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

- Rogue Medic

The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia

Wed, 17 Aug 2016 13:30:50 -0400 by
ResearchBlogging.org
 

This is a very interesting trial that may surprise the many outspoken amiodarone advocates, but it should not surprise anyone who pays attention to research.

ALPS showed that we should stop giving amiodarone for unwitnessed shockable cardiac arrest. The lead researcher is still trying to spin amiodarone for witnessed shockable cardiac arrest, even though the results do not show improvement in the one outcome that matters – leaving the hospital with a brain that still works.[1],[2],[3]

There is an excellent discussion of the study on the podcast by Dr. Salim Rezaie and Dr. Anand Swaminathan REBELCast: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia.

One problem with the study that they do not address on the podcast is that the patients in the study appear to have had time to watch Casablanca before treatment started. Here’s looking at you, while we’re waiting, kid. This is apparently unintentional one way of doing a placebo washout. If we wait long enough . . . .
 

Time from arrival to start of infusion was 87 ± 21 min for procainamide and 115 ± 36 min for amiodarone patients (P = 0.58).[4]

 

If nothing else, this demonstrates how little we need to worry about immediately pushing drugs for stable monomorphic VT (V Tach or Ventricular Tachycardia). Should we expect much from antiarrhythmic treatment?

Research shows that for stable monomorphic VT (V Tach or Ventricular Tachycardia) amiodarone is not very likely to be followed by an improvement. Only 29%[5] or only 25%[6] or only 15% within 20 minutes, but if we don’t mind waiting an hour it can be as much as 29%.[7] For those of you who are not good at math, that means amiodarone is about the same as doing nothing, only it comes in a syringe. Even though these poor outcomes ignore the side effects, they are the best evidence in favor of amiodarone, so what Kool-Aid are the advocates drinking?

Adenosine, yes adenosine the SVT (SupraVentricular Tachycardia) drug, appears to be more effective at treating ventricular tachycardia than amiodarone – and adenosine is faster and safer than amiodarone.[8]

What if the patient becomes unstable? First start an IV (IntraVenous) line. Then sedate the patient. Then apply defibrillator pads. After the patient is adequately sedated, then cardiovert. We do not need the pads on the patient first. If it takes a while to put the pads on, that is a problem with the ability of the doctors and nurses, not a medical problem.

It does not appear as if any patient received amiodarone or procainamide until after waiting in the ED (Emergency Department) for over an hour. Were some patients cardioverted in well under an hour? Probably. The important consideration is that the doctors and nurses be able to apply the defibrillator pads properly and quickly and deliver a synchronized cardioversion in less than a minute. If the patient has not yet been sedated, the cardioversion should be delayed until after the patient is adequately sedated, so the intervention that depends most on time is the sedation of the patient.
 

VT + Amiodarone Cardioversion
 

Is there a better treatment than amiodarone? Sedate the patient before the patient becomes unstable, then cardiovert. How do the MACEs (Major Adverse Cardiac Events) compare with sedation and cardioversion vs. antiarrhythmic treatment.
 

5.4 Proarrhythmia
Amiodarone may cause a worsening of existing arrhythmias or precipitate a new arrhythmia. Proarrhythmia, primarily torsade de pointes (TdP), has been associated with prolongation, by intravenous amiodarone, of the QTc interval to 500 ms or greater. Although QTc prolongation occurred frequently in patients receiving intravenous amiodarone, TdP or new-onset VF occurred infrequently (less than 2%). Monitor patients for QTc prolongation during infusion with amiodarone. Reserve the combination of amiodarone with other antiarrhythmic therapies that prolong the QTc to patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent.[9]

 

All antiarrhythmic drugs can cause arrhythmias. In the absence of information about a specific problem that is best addressed by a specific drug (amiodarone is the opposite of specific), we should avoid treatments that have such a high potential for harm.

Amiodarone doesn’t even do a good job of preventing arrhythmias.
 

Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion.[10]

 

Is anything worse than amiodarone? Even epinephrine, yes epinephrine the inadequately tested cardiac arrest drug, has been followed by improved outcomes from V Tach after amiodarone failed.[11]
 

What is best for the patient?

Sedation, search for reversible causes, apply defibrillator pads, and be prepared to cardiovert.

Maybe sedation isn’t that important? This is by Dr. Peter Kowey, one of the top cardiologists in the world.
 

The man’s very first utterance was, “If it happens again, just let me die.”

As I discovered, the reason for this patient’s terror was that he had been cardioverted in an awake state. Ventricular tachycardia had been relatively slow, he had not lost consciousness, and the physicians, in the heat of the moment, had not administered adequate anesthesia. Although the 5 mg of intravenous diazepam had made him a bit drowsy, he felt the electric current on his chest and remembered the event clearly.

The patient’s mental state complicated the case considerably.[12]

 

How unimportant is sedation? How unimportant is consent?

For sedation, I would recommend ketamine, but etomidate was recommended in the podcast. Both work quickly and the most important obstacle to immediate treatment of a patient who suddenly deteriorates is the time to effect of sedation. Neither drug is expected to interfere with perfusion, which is the main excuse given for avoiding sedation for cardioversion.

