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.
Chest pain, HR 190
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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):
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.
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.
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.
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.
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epipusher
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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.
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.
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.
(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.
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.]
(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
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What....what? :unsure:
Smash
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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
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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.
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.
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.
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.
I agree that it would be wise to avoid cardioversion in a.fib of unknown duration.
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.]
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.
Sorry for the red, just easier.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.
There is...but every decision we make has the possibility of being wrong; just need to do everything possible to reduce that possibility. I'll go beyond just saying "I think" and say that it can be done, but then the question still remains, would it be better for for the patient? Don't have a solid answer for that.
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.
Yeah. Like I said above, it would be better to have a med that would work for most tachyarrhythmias, though still having the option of using one that was more specific IF you were completely certain in your analysis. Amiodarone will work for most rhythms, but that doesn't make it the best choice.
I agree good oversight and med consult can help mitigate the risks.
Of course that's the rub though, so all this really would have to on a service by service basis.
Then maybe 5mg metoprolol SIVP over 1-2 min q 5 min to a max of 15mg.
Curious, why the beta-blocker instead of a calcium channel blocker? Preference, or did I miss something?
I agree that it would be wise to avoid cardioversion in a.fib of unknown duration.
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.]
Sounds fine so far. There it is again, just because we can do something, should we, and is it best for the patient? I know there's some ER's that would be pissed if you brought it a patient that they knew you could have treated, others that won't care, and others that will be happy about it. And I know that really, this all will come down to the individual provider and service. Most tachycardia's don't need truly emergent treatement; many patient's can sustain it. But, at a certain point it does become an issue that needs treatement.
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.
Absolutely. You'll get as much variation in the treatement that's done by different ER doc's as you will by different field providers. And, as long as what's being done is appropriate, and in the best interest of the patient...all good.
All the best.