What is the origin of this tachycardia?

[fiznat]

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This was a patient I had the other day, complaining of an acute onset of weakness and "dull" 3-10 chest "discomfort not pain." He admitted to minor SOB. Blood pressure was 118/70 or so.

I wanted to see what you experts thought about the origin of this rhythm, and what your order might have been as far as treatment.

Personally I did not believe this was VT although I am not so sure now. Since the BP was stable I tried 3 rounds of adenosine which didn't touch it. I next tried a round of Cardizem, which also didn't work. In the ED they tried more Adenocard which of course didn't work, and then Amiodorone which also didn't work. At the exhaustion of meds they finally decided to sedate and cardiovert, which worked on the first shot.

What do you guys think?

 

[DocVirk]

So I'm just a 4th year med student, so take everything I say with a grain of salt...
Any chance this is WPW? I can seriously convince myself of a short PR and upsloping QRS that looks like delta waves.
It doesn't really look like Vtach in the anterior leads, like V1, V2, and I.
If it is WPW, you would expect everything except electricity to not work, and maybe even make the situation worse (except procainamide)

 

[njac]

I'm just a lowly pharmacy student, but I just had ACLS 2 weeks ago. It sounds like you guys did the right thing - if the patient is otherwise stable, go to meds, if that doesn't work or pt becomes unstable, cardiovert.

Doesn't Cardizem primarily work on the SA node? Will that help with a ventricular tachy? Since he was relatively stable, would Lidocaine be an option to diagnose where the arrhythmia was originating?

I'm interested to hear what others have to say.

 

[Derek]

Looks to me like you have a wide complex tachycardia with concordance in V1-V6, thus favoring V-tach. History sometimes help sort these things out: age> 55 prior hx of CAD also favors V-tach. My personal approach to this clinical situation is Amiodarone 150mg IV x's 1 if no resolution then Synch Cardiovert at 100J (Monophasic) assuming the patient maintains stable vitals the whole time. If this was an SVT with underlying WPW causing the widening of the QRS the medications that were given, Adenocard and Cardizem would have resulted in cardiac decompensation, kind of a gamble to give these meds, but it looks like no harm was done.

 

[hyperbaric]

Why adenosine for a wide complex tachycardia?

 

[WilcoWorld]

njac - It's a good thing someone around here knows ACLS (inside joke folks).

Is the patient stable? If not, shock. If so, then we have some time to play.

Start with a description of what your are looking at:
-Fast
-Wide complex
-Regular

This rules out v fib, a fib, and a simple SVT (but not SVT with abberancy).
It almost looks like a flutter with aberrancy, but the rate isn't right (should be about 300, 150, or 75).

An old EKG and some PMH would be very helpful now. EKG could reveal preexisting WPW, or a conduction abnormality that might elucidate the arrhythmia.

WPW is an interesting thought. In order to treat this you need to a) think of it, and b) differentiate orthodromic from antidromic. Orthodromic WPW tachydysrhythmias will conduct down the AV node, and will thus be NARROW, and can be treated like any old SVT. Antidromic ones will conduct down the acessory pathway and will thus be wide complex, and treating with AV nodal blockers can worsen the situation.

The PMH, as mentioned before, can make the pretest probability of V-tach so high, that you should just asume it's v-tach unless you're very convinced otherwise.

In the precordial leads, I think I am seeing retrograde p waves, but I'm not sure.

In any case, I think the safest bet is to treat any wide complex tachydysrhthmia as v tach until proven otherwise. This will minimize your chances of hurting the patient while allowing you to treat them.

Some would argue that adenosine is so short-acting that it may be used with impunity. I would disagree, and would add that electricity has a darn short half-life and a low side effect profile (especially when the condition has been present for <48 hours), making it a pretty great drug.

So, I probably would have skipped the adenosine and the cardizem. If the PMH suggested v tach I would have either shocked or given amio or lido (depending on what my resident felt like doing). If the Fam Hx or prior EKG suggested WPW, I would have used either procaine or electricity (again, depending on my resident's preference).

If I were the patient, I would ask for a slug of versed with a Joules chaser.

 

[fiznat]

This is prehospital so there is no old ECG (you hospital folks are spoiled!). History was unhelpful as well, patient said he had none.

As far as the ECG, I see the precordial concordance, but the axis is wrong for VT at only 109* or so. I understand we usually see extreme right axis deviation in true VT? I was also pretty sure I could see P waves, most prominently in II, III, and aVF. My working diagnosis was a SVT (possibly a flutter) with a (RBBB) abbarancy. I was not willing to rule out any kind of specific atrial tachycardia as the rate makes it really hard for an accurate determination.

I didn't think about WPW till after the fact. I think about it all the time with a-fib but for some reason it didn't click with this patient. There does appear to be some slurring but I'm not convinced it is a delta wave. That might be accounted-for by the ?RBBB. Also the p-wave (if it is that) is a strike against.