This study is very small (not the fault of the authors), but it adds to the evidence that amiodarone is not a good first treatment for the patient.
 

Go listen to the podcast by Dr. Salim Rezaie and Dr. Anand Swaminathan REBELCast: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia

 

Over the years, I have written a bit about cardioversion and the importance of sedation –

Cardioversion – I’m not doing that, you do it! – Mon, 24 Mar 2008

Cardioversion – 2010 ACLS – Part I – Mon, 25 Oct 2010

Cardioversion – 2010 ACLS – Part II – Sun, 31 Oct 2010

Cardioversion – 2010 ACLS – Part III – Thu, 11 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part I – Thu, 11 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part II – Fri, 12 Nov 2010

Synchronized Cardioversion Without Sedation – Part II Scallywag’s Response – Sun, 14 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part III – Tue, 16 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part IV – Wed, 24 Nov 2010

Comments on Cardioversion – 2010 ACLS – Part II – Mon, 16 Apr 2012
 

I have also written a bit about amiodarone –

Merit Badge Courses, Amiodarone, and tPA – Fri, 17 Sep 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part I – Wed, 01 Dec 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part II – Fri, 03 Dec 2010

Is Nexterone the Next Amiodarone? – Sat, 04 Dec 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part III – Mon, 06 Dec 2010

Where are the Black Box Warnings on These Drugs – I – Mon, 05 Dec 2011

Where are the Black Box Warnings on These Drugs – II – Sun, 11 Dec 2011

Is Amiodarone the Best Drug for Stable Ventricular Tachycardia – Wed, 14 Dec 2011

V Tach Storm – Part I – Wed, 28 Dec 2011

V Tach Storm – Part II – Thu, 29 Dec 2011

Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia – Wed, 04 Jan 2012

NIH launches trials to evaluate CPR and drugs after sudden cardiac arrest – Sun, 29 Jan 2012

What Will Be the Next Standard Of Care We Eliminate – Wed, 28 Mar 2012

Happy Adenosine Day – Tue, 12 Jun 2012

Too Much Medicine and Evidence-Based Guidelines – Part I – Tue, 26 Jun 2012

Too Much Medicine and Evidence-Based Guidelines – Part II – Tue, 03 Jul 2012

Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part I – Mon, 02 Jul 2012

Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part II – Thu, 05 Jul 2012

Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium – Part I – Mon, 17 Sep 2012

Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium – Part II – Tue, 18 Sep 2012

How do we measure the QT segment when there are prominent U waves? – Thu, 13 Dec 2012

Woman with Risks for Torsades de Pointes Dying within Hours of Leaving the Emergency Department – Wed, 02 Jan 2013

Examples of Ventricular Tachycardia Caused by Amiodarone – Part I – Tue, 28 May 2013

Publication Bias – The Lit Whisperers – Tue, 11 Jun 2013

Standards Of Care – Ventricular Tachycardia – Wed, 31 Jul 2013

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Footnotes:

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[1] Dr. Kudenchuk is Misrepresenting ALPS as ‘Significant’
Tue, 12 Apr 2016
Rogue Medic
Article

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[2] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest
Mon, 04 Apr 2016
Rogue Medic
Article

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[3] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest.
Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P; Resuscitation Outcomes Consortium Investigators.
N Engl J Med. 2016 May 5;374(18):1711-22. doi: 10.1056/NEJMoa1514204. Epub 2016 Apr 4.
PMID: 27043165

CONCLUSIONS
Overall, neither amiodarone nor lidocaine resulted in a significantly higher rate of survival or favorable neurologic outcome than the rate with placebo among patients with out-of-hospital cardiac arrest due to initial shock-refractory ventricular fibrillation or pulseless ventricular tachycardia.

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[4] Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study.
Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J; PROCAMIO Study Investigators.
Eur Heart J. 2016 Jun 28. pii: ehw230. [Epub ahead of print]
PMID: 27354046

Free Full Text from European Heart Journal.

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[5] Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison.
Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT.
Acad Emerg Med. 2010 Mar;17(3):297-306.
PMID: 20370763 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

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[6] Amiodarone is poorly effective for the acute termination of ventricular tachycardia.
Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN.
Ann Emerg Med. 2006 Mar;47(3):217-24. Epub 2005 Nov 21.
PMID: 16492484 [PubMed – indexed for MEDLINE]

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[7] Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?
Tomlinson DR, Cherian P, Betts TR, Bashir Y.
Emerg Med J. 2008 Jan;25(1):15-8.
PMID: 18156531 [PubMed – indexed for MEDLINE]

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[8] Adenosine for wide-complex tachycardia – diagnostic?
Thu, 23 Aug 2012
Rogue Medic
Article

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[9] AMIODARONE HYDROCHLORIDE- amiodarone hydrochloride injection, solution
DailyMed
5 WARNINGS AND PRECAUTIONS
FDA Label

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[10] Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.
Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, Ceremuzyński L.
Europace. 2000 Jul;2(3):207-15.
PMID: 11227590 [PubMed – indexed for MEDLINE]

Free Full Text PDF + HTML from Europace

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[11] 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.

