Day: October 3, 2020

This article was written for adult cardiac arrest patients which are non-traumatic and cardiac related, When we have a patient in cardiac arrest, what is our main goal? Is it to obtain return of spontaneous circulation (ROSC)? Well obviously yes, but our end goal is to have the patient neurologically intact at discharge. It's become common knowledge that antiarrhythmic drugs such as lidocaine and amiodarone do not increase the probability of patients being discharged neurologically intact. Yes they increase the chance of ROSC in comparison to placebos being administered, but ROSC is only half of the equation. So before we go into epinephrine in cardiac arrest, lets first hit on the cardiac arrest phases. Cardiac Arrest Phases https://aneskey.com/defibrillation-practice/ As you can see, there are three phases to a Ventricular Fibrillation cardiac arrest. Electrical Phase- Occurs 0-4 minutes after the patient goes into cardiac arrest. Myocytes start to use the oxygen/energy reserves (ATP). This is where you get your course VF (seen below)Circulatory Phase- Occurs from 4-10 minutes after onset of cardiac arrest. Myocytes use up all of their energy reserves and start performing anaerobic metabolism. This is where you get your fine VF (seen below)Metabolic Phase- 10 minutes after the onset of cardiac arrest. Myocytes can no longer operate on anaerobic metabolism and will lyse (rupture). https://slideplayer.com/slide/6131710/ When it comes to a VF cardiac arrest, early defibrillation is key. Now I am sure you have heard that a million times, but why is it important? Well let's think about it in a metabolic way. Because VF is your ventricles quivering at a rate over 150 bpm, it uses a lot of energy (ATP), especially in comparison to a normal sinus rhythm. The longer the ventricles are fibrillating, the more energy is used. Sometimes when you defibrillate a patient you get ROSC and other times they go straight into the most stable of all rhythms... asystole. The reason why is because ATP runs all functions of a cell. When ATP is depleted, the cells will not function as well in comparison to a cell with max ATP reserves. ATP is necessary for the cellular functions so when you defibrillate the patient with no ATP reserves, there is no energy to support spontaneous repolarization in the pacemaker cells... Therefore they become asystolic. If they have enough ATP reserves, the pacemaker cells will be able to repolarize and that is when you will obtain ROSC. Insert- Your course VF has a higher amplitude in comparison to fine VF on the ECG because the cells have more energy. That's why early defibrillation is a key factor in obtaining ROSC and ensuring that your patient has the best outcome possible. https://sydneyhems.com/training/2cheer-study-main/physiology-of-cpr/ https://aneskey.com/defibrillation-practice/ Now that you understand the importance of early defibrillation down to the cellular level, let's talk about epinephrine in our adult patients? Epinephrine in Cardiac Arrest Epinephrine administration in cardiac arrest patients has been a hot topic for quite some time. Your standard dose for epinephrine in adult cardiac arrest patients is 1 mg IV/IO push every 3-5 minutes per ACLS guidelines. https://www.ahajournals.org/doi/10.1161/CIR.0000000000000261 So now a little pharmacology on our friend Mr. Epinephrine: Epinephrine is a nonselective adrenergic agonist that acts on α₁, α₂, β₁, and β₂ receptors. So before you start banging your head on a wall, lets talk about these. https://www.sciencedirect.com/topics/medicine-and-dentistry/adrenergic-receptor-function So when we administer epinephrine to our cardiac arrest patients, studies show that during the circulatory phase the use of epinephrine can increase coronary perfusion because of its α-adrenergic effects. Unfortunately, studies also show that epinephrine may be harmful in our ROSC patients due to the beta effects because it can increase myocardial oxygen requirements. But because this is a nonselective, we can't decide what epinephrine can impact. So at the end of the day, does epinephrine increase the probability of our patients being discharged neurologically intact? The answer is Yes and No. When used during the circulatory phase, epinephrine in conjunction with high quality chest compressions could cause an increase. But administering it during the metabolic phase can be detrimental to the patient's outcome. There is not enough conclusive research out there as of yet to completely come up with the right answer. Maybe one day someone will do a meta-analysis on studies of providers only giving epinephrine during each of the phases and comparing it to the success rate of neurologically intact patients that are discharged. What Has Been Proven to Work The only consistent interventions that show statistically higher amounts of neurologically intact patients being discharged from the hospital are: Early bystander CPREarly defibrillationMinimizing hands-off of chest time And funny enough those can easily be done by anyone because it is all BLS care. Unfortunately, a lot of patients do not receive bystander CPR which increases mortality in cardiac arrest patients. Public education in the issue will be health cares best bet to combating this. And if you aren't performing high performance CPR and are having periods of 10 seconds or more to defibrillate or during pulse checks, you should really look into switching your cardiac arrest approach. Every time I see people not doing high performance CPR, I start getting a headache which I can only assume it is from an aneurysm or hypertensive crisis. This site is meant to be used for educational use only. We strive to push evidence based medicine with no bias to help you obtain all the important information. You should always follow your protocols that have been set in place. Follow our social media to stay updated! https://m.facebook.com/SCOPEeducation20/ https://twitter.com/scopeducation?lang=en -Scopeducation Team (Matt) References Goodloe, J., Wayne, M., Proehl, J., Levy, M., Yannopoulos, D., Thigpen, K., & O'Connor, R. (2014, November). Optimizing neurologically intact survival from sudden cardiac arrest: A call to action. Retrieved October 02, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4251222/ Jung, J., Rice, J., & Bord, S. (2018, December). Rethinking the role of epinephrine in cardiac arrest: The PARAMEDIC2 trial. Retrieved October 02, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6330609/ Link, M., Berkow, L., Kudenchuk, P., Halperin, H., Hess, E., Moitra, V., . . . Donnino, M. (2015, November 03). Part 7: Adult Advanced Cardiovascular Life Support. Retrieved October 02, 2020, from https://www.ahajournals.org/doi/10.1161/CIR.0000000000000261 Mcleod, S., Brignardello-Petersen, R., Worster, A., You, J., Iansavichene, A., Guyatt, G., & Cheskes, S. (2017, October 14). Comparative effectiveness of antiarrhythmics for out-of-hospital cardiac arrest: A systematic review and network meta-analysis. Retrieved October 02, 2020, from https://pubmed.ncbi.nlm.nih.gov/29037886/ Moon, M. (2019, January 18). Prehospital epinephrine tied to lower neurologically intact survival. Retrieved October 02, 2020, from https://www.mdedge.com/chestphysician/article/89069/acute-coronary-syndromes/prehospital-epinephrine-tied-lower Mosesso Jr, V., & Rickens, C. (2016, June 04). Defibrillation: Practice. Retrieved October 02, 2020, from https://aneskey.com/defibrillation-practice/ Patil, K., Halperin, H., & Becker, L. (2015, June 05). Cardiac Arrest. Retrieved October 02, 2020, from https://www.ahajournals.org/doi/full/10.1161/circresaha.116.304495 Shao, H., & Li, C. (2017, September 5). Epinephrine in Out-of-hospital Cardiac Arrest: Helpful or Harmful? Retrieved October 02, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5586182/

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