# Chest pain, HR 190



## rhan101277 (Dec 7, 2011)

Here are the details, this happened a couple days ago.

Age: 56 y/o male
Pmhx: COPD, CHF, previous Dysrhythmia requiring non-emergency DC cardioversion.
Meds: Amiodarone, Furosemide, Albuterol, Crestor, Lipitor, ASA


Scenario:

I get a call about chest pain around 4am, pt is mildly SOB, has substernal chest pain 9/10 - non radiating, that started while sitting still.  He has previously taken 350mg ASA today and our protocols state to not administer any ASA if they have had some.  He has wheezing but it is not acute, says he has had it for "years.:

The patient is alert and oriented x 3, GCS 15.  His diaphoretic, pulse is 190 wide complex tach with QRS 138ms, but he has RBBB also and takes amiodarone (200mg x 3 daily) so I think it could be widened due to that.  Pt was admitted two weeks ago for this and they waited 3 days before electrical cardioversion.  I initially think this is SVT w/ aberrancy due to the rate is regular and I think QRS is wide due to reasons stated above.  The reason I think this is that the axis deviation is not extreme right axis and also V1-V6 are not in concordance.

Vitals:

BP: 84/54
HR: 190
Pulse ox: 99 on 4L oxygen
12 Lead: No st elevation or depression ( can't really detect ST elevation with a BBB in place).

I try vagal maneuvers and rate doesn't slow, I try using adenosine as a diagnostic tool to slow rate 6mg, 12mg then 12mg and no slowing.  We arrive at ER before I have time to mix amiodarone 150mg over 10 min.  He remains AAOx3 and systolic BP never drops below 80.  Transport time was 15 minutes.

ER doc opts to cardiovert, but contacts cardiology for a consult.  He gives etomidate, starts up amiodarone drip and before he can cardiovert the pt goes into a flutter with 3:1 conduction and he doesn't cardiovert.  I didn't find out any more behind what went on but I was definitely more stressed on this call than usual.  Dr first thinks this is vtach but then says it is afib with RVR but it is regular, he said sometimes rate can be so fast it always looks regular.

Would you have cardioverted this patient?  I elected not to.


----------



## Handsome Robb (Dec 7, 2011)

That's a puzzler. I would have tried the adenosine then if that didn't work sedated and cardioverted him. I'm thinking with him taking amiodarone PO daily and it isn't working there's no reason for me to give him more while risking the possibility of dropping his BP.

He's AAO however symptomatic, that's why I say sedate and cardiovert after trialing the adenosine. My instructor has always told me not to be afraid of electricity.

Just my .02, remember, I'm young, dumb and not very experienced


----------



## Dwindlin (Dec 7, 2011)

NVRob said:


> That's a puzzler. I would have tried the adenosine then if that didn't work sedated and cardioverted him. I'm thinking with him taking amiodarone PO daily and it isn't working there's no reason for me to give him more while risking the possibility of dropping his BP.
> 
> He's AAO however symptomatic, that's why I say sedate and cardiovert after trialing the adenosine. My instructor has always told me not to be afraid of electricity.
> 
> Just my .02, remember, I'm young, dumb and not very experienced



Agree with NV. As long as he is compliant with his meds I think I would skip the Amio.


----------



## Handsome Robb (Dec 7, 2011)

I would love to see the 12 lead as well if you have a copy of it to post up.


----------



## rhan101277 (Dec 7, 2011)

Yeah I have a copy, I am not afraid to use electricity but I would not have been able to sedate him with his pressure.  We carry versed for that and he was hypotensive but not by much.  I will try to post up the 12 lead tomorrow.


----------



## Handsome Robb (Dec 8, 2011)

rhan101277 said:


> Yeah I have a copy, I am not afraid to use electricity but I would not have been able to sedate him with his pressure.  We carry versed for that and he was hypotensive but not by much.  I will try to post up the 12 lead tomorrow.



What about a 500cc bolus then see how his pressure is?

 Theoretically you could cardiovert him _then_ push the versed for the retrograde amnestic effects but that is also banking on the rhythm converting on the first try. I'd personally try the bolus first though since I'm not a very lucky human being.

I'm waiting for someone way smarter than me to come in here and tell me I'm way off base h34r:


----------



## Nervegas (Dec 8, 2011)

NVRob said:


> What about a 500cc bolus then see how his pressure is?
> 
> Theoretically you could cardiovert him _then_ push the versed for the retrograde amnestic effects but that is also banking on the rhythm converting on the first try. I'd personally try the bolus first though since I'm not a very lucky human being.
> 
> I'm waiting for someone way smarter than me to come in here and tell me I'm way off base h34r:



I wouldn't call it way off base, but I would trial the fluid challenge first, and then see where I was at before sedation. 