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[12] The calamity of cardioversion of conscious patients.
Kowey PR.
Am J Cardiol. 1988 May 1;61(13):1106-7. No abstract available.
PMID: 3364364

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Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P, & Resuscitation Outcomes Consortium Investigators (2016). Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. The New England journal of medicine, 374 (18), 1711-22 PMID: 27043165

Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J, & PROCAMIO Study Investigators (2016). Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. European heart journal PMID: 27354046

Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, & Ellinor PT (2010). Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17 (3), 297-306 PMID: 20370763

Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, & Ruskin JN (2006). Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Annals of emergency medicine, 47 (3), 217-24 PMID: 16492484

Tomlinson DR, Cherian P, Betts TR, & Bashir Y (2008). Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emergency medicine journal : EMJ, 25 (1), 15-8 PMID: 18156531

Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, & Ceremuzyński L (2000). Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology, 2 (3), 207-15 PMID: 11227590

Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, & Fontaine G (2012). Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia. World journal of cardiology, 4 (10), 296-301 PMID: 23110246

Kowey PR (1988). The calamity of cardioversion of conscious patients. The American journal of cardiology, 61 (13), 1106-7 PMID: 3364364

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Filed Under: ACLS, Adenosine, Assessment, Cardioversion, Critical Judgment, Ethics, Ketamine, Pharmacology, Research Blogging, Sedation, Toxicology, V Tach

1-Union-801 Podcast Discussing Epi for V Tach, Cardioversion, Procainamide, Paralytics During Hypothermia, Quality of CPR, and DNA Transfer

Thu, 01 Aug 2013 21:00:14 -0400 by

 

 
On 1-Union-801 John Broyles and I discussed some things that I had written. I was supposed to be on the podcast two weeks earlier, but I am on duty at the time of the podcast, and I had a call a few minutes before the show. This podcast was not interrupted by any calls.[1]
 

Go listen to the podcast.
 

Epinephrine for V Tach – Instant Death or Effective Treatment?

What might happen if epinephrine is given for this V Tach (Ventricular Tachycardia)?
 

Click on images to make them larger. Image credit and article about epinephrine for V Tach.[2]
 

We also discuss sychronized cardioversion and procainamide.
 
Other things we discussed (in order) were –

Do Paralytics Improve Outcomes Following Resuscitation?

We want to minimize movement after starting therapeutic hypothermia. Is the use of paralytics the right way to do this?
 

Un-extraordinary measures: Stats show CPR often falls flat

The author appears to take the comments of Dr. David Newman completely out of context in order to make a point that I do not think Dr. Newman would ever make.

Who is Dr. Newman?
 

 

SMART EM

Dr. David Newman, and sometimes Dr. Ashley Shreves, write and podcast about research and emergency medicine. There is an excellent deconstruction of the ACLS (Advanced Cardiac Life Support) guidelines and the lack of evidence for the drugs recommended in the guidelines.

The NNT is another excellent site that is here, too.

At Annals of Emergency Medicine, Dr. Newman and Dr. Ashley Shreves present excellent summaries of the articles in each issue. Annals of Emergency Medicine Podcast

I also mentioned Dr. Richard Levitan’s No Desat approach of using high flow oxygen by nasal cannula, which works wonders. Read about No Desat!
 

Apparent DNA Transfer by Paramedics Leads to Wrongful Imprisonment

Do we use gloves properly?

Is DNA transfer between patients an indication of a lack of use of gloves?
 

Go listen to the podcast.
 

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Footnotes:

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[1] Rogue Medic Saved Our Bacon 20 Jul 13
1-Union-801
John Broyles
Podcast page.

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[2] 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.

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Filed Under: ACLS, Cardioversion, Epinephrine, Heresy, Research, V Tach

Another Sinus Tachycardia that F&B Medics Want to Shock

Mon, 11 Feb 2013 08:00:53 -0500 by

 

In Worst test question ever! – Maybe, I pointed out some of the problems with the way we “educate” people in EMS. The following question was provided with the rhythm above.
 

You are dispatched emergency traffic to the scene of a 24 yo F with “palpitations.” You arrive to find her pale, sweaty and lethargic. You palpate a radial pulse with an extreme rate. You hook her up to the monitor and find the following rhythm? You have a 45 minute transport time. Which of the following is the most appropriate initial treatment for this condition?

1.) Nitroglycerin 0.4mg SL
2.) Immediate synchronized cardioversion
3.) Adenosine 12mg Rapid IV push followed by 20cc NS bolus
4.) Epinephrine 1mg 1:10000 q-3-5m IVP

 

If a test question is so poorly written that there is no justifiable answer, why would anyone competent defend the question?

The answer is that we have dangerous people as “educators” and no really good method of eliminating them from EMS classrooms.

If there are no correct answers, can there be one best answer?

If there are no correct answers, can the most deadly answer possibly be the best answer?

We are supposed to be providing patient care, not making “educators” feel good about being dangerous.

Could the rhythm be atrial flutter?

