Sim #1
The patient is a 50M hx COPD p/w pneumonia, currently being treated with IV azithromycin. He begins to vomit when the team walks into the room. The nurse asks the team if they want him to give Zofran, and the team decides to do that. Shortly after administration of the Zofran, the patient becomes altered, hypotensive to the 80s systolic, and tachycardic to the 200s. (It was a trap!) The monitor shows polymorphic ventricular tachycardia. An EKG obtained before the event shows a prolonged QT interval. The patient is given IV magnesium, but does not convert to sinus rhythm. The patient then goes into asystole, and the team begins CPR. The patient is given another dose of Mg 2mg and shocked once, with ROSC. Cardiology is called prior to TVP insertion.
Learning points:
– If the patient is in cardiac arrest due to torsades, just push the magnesium, rather than drip it in. ACLS recommends giving 1-2 grams of MgSO4 IV/IO if the patient is in arrest; it can be slowed over 5-60 minutes only if the patient has torsades with a pulse.
– Stop all QT-prolonging medication drips immediately in the torsades patient, including in this case the azithromycin.
– If the stable torsades patient doesn’t respond to magnesium, try overdrive pacing.
– However, in an unstable patient, such as this one (due to AMS), don’t fool around with overdrive pacing; just cardiovert.
– For a wide, regular tachycardia causing instability, you can give 100J, but multiple attendings recommend starting at 200J biphasic to be sure that you will convert the rhythm.
**MIND-BLOWING PEARL** – Not only can you place a transvenous pacer while transcutaneous pacing is ongoing, but you might even be able to continue CPR during defibrillation. (!!!?@$*@!) Hang in there with me. Since we now use fancy self-adhesive electrodes to perform cardioversion and defibrillate, rather than the old paddle electrodes, some daredevils have wondered if you need to bother with the “I’m clear, you’re clear, we’re all clear” mantra we all know and love. If you’re wearing proper PPI, why not just continue CPR during defibrillation, they ask, and thereby minimize interruptions to compression? Obviously, a good way to join the patient in cardiac arrest, right? Actually, there is an argument to the contrary HERE.
This summary was written by Brendan Barrett, MD – PGY2
No one dies from a dose of azithro. This is like beta-blockers and cocaine, there’s a disconnect between theory and reality.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4040726/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404501/
On the other hand, I hate this shotgunning of abx created by sepsis quality measurements. I doubt that anyone ever stops an abx because it may kill the pt (every time I tell a resident that they’re going to kill the pt with a z-pack, they give it anyway).
Torsades usually degenerates into vfib, not asystole.
It sounds like the pt was shocked during asystole?!?
I doubt that the patient went back into torsades after rosc. If he did, he wouldn’t have a pulse.
Torsades is a form of vtac, so lido is an option. Don’t give the other drugs used in ventricular arrhythmias (amio, procainamide) – they prolong QT.
A quicker way to overdrive pace is to start an isoproterenol drip, but we usually don’t do that in torsades.
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