Measurements of subcutaneous oxygen tension (PscO₂), subcutaneous carbon dioxide tension (PscCO₂) and subcutaneous pH (pHsc) were used for evaluation of peripheral oxygenation in pigs subjected to oleic acid-induced lung injury during ventilation with increasing levels of positive end-expiratory pressure (PEEP). Lung injury resulted in a decrease of arterial oxygen tension (PaO₂) from 93 to 37 mm Hg (p < 0.01) with maintained cardiac output. PscO₂ decreased from 45 to 17 mm Hg (p < 0.01) and pHsc from 7.47 to 7.39 (p < 0.05), and PscCO₂ increased from 46 to 59 mm Hg (p < 0.05). Increase of PEEP level between 5 and 20 cm H₂O resulted in a continuous increase of PaO₂ from 45 to 145 mm Hg and a decrease of cardiac output from 4.1 to 2.0 liters/min (p < 0.01). PscO₂ increased up to a PEEP level of 15 cm H₂O, reaching 26 mm Hg. Further increase of PEEP level up to 20 cm H₂O resulted in an increase of PscCO₂ from 65 to 71 mm Hg (p < 0.05) and a decrease of pHsc from 7.31 to 7.29 (p < 0.05). In conclusion: measurements of tissue gases and pH can be used to evaluate optimum peripheral tissue oxygenation during titration of PEEP level. Whether these measurements can be used as the only indicator to guide therapy in an individual case remains to be studied.

The new Paratrend 7 and the old Biogenesis sensors generate almost equal tissue oxygen-tension values in response to changes in arterial oxygen tension. The Continucath sensor generates almost 50% higher values compared with the Paratrend 7 and Biogenesis sensors, both with and without tonometer.

The effect of different fractions of inspired oxygen on subcutaneous oxygen tension, carbon dioxide tension and pH in relation to arterial and mixed venous blood gases and pH and hemodynamic variables was evaluated in 13 domestic pigs. Subcutaneous, arterial and mixed venous oxygen tensions were closely correlated (r = 0.94). A minor significant increase in subcutaneous carbon dioxide tension was noted during hyperoxia (p < 0.05). A major increase (33%) was noted during the last step of hypoxia, when arterial and mixed venous carbon dioxide tensions increased only 12 and 17%, respectively. A minor decrease in subcutaneous pH was noted during hyperoxia (p < 0.05) and a major decrease during hypoxia (p < 0.05). Measurements of subcutaneous tissue gases and pH are indicators of oxygen utilization during hyper- and hypoxia.

Evaluation of splanchnic perfusion and oxygenation was performed by measurements of serosal tissue oxygen tension (PserO₂) and intramucosal pH (pHi) in relation to subcutaneous oxygen tension (PscO₂), subcutaneous carbon dioxide tension (PscCO₂) and subcutaneous pH (pHsc) in pigs subjected to oleic acid-induced lung injury during ventilation with increasing levels of positive end-expiratory pressure (PEEP). Lung injury resulted in a general hypoxia and redistribution of perfusion away from the subcutaneous and splanchnic tissues, illustrated by a decrease in PaO₂ from 93 to 37 mm Hg (p < 0.01), PscO₂ from 45 to 17 mm Hg (p < 0.01), PserO₂ from 80 to 30 mm Hg (p < 0.01) and pHi from 6.84 to 6.74 (p < 0.05) and a decrease of porta flow from 0.77 to 0.57 l/min. Application of PEEP up to 10–15 cm H₂O resulted in an increase of portal vein oxygen tension (PportaO₂) from 21 to 34 mm Hg (p < 0.01), PscO₂ from 17 to 26 mm Hg (p < 0.05) and PserO₂ from 30 to 55 mm Hg (p < 0.05). At PEEP 20 cm H₂O PserO₂ decreased to 47 mm Hg (p < 0.05). Porta flow decreased continuously with increasing levels of PEEP. PserO₂ correlated with PportaO₂ (r = 0.7, p < 0.001). pHi correlated poorly with PportaO₂ (r = 0.2) and porta flow (r = 0.4). PscO₂ and PserO₂ correlated well (r = 0.8, p < 0.001). In summary, splanchnic perfusion and oxygenation was better reflected by serosal oxygen tension than pHi in the colon. Changes in serosal oxygenation of the colon paralleled changes in subcutaneous tissue oxygenation.

Peripheral tissue oxygen utilization was studied during hypoxic-induced acidosis and sodium bicarbonate-induced alkalosis in 8 domestic pigs by measurements of subcutaneous oxygen tension (P_scO₂), carbon dioxide tension (P_scCO₂) and pH (pH_sc) in relation to central hemodynamic parameters and oxygenation. Hypoxic-induced acidosis resulted in a decrease in P_scCO₂ and arterial oxygen tension (P_aO₂) to one third of baseline values (p < 0.05), an increase in P_scCO₂ and arterial carbon dioxide tension (P_aCO₂) from 41 to 55 and 34 to 39 mm Hg, respectively (p < 0.05), and a decrease in pH_sc from 7.47 to 7.30 (p < 0.05). P_scO₂ and P_aO₂ increased during reversal of hypoxia and infusion of bicarbonate (p < 0.05), without reaching baseline values. In parallel P_scCO₂ decreased and pH_sc increased but changes lagged behind changes in blood gases. Alkalosis established by further infusion of bicarbonate resulted in a decrease in P_aO₂ to 62 mm Hg whereas P_scO₂ remained below baseline values (p < 0.05). Correction of oxygen utilization in the subcutaneous tissue as measured by the markers P_scCO₂ and pH_sc is slower than indicated by changes in tissue oxygen tension, blood gases and pH. Overcompensation of acidosis with bicarbonate resulting in alkalosis impairs oxygenation.