoglobin dissociation and the movement of O₂ from the blood to the tissues. Oxygenation of tissues is not only influenced by blood O₂ transport and perfusion, but also tissue oxygen tensions. The closer the blood borne and tissue O₂ tensions are to each other, the smaller the “driving force” (gradient) for O₂ to move into tissues.

Nitrogen tensions in the SQ increased by 25% as a result of being compressed in 2 ATA air, while the MM tensions increased by 60%. Tissue N₂ tensions did not achieve steady-state values by the time the 30-min 2 ATA air exposure was completed (Figures 3 and 4). The increased wash-in of N₂ in MM compared with SQ to this point reflects, in our opinion, the differences in perfusion of the MM and SQ tissues.

Paradoxically, MM CO₂ decreased significantly (0.03), and the SQ increased significantly (P < .001). This observation is consistent with earlier SQ pocket CO₂ measurements noting hyperbaric air exposures cause a slight rise in CO₂ tensions.24,25

Tissue Gas Tensions in Hyperbaric Oxygen

Protocol A’s 90-min exposure at 2 ATA O₂ increased the MM O₂ tensions to 158 mm Hg or 5.7-fold (33.4 to 192 mm Hg), and SQ O₂ tensions rose 4.47-fold (53.3 to 238.4 mm Hg). Protocol B’s longer, air break-punctuated HBO exposure increased MM O₂ tension 176 mm Hg, also 5.6-fold (38 to 214 mm Hg) (Table 10). These findings are reasonably consistent with results of previous limited polarographic26,27 and mass spectrometer studies.13,14      

Our studies show that the representative monoplace and multiplace treatment protocols were essentially equally effective in elevating tissue O₂ tensions – the objective of clinical hyperbaric O₂ therapy.

The mean SQ O₂ tension of protocol A, after a 90 minute 2 ATA O₂ exposure, was 12 % higher than that in Protocol B’s 120 minute 2 ATA O₂ exposure. This difference may be due to air breaks in protocol B’s or from differences in O₂ diffusion through the skin, because the chamber was pressurized with O₂ in protocol A and with air in protocol B.28–31 In protocol B, the increase in muscle O₂ was more rapid in the initial 20 minute O₂ exposure. This is attributed to the immediate breathing of 100% O₂ at 2 ATA via the regulator in protocol B, whereas in protocol A, replacing the 2 ATA air in the chamber to 2 ATA 100% O₂ (without a regulator) requires approximately 20 minutes at an ideal inflow rate of O₂ at 400 L/min.32

The effectiveness of reduction in N₂ tensions was different in the two protocols. Muscle N₂ was reduced 653 mm Hg (720 to 67 mm Hg) or to 9.3% of its maximum 2 ATA air starting point in protocol A. In protocol B, the reduction was 602 mm Hg (733 to 131 mm Hg) to 17.98% of its maximum 2 ATA air starting point. The differences were significant (P < .001). This may have important ramifications for extravehicular space activities, because a 90-min 2 ATA O₂ exposure would lessen the N₂ washout time by less than one third of what it is for breathing O₂ at sea level.33 In addition, the diffusion of gases through the skin may be important.34–37 Compression in air, as in the multiplace protocol, establishes a transcutaneous gradient favoring tissue uptake of N₂. Conversely, compression in O₂ as in the monoplace protocol establishes a transcutaneous N₂ gradient favoring tissue N₂ loss through skin. Hyperbaric air breaks, used primarily in multiplace protocols in an effort to reduce O₂ toxicity, cause periodic tissue increments of N₂ and decrements in O₂ tensions. The initial report of this technique used a normoxic gas mixture at 3 ATA (7% O₂ with 93% N₂) to prevent in O₂ toxicity.38 The effects of air breaks on tissue gas tensions are most apparent in MM but are also seen in the SQ tissues (Figure 4). This information provides a rationale for treating decompression illness without air breaks, such as the Hart treatment table.39,40

