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

- Rogue Medic

Is placebo better than aggressive medical treatment for patients NOT having a heart attack?

Also to be posted on ResearchBlogging.org when they relaunch the site.

Is cardiac catheterization placebo better than aggressive medical treatment for patients not having a heart attack?


The answer is not really different from before. This should not be surprising for anyone who pays attention to EBM (Evidence-Based Medicine). We should all pay attention to EBM, because it is the best way to find out what works.

Many routine treatments are not beneficial to patients, but are considered to be standards of care. We continue to give these treatments out of unreasonable optimism, a fear of litigation, or fear of criticism for not following orders. The difference between the banality of evil and the banality of incompetence does not appear to be significant in any way that matters.

PCI (Percutaneous Coronary Intervention) treatment does not add any benefit – unless you are having a heart attack.

The placebo group received sham PCI in addition to optimized medical treatment. this did not provide any benefit over actual PCI in addition to optimized medical treatment. The patients in the placebo group received all of the same medications that the patients in the PCI group received.

Why is this news today?

A recent article in The Lancet is encouraging snake oil salesmen and snake oil saleswomen to claim that it shows the miracle healing power of placebos, but this is not true.

Apparently, Big Placebo (the multi-billion dollar alternative medicine industry) is trying to use this to promote their scams (homeopathy, acupuncture, Reiki, naturopathy, prayer, . . . ).

Big Placebo seems to think that this study shows that placebo is better than medical treatment. A placebo is an inactive intervention that is undetectable when compared with the active treatment. The placebo group received the same aggressive medications that the treatment group received.

All patients were pretreated with dual antiplatelet therapy. In both groups, the duration of dual antiplatelet therapy was the same and continued until the fial (unblinding) visit. Coronary angiography was done via a radial or femoral arterial approach with auditory isolation achieved by placing over-the-ear headphones playing music on the patient throughout the procedure.[1]


What is new about this?

A much larger study a decade ago showed that aggressive medical therapy was as good as PCI and aggressive medical therapy. The difference is the use of sham PCI to create a placebo group for comparison, rather than using a No PCI group for comparison.

As an initial management strategy in patients with stable coronary artery disease, PCI did not reduce the risk of death, myocardial infarction, or other major cardiovascular events when added to optimal medical therapy.


Compare that with the conclusion (interpretation) of the new paper.

In patients with medically treated angina and severe coronary stenosis, PCI did not increase exercise time by more than the effect of a placebo procedure. The efficacy of invasive procedures can be assessed with a placebo control, as is standard for pharmacotherapy.


The unfortunate outcome is that we will have fewer hospitals providing PCI, so patients with heart attacks (STEMI – ST segment Elevation Myocardial Infarctions) may have to wait longer for emergency PCI, which really does improve outcomes.

What other Standards Of Care are NOT supported by valid evidence?

Amiodarone is effective for cardiac arrest, whether unwitnessed, witnessed, or witnessed by EMS.

Kayexalate (Sodium Polystyrene) is a good treatment for hyperkalemia. Anything that causes diarrhea will lower your potassium level, but that does not make it a good treatment, unless you are in an austere environment (in other words – not in a real hospital).

Amiodarone is effective for VT (Ventricular Tachycardia).

Backboards are effective to protect against spinal injury while transporting patients.

Blood-letting is effective for anything except hemochromatosis (and some rare disorders).

More paramedics are better for the patient.

Prehospital intravenous lines save lives.

IV fluid saves lives in hemorrhagic shock.

Oxygen should be given to everyone having a heart attack.

The Golden Hour is important.

Driving fast saves lives. For only some rare conditions, it probably does – and that depends on traffic.

Flying people to the hospital saves lives. Again, for only some rare conditions, it probably does – and that depends on traffic and distance.

Tourniquets are dangerous. As with anything else, if used inappropriately, they are dangerous, but tourniquets save lives.

Prehospital intubation saves lives.

Ventilation in cardiac arrest improves outcomes (other than for respiratory causes of cardiac arrest, which are easy to identify).

