Okay, so today we're going to be going over av blocks. As always,
a big thank you to everybody who's supported the channel all of the really
nice comments. I truly do appreciate it, so thank you so much.
And also a big thank you to today's sponsor of the podcast, True Learn.
All Right, So, av blocks they are a super high old topic.
They always come up on exams. If you're going to get a dysrhythmi
a question, very good chance it's going to be on AV blocks. So
I wanted to dedicate a podcast going over all of the high old info you
need to know, as well as sharing some new monics for this topic.
Before we begin, I want to go over some key concepts, some basic
foundation you need to have an understanding to better understand AV block. So let's
first quickly review the normal electrical conduction system of the heart, because, like
most things in medicine, identifying abnormalities requires a solid understanding of what constitutes normal.
So normal electrical activity of the heart. It's like this long road and
there's checkpoints along the road. The very beginning of this journey starts at the
say node, which is located in the right atrium. The essay node sends
an electrical signal through the walls of the atrium, causing them to contract,
and then it hits its first checkpoint on the road, the AV node,
which is very important for today's topic. So the signal stops here very briefly
to allow the ventricles time to fill, and then proceeds down into the lower
chamber of the heart through the bundle of hiss. The signal then travels into
the left and right bundle branches, and then finally into the perkine fibers,
which transmit the electricity to the ventricles, causing them to contract. If you
ever need help remembering this pathway, just remember the sentence send a big bounding
pulse, Send a big bounding pulse. The letters are SABBP S stands for
s A node, A stands for AV node, B stands for bundle of
his second B stands for bundle branches, and the P stands for perkine fibers.
So that's the past pathway you need to know now. In an ECG,
the area you need to be very familiar with for AV blocks is something
known as the pr interval. The pr interval is a measurement of the time
it takes the electrical impulse to travel through the atria across the AV node to
the ventricles, so part of that measurement includes that delay at the AV node.
That first little checkpoint we discussed before on your ECG, your pr interval
is a point measured from the beginning of the P wave to the beginning of
the QRS complex. Now, a normal pr interval, this is really important,
is between one hundred and twenty to two hundred milliseconds. Two hundred milliseconds
is five little boxes on an ECG or one large box. Anything larger than
that we got an issue, likely an AV block, which we'll be talking
about today. All right, So those are the basic concepts you need to
understand before we get started. Now, AV blocks are broken down into a
few subtypes. Will go over today. You have a first degree AV block,
a second degree AV block, which is further classified into a Mobitz type
one aka Wanki block, and a Mobitz type two. And then finally we
have a third degree block or a complete AV block, which it's also known
as So let's break each of them down talk about everything you need to know,
and let's first start with our first degree AV block, So a first
degree av is a cardiac condition characterized by abnormally slow electrical conduction from the atrium
to the ventricles. So first degree block, it's not really a block per
se as every impulse is still getting through to the ventricles. It's just getting
there really slowly. It's taking its time, so more of a traffic type
situation rather than the road being completely shut down in this case. So we
have slow conduction through the heart, most commonly occurring at the AV node,
although it can affect the hisper kinjee system as well. So why is this
happening? Let's talk about some etiologies. So the first thing I want you
to be aware of is this can be a normal finding, especially in athletes
that have a slow resting heart rate. So those really well trained athletes who
have a heart rate of like forty beats per minute, they can have a
first degree AV block without any structural abnormalities of the heart. So a first
degree AV block can be normal. But what about the abnormal stuff? So
in all types of AV blocks, medications can be to blame. There's a
number of medications that can cause an AV block. Essentially any drug that impairs
or slows. A v noodal conduction can cause a first degree heart block.
The ones you need to know your AV noodal blocking drugs include dijoxin, beta
blockers, some calcium channel blockers specifically, your non dihydroperioding agents like for Wrappamil
or deltai zem. They can all cause av blocks, so on your exam
if they ask you what the underlying cause may be, make sure you're looking
for one of these meds. And if you need an easy way to remember
the common A V noodal blocking drugs, you can remember ABCD, ABCD your
main A v noodal blocking drugs start with A, B, C or D.
A standing for adenasine, B standing for beta blockers, C standing for
calcium channel blockers, your non dihydropiodin specifically, and then finally D for dijoxin.