As far as this scenario, I would have checked lung sounds before going ahead with a fluid challenge, then trial Adenosine. Rapid Tx to the appropriate facility. I would avoid additional Amiodarone, he is already hypotensive, even with a fluid challenge, no reason to risk it. I would also consider some fentanyl for pt comfort depending on our ETA.

If the pt continues to deteriorate enroute, then I would have moved towards cardioversion. But I think you handled this one the right way.


----------



## firetender (Dec 8, 2011)

NVRob said:


> I'm waiting for someone way smarter than me to come in here and tell me I'm way off base h34r:


 
I'd like to but my world is still defined by phones at home!

What I'd be looking for are signs of decreasing perfusion. Does the elevated heart rate continue to increase? The BP doesn't appear to be getting affected.

For me, this was a major tip-off (from the OP):



> Pt was admitted two weeks ago for this and they waited 3 days before electrical cardioversion.


 
This alone tells me there may have been good reason NOT to be concerned about the aberrancy of an increased pulse that's not getting worse. Or even more reason to suspect other things need to be in better balance first that are not related to emergency interventions. 

So as far as urgency goes, electrical intervention would not be appropriate unless it was treating something moving toward life-threatening. This doesn't sound like a situation getting worse; There is stability here. 

And that's what you're working with. It's a matter of supporting what is working rather than interposing a treatment that has the potential to upset the applecart. The hospital is only 15 minutes away. Don't kid yourself, cardioversion at any level holds the potential to make a working heart stop.

An important point I would have liked to have been made more clear is How was the patient (subjectively) doing on fiirst presentation compared to once in the back of the ambulance? How was he feeling? Any change?


----------



## Chief Complaint (Dec 8, 2011)

I think you handled it well.  With the hospital so close i wouldn't have cardioverted either.  As mentioned above, its possible that it might make things worse.  Sometimes less is more if you arent exactly sure what's going on with your patient.


----------



## systemet (Dec 8, 2011)

A couple of quick opinions:

* Deciding a WCT is supraventricular in origin with aberrancy is a very hazardous thing to do.  You may be right, and certainly if the axis isn't extreme right, and there's a classic RBBB pattern in V1, you may be right a lot of the time.  But you'll also be wrong, and giving metoprolol or diltiazem to a VT is going to disastrous.

* Have you considered the possibility for WPW?  The patient has had a previous tachycardia requiring cardioversion.  I know many of these patients don't have a clue as to what happened, what meds they're taking, what they did last time they were in hospital, etc.  But it would be nice to know if this has been considered.

* You can still see ST elevation in RBBB.  It doesn't prevent you from diagnosing a STEMI.  Even with LBBB, the Sgarbossa criteria allow the identification of STEMIs, although the sensitivity is poor.

* I'm not saying you did the wrong thing here.  But, be aware that it's not usually a sin to bring in a stable patient with an untreated tachycardia.  A lot of these patients develop an arrhythmia, spend a couple of hours feeling funny, drive themselves to the ER, sit around in the waiting room for a while, and then lie in a bed for an hour while the doctors decide the best course of action.


----------



## rhan101277 (Dec 8, 2011)

The patient did not have any change in the back of the ambulance.  He did not get worse but he also did not get better.  Through the whole trip he was AAOx3 and his mentation was great, this was a key factor in my decision making.  If he is talking to me his brain is perfusing well despite him being borderline hypotensive (our protocols use 90mmHg as hypotension).  It is normal for the body to shunt flow to the core and just because you are seeing a blood pressure of 84/56 or what not when taking from an extremity does not mean you would see that same number if you had an arterial line in.

I have seen people with manual pressures like this only to have a femoral artery pressure of around 100 systolic, not to say it always works like this but still.  I am still going to post up the 12 lead, I got it in the car but it is to cold to walk outside right now.


----------



## rhan101277 (Dec 8, 2011)

Here is the strip


----------



## 46Young (Dec 8, 2011)

rhan101277 said:


> The patient did not have any change in the back of the ambulance.  He did not get worse but he also did not get better.  Through the whole trip he was AAOx3 and his mentation was great, this was a key factor in my decision making.  If he is talking to me his brain is perfusing well despite him being borderline hypotensive (our protocols use 90mmHg as hypotension).  It is normal for the body to shunt flow to the core and just because you are seeing a blood pressure of 84/56 or what not when taking from an extremity does not mean you would see that same number if you had an arterial line in.
> 
> I have seen people with manual pressures like this only to have a femoral artery pressure of around 100 systolic, not to say it always works like this but still.  I am still going to post up the 12 lead, I got it in the car but it is to cold to walk outside right now.



