SVT vs. V-tach

[hellofirstresponders]

Whats the difference? Why do we not make the pt bare down, and act like their going to take a dump? Like, why won't it work on v-tach but it does on SVT?

 

[triemal04]

Read up on the vagus nerve and how vagal manuevers work (physiologically). Follow that with where the stimuli for an SVT is coming from versus in vtach. If you still don't understand, then ask again.

And if you're really lazy this is a pretty brief overview but it'd help to learn more. http://medinfo.ufl.edu/~ekg/Rate and Rhythm.html

 

[Akulahawk]

The difference between SVT and VTach is all in the A&P of the heart... Vagal Stimulation only works on one of them... Once you understand the Physiology of normal cardiac conduction, how the Vagus Nerve affects that and where, and how SVT and VTach happen, it'll be a LOT clearer why these two conditions are treated differently.

It's good that you're asking this stuff. You'll be further ahead of the game than other EMTs and by asking the WHY behind the WHAT, you'll end up being a better EMT for it... especially when you learn the answers...

 

[el Murpharino]

VT - originates in the ventricles
SVT - originates in the atria

The right vagus nerve innervates the SA node, which too, is in the atria.

So oversimplified I feel horrible putting it this way.

 

[maxwell]

The reason we don't try vagal manuvers on pts in VT is ... well, VT is neither a rhythm triggered by vagal stimuli nor helped by the administration of vagolytics (VT is a rhythm of distal origin where SVT is a rhythm of proximal origin). I.e. we don't give atropine for VT (atropine is a vagolytic [...whence increasing the HR]). SVT *can* look like VT on an ECG (with aberrant conduction: A-Fib with weird pathways like LGL, WPW, etc h34r. Symptoms can be similar (AMS, CP, SOB), however, the treatment is different. SVT: most automatic tachycardias are AVNRT (like 80% or so) hence the tx is to break the re-entry cycle (or control the rate if it's just A-Flubber)....VT: there's an underlying pathology (the heart doesn't like VT and doesn't do it unless it has to)..so we should treat the K+ of 9.1, etc :deadhorse:.

 

[Shishkabob]

(or control the rate if it's just A-Flubber)

???

 

[Melclin]

Clearly you know you could look it up in a textbook but seeing as though you're asking here, I figure you want someone to explain it too you rather than refer you to a textbook with a emoticon sarcastic face so:

I'm no expert so everyone feel free to point out if I've gone wrong somewhere and please do so I don't end up sending people down the wrong path.

Hyrisk, I don't know where you're at in terms of learning so I'll just start from the start. I assume you understand the conduction of an impulse down through the heart at a basic level and the basic anatomy of the heart.

SVT just means any tachy that originates outside the ventricles so SVT can mean alot of things.

-SVT can originate in SA node (you could consider sinus tachy to be a form of SVT but clearly that would confuse matters, its more appropriate to call it sinus tach) but I believe there are other forms or more rare SVT that do originate in the SA node..

-SVT can originate in the atria (things like multifocal atrial tachy, a-fib, a-flutter, although people then tend to call these things by their specific names rather than referring to them as SVT, although this may change depending on where you are, it might be normal to call a-fib SVT in some places, who knows.)

-SVT can originate in the AV node/junction. When people refer to SVT they are typically talking about a type of SVT that originates here called junctional (supraventricular) tachycardia. So, as an impulse travels into the AV junction some of the pathways through the junction may not yet be ready to conduct it (for a number of reasons), while other pathways are. When the impulse gets to the end of the pathway it was able to travel along, it may then find that the pathway that wasn't ready for it before, now is ready so it travels back up the wrong way to the start of the junction. Here it finds the pathway it was on originally, ready to take it again and it just continues in that loop hence the name re-entry (this can happen in the atria as well- paroxysmal atrial tachycardia- to the same affect).

The problem is that each time it gets to the bottom of the AV junction and 're-enters' the junction through that other pathway, it also shoots off an impulse to the ventricles and because the loop is short, it happens very quickly, hence the tachycardia. I'm a little sketchy on some of the different types of re-entry and so on but I don't think its that important in this context.

----------------------------
When the vagus nerve is stimulated by one of those maneuvers you mentioned it dumps acetylecholine into the neuromuscular junction. This does two things. It lowers the inherent rate of the sinus node, but more importantly, it lowers the excitability of the AV node fibers.

