HYPOTHESIS: Corticosteroids will improve the rate of resuscitation from cardiac arrest. DESIGN: Prospective blinded randomized placebo-controlled trial. INTERVENTION: An 8-min cardiac arrest was induced by KCl infusion and chest restriction in 36 male Sprague-Dawley rats with continuous EKG and arterial blood pressure monitoring. At the start of CPR the rats received one of three study drugs: normal saline (placebo); 0.05 mg hydrocortisone (Group A) and 0.25 mg hydrocortisone (Group B). Mechanical ventilation, chest compressions and ACLS drug administration were provided following a standardized algorithm. RESULTS: The resuscitation rate was significantly higher (P < 0.05) in Group B (92%) compared to Group A (50%) and placebo (50%). For the rats resuscitated, the duration of CPR (placebo = 163 s, Group A = 126 s, Group B = 120 s) and the amount of epinephrine used (placebo = 0.007 mg, Group A = 0.005 mg, Group B = 0.005 mg) did not reach statistical significance (P = 0.15 and P = 0.21). CONCLUSION: Hydrocortisone significantly increased the rate of ROSC from cardiac arrest. There also appears to be a trend of decreasing duration of CPR and epinephrine requirements with hydrocortisone. Further studies evaluating the mechanism of action and long term effects of hydrocortisone in cardiac arrest need to be conducted.
HYPOTHESIS: Corticosteroids will improve the rate of resuscitation from cardiac arrest. DESIGN: Prospective blinded randomized placebo-controlled trial. INTERVENTION: An 8-min cardiac arrest was induced by KCl infusion and chest restriction in 36 male Sprague-Dawley rats with continuous EKG and arterial blood pressure monitoring. At the start of CPR the rats received one of three study drugs: normal saline (placebo); 0.05 mg hydrocortisone (Group A) and 0.25 mg hydrocortisone (Group B). Mechanical ventilation, chest compressions and ACLS drug administration were provided following a standardized algorithm. RESULTS: The resuscitation rate was significantly higher (P < 0.05) in Group B (92%) compared to Group A (50%) and placebo (50%). For the rats resuscitated, the duration of CPR (placebo = 163 s, Group A = 126 s, Group B = 120 s) and the amount of epinephrine used (placebo = 0.007 mg, Group A = 0.005 mg, Group B = 0.005 mg) did not reach statistical significance (P = 0.15 and P = 0.21). CONCLUSION:Hydrocortisone significantly increased the rate of ROSC from cardiac arrest. There also appears to be a trend of decreasing duration of CPR and epinephrine requirements with hydrocortisone. Further studies evaluating the mechanism of action and long term effects of hydrocortisone in cardiac arrest need to be conducted.
Authors: Lars W Andersen; Birthe Sindberg; Mathias Holmberg; Dan Isbye; Jesper Kjærgaard; Stine T Zwisler; Søren Darling; Jacob Moesgaard Larsen; Bodil S Rasmussen; Bo Løfgren; Kasper Glerup Lauridsen; Kim B Pælestik; Christoffer Sølling; Anders G Kjærgaard; Dorte Due-Rasmussen; Fredrik Folke; Mette Gitz Charlot; Kasper Iversen; Martin Schultz; Sebastian Wiberg; Rikke Malene H G Jepsen; Tobias Kurth; Michael Donnino; Hans Kirkegaard; Asger Granfeldt Journal: Resusc Plus Date: 2021-01-30