In accordance with previous reports, in our study early post resu

In accordance with previous reports, in our study early post resuscitation phase was characterized by significant abnormalities in microvascular flow.14 This returns to normal within the next 24 h. Donadello et al. observed in TTM33 a MFI of 2.1 (±0.5) in the first 12 h after ICU admission and an MFI of 2.8 (0.2) after 24–48 h. In our study the TTM36 group seemed to have a slightly higher MFI in comparison to the TTM33 group, but this was not statistically significant. Moreover, in both groups MFI normalized over time. Hypothermia does not seem to have a relation with microvascular alterations. Van Genderen et al.15 investigated

the microcirculatory perfusion and alterations and concluded that the abnormalities in sublingual microcirculation were independent of systemic hemodynamics and suggested that the observed alterations were probably due to hypothermia-induced XL184 datasheet vasoconstriction. However, the fact that in our data microcirculatory alterations were not different between two target-temperatures, suggests alternative causes, although

a targeted temperature of 36 °C may be considered hypothermia to some extent In septic patients it is known that presence and persistence of alterations in tissue oxygenation (StO2) in the first 24 h are associated with worse outcome.4 Donadello et al.14 found no changes in StO2 over time during hypothermia. In our study we observed a significant difference at time point 1 (start study) between groups; StO2 was significantly lower Tolmetin in TTM36 as Vemurafenib datasheet compared to TTM33 (59.8 (±13.7) and 44.6 (±15.8), p = 0.03). But this difference disappeared after 12 and 24 h. A higher StO2 in the TTM33 group may be explained by a lower oxygen consumption in response to hypothermia. Alternatively, a higher

StO2 may be present during shunting. Since the catchment area of the StO2 probe incorporates both capillary and venous blood, this cannot be ruled out, and is in line with the observed higher lactate levels. However, the data on the microcirculation, especially the MFI, which was found to be low in these patients, did not support shunting as an explanation for the increase in StO2 and lactate. An alternative explanation for the higher lactate levels in TTM33 could be metabolic: the liver might not be able to metabolize sufficient lactate under conditions of hypothermia. It is of note, however that the difference in StO2 between groups disappeared over time despite maintenance of the target temperature level during this observation period. This may be in line with the concept of oxygen deficit and oxygen debt. An initial greater misbalance between oxygen delivery and consumption in the TTM36 maybe reflected by a prolonged recovery period of the StO2.

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