Without explaining the idea of action potentials and refractory periods (which is something you may want to read up on to get all this properly. It has to do with why the fibers may or may not be ready to conduct an impulse), let us just say that lowering the excitability means that those pathways that were and weren't ready at the wrong times that were causing the problem, have their timing adjusted to stop, or discourage, that loop.
-----------------------------
VT originates entirely in the ventricles and while it can be due to a similar re-entry circuit as explained above, it isn't necessarily. However, it doesn't matter because the vagus nerve innervates very little of the ventricles, if any. Example:

So, in VT, the vagal maneuver still dumps acetylcholine into the top part of the heart, but not the ventricles, so it doesn't effect the the VT. Even in cases where SVT has caused VT, the problem has moved onto the ventricles out of the reach of the vagus nerve so it can't do anything stop the problem.

 

[dmiracco]

Down and dirty answer is that the vagus nerve does not intervate through the ventricles only the sympathetic system by way of the cardiac plexus

 

[medic417]

If it is VT many times they will have Extreme Right Axis Deviation ( ERAD leads I,II,III pointed down) combined with an upright V1. There are other indicators on a 12 lead that can prove VT as well.

 

[dmiracco]

If it is VT many times they will have Extreme Right Axis Deviation ( ERAD leads I,II,III pointed down) combined with an upright V1. There are other indicators on a 12 lead that can prove VT as well.

Exactly, extreme right axis deviation, aka no mans land, and concordance in the V leads is also key to determine VTB)

 

[medic417]

Exactly, extreme right axis deviation, aka no mans land, and concordance in the V leads is also key to determine VTB)

And don't forget that to get accurate axis you must place limb leads on the limbs.

 

[Shishkabob]

-90 to -180 on the EKG for people who want to know ^_^

 

[TomB]

Be careful when using this criterion. Most cases of VT do not present with extreme axis deviation. In other words, by no means does the absence of an extreme axis deviation imply a supraventricular origin of a wide complex tachycardia. The default dx should always be VT for a wide complex tachycardia, and I would be very cautious using morphology as evidence that a tachycardia is SVT. Ruling in VT is fine, but failure to rule in VT does not rule it out, and that point cannot be overemphasized, especially if you're considering a calcium channel blocker.

 

[Smash]

The Brothers Brugada (and their cousin I think) developed a 4 step criteria (Brugada! We're not just a Syndrome anymore!) for discerning whether a rhythm is VT or SVT with aberrant conduction.

However, as TomB rightly points out, it is really largely irrelevant to a prehospital provider; any wide complex tachycardia should be considered VT and treated accordingly.

 

[emtbill]

On drug therapy for VT vs. SVT...

I understand that lidocaine is a sodium channel blocker, which decreases the action potential of the myocardium, which makes it less likely impulses from the pacemaker in the ventricles will be transmitted to the myocardium to depolarize, but I don't know why this would be counterproductive in a supraventricular tachycardia, even though I know lidocaine is not indicated in these arrhythmias. I have always been taught that lidocaine suppresses the AV node, and if the patient is in a-fib or a-flutter, the hundreds of impulses per minute from the atria, now unchecked by the AV node, will likely cause the ventricles to fibrillate. This is why it is important to be able to read aberrant a-fib on the 12 lead right? Why can lidocaine cause this to happen then if its action is to inhibit the ion movement that caries the impulses responsible for myocardium depolarization? Why is this (evidently) less dangerous than a CCB for VT, and why is a CCB for VT more dangerous?

 

[medic417]

The Brothers Brugada (and their cousin I think) developed a 4 step criteria (Brugada! We're not just a Syndrome anymore!) for discerning whether a rhythm is VT or SVT with aberrant conduction.

However, as TomB rightly points out, it is really largely irrelevant to a prehospital provider; any wide complex tachycardia should be considered VT and treated accordingly.

I disagree. Improper diagnosis in the field could delay the care they need. You need to learn all steps involved. I listed one thing to check already. I check others as well and it takes me just about 3 seconds total after I take the 12 lead.

The 12 lead is 96% diagnostic for VT identification.

So patient has HR 150+. 12 lead with limb leads on limbs not torso. If any step shows VT no need to go to next step.

Step 1 ERAD(described above in my post) and upright V1

Step 2 Is lead V1 shaped as a fireman's hat, single upright steeple, or two peaks with the first taller ( big mountain little mountain )

Step 3 V1 downward and either flat R wider than 40ms or slurred or notched initial down stroke.

Step 4 V6 Any negative deflection.

Always go in order.

 

[medic417]

On drug therapy for VT vs. SVT...

I understand that lidocaine is a sodium channel blocker, which decreases the action potential of the myocardium, which makes it less likely impulses from the pacemaker in the ventricles will be transmitted to the myocardium to depolarize, but I don't know why this would be counterproductive in a supraventricular tachycardia, even though I know lidocaine is not indicated in these arrhythmias. I have always been taught that lidocaine suppresses the AV node, and if the patient is in a-fib or a-flutter, the hundreds of impulses per minute from the atria, now unchecked by the AV node, will likely cause the ventricles to fibrillate. This is why it is important to be able to read aberrant a-fib on the 12 lead right? Why can lidocaine cause this to happen then if its action is to inhibit the ion movement that caries the impulses responsible for myocardium depolarization? Why is this (evidently) less dangerous than a CCB for VT, and why is a CCB for VT more dangerous?

