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The difference in CO2 tension between venous and arterial blood (delta PCO2) increases in low-flow states. Therefore, delta PCO2 has been suggested as an additional variable in the monitoring of perfusion. We measured CO2 tensions in arterial, mixed venous, hepatic venous, and femoral venous blood in 42 postoperative cardiac surgery patients. Splanchnic and leg blood flow was measured with dye dilution. Forty-three preoperative abdominal surgery patients served as controls. Systemic and femoral delta PCO2 was increased in cardiac patients, whereas there was no difference in splanchnic delta PCO2 between the groups. In cardiac patients, systemic delta PCO2 correlated well with both splanchnic and femoral delta PCO2 (r2 = .74 and r2 = .56, respectively). Femoral delta PCO2 was higher than splanchnic delta PCO2 (1.27 +/- .44 kPa versus .66 +/- .41; p < .001) after cardiac surgery, but not in the control group. The correlation between delta PCO2 and respective blood flow was weak in the whole body, the splanchnic region, and the leg. When splanchnic blood flow was low, systemic and splanchnic delta PCO2 varied widely. In the cardiac patients with an increased systemic delta PCO2 (> .93 kPa), systemic and regional blood flow was low, but there were no differences in systemic or regional oxygen consumption or lactate levels. After cardiac surgery, high systemic delta PCO2 is associated with marginal systemic and regional perfusion. The adequacy of regional blood flow cannot be assessed on the basis of the systemic delta PCO2.

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BACKGROUND AND METHODS: Hepatic dysfunction after severe hemorrhagic shock is common and may be a consequence of visceral tissue hypoxia. Peripheral tissue PO2 has been suggested to correlate with the development of visceral hypoxia. To test the hypothesis that changes in peripheral tissue PO2 reflect changes in hepatic PO2, we measured subcutaneous PO2, transcutaneous PO2, transconjunctival PO2, and liver tissue PO2, and their relationship with changes in mean arterial blood pressure (MAP) and systemic oxygen transport (DO2), during progressive bleeding in pigs (n = 23). In addition to the tissue PO2, portal vein PO2 and circulating lactate concentrations were also measured in six of the animals. The animals were anesthetized and bled to an MAP of 50 mm Hg within 1 hr. RESULTS: After an induced 10% reduction of MAP, only the DO2 decreased significantly (p less than .05). After a 20% reduction of MAP, the DO2 decreased further and was associated with a significant (p less than .05) reduction of all peripheral tissue PO2 values. A significant (p less than .05) reduction of liver tissue PO2 was observed later during bleeding, after induction of a 30% reduction in MAP. In the subgroup with portal venous PO2 and lactate measurements, reductions of all peripheral tissue PO2 and portal venous PO2 values occurred after a 20% reduction (p less than .05) of MAP. An increase (p less than .05) in the portal venous lactate concentration was observed after a 50% reduction of MAP, and a decrease (p less than .05) in liver tissue PO2 was noted after a 60% reduction of MAP. CONCLUSIONS: Reductions of both peripheral and portal venous PO2 values occur early during hemorrhage. The liver tissue PO2, though initially low, appears to be better defended, suggesting either redistribution of splanchnic blood flow or adaptation in hepatic oxygen demand.

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We compared the 95% response time (95% RT) of two tissue oxygen tonometers under two sets of circumstances. We first evaluated the devices during normoxia, hyperoxia, and anoxia in vitro, using a transcutaneous PO2 electrode (PtcO2) as the reference. The responses to normoxia and to different grades of hyperoxia were examined in vivo in 8 healthy volunteers to assess the relationship between changes in subcutaneous PO2 and PtcO2, an estimate of arterial PO2 (PaO2). One subcutaneous method (ScA) used a technique based on a polarographic needle electrode in situ connected to an ammeter; the second method (ScB) was based on a blood gas analyzer system first described by Hunt (Lancet 164;2:1370). ScA and PtcO2 both responded to stepwise changes in ambient oxygen concentration (21-100%) in vitro within 10 seconds; the 95% RT of ScA was 1.39 +/- 0.5 to 2.39 +/- 0.8 minutes and that of PtcO2 was 0.32 +/- 0.1 to 0.49 +/- 0.1 minutes. ScB had a lag of 3 minutes, and the 95% RT was 6.75 +/- 0.5 to 8.2 +/- 0.8 minutes. In contrast to the results in vitro, the response of ScA to changes in FiO2 in vivo was delayed compared with the rapid response of PtcO2, reflecting the physiologic delay of tissue PO2 in response to increased PaO2. The time lag and the long 95% RT of ScB were even more evident in vivo. ScA reacted three to four times faster than ScB, both in vitro and in vivo, to changes in the oxygen environment. The in vitro 95% RT of ScA to changes in ambient oxygen varied from 2 to 3.5 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

