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Increased Partial Pressure of Oxygen

Breathing O2 at increased ambient pressure will lead to elevation of alveolar O2 tension (PAO2 ), which can be calculated according to the alveolar gas equation for O2 :





where PIO2 and FIO2 are the inspired partial pressure and fractional O2 concentration, respectively; PACO2 is alveolar PCO2 , assumed to equal arterial PCO2 (PaCO2 ); and R is the respiratory exchange ratio (usually ≅0.8 at rest). Calculated values are shown in Table 70-4 . Arterial PO2 (PaO2 ) has


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Figure 70-2 Ambient pressure as a function of altitude and water depth. Whereas ambient pressure increases linearly with depth, pressure and altitude are not linearly related. As air is inspired and humidified, there is a small and usually insignificant drop from atmospheric PO2 to inspired PO2 . At altitude, however, this decrease accounts for a greater proportion of the total ambient pressure. The O2 partial pressure line in the water is shown for a constant FIO2 of 21%. At increasing depth, the inspired PO2 eventually exceeds the pulmonary toxic limit (≅14 m in depth) and the central nervous system toxic limit (≅70 m in depth). The threshold for high-pressure nervous syndrome and pressure reversal of anesthesia (observed in non-narcotic atmospheres) is around 150 to 200 m in depth. The shaded red bars represent the depth or altitude ranges over which risk progresses from low (light shading) to high (dark shading). AMS, acute mountain sickness; HACE, high-altitude cerebral edema; HAPE, high-altitude pulmonary edema.

been estimated from calculated values of PAO2 , assuming that the arterial-alveolar PO2 ratio remains constant.[64] Whereas at 1 ATA the fraction of O2 in arterial blood that is carried dissolved in plasma is minimal, it can be seen that at elevated PaO2 in the range of 1000 to 2000 mm Hg, significant quantities of O2 may exist in dissolved form ( Fig. 70-3 ).


TABLE 70-3 -- Units of pressure
Atmospheres Absolute (ATA) Absolute Pressure (mm Hg) Gauge Pressure (mm Hg) Feet of Sea Water (fsw) Meters of Water (msw)
1  760    0   0  0
2 1520  760  33 10
3 2280 1520  66 20
6 4560 3800 165 50


TABLE 70-4 -- Theoretical * gas tensions and arterial blood O2 content at various ambient pressures in a normal individual (Hb, 14 g/dL)
Pressure (ATA) FIO2 Inspired PO2 (mm Hg) PAO2 (mm Hg) PaO2 (mm Hg) CaO2 (Total) (mL/dL) CaO2 (Dissolved) (mL/dL) PaCO2 (mm Hg)
1 0.21  150  102   87 18.7 0.3 40
1 1.0   713  673  572 21.2 1.7 40
2 1.0  1473 1433 1218 23.1 3.7 40
3 1.0  2233 2193 1864 25.1 5.6 40
*Assuming constant PaO2 /PAO2 ratio.[64]




Increased PaO2 has at least four pharmacologic effects:

Increased blood O2 content

Vasoconstriction

Antibacterial action, particularly against anaerobic bacteria

Inhibition of endothelial neutrophil adhesion in injured tissue


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Figure 70-3 Blood O2 content versus PO2 . Virtually complete saturation of hemoglobin with O2 occurs at a PO2 of 100 mm Hg. Further increases in PO2 do not alter the quantity of O2 bound to hemoglobin. However, there is a linear increase in total blood O2 content with PO2 because of increasing quantities of O2 dissolved in plasma.

The increased arterial O2 content underlies the rationale for administering HBO for the treatment of ischemic conditions, for example, ischemic, nonhealing wounds. The elevation in PaO2 leads to an increase in tissue PO2 , which can be estimated by using transcutaneous PO2 electrodes, even in ischemic tissue.[65] [66] The second effect is an explanation for the effectiveness of HBO in the treatment of traumatic edema (e.g., crush injury). The mechanism of HBO-induced vasoconstriction appears to be inactivation of nitric oxide (NO) as a result of increased production of superoxide[67] [68] and possibly decreased release of NO from circulating S-nitrosohemoglobin. [67] [69] [70]

These two effects, increased O2 content and vasoconstriction, lead to hemodynamic changes,[70] [71] which are shown in Table 70-5 . The elevation in PaO2 that occurs while breathing 100% O2 at 3 ATA results in a drop in cardiac output and heart rate and an increase in total peripheral resistance. There is also a slight increase in mean arterial pressure.

The other major pharmacologic effect of increased PaO2 is the inhibition of toxin production and growth of certain anaerobic bacteria. Additionally, increased PaO2 has been shown to return phagocytic function and the ability of aminoglycosides to kill aerobic bacteria in ischemic tissue to normal.[31] [72]

HBO also has some poorly characterized microcirculatory and cellular effects. Zamboni and colleagues[36] [37] [73] described a reduction in blood flow on reperfusion of ischemic myocutaneous tissue flaps. This decrease in flow appears to be due to leukocyte adherence to the capillary endothelium mediated by leukocyte adhesion glycoprotein CD18,[74] an effect that is prevented and ameliorated by HBO treatment.[36] [37] [73] [75] In an animal model, timely administration of HBO also appears to decrease the lipid peroxidation in the brain that occurs after treatment of carbon monoxide (CO) poisoning.[76]

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