Epinephrine improves outcomes in cardiac arrest. It does produce a pulse more often, but at what cost to the long-term survival of the patient and the patient’s brain? PARAMEDIC2 should help us to identify which patients benefit from epinephrine, since it is clear that many patients are harmed by epinephrine in cardiac arrest. If we limit treatment to patients reasonably expected to benefit from the treatment, we can improve long-term survival.

And there are many more.


[1] Percutaneous coronary intervention in stable angina (ORBITA): a double-blind, randomised controlled trial.
Al-Lamee R, Thompson D, Dehbi HM, Sen S, Tang K, Davies J, Keeble T, Mielewczik M, Kaprielian R, Malik IS, Nijjer SS, Petraco R, Cook C, Ahmad Y, Howard J, Baker C, Sharp A, Gerber R, Talwar S, Assomull R, Mayet J, Wensel R, Collier D, Shun-Shin M, Thom SA, Davies JE, Francis DP; ORBITA investigators.
Lancet. 2017 Nov 1. pii: S0140-6736(17)32714-9. doi: 10.1016/S0140-6736(17)32714-9. [Epub ahead of print]
PMID: 29103656

[2] Optimal medical therapy with or without PCI for stable coronary disease.
Boden WE, O’Rourke RA, Teo KK, Hartigan PM, Maron DJ, Kostuk WJ, Knudtson M, Dada M, Casperson P, Harris CL, Chaitman BR, Shaw L, Gosselin G, Nawaz S, Title LM, Gau G, Blaustein AS, Booth DC, Bates ER, Spertus JA, Berman DS, Mancini GB, Weintraub WS; COURAGE Trial Research Group.
N Engl J Med. 2007 Apr 12;356(15):1503-16. Epub 2007 Mar 26.
PMID: 17387127

Free Full Text from N Engl J Med.


Normal Sinus Rhythm is Not a Good Description

What is the rhythm 1a

Is Normal Sinus Rhythm a good description of this rhythm?

Is it sinus?

Is it normal?

Dr. Steven Novella writes about normal and some of the meanings of normal.

This findings, if confirmed, has several implications. First, it is just good to know how our brains typically work. “Normal” is a combined judgment about what is actually happening and what “should” be happening. This confirms what was observed in health care, especially psychiatry, that there is a moral judgment in deciding what is normal.[1]


Too often, we seem to try to apply what we think something should be to our mistaken description of what something is.

As an example, an ECG (ElectroCardioGram) showing a regular, or slightly irregular, sinus rhythm is often described using the misleading term normal sinus rhythm.

Normal suggests that there is nothing wrong with the rhythm, or with the heart, when it is not unusual for a patient to have a heart attack with a normal sinus rhythm being accurately displayed on the ECG.

We are subconsciously telling ourselves, Nothing to see here. Move along.

We are fooling ourselves and discouraging investigation of what may be causing problems by unnecessarily adding the term normal.

In this setting, normal does not add any information, but suggests that we know more than we actually know.

Why lie to ourselves?

Because we trust ourselves and don’t bother to check our assumptions to see if they are valid.

What is the rhythm 1

It is clearly sinus, but what information do we add by calling it normal?


[1] What Is Normal?
Steven Novella
Feb 02, 2017


Valsalva the SVT or Shock the Monkey?


The Skeptics’ Guide to Emergency Medicine should be on your podcast list. The podcasts are short, so there is not much reason to avoid them. This one is 13 minutes.

Valsalva for SVT (SupraVentricular Tachycardia) is supposed to come before medication. At least that is the order of treatments of every EMS SVT protocol I have seen. Since medicine is expected to have more, and more serious, side effects, this is reasonable.

What medicines?

Adenosine has the side effects of –


Prolonged asystole, ventricular tachycardia, ventricular fibrillation, transient increase in blood pressure, bradycardia, atrial fibrillation, and Torsade de Pointes



Central Nervous System

Seizure activity, including tonic clonic (grand mal) seizures, and loss of consciousness.[1]


It appears to be reasonable to try to avoid those side effects.

