The paramedic swung the stretcher into the resus bay, and started giving report. As the team of RNs, techs, and residents swung into action, I noted that the young adult patient didn’t look very sick at all. Confused, yes, and perhaps a bit anxious, but this seemed like an over-triage.
“Paramedic Battistelli,” I called out, “why is this 38 year-old female patient here, instead of in fast track?”
“Hey Dr. Walsh! We were called for a seizure, but she looked fine when we got to the house. She denied any problems, but family said she was just lying on the bed, no warning, when she started convulsing. Vitals and sugar were fine. Listen, I didn’t think I should call in the cath lab team, but I didn’t like the looks of this.” And he handed me his 12-lead:
“Well,” I responded, “look at these deep T-wave inversions in V1-V4. This looks like Wellens syndrome. We better get the cath lab rolling! When did she stop having chest pain?”
“Doc, she denied chest pain, pressure, burning – everything.”
“Okay. Then this is probably the anterior T-wave inversions you see with a massive pulmonary embolism! We might need to give her tPA. Was she very hypoxic?”
“No, in fact she never so much as coughed. No trouble breathing, sats were great.”
“Well, it’s kind of rare, but you can see these sorts of inversions with takotsubo cardiomyopathy too. Let me guess,” I asked loudly, “she must have had a terrible scare right before the seizure. Or maybe a nasty argument, or some other emotionally charged moment?”
“Nope. She had been napping on the bed with her mother.”
I asked to repeat the ECG, figuring that the leads had been misplaced, or there was some artifact, or the EMS monitor had some bad filter setting..
Crud, this looked worse.
“Medic Battistelli, this shows clear signs of Wellens at this point. As you know, women often don’t feel any pain with their MIs. I’m activating the cath lab.”
“Ok, sounds fine,” he interjected, “but I saw something else on the ECG. It sounds crazy, but…”
“Dr. Walsh!” The RN grabbed my arm. “She’s seizing again – and look at the monitor!”
Palpation of her carotid confirmed pulselessness. CPR was started, and the a single defibrillation restored sinus rhythm, as well as consciousness. “Looks like that was VT triggered by ischemia,” I told the team, “let’s focus on getting her to the cath lab as quickly as possible.”
“Doctor Walsh, I was wondering,” asked Mike, “should we try one thing before sending her to the lab?”
What was Mike suggesting for therapy?
Magnesium, as therapy for Torsades de Pointes (TdP).
The arrest rhythm was a wide-complex tachycardia, and thus overwhelmingly likely to be a form of ventricular tachycardia. This VT does not have the usual monomorphic morphology, however, and is instead called polymorphic VT (PVT). One might leap to calling this TdP based on this rhythm, given the dramatic appearance of the “twisting points”, but it’s crucial to remember that you can only diagnose TdP when the QTc is long. If the QTc was not prolonged here, this would be just PVT, which is usually caused by cardiac ischemia.
A look back at the EMS ECG shows that the QTc is quite prolonged, > 600 ms, and so we can diagnose TdP.
Why does this matter for therapy?
Well, as mentioned, PVT is usually caused by cardiac ischemia, so evaluation and treatment should first focus on ACS. TdP, by contrast, often has a metabolic (± genetic) cause, and these should be sought and corrected.
Most importantly, distinguishing between PVT and TdP is crucial when selecting an antiarrhythmic medication.
- For PVT associated with cardiac ischemia, beta-blockers and amiodarone are considered a class I intervention.
- For TdP, however, magnesium plays a central role (after defibrillation!), while amiodarone has no established or theorized benefit.
Interestingly, many clinicians have been taught that amiodarone is dangerous in TdP, since it is well-recognized as causing a prolonged QTc. There seems to be little evidence for this, and it appears that amio only rarely is implicated as a cause of TdP.