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Survival EKG! Narrow Complex Tachycardias (Miguel Valderrábano, MD) — Transcript

by Houston Methodist DeBakey CV Education · 1,731 words · 260 segments · language en · Watch on YouTube

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0:00so next I think is the EKG session svt's
0:06you must be aware of the different kinds
0:08of SVT's av nodal reentrant a most
0:10common where the reentry is electricity
0:12spinning around the tissues surrounding
0:14the AV node as I will explain later
0:16later avrt
0:18a ventricular reentry that means there's
0:21an accessory pathway and the reentry
0:23mechanism involves an accessory pathway
0:26deliberating electricity either ortho
0:29trauma CLE from the atria to the
0:30ventricles and electricity goes back up
0:33through the accessory pathway and aunt
0:37atomically is where electricity goes
0:38down the accessory pathway and up the AV
0:40node a Tata acharya typically is
0:42automatic it of focus in it the eight in
0:45the eight or tissue firing electricity
0:47and then it conducts down to ventricles
0:49atrial flutter these are typically macro
0:51reentrant mechanisms around and the
0:54different structures of the of both the
0:57right item or the left atrium multifocal
0:59today acharya and it or fibrillation
1:01okay so when we talk about av nodal
1:04reentry it's really really in the
1:07tissues that surround the AV node the AV
1:09node we call the compact AV node this
1:12comma-shaped structure in the anterior
1:15aspect of the right atrium very close
1:20[Music]
1:24the AV node connects with HL tissues
1:27through two main pathways the fast
1:30pathway which is right on top of the and
1:34the slow pathway which are extensions of
1:37the gray neural tissue around the corner
1:39I'm sense between the tricuspid annulus
1:41and the core Exynos ostium there's a
1:43connection the rise of the with the AV
1:45node that becomes the slow pathway in
1:48normal sinus beats so keep in mind this
1:51is normal anatomy we all have this this
1:54is nothing nothing anomalous in some
1:58patients this constitute the substrate
2:00for reentry and again I don't know how
2:02the so what happens is that the fast
2:07pathway is not just fast it also has a
2:10longer refractory period and this low
2:13pathway is not only slower it also has a
2:16shorter refractory period we'd like this
2:18analogy which is mostly for the morning
2:20purposes distance compared to a slow
2:31boat just to remember that the fast
2:33pathway has a longer refractory period
2:35so if you have a PhD that tries to
2:37invade the fast pathway shortly after it
2:40has been activated chances are it will
2:42be refractory and that activation will
2:44may proceed through the slow pathway so
2:48this is normal sinus rhythm where
2:50collides where activations collide but
2:54then in a beam or all three entry well
2:57if if the fast pathway is refractory
2:58then the slow pathway conducts hangs
3:01around perpetuating mechanism of reentry
3:09is it truly AV nodal not really is is
3:13the perineural tissues around the
3:15complex AV node and this allows us to be
3:17able to cure this how do we cure this
3:25the slow pathway is anatomically in a
3:28distinct area separate from the fast
3:30pathway so when we burn it we take care
3:32of it how do we recognize it on the EKG
3:35well
3:36as you saw in the previous slide
3:38electricity when was going up the slow
3:40pathway then split one limb of the
3:42electricity went down the ventricles and
3:44activated the ventricles and in parallel
3:46electricity went up to the atrium so
3:48atria and ventricles activate at the
3:50same time that's why the piece and the
3:52key horses are superimposed to either
3:54see no piece this is the retrograde
4:00p-wave by comparing with the baseline
4:07sinus EKG if it's retrograde conduction
4:18it'll be midline in the atrium will be
4:21in the septum between the right atrium
4:22and the left atrium and it will go from
4:24low to high so it would be a negative P
4:26within two three and a VF and it would
4:27be narrow in two three and V 1 V 2 V 3
4:30because it's septal as opposed to a
4:34sinus P wave that goes first ready to
4:36man in the left atrium and it's wider
4:38the p-waves much wider than the
4:40retrograde P we give adenosine it stops
4:42because we block conduction in the in
4:45the April to India V neural tissue this
4:47is this illustrates that the avnrt
4:51depends on the AV node when you when you
4:53block conduction in the AV node without
4:55anything it'll stop adenosine block
4:57conduction in the AV node if the AV node
4:59is mechanistically involved with the
5:01tachycardia it will stop the tachycardia
5:02if it's not mechanistically involved it
5:05will unmask it if it's a tour flutter
5:07which doesn't care about the AV node you
5:09will see the flutter waves but avnrt
5:11will stop with adenosine provided you
5:13give enough and enough attention makes
5:15it to the AV node alright let's go to
5:17the next one so this is how we ablated
5:19we put
5:24we can record a hispano single next week
5:28hello in most patients at CC in some
5:32patients it gets tough because there's
5:33no pathway and the fast path we can be
5:35very close so there is a one two percent
5:37risk of AV block when we oblate this
5:40slow pathway so a VRT is a situation
5:53which is the Delta wave that has a
5:56signature on the EKG and when you get a
6:00piece that would be also trauma Cree
