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Also posted over at Paramedicine 101 and at Research Blogging.
Go check out the excellent material at both sites.
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In the current JEMS, there is an embarrassing article. Drug Shortage Possible in N.Y.
It seems that the drugs that people are worried about are lidocaine, furosemide, 50% dextrose, and epinephrine 1:10,000 preloaded syringes. Here, I will discuss lidocaine.
Lidocaine is not appropriate for EMS patients, because there are more appropriate drugs. Lidocaine is still used for cardiac arrest, even though there is absolutely no reason to believe that it does anything positive for the patient.
There is no evidence that any antiarrhythmic drug given routinely during human cardiac arrest increases survival to hospital discharge. Amiodarone, however, has been shown to increase short-term survival to hospital admission when compared with placebo or lidocaine.[1]
In other words, amiodarone doesn’t work, but lidocaine is even worse.
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Lidocaine is also used for ventricular tachycardia
with similar lack of effect.
Lidocaine terminated ventricular tachycardia in four of 31 patients, ajmaline in 19 of 30 patients (P<0.001).[2]
Lidocaine is no better than holding the patients hand or any other placebo. Spontaneous remission of ventricular tachycardia should occur in more than 4 out of 31 patients.
DC shock was used in 16 nonresponders (22.9%) to procainamide and 10 non-responders (50%) to lidocaine.[3]
Only 35% of patients improved after lidocaine. Maybe they improved because of lidocaine – maybe not. More important is that 50% of patients who received lidocaine ended up being cardioverted. Did they require cardioversion because of the lidocaine?
Would you recommend a drug that leads to half of patients being cardioverted?
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Footnotes:
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[1] Medications for Arrest Rhythms
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 7.2: Management of Cardiac Arrest
Free Full Text
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[2] Electrophysiological and haemodynamic effects of lidocaine and ajmaline in the management of sustained ventricular tachycardia.
Manz M, Mletzko R, Jung W, Lüderitz B.
Eur Heart J. 1992 Aug;13(8):1123-8.
PMID: 1505562 [PubMed – indexed for MEDLINE]
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[3] Efficacy of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia.
Komura S, Chinushi M, Furushima H, Hosaka Y, Izumi D, Iijima K, Watanabe H, Yagihara N, Aizawa Y.
Circ J. 2010;74(5):864-9. Epub 2010 Mar 26.
PMID: 20339190 [PubMed – indexed for MEDLINE]
Table 3 is from this paper. As you can see, lidocaine is a joke compared to procainamide.
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Manz M, Mletzko R, Jung W, & Lüderitz B (1992). Electrophysiological and haemodynamic effects of lidocaine and ajmaline in the management of sustained ventricular tachycardia. European heart journal, 13 (8), 1123-8 PMID: 1505562
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Komura S, Chinushi M, Furushima H, Hosaka Y, Izumi D, Iijima K, Watanabe H, Yagihara N, & Aizawa Y (2010). Efficacy of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Circulation journal : official journal of the Japanese Circulation Society, 74 (5), 864-9 PMID: 20339190
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The key words are “routinely given”. Lidocaine is probably a better choice for Torsades if (or when) the MgSO4 doesn’t convert the rhythm because unlike amiodarone, lidocaine doesn’t prolong the QT-interval.. It’s also good for flushing an IO line.
Tom
Tom B.,
I agree about the IO line use.
I am not so comfortable with the use of lidocaine for Torsades de Pointes after magnesium is unsuccessful. While lidocaine may not cause the rhythm to deteriorate to Torsades de Pointes, it may still cause the rhythm to deteriorate to the point where cardioversion is indicated.
Does lidocaine improve the rhythm more often than placebo?
We do not know.
Does lidocaine cause the rhythm to deteriorate more often than placebo?
We don’t know.
Should EMS be using lidocaine for arrhythmias?
I don’t think so.
I agree about the use of the term routinely given. Calcium is an excellent treatment for hyperkalemia. Magnesium is similarly excellent for Torsades de Pointes. Neither of these are given routinely.
Unless I missed something, the lack of benefit described in 2005 continues. There are so many other treatments we should be focusing on, rather than looking for a magic drug treatment.
We are experimenting on huge numbers of patients, based solely on the excuse – What if drug X works? That is not medicine.