Too much of this could become more of a problem than an SVT.

Click on images to make them larger. Image credit.[2] This is not the actual strip, but a strip of an adenosine pause edited to produce more asystole, which I have seen.

The side effect becomes much more of a problem when someone decides to treat the side effect, rather than wait for it to wear off.

We SLAM adenosine in because it wears off quickly. A minute, or two, of asystole is not a problem.

Giving a dose of epinephrine to a patient who had an SVT a minute ago and now has adenosine quickly wearing off – that may be a fatal problem.

But how effective is the Valsalva maneuver (VM)?

The VM is a non-invasive way to convert patients from SVT to sinus.It increases myocardial refractory period by increasing intrathoracic pressure thus stimulating baroreceptors in the aortic arch and carotid bodies Increases vagal tone (parasympathetic).[3]


Here is a big problem with the use of the Valsalva maneuver. It is just one method of attempting to stimulate the vagus nerve.

There are many other methods and they may be more successful. Carotid sinus massage (after auscultation for bruits), facial immersion in ice water (assuring that the airway does not become a problem), bearing down, blowing through a straw (even better may be a swizzle stick), digital circumferential sweep of the anus, coughing, . . . .

There are many ways of activating the vagal nerve, but my favorite is to act as if I have not started an IV before, go very s l o w l y with the insertion of the largest IV catheter I think I can get in the vein, and this has almost always broken the rhythm.

Yes, that is anecdotal, but I have only rarely needed to follow that with medication.

Yes, pain is not a nice thing, but it is much nicer than the side effects listed above.

Bottom Line: There is no standardized methods to perform a VM to terminate uncomplicated SVT that are evidence based.

Clinical Application: VM is a viable technique that is poorly researched for the conversion of SVT and should not be considered essential to attempt prior to chemical cardioversion.[2]


We need better vagal maneuvers.

We need good evidence on what works.

Go read the article and listen to the podcast.


[1] ADENOCARD (adenosine) solution
[Astellas Pharma US, Inc.]

FDA Label

[2] Atrioventricular Re-entrant Tachycardia
Thumbnail Guide to Congenital Heart Disease
edited version of their adenosine ECG strip

[3] SGEM#67: Shock the Monkey Tonight (Valsalva Maneuver for SVT)
Podcast Link: SGEM67
Date: March 23, 2014
Skeptics’ Guide to Emergency Medicine
Article and link to podcast


Who Needs a 12 Lead ECG?


Do we do too many 12 lead ECGs on patients who do not have chest pain?

This is something that some people worry about.

Save the electrodes!

Those poor little electrodes are being abused!

Are electrodes being abused?

Women and the elderly with STEMI are particularly likely to present with atypical chief complaints such as dyspnea and weakness. Such patients experience significant delays in door-to-ECG time and treatment and have increased morbidity and mortality compared with patients who present with chest pain.5,9-12 [1]


Tiredness/weakness is the second best predictor of STEMI (ST segment Elevation Myocardial Infarction).

After chest pain (pressure, tightness, heaviness, squeezing, et cetera), the best predictor of STEMI is dyspnea in akll age ranges, but dyspnea indicates 20% of STEMIs in patients over 80 years old.

Are we helping anyone by avoiding 12 lead ECG (ElectroCardioGram) assessment?

Presenting chief complaints among 6,464 patients with STEMI. Chest pain decreased in frequency with age, whereas a chief complaint of dyspnea, weakness, syncope, or altered mental status all increased in frequency with age.[1]


Click on images to make them larger.


The advantage of a logarithmic chart is that there is greater distinction among the smaller numbers (such as the other complaints that make up less than 5% in the image above). The disadvantage is that large changes are flattened. I modified the dyspnea line to show how it would look on a linear scale (from 5% to 20%). As you can see, the ability to predict STEMI increases dramatically with age – more dramatically than the logarithmic scale suggests.


How should we remember all of this?