It is not a bad idea to suspect flutter when the ECG rate is an even fraction of the ≈300 rate that is typical of flutter waves e.g. ≈75, ≈100, and ≈150)?

Is there another wave half way between the P waves seen in this rhythm, which would make both waves F waves?

I do not see any Flutter waves.
 

 

That is the same rhythm. Do you see any F waves?

If the rhythm is sinus, then cardioversion/defibrillation is not going to help, but can make things a lot worse.

We can produce anything from pain to death by shocking this rhythm.

Why would we do that to satisfy an incompetent “educator”?

This might be a good question to identify people who should not be trusted to care for patients. If we are willing to make a choice that is the equivalent of harming patients in order to come up with the one best answer right answer in a testing environment, what might we do when faced with a real patient, but a protocol that we think needs to be followed?

Is cardioversion the way to avoid the QA/QI/CYA spanking?

Should we be trying to figure out how to intervene?

Should we be trying to figure out when to intervene?

If the intervention is a heart-stopping dose of electricity (cardioversion), should we be looking for excuses to shock, or should we be trying to figure out if the patient is likely to benefit from that treatment?

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What about this 80+ year old patient, who is pale, and lethargic, but is not confused?
 

 

 
 

Here is a different EMS 12 Lead Facebook post.
 

More ACLS…
Your pt is a 54 yo male found in bed, with AMS. He looks pale, has BP of 84/52 with the rhythm below. No other hx is available right now. What’s the treatment?

 

The earlier post looked like a sinus tachycardia from a rhythm generator. With the HeartSim, to get a good fast narrow complex rhythm use atrial tachycardia and hit the faster button once or twice – that produces a rhythm that is not obviously sinus. There were 25 comments choosing from among the choices given, before there was a comment from someone smart enough to recognize that all of the choices were wrong.

Yes, the National Registry does encourage the fraud of one best answer. Why do medics choose a dangerous treatment, when we know it is dangerous?

We have been taught to choose try to figure out what would be most pleasing to the instructor/evaluator – not to do what is best for the patient.

Why aren’t the instructors/evaluators looking for what is best for the patient?

 
One of the reasons for fewer indefensible answers at EMS 12 Lead is that many of the people following EMS 12 Lead are already medics, nurses, and/or doctors, rather than students looking to please an instructor/evaluator.

This time, there were four good answers before anyone suggested cardioversion, but why are so many of us looking for excuses to use electricity to stop the hearts of patients?

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Filed Under: ACLS, Cardiology, Cardioversion, Critical Judgment, Heresy

Happy Adenosine Day

Tue, 12 Jun 2012 16:30:04 -0400 by
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6-12-12
 

The dosing of adenosine (Adenocard) for PSVT (Paroxysmal SupraVentricular Tachycardia or just SVT – SupraVentricular Tachycardia) is 6 mg, followed by an immediate 20 ml flush, wait a minute, 12 mg, followed by an immediate 20 ml flush, wait a minute, and then another 12 mg, followed by an immediate 20 ml flush.

This only comes twice a century according to the Gregorian calendar. Once in the US style and once in the European style (December 06, 2012 – where the month comes after the day).
 

Wait!
 

O frabjous day! Callooh! Callay!

The AHA (American Heart Association) has decided that we should be able to celebrate Adenosine Day twice a year, rather than twice a century.
 

Adenosine. If PSVT does not respond to vagal maneuvers, give 6 mg of IV adenosine as a rapid IV push through a large (eg, antecubital) vein followed by a 20 mL saline flush (Class I, LOE B). If the rhythm does not convert within 1 to 2 minutes, give a 12 mg rapid IV push using the method above.[1]

 

Where is the third dose?

Is it wrong to give a second dose of 12 mg? No, but it also isn’t wrong to celebrate Adenosine Day twice a year. 😉

It never did make sense to wait a minute to repeat the same dose of a medication that is supposed to be completely metabolized in less than a minute. Unless there is something cumulative about the administration, the same dose should produce the same result.

Since the second dose of 12 mg occasionally has been followed by a change in rhythm, maybe the metabolism of adenosine is not as fast as we expect.

I have seen a strip of over a minute of asystole following adenosine administration – the initial 6 mg dose. Apparently, that patient did not metabolize adenosine as rapidly as we would expect.
 


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.
 

What should we do for that asystole?

Check a pulse.

Yes. There is no pulse. The leads are connected. The axis of the heart has not suddenly changed, so checking another lead will not change anything, but feel free to satisfy do your protocol thing.

Check for responsiveness.

The patient states that she feels awful and wants to know what you did to her.

Begin CPR?

Not on an awake and talking patient.

Give epinephrine?

Hell No!

Epinephrine, if it provides any benefit, only helps the chest compressions of CPR to perfuse. We are not starting CPR, so we are not giving epinephrine.

What dose would we give to this living patient? the appropriate dose for a living patient 0.002 mg (2 μg) to start or the dead person dose of 1 mg (1,000 μg)?

What was the initial rate?

Very very fast.

How quickly is adenosine metabolized?

Very very quickly.