Early observations suggest that HBO exposure had little effect or slightly elevated tissue CO₂ tensions.41–43 Subsequent mass spectroscopic analyses revealed that HBO depressed CO₂ tension.13,14 We noted that protocol A’s HBO exposure reduced CO₂ tension by 11% (approximately 4.3 mm Hg), while protocol B’s HBO exposure reduced it by 16% (approximately 7.5 mm Hg). Subcutaneous tissue CO₂ tensions responded similarly (P < .001). Tissue CO₂ tension declines seen by mass spectroscopy may reflect respiratory compensation (such as imperceptible hyperventilation) caused by the reduction in venous hemoglobin’s buffering capacity and acidosis. Venous hemoglobin’s CO₂ carrying capacity is reduced in the presence of elevated O₂ tensions due to the displacement of CO₂ by the more firmly attached O₂ molecules.44–46

Tissue Gas Tensions During Recovery in 1 ATA Air

Thirty minutes of recovery in 1 ATA air was not sufficient for any measured gas to return to the precompression level. The O₂ tensions in the SQ decreased less rapidly than those in MM, as has been observed before.3 A recent report using MRI noted that MM O₂ tensions fell rapidly in contrast to those in solid tumor tissue, which remained elevated for at least 60 minutes after the HBO exposure.47 Change in CO₂ tension during the recovery interval is remarkable, because there is a highly significant rise (P < .001) toward precompression levels. The MM N₂ tensions returned to normal levels and the SQ N₂ tensions responded less rapidly during the air breathing period.

CONCLUSIONS

Multiple mass spectroscopic analyses of the tensions of O₂, CO₂, and N₂ in MM and adjacent SQ tissues were measured using two protocols. Protocol A approximated an exposure typical of an HBO treatment in monoplace chamber HBO treatment pressurized with O₂ and without air breaks while protocol B approximated a multiplace chamber HBO treatment where the chamber is pressurized with air, and the subject breathes O₂ through a regulator with intermittent air breaks.    

The objectives were to provide better resting human muscle and subcutaneous tissue O₂, CO₂, and N₂ tension values than previously available and to compare the effects of representative HBO protocols on tissue O₂ accumulation and tissue N₂ washout.

From more than 16,000 individual human tissue gas determinations we observed the following: (1) Normal room air values for resting human MM and SQ tissue O₂, CO₂ and N₂ tensions ([MM O₂: 28 mm Hg ± 7, MM N₂:437mm Hg ± 47, MM CO₂: 45mm Hg ± 4] [SQ O₂: 44mm Hg ± 10, SQ N₂:540mm Hg ± 55, SQ CO₂: 38mm Hg ± 4])

There are differences in gas exchanges with protocols A and B. In protocol A, MM N₂ tension decreased 9% more than protocol B with 11% less O₂ exposure time. In protocol A, SQ O₂ tension increased 12% more than protocol B with 9% less time. In protocol B, MM O₂ tension was 9% higher than protocol A, with 11% more exposure time at 2 ATA O₂. The skin acts as an organ for gas exchange for O₂, N₂, and CO₂

Air Breaks as used in protocol B are a source of rapid N₂ deposition into the tissues and may be a possible explanation why patients with mixed air embolism and decompression sickness deteriorate with tables analogous to protocol B.48,49 Absence of air breaks in Protocol A was not a cause of O₂ toxicity in our study group.

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Table 1. Anthropomorphic Characteristics of Subjects

 

Item                                                  Men                Women                Total

Protocol A

Number (%)                                    15(44)               21(66)               36(100)

Mean Age (y ±)                        38.9 Yrs ± 13     31 Yrs ± 6.5        34.5 ± 10.9

Mean Height/Inches (± SD)           70 ± 2.8           64.5 ± 2.2          66.8 ± 3.72

Mean Weight/Pounds (± SD)     184.4 ± 23.9      131.3  ± 18.7      153.4 ± 34.1

Protocol B

Number (%)                                    12(36)               21(64)               33(100)

Mean Age (y ± SD)                     41.6 ± 13.4        31Yrs ± 6.5          35 ± 11.2

Mean Height (in ± SD)                  70.3 ± 2.8          64.5 ± 2.2           66.8 ± 3.8

Mean Weight (lb ± SD)               184.5 ± 25.9      131.3 ± 18.7          150 ± 33

‡Atmospheres absolute.