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We investigated the effects of clinically appropriate doses of NaHCO3 on tissue oxygenation when hemorrhagic shock was corrected with hydroxyethyl starch (hetastarch) in 12 piglets. Six animals received colloid only while six received colloid and bicarbonate. Both groups recovered rapidly hemodynamically, but conjunctival, subcutaneous, and liver tissue PO2 values returned to baseline more slowly after bicarbonate administration. In the NaHCO3 group, pulmonary artery wedge pressure and arterial bicarbonate concentration were higher during early resuscitation, and arterial plasma lactate remained higher than in the control group at the end of the follow-up period. The delayed increase in tissue PO2 values after bicarbonate infusion may be explained, at least partly, by decreased arterial blood oxygenation and a shift of the oxyhemoglobin curve to the left. NaHCO3 adjunct has no added beneficial effect on hemodynamics and may be harmful to tissue oxygenation in hemorrhagic shock resuscitated with hetastarch.

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Liver oxygenation was studied with hemorrhagic hypotension and corrected using whole blood, a synthetic colloid (hydroxyethyl starch or hetastarch, HES; mol. wt. 120,000), or a crystalloid solution. Measurements were performed directly by recording pig liver tissue oxygen tension with an implanted silicone elastomer (Silastic) tube, and indirectly by calculating blood oxygen contributions. The direct method seems fairly reliable and accurately reflects different levels of bleeding and shock and their correction. Liver tissue oxygen tension (PlO2) may thus be used as an indicator of central organ response to shock management. PlO2 decreased during bleeding from 33.5 +/- 0.5 to 16.0 +/- 0.5 torr, and normalized rapidly after retransfusion. The baseline values were significantly exceeded after hetastarch infusion but were never reached with Ringer's solution. The correction of liver oxygen consumption was less complete after crystalloid infusion as well. On the other hand, the difference in liver oxygenation was less marked after crystalloid infusion and retransfusion, which restored perfusion to the baseline. The total amount of Ringer's solution needed to keep the animals hemodynamically stable during the 2-h follow-up period was four times higher than with hetastarch and some five times the blood volume shed. The cause of defective correction of liver oxygenation seems to be the poor response of liver blood flow to refilling in the Ringer group, in addition to apparent tissue edema after crystalloid infusion. According to our study, hemorrhagic hypotension related to liver oxygenation is more promptly and completely corrected with the colloid hydroxyethyl starch than with a crystalloid solution in the early phase of treatment.

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Because it is difficult to verify the efficacy of hemorrhagic shock treatment, we compared subcutaneous O2 tension (PscO2) with liver oxygenation in efforts to correct shock in piglets with two different colloids, hydroxyethyl starch (HES-120) and dextran-70. Nineteen animals were bled to shock and the shed blood was retransfused in the control group. Liver oxygenation was measured directly by means of a silicone tube used as a tonometer, and indirectly by calculating liver O2 consumption (VO2). PscO2 was monitored with a needle electrode. The two colloid groups were compared by measuring plasma lactate, and the plasma colloid osmotic pressure (COPp). PscO2 followed closely the changes in liver tissue PO2 during the experiment; it seems to be a useful tool in estimating volume filling during the treatment of hemorrhagic shock. A wider variation was noted in calculated liver VO2 compared with hepatic venous PO2 or liver tissue PO2. Despite the fact that COPp increased to a higher level after the administration of dextran, HES proved to be at least as effective as dextran in restoring mean arterial pressure, cardiac output, liver oxygenation, PscO2, arterial pH, arterial plasma lactate, and liver lactate uptake.

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