Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

The Kitchen Sink Approach to Cardiac Arrest

When faced with death, we can become desperate, stop thinking clearly, and just try anything.

Alternative medicine thrives on the desperation of people who are not thinking clearly. We should be better than that, but are we?

A recent comment on The Myth that Narcan Reverses Cardiac Arrest[1] proposes that I would suddenly give kitchen sink medicine a try, if I really care about the patient.

Kitchen sink medicine? It’s better to do something and harm the patient, than to limit treatment to what works. Throw everything, including the kitchen sink, at the patient.

Mike Karras writes –

I will leave you with this question sir and I am interested to hear your answer. You walk in to find your 14 year old daughter that intentionally overdosed on morphine in a suicide attempt and she is in cardiac arrest. How would you treat her? Would you give her Narcan? I think you would.[2]


Mike, I am thrilled to read that you do not think that I care about the outcomes of my patients, unless the patient happens to be my daughter. I am even more thrilled that you made my imaginary daughter suicidal.

No, I would not use naloxone (Narcan).

I would also not use homeopathy, acupuncture, sodium bicarbonate, incantations, or magic spells to treat my daughter during cardiac arrest. Voodoo only works on believers, because voodoo is just a placebo/nocebo.[3]

Image credit.

Does really wanting something to be true make it true? If you believe in magic, the answer is Yes, believing makes it true. If you examine the evidence for that belief, you have several choices. You can acknowledge your mistake, or you can employ a bit of cognitive dissonance, or . . . . Cognitive dissonance is the way our minds copes with the conflict, when reality and belief do not agree, and we choose to reject reality.[4]

According to the ACLS (Advanced Cardiac Life Support) guidelines –

Naloxone has no role in the management of cardiac arrest.[5]


If the patient is suspected of having a cardiac arrest because of an opioid overdose (overdose of heroin, fentanyl, morphine, . . . ), the treatments should include ventilation and chest compressions. If those do not provide a response, epinephrine (Adrenaline in Commonwealth countries) is added.

An opioid overdose can produce respiratory depression and/or vasodilation. I can counter both of those with chest compressions, ventilation, and maybe epinephrine. Naloxone works on opioid receptors. What does naloxone add?

Does naloxone’s stimulation of an opioid receptor produce more ventilation than bagging/intubating?

Does naloxone’s stimulation of an opioid receptor produce more oxygenation than bagging/intubating?

Does naloxone’s stimulation of an opioid receptor produce more vasoconstriction than chest compressions and epinephrine?*

Also –

Don’t confuse post- or pre–arrest toxicologic interventions with the actual cardiac arrest event.[6]


Dead people do not respond to treatments the same way living people do.

See also –

Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions – Tue, 01 Nov 2011

Naloxone in cardiac arrest with suspected opioid overdoses – Thu, 05 Apr 2012

The Myth that Narcan Reverses Cardiac Arrest – Wed, 12 Dec 2012

Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest – Sun, 03 Aug 2014

* Late edit – 02/17/2015 10:52 – added the word naloxone’s to the three sentences about the relative amount of stimulus provided by standard ACLS and by the addition of naloxone. Thanks to Brian Behn for pointing out the lack of clarity.


[1] The Myth that Narcan Reverses Cardiac Arrest
Wed, 12 Dec 2012
Rogue Medic

[2] Comment by Mike Karras
The Myth that Narcan Reverses Cardiac Arrest by Rogue Medic
Mon, 16 Feb 2015

[3] Nocebo

A nocebo is an inert agent that produces negative effects. What this means is that nocebo effects are adverse placebo effects. There is no reason to believe that placebos only produce positive effects or no effects at all.

[4] Cognitive dissonance

[5] Opioid Toxicity
2010 ACLS
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 12.7: Cardiac Arrest Associated With Toxic Ingestions
Free Full Text from Circulation

[6] Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions
Emergency Medicine News:
October 2011 – Volume 33 – Issue 10 – pp 16-18
doi: 10.1097/01.EEM.0000406945.05619.ca
Roberts, James R. MD

Read the whole article about antidotes and cardiac arrest.


Does a Placebo vs. Adrenaline Study Deprive Patients of Necessary Care According to the Resuscitation Guidelines?

