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

- Rogue Medic

V Tach Storm – Part II


Continuing from Part I.

What is amiodarone?

Mechanism of Action
Amiodarone is generally considered a class III antiarrhythmic drug, but it possesses electrophysiologic characteristics of all four Vaughan Williams classes.
[1]

If you use ventilators, do you change all of the settings at once, or do you adjust one at a time? Amiodarone changes all of the conduction at the same time, just not in ways that are as controllable as the settings on a ventilator.


Image credit.

Amiodarone is the napalm of antiarrhythmics. Amiodarone hits everything all at once. Amiodarone interferes with all of the Vaughn Williams classes. Some people think that a broad-spectrum antiarrhythmic is somehow a good thing. That might be the case, if there were a reason to believe that the patient is experiencing problems with all 4 of these conduction systems and the amiodarone is going to improve all 4 of these conduction systems.

What are the chances of that?

Imagine trying to guess the combination to a very simple 4 digit combination lock. We will make the digits binary, since the choices are more conduction or less conduction. No change is not really a possibility with amiodarone. How would we calculate the odds of reaching the right combination?

Each class has only 2 possibilities, so the calculation is 2 X 2 X 2 X 2 = 16. [2] Four different conduction systems being manipulated – all at the same time.

But it isn’t even that complicated. We know what the expected direction of effect of the amiodarone will be. The only question is whether the effect of amiodarone makes things better for that class, or if amiodarone makes things worse. This is still a binary consideration, so the calculation does not change.

Of course, this is an over-simplification, but Just give amiodarone is also an over-simplification.

He’s got an odd rhythm on the ECG.

Just give amiodarone.

Don’t you want to know what the rhythm is?

Just give amiodarone.

But what if amiodarone makes things worse?

Just give amiodarone.

As simple as pointing a diagnostic device and pressing Go or pointing at a drug and grunting. 21st Century Emergency Medical Care.

If amiodarone is so good, why do so many patients end up being cardioverted?

For monomorphic V Tach – less than 30% success[3],[4],[5] – and monomorphic V Tach is what amiodarone is best at.

If amiodarone is safe, that may not be a bad idea, but . . . .

Pharmacodynamics
Amiodarone I.V. has been reported to produce negative inotropic and vasodilatory effects in animals and humans. In clinical studies of patients with refractory VF or hemodynamically unstable VT, treatment-emergent, drug-related hypotension occurred in 288 of 1836 patients (16%) treated with amiodarone I.V. No correlations were seen between the baseline ejection fraction and the occurrence of clinically significant hypotension during infusion of amiodarone I.V.
[1]

16% develop hypotension?

Isn’t hypotension one of the things we are trying to avoid?

Yes.

Less than 30% improve, but 16% get worse?

Maybe that is why the FDA (Food and Drug Administration) label only says that we should be using amiodarone after other treatments do not work.

INDICATIONS AND USAGE
Amiodarone HCI Injection is indicated for initiation of treatment and prophylaxis of frequently recurring ventricular fibrillation and hemodynamically unstable ventricular tachycardia in patients refractory to other therapy.
[1]

Amiodarone may not be a good starting point for treatment, but more of a last ditch – It can’t possibly get any worse, so what has the patient got to lose? treatment.

In Dr. Orman’s podcast – V Tach Storm – hemodynamically unstable is where the patient ended up after amiodarone. The patient’s heart rate is 207, but he is hypertensive. 150 mg of amiodarone is reported to have been given over 5 to 10 minutes, even though ACLS and the FDA label state that the initial dose should be given over 10 minutes. He later repeats the dose of amiodarone and adds 2 gm magnesium. A couple of sinus beats emerged, but went away, but now his heart rate is over 220.

Dr. Orman states, “You’re making some headway. Probably what you are doing is having some effect on him, but it’s not quite getting you where you want to go.”

The patient becomes hypotensive – from 175 systolic to 90/55 and he became short of breath. Is it the amiodarone, or the magnesium, or the rhythm, or something else, or some combination of these?

Then he appears to have been given some propofol for sedation and cardioverted at 200 joules, then 300 joules, then 360 joules. The doctor feels the need to apologize for repeating cardioversion, which I don’t understand. Why not sedate and cardiovert earlier?

