Role of Epinephrine in ACLS

During a code, epinephrine increases coronary perfusion pressures, and generally constricts all blood vessels large and small. This is useful because your compressions alone often do not provide enough pressure to deliver adequate perfusion.

Yes, epinephrine can increase myocardial oxygen demand, and constricting vessels that are already occluded is not always a good idea. But some blood flow is better than no blood flow, and alive is generally better than dead. In a code, they're already dead. If they're a STEMI coming in from an external hospital, Epi probably wouldn't be the first drug I'd ask for, but this isn't that.

Yes, there have been some small, observational studies indicating that despite increasing coronary perfusion pressures and CI/CO, myocardial and cerebral perfusion (in rats) are actually decreased. I look forward to further research in this area but it's not as though it's some well-researched topic. There's a handful of poorly-designed studies , albeit with interesting results.

Taking vasopressin out of the guidelines was dumb. I'm glad I don't need to use the guidelines.

Epi is used to increase the diastolic blood pressure and thus increase coronary artery perfusion, which will increase the chance of ROSC. However, the ACLS dosing of epinephrine was extrapolated from dog studies decades ago and have not been validated in human trials. The old mantra of "just give them a ton of epi, they can't get any deader" is misguided in my opinion. Especially in ischemic heart disease (coronary vasoconstriction) and refractory VFib (precipitates beta receptor storm). Scott Weingart recommends hemodynamic dosing of epinephrine to achieve a coronary perfusion pressure greater than 20 which has been shown to lead to greater likelihood of ROSC. Also agree that vasopressin has at least as much evidence to support its use as epi and peobably more... we got rid of it too because the manufactures suddenly decided it needed to be refrigerated and pharmacy didn't want to deal with the hassle of making that happen. ACLS, like ATLS, is written to bring everyone up to a bare minimal level of competence. Anyone who deals with critically ill patients should be identifying the cause of the arrest and modifying their treatment based on this, not blindly shoving milligram after milligram of epi into everyone.

Also agree that vasopressin has at least as much evidence to support its use as epi and peobably more... we got rid of it too because the manufactures suddenly decided it needed to be refrigerated and pharmacy didn't want to deal with the hassle of making that happen. ACLS, like ATLS, is written to bring everyone up to a bare minimal level of competence. Anyone who deals with critically ill patients should be identifying the cause of the arrest and modifying their treatment based on this, not blindly shoving milligram after milligram of epi into everyone.

It was more dumbing down of the guidelines than refrigeration. Mine is just in the omnicell.

Then our pharmacy is full of it... shocking!!!! (Also claims that this is why we can't have ketamine and rocuronium in the Pyxis and need to get them tubes from pharmacy...)

Then our pharmacy is full of it... shocking!!!! (Also claims that this is why we can't have ketamine and rocuronium in the Pyxis and need to get them tubes from pharmacy...)

We have both in our OmniCell (Pyxis equivalent)

refractory VFib (precipitates beta receptor storm.

Can you elaborate? I'm not familiar with the concept.

As opposed to an asystolic arrest where the electrical system of the heart isn't functioning, ventricular fibrillation happens when the heart's electrical system is overactive (tons of dyssynchronous firing that causes non-functional contractions which are the fibrillations). It is like afib but it affects the whole heart. Would you give an arrythmogenic medication like epi in afib? Of course not. The epi, especially a huge dose like 1mg, will cause an increase in dromotropy and chronotropy which will potentiate the vfib (this is the beta storm or over stimulation of beta receptors). There is emerging evidence that giving a drug like esmolol in refractory vfib may be enough to block the beta receptors and allow the native pacemaker of the heart to reset when defibrillated and allow the patient to be shocked out of the vfib. If the beta stimulation continues it will be impossible to shock the pt out of the vfib.

As opposed to an asystolic arrest where the electrical system of the heart isn't functioning, ventricular fibrillation happens when the heart's electrical system is overactive (tons of dyssynchronous firing that causes non-functional contractions which are the fibrillations). It is like afib but it affects the whole heart. Would you give an arrythmogenic medication like epi in afib? Of course not. The epi, especially a huge dose like 1mg, will cause an increase in dromotropy and chronotropy which will potentiate the vfib (this is the beta storm or over stimulation of beta receptors). There is emerging evidence that giving a drug like esmolol in refractory vfib may be enough to block the beta receptors and allow the native pacemaker of the heart to reset when defibrillated and allow the patient to be shocked out of the vfib. If the beta stimulation continues it will be impossible to shock the pt out of the vfib.

Thank you so much for explaining it so well! :)