 Some in the media have been critical of the upcoming British study of adrenaline (epinephrine) vs. placebo for cardiac arrest.[1] They assume that the guidelines require that we give adrenaline, but that is not true.

The guidelines only state that adrenaline may be considered.

If you are a dog, pig, or rat in a laboratory and you have had an artificially induced cardiac arrest, then adrenaline will help resuscitate you. If you are a human who has a cardiac arrest for any one of a variety of reasons, then there is not a good reason to give this rat resuscitation drug, which has not been adequately studied in humans.

There probably are some human patients who do benefit from adrenaline in cardiac arrest, but we have no idea which patients those are and there probably are humans who are harmed by adrenaline. The most common cause of cardiac arrest is heart attack, but you were having a heart attack while still alive, is there a worse drug we could give you than adrenaline? Does adrenaline suddenly become sugar and spice and everything nice, just because we cannot feel a pulse? Maybe, but should we assume that?

What if you have lost so much blood that your heart is not able to produce a pulse, even though your heart is beating as hard as it can? Adrenaline is indicated according to the same guidelines. Why? Unreasonable optimism.

Which patients benefit from adrenaline? We don’t know.

Which patients are harmed by adrenaline? We don’t know.

How do we find out? Research, such as the upcoming study of adrenaline (epinephrine).

What do the guidelines say about conducting this research?

Given the observed benefit in short-term outcomes, the use of epinephrine or vasopressin may be considered in adult cardiac arrest.

Knowledge Gaps

Placebo-controlled trials to evaluate the use of any vasopressor in adult and pediatric cardiac arrest are needed.[2]


Vasopressors are adrenaline, vasopressin, norepinephrine, and phenylephrine. We need evidence to find out if any of them work.

When the 2010 guidelines were written there was an inescapable need for placebo studies.

Has anything changed?


There was a placebo study in 2012 that was aborted by pressure from media and politicians before any useful results could be obtained.[3]

There is evidence that adrenaline improves the return of a pulse, but that appears to just produce comatose patients who die in the hospital without waking up, so the initial improvement appears to be very misleading.

We could try real medicine, where we find out what the right treatment is and give the right treatment to the right patient, but that seems to be asking too much for some people.

The Media are Just As Bad at Ethics As They are at Science


[1] The Controversy of Admitting ‘We Do Not Know What Works’
Wed, 13 Aug 2014
Rogue Medic

[2] Part 8: Advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations.
Morrison LJ, Deakin CD, Morley PT, Callaway CW, Kerber RE, Kronick SL, Lavonas EJ, Link MS, Neumar RW, Otto CW, Parr M, Shuster M, Sunde K, Peberdy MA, Tang W, Hoek TL, Böttiger BW, Drajer S, Lim SH, Nolan JP; Advanced Life Support Chapter Collaborators.
Circulation. 2010 Oct 19;122(16 Suppl 2):S345-421. doi: 10.1161/CIRCULATIONAHA.110.971051. No abstract available.
PMID: 20956256 [PubMed – indexed for MEDLINE]

Free Full Text from Circulation.

[3] Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial
Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.
Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2.
PMID: 21745533 [PubMed – in process]

Free Full Text PDF Download from semanticscholar.org

This study was designed as a multicentre trial involving five ambulance services in Australia and New Zealand and was accordingly powered to detect clinically important treatment effects. Despite having obtained approvals for the study from Institutional Ethics Committees, Crown Law and Guardianship Boards, the concerns of being involved in a trial in which the unproven “standard of care” was being withheld prevented four of the five ambulance services from participating.


In addition adverse press reports questioning the ethics of conducting this trial, which subsequently led to the involvement of politicians, further heightened these concerns. Despite the clearly demonstrated existence of clinical equipoise for adrenaline in cardiac arrest it remained impossible to change the decision not to participate.


Edited 12-27-2018 to correct link to pdf of Jacobs study in footnote 3.


Remote CPR Skills Testing Online – A Crazy Idea?


On the MedicCast, Jamie Davis interviews Roy Shaw of SUMO about a method of remote CPR certification for health care providers.

The Single Use Manikin Option, or SUMO™, is an AHA-compliant way of getting certified in CPR completely online.[1]



It looks too simple, but how complicated should we make it?

