Malignant Arrhythmias During Induction of Target Temperature Management After Cardiac Arrest

The aim of this study was to evaluate the incidence and determinants of malignant arrhythmias (MA) in patients with shock following out-of-hospital cardiac arrest (OHCA) treated with targeted temperature management. Risk factors for the development of MA were prospectively analyzed in patients after OHCA. MA were defined as ventricular tachycardia or fibrillation with a duration >30 seconds, which had to be terminated by defibrillation. All patients were treated with therapeutic hypothermia for 24 hours. Demographics, OHCA details, interventions, and intensive care unit (ICU) treatment were recorded. A total of 55 patients were included, 11 (20%) of whom developed MA during the ICU stay. All MA occurred within the first 18 hours after admission. Patients who developed MA showed a stronger decrease in body temperature (Delta -2.4 degrees C +/- 0.8 degrees C vs. Delta -1.3 degrees C +/- 1.3 degrees C; p = 0.016) and in serum potassium levels (Delta -0.9 +/- 1 mmol/L vs. Delta -0.3 +/- 0.6 mmol/L; p = 0.037) during the cooling period compared with patients without MA. In the multivariable analysis, fast temperature decline as well as lower potassium levels were associated with MA. In addition, higher number of shocks during resuscitation and higher ICU epinephrine use were independent predictors of MA in patients with OHCA. The use of epinephrine as well as hypokalemia in context with intense cooling may increase the incidence of MA in patients with shock after cardiac arrest. Therefore, these therapeutic strategies should be applied with caution in this vulnerable group of patients

TIMP-2/IGFBP7 predicts acute kidney injury in out-of-hospital cardiac arrest survivors

Background: Acute kidney injury (AKI) is a common complication after cardiopulmonary resuscitation (CPR) and predicts in-hospital mortality. To which extent post-resuscitation disease or the initial event of cardiac arrest and the duration of insufficient cardiac output triggers AKI is challenging to discriminate. Knowledge on molecular mediators of AKI is scarce. Early identification of patients at high risk of AKI is hampered by the low sensitivity of the established tests in clinical routine practice. The present study aimed to determine the diagnostic utility of the novel urine biomarkers tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) for the early recognition of AKI in patients with non-traumatic shock. Methods: The performance of [TIMP-2].[IGFBP7] was prospectively analysed in 48 patients with shock following out-of-hospital cardiac arrest (OHCA). All patients were treated with target temperature management (TTM) for 24 h. Urinary [TIMP-2].[IGFBP7] samples were collected at 3 and 24 h after determination of OHCA. Results: Patients (n = 31 (65%)) developed AKI after an average of 26 +/- 12 h. Patients who developed AKI had significantly higher [TIMP-2].[IGFBP7] compared to individuals that did not develop AKI (1.52 +/- 0.13 vs. 0.13 +/- 0.14; p < 0.05) as early as 3 h after determination of OHCA,. For urine [TIMP-2]*[IGFBP7], the area under the curve (AUC) for the development of AKI was 0.97 (CI 0.90-1.00) at 3 h after OHCA. The optimal [TIMP-2].[IGFBP7] cut-off value for the prediction of AKI was 0.24. The sensitivity was 96.8% and specificity was 94.1%. Conclusions: Urinary [TIMP-2].[IGFBP7] reliably predicts AKI in high-risk patients only 3 h after determination of OHCA with a cut-off at 0.24. This novel test may help to identify patients at high risk of AKI to enrol into clinical studies to further elucidate the pathophysiology of AKI and devise targeted interventions in the future

Additional file 1: of TIMP-2/IGFBP7 predicts acute kidney injury in out-of-hospital cardiac arrest survivors

Table S1. Hemodynamic parameters and cumulative amount of administered norepinephrine and fluid over the observational period of the initial 48 h upon hospital admission. MAP, mean arterial pressure; GEDI, global end diastolic volume index; ELWI, extravascular lung water index. (DOC 36 kb