Did you consider using quantitative capnography on this pt (assuming that you have it)? You can get real time feedback as to their hemodynamic status. For example, in a low flow state you can expect the ETCO2 to be below the norm, for example. A downward trend in ETCO2 capnometry values could suggest the progression of cardiogenic shock in this case. Less blood flow to the lungs will result in less CO2 being delivered for exhalation. Also realize that in the presence of rales, which could develop w/ heart failure secondary to this tachydysrhythmia, CO2 is 20 times more soluble than O2 (IIRC), so it will move through fluid the same speed as through air. Peripheral SPO2 readings have a delay in representing the pt's true status, but quantitative ETCO2 gives immediate feedback.

This would be another vital assessment tool to determine if your pt is stable or unstable to help determine treatment.


----------



## rhan101277 (Dec 8, 2011)

46Young said:


> Did you consider using quantitative capnography on this pt (assuming that you have it)? You can get real time feedback as to their hemodynamic status. For example, in a low flow state you can expect the ETCO2 to be below the norm, for example. A downward trend in ETCO2 capnometry values could suggest the progression of cardiogenic shock in this case. Less blood flow to the lungs will result in less CO2 being delivered for exhalation. Also realize that in the presence of rales, which could develop w/ heart failure secondary to this tachydysrhythmia, CO2 is 20 times more soluble than O2 (IIRC), so it will move through fluid the same speed as through air. Peripheral SPO2 readings have a delay in representing the pt's true status, but quantitative ETCO2 gives immediate feedback.
> 
> This would be another vital assessment tool to determine if your pt is stable or unstable to help determine treatment.



No I didn't, I thought about it.  I was interested in focusing on terminating the Dysrhythmia.  I get better at this job everyday though.


----------



## triemal04 (Dec 8, 2011)

That isn't vtach.  Hopefully TomB will chime in on this and correct me if I'm wrong, but I'm fairly confident in my assessment.  

There are several things that would point to vtach; negative QRS in V6 and initial R-wave in avr are both indicative, as well as the right axis deviation (not as good as extreme right access deviation though).  If there was no responce whatsoever to adenosine, that would point to it as well. 

But, the QRS really isn't that wide; for a RBBB that's pretty decent looking.  AVR can look like that without a ventricular origin, though it's rare.  It's hard to say for sure (may be some in 2 or that's just movement) but there aren't any fusion beats, and if you look at V2 and AVL you can see atrial activity; specifically what looks to be flutter waves.  That part is backed up by the patient's history; a 3 day wait for cardioversion would make sense if he needed to be placed on anticoagulants.  (that also does not mean that he had a rapid arrhythmia for 3 days, just that he had an aberrant rhythm).  And amiodarone is sometimes prescribed for afib/aflutter.

That being said, this patient still get's the sedative of your choice and then cardioversion.  While I'm confident about it being aflutter, and there aren't any delta waves and the QRS's within each lead are the same, I still wouldn't try to give cardizem or amiodarone (or procainamide if you carry that).

The best choice for this is to call it a wide complex tachycardia of unknown origin, and treat it as such...which means treating for vtach. 

Sedate and cardiovert.


----------



## rhan101277 (Dec 8, 2011)

triemal04 said:


> That isn't vtach.  Hopefully TomB will chime in on this and correct me if I'm wrong, but I'm fairly confident in my assessment.
> 
> There are several things that would point to vtach; negative QRS in V6 and initial R-wave in avr are both indicative, as well as the right axis deviation (not as good as extreme right access deviation though).  If there was no responce whatsoever to adenosine, that would point to it as well.
> 
> ...



I didn't cardiovert him, if I did I would have to have done so without sedation.  Because of his BP.  Do you think it was wrong for me not to cardiovert?  Another thing I took into consideration in not doing so was his stay just two weeks ago where they waited three days to cardiovert, true his BP may have been better.  I just know that anytime you use electricity there comes a chance of causing asystole that will not recover.  It would be tough me having to tell the family how did he die in route, he was talking when you left.


----------



## lightsandsirens5 (Dec 8, 2011)

I could be way off, having just been introduced to 12 leads, but isn't her getting pretty close to being ERAD based off of that 12 lead?

Like I said, I could be way off.


