Anti-dysrhythmic therapy for Malignant Hyperthermia

[Brenna's Dad]

My instructor proposed the following question during class:

What antidysrthymic would be most effective for treating hyperkalemic induced dysrhythmias in the malignant hyperthermia patient?

Procainamide appears to be the historical agent of choice. But is this the best chocie? What agent would you choose and why (receptors)?

I know what my answer would be, but are there any other takers?

[pasgasser]

I have not posted on this board before so I will introduce myself. I follow this board and read primarily the posts regarding clinical questions and do not desire to be involed in politcal discussions about MDA and CRNA. With that said I am a private practice anesthesiologist and do 100% of my own cases (no supervision).

With regards to your question concerning MH and anti-arrhythmics for hyperkalemia the answer is still calcium, eventhough this seems counterintuitive. MH is a problem in the sarcoplasmic reticulum in which intracellular Ca++ cannot be retaken up thereby causing sustained contraction in cells leading to hyperpyrexia, hypercarbia, etc. The intravascular Ca++ in these patients is not elevated and Ca++ is still the med of choice to stablize myocardial tissue when exposed to hyperkalemia. Giving bicarb also decreases intravascular potassium level and helps the situation by causing a shift of potassium back into cells.

[Brenna's Dad]

Thank you for your response.

I agree that treatment of hyperkalemia should be first line treatment for dysrythmias in MH. Besides bicarb, you can also use insulin and dextrose.

According to my quick literature search last night, the Ca++ receptor on the sacroplasmic reticulum is the Ryanodine receptor. Dantrolene apparently antagonizes this receptor and prevents the release of Ca++ from the SR into the cell.

But, if you needed to give an antidysrythmic because you patient was in VF and your potassium lowering interventions along with defibrillation was not effective, what would be your agent of choice and why?

[pasgasser]

Until the potasium is lowered the pt's arrhythmia will likely be resistant to all measures. After the potassium is lowered I would use the usual protocol (ACLS) to treat arrhythmias and would start with amiodarone.

[charles-thor]

Since amiodarone displays weak class IV effects and Ca++ blockers are contraindicated, then why use something that may contribute to the problem? From my understanding, after the acidosis and hyperkalemia are corrected (HCO3- supplementation), the arrthymias should subside. However, procainamide seems like a logical selection as it not only helps to control arrhythmias, but it also inhibits abnormal drug induced contraction in MH susceptible muscle in vitro.

[Tenesma]

i would shock VF... that is my favorite form of "dysrhythmic"!!!!

[Brenna's Dad]

According to my quick literature search last night, it seems that it was previously thought that Procainamide helps relieve muscle contraction, but that this was disproven. (Feel free to refute this)

Like pasgasser, I initially liked Amiodarone based on its multiple channel and receptor blockade (Na+, K+, Ca++, and Beta 1), but also started thinking about the effects Ca++ channel blockade would have on smooth muscle (hypotension).

The thing about Procainamide, is that its metabolite NAPA is Class III (K+ channel blockade) , which might assist with the hyperkalemic situation. (Theoretically). However, I also find it hard to argue with Lidocaine, which suppresses ventricular tissue.

Any other thoughts??