Microvascular reactivity as expressed in the descending and ascending slope of the StO2 was unpredictable and gave a large inter-individual variability. There
was no significant difference in reactivity between TTM33 and TTM36. This variability was also described by Donadello et al.14 in a group of hypothermic patients. Limitations of the study were related to the small sample size. In our sample size calculation, we anticipated a MFI of 2.5 with a SD of 0.4, but this is not in agreement with the actual observations. With regard to the reliability, the observed differences between the groups PLX-4720 are well beyond the described coefficients of variation of both SDF and NIRS.16 and 17 Secondly, there was a large inter-individual variability in the microvascular reactivity. Therefore, a small difference between groups may have been undetected in this study. Although this is a small sample size study, our data suggest that after OHCA, the microvascular flow index is altered, independent of TTM33 or TTM36. Since there was found no statistical difference between groups, we reject our hypothesis that a difference in temperature management under TTM is associated with alterations in microvascular blood flow. Since tissue oxygenation at the start
of the study appears to be higher in the TTM33 group, without a rise in shunt fraction, reduction of oxygen consumption, or attenuation of oxygen debt seems to be the most logical explanation for this outcome. This suggests that in clinical practice elevation of lactate levels during hypothermia may not only reflect impaired organ perfusion and other causes should be considered. ERK inhibitor All authors declare no conflicts of interest. We express our gratitude to all intensivists and
nurses of both intensive care units for Depsipeptide mw their efforts to include patients and collect data. “
“Cardiac arrest is a major cause of death in the modern world with few therapies.1 In the US, every year approximately 300,000 people experience a sudden cardiac death, approximately 92% of these patients die.2 In the last years, several studies showed that mild therapeutic hypothermia improves outcome when induced after cardiac arrest in humans.3 and 4 In 2010, the American Heart Association (AHA) and the European Resuscitation Council (ERC) published revised recommendations for temperature regulation in patients successfully resuscitated from cardiac arrest.5 and 6 Recently, controversy has risen on the need for cooling patients after cardiac arrest. A recent publication did not find any differences in outcome between temperature management of 33 °C vs. 36 °C,7 however AHA and ERC have not change their guidelines yet. Concerning timing of cooling, the European Resuscitation Council stated earlier: “… but, as yet, there are no human data proving that earlier time to target temperature produces better outcomes”.