----------



## triemal04 (Dec 8, 2011)

rhan101277 said:


> I didn't cardiovert him, if I did I would have to have done so without sedation.  Because of his BP.  Do you think it was wrong for me not to cardiovert?  Another thing I took into consideration in not doing so was his stay just two weeks ago where they waited three days to cardiovert, true his BP may have been better.  I just know that anytime you use electricity there comes a chance of causing asystole that will not recover.  It would be tough me having to tell the family how did he die in route, he was talking when you left.


Holding off based on what happened before isn't the best idea without knowing all the facts about what happened then.  Just because he was cardioverted before does NOT mean it was for the same type of situation.

Beyond that, you have someone who has a moderately low BP, in this case most likely caused by his rapid heartrate and maybe his meds (IV amiodarone usually causes hypotension due to the chemicals in the solution not neccasarily because of the drug itself), who is sweaty (can't fake that), mildly short of breath and complaining of chest pain (you didn't elaborate but we'll assume cardiac type chest pain) most likely due to his rapid rate.  

So, does something need to be done?  Yes.  In a hugeohmygodhe'sgoingtodiedoitnownownownow rush?  Not neccasarily.  If you had access to better sedatives than versed (like etomidate) then there wouldn't be any reason to delay to long, but giving a fluid bolus at the same time as a small dose of versed (say 2.5-5mg depending on his size) and waiting a couple minutes for in to take effect, while being ready to immedietly shock if needed would be ok too.

If you think the hypotension is caused by his meds, then you need to be looking at alternative therapies to raise his BP (or leaving it alone, depending), and if you think it's caused by his rate...that should soon be fixed.  

I'd still stay away from treating this with medications, other than a sedative.

And actually, in looking at the LP's interpretation of the QRS axis, that is ERAD.  The quick method of checking axis deviation doesn't bear that out, so someone else can answer that one.


----------



## 46Young (Dec 8, 2011)

rhan101277 said:


> I didn't cardiovert him, if I did I would have to have done so without sedation.  Because of his BP.  Do you think it was wrong for me not to cardiovert?  Another thing I took into consideration in not doing so was his stay just two weeks ago where they waited three days to cardiovert, true his BP may have been better.  I just know that anytime you use electricity there comes a chance of causing asystole that will not recover.  It would be tough me having to tell the family how did he die in route, he was talking when you left.



I agree with post # 15. Any bradycardia protocol I've come across advises to sedate prior to cardioversion, time permitting, if the pt is unstable. Hypotension is one of the criteria to call the pt unstable. Just have a bag of NS hanging, and monitor L/S after the fluid bolus if needed. Mix some dopa and keep it nearby as well if you want to stay ahead of your pt.

Again, an ETCO2 capnoline would be of good use here. If the pt's ETCO2 values are dropping, the shock is progressing (less flow, lower ETCO2), and you need to cardiovert. If the pt's pressure holds, along with the pt's mentation and a normal ETCO2, you would be more justified in withholding electrical therapy in this case. Otherwise, if you fail to cardiovert, and the pt has an untoward outcome, you can be found negligent for withholding therapies. 

BTW, if it's too difficult to tell if the rhythm is regular or irregular, consider turning up the QRS volume. You'll pick up an irregular beat with your hearing well before you will by sight.


----------



## rhan101277 (Dec 8, 2011)

46Young said:


> I agree with post # 15. Any bradycardia protocol I've come across advises to sedate prior to cardioversion, time permitting, if the pt is unstable. Hypotension is one of the criteria to call the pt unstable. Just have a bag of NS hanging, and monitor L/S after the fluid bolus if needed. Mix some dopa and keep it nearby as well if you want to stay ahead of your pt.
> 
> Again, an ETCO2 capnoline would be of good use here. If the pt's ETCO2 values are dropping, the shock is progressing (less flow, lower ETCO2), and you need to cardiovert. If the pt's pressure holds, along with the pt's mentation and a normal ETCO2, you would be more justified in withholding electrical therapy in this case. Otherwise, if you fail to cardiovert, and the pt has an untoward outcome, you can be found negligent for withholding therapies.
> 
> BTW, if it's too difficult to tell if the rhythm is regular or irregular, consider turning up the QRS volume. You'll pick up an irregular beat with your hearing well before you will by sight.



Two separate doctors confirm it isn't vtach.  One says it isn't because v1-v6 are not in concordance.  The other says it could be afib with RVR and that the rate is so fast you won't be able to see it being irregular.  At least I didn't kill anybody, sometimes you have to make tough decisions with few facts.


