# 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?


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## 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


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## 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...


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## 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.


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## 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:.


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## Shishkabob

maxwell said:


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









???


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## 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. 

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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.


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## 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


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## 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.


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## dmiracco

medic417 said:


> 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)


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## medic417

dmiracco said:


> 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.


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## Shishkabob

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


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## 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.


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## 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.


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## 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?


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## medic417

Smash said:


> 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.


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## medic417

emtbill said:


> 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.


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## TomB

medic417 said:


> 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.



medic417 said:


> 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.



medic417 said:


> 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.



medic417 said:


> 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.



medic417 said:


> 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.



medic417 said:


> 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.



medic417 said:


> 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.



medic417 said:


> 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.



medic417 said:


> 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?


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## TomB

medic417 said:


> 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).


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## TomB

emtbill said:


> 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!


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## medic417

TomB said:


> 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.
> 
> 
> 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.



The delay is deciding where to take them or even on not doing anything when you should do something.  

As to the research contact Bob Page at St Johns for that.

Yes you can still have VT w/o it showing but in most cases it is there.


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## boingo

Tom's point is that if they are sick, they get cardioversion, regardless of point of origin, if not, a "drug free" approach may be the safest for the patient.  Tom being a firefighter knows the drug box is bad!  Just kidding....

I'm not sure why a patient with VT would be taken to a seperate hospital than one with SVT, so don't know why the actual dx would factor into that.

One can mentally masturbate the nuances of VT v.s. SVT, however if ANY doubt, one must tx as VT until proven otherwise.  There are plenty of examples of EKG's meeting criteria, brugada's, Marriots, etc...that don't appear to be VT but in fact are.  First do no harm.


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## TomB

boingo said:


> Tom's point is that if they are sick, they get cardioversion, regardless of point of origin, if not, a "drug free" approach may be the safest for the patient.  Tom being a firefighter knows the drug box is bad!  Just kidding....
> 
> I'm not sure why a patient with VT would be taken to a seperate hospital than one with SVT, so don't know why the actual dx would factor into that.
> 
> One can mentally masturbate the nuances of VT v.s. SVT, however if ANY doubt, one must tx as VT until proven otherwise.  There are plenty of examples of EKG's meeting criteria, brugada's, Marriots, etc...that don't appear to be VT but in fact are.  First do no harm.



Hahaha! 

Mongo like drug box!


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## emtbill

None of the services I have ever worked at have carried cardizem for (what I suspect are) these very reasons (misdiagnosing wide complex as SVT). We have metoprolol for SVT's unresponsive to adenosine. What do the veterans here think about giving adenosine to a wide complex tachycardia that is suspected of being SVT (using whatever algorithm you choose)? If it's an aberrantly conducted reentrant SVT this should fix it, otherwise you may be able to see atrial fib or flutter waves. Adenosine should not make VT worse right? What about sedating and cardioverting every wide complex tachycardia to avoid having to give these cardiotoxins all together?

@medic417: I also took Page's seminar and learned the same criteria you mentioned. I don't know about in your class, but with mine he never once talked about SVT. He only talked about how to rule in VT. He also did not talk about therapy to consider when his VT criteria failed, suggesting SVT. Well...if memory serves I think he talked about a tachycardia that failed his criteria for VT, the medic gave adenosine, saw it was AF, then gave cardizem with successful conversion, but largely Page doesn't advocate giving CCB's to a wide complex tachycardia...maybe he's worried about being liable if a bunch of people start killing patients in VT with cardizem after taking his class .

@Tom: are you suggesting taking all stable patients with wide complex tachycardias to the ER and not giving drugs, or just the ones that might be in SVT, while still giving drugs to a suspected stable VT?


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## medic417

TomB said:


> 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).



If we have whats needed in the field to start treatment prior to transport patient benefits as ever second heart cells are dieing.  

Also note on 96% diagnostic of VT, in other words if my method shows VT odds are it is VT.  There are other methods that have proven much less reliable yet patients are being treated by them.


