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Am I seeing R' in V1 -V4?
 
I agree it looks like a narrow QRS, but the other criteria you list do not suggest a non-VT diagnosis. AV dissociation is only present about half the time with VT and is often difficult to appreciate. VT can show a normal axis, right axis deviation, or left axis deviation. Negative concordance favors VT, but an absence of concordance does not rule it out. Just clarifying because wide and fast is VT until proven otherwise! That's one of the most important rules of ECG interpretation.

Thanks for the clarification, but I thought VT almost always presents with an extreme right axis deviation? Anyway, good to know. Of course I would always treat wide and fast like VT. I'm very new to advanced 12 lead interpretation like I just tried to do.

What if it was aberrant SVT though and you gave lidocaine? Won't that make the situation worse if you gave lidocaine to a supraventricular dysrhythmia? Personally I would give amiodarone as the AHA recommends since it is also effective on supraventricular rhythms.

What if one incorrectly interprets a rhythm as supraventricular with aberrant conduction and decides to give adenosine when it is in fact of ventricular origin? On first thought I wouldn't think adenosine would make VT any worse since it works on the AV node and in VT the pacemaker is in the ventricles, but evidently I am wrong since it is always a major point to treat wide and fast like VT until proven otherwise.

What about giving adenosine to peds with wide complex tachycardia? In the PALS algorithm they advocate giving a trial of adenosine to apparent VT prior to cardioverion. I suppose aberrantly conducted SVT's are more common in peds than adults?
 
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What if it was aberrant SVT though and you gave lidocaine? Won't that make the situation worse if you gave lidocaine to a supraventricular dysrhythmia? Personally I would give amiodarone as the AHA recommends since it is also effective on supraventricular rhythms.

Ami is the drug of choice now for VT and Adenosine/Ami for SVT. For us here the alternative is Verapamil for SVT and Ami for VT. A bit nasty to give a VT Verapamil - a calcium channel blocker - kills off the pacemaker and asystole results. OOps!!! Lido (we use to use it) might drop BP but won't stop conduction through to the ventricles. Lesser of two potential evils.

Mechanical action is generated via the myocardium/ventricles via calcium -the VT pacemkaer site is the only thing producing output so lose your pacemaker and you get.... nothing.

Effects and side effects - the great balancing act.

MM
 
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Thanks for the clarification, but I thought VT almost always presents with an extreme right axis deviation? Anyway, good to know. Of course I would always treat wide and fast like VT. I'm very new to advanced 12 lead interpretation like I just tried to do.

VT usually has an other-than-extreme axis. The best way to get a feel of this is to start collecting 12 lead ECGs of arrhythmias, do a Google search, or check out the VT page at the ECGpedia.

What if it was aberrant SVT though and you gave lidocaine? Won't that make the situation worse if you gave lidocaine to a supraventricular dysrhythmia? Personally I would give amiodarone as the AHA recommends since it is also effective on supraventricular rhythms.

Lidocaine shouldn't hurt SVT and may even help. On the other hand, as someone else already mentioned, you can kill a patient by giving a CCB to VT. Think twice before giving antiarrhythmics to irregular or polymorphic wide complex tachycardias. Amiodarone could make Torsades or AF with WPW worse.

What if one incorrectly interprets a rhythm as supraventricular with aberrant conduction and decides to give adenosine when it is in fact of ventricular origin? On first thought I wouldn't think adenosine would make VT any worse since it works on the AV node and in VT the pacemaker is in the ventricles, but evidently I am wrong since it is always a major point to treat wide and fast like VT until proven otherwise.

Adenosine probably won't hurt a stable regular wide complex tachycardia with a rate < 250, but it's not indicated. It used to be part of the algorithm for wide complex tachycardia of unknown origin, but not anymore.

What about giving adenosine to peds with wide complex tachycardia? In the PALS algorithm they advocate giving a trial of adenosine to apparent VT prior to cardioverion. I suppose aberrantly conducted SVT's are more common in peds than adults?

Yes, I noticed that last time I took PALS.
 
Two words: Drive Faster.
It is very crowded with the patient, the tech, and the Grim Reaper.
 
What rhythm is that - conga or quickstep?

Venty where are you on this one? Theres been a few stabs but a few to many chickens as well. Come on troops we may have to treat a pt like this one day - somebody obviously had to before. For the guys infering this is a nasty looking rhythm please explain in a bit of detail. Some of us EKG fumblers need some pointers.

(all in good fun troops) I'm sure there are light bulb jokes about cardiologists and their respective multiple interpretations of rhythms like this one.

MM
 
Venty where are you on this one? Theres been a few stabs but a few to many chickens as well. Come on troops we may have to treat a pt like this one day - somebody obviously had to before. For the guys infering this is a nasty looking rhythm please explain in a bit of detail. Some of us EKG fumblers need some pointers.

Go back to your basics.
Activate Cath Lab, 2 large bore IVs, monitor vitals, ASA, nitro, Lopressor (if applicable) Morphine or Fentanyl, O2 via most appropiate device, and a healthy diesel bolus.

Also, if you draw labs, draw em up.
 
The rhythm, the rhythm

Go back to your basics.
Activate Cath Lab, 2 large bore IVs, monitor vitals, ASA, nitro, Lopressor (if applicable) Morphine or Fentanyl, O2 via most appropiate device, and a healthy diesel bolus.

Also, if you draw labs, draw em up.

I don't disagree with the basics though we don't know anything about the pt. For all we know this might be a paediatric.

Rather I was getting at analysis of the rhythm and an interpretation with explanation for all - that was the original premise of the post.

MM
 
If you want more evidence this is atrial flutter and not acute injury, take a pair of calipers and set it for whatever you think the QT interval is. Now place the calipers at the beginning of the QRS complex in each lead. Take leads V3 and V4 as examples. Now compare to leads III and V6. What could possibly account for such wild variations in the QT interval? The conclusion is that we're looking at flutter waves superimposed on T waves. The QT interval should be constant across all 12 leads.
 
I'm going with the RBBB with ischemia.

If you look at AVF and V5, there's definite flipped T waves. Depending on where you place the J point, you can rule out elevation in place of RSR' with flipped T's as well as depression in most leads.

Any thoughts?
 
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