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Case Study with EKG's: Transient Tachycardia


fiznat

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I am presenting this on behalf of a friend at work (who is also a member here), so please excuse anything that I may be missing.... I wasn't there.

Pt

Dispatched for chest pains, on arrival found 88y/o male at home complaining of chest pains that have since resolved. He is currently without any complaint whatsoever, but would like an evaluation at a local ED.

Hx: A-Fib, HTN, IDDM

Rx: Digoxin, Lopressor, ASA, Lantus

NKDA

VS

HR: 90-120 variable

BP: 160/90

RR: 20

SPO2: 94%-->100% with O2

EKG

Bretts.jpg

Bretts2.jpg

Unfortunately unable to capture much of the wide rhythm on 12 lead. Again, calling it transient wide complex tachycardia of unknown origin. ?P-VT. The wide rhythm came in and out every few seconds, lasting at a maximum of 7 seconds. The patient states he feels "fine" despite the changing rhythm.

Tx

Routine ALS.

Pt was given 324mg PO ASA, 1 x 0.4mg SL NTG. Pt remained without complaint throughout, no significant BP/RR/Mental status changes, etc

After administration of the NTG, the wide complex tachycardia ceased completely- leaving behind only a-fib at a rate of about 90.

Discussion

It is tough without much of the wide complex stuff on the 12 lead, but what would you call this rhythm? It is regular, wide, and of a consistent morphology, which definitely suggests paroxysmal ventricular tachycardia, although I know that aberrancies can really widen a rhythm when it suddenly speeds up like this. I recently had a similar patient in which that was the case. It would be easier with the aid of axis on a 12 lead, but the provider wasn't able to capture any of it in that mode.

What do you think of the treatment? The patient had no complaints, but obviously had a profoundly irritable heart. We don't have a specific protocol for this kind of situation, but the obvious answers are amiodorone, lidocane, etc. ...Although the patient remained stable and without complaint throughout, so perhaps medication isn't indicated. What do you think about ASA + NTG in the absence of chest pain or ischemic changes?

Discuss! :P

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I'd probably consider holding off on the ASA, just because the patient is already on it daily. It might be reasonable to use a lower dose even.

The ECG is pretty interesting, just because you don't often get to see this mechanism in action. On the three lead, continuous strip, it appears that when the rate speeds up the QRS complexes narrow, and when it slows down, they widen. Much more common to see the reverse happen (ie, faster-wider, slower-narrower).

This looks like a rate control issue more than an irritable foci. With the history, it could be any number of things, but it might be useful to consider rate control of the atrial fibrillation. The patient being asymptomatic leads me to think that it would be acceptable to just watch things as they happen, and not jump to any specific, possibly detrimental, actions.

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The underlying rhythm remains afib. While i think that an aberrant conduction may produce a whide complex, I would think were looking more towards runs of Vtach. Since HAD chest pain, id be happy to give the ASA. Nitro I wouldnt mind, though if the asa stemmed the pain and bouts of vtach, i wouldnt much bother with it.

That being said, this guy has risk factors for ischemia up the wazoo. Even in the abscence of the obvious ST-segment eleveation demonstrative of an MI, runs of Vtach are indicative of ischemic tissue. So the administration of ASA and nitro arent a bad idea. I just dont know if id think to do it (its outside protocol). Id probably be more likely to pull out the Amio, draw it up, and watch for a sustained Vtach. I probably would not give lido or amio in the absence of symptomy, though i would be ready for that irritable heart to move to sustained.

I doubt it is an 'abberant conduction disorder.' I mean, if he suffering from runs of Vtach, there is probably some ischemic/necrosed neural tissue that leads to the disorder or the predisposition in the first place. What i mean is that there probably is not any major conduction block / hemiblock that forces the wide complex from what seems to be a fairly narrow complex even at fairly fast rates.

In retrospect, since the ASA and NTG ceased the Vtach, it was probably a mild ischemic event that induced a potentially life threatening injury. Id say hell of a job if that was the thought process going in, thats excellent forsight. To be honest, I would not have given the NTG if the patient remains pain free. (Keep in mind im trying to know the outcome, but put myself in the providers position as it is unfolding). I dont think id go along with amio either, unless the runs went into a sustained vtach.

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Ok well I'll own up to this call... It was mine and thanks to Fiznat for posting it for me. He's a much better writer than I. Overactive hit it right on the head. With the patients Hx of IDDM and having HAD chest pain as the reason for the call. I was leaning toward the V-tach being due to irriatable tissue secondary to ischemia. Even though the 12-lead doesnt have any ST changes jumping out at us. Ectopy is a sign of ischemia, so I increased his 02 from a n/c at 4lpm to an NRB at 12lpm and i moved forward with the ACS protocol. After the first NTG his runs of V-tach stopped and he remained in a-fib for the next 5 mins of transport. I didnt go with Amio or lido because I felt if i could increase perfusion to the heart the v-tach would stop... and it did... There is a better strip of the V-tach if Fiznat can post it.

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I have to admit that was quite impressive foresight. Of course also potentially dangerous. Had the Vtach been an electrical disturbance not induced by an acute ischemia, but caused by an older injury, you might have induced them into a non-perfusing rhythm. What i mean is if the electrical disturbance continued and sustained a tachy-dysrythmia and they have nitrates on board, the decreased venous return and filling time might have tanked their cardiac output. Its the only reason Id be worried about it. However, given the history and story, it sounds like it was likely an acute event. Again, i dont know if I would be so bold to make that step, even with a fairly sure story.

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with the pt moving back and forth between v-tach and a-fib, I was pretty confident that it wasn't an electrolyte imbalance. And had the pt gone into full on v-tach with out a pulse cpr could have been more effective at perfusing the heart tissue if he was alittle bit vasodialated. And im sure the first round of epi would counter act my NTG.

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You do realize that the rhythm is irregular, right? It is subtle, but it is definitely there.

Ah I gotta disagree with ya there dude. That rhythm is regular. No question about it.

Here, I'll demonstrate. All of the (S-S) red lines are of the exact same length (cut and paste elements in photoshop)

regular.jpg

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