Pulseless torsades

Not the current ACLS recommendation or what I learned...
 
chaz90 said:
It should still sync up...
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It does, at least with our rhythm generators at school..

Never had a tdp patient in real life
 
teedubbyaw said:
Not the current ACLS recommendation or what I learned...
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Well, ACLS does sometimes cater to the lowest common denominator to ensure no provider is left behind or fails to meet minimum competencies. If the patient is still perfusing enough to have a pulse (albeit weak) and some level of consciousness and BP, I would attempt to deliver the shock at the best time of the cardiac cycle to convert whilst attempting to avoid R on T. As mentioned in a recent thread, some have even considered high dose synchronized cardioversion of pulseless V Tach, though this has been discarded by ACLS due to time constraints and perceived confusion. As Desert mentioned, I would jump to high dose cardioversion of persistent TDP as it is notoriously refractory to electricity. I'd also certainly be setting up my magnesium drip post haste.
 
You can "attempt" to cardiovert TDP. As the name implies, twisting of the points, there are moments of monomorphic like complexes that are cyclically changing. There is a chance you will be able to sync and shock on the R wave before a change in axis however I would think there would be a fairly high chance that it would end up being unsyncronized. But I agree that it does not hurt to try, worst case scenario it ends up being a defibrillation.
 
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teedubbyaw said:
Not the current ACLS recommendation or what I learned...
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I actually had a TDP thrown in for my ACLS team leader scenario on this last Thurs.
Defib is the correct answer per ACLS. Defib at 150 with adjunct of mag sulfate drip.

I do have another question, though. Would amio hurt a TDP patient? For the life of me I could not remember during the scenario if you were supposed to give amio along with mag. I did anyways and no one commented on it, either way.
Forgot to ask either way if that was proper or not.
Anyone have some insight for me? Per my protocols/ drug profiles, it looks like it would be indicated, although I've never heard it mentioned with treatment per ACLS.
 
Long term amio can cause long qt, which is a common cause of tdp. no studies have directly linked amio induced long qt with tdp though.
 
Bearamedic said:
Long term amio can cause long qt, which is a common cause of tdp. no studies have directly linked amio induced long qt with tdp though.
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There are many common meds that prolong the QT.
 
A couple of points.

  • TdP is polymorphic VT in the presence of an underlying prolonged QT interval.
  • The dividing line between polymorphic VT and VF is a bit arbitrary. Some might say that polymorphic VT should have a cyclic rate less than 300. However, I've seen TdP with a cyclic rate greater than 300 and I've seen VF start out with a cyclic rate less than 300 (which then increased 0ver time). Since then I've been paying attention and VF often starts out slow(ish) and then speeds up, sometimes to a cyclic rate as high as 720 or more.
  • The best definition of PEA is "any rhythm on the monitor which should be producing a palpable pulse but is not". Polymorphic VT could go either way so does not meet that standard, IMHO.
  • Anecdotally, most cases of (alleged) TdP I've reviewed end up not having a prolonged QT in the underlying rhythm.

Tom
 
I have always been told PEA is any "organised rhythm" that should have a pulse but doesn't ... so I wouldn't consider torsades to be PEA.

Now, as far as amiodarone, local guidance is as follows

"Torsade may be self limiting (with spontaneous reversion into sinus rhythm) or it may deteriorate into VF. It is relatively unusual for a patient to remain in torsade VT for very long and for this reason it is relatively rare to have to treat it pharmacologically.

Amiodarone is relatively contraindicated in torsade VT because further prolongation of the QT interval may make it worse. However, as described previously prolongation of the QT interval from amiodarone is more likely with chronic administration than acute administration.

If the patient is in torsade VT and significantly compromised the treatment of choice is synchronised cardioversion. If the patient is in torsade VT and not compromised it would be worth waiting a few minutes (being prepared to immediately cardiovert if the patient changes) to see if the rhythm spontaneously reverted. If the rhythm did not revert and the patient was not compromised it would be appropriate to administer amiodarone"
 
Clare said:
I have always been told PEA is any "organised rhythm" that should have a pulse but doesn't ... so I wouldn't consider torsades to be PEA.
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That was my initial thought on this topic.

