Posted by: medicblog999 | February 6, 2010

The Conclusion – What would you do? – ECG Geek 6

choices

I think its time to wrap this little episode up now……

As I said in the last post, after stating that he ‘didn’t feel very well’ I noticed the trace on the monitor to be as was shown on the rhythm strip.

ECG pt 3

Jim remained conscious whilst I quickly explained what I was doing

“I am just putting these special pads on your chest to keep an eye on you a little bit closer, Okay?”

I placed the defib pads onto his chest which gave me a couple of seconds to take in what actually was happening with his heart.

I know there has been some conflicting ideas of what this trace may actually be, but in my opinion, on looking at the screen when I was putting on his pads, there was a very definite ‘twisting’ of the chaotic activity seen on the monitor. Also the fact that he remained conscious for the next few seconds was also reassuring (but a little bit surprising)

What clinched the diagnosis for me though was the fact that after about 15 seconds, he reverted back into his wide complex, ventricular escape rhythm that was evident before his rhythm changed.

Following going back to his ‘normal’ rhythm, Jim began to feel better again. We were now only about two minutes away from the hospital when it happened again. This time it I didn’t need the time to put on the pads etc, as they were already done. I closely watched the monitor and Jim. The only treatment we have for Torsades is to cardiovert them if they become unconscious, or if they remain conscious, its hands off and hope to god that it is only a short burst!

Which again, this was.

I didn’t have a time to put in a pre-alert for the Torsade, so they were expecting a 3rd degree heart block bradycardic patient. When I explained what had happened, I got the usual look of ‘are you really sure?” from the medical staff, but once I showed the Doc the ecg strip, he suddenly believed me too.

I gave my handover and obviously included the administration of the 500mcg atropine, which I was now getting a little nervy about, however the doctor just said “champion” then continued with his assessment of the patient. Can you guess what the first thing that the doctor did?

That’s right my friends, more Atropine!

Before long, and following no improvement with another 2 doses of atropine, he was attached to the pacer and the transcutaneous pacing pads and things began to settle down a bit. I didn’t get back to follow up on him and what caused the torsades (if that is actually what it was? – more on that in a moment), but I certainly made sure that I grabbed hold of my favorite A&E Consultant, so that I could pick his brains.

The one question I needed answering?

“So did my single dose of Atropine change his 3rd degree heart block from a narrow complex into a wide complex? If that was the case, does that mean that the wide complex escape rhythm contributed to his Torsade de Pointe?”

I can honestly say that all of the significant learning that has taken place in my career has come from finding a superior brain to mine, and then gorging myself on the knowledge that is held in there. I wasn’t entirely sure what had just happened with my patient and I needed to know why it had happened, so that I could maybe do better next time.

The answer?

“I’m sure that the small amount you gave didn’t affect anything that was, or wasn’t going to happen to that patient”

Maybe he was just being kind?

Which still leaves me with my main dilemma and the real reason for bringing you through this whole story. I still am not entirely sure if I would do the same thing again if it all happened again in a different patient. At the end of the day, if my patient fits the JRCALC guidelines for treatment with Atropine, then do I give it to keep right with my guidelines or do I use the experience I have gained as a practicing and reflecting paramedic and use that to shape my future practice?

My conclusion is that I will do whatever I think is in the best interests of the patient and if I am asked to account for my actions or inactions, I will have experience, knowledge and research behind my clinical rationale.

Up until this series of posts I certainly had the experience to fall back on along with the knowledge of what I gained from the case in question. But what I have valued more than anything is the comments you have all made to the last three posts. You have made me go and read up on some areas which I hadn’t thought about in the past. You have made me question my own diagnosis of my patient (specifically if it was a true Torsade de point or not) and you have opened my eyes to many paramedics who are far more knowledgeable than I.

I have never claimed to be an EMS educator per se, but I know that writing and running a successful blog can lead some readers to think that whatever you right must be true. Now whilst that is certainly the case in some blogs out there, I realise that with this blog, I have always wanted it to be a two way street. I have had real enjoyment reading your comments (as has Mrs999), and they have caused quite a bit of discussion between the two of us over the past week, so thank you all for that!!

But finally, about the Torsades (or not). Let’s look at it in a number of stages and compare it to the ECG from Part 3:

ECG pt 3

  • The classical definition of Torsade de Pointe is that it is a variant of Ventricular tachycardia, it is classed as polymorphic which is what gives it its unique shape, form and loss of uniformity that differentiates if from VT.  – CHECK!
  • The normal rate of ventricular contraction should be between 150 and 250 bpm – As Tom Bouthillet from Pre-hospital 12 lead ECG blog states : “Typically Torsades will be < 300 BPM. Using the small block method we can place the ventricular rate between 375 and 500 (probably averaging around 425)” – Okay….Err….Not Check!
  • There is usually a distinct regular variation of the morphology of the QRS vector from positive to negative and back again, which is what gives it its name of ‘twisting of the points’ – If you have looked at the full page version of the tracing, I would argue that it fits the shape and morphology of a ‘twisting pattern’ – Possibly Check?
  • The definition also requires that the QT interval be increased markedly (usually to 600 msec or greater) – There was a great discussion between Tom Bouthillet and Matt (complete with diagrams) on part 3, as they discussed what the QTc was for my patient, so go and have a look to see which side you come down on. Matt came out with a QTc of 563msec, whilst Tom came out with 422msecs! It amazes me that things can come down to such minute numbers, however, even if we go with Matt’s higher number then we are still a little short of the defined QTc interval for the likelihood of the onset of Torsades  – So that’s a ….Not Check!
  • Torsade de Pointe is usually associated with short burst of the dysrhythmia which will usually revert to the prior rhythm afterwards. Although there is a high risk of the patient continuing into VF, especially if antiarrhythmic medication is given, in my patient, both episodes lasted less than 20 seconds and reverted to his normal without intervention – Definite Check and probably the most important one in this case!