 

Table 2. Comparison of Protocols A and B

 

                             Protocol A*                                                                       Protocol B†

                                      Exposure     Accumulated                                            Exposure      Accumulated
Step    ATA‡     Gas          Time             Time                   ATA‡       Gas           Time               Time

1             1          Air       Baseline              0                           1           Air         Baseline               0

2             2          Air         30 min           30 min                      2           Air           30 min             30 min

3             2          O₂         90 min          120 min                     2            O₂           20 min             50 min

4             1          Air         30 min          150 min                     2           Air            5 min              55 min

5                                                                                             2            O₂           20 min             75 min

6                                                                                             2           Air            5 min              80 min

7                                                                                             2            O₂           20 min            100 min

8                                                                                             2           Air            5 min             105 min

9                                                                                             2            O₂           20 min            125 min

10                                                                                           2           Air            5 min             130 min

12                                                                                           2            O₂           20 min            150 min

13                                                                                           1           Air           30 min            180 min

*Compressed in O₂ and breathing O_2.

†Compressed in air and O₂ breathing by SCUBA regulator.

 

 

 

Table 3. Correction Constants (K) For Tissue Temperature

 

                                                     Male                                        Female

                                          MM                 SQ                      MM               SQ

Mean Temperature          36.2 C           33.32 C                36.83 C        34.02 C

O₂ K                                   1.45                 1.6                      1.41             1.56

N₂ K                                   1.39                1.55                     1.35             1.51

CO₂ K                                1.12                1.17                     1.11             1.16

 

Table 4. Two ATA Air, Protocol A

 

                       A: SQ Vs MM N₂                             A: SQ Vs MM O₂                         A: SQ Vs MM CO₂

ISA            P1            P2            P3                 P1            P2            P3                 P1          P2

A20           NS       0.000001    1E–07           0.0012     1E–07      1E–07              NS       1E–07    0.0007

A21           NS       0.000017    1E–07            0.001      1E–07      1E–07              NS       1E–07     0.009

A22           NS         0.0073      1E–07           0.0001     1E–07      1E–07              NS       1E–07     0.014

A23           NS            NS         1E–07          0.00009    1E–07      1E–07              NS       1E–07     0.017

A24           NS            NS         1E–07          0.00002    1E–07      1E–07              NS       1E–07     0.021

A25           NS            NS         1E–07          0.00003    1E–07      1E–07              NS       1E–07     0.035

A26           NS            NS         1E–07          0.00002    1E–07      1E–07              NS       1E–07       NS

A27           NS          0.043       1E–07          0.00001    1E–07      1E–07              NS       1E–07       NS

A28           NS          0.043       1E–07          0.00001    1E–07      1E–07              NS       1E–07       NS

O0             NS          0.045       1E–07          0.00009    1E–07      1E–07              NS       1E–07       NS

 

Table 5. Protocol B

 

                       B: SQ Vs MM N₂                             B: SQ Vs MM O₂                         B: SQ Vs MM CO₂

ISA            P1            P2            P3                 P1            P2            P3                 P1          P2          P3

A20           NS         1E–07       1E–07              NS         1E–07      1E–07             0.05      1E–07     0.025

A21           NS          0.042       1E–07              NS      0.000009    1E-07            0.036     1E-07      0.023

A22           NS            NS          1E-07               NS       0.00012     1E-07            0.027     1E-07      0.018

A23           NS            NS          1E-07               NS       0.00014     1E-07            0.034     1E-07      0.024

A24           NS           0.03        1E-07               NS       0.00009     1E-07              NS        1E-07      0.046

A25           NS          0.005       1E-07               NS       0.00006     1E-07             0.04      1E-07        NS

A26           NS         0.0012      1E-07               NS       0.00005     1E-07              NS        1E-07        NS

A27           NS        0.00015     1E-07               NS       0.00003     1E-07              NS        1E-07        NS

A28           NS         0.0007      1E-07               NS       0.00002     1E-07              NS        1E-07        NS

O0             NS          0.029       1E-07               NS           NS         1E-07              NS        1E-07        NS

 

SQ = subcutaneous tissue; MM = muscle; A2 = 2 ATA air; NS = no significant difference.