What do we expect the rate to be when the adenosine wears off and the epinephrine kicks in?

If the hear can go any faster before it quits, it will, but epinephrine (heart failure in a syringe) is only going to make the heart fail sooner.

The only thing to do is to wait at least a minute for the adenosine to wear off. This is a good time to review the medications the patient is taking for drugs that alter the effective period of adenosine –
 

Adenocard is antagonized competitively by methylxanthines such as caffeine and theophylline, and potentiated by blockers of nucleoside transport such as dipyridamole. Adenocard is not blocked by atropine.[3]

 

Benzodiazepines can also potentiate adenosine.[4] If we have any expectation of cardioversion, we should sedate early. Benzodiazepines are not the best, or second best, or even the third best sedative for cardioversion, but benzodiazepines are all that some of us have. Also, I have been told by one person that cardioversion is less painful that adenosine. If cardioversion is preferable to adenosine, maybe we should consider giving a sedative before adenosine for some people.

And then there is the myth that adenosine diagnoses SVT. This is not true. Some V Tach (Ventricular Tachycardia) does respond to adenosine,[5] just as some V Tach does respond to amiodarone.

The only questions are –

Do more V Tach patients respond to adenosine than to amiodarone?

Should we finally give up the ineffective amiodarone (barely more effective than placebo, but with the potential for more harm – hypotension, QT segment prolongation, torsades, et cetera – and it is the only commonly used antiarrhythmic banned for pregnant patients) and sedate the patient in preparation for cardioversion?

Almost all of the patients who receive amiodarone will receive cardioversion because of the ineffectiveness of amiodarone. Why do we treat patients as if amiodarone will work this time?

Because we are hopeless optimists who do not understand what we are doing. 😳

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Footnotes:

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[1] Adenosine
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.3: Management of Symptomatic Bradycardia and Tachycardia
Free Full Text from Circulation

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

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[3] ADENOCARD (adenosine) solution
[Astellas Pharma US, Inc.]
DailyMed
FDA Label

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[4] Therapeutic concentrations of diazepam potentiate the effects of adenosine on isolated cardiac and smooth muscle [proceedings].
Clanachan AS, Marshall RJ.
Br J Pharmacol. 1980 Jan;68(1):148P-149P. No abstract available.
PMID: 7357161 [PubMed – indexed for MEDLINE]

Free Full Text from PubMed Central

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[5] Effects of adenosine triphosphate on wide QRS tachycardia. Analysis in 18 patients.
Hina K, Kusachi S, Takaishi A, Yamasaki S, Sakuragi S, Murakami T, Kita T.
Jpn Heart J. 1996 Jul;37(4):463-70.
PMID: 8890760 [PubMed – indexed for MEDLINE]

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Filed Under: 2010 AHA Guidelines, Cardiology, Cardioversion, Heresy, Pharmacology, Research

Comments on Cardioversion – 2010 ACLS – Part II

Mon, 16 Apr 2012 15:35:01 -0400 by
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In response to Cardioversion – 2010 ACLS – Part II, there are some new comments. Chris from Sweden, had written –

What meds do you use in the hypotensive, but still conscious patient for sedation? Could ketamine and low dose of midazolam be of use here?

Gerardo Gastélum comments –

Not Ketamine for cardioversion. Ketamine rises heart rate and coronary O2 requirements.

Benzos like Midazolam or Diazepam + Opiates such as Fentanyl or Morphine can do the works. AHA also recomends etomidate, thiopental and propofol, but out of these I chose etomidate due to it´s cardiovascular stability.

I disagree.

There may be more of a desire to avoid sedatives that vasodilate and depress cardiac activity. This is one of the reasons that etomidate is recommended. I think that either effect is going to be short-term – if the cardioversion, or series of cardioversions, works.

Some people discourage sedation. One of the things that they do not appear to consider is the possibility of needing to cardiovert more than once.

I can get away with shocking her without sedation, justify it as saving her life, and sedate her afterward to deal with the side effects of such brutal treatment, but the idea of appropriate sedation prior to cardioversion almost scares me into an unstable tachycardia.

Fortunately, nobody here is recommending that we not sedate for cardioversion.

With comments on this topic, I tend to wonder, Has this been covered in an EMCrit podcast? What would Dr. Scott Weingart do? Maybe he can make up some EMCrit screensavers with the slogan WWWD? (What Would Weingart Do?). Dr. Weingart is trying to smooth the transition from treatment in the ED (Emergency Department) to treatment in the ICU (Intensive Care Unit) and possibly take over the world of emergency education.

I think the clever something to give is probably a low dose of etomidate, maybe 5 or 7 mg of etomidate. They’re not going to be fully unconscious, like when we gave the 10 or 15 mg, but it’ll take the edge off.

They’re getting no pain control whatsoever from that, so if you were really a smart guy, give a little etomidate with some ketamine, or even just ketamine alone.[1]

Listen to the whole podcast – all 9 minutes of it. I just copied a few sentences, but this very short podcast covers a lot of material that is very important to understand before dealing with the unstable tachyarrhythmia patient.

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Image credit.