----------



## 46Young (Dec 8, 2011)

rhan101277 said:


> Two separate doctors confirm it isn't vtach.  One says it isn't because v1-v6 are not in concordance.  The other says it could be afib with RVR and that the rate is so fast you won't be able to see it being irregular.  At least I didn't kill anybody, sometimes you have to make tough decisions with few facts.



Nobody's trying to beat you up over this call, just making suggestions while in a low stress environment with plenty of time to think.


----------



## coolidge (Dec 8, 2011)

*v1-v6 are not in concordance*

Can you explain what this means:  v1-v6 are not in concordance
Thanks


----------



## triemal04 (Dec 9, 2011)

46Young said:


> Nobody's trying to beat you up over this call, just making suggestions while in a low stress environment with plenty of time to think.


Actually...I am, at least a little bit.

This patient really should have been treated in the field.  There's an arguement to be made for delaying treatement, but as presented the risks of converting him to a sinus rhythm are less than leaving him alone.  It worked out fine to not do anything, and often will, but you are playing with fire doing that.  Choosing meds or electricity is something that can be debated, but regardless, one needed to be choosen and initiated (beyond adenosine which you he gave).

That's not really the problem I have though; chalk it up to a learning experience, no big deal.  What really bothers me is this (and if you left something out that negates what I'm saying then my apologies):


> Pt was admitted two weeks ago for this and they waited 3 days before electrical cardioversion.





> Another thing I took into consideration in not doing so was his stay just two weeks ago where they waited three days to cardiovert


Do you really know that "this" is the same thing that happened 2 weeks ago?  In the exact same circumstances?  No?  Then that is a huge problem.  Essentially you were basing your treatement path, at least in part, on incomplete information that YOU KNEW, or should have known, was incomplete.

Look at this patient clinically.  As you presented him, is that a normal, healthy guy?  Do you think that someone like that would tolerate that state for 3 days?  Did the ER doctor?  It looks like you let an incomplete story that only clears up some parts of the patient's history talk you into not doing something that you didn't want to in the first place.

You were with this guy for, what?  30 minutes?  More?  Think of everything else you could have done.  You say you can't give versed with a pressure like that?  Treat his BP.  Call for orders for versed if you need to; more than likely they would have said to just bring him in, but at least you're thinking things through.  You planned to give amiodarone.  What if that dropped his BP?  What if it didn't work?  What if he got worse? 

You need to evaluate the history that you are given just as you do the results of your exam.  Misinterpreting it can have just as disastrous consequences.

Anyway.  It all worked out...learn from it and move on.  No biggie.


----------



## triemal04 (Dec 9, 2011)

coolidge said:


> Can you explain what this means:  v1-v6 are not in concordance
> Thanks


If V1-V6 all have a QRS going in the same direction (generaly a negative deflection) it's something like 95% specific for vtach.  In this case concordance just means they are all the same.


----------



## systemet (Dec 9, 2011)

I think your doctors are wrong. I think this is VT.  I have to do some work here, but I'll explain my reasoning later.

I may be wrong.  But I don't think I am.

Just quickly note a couple of things:

* You do have extreme right axis deviation.  Look at lead II.  It's mostly negative.  Even if we trust the machine, which we shouldn't, it's giving an axis of 193 degrees, which is indeterminate / extreme right.

* There's no classic RBBB pattern in V1.

* I think I can see P waves appeared in the S wave in V4, II, aVL and other places.  I think this is AV dissociation.


----------



## epipusher (Dec 9, 2011)

Strong statement to say two doctors in agreement are wrong. I think you did just fine on this run. It seems as though you may have had some sort of "gut feeling" on this run that none of us are going to experience via a forum post. Good job.


----------



## systemet (Dec 9, 2011)

epipusher said:


> Strong statement to say two doctors in agreement are wrong.



Agreed.  The probability of me, a random paramedic, being wrong is much higher than the probability of two different physicians being wrong at the same time.  Especially if either of them are working in specialties / settings where they encounter this relatively rare population of patients on a regular basis.

But I think I'm right, and when I have a few minutes to write a coherrent post, I'll try and explain why.


----------



## systemet (Dec 9, 2011)

Ok.  Here we go.

(1) So the first thing, which needs stating just because it's _so important_, when we see WCT, we should always bias our decision-making process towards VT, not SVT.  Why?  Because second-line therapies for SVT with aberrancy, e.g. diltiazem, metoprolol,  run a very high risk of *killing* someone with VT.  And remember, this is a stable patient we're talking about here.  I would argue that, in EMS, we almost never need to be able to differentiate SVT with aberrancy, and can probably just assume WCT = VT.  Most of us use amiodarone as a first-line agent for VT, which may help in some cases of SVT.  The only real risk of missclassifying a WCT as VT instead of SVT with aberrancy is that the receiving center may choose to place a pacemaker to prevent recurrence.  But if you've been able to obtain a 12-lead prior to conversion this risk is minimised.