One of the problems with EMS is that we do not maintain skills that we do not use frequently. We know that we lose our skills very quickly, but we only retrain every couple of years (or every year) for the skills considered most important. If we care about our patients’ outcomes, we need to do better.

Not only have varying rates of skill acquisition been documented after traditional American Heart Association (AHA) training classes, but also universally poor skill performance of varying providers 3 to 6 months after CPR training has been established.11,–,15 [2]


Supervised on-line mannequin practice may be the most practical way for us to increase the rate of providing hands-on practice. As cameras become cheaper and smaller, as cell phones become much more interactive, we may have a way to do the same for intubation. Is there any good reason for practicing intubation less than once a month?

We need to improve our intubation, but everyone seems to think that the problem is with other medics and they do not need any practice. When the research is done, the problems continue. We like to intubate. We assume we are good at it. We hate to practice. we really like to make excuses. Our patients are the ones who are harmed. Other than bad assessment, bad intubation is probably the most deadly skill we have.

Training sessions occurred at entry into the study (time 0: initial skill acquisition) and then 1, 3, and 6 months after study entry.[2]


Each training session was less than five minutes long (one minute of testing, then two minutes of training), so the interference with work would be minimal, while the benefit would be significant.

In this study, lower rates of retention were observed in the training group that did not use a live instructor (automated defibrillator feedback only) compared with the group that used an instructor without automated feedback (instructor-only training).[2]


They suggest that the participants relied on the feedback from the automated devices and may not have learned to assess their performance themselves. During testing, the lack of machine feedback may have put them at a disadvantage. If machine feedback can be provided at the time of initiating compressions, The machine feedback could help. currently, that does not seem likely, so the use of only machine feedback is not as good an option as feedback from an instructor or from an instructor and a machine.

Although the automated feedback provided was targeted to CPR psychomotor skill errors, these systems do not provide constructive positive feedback. Instructors have an advantage: they were able to comment not only on skills done incorrectly, but also praise good performance.[2]


How well would this work in EMS?

We could make this something that is done once a week, or even at the beginning of each shift, on a different skill each time. Intubation/Airway management is the weak spot of EMS, so we could use this to improve.

If are only retraining on intubation/airway management once a year, or once every other year, we obviously are not taking patient care seriously and are trusting our luck, rather than any skill.

Go listen to the podcast on the Single Use Manikin Option (SUMO™) and consider if that would be a better way of recertifying. Maybe it is one way of implementing brief low-dose, high-frequency booster training in addition to recertification.

Also check out the site –



[1] SUMO Remote CPR Skills Testing Online and Episode 392
By podmedic
June 30, 2014
Podcast/videocast page

[2] Low-dose, high-frequency CPR training improves skill retention of in-hospital pediatric providers.
Sutton RM, Niles D, Meaney PA, Aplenc R, French B, Abella BS, Lengetti EL, Berg RA, Helfaer MA, Nadkarni V.
Pediatrics. 2011 Jul;128(1):e145-51. doi: 10.1542/peds.2010-2105. Epub 2011 Jun 6.
PMID: 21646262 [PubMed – indexed for MEDLINE]

Free Full Text from Pediatrics.

Sutton RM, Niles D, Meaney PA, Aplenc R, French B, Abella BS, Lengetti EL, Berg RA, Helfaer MA, Nadkarni V. (2011). Low-Dose, High-Frequency CPR Training Improves Skill Retention of In-Hospital Pediatric Providers PEDIATRICS, 128 (1) DOI: 10.1542/peds.2010-2105d


A Resuscitation Question So Obvious That . . . .


Here is a question that was asked as an example of something so obvious only an idiot would get it wrong.

I cannot come up with any right answer.

The immediate treatment of cardiac arrest includes all except:

A:       intubation

B:       Open cardiac massage

C:       IV (IntraVenous) access

D:       IV adrenaline

E:       USG (UltraSonoGraphy)

Who gets that wrong?


Open-chest cardiopulmonary resuscitation: past, present and future.

Define wrong.

Define immediate.

Are these supposed to be treatments that work?

In that case, we should define treatments that work.