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In the second comment, Gerardo Gastélum provides a quote from the 2010 ACLS guidelines that is important for the understanding of the difference between unstable and just symptomatic.[2]

Thank you for the great description from ACLS.

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Footnotes:

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[1] EMCrit Podcast 20 – The Crashing Atrial Fibrillation Patient
by EMCRIT on FEBRUARY 12, 2010
Podcast page

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[2] Management of Symptomatic Bradycardia and Tachycardia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.3: Management of Symptomatic Bradycardia and Tachycardia
Free Full Text from Circulation

Unstable and symptomatic are terms typically used to describe the condition of patients with arrhythmias. Generally, unstable refers to a condition in which vital organ function is acutely impaired or cardiac arrest is ongoing or imminent. When an arrhythmia causes a patient to be unstable, immediate intervention is indicated. Symptomatic implies that an arrhythmia is causing symptoms, such as palpitations, lightheadedness, or dyspnea, but the patient is stable and not in imminent danger. In such cases more time is available to decide on the most appropriate intervention. In both unstable and symptomatic cases the provider must make an assessment as to whether it is the arrhythmia that is causing the patient to be unstable or symptomatic. For example, a patient in septic shock with sinus tachycardia of 140 beats per minute is unstable; however, the arrhythmia is a physiologic compensation rather than the cause of instability. Therefore, electric cardioversion will not improve this patient’s condition. Additionally, if a patient with respiratory failure and severe hypoxemia becomes hypotensive and develops a bradycardia, the bradycardia is not the primary cause of instability. Treating the bradycardia without treating the hypoxemia is unlikely to improve the patient’s condition. It is critically important to determine the cause of the patient’s instability in order to properly direct treatment. In general, sinus tachycardia is a response to other factors and, thus, it rarely (if ever) is the cause of instability in and of itself.

One of my earliest posts was a variation on the distinction between unstable and symptomatic –

Cardioversion – I’m not doing that, you do it!

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Filed Under: 2010 AHA Guidelines, Cardioversion, EMCrit, Heresy, Ketamine, Pharmacology, Sedation

When Does Post-Resuscitation Care Begin

Wed, 18 Jan 2012 22:22:13 -0500 by
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In the comments to Cardiac Arrest Management is an EMT-Basic Skill, AZCEP wrote –

True enough, but it is an important part of resuscitation all the same. Post-arrest management has been de-emphasized to the point of absence from AHA guidelines until the latest version reintroduced it to us.

When we start post-resuscitation care before the patient is resuscitated, we are not doing any good. Post means after. Post-resuscitation means after resuscitation, not during resuscitation and definitely not before ROSC.

We are just making excuses for interrupting compressions and continuing experimental treatments that most likely decrease survival.

Post-resuscitation treatment should not be de-emphasized. I have always spent time teaching people what to do after ROSC (Return Of Spontaneous Circulation).

First. Assess. Don’t do too much.

Find out what is going on before doing anything.

Suppose the patient’s initial pressure is 60 by palpation.

What do we do?

Second. Reassess.

Things change, so we want to know what the trend is. We do not care what normal is. We are dealing with a patient who is not at all representative of what we do.

60/palp is not a good pressure for a normal patient, but there is nothing normal about this patient. We want to know what direction the blood pressure is going. A minute ago the pressure was 0/0, so things have improved. Rushing to give a catecholamine (something that is just a weaker version of epinephrine, or just epinephrine by drip) is a bad idea. The patient just had his systolic pressure rise by 60 points in one minute without any pressors. Adding a pressor to a dramatically rising blood pressure is a bad idea.

If the pressure stays at 60/palp, then some fluids are not a bad idea. Always listen to lung sounds before giving fluids, but crackles are not an absolute contraindication for a fluid challenge. Crackles may even be an indication for a fluid challenge.

If the next pressure is lower, then a fluids challenge is the first treatment – not a catecholamine!

We just resuscitated the patient. Let’s hold off on the drugs that can kill the patient. At least let him live for a few minutes.

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What about cardioversion?

This patient definitely meets criteria for cardioversion.

No. This patient only meets criteria for cardioversion after a full assessment and not after cardiac arrest.

How much epinephrine has the patient received?

Is cardioversion going to metabolize any of that massive dose of epinephrine?

Absolutely not.

Just say NO.

Reassess and then reassess again.

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The best management of a cardiac arrest is to prevent it from ever happening to begin with.

Preventing cardiac arrest is much better than responding to cardiac arrest, but should we assume that ALS that failed to prevent cardiac arrest is going to reverse cardiac arrest? These are very different medical presentations, even though they may be in the same patient.

I wrote about this in Dissecting the ACLS Guidelines on Cardiac Arrest from Toxic Ingestions. Calcium chloride is safe and effective at preventing arrest from hyperkalemia. Once the patient is dead (maybe medical command refused orders for calcium chloride, maybe the patient arrested prior to arrival, maybe we didn’t think it was that serious, . . . ), giving calcium chloride may not be anywhere near as successful.

There is an important difference in the way dead people and living people respond to treatments.