But that still doesn’t leave me fulfilled with a definite answer. Was this Torsade de Pointe or was it something more obscure that I have never heard off and need to go and look up.

For those of you following the Chronicles of EMS and my trip to San Francisco, you will be aware of my wish to have some of the cardiac interventions that US medics have. I know there would have been far more medications and interventions that you could have done with this patient as compared to what I have, but ultimately, I feel that this case appears to have been, with hindsight, a definite ‘hands off’ approach. (That will make TOTWTYTR happy!!)

So what do you think?

Let me know please and once again, thanks for all the comments!

I hope you have enjoyed it as much as I have!

Advertisements

Responses

  1. Mark – Keep in mind that Torsades is just a particular variety of polymorphic VT (as is VF for that matter). Although we typically think of VF as “all or nothing”, the literature shows the existence of so-called transient VF (Google “paroxysmal VF”, click on the first Google book link, scroll up and look at the image). In the absence of a clinically significant prolonged QTc in the underlying rhythm, it's still a polymorphic VT (assuming it was not artifact). At what point does extremely fast polymorphic VT become VF? Well, good question. Perhaps at the point that the patient becomes pulseless. Either way, the decision point for antiarrhythmic drugs is the QTc of the underlying rhythm, if obtainable.

  2. Thanks Mark for this case set. It was really interesting to see how the patient's condition developed in a way I would not have predicted. It's really good for me as a student to read about cases like these to learn the possibilities of different outcomes occurring to patients – this would not be a typical 'text book case', to put it one way! I think you've summed up this case quite well, big ups for including the criteria for Torsade de Pointe.I've also found it fantastic reading other readers comments with different backgrounds and experience. Thanks for creating a forum for learning and discussion.Cheers!

  3. This was a good one Mark. So I printed the EKG's out and took them to work with me yesterday on the off chance that I would get to one of our cardiac units during a flight. I got lucky and ran this by 2 cardiology residents and a fellow. One resident said TDP the other said it could be VF that self terminated as tbouthillet recommended. The fellow said he leans towards TDP and the reason he gave is that 1) TDP is a rare occurrence when compared to most other arrhythmias and that a self terminating VF with no LOC is even more rare. 2) Treating TDP with an antiarrhythmic most likely amiodarone would not improve the QT but make it worse. 3) Treating a self terminating VF with magnesium will not have bad effects but may work for both. 4) If the patient has (+) LOC the treatment for both is Defibrilation. This just hilights the old saying about asking 3 cardiologists a question and getting 3 different answers so I'll have to find a 4th to even out the mix.

  4. It looks like a sinus arrest only seen it once before where the heart went into vf then came back as i lay him flat to put the pads on .

  5. My Girlfriend and I are both Paramedics and have spent the morning reading this series of blogs and have come to the consensus that we would have the Pt on O2, have the pacing patches in place and the drug box within reach and ready in the event that this patient becomes unstable. We would only consider pacing this patient if there were an extended transport distance and then only once the patient showed further signs of decompensation. Far be it for me to begin intervening and unintentionally knock out a perfusing rythmn and put this patients already overworked heart into an even more unstable prediciment. This is clearly one of those cases where we act because we have to, not because we can! I would be interested in learning what the final diagnosis was for this patient and what treatments he underwent to correct it.

  6. Mark, that was a great read, especially for a green medic such as myself. We only really ever talk about Torsades in class, I've never seen it, nor have I heard about it presenting to anyone I know at any point in recent years. Anyway, I do agree with your treatment as far as the O2 and Atropine go – completely within protocol here in PA for me to do that as well, and the 0.5mg of Atropine is suggested as a “test” dose, insofar that if it does help conduct some P's down, then at least we're getting somewhere.I do have a few questions, though. Do you happen to have any sedatives, e.g. Benzos? According to the AHA's ACLS here, he certainly would meet criteria for TCP, although sedation goes a long way when you're taking over somebody's heart, electrically, from the outside. Then again I'm remembering you said you can't pace in the field… is that absolute, or can you call in for orders to do that?My other question is, do you carry Magnesium? I've been taught that's the “definitive” field treatment for Torsades (and for eclamptic seizures). I'm also interested to know what his 12-lead looked like… and what the LP12 said about his axes/other numbers.

  7. Mark, that was a great read, especially for a green medic such as myself. We only really ever talk about Torsades in class, I've never seen it, nor have I heard about it presenting to anyone I know at any point in recent years. Anyway, I do agree with your treatment as far as the O2 and Atropine go – completely within protocol here in PA for me to do that as well, and the 0.5mg of Atropine is suggested as a “test” dose, insofar that if it does help conduct some P's down, then at least we're getting somewhere.I do have a few questions, though. Do you happen to have any sedatives, e.g. Benzos? According to the AHA's ACLS here, he certainly would meet criteria for TCP, although sedation goes a long way when you're taking over somebody's heart, electrically, from the outside. Then again I'm remembering you said you can't pace in the field… is that absolute, or can you call in for orders to do that?My other question is, do you carry Magnesium? I've been taught that's the “definitive” field treatment for Torsades (and for eclamptic seizures). I'm also interested to know what his 12-lead looked like… and what the LP12 said about his axes/other numbers.


Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s

Categories

%d bloggers like this: