Case discussion, EKG

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Noyac

Noyac

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This was my Pt today. 21 yo male reportedly healthy. Vague history of anxiety, SOB, syncope. Punched a wall which unfortunately had a 2X4 stud just behind it. Dumb*ss!
Booked for a 4th and 5th MC ORIF (Boxers fx).
This is the EKG strip on my monitor when I hooked him up.
What is it?
What’s your plan?
 
I assume you are concerned about WPW/delta wave...but was this on the monitor only or also on 12-lead EKG?

HH
 
12 lead ekg confirmation
Would get cards to see pt re long term follow up
But given open fx wound they will probably only have time to give recs..

Crash cart in room
Lidocaine, adenosine available
Bblocker if HR and BP tolerates
Avoid excess sympathetic activity that can trigger dysrhythmia.

Versed premed
Consider regional (scb?) but GA should be ok

Have art line equipment available, but wouldnt necessarily put one in unless pt had runs
 
eikenhein said:
12 lead ekg confirmation
Would get cards to see pt re long term follow up
But given open fx wound they will probably only have time to give recs..

Crash cart in room
Lidocaine, adenosine available
Bblocker if HR and BP tolerates
Avoid excess sympathetic activity that can trigger dysrhythmia.

Versed premed
Consider regional (scb?) but GA should be ok

Have art line equipment available, but wouldnt necessarily put one in unless pt had runs
Click to expand...

Small point: Adenosine and beta blocker ok for wpw with re-entry tachycardia, but not for wpw with a fib.
 
ahh thats right we learn about procainamde and amiodarone for wpw for rx

BB and adenosine in WPW w Afib promotes electrical activity through aberrant tract by preferentially blocking AV node conduction.
not sure if it leads to vfib, but i think makes arrhythmia worse
 
Yes, when a fib present in WPW or other reentrant phenomenon then
eikenhein said:
ahh thats right we learn about procainamde and amiodarone for wpw for rx

BB and adenosine in WPW w Afib promotes electrical activity through aberrant tract by preferentially blocking AV node conduction.
not sure if it leads to vfib, but i think makes arrhythmia worse
Click to expand...
 
Because you have an accessory pathway as an additional connection between the atria and ventricle. Adenosine bblocker calcium channel blocker works on the av node to slow conduction but if you have atrial activity going at 200, it will all get transmitted to the ventricles regardless through the accessory pathway. The history of syncope tells you this is likely the case. You need meds that work on the ventricle like class 1a 1c 3
 
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So it sounds like most people would proceed with the case. Is that the general consensus?
 
do the case, sounds like it can't really wait that long anyways, be prepared to deal with consequences if they arise
pt should know his risk is increased from this presumptive diagnosis of WPW
should definitely get cards followup
 
dhb said:
I'd do a strait regional and have cards evaluate him.
Click to expand...

so you'd inject a bunch of local anesthetic that can cause arrythmias in large doses?

caligas said:
Agree. These folks drop dead when we are NOT around, not when we are there watching every heartbeat with a defibrillator locked and loaded.
Click to expand...

The incidence of sudden cardiac death from WPW is extremely low. The overwhelming majority would never drop dead from it at any point even if untreated.
 
Pretty easy case for you studs and studettes.
Now let’s say the Pt has a run of stable SVT WITHOUT A FIB. What’s your first intervention? Second?
Does this change depending on if the Pt is asleep or not?
 
dhb said:
No just 5-10cc will do thank you (never put epi in my blocks)
But then we Europeans like a little finesse
Click to expand...
I think it would be totally reasonable to do a lidocaine (or mepivicaine) block without epi at 5-10cc. I’d do the axillary approach but could see a SCB or ICB working as well. I like the ability of seeing the three branches when doing the axillary though.
 
Noyac said:
I think it would be totally reasonable to do a lidocaine (or mepivicaine) block without epi at 5-10cc. I’d do the axillary approach but could see a SCB or ICB working as well. I like the ability of seeing the three branches when doing the axillary though.
Click to expand...

You can see all 3 on a ICB too. :prof:
 
Noyac said:
Pretty easy case for you studs and studettes.
Now let’s say the Pt has a run of stable SVT WITHOUT A FIB. What’s your first intervention? Second?
Does this change depending on if the Pt is asleep or not?
Click to expand...

*I am attempting to answer this with 0 actual experience of the described situation.
And thank you for contributing this to our learning.

Hemodynamically stable:
Awake: ask what the pt does to make the jitters go away when they're having them -> AGGRESSIVE vagal maneuvers -> esmolol 30mg -> consult EP, adenosine/zoll pads ready
Asleep: try carotid massage -> esmolol 30mg -> connsult EP, adenosine/zoll pads ready

Hemodynamically stable a fib:
Awake: flecainide PO 200mg, consult EP
Asleep: procainamide 100mg IV, consult EP

Hemodynamically unstable:
Awake/asleep: call code blue, crash cart, procainamide 100mg push q 1 min for 2-3 mins while they getting the machine -> adenosine/zoll pads -> synchronized cardioversion@ 120 joulse biphasic

Now i've typed this out, i'm questioning why i don't just give everyone with WPW flecainide/procainamide anyways and skip the beta blockade... (prob due to my comfort of having used esmolol and adenosine before)
 
Last edited:
dchz said:
*I am attempting to answer this with 0 actual experience of the described situation.
And thank you for contributing this to our learning.