P-Values:                               

F- Test = P1          

t-Test = P2

Chi-square test = P3

 

 

Table 6. Two ATA O2 , Protocol A

 

                       A: SQ Vs MM N₂                             A: SQ Vs MM O₂                         A: SQ Vs MM CO₂

ISA            P1            P2            P3                 P1            P2            P3                 P1          P2          P3

O0             NS          0.045       1E-07           0.00009     1E-07       1E-07              NS        1E-07        NS

O1            0.03          NS          1E-07              0.04       0.0092      1E-07              NS        1E-07        NS

O2           0.054       0.054       1E-07             0.057         NS         1E-07              NS        1E-07        NS

O3             NS        0.00003     1E-07               NS           NS         1E-07              NS        1E-07        NS

O4             NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O5             NS         1E-07       1E-07             0.037         NS         1E-07              NS        1E-07        NS

O6             NS         1E-07       1E-07             0.035         NS         1E-07              NS        1E-07        NS

O7             NS         1E-07       1E-07             0.027         NS         1E-07              NS        1E-07        NS

O8             NS         1E-07       1E-07             0.018         NS         1E-07              NS        1E-07        NS

O9             NS         1E-07       1E-07             0.015         NS         1E-07              NS        1E-07        NS

O10           NS         1E-07       1E-07            0.0089        NS         1E-07              NS        1E-07        NS

O11           NS         1E-07       1E-07             0.008         NS         1E-07              NS        1E-07        NS

O12           NS         1E-07       1E-07             0.007         NS         1E-07              NS        1E-07        NS

O13           NS         1E-07       1E-07             0.013         NS         1E-07              NS        1E-07        NS

O14           NS         1E-07       1E-07             0.017         NS         1E-07              NS        1E-07        NS

O15           NS         1E-07       1E-07             0.012         NS         1E-07              NS        1E-07        NS

O16           NS         1E-07       1E-07             0.015         NS         1E-07              NS        1E-07        NS

O17           NS         1E-07       1E-07             0.016         NS         1E-07              NS        1E-07        NS

O18           NS         1E-07       1E-07             0.013         NS         1E-07              NS        1E-07        NS

O19         0.031       1E-07       1E-07             0.012         NS         1E-07              NS        1E-07        NS

O20         0.013       1E-07       1E-07              0.01          NS         1E-07              NS        1E-07        NS

O21         0.015       1E-07       1E-07             0.008         NS         1E-07              NS        1E-07        NS

O22        0.0017      1E-07       1E-07             0.013         NS         1E-07              NS        1E-07        NS

 

Table 7. Two ATA Air, Protocol B

 

                       B: SQ Vs MM N₂                             B: SQ Vs MM O₂                         B: SQ Vs MM CO₂

ISA            P1            P2            P3                 P1            P2            P3                 P1          P2        P3

O0             NS          0.029       1E-07               NS           NS         1E-07              NS        1E-07        NS

O1            0.17          NS          1E-07            0.0001      0.003       1E-07              NS        1E-07        NS

O2             NS        0.00002     1E-07            0.0006     0.0007      1E-07              NS        1E-07        NS

O3             NS         1E-07       1E-07            0.0011      0.001       1E-07              NS        1E-07        NS

O4             NS         1E-07       1E-07             0.003       …002      1E-07              NS        1E-07        NS

O5             NS         1E-07       1E-07             0.008         NS         1E-07              NS        1E-07        NS

O6             NS         1E-07       1E-07               NS         0.027       1E-07              NS        1E-07        NS

O7             NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O8             NS         1E-07       1E-07              0.02        0.025       1E-07              NS        1E-07        NS

O9             NS         1E-07       1E-07             0.014       0.014       1E-07              NS        1E-07        NS

O10           NS         1E-07       1E-07             0.008       0.015       1E-07              NS        1E-07        NS

O11           NS         1E-07       1E-07             0.045         NS         1E-07              NS        1E-07        NS

O12           NS         1E-07       1E-07               NS         0.016       1E-07              NS        1E-07        NS

O13           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O14           NS         1E-07       1E-07             0.021         NS         1E-07              NS        1E-07        NS

O15           NS         1E-07       1E-07             0.059         NS         1E-07              NS        1E-07        NS

O16           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O17           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O18           NS         1E-07       1E-07               NS         0.057       1E-07              NS        1E-07        NS

O19           NS         1E-07       1E-07               NS         0.024       1E-07              NS        1E-07        NS

O20           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O21           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O22           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O23           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O24           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O25           NS         1E-07       1E-07             0.005      0.0005      1E-07              NS        1E-07        NS

O26           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O27           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O28           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O29           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

O30           NS         1E-07       1E-07               NS           NS         1E-07              NS        1E-07        NS

 

SQ = subcutaneous tissue; MM = muscle; A2 = 2 ATA air; NS = no significant difference.