Interesting someone mentioned 100J for the sync-cardioversion. That's what I would have done as well (I actually called the doc to see if he wanted me to, but was turned down since we were fairly close to the hospital). Poor guy, the ED shocked at freaking 360 😱.

 

[kungfufishing]

'lectricity

 

[coldcoldworld]

Agree with some of what was said but here's how I would break it down.

Wide complex regular tachy, so your choices are basically VT or SVT with aberrancy. Obviously shock if unstable.

Someone mentioned ?WPW findings but its hard to have a shortened PR if there aren't any clear P waves to begin with, which you don't have with either VT (usually, unless you get lucky and see AV dissociation) or with SVT (maybe see some buried retrograde P's). The "slurred upstroke" you're describing looks that way because the ventricle is depolarizing through an abnormal pathway, either through a slow accessory or cell to cell in the ventricle so again can't really be relied on.

This is the classic time when you could either apply Brugada criteria or as Wilco mentioned, just treat as VT. While Adenosine is an okay place to start as you may see P waves march through, I would strongly caution against just throwing Dilt or a beta blocker at an undifferentiated WCT. May do okay if truly SVT with aberrancy but can do very poorly and crump and die if given in VT. On the same note, if you treat for VT and they're in SVT, they won't usually crump.

For those interested in Brugada, here it is.
Step 1: Do you see an RS complex in any precordial lead? If no, its VT. If yes, you have to keep going. Our guy has RS complexes in V1 and V2.

Step 2: Is the RS interval >100 msec? This is measured from the start of R upslope to the nadir of the S. If >100 ms, its VT and you're done. If no, keep going. So its hard to tell from the EKG provided but to me it looks like the RS intervals seen in V1 and V2 are closer to 120 ms (3 boxes) so I would probably stop here and call it VT unless they had some other big reason like known aberrancy in the past. Amio 150 or Lido 100 would both be reasonable.

If the RS is <100 msec, you go to step 3.
Step 3: Any evidence of AV dissociation? This would include actually seeing P waves coming through. Others would be fusion beats or capture beats. I don't think I see any of these.

If you see AV dissociation, its VT. If not you move on to step 4. Step 4 is a bunch of morphology criteria for RBBB and LBBB appearing QRS. For me these are quite esoteric and beyond my scope or interest level. If I get to Step 4, they're either getting treated for VT or there will be a cardiologist on board.

While its obviously nice to know these criteria, I think the more important point here is that SVT w/ aberrancy is definitely a diagnosis of exclusion.

Hope this helped anyone who is still awake after all of that internal medicine like mental m asturbation. How did the guy end up doing??

 

[Jeff698]

From an identification standpoint, I'm leaning more towards VT for many of the same reasons stated.

The nice thing is, from a treatment standpoint, there are safe interventions that work equally well for VT and SVT w/ abberrancy.

I'd probably go with procainamide then electricity or just electricity.

Thanks for the interesting tracing.

Take care,
Jeff

 

[fiznat]

Yeah so I probably should have done the Amio instead of the Cardizem, since that drug is supposed to work both high and low. ...Not that Amio worked in the ED either, though.

I understand the urge to go right to cardioversion. I felt the same thing but we've got protocols we have to follow as prehospital providers, and I would most definitely get my pee-pee slapped if I skipped straight to the bottom of the ACLS algorithm.

We carry Procanimide but our docs decided to take it out of the adult treatment protocol for some reason. We use it only for kids these days, which means we never use it ever haha.

The guy eventually got cardioverted and dropped right out of the rhythm into a sinus in the 80s. He looked and said he felt worlds better. Amazing the difference a couple hundred points in heart rate makes.

 

[southerndoc]

It's very rare to have VT at a rate of 220. Likewise, it's rare to have monomorphic VT in a young adult. Usually they only get VT when they have a predisposing condition (Brugada, prolonged QT, etc.), and those are almost always polymorphic VT (Torsades).

Given the patient's age, the rate, and the questionable retrograde P's, I would have given the patient procainamide.

A couple things:

1. Be very careful of giving adenosine to patients with wide complex tachycardia. WPW patients can have some serious detrimental outcomes. The same is true of beta blockers and calcium channel blockers.

2. Amiodarone is a wicked drug. Although it works great for those with known VT and in cardiac arrests, keep in mind the side effects. A small but not insignificant number of patients (8%) get pulmonary fibrosis, with as many as 30% of those dying from the disease. One dose of amiodarone will linger in a person's system for up to 180 days.