Does work mean that the treatments are in some guidelines?

That is not the way I would interpret it.

Does work mean that the treatments improve survival to discharge (preferably much longer) with little, or no, neurological impairment.

If we ask patients, before they have a cardiac arrest, What do you want from treatment for cardiac arrest? – Isn’t that the way we would expect patients to define treatments that work?

Do we expect patient to answer with –

I want to spend a few days in a coma, have several more cardiac arrests, and never wake up. Don’t worry about the cost, because this kind of experience is priceless.

But that is the result of the treatments in the guidelines – except for continuous compressions and defibrillation.

So, if we look at the choices in the question –

Does intubation (any ventilation) improve outcomes in cardiac arrest?[1]

Does cracking the chest to squeeze the heart improve outcomes in cardiac arrest?[2]

Does IV access improve outcomes in cardiac arrest?[3]

Does IV adrenaline (epinephrine in non-Commonwealth countries) improve outcomes in cardiac arrest?[4]

Does USG improve outcomes in cardiac arrest?[5]

They are all supposed to work – except for one.

There are at least five problems with that question (not all of the choices are treatments).

None of these treatments can be shown to improve outcomes.


I mentioned the lack of efficacy of these treatments and received a bunch of links about intubation vs. supraglottic airways. I appreciate when people provide evidence to support their position. It makes a discussion much more reasonable.

The problem is that I was not looking to make a choice between endotracheal intubation and supraglottic airway. I am looking for evidence that any kind of ventilation improves outcomes that matter. The same is true for open chest massage, IV access, IV adrenaline, and USG.

Why send me irrelevant research? 😳

Will I be so impressed with some research, that I do not realize that the papers are irrelevant to the question being discussed?

The thread of questions and the responses promptly went down a memory hole.[6]

Why do we care so little about our patients that we use treatments that are harmful?

Why do we care so little about our patients that we use treatments where we haven’t even bother to find out how much harm they do?


[1] Prove it – Ventilation improves survival from cardiac arrest
Tue, 11 Sep 2012
Rogue Medic

[2] Open-chest cardiopulmonary resuscitation: past, present and future.
Alzaga-Fernandez AG, Varon J.
Resuscitation. 2005 Feb;64(2):149-56. Review.
PMID: 15680522 [PubMed – indexed for MEDLINE]

The object effective CPR is to restore the spontaneous systemic circulation as soon as possible to avoid any neurological damage and to obtain higher survival and outcome rates. Experimentally, OCCPR increases the time window for successful resuscitation and has demonstrated to be superior in maintaining hemodynamic variables almost in the normal physiological range. Hence, OCCPR should be integrated with CCCPR into a logical resuscitation protocol which will assure better survival opportunities.


It should be studied, but the evidence is most from studies of dogs.

[3] I do not know of any research addressing this. It would be foolish to assume that outcomes are improved without evidence.

[4] Killing Patients Just to Get a Temporary Pulse With Epinephrine
Wed, 21 Mar 2012
Rogue Medic

[5] I do not know of any research addressing this. It would be foolish to assume that outcomes are improved without evidence.

[6] Memory hole


Dark Ages of ACLS Comment on Part II of ‘Why Did We Remove Atropine From ACLS?’


In the response to Why Did We Remove Atropine From ACLS? Part II is the following from mpatk –

What does that leave us with?

Compressions in cardiac arrest.

Defibrillation in VF cardiac arrest.

Therapeutic hypothermia after resuscitation.

The problem is that people (AHA in particular) insist on looking at all cardiac arrests as the same. We don’t treat all forms of shock the same way, why do we do so for cardiac arrest? The only distinction we draw is “shockable vs. non-shockable rhythms”; why not other decision points?


Valid science requires that we control for as many variables as possible and acknowledge when we cannot adequately control for all relevant variables.

Many people in medicine, perhaps especially those writing guidelines, have ignored that.

The AHA (American Heart Association) is getting better at eliminating the wishful thinking from ACLS (Advanced Cardiac Life Support), but there is still a long way to go. The list of treatments based on wishful thinking is much longer than the list of treatments based on valid evidence of improved outcomes.

For example, ventilations are bad for SCA of cardiac origin; on the other hand, for cardiac arrest secondary to respiratory arrest (e.g. drownings), the ventilations are critical.


