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Discussion

Stable Vtach

Hello, Here for learning. I have a question can we shock stable Vtach with a HR 140s to 160s? SBP 113/60s, alert and oriented, no chest pain.  Asymptomatic. Amio bolus was not even finished was only half way through. Decision was made to shock at 100J. He turned pale, hypotensive and rapidly decompensated. Not sure what the right decision was. Asking for medical advice. TY

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All things being equal because you included no history at all, stable, asymptomatic VT (assuming that's what it really was) is treated pharmacologically before DCCV. Sounds like there were a couple of steps to go before cardioversion was indicated. But, again, very little information here. And you don't say what the rhythm was after cardioversion. 

Agree with offlabel, there is not sufficient history make any sort of determination. With that being said typically VT will be faster than the rate you mentioned, sometimes VT can be confused for a wide complex tachyarrhythmia. 

  • Author

Sorry, Hx of afib newly diagnosed, DM, EF 50%, I forgot most of the HX. Admitted for DKA. Ph 7.1 and lactic 9. Normal WBC. No open wounds. Nothing on XR. Provider only gave half of amio. Pt a and o x3, asymptomatic, VS stable. Shocked pt converted to NSR at 60s. 

Thank you so much for the reply. HR was only in the 140s. Occasionally would go up to 160s. 

Looks like there was a lot of metabolic derangements that could have caused the tachycardia as a compensatory mechanism. 

Matthew89 said:

Sorry, Hx of afib newly diagnosed, DM, EF 50%, I forgot most of the HX. Admitted for DKA. Ph 7.1 and lactic 9. Normal WBC. No open wounds. Nothing on XR. Provider only gave half of amio. Pt a and o x3, asymptomatic, VS stable. Shocked pt converted to NSR at 60s. 

Thank you so much for the reply. HR was only in the 140s. Occasionally would go up to 160s. 

OK...so it sounds like whomever decided to cardiovert didn't want to wait for v-fib (believing what they were seeing was actually VT). At that point (SR with hypotension) running in a liter of fluid real fast and maybe a pressor to bridge the volume while waiting for the bp to flatten out would be what I would have done without anymore information, which, it sounds like there's a lot more.

There's really no such thing as stable v-tach..  I get it, your patient was "asymptomatic" but v-tach by its very nature is unstable and arrest should be considered imminent if it's not fixed.

VT isn't inherently stable. Your patient might be asymptomatic but that's going to be temporary. My only real concern in this is having only a 1/2 dose of an antiarrythmic onboard before cardioverting. If the patient is asymptomatic, I'd want that full dose onboard. That's only a couple minutes. That being said, if there's any indication that the patient is becoming symptomatic, then the next step is sync cardioversion. IMHO if you have time to sedate, you have time to administer that antiarrythmic. 

Also with VT, because this will lead into (eventually) pulseless VT or VF, you want to convert this even if the patient has an underlying AFib. While there's a risk of stroke or PE in that instance, that risk is lower than what will happen if the patient isn't converted out of VT into a more stable rhythm. 

  • Guides

Agree with responses. It is also good to think about VT causes. Not knowing much about the cardiac history other than new AFib and a somewhat normal EF, perhaps VT was induced by the acidemia from DKA and other electrolyte imbalance (was the serum potassium low?).  If the patient converted to SR after the synchronized cardioversion, then the hypotension and decompensation is from something else likely from under-resuscitation and electrolyte imbalance knowing that the patient was admitted with DKA.

However, VT can be from a host of other etiologies...ischemic scar, MI, HOCM, PE, etc.

FiremedicMike said:

There's really no such thing as stable v-tach..  

That's what I thought LOL. It's kind of an oxymoron. Like "runs of asystole" 

We have had 2 pts in the last 10 days to come to us with A-fib w/RVR. We converted both with an amio bolus and a gtt for about 12 hours (if they wouldn't convert, they were going to shock). Both cardioverted with the amio. 

It was a fascinating experience as I work on an ortho floor. We love learning new things. Not sure I am super comfortable with more advanced cardiac stuff, but it's better than pulm/trach stuff. ?

I have some serious concerns for the treatment here & MD/PA/NP decisions. 

DKA patients can have extreme electrolyte imbalance. That wide complex can be from that. The pH & lactic are common on these patients until corrected. Generally they need at least 4L of fluid for dehydration (which also causes tachycardia)  as well as insulin infusion. K & Mg need fixing.

HR 140's = not VT. Not fast enough. Sounds like an AFib RVR, tachycardia with BBB. Did you use adenosine to see what's there and /or chemically convert? Or Vagal maneuvers? 

Second, ACLS guideline for stable VT recommended DCCV as last resort or if decompensating. An EKG needs to be done to determine the actual rhythm. If wide complex, did you use the "stop & restart the heart" drug adenosine?  Did they consult "expert" aka Cards/EP? 

The underlying cause needed treatment which was probably causing the tachycardia. Even if not ACLS certified,  most facilities attach copies of the guideline cards to their code carts. See the AHA site below.

https://CPR.heart.org/en/resuscitation-science/CPR-and-ecc-guidelines/algorithms

  • Author

Thank you for everyone's reply. Appreciate all the input and shared knowledge. For that patient all electrolytes were normal k, mag, phos. 2L bolus and bicarb was being given assuming it was acedemia. In terms of hx patient was not compliant so that is the only hx I have. 
 

He was originally in afib. But then he would have ventricular tachyarrythmias. Wide complex and were regular. That's what I was wondering half a bag of amio was infusing but the provider wanted to cardiovert. The VS was stable. HR did go up to 160s but maintained at 140s. 
No adenosine was given. 

I was wondering if amio should have been given and if he did not convert how long do we wait. And what other meds. Should Adenosine been given after amio bolus?

Was not sure. Pt was cardioverted and became pale. I don't know if he went to cardiogenic shock. Liver enzymes doubled. Pt eventually decompensated. Had a cardiologist read the EKG. He did say VTach. 
 

 

Adenosine works on the AV node so it would be ineffective in afib. Amio is a good first-line drug, but procainamide and sotalol can be effective. I don't know that there's a time per se to wait before a patient is shocked. I know stable vs unstable vtach is controversial, but I've seen it go on for some time in a perfectly awake and happy patient. 

It sounds like the patient was sicker than he looked and tachycardic as a compensatory mechanism to maintain their cardiac output (CO = HR x SV). When they were shocked into a normal rhythm their output plummeted and their hemodynamic status with it.

You can't always predict it. It doesn't sound like anything was done wrong. Sometimes sick bodies don't play nice.

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