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## TomB

medic417 said:


> If we have whats needed in the field to start treatment prior to transport patient benefits as ever second heart cells are dieing.
> 
> Also note on 96% diagnostic of VT, in other words if my method shows VT odds are it is VT.  There are other methods that have proven much less reliable yet patients are being treated by them.



I wouldn't criticize you for giving 150 mg amiodarone over 10 minutes, but generally speaking, if the heart is experiencing demand side ischemia to the point of myocardial damage there will be symptoms like CP and SOB.


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## TomB

Billy -

I'm saying that a perfusing rhythm is a good thing. If you consider you Hs and Ts, correct hypoxia, acidosis, hypovolemia, electolyte derangement, and you make the reasoned clinical decision to try an indicated antiarrythmic, then go for it. Just realize it's a big responsibility and any antiarrythmic can be proarrhythmic. I just get nervous when I see discussion about using morphology to rule out VT. It's dangerous.

Tom


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## medic417

TomB said:


> Billy -
> 
> I'm saying that a perfusing rhythm is a good thing. If you consider you Hs and Ts, correct hypoxia, acidosis, hypovolemia, electolyte derangement, and you make the reasoned clinical decision to try an indicated antiarrythmic, then go for it. Just realize it's a big responsibility and any antiarrythmic can be proarrhythmic. I just get nervous when I see discussion about using morphology to rule out VT. It's dangerous.
> 
> Tom



Not rule out rule in.  If I said rule out I apologize.  Because if I rule it to be VT I will have treatment options that differ from SVT.  

*Since I may have confused someone let me clarify you can not rule out anything with an EKG alone.  *

I do feel it is important that we start treatment in the field rather than waiting for the hospital as there are often long delays there.  So an extra 5 minutes on scene getting treatment started may actually save 30 minutes or more of cardiac tissue when you factor in the waits at the ER.


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## Akulahawk

emtbill said:


> None of the services I have ever worked at have carried cardizem for (what I suspect are) these very reasons (misdiagnosing wide complex as SVT). We have metoprolol for SVT's unresponsive to adenosine. What do the veterans here think about giving adenosine to a wide complex tachycardia that is suspected of being SVT (using whatever algorithm you choose)? If it's an aberrantly conducted reentrant SVT this should fix it, otherwise you may be able to see atrial fib or flutter waves. Adenosine should not make VT worse right? What about sedating and cardioverting every wide complex tachycardia to avoid having to give these cardiotoxins all together?
> 
> @medic417: I also took Page's seminar and learned the same criteria you mentioned. I don't know about in your class, but with mine he never once talked about SVT. He only talked about how to rule in VT. He also did not talk about therapy to consider when his VT criteria failed, suggesting SVT. Well...if memory serves I think he talked about a tachycardia that failed his criteria for VT, the medic gave adenosine, saw it was AF, then gave cardizem with successful conversion, but largely Page doesn't advocate giving CCB's to a wide complex tachycardia...maybe he's worried about being liable if a bunch of people start killing patients in VT with cardizem after taking his class .
> 
> @Tom: are you suggesting taking all stable patients with wide complex tachycardias to the ER and not giving drugs, or just the ones that might be in SVT, while still giving drugs to a suspected stable VT?


Sacramento doesn't use adenosine, Cardizem, or metopralol for tachycardias. If they're stable, they get watched. If the patient becomes unstable, we sedate (if necessary) and Sync Cardiovert. For Wide Complex Tachycardias, regardless of etiology, after 4 shocks, we begin using Lidocaine. If they go into cardiac arrest, we switch protocols and treat that rhythm instead. 

Is this ideal? Not for most places. However, here, most of the time, if you've begun transport early, you're not likely to reach the end of the protocol before you reach the emergency room, unless you're starting from way out along the eastern or very southern portions of the County.

Other Counties I've worked in use adenosine, but for unstable tachycardias, they go straight to cardioversion. Consider this: if you're having to give amiodarne (Cordorone) over 10 minutes, chances are your patient is not exactly emergently unstable. Adenosine, if you have it handy, works. Cardizem and metopralol also work... but you've got a patient who's got pulses and isn't so unstable that you need to go straight to electrical therapy. 

Personally, I'd like to have the tools to use those other medications for chemical cardioversion... but that's not an option here.


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