P-Values: F- Test = P1, t-Test = P2, Chi-square test = P3

 

 

 

Table 8. One ATA Air, Protocol A

 

                       A: SQ Vs MM N₂                             A: SQ Vs MM O₂                         A: SQ Vs MM CO₂

ISA            P1            P2            P3                 P1            P2            P3                 P1          P2        P3

A0           0.007       1E-07       1E-07             0.002         NS         1E-07              NS        1E-07        NS

A1           0.051       1E-07       1E-07            0.0002     0.0016      1E-07              NS        1E-07        NS

A2             NS         1E-07       1E-07          0.000003  0.00002     1E-07              NS        1E-07        NS

A3             NS         1E-07       1E-07            1E-07    0.000003    1E-07              NS        1E-07        NS

A4             NS         1E-07       1E-07            1E-07    0.000003    1E-07              NS        1E-07        NS

A5             NS         1E-07       1E-07            1E-07    0.000004    1E-07              NS        1E-07        NS

A6             NS         1E-07       1E-07            1E-07    0.000006    1E-07              NS        1E-07        NS

A7             NS         1E-07       1E-07            1E-07    0.000008    1E-07              NS        1E-07        NS

A8             NS       0.000001    1E-07            1E-07    0.000011    1E-07              NS        1E-07        NS

 

Table 9. Protocol B

 

                       B: SQ Vs MM N₂                             B: SQ Vs MM O₂                         B: SQ Vs MM CO₂

ISA            P1            P2            P3                 P1            P2            P3                 P1          P2        P3

A0             NS         1E-07       1E-07               NS         0.025       1E-07              NS        1E-07        NS

A1             NS         1E-07       1E-07               NS       0.00053     1E-07              NS        1E-07        NS

A2             NS         1E-07       1E-07             0.005    0.000008    1E-07              NS        1E-07        NS

A3             NS         1E-07       1E-07           0.00004  0.000001    1E-07              NS        1E-07        NS

A4             NS         1E-07       1E-07          0.000002 0.000001    1E-07              NS        1E-07        NS

A5             NS         1E-07       1E-07          0.000001 0.000002    1E-07              NS        1E-07        NS

A6             NS         1E-07       1E-07            1E-07    0.000004    1E-07              NS        1E-07    0.00001

 

SQ = subcutaneous tissue; MM = muscle; A2 = 2 ATA air; NS = no significant difference.

P-Values: F- Test = P1   

t-Test = P2

Chi-square test = P3

 

 

Table 10. Summary of Mean Gas Tensions mm Hg

 

Exposure                  1ATA Air                    2 ATA Air                    2 ATA O₂                     ATA Air

Protocol                A                    B            A                    B            A                 B            A                B             

MMCO₂                45.4               45.6       45.1               45.2        40.8             37.7        41.9            40.4

MMN₂                   430                445        720                733          67             131.3       290             352

MMO₂                    28                  30          34                  38          192              214         41.9            44.3

SQCO₂                  39                  39         39.6               39.8        35.9             34.3        37.4            36.4

SQN₂                    540                540        676                677         376              389         404             416

SQO₂                    45                  43          54                  53          238              211         114              97

 

A = Protocol A-36 subjects; B = Protocol B-33 subjects; MM = muscle;  SQ = subcutaneous, Baseline gases,

 

Figure 1. Mass Spectroscopy Probe. Wet membrane calibration from: Dry Gas: N₂-380mm, 0₂-152mm, CO₂-38 mm, and Ar-190 mm Hg.

 

Figure 2. Adiabatic change in an occupied monoplace chamber: subcutaneous and muscle N2 and O2: Protocol A.

 

Figure 3. Subcutaneous and muscle N2 and O2: Protocol A.

 

Figure 4. Subcutaneous and muscle N2 and O2: Protocol B.

 

Figure 5. Subcutaneous and muscle CO2, Protocols A and B.