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Filed Under: 2010 AHA Guidelines, Cardioversion, Heresy, Pharmacology

Is Ketamine an EMS Wonder Drug

Sun, 01 Jan 2012 06:30:42 -0500 by
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Too Old To Work responded to my description of the benefits of keatamine in What I Wanted from EMS Santa But Did Not Get.

Funny, I’ve used Lidocaine and Amiodarone a number of times to terminate antiarrhythmias, although I still contend that Lidocaine works better than Amio. I’ve only used cardioversion a couple of times and only when there was no other alternative. The last time I used it, we were using Valium for sedation, it’s been that long.

That is why we ignore anecdotal evidence of benefit. When we look at numbers large enough to provide predictable results, the memories of good outcomes from amiodarone and lidocaine are found to be the result of statistical variation, or bad memory, or both. We tend to forget the times that our antiarrhythmics do not work for V Tach (Ventricular Tachycardia).

Different studies show that amiodarone is only 29% effective at terminating V Tach,[1] only 25% effective at terminating V Tach, [2], and only 15% effective at terminating V Tach within 20 minutes, but if we don’t mind waiting an hour it can be as much as 29% effective.[3]

If we are not trying to convert the rhythm promptly, should we even consider V Tach an emergency? If lights and sirens only make a difference of a minute, or two, V Tach is obviously not a lights and sirens emergency. Maybe we need a treatment that works.

Over 60% of the patients were cardioverted, for which they should receive a sedative that does not produce/worsen hypotension. We might as well start acknowledging that our anecdotes often do not match reality.

When the patient is awake and alert with a systolic blood pressure of 70, should we give a vasodilator, such as midazolam, or should we give a drug that does not decrease cardiac output, such as ketamine?

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Image credit.

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Amiodarone works just as well as Ketamine for sedation, Versed or Ativan work better for excited delirium.

Amiodarone can produce hypotension, arrhythmias, and cardiac arrest, but that is not the kind of sedation I want. Was this a typo?

Since you do not appear to have listened to any of the EMCrit podcasts I linked to, here is another opportunity to learn. Dr. Weingart describes the lack of effectiveness of benzodiazepines (midazolam [Versed], lorazepam [Ativan], and diazepam [Valium]). He does not discourage their use to minimize emergence reactions, but he does not suggest that they are appropriate as sole treatments for excited delirium, unless that is all you have available.[4]

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Fentanyl probably works better for pain management, especially cardiac related pain.

Which is great – if the patient does not require doses that produce respiratory depression, or if the only pain we treat is cardiac pain. Let me quote from the anonymous comment that you followed, but do not appear have read.

It facilitates extrication of critical patients who are still awake and who often have compound fractures. Given the choice of struggling to hold a combative head patient down while trying to get them in a c-collar and a backboard vs. IM Ketamine and a cooperative patient within a minute or two, Ill take the latter. It’s a beautiful thing when used responsibly. It certainly is safer than trying to sedate and paralyze a hypoxic patient.

If we want to be very limited in our options, then we should not ask for ketamine from our medical directors.

If we do not like using safe drugs, then we should not ask for ketamine from our medical directors.

I am stating that we should ask for ketamine from our medical directors. Our patients deserve it.

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I’m not following the last part of you post, because you haven’t set the circumstances requiring Ketamine and a NRB.

I linked to the EMCrit podcast covering DSI (Delayed Sequence Intubation). I think that podcast more than adequately describes the circumstances in under 20 minutes.[5]

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Ketamine might be an all in one wonder drug, but why do we need an all in one wonder drug when we can have a selection of wonder drugs?

No drug is a wonder drug.

Ketamine does a lot of things very well – better than the usual EMS drugs. We should not allow our lack of familiarity to discourage us from using this drug that is used frequently, safely, and effectively all over the world.

At Free Emergency Medicine Talks you should listen to Mel Herbert – Updates on Ketamine. Unfortunately, the video is not included, but the information is still very clear and very thorough.

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Ketamine is recommended for use in the patient whose stomach is not empty when, in the judgment of the practitioner, the benefits of the drug outweigh the possible risks.[6]

You may only treat patients who have been fasting, but I end up with patients with full bellies. I would prefer better ways to keep the stomach contents out of the lungs.

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Ketamine has a wide margin of safety; several instances of unintentional administration of overdoses of ketamine (up to ten times that usually required) have been followed by prolonged but complete recovery.[6]

Is any other sedative that safe?