My experience has been that cardioversion is frequently done incorrectly. That is one of the reasons I would spend a lot of time on cardioversion in ACLS classes. The ACLS procedures most commonly fouled uo are cardioversion, transcutaneous pacing, needle decompression of tension pneumothorax, and needle decompression of cardiac tamponade.

Not many people are comfortable cardioverting patients.

Eventually, the cardiologist gave another 150 mg of amiodarone and 5 mg of metoprolol and soon after the arrhythmia changed to a 50/50 mix of sinus tachycardia and V Tach.


Click on the image to make it larger.

A stable 75 year old patient with V Tach at a rate of almost 200. An unknown dose of disopyramide (Norpace), 135 mg lidocaine, cardioversion X 4, 150 mg amiodarone, 2 gm magnesium, 150 mg amiodarone, an unknown dose of propofol, cardioversion X 3, 150 mg amiodarone, and 5 mg metoprolol. After deterioration, he improves to an alternating V Tach and sinus tachycardia with each present about half of the time.

How much did the drugs help?

How much did the drugs hurt?

We do not know.

Procainamide was not given. Sotalol was given in the ICU.

The patient was taking disopyramide (Norpace), which is mentioned as being proarrhythmic, but lidocaine is proarrhythmic. Amiodarone is proarrhythmic. Why are the proarrhythmic effects of these drugs not also mentioned?

When do we stop throwing proarrhythmic medications at a rhythm?

At the end, there is a good discussion of other possible treatments, which you should listen to. V Tach Storm.

Footnotes:

[1] AMIODARONE HYDROCHLORIDE injection, solution
[Bedford Laboratories]

FDA label
Label

Like class I drugs, amiodarone blocks sodium channels at rapid pacing frequencies, and like class II drugs, it exerts a noncompetitive antisympathetic action. One of its main effects, with prolonged administration, is to lengthen the cardiac action potential, a class III effect. The negative chronotropic effect of amiodarone in nodal tissues is similar to the effect of class IV drugs. In addition to blocking sodium channels, amiodarone blocks myocardial potassium channels, which contributes to slowing of conduction and prolongation of refractoriness. The antisympathetic action and the block of calcium and potassium channels are responsible for the negative dromotropic effects on the sinus node and for the slowing of conduction and prolongation of refractoriness in the atrioventricular (AV) node. Its vasodilatory action can decrease cardiac workload and consequently myocardial oxygen consumption.

[2] Here is a list of the possibilities, for those wanting to see the math.

1. BetterBetterBetterBetter.

2. BetterBetterBetter – Worse.

3. BetterBetter – Worse – Better.

4. Better – Worse – BetterBetter.

5. Worse – BetterBetterBetter.

6. BetterBetter – Worse – Worse.

7. Better – Worse – Better – Worse.

8. Worse – BetterBetter – Worse.

9. Better – Worse – Worse – Better.

10. Worse – Better – Worse – Better.

11. Worse – Worse – BetterBetter.

12. Better – Worse – Worse – Worse.

13. Worse – Better – Worse – Worse.

14. Worse – Worse – Better – Worse.

15. Worse – Worse – Worse – Better.

16. Worse – Worse – Worse – Worse.

[3] 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]

[4] 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.

[5] 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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Comments

  1. Just for clarification, aren’t all antiarrhythmics also proarrhythmics? At least this is what I was taught in ACLS…. And this makes sense since they interfere with electrolyte channels. By reducing Sodium/Potassium, what are we doing to the Calcium and/or Magnesium levels? How do they respond to rapid infusions of “Broad Spectrum” electrolyte channel blockers? I guess by going into V-Tach…. 🙂

  2. yeah i had vtach from sports. young and healthy. potassium gave in er, seemed ok. lidocaine worked after vtach on stress tests. EP cured it. I think ortho problems can cause vtach. shoulder and/or hip probs leading to reduced portal flow into the right ventrical causes r.v. to speed up to compensate. think i tore something in my right hip 20 y.a. playing tennis, and left shoulder separated 10.y.a. from impacting winshield. Just my 2cents. “not a doctor” haha. :/ Wish i could get hip mri’s to confirm. “too expensive”. yeah but what about 1 week in ICU?! pfffft

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