ACLS 2011 is pretty clear about this:

"_The first step in the management of any tachycardia is to determine if the patient’s condition is stable or unstable (Figure 4, Box 3). An unstable patient with a wide-complex tachycardia should be presumed to have VT and immediate cardioversion should be performed (Figure 4, Box 4 and see above). Precordial thump may be considered for patients with witnessed, monitored, unstable ventricular tachycardia if a defibrillator is not
immediately ready for use (Class IIb, LOE C). If the patient is stable, the second step in management is to obtain a 12-lead ECG (Figure 4, Boxes 6 and 7) to evaluate the rhythm. At this point the provider should consider the
need to obtain expert consultation._"


(2) Speaking to concordance:  The idea that either (i) all precordial complexes are R waves (positive concordance), or (ii) all precordial complexes are QS waves, indicating that ventricular activation occurs from either the anterior or posterior wall.  This is very _*specific*_ for VT.  What it is not, is *sensitive*, with some studies reporting sensitivities in the range of 21%. Now I got myself in trouble recently for pointing out the difference between sensitivity and specificity in another thread recently, but here is another case in point.  A sign that is specific is something that when it is present the patient exhibits the disease in question.  So in this case, we know that when we see precordial concordance, it's very likely that we're seeing a VT.  However, we can't assume that the reverse is true, i.e. that because it's absent, the disease isn't present.  This is a false equivocation, this is something that is better described by the concept of sensitivity.  Sensitivity is the percentage of patients with a disease that exhibit a certain sign.  So, in some published research studies only 21% of the patients later found to be in VT showed concordance.  Or, put another way, 79% of patients in VT had no evidence of concordance.  Thus the absence of precordial concordance tells us nothing, as most of our patients in VT probably won't have it.  When it's present, great, it's a very useful finding, but it's absence doesn't mean much.

(3) Axis: speaking very generally, the axis tells us the direction the ventricular myocardium is depolarising in.  This patient has a extreme rightward or "indeterminate" axis (-90 to +180), meaning that depolarisation is beginning in the bottom of the left ventricle, and spreading upwards and towards the right shoulder.  Note how this produces a negative complex in lead II (which is looking in the opposite direction), and a strongly positive complex in aVR (more on this later).  This is 96% specific for VT, meaning that only 4% of patients exhibiting extreme right axis deviation will have SVT with aberrancy.

---------------------> SORRY, GOT TO RUN; will finish these thoughts later.


----------



## systemet (Dec 9, 2011)

Moving on....

(4) BBB -- It's been suggested here that this patient has a previous hx of RBBB, and that this tachycardia might SVT with previous abberrancy. However, there's not a classic rSR' pattern in V1 (I guess if you're feeling really generous you could make an argument for counting the initial positive deflection as r wave, but then the complex becomes > 0.14 seconds, which is rare for aberrancy / preexisting BBB.  We normally see predominantly positive complexes in I and V6, although here they're absent, which speaks as much to axis as anything else, and when you look, the R < S in V6, which favours VT, although again, this is an effect of axis.  This raises a similar issue, that of why is the axis so rightward?  RBBB alone doesn't cause RAD.  It's possible, I guess, that the patient has pre-existing RVH or something, but this is unlikely here as well, because of the degree of axis deviation.

(5) Brugada criteria - these guys looked at a few hundred WCTs, and compared the ECG characteristics.  Amongst other criteria, in one cohort they examined, they identified that an R wave >  S wave in V6 was 94% specific and 41% sensitive for VT.  [These are almost exactly the same numbers for ST changes in the anterior leads and STEMI, by coincidence.]  They also noted an R wave in V1 or V2 was 60% sensitive and 84% specific.  I think it could be argued that both are the case in our ECG.

I'm not saying that I'm definitely right and that the physicians are definitely wrong.  Except for the guy who said it couldn't be VT because there wasn't precordial concordance.  He was just wrong.  The various morphological criteria for VT versus SVT with aberrancy aren't iron clad, although they're pretty good.  What I will say is this:-

* I think the adenosine was ok, considering the recent guidelines change, provided we've done our best to ensure that the patient doesn't have WPW.

* There is no way I would be comfortable giving nodal blockers beyond adenosine to this patient, and would actively intervene in front of bystanders if someone else attempted to on a call when I was present.