It would be nice to have good evidence to support this, but it is the kind of treatment that is correcting an obvious deficit, so it is not unreasonable without evidence.

We should still try to obtain valid evidence that minimizes the roles of non-ventilation variables.

Sodium bicarbonate isn’t recommended any more….unless it’s a known dialysis patient who missed his dialysis; then bicarb and calcium are life-saving.


I agree with calcium chloride for cardiac arrest that is suspected of being due to hyperkalemia.

I think that dialysis patients should be given 1 gram of calcium chloride as the first treatment after initiation of chest compressions in cardiac arrest.

Again, it would be nice to have good evidence. There are plenty of case reports of cardiac arrest responding to calcium and some other good evidence.[1]

Image credit.

Similarly, epinephrine seems to have a negative effect; but may be beneficial in e.g. beta-blocker overdose.


Are beta blockers competitive antagonists that are reversible with higher doses of what they are supposed to block?

Do you have any evidence?

We need to do the research; and we need to mine the data to look for different treatments for different causes rather than trying to cure “cardiac arrest” as a single problem.



The problem is that so many treatments have become standards of care/ACLS requirements, that researchers are prevented from randomizing patients to placebo and treatment groups.

The treatment is based on wishful thinking, so all that patients are being deprived of is wishful thinking.

Wishful thinking is dangerous nonsense.


[1] EMCrit Podcast 32 – Treatment of Severe Hyperkalemia
Podcast page.


Why Did We Remove Atropine From ACLS? Part II


Continuing from Part I.

The AHA (American Heart Association) stopped recommendeding use of atropine for the treatment of PEA (Pulseless Electrical Activity) or asystole in the 2010 ACLS (Advanced Cardiac Life Support) guidelines.

There is not much information given, but that little bit of information just makes it more clear that we never had a good reason for making atropine a standard part of ACLS.

One sentence at a time, look at the reasoning –

Interventions Not Recommended for Routine Use During Cardiac Arrest

Atropine sulfate reverses cholinergic-mediated decreases in heart rate and atrioventricular nodal conduction.[1]


There is a hypothetical justification for atropine based on physiology/pathophysiology.

There has been a hypothetical justification for every treatment found to be harmful. That hypothetical justification did not protect patients from real harm.

No prospective controlled clinical trials have examined the use of atropine in asystole or bradycardic PEA cardiac arrest.[2]


Why was a treatment that had never been demonstrated to improve outcomes recommended and the standard of care?

Without evidence of improved outcomes, should any treatment be used outside of controlled trials?

Lower-level clinical studies provide conflicting evidence of the benefit of routine use of atropine in cardiac arrest.34,295,–,304 [1]


To translate – Useless information is . . . useless.

There is no evidence that atropine has detrimental effects during bradycardic or asystolic cardiac arrest.[1]


Is atropine the alternative medicine of cardiac arrest?

This sentence contradicts the evidence review that led to the removal of atropine from the guidelines.

Here is a listing of the evidence that opposes the use of atropine for cardiac arrest.

Click on image to make it larger.[2]

While the evidence of harm is not great, the evidence of benefit is not great, either.

Evidence of worse outcomes from cardiac arrest is evidence of harm.

There are four studies – three that show a negative correlation with atropine and survival to discharge.

no evidence that atropine has detrimental effects?

The positive studies are also just showing correlation. Poor studies mean poor information. Why were we giving atropine based on poor information?

We were giving atropine based on wishful thinking.

Available evidence suggests that routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit (Class IIb, LOE B).[1]


We should not include treatments that do not have evidence of therapeutic benefit.

For this reason atropine has been removed from the cardiac arrest algorithm.[1]


For this reason, atropine should never have been included in the cardiac arrest algorithms.

For this reason, all treatments that do not have evidence of therapeutic benefit should have an expiration date.

If no evidence is provided, the treatment is removed from the guidelines.

This would apply to ventilations, epinephrine (Adrenaline), vasopressin (Pitressin), norepinephrine (Levophed), and phenylephrine (Neo-Synephrine) in cardiac arrest.