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Footnotes:

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[1] Amiodarone is poorly effective for the acute termination of ventricular tachycardia.
Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN.
Ann Emerg Med. 2006 Mar;47(3):217-24. Epub 2005 Nov 21.
PMID: 16492484 [PubMed – indexed for MEDLINE]

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[2] Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison.
Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT.
Acad Emerg Med. 2010 Mar;17(3):297-306.
PMID: 20370763 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

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[3] Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?
Tomlinson DR, Cherian P, Betts TR, Bashir Y.
Emerg Med J. 2008 Jan;25(1):15-8.
PMID: 18156531 [PubMed – indexed for MEDLINE]

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[4] On Human Bondage and the Art of the Chemical Takedown
EMCrit
November 13, 2011
Page with podcast and supplemental information

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[5] Delayed Sequence Intubation (DSI)
EMCrit
January 31, 2011
Page with podcast and supplemental information

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[6] Ketamine Hydrochloride (ketamine hydrochloride) Injection, Solution, Concentrate
[Bedford Laboratories]
FDA Label
DailyMed
Label

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Filed Under: Airway Management, Cardioversion, EMCrit, Excited Delirium, Heresy, Intubation, Ketamine, Pharmacology, Research, Sedation

Is Amiodarone the Best Drug for Stable Ventricular Tachycardia

Wed, 14 Dec 2011 06:30:47 -0500 by
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Is Amiodarone the Best Drug for Stable Ventricular Tachycardia?

What do the cardiologists recommend?

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D. Sustained Monomorphic Ventricular Tachycardia
Recommendations

Class I

1. Wide-QRS tachycardia should be presumed to be VT if the diagnosis is unclear. (Level of Evidence: C)

2. Direct-current cardioversion with appropriate sedation is recommended at any point in the treatment cascade in patients with suspected sustained monomorphic VT with hemodynamic compromise. (Level of Evidence: C)

Class IIa

1. Intravenous procainamide (or ajmaline in some European countries) is reasonable for initial treatment of patients with stable sustained monomorphic VT. (Level of Evidence: B)

2. Intravenous amiodarone is reasonable for patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents. (Level of Evidence: C)

3. Transvenous catheter pace termination can be useful to treat patients with sustained monomorphic VT that is refractory to cardioversion or is frequently recurrent despite antiarrhythmic medication. (Level of Evidence: C)[1]

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Class I –

Cardioversion.

Class IIa –

1. Procainamide.
2. Amiodarone.
3. Transvenous pacer.

OK, but that is not from the current ACLS.

Amiodarone must have been moved up in the rankings in the current ACLS, because that is what we were taught.

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The guidelines above came out in 2006.

Amiodarone was was not moved up, but was downgraded to Class IIb in the current (2010) ACLS Guidelines.

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Image modified from Paramedicine 101 – 2010 AHA Updates.

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For patients who are stable with likely VT, IV antiarrhythmic drugs or elective cardioversion is the preferred treatment strategy. If IV antiarrhythmics are administered, procainamide (Class IIa, LOE B), amiodarone (Class IIb, LOE B), or sotalol (Class IIb, LOE B) can be considered. Procainamide and sotalol should be avoided in patients with prolonged QT. If one of these antiarrhythmic agents is given, a second agent should not be given without expert consultation (Class III, LOE B). If antiarrhythmic therapy is unsuccessful, cardioversion or expert consultation should be considered (Class IIa, LOE C).[2]

Class I –

Still cardioversion.

Class IIa –

Procainamide.

Class IIb –

Amiodarone.

Maybe in the 2015 ACLS Guidelines there will not be any mention of amiodarone, except as a historical footnote. Maybe amiodarone will be replaced by something more effective at treating ventricular tachycardia, such as adenosine. 😳

More likely is that we use more procainamide, but we should also consider being much more aggressive in sedating patients in anticipation of cardioversion. Amiodarone is associated with improvement from ventricular tachycardia in less than 30% of patients with stable ventricular tachycardia.

We need better sedatives. Ketamine would probably be the safest sedative for EMS to use.

Why don’t more of us have ketamine?

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Footnotes:

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[1] D. Sustained monomorphic ventricular tachycardia
XIII. Acute management of specific arrhythmias
ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death–executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society.
Zipes DP, Camm AJ, Borggrefe M, Buxton AE, Chaitman B, Fromer M, Gregoratos G, Klein G, Moss AJ, Myerburg RJ, Priori SG, Quinones MA, Roden DM, Silka MJ, Tracy C, Blanc JJ, Budaj A, Dean V, Deckers JW, Despres C, Dickstein K, Lekakis J, McGregor K, Metra M, Morais J, Osterspey A, Tamargo JL, Zamorano JL, Smith SC Jr, Jacobs AK, Adams CD, Antman EM, Anderson JL, Hunt SA, Halperin JL, Nishimura R, Ornato JP, Page RL, Riegel B; American College of Cardiology/American Heart Association Task Force; European Society of Cardiology Committee for Practice Guidelines; European Heart Rhythm Association and the Heart Rhythm Society.
Eur Heart J. 2006 Sep;27(17):2099-140. No abstract available.
PMID: 16923744 [PubMed – indexed for MEDLINE]

Free Full Text from European Heart Journal with link to PDF Download

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[2] Therapy for Regular Wide-Complex Tachycardias
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Part 8: Adult Advanced Cardiovascular Life Support
Part 8.3: Management of Symptomatic Bradycardia and Tachycardia
Wide-Complex Tachycardia (Figure 4, Boxes 5, 6, and 7)
Free Full Text from Circulation with link to PDF Download

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Filed Under: 2010 AHA Guidelines, ACLS, Cardiology, Cardioversion, Heresy, Ketamine, Pharmacology
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