* I think in this situation "expert consultation" means more than "some guy who rocked the ACLS megacode station, and has been a medic for 10 years".  If the patient's stable, amiodarone seems reasonable enough, but then again, so does doing nothing until you get to the hospital, or giving med consult a call and seeing what they'd prefer.

* I think OP did a fine job.  But I think we should all be very cautious in attempting to differentiate WCT in the field.  Assuming it is VT is probably the best choice.

* I'm really not trying to be a ****head.  I just have strong feelings about this.

[As an aside, I took another look at the ECG, and think that the P waves I saw were retrogradely conducted -- this happens in a lot of VT, it's not just a junctional tachycardia thing.  So I don't think there's AV dissociation here, but that's not necessary for it to be VT.]


----------



## lightsandsirens5 (Dec 9, 2011)

46Young said:


> I agree with post # 15. Any *bradycardia* protocol I've come across advises to sedate prior to *cardioversion*, time permitting, if the pt is unstable. Hypotension is one of the criteria to call the pt unstable. Just have a bag of NS hanging, and monitor L/S after the fluid bolus if needed. Mix some dopa and keep it nearby as well if you want to stay ahead of your pt.



What....what? :unsure:


----------



## Smash (Dec 10, 2011)

Systemet, the ECG also appears to rule in for VT using Vereckei criteria


----------



## systemet (Dec 10, 2011)

Smash said:


> Systemet, the ECG also appears to rule in for VT using Vereckei criteria



It's crazy how many different systems there are; Wellens, Brugada, Vereciki, Griffith, etc.  

Myself, I just don't see the point in trying to differentiate SVT with aberrancy in the field, unless you're in a truly remote setting.  Otherwise it just seems smarter to treat as VT, take them to the ER, where the ER doc will probably sit on their hands are consult with cardiology before doing anything further.

I'm hugely pro-EMS, but I just can't see the benefit of trying to differentiate SVT with aberrancy in most 911 responses.  It seems safer to assume VT.  I can appreciate that maybe flying into a rural / remote hospital/outpost and being able to recognise VT when they've decided to treat a WCT patient with inappropriate agents, but I can't really see making the decision the other way.  If you show up, they've tried to convert with adenosine / amiodarone / whatever and you suspect SVT with aberrancy, it seems like sedation and cardioversion is probably safer than going with nodal blocking agents, even if you've got an hour flight ahead of you.


----------



## Smash (Dec 10, 2011)

I agree with that, merely pointing out that if one were to engage in what is ultimately an academic enterprise, the rhythm appears to rule in for VT using a couple of different algorithms.


----------



## triemal04 (Dec 11, 2011)

systemet said:


> I'm hugely pro-EMS, but I just can't see the benefit of trying to differentiate SVT with aberrancy in most 911 responses.  It seems safer to assume VT.  I can appreciate that maybe flying into a rural / remote hospital/outpost and being able to recognise VT when they've decided to treat a WCT patient with inappropriate agents, but I can't really see making the decision the other way.  If you show up, they've tried to convert with adenosine / amiodarone / whatever and you suspect SVT with aberrancy, it seems like sedation and cardioversion is probably safer than going with nodal blocking agents, even if you've got an hour flight ahead of you.


Fair enough.  I think you allready mentioned it, but it is always better to use the criteria to rule vtach in, not out.  

Not fair to say that we shouldn't be at least attempting to differentiate between an SVT or afib/flutter with aberency and vtach in the field though.  I agree, if you aren't absolutely sure then it is better to treat as vtach and if it's a borderline case to treat as vtach.  People can be taught to accurately decide what rhythm the patient is in though; if they are then there is no reason they shouldn't be treating what they find.  It will increase the risks to a certain extent, but a good education and medical oversight can help lower those.

I'm sure there are a fair number of places that don't carry amiodarone for one reason or another, and there are some, not many but some, people with allergies to amiodarone.  If you have the patient that you decide does have afib with aberrancy but is truly stable, how would you treat them?  There is always the option of doing nothing and that might be the best course, or going directly to cardioversion, which has it's own risks (that are increased if it's afib).  Take the OP's patient.  Say he has a normal BP, no complaints other than palpations, and you are 30 minutes from a hospital.  For arguements sake you decide this probably isn't vtach but afib.  You don't carry amiodarone.  What is your treatement plan?

I'm not pointing fingers by any means, just honestly curious.