Good discussion.
 
Pimp question: Anyone want to guess how Isuprel is used in the management of TDP?
 
Chase said:
Pimp question: Anyone want to guess how Isuprel is used in the management of TDP?
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I know it used to be used prehospital as a dromotropic for refractory bradycardia, so I'm guessing it's something to do with shorting the QT interval?
 
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DEmedic said:
I know it used to be used prehospital as a dromotropic for refractory bradycardia, so I'm guessing it's something to do with shorting the QT interval?
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Bingo. It is rarely used but i have seen it with an infected pacemaker w/ sepsis. Their underlying rhythm was bradycardic with long QT and would constantly R-on-T into TDP and occasionally arrest. Refractory to multiple mag infusions. Isuprel increased the HR and shortened the QT enough to avoid the R-on-Ts and get them through the couple days needed for antibiotics and reinsertion.
 
I totally just pulled that one out of my…

For some reason, isoproterenol was on the drug list that we had to know while in paramedic school.
 
Chase said:
Bingo. It is rarely used but i have seen it with an infected pacemaker w/ sepsis. Their underlying rhythm was bradycardic with long QT and would constantly R-on-T into TDP and occasionally arrest. Refractory to multiple mag infusions. Isuprel increased the HR and shortened the QT enough to avoid the R-on-Ts and get them through the couple days needed for antibiotics and reinsertion.
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TdP is typically pause dependent, meaning if you can get rid of any long pauses (often post-VPB) during bradycardia you can likely avoid the TdP.
 
Chase said:
You can "attempt" to cardiovert TDP. As the name implies, twisting of the points, there are moments of monomorphic like complexes that are cyclically changing. There is a chance you will be able to sync and shock on the R wave before a change in axis however I would think there would be a fairly high chance that it would end up being unsyncronized. But I agree that it does not hurt to try, worst case scenario it ends up being a defibrillation.
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Our monitors won't discharge if they're set to sync and it's not able to sync with the ECG correctly.
 
Bearamedic said:
Obviously, but the post directly above mine was asking about amio, not "many common meds" in relation to tdp.
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He wasn't asking about "long term amio" therapy, though. He was asking about a loading dose.

With that in mind, I doubt my input was any less relevant to his question than yours was.

Many folks seem quite unaware at just how many meds can cause QT prolongation, and so it seemed a relevant thing to point out.
 
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Ok I have a Torsades case for you guys. (My own call) 42 YOM on the side of the road having chest pains. Pt was just biking (Not any biking, spandex road bike, the hole deal) Pt's friend states they just biked 30 miles. Pt was, CAO x 4, pale, skin tone moist, HR 90, Resp. 22, complaining of mid-sternal chest pain. No medical history. Very healthy! While getting a BP and my partner fetching the monitor, the pt states, "I'm getting dizzy", faints and vomits. Pt laid left lateral. [-] carotid pulses. Performed pre-cordial thump. CPR performed for a brief few seconds. Applied monitor - Torsades. Immediately d-fib @ 360. Pt regained consciousness with pulses and asked, "what just happened?" 12 lead - NSR @ 92bpm w/ an anterior-lateral wall MI. Pt loaded, EKG transmitted and en route to a hospital. O2 via nasal cannula. Bilateral IV's established. BP now 132/60. NSS fluids @TKO. ASA 325 and 1 nitro administered. Zofran 4mg administered. continued w/ 2 more doses of nitro q 5min. and monitored the rest of the transport. repeat 12 leads performed. Pt remained conscious throughout remainder of transport. Pt taken directly to hospital cath lab. Overall the call took approximately 30 mins. Pt had a 100% recovery!

In a nutshell this is the short version! :D But I hope it helps with decision making! It was also a scary situation for those you who are healthy and young!

Now for all the talk on Torsades, do I sync, d-fib? the story doesn't lie. Medical director gave kudos! This treatment would have been different of course with a stable pt...but this would be a typical ACLS algorythm.
 
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