If not sure if VT or SVT better to use adenisone to find underlying rhythm than to kill them with lidocaine.

 

[TomB]

I disagree. Improper diagnosis in the field could delay the care they need.

Why should it delay the patient's care? For unstable patient, the therapy is identical. If the patient is hemodynamically stable, then I would rather the treating paramedic show restraint. A delay in care is far superior to a clinical misadventure -- the kind the patient suffers when VT is misclassified as SVT with aberrant conduction.

You need to learn all steps involved. I listed one thing to check already. I check others as well and it takes me just about 3 seconds total after I take the 12 lead.

Let's look at them one by one.

The 12 lead is 96% diagnostic for VT identification.

I'd like to see you back that up with peer reviewed literature. Even if it were true (which I doubt) the failure to rule in VT does not rule out VT, and that is the pointed issue.

So patient has HR 150+. 12 lead with limb leads on limbs not torso. If any step shows VT no need to go to next step.

Noted.

Step 1 ERAD(described above in my post) and upright V1

For the record, bifascicular block RBBB/LPFB sometimes presents with RBBB morphology in lead V1 and extreme right axis deviation. But what does it matter? VT should be your default diagnosis anyway. Misclassifying SVT as VT is not nearly as dangerous as misclassifying VT as SVT. Regardless, in Wellens' series, left axis deviation was the most frequently occurring axis deviation for VT regardless of polarity in lead V1.

Step 2 Is lead V1 shaped as a fireman's hat, single upright steeple, or two peaks with the first taller ( big mountain little mountain )

In Wellens' series, only 4 of 93 patients had this finding, but all 4 were experiencing VT. In other words, very low sensitivity but high specificity (in a small case series). On the other hand, of the 30 patients with an rR' complex in lead V1, 19 were experiencing SVT with aberrent conduction and 11 were experiencing VT. What's the message? Failure to rule in VT does not rule out VT.

Step 3 V1 downward and either flat R wider than 40ms or slurred or notched initial down stroke.

In a LBBB type wide complex tachycardia with a rS complex in lead V1, it's true that a slurred upstroke of the R wave favors VT. But that should be your default diagnosis anyway. Don't suppose that in the absence of this finding you're dealing with SVT. That's how patients get killed.

Step 4 V6 Any negative deflection.

An S wave in lead V6 is a normal variant for LBBB, especially for patients with coexisting RVH, but again, I have no quarrel with ruling in VT.

Always go in order.

Okay, so you've listed some criteria that help shore up the dx of VT. The question is, what do you do when these criteria are absent?

For example:

Extreme axis? No.
Lead V1 is not upright so next criterion does not apply.
Lead V1 shows LBBB morphology, but it's a QS complex, so no R wave and criterion does not apply.
Upright QRS complex in lead V6.

Conclusion?

 

[TomB]

If not sure if VT or SVT better to use adenisone to find underlying rhythm than to kill them with lidocaine.

Better to leave the drugs in the drug box altogether! Having said that, lidocaine and adenosine used to both be a part of the "wide complex tachycardia of uncertain etiology" algorithm in the AHA ECC guidelines. There are much worse drugs you could try (a calcium channel blocker for example). However, none of these drugs are currently indicated. What's the rush? If it's unstable, cardiovert. If it's stable, consider capturing a 12 lead ECG, starting an IV, providing supportive care, and taking the patient to the hospital, especially if there's anything particularly disturbing about it (irregular, polymorphic, or extremely fast rate).

 

[TomB]

On drug therapy for VT vs. SVT...

I understand that lidocaine is a sodium channel blocker, which decreases the action potential of the myocardium, which makes it less likely impulses from the pacemaker in the ventricles will be transmitted to the myocardium to depolarize, but I don't know why this would be counterproductive in a supraventricular tachycardia, even though I know lidocaine is not indicated in these arrhythmias. I have always been taught that lidocaine suppresses the AV node, and if the patient is in a-fib or a-flutter, the hundreds of impulses per minute from the atria, now unchecked by the AV node, will likely cause the ventricles to fibrillate. This is why it is important to be able to read aberrant a-fib on the 12 lead right? Why can lidocaine cause this to happen then if its action is to inhibit the ion movement that caries the impulses responsible for myocardium depolarization? Why is this (evidently) less dangerous than a CCB for VT, and why is a CCB for VT more dangerous?

Interesting question, emtbill! I'm not sure what the answer is, but I like the question!