AMSA and Amiodarone Study in Cardiac Arrest

Overview

Investigators' aim is to assess whether the administration of amiodarone during resuscitation could cause a reduction of the values of the amplitude spectral area (AMSA). Amiodarone is recommended for the treatment of cardiac arrest due to ventricular tachycardia/ventricular fibrillation (VT/VF) ( with a low level of recommendation cause of conflicting results. AMSA is a parameter expressing the amplitude of VF and it has been shown to predict defibrillation success and the return of spontaneous circulation (ROSC). No data are available so far about the impact of amiodarone administration on AMSA values.

The primary study endpoint of the present study is to determine whether patients who received amiodarone during advanced resuscitation had lower values of AMSA as compared to those who did not receive amiodarone. Secondary endpoints The secondary endpoints of this study are: 1. To assess, after correction for confounders, the rate of successful defibrillation, the rate of ROSC and the rate of short-term survival (survived event or survival to hospital discharge according to the available data) both in the amiodarone and non-amiodarone group. 2. To assess the role of AMSA for shock success and ROSC prediction in amiodarone group and in non-amiodarone group. Type of study. This is a multicentre study based on a retrospective analysis of prospectically collected data. Study population All the out-of-hospital cardiac arrests (OHCA) which occurred from January 1st, 2015 to December 31st, 2020 will be considered for the present study. In the analysis the investigators will include only those patients who received at least one shock for ventricular fibrillation during advanced resuscitation regardless whether or not the presenting rhythm was shockable or non-shockable. The study cohort will involve cases retrieved from the Lombardia CARe registry (Lombardia Cardiac Arrest Registry NCT03197142), from the registry of Oslo and Vestfold Data Collection Data from different databases will be integrated and combined in a single ad hoc database for statistical analysis. For every shock, both pre-shock carbon dioxide at the end ot the tidal volume (ETCO2) and pre-shock AMSA will be calculated. The median ETCO2 value in the minute before the shock (METCO2) will be computed automatically either from a capnogram, when available, applying the algorithm described by Aramendi et al, or from the defibrillator with a ETCO2 monitoring feature. AMSA will be computed using a 2-second-pre-shock ECG interval, free of chest compression artifacts, leaving a 1-second guard before the shock. The electrocardiogram (ECG) will be bandpass filtered (0.5-30Hz) and the fast Fourier transform computed to obtain AMSA in the 2-48 Hz bandwidth. For each patient all the pre-hospital variables will be included according to the 2014 Utstein recommendations and the number of shocks will be computed. The mean value of both ETCO2 and of AMSA will be calculated. Statistical analysis Categorical variables will be compared with the Chi-square test and presented as number and percentage. Continuous variables will be compared with the t-test and presented as mean ± standard deviation, or compared with the Mann-Whitney test and presented as median and interquartile range (IQR) according to normal distribution tested with the D'Agostino-Pearson test. A multivariable regression model will be fitted both for shock success and for ROSC (including all non-correlated potential predictors) and to test the effect of amiodarone on AMSA values after correction for confounders. The values of AMSA in the amiodarone and in the non-amiodarone group will then be compared in two groups of shocks randomly matched and identified via propensity score matching, so that they are homogeneous for time to shock, pre-shock ETCO2, outcome of defibrillation and the age of the patients.

Conditions

Interventions

Eligibility

Locations (4)

Outcomes