This would also apply to amiodarone (Cordarone), lidocaine (Xylocaine), and Magnesium in VF (Ventricular Fibrillation) cardiac arrest.

What does that leave us with?

Compressions in cardiac arrest.

Defibrillation in VF cardiac arrest.

Therapeutic hypothermia after resuscitation.

In Part III I will look at the most positive study supporting the use of atropine for cardiac arrest.


[1] Atropine
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8.2: Management of Cardiac Arrest
Interventions Not Recommended for Routine Use During Cardiac Arrest
Free Full Text from Circulation.

[2] Atropine for cardiac arrest
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Appendix: Evidence-Based Worksheets
Part 8 ALS
Swee Han Lim
Evidence-Based Worksheet Download in PDF format.

That link is no longer available, but the overall page of evidence-based worksheets is available in PDF format here.


Why Did We Remove Atropine From ACLS? Part I


As of 2010, atropine is gone from the ACLS (Advanced Cardiac Life Support) treatment guidelines and nobody seems to be upset. We never had good evidence to support treatment of dead people with atropine, but we practiced this witchcraft because we chose optimism over evidence.

Some people claim that the constant changes to ACLS are evidence that evidence does not work.

That is not true. We ignored the lack of valid evidence. We chose to be ignorant.

We keep changing guidelines as we keep learning more. We should require valid evidence before adding treatments to guidelines, but too many of us are overly optimistic about treatments that are not supported by valid evidence. We believe that this time will be different. After we study treatments, we generally find out that we have been harming more patients than we have been helping.

Atropine is one example.

Look at all of this evidence of benefit.

Click on images to make them larger.[1]

What do the LOE (Level Of Evidence) and Good, Fair, and Poor categories mean?

The LOEs were subdivided into three major categories, depending on the type of question being asked: intervention, diagnosis, or prognosis. The quality of evidence categories were reduced from five categories in 2005 to three (good, fair, poor) in 2010.[2]


There is no further explanation of how Good, Fair, and Poor were to be decided, but there is an explanation of what the LOEs mean.

Level A is the evidence least likely to be misleading –


Level B is evidence that is much less likely to provide an accurate representation of the true effect of the intervention, because there are many more variables that are not controlled for –


Level C is the lowest evidence possible and even includes a category that is not really evidence – Expert Opinion


Expert Opinion is lower than the lowest of the low evidence.

In the chart Evidence Supporting Clinical Question, there is no column for expert opinion, because there is no good reason to include expert opinion in the analysis of evidence.

But what about the evidence that is there supporting the use of atropine?

Why is everything poor evidence?

Why isn’t there anything better than LOE 3: Studies using retrospective controls?

If the most positive study was back in 1984, and it was only LOE 3, why did we only remove atropine from the cardiac arrest guidelines in 2010?

The supporting evidence is not the only evidence, but that is not a good answer to my question.

The weak evidence in support of atropine in cardiac arrest is more than matched by stronger evidence that atropine does nothing useful –


There is also weak evidence that atropine is harmful –



How did atropine ever make it into the ACLS guidelines based on such poor evidence?

To be continued in Part II and Part III.


[1] Atropine for cardiac arrest
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Appendix: Evidence-Based Worksheets
Part 8 ALS
Swee Han Lim
Evidence-Based Worksheet Download in PDF format.

That link is no longer available, but the overall page of evidence-based worksheets is available in PDF format here.

[2] Classification of Evidence
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 2: Evidence Evaluation and Management of Potential or Perceived Conflicts of Interest
Evidence Evaluation Process
Free Full Text from Circulation.


Epinephrine for V Tach – Instant Death or Effective Treatment?


The patient has V Tach (Ventricular Tachycardia) with a pulse. After amiodarone is given the patient’s blood pressure drops and the patient becomes unstable. The patient is still awake, so cardioversion would be very painful and these physicians would need to get anesthesia to sedate the patient. I know – that anesthesia requirement is a bad policy and completely unnecessary for the safety of the patient, but it is politics in that facility. However, sedation for emergency cardioversion is very important.

There are other medications that might be effective at terminating V Tach.

What might happen if epinephrine is given?

Click on images to make them larger.

If take an ACLS (Advanced Cardiac Life Support) class, where the protocolized treatment of arrhythmias is taught, the instructor may tell you that you just killed the patient with epinephrine.

