Recently, Nielsen et al.,7 showed in a large multicenter study no difference in neurological outcome between patients cooled to 33 °C vs. a control group treated with a target temperature at selleck products 36 °C. There may be several explanations for this finding: first, in the historical cooling trials,3 and 4 the control group was not treated with targeted temperature management, and thus post ROSC fevers may have worsened outcome

in the control group. Also, the time from arrest to inclusion in the study was 4 h and thus delay in cooling may have played a role. Therefore, further studies are needed, particularly studies of the application of more rapid approaches to cooling. Interestingly, in our cohort, time from ROSC to hospital admission was significantly

longer in the prehospital group than the IH group with a median difference of 9 min. This longer time period in the prehospital group could be possibly explained by the time necessary to initiate the cooling procedure including insertion of a temperature probe, removing the patient’s clothing, movement of the cooling equipment from the ambulance to the arrest location and/or positioning the cooling pad on the patient in the field. Although patients cooled in the prehospital setting showed only 0.6 °C difference Tes measured after admission in the emergency department vs. IH patients, target temperature was reached significantly faster in the prehospital cooling group with a substantial median time difference of 50 min. This might reflect the possibility that in the prehospital group, the cooled skin has facilitated a subsequent Selleck RG7420 decrease in core body core temperature, which ultimately

results in a shorter time to target temperature. Galactosylceramidase Furthermore, although we noted a shorter time to target temperature in the prehospital group, cooling rate in °C/h was not different between the two groups (2.0 °C/h vs. 2.3 °C/h, p = 0.41). Another possible explanation for a longer time to target temperature in the IH group could be the simple fact that cooling was initiated at median of 55 min after hospital admission. Retrospectively, this extensive time period could partly be explained by different examinations, procedures and interventions performed before the initiation of cooling, but detailed data on this issue were not available. This cooling delay could also explain the longer time to target temperature in comparison to the prehospital cooling group. Another interesting observation was a significantly lower potassium value, albeit within the normal range, in the prehospital group on admission before reaching target temperature. During mild therapeutic hypothermia this side effect is well known and has been previously described in patients after reaching target temperature.34 and 35 Our finding shows that a decline of potassium value may already begin immediately after the onset cooling.