----------



## systemet (Dec 12, 2011)

triemal04 said:


> Not fair to say that we shouldn't be at least attempting to differentiate between an SVT or afib/flutter with aberency and vtach in the field though.  I agree, if you aren't absolutely sure then it is better to treat as vtach and if it's a borderline case to treat as vtach.  People can be taught to accurately decide what rhythm the patient is in though; if they are then there is no reason they shouldn't be treating what they find.  It will increase the risks to a certain extent, but a good education and medical oversight can help lower those.



Maybe you're right.  I don't know.  It just seems very risky to me, given the repeated problems that even EM physicians have with misdiagnosing VT as SVT w/ aberrancy.

As we've discussed here there's a lot of different evidence-based guidelines for distinguishing between VT and SVT w/ aberrancy.  These are used by cardiology and EM to differentiate the two.  But even then, it's tricky, and there's a certain error rate.  

I would argue that a stable patient presents with a WCT to the ER, it's probably first going to get treated with amiodarone, and if this fails to convert, there's probably going to be a cardiology consult.  If there's uncertainty in the initial presentation as to SVT versus VT, I think that's going to go by cardiology as well, in a larger center.  While I'm not sure how logically valid my argument is, I'd suggest if the EM docs are willing to sit on these patients and consult, that perhaps we should be willing to sit on them too.

I agree good oversight and med consult can help mitigate the risks.



> I'm sure there are a fair number of places that don't carry amiodarone for one reason or another, and there are some, not many but some, people with allergies to amiodarone.  If you have the patient that you decide does have afib with aberrancy but is truly stable, how would you treat them?



If:

(A)

(i) clearly irregular on presentation OR
(ii) vagals reveal underlying atrial fibrillation OR
(iii) adenosine response reveals underlying a.fib 

and

(B)

I'm sure that the patient is symptomatic due to the a.fib, and not due to another underlying pathology (which I would argue is going to be the case 95% of the time)

and

(C) I don't suspect WPW from history or ECG findings

and

(D) I'm not on the hospital's doorstep

and

(E) No COPD / severe CHF / hx of reactive airway disease 

Then _maybe_ 5mg metoprolol SIVP over 1-2 min q 5 min to a max of 15mg.  




> There is always the option of doing nothing and that might be the best course, or going directly to cardioversion, which has it's own risks (that are increased if it's afib).



I agree that it would be wise to avoid cardioversion in a.fib of unknown duration.  



> Take the OP's patient.  Say he has a normal BP, no complaints other than palpations, and you are 30 minutes from a hospital.  For arguements sake you decide this probably isn't vtach but afib.  You don't carry amiodarone.  What is your treatement plan?



No complaints other than palpitations?  Evaluate the 12-lead for evidence of ischemia or infarction.  Give a small fluid bolus providing there's no acute renal failure or major CHF issues, consider chatting with a doc regarding treatment options (we may hate medical consult as paramedics, but this is one of those situations where it's not a bad idea), and drive to the ER.  30 minutes isn't a long time.  Re-evaluate that decision if the patient condition changes.

If the patient becomes more symptomatic, then we can look at the other options, e.g. beta-blockers, CCBs, and such.  My expectation would be that a patient this stable wouldn't change significantly over the course of transport.  But of course they might.

[Now, you should take my opinion here for what it's worth, I haven't worked EMS in a couple of years, so it may not be worth much.]




> I'm not pointing fingers by any means, just honestly curious.



Hey, no problem.  This is just my opinion based on prior experience.  A couple of years ago it was supported by medical consult in the area I worked in.  I think we can probably agree that this is a grey area where clinical judgment has to be applied.

All the best.


----------



## systemet (Dec 12, 2011)

Smash said:


> I agree with that, merely pointing out that if one were to engage in what is ultimately an academic enterprise, the rhythm appears to rule in for VT using a couple of different algorithms.



Yep, not trying to argue with you in any way!


----------



## triemal04 (Dec 12, 2011)

systemet said:


> Maybe you're right.  I don't know.  It just seems very risky to me, given the repeated problems that even EM physicians have with misdiagnosing VT as SVT w/ aberrancy.
> Awesome!  I don't know for sure either.   I just think that it can be done, and done safely and treated appropriately by field based providers.  It would be safer to just ensure that everyone had amiodarone (or procainamide which seems to be making a comeback if you look at AHA), decide what the rhythm was, and then use a med that didn't have a big chance of causing problems if their interpretation was wrong.
> 
> As we've discussed here there's a lot of different evidence-based guidelines for distinguishing between VT and SVT w/ aberrancy.  These are used by cardiology and EM to differentiate the two.  But even then, it's tricky, and there's a certain error rate.
> ...


Sorry for the red, just easier.


----------

