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The underlying cause will still be present and therefore the rhythm is likely to recur. We need to prevent it from recurring while we search for and treat the underlying cause. However you got your patient out of Torsades, your first line agent to keep them out is magnesium.
Use as described above. Hypokalemia and hypocalcemia should be treated, if present. This can be done either medically using isoproterenol or electrically. It you choose to electrically pace the heart , you can use the transcutaneous approach, but the transvenous approach is preferred because of a higher capture rate and the ability to perform without sedation. Once the rhythm has been adequately suppressed, you can titrate the rate down to the lowest that continues to suppresses dysrhythmias.
The most important thing to mention about the management of torsade de pointes is that there is essentially no evidence. The best available evidence is for the standard ACLS algorithm, with no differentiation made between torsades and standard monomorphic ventricular tachycardia. The largest review, covering 18 patients, demonstrated that pacing to a rate of 70 beats per minute was successful at suppressing torsades des pointes.
Torsades de Pointes on ERCast. Magnesium infusions on PulmCrit. A better approach to Torsade de Pointes on PulmCrit. QT Interval on Life in the Fastlane. In the Rapid Review series, I briefly review the key points of a clinical review paper or two. The topic this time: […]. This will be the final post this week about status epilepticus. I have long argued that our current status algorithms leave too […]. On paper, most of resuscitation is actually pretty easy.
On paper, there are basic algorithms to follow. On paper, the steps are […]. I have never prescribed tramadol. In Canada, everyone seemed […]. Thanks Taft I knew including a list was a mistake. Methadone is definitely an important medication to include it has been added.
It was inevitable that I was going to miss some and a number on this list may not actually cause clinically important QT prolongation. I tried…. The case originally stated that the patient was on azithromycin.
The magnesium protocol, doses, and target levels listed above are consistent with the bulk of published evidence on TdP including standard references such as UpToDate and Tintinalli's. However, recommended doses vary widely, with some authors recommending low doses.
For example, Charlton et al. I suspect that an adequate magnesium infusion regimen would have been successful, thereby abrogating the need for overdrive pacing.
Interesting post, thanks. Can we have it in SI units as well please? After all pretty much everywhere in the world outside the US uses SI units. Dear dr. I have one question — I was double-cheking the conversion to SI units and found two different formulas in my sources.
One of them gives the same numbers as stated in your protocol but according to the other 1 g of magnesium sulfate is equivalent to about 4 mmols of magnesium, 4 grams thus being equal to 16 mmols. Could you double check these calculations? Thank you! Thank you Dr. What a-fib patients would you recommend treating with mag? In my service area Cardizem has become scarce and our treatment protocols now edge us in the direction of utilizing Lopressor as a first line treatment in stable patients with rapid a-fib.
Any thoughts you have are appreciated. Often used as an adjunct with another agent because alone it may not be sufficient. Very cool, as usual, Josh. Very important topic! Is there a ideal concentration of the solution? Very important topic!! Is there a ideal concentration?
We are the EMCrit Project , a team of independent medical bloggers and podcasters joined together by our common love of cutting-edge care, iconoclastic ramblings, and FOAM. Why the standard approach fails This is largely a matter of pharmacokinetics: Magnesium is poorly absorbed by cardiomyocytes. Following a bolus of grams of magnesium, relatively little magnesium gets into cardiac tissue. Most is excreted in the urine.
Unless the patient has severe renal failure, magnesium levels will drop back to baseline over several hours figure below. For example, dofetilide is a common cause. With a half-life of 10 hours, dofetilide will lurk around long after the magnesium bolus has worn off.
Like a naloxone infusion for methadone poisoning, this will allow magnesium to out-last other drugs that caused the TdP e. Many patients with TdP have an intracellular magnesium deficiency which can occur despite normal serum levels, since most magnesium is located intracellularly. However, a hour exposure to elevated serum magnesium allows magnesium to eventually soak into the cardiomyocytes. Repletion of intracellular magnesium stores provides ongoing protection against TdP, even after the infusion is stopped and the patient leaves the ICU.
A protocolized magnesium infusion is quite safe. Compared to the risk of recurrent arrhythmia and cardiac arrest from inadequately treated TdP, magnesium infusion is almost certainly the safer route to go. Some more detail about the magnesium infusion The magnesium protocol shown above is based on clinical trials involving atrial fibrillation in fact, it is more conservative than these studies, to establish a greater margin of safety.
My impressions are as follows: The protocol is easy to use even for folks without experience using magnesium infusions. The protocol appears to be quite safe. Very rarely a patient might accumulate magnesium and develop a rather high level e. My guess is that the infusion has been used by us for about a dozen patients with TdP. It has been uniformly effective for TdP, including recalcitrant cases which outside hospital cardiologists were struggling with.
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