6:09entry auto go the opposite block in
6:12which case you will have a very wide QRS
6:15and you will have a retrograde
6:18conduction through the AV node back up
6:20to the acre so these are the two types
6:22ortho drumming like I said here so it's
6:37closer to the left bundle branch right
6:43[Music]
6:54so the Takara will become slower alright
6:58this is an important concept we not all
7:02the accessory pathway are equal
7:04obviously there's right side paths which
7:07are much more common easier to operate
7:09through the mitral annulus it's less
7:12mobile and the tricuspid annulus and
7:13these are the nomenclature you don't
7:17need to know about this but the idea is
7:19when you have pre excite-ation you have
7:29our way and when we go into into SVT
7:39next slide please
7:41the you will see that
7:50this bundle branch block but the QRS
7:58becomes narrower than in sinus rhythm
8:00that's consistent with orthodontic now
8:02we talked about the fact that depending
8:06on where it takes longer to complete
8:30that whole circuit so with aberrancy
8:38left-side accessory pathway will have
8:40slower technique area when the left
8:42bundle branch goes away he may become
8:45faster
8:46now that's something that it's not
8:49intuitive but you can see it in this EKG
8:57without any interruption okay whenever
9:00you see a wide Peggy Carter what compass
9:02take area becoming narrow without any
9:05interruptions that's SVT with aberrancy
9:07a definition it cannot be an AV slower
9:15when there is live bundle branch block
9:18so what is the diagnosis this is
9:20orthodontic av AV RT using a lip sorry
9:23to say pathway that will make you
9:31alright next light all right other forms
9:35of like a car EKG changes modulated by
9:41an accessory pathway this is an
9:42irregular rhythm that has varying
9:45degrees of QRS widths alright you have
9:48to think atrial fibrillation with an
9:49accessory pathway and and intermittent
9:52degrees of varying degrees of P
9:54excitation that will be in your boards
9:56they're more classic examples next this
10:00is um perhaps a more classic example
10:02wide complex tachycardia irregularly
10:05irregular with varying degrees of QRS
10:08width so bring the really excite agent
10:11this is a terrible a sham with an
10:13accessory pathway
10:14it'll be your board each of the Acharya
10:16again it's usually focal in mechanist
10:19mechanism and it doesn't care about
10:22every conduction all right so you will
10:24see that's an effective technique area
10:41when the PR interval and any conduction
10:43does not affect Acharya you have to
10:45think that AV conduction is irrelevant
10:47to it and that's most common in a
10:50totally Korea's next okay atrial flutter
10:53very common typical atrial flutter is
10:55caused by counterclockwise reentry in
10:58the tricuspid annulus as you can see
11:01here what is typical later flutter you
11:06will see the negative sawtooth waves in
11:08two three and AVF and mechanistically
11:12this is this is what's going on it
11:14typically happens in in normal hearts or
11:17perhaps hypertensive heart typically to
11:20a flutter is a close cousin of
11:22paroxysmal atrial fibrillation you see
11:24many patients that present with
11:25palpitations age in their mid-40s for
11:28years
11:29nothing happens nothing is picked up on
11:31monitor then one day they show up on
11:32flutter when you take care of those
11:36flutters many of those patients about
11:3760% over the next five years will show
11:39up with Parsees monitored fibrillation
11:41atrial flutter occurs whenever
11:43electricity organ whenever fibrillation
11:46organizes itself into this whenever one
11:49wave of electricity starts spinning
11:50around it
11:53for the next turn and it's like a dog
11:56chasing its own tail it's more likely to
11:59perpetuate itself than paroxysmal atrial
12:00fibrillation this is how it looks on the
12:04EKG you see and there are different
12:19variants they're reversed typical ATAR
12:21flutter where you have a clockwise
12:23reentry in the same anatomical substrate
12:26and then there are many a typical forms
12:28of atrial flutter that occur most
12:31commonly after ablation evader
12:34fibrillation and are typically left
12:36atrial macrorry in turn circuits the way
12:39we ablated I don't know if I have a
12:40movie of that of course when you give a
12:42Tennyson you unmasks the p-wave the far
12:46away's you do not treat you do not stop
12:49the atrial flutter then our scene is
12:51used primarily for diagnostic purposes
12:53when you cannot see the flutter waves
12:55typically when you have two to one AV
12:57conduction but it's hard to discern mask
13:06and mask the flutter waves please don't
13:09you don't need to do this more than once
13:10once you have a diagnosis you don't use
13:13adenosine for rate control and as I
13:16described later fara can occur after a
13:18few ablation that's unfortunately the
13:21more common scenario for us in ep and
13:23these are typically macro reentry's
13:25usually the roof dependent in the left
13:27atrium or pay my trough also in the left
13:30atrium multifocal atrial tachycardia
13:32occurs in the setting of hypoxia and
13:34usually lung disease and is define as an
13:38atrial tachycardia that does not has at
13:40least three different p-wave
13:42morphologies and not a single dominant
13:44one so you will see sinus and it occurs
13:52also in the context of digoxin toxicity
14:02you

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