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why do we give adrenaline in cardiac arrest

Epinephrine is the primary drug administered during cardiopulmonary resuscitation (CPR) to reverse cardiac arrest. Epinephrine increases arterial blood pressure and coronary perfusion during CPR via alpha-1-adrenoceptor agonist effects. However, the dose, timing and indications for epinephrine use are based on limited animal data. Recent studies question whether epinephrine provides any overall benefit for patients. A randomized controlled trial indicates that epinephrine for out-of-hospital cardiac arrest increases return of pulses, but does not significantly alter longer-term survival. Very large, well-controlled, observational studies suggest that, despite increases in return of pulses, epinephrine reduces long-term survival and functional recovery after CPR. Detrimental effects were greatest in patients found in ventricular fibrillation. Laboratory data suggest that harmful epinephrine-induced reductions in microvascular blood flow during and after CPR may offset the beneficial epinephrine-induced increase in arterial blood pressure during CPR. The available clinical data confirm that epinephrine administration during CPR can increase short-term survival (return of pulses), but point towards either no benefit or even harm of this drug for more patient-centred outcomes (long-term survival or functional recovery). Prospective trials are needed to determine the correct dose, timing and patients for epinephrine in cardiac arrest.
Descriptive statistics were used to characterize the study population.

Continuous variables are reported as medians with interquartile ranges and categorical variables are reported as counts with relative frequencies. Categorical data were compared with о test and continuous data with the Wilcoxon rank sum test. The Cochran-Armitage test was used to assess for trends over time. The goal of the main analysis was to determine survival to hospital discharge in those who received epinephrine within the two minutes after the first defibrillation (that is, before the recommended second defibrillation) compared with those who did not receive epinephrine or received epinephrine more than two minutes after the first defibrillation. To assess the adjusted relation we performed propensity score matching. The propensity score was calculated with multivariable logistic regression with generalized estimating equations with an exchangeable variance-covariance structure to account for clustering within hospitals. For the calculation of the propensity score, the dependent variable was administration of epinephrine within two minutes after the first defibrillation. We included all variables presented in tables 1, 2, and 3 in the propensity score model. These variables have been defined elsewhere. We included quadratic and cubic terms of age, and year of the cardiac arrest was treated as a categorical variable.

We also included an interaction term between time to defibrillation and intubation within the first minute as these factors could theoretically affect (timing of) epinephrine. We chose all variables a priori based on prior work and/or clinical reasoning. We next performed 1:1 matching on the propensity score using nearest neighbor matching with a maximum caliber of 0. 01 of the propensity score. Patients who received epinephrine at either zero, one, or two minutes after the first defibrillation were separately matched on the propensity score with a patient who was Бat riskБ of receiving epinephrine within the same time frame. БAt riskБ patients included those still undergoing resuscitation (that is, patients who did not have return of spontaneous circulation or in whom resuscitation was terminated) and who did not receive epinephrine before or within the same minute, including patients who received epinephrine at a later time point (Бas yet untreatedБ patients). The matching was performed separately for minutes zero, one, and two after the first defibrillation with replacement of controls to optimize the sample size. If we included a patient with return of spontaneous circulation within or before this time period, and who was therefore never Бat riskБ for receiving epinephrine, in the analysis this could bias the results towards a harmful effect of epinephrine because early return of spontaneous circulation (that is, short duration of arrest) is associated with improved survival.

To assess the performance of the matching, we compared baseline categorical variables between the matched groups using the Cochran-Mantel-Haenszel test and calculated standardized differences. Using the matched cohort, we next performed conditional logistic regression to assess the association between epinephrine administration and survival to hospital discharge. Given the potential importance of time to defibrillation, we included this variable in the regression model as a categorical variable. We report the results from the regression model as odds ratios with 95% confidence intervals. We performed similar conditional logistic regression analyses for the secondary outcomes of return of spontaneous circulation and good functional outcome. To compare the number of total defibrillations, the time to the second defibrillation, total dose of epinephrine, and the time to the end of resuscitation in the two groups we used Poisson regression with robust variance estimates while accounting for the correlation between matched participants. The results of these analyses are presented as relative increases with 95% confidence intervals.

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