My point is that cardioversion (actually defibrillation since you can’t “sync” Torsades) often does not prevent Torsades from recurring when drug (or electrolyte) induced prolonged QT-interval is the underlying cause. So if the patient is unstable and shocking isn’t working, it makes sense to give the only anti-arrhythmic that shortens the QT-interval. That is medicine. You can’t have a randomized, multi-centered, double-blind, placebo controlled clinical trial for everything.
Tom
Tom B.
Cardioversion, defibrillation, or medication is only a temporary measure.
We are not curing the patient. If the problem is a drug induced QT prolongation, then the cure is to treat the QT prolongation.
Lidocaine does not do that. Lidocaine is an antiarrhythmic that isn’t supposed to make the QT prolongation worse. That is far from being a good treatment.
Magnesium, potassium, overdrive pacing, and isoproterenol can be very effective.
Cardioversion is possible for TDP. The textbook states otherwise, but reality is not limited to what is in the textbook. All that matters is whether the monitor synchronizes on the QRS. This is possible, even though the QRS wanders between positive and negative, because the wandering is predictable.
I don’t demand a randomized placebo controlled trial for everything. I never stated that I do. The evidence needs to be appropriate to the treatment. Rarely used treatments need to be evaluated by different methods.
Where is some good evidence that lidocaine is effective for TDP?
You may find the rare case where a patient improved after lidocaine, but it is unlikely to be because of lidocaine.
Unfortunately, I do not have access to the following full article:
The withdrawal of the offensive drug or the correction of a treatable cause was sufficient to prevent torsade de pointe while the use of isoproterenol was effective in 7 patients who received this drug alone or prior to the ventricular pacing which was successfully used in 9 patients. Lidocaine was ineffective or had deleterious effects in 15 patients where electrical cardioversion required repeated use with an average of 5 times/patient.
Torsade de pointe. Report of 18 cases.
Chalak W, Taha A, Araoya M, Rifaat M.
J Med Liban. 1993;41(2):62-8; discussion 68-9. Review.
PMID: 8057345 [PubMed – indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/8057345
That does not suggest that TDP is an indication for lidocaine.
Lidocaine is a Class IIb intervention for polymorphic VT with a prolonged QT-interval according to the ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death.
That means that the experts have reviewed all the available evidence and determined that it may help and probably won’t hurt, your 15 patient series notwithstanding. Magnesium sulfate is Class IIa (hence the reason I said, “if /when MgSO4 doesn’t convert the rhythm).
I am aware of cases where lidocaine has helped patients with shock resistent and magnesium sulfate resistent polymorphic VT. Dr. Wes featured just such a case on his blog last year.
We don’t give potassium in the field and we don’t give isoproterenol. Overdrive pacing is rarely performed transcutaneously, and that’s probably a good thing considering how well this procedure is performed.
So again, it’s risk/benefit. If you have an unstable patient who is not responding to cardioversion or mag sulfate I think the risk/benefit equation favors lidocaine. You’re trying to make it sound like it’s voodoo but it’s not.
Sometimes I think you just get a kick out of being stubborn.
Tom
Tom B.,
They also recommend antiarrhythmics for VF/pulseless VT cardiac arrest. There is no evidence that lidocaine or amiodarone or procainamide or bretylium lead to improved outcomes.
Without evidence of improved outcomes, this is voodoo, just without the dolls and without the needles.
Magnesium is very effective for TDP. We should be transporting the patient to the cardiologist quickly and not worrying about what to give, if the magnesium is not effective, just to give something.
We should avoid treatments that have not been shown to be effective.
Just because a patient, or two, gets better after lidocaine does not mean that the patient got better because of the lidocaine. Maybe it took that long for the magnesium to work. Maybe it is just a case of spontaneous resolution.
Spontaneous resolution is much more common with ventricular tachycardia than people think.
I don’t just get a kick out of being stubborn, I dislike voodoo.
The 2005 AHA ECC guidelines make this statement quite clearly:
“There is no evidence that any antiarrhythmic drug given routinely during human cardiac arrest increases survival to hospital discharge. Amiodarone, however, has been shown to increase short-term survival to hospital admission when compared with placebo or lidocaine.”
That’s why lidocaine is Class Indeterminate and amiodarone is Class IIb.
I can’t even believe I’m engaging in this debate since I’m not a huge fan of prehospital antiarrhythmics.
On the other hand, there’s no question that antiarrhythmics, under select circumstances, can have therapeutic effects (or pro-arrhythmic effects).
What it boils down to is this: I’m saying, “Use them responsibly” and you’re saying “Don’t use them.”
Tom