That's an easy way to remember the ones that you need to know for
the exam. Myocarditis is another potential cause, and while there's many causes of
myocarditis, viral illness, etc. For the exam, you absolutely have to
remember lime disease. Lime disease can lead to AV blocks and the people who
make exam questions they just love to ask about this. So in patients with
limecarditis, the degree of AV block can actually fluctuate pretty quickly. You can
start with the first degree AV block, but it can quickly progress to second
degree or even a complete AV block a third degree block. Main takeaway though,
if there's a harp block in the question, make sure you're looking for
lime disease and the answer choices. And then another one is myocardial infarction.
This is another potential cause, often an inferior wall am I, as the
a V node and the inferior wall are both fed by the right coronary artery.
There's, of course, plenty of other causes infiltrated and dilated cardiomyopathies like
sarcoidosis, certain muscular dystrophees leve disease. But for the exam, focus on
your meds, your beta blockers, calcium channel blockers, etc. Lime disease,
m I, and your normal variant, as those are the ones most
likely to come up. All right, what about clinical manifestations next? The
main thing you need to know for clinical manifestations is asymptomatic. Asymptomatic is what
you need to know because patients with first degree AV block are generally going to
be asymptomatic. It's not impossible to have some nonspecific symptoms such as dizziness,
fatigue, etc. But overall, most patients with the first degree block are
not going to present with any symptoms at all. Let's talk about diagnosis next.
This is obviously very important for all AV blocks. So you diagnose your
AV blocks with an ECG. Your first ree AV block is going to be
diagnosed with an ECG. Now what are you looking for on the ECG.
Well, we know a first degree AV block is caused by delayed conduction from
the atria to the ventricles, So knowing that where on ECG should we be
looking to calculate this delay. While, as we discussed before, you determine
that delay by looking at the pr interval, which measures the time it takes
the electrical impulse to travel through the atria across the AV node to the ventricles.
And as we know, the normal amount of time for this to take
place should be a max of two hundred milliseconds or one large box. When
the first degree AV block, there's a traffic jam and while the signals still
getting through the ventricles, taking a lot longer than it's supposed to, and
this leads to a prolonged pr interval, specifically a pr interval over two hundred
milliseconds. That's all you need to know for a first degree block, pr
interval over two hundred milliseconds, more than one big box. It's nice and
simple. And the key which will be different from all other AV blocks,
which we'll talk about next, is the conducted impulse. It's always going to
get through to the ventricles, all of that electricity it's still getting through,
which means there's always going to be a QRS complex following that P wave.
Even though the pr interval is prolonged, it's always going to be followed by
a QRS complex, it's just taking longer to get there. So again,
ECG diagnosis is made with a pr interval over two hundred milliseconds. So there's
a lot of mnemonics for HART blocks, a lot of ways to remember these,
and for a first degree block, you remember the ECG findings by remembering
the rhyme. If the R is far from the P, then you have
a first degree. If the R is far from the P, then you
have a first degree. That wideen pr interval over two hundred milliseconds. All
right, let's talk about treatment next. So we do an ECG. We
see the patient has a first degree block. How are we going to treat
this? Do we even need to treat this? Most of the time the
answer is no, but it does depend on a couple of factors, mainly
related to whether or not they're symptomatic and treatment for a first degree block,
it's pretty simple. You really just have two options. You either do nothing
or you give them a pacemaker. So if they're asymptomatic, you're just going
to observe. They don't require any treatment. Obviously, if there's an underlying
cause like a medication that can be discontinued or another underlying treatable cause that should
be addressed. But otherwise, asymptomatic doesn't require any intervention. And then there's
some rare cases that will get a pacemaker. So a patient with a y
q r S complex in conjunction with prolongation of the pr interval, patients with
something known as pseudo pacemaker syndrome. I don't think you should memorize any of
that. Just remember most patients with the first degree av block just observed pacemaker
only in some rare cases. All right, quick recap of a first gree
Hart block. This is a cardiac condition characterized by slow conduction from the atrim
to the ventricles. All the beats are getting through, They're just taking their
damn time. It can be a normal finding, especially in a well trained
athlete with a slow heart rate. Most patients are going to be asymptomatic diagnosed
with ECG pr interval over two hundred milliseconds. Most of the time you'll just
observe pacemaker only in some rare cases. That's the first Threehart block. Moving
on to our second degree AV block. Remember this is broken into two subtypes,
Mobitz type one and Mobitz type two. Let's start with Mobitz type one
aka Winkiebock, named after the Dutch physician Carl Frederick Winkibock. So this is
a progressive lengthening of the pr interval, often due to impaired conduction within the
AV node, resulting in occasional non conducted impulses. So this is similar to
a first degree AV block where there is some traffic on the road to the
ventricles, so we have this prolonged pr interval. The difference is though in
a Mobit's one that traffic it keeps getting worse and worse, leading to the
pr interval getting longer and longer, until eventually everything just comes to a standstill.