3. Electricity is probably not the best option in the back of an ambulance if the person has a decent blood pressure. Sure, it's really cool to juice somebody, but it's best done in the emergency department. In fact, many patients actually get defibrillated by the cardiologist and not the emergency physician if they are stable. Electricity is not benign. I've seen two cases where patients were cardioverted (synchronized) into asystole and required medications to be resuscitated. It's not a pleasurable experience, and definitely not something that a lone paramedic should be dealing with. If they are unstable, then sure, by all means, give 'em the juice.

 

[theCamel]

It's very rare to have VT at a rate of 220. Likewise, it's rare to have monomorphic VT in a young adult. Usually they only get VT when they have a predisposing condition (Brugada, prolonged QT, etc.), and those are almost always polymorphic VT (Torsades).

Given the patient's age, the rate, and the questionable retrograde P's, I would have given the patient procainamide.

A couple things:

1. Be very careful of giving adenosine to patients with wide complex tachycardia. WPW patients can have some serious detrimental outcomes. The same is true of beta blockers and calcium channel blockers.

2. Amiodarone is a wicked drug. Although it works great for those with known VT and in cardiac arrests, keep in mind the side effects. A small but not insignificant number of patients (8%) get pulmonary fibrosis, with as many as 30% of those dying from the disease. One dose of amiodarone will linger in a person's system for up to 180 days.

3. Electricity is probably not the best option in the back of an ambulance if the person has a decent blood pressure. Sure, it's really cool to juice somebody, but it's best done in the emergency department. In fact, many patients actually get defibrillated by the cardiologist and not the emergency physician if they are stable. Electricity is not benign. I've seen two cases where patients were cardioverted (synchronized) into asystole and required medications to be resuscitated. It's not a pleasurable experience, and definitely not something that a lone paramedic should be dealing with. If they are unstable, then sure, by all means, give 'em the juice.

i'd like to echo southerndoc's points, and suggest that if stable holding off on adenosine and the anti-arrhythmetics might be the way to go. this month's EM:RAP has an excellent, pertinent section on how to handle situations like this one as well.

even just recognizing wide versus narrow, and then getting comfortable with concepts like concordance can help steer you away or towards VTach - and then you won't get in trouble by giving them potentially harmful meds.

p.s. to me i'd read this as VTach vs. SVT with aberrancy

 

[fiznat]

The patient was 48 years old. Is that still considered a young adult?

In regards to holding off on all treatment on this patient since he has a stable BP...

I had another tachycardic patient a few months ago with a similar rate. His complexes were narrow, though, and the BP was much lower necessitating sync-cardioversion enroute to the ED. Cardioversion worked fine, but what I found interesting was in a conversation with the ED doc afterwords, he made the point that the longer we "sit" on a tachy rate like this the harder the rhythm is to break. He commented that it was good we jumped in and cardioverted as soon as we did, because it might not have worked so well 15 minutes later in the ED.

Would the same maxim hold for this patient I just presented? Is holding off on a stable/symptomatic tachycardia like this detrimental to the patient in that his chances of breaking go down with time?

Sometimes its hard to tell what is real and what is anecdotal when you get advice like this.

 

[SoCuteMD]

Do you havea f/u EKG on this guy? Did he have WPW?

 

[fiznat]

^^

I don't at the moment. I'll check and see if one of the nurses will let me look up his chart next time I stop by that hospital. Pretty sure it was sinus with no evidence of WPW though.

 

[njac]

njac - It's a good thing someone around here knows ACLS (inside joke folks).

srsly. no insulin! no pulse! omg!

I have 2 days left on the rotation and we still haven't opened a crash cart. This is ridiculous.😴

 

[Rendar5]

could be lots of stuff. vtach, aflutter with 2:1 conduction and intraventricular conduction delay, WPW. Did adenosine even slow it down for a second or two before it went back to this or did absolutely nothing happen at all when u gave adenosine? EKG during a temporary slowdown from adenosine would be very useful.

EDIT ignore aflutter remark, speed is wrong for 1:1 or 2:1

 

[fiznat]

Did adenosine even slow it down for a second or two before it went back to this or did absolutely nothing happen at all when u gave adenosine? EKG during a temporary slowdown from adenosine would be very useful.

Adenosine did absolutely nothing. In fact, the 3 lead you are looking at actually was captured during adenosine administration.

 

[southerndoc]

Sorry, for some reason I thought the patient was in his 20's. Not sure where I came up with that.

Even at 48, I still don't think this is VT. The rate is too fast. Usually VT is 150-180. SVT from WPW is often in the 220's.

 

[BADMD]

I'm going to echo SouthernDoc. I'd think twice about using a BB, CCB or adenosine. If the guy is stable, with no hx of CAD and you don't suspect a low EF, I'd choose Procainamide.

We've gotten away from the stuff now that amiodarone in on the ACLS pathway. I don't like amio (and I think its inclusion in ACLS had as much to do with lobbying as it does to actual evidence). In the right patient, procainamide is like holy water.