The authors came up with a nice simple flow chart (below).

This is for the ED, but is there a good reason for EMS to ignore these STEMIs?


Even in the 18-49 year old patients, dyspnea is about as likely to predict a STEMI as weakness is likely to predict a STEMI in an 80+ year old patient.

Chest pain still indicates about 50% of STEMI patients over 80, but we will miss half of STEMIs in this population if we only do 12 leads on chest pain patients.

Can an 80+ year old patient have a good quality of life after a STEMI?


Also see When should you get an ECG? at Mill Hill Ave Command.


[1] Development and validation of a prioritization rule for obtaining an immediate 12-lead electrocardiogram in the emergency department to identify ST-elevation myocardial infarction.
Glickman SW, Shofer FS, Wu MC, Scholer MJ, Ndubuizu A, Peterson ED, Granger CB, Cairns CB, Glickman LT.
Am Heart J. 2012 Mar;163(3):372-82. doi: 10.1016/j.ahj.2011.10.021.
PMID: 22424007 [PubMed – indexed for MEDLINE]

Glickman SW, Shofer FS, Wu MC, Scholer MJ, Ndubuizu A, Peterson ED, Granger CB, Cairns CB, & Glickman LT (2012). Development and validation of a prioritization rule for obtaining an immediate 12-lead electrocardiogram in the emergency department to identify ST-elevation myocardial infarction. American heart journal, 163 (3), 372-82 PMID: 22424007


A Recalled AED is Better Than No AED

Cardiac arrest. CPR in progress. Do not use the AED, because it has been recalled!



HeartStart automated external defibrillators from Philips Healthcare have been recalled.

What does the FDA (Food and Drug Administration) mean by recall?

Well, why was the recall issued?

Certain HeartStart automated external defibrillator (AED) devices made by Philips Medical Systems, a division of Philips Healthcare, may be unable to deliver needed defibrillator shock in a cardiac emergency situation, the U.S. Food and Drug Administration said today in a new safety communication for users of these previously recalled devices.[1]


A shock might not be delivered.

What does the FDA recommend?

“The FDA advises keeping all recalled HeartStart AEDs in service until you obtain a replacement from Philips Healthcare or another AED manufacturer, even if the device indicates it has detected an error during a self-test,” said Steve Silverman, director of the Office of Compliance in the FDA’s Center for Devices and Radiological Health.[1]


Do not take these AEDs out of service service until a replacement is present.


What about the lawyers?

But it’s defective!

Thinking is dangerous!

“Despite current manufacturing and performance problems, the FDA considers the benefits of attempting to use an AED in a cardiac arrest emergency greater than the risk of not attempting to use the defibrillator.”[1]


The benefit is greater than the risk.

There is risk with everything.

Anyone who tells you otherwise is selling something.

There is not benefit with everything.

Since the detection of an error during the self-test does not guarantee that the AED will not deliver a shock when needed, removing the AED without a replacement is more dangerous than leaving the AED in service.

These recalled AEDs are better than no AED.

Of course, if needed for use in an emergency, make every attempt to clear the error and use the device normally, as described in the Owner’s Manual.[2]


The manufacturer and the FDA agree that, in the case of these AEDs, something is better than nothing.

Are we really going to make a dead patient more dead by using a defective AED?


[1] FDA issues safety communication on HeartStart automated external defibrillators from Philips Healthcare
FDA News Release
For Immediate Release: Dec. 3, 2013
Media Inquiries: Jennifer Rodriguez, 301-796-8232, jennifer.rodriguez@fda.hhs.gov
Consumer Inquiries: 888-INFO-FDA
News Release

[2] Philips HeartStart FRx and OnSite (HS1) automated external defibrillators (AEDs)
Phillips Healthcare
Maintenance Advisory


Is Earlier Better for Therapeutic Hypothermia? Part I


When is the right time to begin TH (Therapeutic Hypothermia) to produce the best outcomes?

In the ICU (Intensive Care Unit)?

In the ED (Emergency Department)?

In the ambulance?

While the patient is still pulseless?

This question was asked in 2010.

Click on image to make it larger.

Favorable outcomes – 47.5% EMS TH vs 52.6% ED TH.

Worse outcome, but not statistically significant.

Discharge to home – 20.3% EMS TH vs 29.3% ED TH.

Worse outcome, but not statistically significant.

Discharge to rehabilitation – 27.1% EMS TH vs 23.3% ED TH.

Worse outcome, because these patients are not well enough to go home, but not statistically significant.

Dead – 52.5% EMS TH vs 46.6% ED TH.

Worse outcome, but not statistically significant.

The great tragedy of Science — the slaying of a beautiful hypothesis by an ugly fact. -Thomas Henry Huxley.

EMS TH was added to many EMS protocols because of a lack of clear evidence of harm. EMS needed to Just do something.

The results did not support EMS administration of chilled IV (IntraVenous) fluid for prehospital therapeutic hypothermia, but the study was stopped early, because –

At the interim analysis of the first 200 patients, the Steering Committee noted that there was no difference in the primary outcome measure and that it was extremely unlikely that such a difference would emerge between the groups. Therefore, the study was stopped because of futility after 234 patients had been enrolled.[1]


In other words – We will not let the numbers convince us that there is no benefit, because numbers that do not support a positive effect are futile?

If the data would have indicated a negative effect, but had not reached statistical significance, should we expect the Steering Committee to support continuing the study, or would they support discontinuing the study early to protect the enrolled patients, but leave the question unanswered?

When studies are discontinued early to protect patients, do they discourage further studies?

When studies are discontinued early to protect patients, do they only endanger future patients?

Or does early termination encourage further studies because there is not clear evidence of harm and we want to believe that our interventions are beneficial?

What if it works?

Most proposed treatments do not work, so this is just an excuse to continue using something dangerous. What if it works? is the logical fallacy that is used to justify harming patients with alternative medicine.

We should not harm vulnerable patients because of our unreasonable belief in wishful thinking.

If it helps just one patient it is worth it.

This is another logical fallacy, because it completely ignores the harm that the treatment causes.

Some patients will improve after almost any treatment – even cyanide.

That means that alternative medicine advocates could should endorse the use of cyanide, because if it helps just one patient . . . .

We need to have unbiased information about the real benefits (if any) and the real harms (if any), before we encourage using anything on vulnerable patients.

Is it good to just do something?


Is it good to help patients?

If our responsibility is to help patients, one of the best ways to help patients is to avoid causing harm.

Just doing something, with no evidence of benefit, is causing harm.

How many EMS agencies have prehospital therapeutic hypothermia protocols because of a desire to just do something?

I have been criticized for not being a supporter of treatments that do not have evidence of benefit.

Am I a killjoy, desiring bad outcomes?


I understand that treatment that does not have evidence of benefit is almost always going to do more harm than good.

Just do something?


Just demand valid evidence of improved outcomes.


[1] Induction of therapeutic hypothermia by paramedics after resuscitation from out-of-hospital ventricular fibrillation cardiac arrest: a randomized controlled trial.
Bernard SA, Smith K, Cameron P, Masci K, Taylor DM, Cooper DJ, Kelly AM, Silvester W; Rapid Infusion of Cold Hartmanns (RICH) Investigators.
Circulation. 2010 Aug 17;122(7):737-42. doi: 10.1161/CIRCULATIONAHA.109.906859. Epub 2010 Aug 2.
PMID: 20679551 [PubMed – indexed for MEDLINE]

Free Full Text from Circulation.

Bernard SA, Smith K, Cameron P, Masci K, Taylor DM, Cooper DJ, Kelly AM, Silvester W, & Rapid Infusion of Cold Hartmanns (RICH) Investigators (2010). Induction of therapeutic hypothermia by paramedics after resuscitation from out-of-hospital ventricular fibrillation cardiac arrest: a randomized controlled trial. Circulation, 122 (7), 737-42 PMID: 20679551


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.


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