Hemodynamically stable:
Awake: ask what the pt does to make the jitters go away when they're having them -> AGGRESSIVE vagal maneuvers -> esmolol 30mg -> consult EP, adenosine/zoll pads ready
Asleep: try carotid massage -> esmolol 30mg -> connsult EP, adenosine/zoll pads ready

Hemodynamically stable a fib:
Awake: flecainide PO 200mg, consult EP
Asleep: procainamide 100mg IV, consult EP

Hemodynamically unstable:
Awake/asleep: call code blue, crash cart, procainamide 100mg push q 1 min for 2-3 mins while they getting the machine -> adenosine/zoll pads -> synchronized cardioversion@ 120 joulse biphasic

Now i've typed this out, i'm questioning why i don't just give everyone with WPW flecainide/procainamide anyways and skip the beta blockade... (prob due to my comfort of having used esmolol and adenosine before)
Click to expand...
What's in the carts? I know for sure we don't have flecainide or procainamide stocked in our anes carts but we do have adenosine and esmolol.
 
MirrorTodd said:
What's in the carts? I know for sure we don't have flecainide or procainamide stocked in our anes carts but we do have adenosine and esmolol.
Click to expand...

Usually pharmacy has a bigger cart that comes to our code blue. And also if they are stable i have time to get procainamide/flecainide...
 
SaltyDog said:
You can see all 3 on a ICB too. :prof:
Click to expand...
I knew someone would say that but i find it extremely easy to pinpoint the one I’m looking to block from the axillary approach. I don’t doubt that it’s doable from the ICB but I’m better at the axillary when focusing on one nerve. Also, the ICB is so easy that I have only used US on that block once. So I’m less familiar with focusing on one nerve here.
 
dchz said:
*I am attempting to answer this with 0 actual experience of the described situation.
And thank you for contributing this to our learning.

Hemodynamically stable:
Awake: ask what the pt does to make the jitters go away when they're having them -> AGGRESSIVE vagal maneuvers -> esmolol 30mg -> consult EP, adenosine/zoll pads ready
Asleep: try carotid massage -> esmolol 30mg -> connsult EP, adenosine/zoll pads ready

Hemodynamically stable a fib:
Awake: flecainide PO 200mg, consult EP
Asleep: procainamide 100mg IV, consult EP

Hemodynamically unstable:
Awake/asleep: call code blue, crash cart, procainamide 100mg push q 1 min for 2-3 mins while they getting the machine -> adenosine/zoll pads -> synchronized cardioversion@ 120 joulse biphasic

Now i've typed this out, i'm questioning why i don't just give everyone with WPW flecainide/procainamide anyways and skip the beta blockade... (prob due to my comfort of having used esmolol and adenosine before)
Click to expand...
I’ll admit that while I proceeded with the case I had to look up exactly what I would do in various situations. A lot of scenarios recommended synchronized cardioversion. Adenosine seemed to be my first line drug for SVT followed by cardioversion. I have never given flecanide or procainamide in the OR. JUST SAYING.
 
Noyac said:
I’ll admit that while I proceeded with the case I had to look up exactly what I would do in various situations. A lot of scenarios recommended synchronized cardioversion. Adenosine seemed to be my first line drug for SVT followed by cardioversion. I have never given flecanide or procainamide in the OR. JUST SAYING.
Click to expand...

I was close to giving flecanide once in a 19 year old G1P0 with ebstein's and reentrant pathway. But she said cold water slowed her heart rate... That was the first and only time vagal maneuvers ever worked in my life...

I think another issue is that it is hard to see P waves when the HR is >140. Since we have mentioned many times that A Fib and SVT should be treated differently. One of the tricks I have is to slow down the strip rate on the EKG monitors. Then you can actually see P waves when the QRS is not so close together.
 
dchz said:
I was close to giving flecanide once in a 19 year old G1P0 with ebstein's and reentrant pathway. But she said cold water slowed her heart rate... That was the first and only time vagal maneuvers ever worked in my life...

I think another issue is that it is hard to see P waves when the HR is >140. Since we have mentioned many times that A Fib and SVT should be treated differently. One of the tricks I have is to slow down the strip rate on the EKG monitors. Then you can actually see P waves when the QRS is not so close together.
Click to expand...
I need to find the manual for the monitors cause there are apparently a great many things one can do aside from the basic stuff.
 
dchz said:
I was close to giving flecanide once in a 19 year old G1P0 with ebstein's and reentrant pathway. But she said cold water slowed her heart rate... That was the first and only time vagal maneuvers ever worked in my life...