There were three patients treated with epinephrine for V Tach. They were not in the artificial environment of an ACLS class, and had not been taught by the epi for unstable V Tach = death ACLS instructors, so the patients did not know that they were supposed to die.

The physicians treating the V Tach patients had read the ACLS books, as well as a lot of other research on the treatment of arrythmias. The physicians chose to treat these patients with epinephrine.

47 year old male, 125/86 mmHg, heart rate of 170 with the rhythm above. 300 mg amiodarone over 5 min did not get rid of the V Tach, but it did appear to drop the blood pressure to 89/46 mmHg with profuse sweating, but without loss of consciousness. Perhaps that was also true of those taking care of the patient.

1 mg (1,000 μg) of 1:10,000 epinephrine given over less than 60 seconds was followed within 30 seconds by the changes below.


Heart rate increased to 180, briefly, blood pressure increased to 130/84 mmHg, then the rhythm converted.

Not to V Fib (Ventricular Fibrillation), but to a stable sinus tachycardia at a rate of 110.

The side effects of epinephrine were chest discomfort, nausea, and anxiousness.[1]


Well, he was only 47, so we got lucky with epinephrine at that young age.

How about a 64 year old male with a heart attack history, low ejection fraction and an AICD (Automated Implantable Cardioverter-Defibrillator), on bisoprolol 10 mg daily and amiodarone 200 mg daily for recurrent NSVT (Non-Sustained V Tach), conscious with a pressure of 85/50 mmHg and now a sustained V Tach at 140 beats/min?

A lower dose of epinephrine was given – 0.5 mg (500 μg) over less than 30 seconds was followed within 30 seconds by an increase of rate from 140 to 148, followed by conversion to a nice slow sinus rhythm.

The third patient had V Tach storm, which might seem even less likely to benefit from epinephrine.

A patient with a history of two heart attacks, taking carvedilol (12.5 mg twice daily) and amiodarone (200 mg daily) with an AICD, presenting with a pressure of 90/45 mmHg and a rate of 140+. He received six AICD shocks within 5 minutes in the hospital, but the rhythm returned to V Tach each time. 150 mg amiodarone was given over 15 min and the pressure dropped to 70/40 mmHg. Overdrive pacing was attempted with only a conversion of V Tach to V Fib, which was shocked by the AICD. Within 60 seconds, the V Tach was back. Blood pressure continued to fall to 65/30 mmHg.

Epinephrine was given – 0.5 mg (500 μg) over less than 30 seconds was followed within 30 seconds by an increase in blood pressure to 125/85 mmHg, followed by termination of V Tach within 90 seconds.

In cases of drug-resistant poorly tolerated VT, immediate external electrical cardioversion must be attempted. However, there are cases in which VT recurs immediately after the shock, and cardioversion involves the need for anesthesia when the patient is still conscious.[1]


Based on the cases reported herein, low doses of IV epinephrine may be able to terminate sustained monomorphic VT, when the arrhythmia is refractory to amiodarone used alone or in combination with beta-blockers and electrical cardioversion.[1]


I would not refer to 1,000 μg epinephrine, or even 500 μg, as low dose.

Dr. Scott Weingart discusses the use of epinephrine as a bolus dose pressor, but at much smaller doses.


0.5-2 ml every 2-5 minutes (5-20 mcg)

No extravasation worries![2]


Do not use epinephrine for V Tach without discussing it with your medical director and obtaining permissions, assuming you work some place where the medical director has the authority. If you are a doctor, discuss this with cardiology before using it.

Read the discussion of the many possible confounders in the full text of the paper and learn a bit about cardiology and the ways that physiology misleads us.


[1] Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia.
Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, Fontaine G.
World J Cardiol. 2012 Oct 26;4(10):296-301. doi: 10.4330/wjc.v4.i10.296.
PMID: 23110246 [PubMed]

Free Full Text from PubMed Central.

[2] Push-Dose Pressors – Podcast 6
Dr. Scott Weingart
Article and podcast.

Bonny, A. (2012). Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia World Journal of Cardiology, 4 (10) DOI: 10.4330/wjc.v4.i10.296