Sinus tach with abarrency or VT...?

This is a 12 lead from a post narrow complex PEA cardiac arrest. History of dementia and type II diabetes. No recent illness, husband states 20 min earlier, the patient had requested assistance to the washroom where she collapsed off the toilet. Fire department arrived first, and state they palpated a weak bradycardic carotid. On EMS arrival, the patient was in a bradycardic PEA. ROSC was established following 3 doses of 1mg Epi Q 3, 500ml NS bolus and intubation. Following ROSC patient was in a bradycardic sinus bradycardia and treated with nondemand transcutaneous pacing at 110mA at a rate of 70. Pulses were subsequently lost approximately 10 min after TCP was initiated. TCP was discontinued and the patient received another round of CPR and 1 dose of EPI, which resulted in ROSC (this time not bradycardic). Once extricated and in the ambulance I noted a wide complex tachycardia running across my monitor, the patient did have a pulse with this rhythm. I opted not to touch it and transport to the hospital.

My question for everyone is, do you think this is a SVT with LBB, VT, massive STEMI or hyperkalemia??

From what I can see, you're up in Lead 1, and down in both avF, and lead 2. IIRC, correctly that meets criteria pathological RAD.

Also, TMK, VT (WCT) will be "up" across the 12 lead, I'm not exactly seeing that here. I'm not seeing any tented, or clear enough "T" waves---let alone have the patients med list, and/ or enough hx (RF non-compliant with dialysis) to rule hyperkalemia in.

My best guess is an "extensive" anterior MI, but no cardiologist I be'z. In short, I think an abberancy, yes. Let's see what our peers think...

Hyperkalemia but does look suspect for infarct. I'd give calcium regardless

Story doesn't really fit hyperK to me. My guess would be AIVR secondary to massive STEMI but who knows.


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About how old? Pt. hx isn't really suggestive of VT, neither is the 12 lead. Rate is right around 100, what appears to be a fairly normal axis, and regularly regular. No classic sine wave appearance. Being post arrest, I don't really doubt that there are some pretty severe metabolic and electrolyte derangements, but the 12 lead just doesn't cut it for me. There is some fairly what I would call classic STe if not so elevated, with reciprocal changes in I and aVL. I'm not appreciating any P-waves anywhere throughout the strip, so I'd call it a junctional rhythm with non-specific interventricular delay with the possibility of acute ischemia.

I do not see anything that would indicate Hyper K, looks like a massive STEMI. The R-R is irregularly irregular, so it is not VT. Good job on the ROSC, thanks for sharing the case! If you can follow up and find out more would love to hear about it!

MonkeyArrow said:

About how old? Pt. hx isn't really suggestive of VT, neither is the 12 lead. Rate is right around 100, what appears to be a fairly normal axis, and regularly regular. No classic sine wave appearance. Being post arrest, I don't really doubt that there are some pretty severe metabolic and electrolyte derangements, but the 12 lead just doesn't cut it for me. There is some fairly what I would call classic STe if not so elevated, with reciprocal changes in I and aVL. I'm not appreciating any P-waves anywhere throughout the strip, so I'd call it a junctional rhythm with non-specific interventricular delay with the possibility of acute ischemia.

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The patient was a 90 year old female :S

How long after ROSC was this 12 lead and did transport time allow serial EKGs?

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GMCmedic said:

How long after ROSC was this 12 lead and did transport time allow serial EKGs?

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This 12-lead was approximately 10 min following ROSC, serial 12 leads were similar. Unfortunately, after cardiac ultrasound and a subsequent loss of pulses resuscitation was not attempted in the ED. There was no blood drawn or other diagnostics performed in the ED .

Reminds me of this.

http://hqmeded-ecg.blogspot.com/2015/07/giant-r-waves-what-are-they.html

Looks like an anterior inferior wall MI from type III LAD occlusion.

Based on the patent and story alone, if I were to not look at the ECG, I would've guess VT and/or MI until proven otherwise. This is why cardiac arrest patients should typically be directly transported to a PCI capable center.

I think I've already made a lot of post about SVT with aberrancy vs VT though. The gist of it is that unless it is antidromic AVRT (which can be indistinguishable from VT), SVT with aberrancy is going to have a very predictable QRS pattern because the electrical follows the same pathway (original from above the ventricles) while VT will have an unpredictable or very varying pattern because the foci can original from anywhere; This is also why VT patterns can be very specific, but not sensitive eg extreme right axis deviation).