I think another issue is that it is hard to see P waves when the HR is >140. Since we have mentioned many times that A Fib and SVT should be treated differently. One of the tricks I have is to slow down the strip rate on the EKG monitors. Then you can actually see P waves when the QRS is not so close together.
Click to expand...
I'll have to learn how to do this.
 
i never thought that the recommendation to avoid adenosine in pre-excited atrial fibrillation made sense with the explanation given.
Don't block the slow pathway so that the impulse travels down the fast pathway? If the bypass tract truly has significantly less decremental conduction physiology (this is very variable among bypass tracts) then the ventricular response should already be very rapid and unstable, regardless of what you've done to the AV node, because the impulses should be exciting the ventricles over the bypass tract preferentially. I believe that if the ventricular response is not super rapid, then blocking the AV node isn't going to make it even more rapid. When a WPW patient develops an SVT with a very RVR, i think you should just light em up and kill that rhythm asap. very rapid RVR is a risk for v fib or v tach.
 
I think the idea is that the conduction pathway preferentially goes through the av node so that if you block that then it is more likely to go to the accessory pathway. If you already have a rapid and unstable ventricular response then giving adenosine is not really going to change anything but doesn't help.
 
Psai said:
Just get a bucket, put some cold water in it and then overturn it unto the patients visage
Click to expand...
Excellent, thank you. Now I just have to figure out how to do that stuff with my monitor.
 
Noyac said:
Also, the ICB is so easy that I have only used US on that block once.
Click to expand...

What's your technique for a blind/nerve stem ICB. I know this block was around long before the advent of U/S. Of all the blocks we do, the ICB is the one I can't imagine doing without U/S. The cords hug the vessels with the medial cord sandwiched between the artery and vein, and the posterior cord right behind the artery. Is it a transarterial approach like an old school ax block? Maybe you aren't doing the block where I'm doing the block?? I'm honestly really curious.
 
SaltyDog said:
What's your technique for a blind/nerve stem ICB. I know this block was around long before the advent of U/S. Of all the blocks we do, the ICB is the one I can't imagine doing without U/S. The cords hug the vessels with the medial cord sandwiched between the artery and vein, and the posterior cord right behind the artery. Is it a transarterial approach like an old school ax block? Maybe you aren't doing the block where I'm doing the block?? I'm honestly really curious.
Click to expand...
I palpate the coracoid process and from there drop down 2cm and then 2cm medically. From here it is a straight shot about 2-4cm deep. Super easy.
 
Psai said:
I think the idea is that the conduction pathway preferentially goes through the av node so that if you block that then it is more likely to go to the accessory pathway. If you already have a rapid and unstable ventricular response then giving adenosine is not really going to change anything but doesn't help.
Click to expand...
This is how I understand it as well.
 
Noyac said:
I palpate the coracoid process and from there drop down 2cm and then 2cm medically. From here it is a straight shot about 2-4cm deep. Super easy.
Click to expand...

I would actually really like to come watch you do blocks the old fashioned way. You ever do any medical mission trips? Would be a cool opportunity to learn/do/practice this stuff.
 
Late to the party.
Great discussion regarding WPW.
 
Psai said:
I think the idea is that the conduction pathway preferentially goes through the av node so that if you block that then it is more likely to go to the accessory pathway. If you already have a rapid and unstable ventricular response then giving adenosine is not really going to change anything but doesn't help.
Click to expand...

Ok but the diffuse electrical rotors and wavelets that sustain AF should be exciting both the accessory pathway and the AV node with the same frequency. The reason conduction is usually down the AV node is that in most cases the AV node is actually the pathway with the smallest refractory period, not the bypass tract. If its a fib with diffuse impulses, and not an ectopic or re-entrant SVT, then whichever pathway is least refractory determines the ventricular rate. So blocking the AV node will either slow the ventricular response (preferential AV conduction) or do nothing (preferential bypass tract conduction).

Is this reality? I don't actually know. But it doesn't make sense, thats for sure.
 
SaltyDog said:
I would actually really like to come watch you do blocks the old fashioned way. You ever do any medical mission trips? Would be a cool opportunity to learn/do/practice this stuff.
Click to expand...
Interested, but haven’t done any trips.
 
The av node will be refractory to most of the a fib impulses as it is so blocking the av node will either cause preferential bypass tract conduction (increase likelihood of excessive ventricular rate) or already be going down the bypass tract (doing nothing positive but maintaining excessive ventricular rate leading to v fib and death)
 
Noyac said:
I palpate the coracoid process and from there drop down 2cm and then 2cm medically. From here it is a straight shot about 2-4cm deep. Super easy.
Click to expand...

how are you able to palpate the coracoid process in your patients. even a moderately fat person, its hard to feel anything ?

what are your go to vagal maneuvers for awake patient?
 
I think one of the issues with blocking the AV node and preferentially allowing conduction down the accessory pathway is that the electrical impulses down the accessory pathway are much more disorganized as they spread around the ventricles. This leads to the development of vfib. When the impulse from the atrium to the ventricle goes through the AV node, the impulse is propagated through the ventricle in a much more organized fashion via the Purkinje fibers.
 
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