The road shuts down, the atrial impulse is filled or reach the ventricles,
and you have a dropped beat. So again, mobits type one aka
Winkie box. There's some traffic on the road, the traffic keeps getting worse
and worse, pr interval getting longer and longer, until all traffic comes to
a stop and you have a non conducted p wave no QRS complex following it.
One important thing to know about mobis type one Winkie box is it usually
occurs within the AV node. Mobitz one usually occurs within the AV node.
This is really important because all of the conditions we're going to go over today,
they're all called AV blocks, but they don't all occur within the AV
node. For instance, Mobitz type two, which we'll talk about next,
almost always occurs from conduction system issues below the level of the AV node,
and it's part of the reason why in ambit's one, which affects the AV
node, we see this progressive pr lengthening where in a mobits two, we
generally do not mob over more detail about that once we talk about mobitz too,
Let's talk about etiologies next. As far as your etiology is there for
the most part, the same as in a first degree heart block. Once
again, this can be a normal finding and patients like athletes with no underlying
cardiac pathology, and actually up to ten percent of long distance runners have been
found to have a MOBITS type one second degree block, which I found was
pretty interesting. Moving on to your meds, of course your av noal blocking
medications like we went over before, dig beta blockers, non to hydro period
in calcium channel blockers can all cause a MOBITS one. Don't forget your myocardidis
from lyme disease, myocardial infarction as well as some other underlying heart diseases,
and then hyperkalemia, which is the only one I didn't mention first degree block
as this is much more common in second and third degree blocks. So those
are the ones to know, because of course many others iatrogenic causes like post
cardiac surgery cardio myyopathy, but the main ones you need to memorize the ones
that will likely come up on an exam question. The way that I used
to remember them was with the mnemonic blocks bloc ks as in AV blocks.
The B stands for beta blockers, the L stands for lime disease O as
an ordinary as in your normal, variant and young healthy athletic patients. C
stands for calcium channel blockers, non dihydroperioding agents. Specifically, K stands for
K increase as in hyperkalemia. Remember the element symbol for potassium as K.
And then finally the S stands for stemi as an st elevation m I to
help you remember your myocardial infarction. So again remember blocks for your etiologies beta
blockers, lime disease, ordinary, calcium channel blockers, K increase, and
stemy. Moving on to clinical manifestation's neck So most patients, just like in
a first degree a V block, will be asymptomatic. Now, with that
being said, if the sinus rate is slow enough and you have a bunch
of non conducted beats, your cardiac output will decline and you may start to
notice some signs of hypoperfusion such as fatigue, lightheadedness, syncope, angina.
But in general, most patients are going to be asymptomatic. Moving on to
diagnosis, of course, this is the highest seal thing to know. So
will you diagnose with your ECG, and you're looking for a progressive prolongation of
the pr interval followed by a non conducted P wave. So when you look
at your ECG for a mob's type one aka winky Bok, you're going to
see this trend of the pr interval progressively lengthening. With each beat, it
gets wider and wider and wider, until eventually, boom, dropped beats.
You'll have a P wave but no QRS complex. And then once this happens,
it starts all over again. Pr interval longer, longer, longer,
dropped beat. This can of course happen in patterns three P waves to every
two Kors complexes, four P waves to every three Kors complexes, et cetera.
So comparing this to a first degree block, remember a patient with a
first gree AV block had a prolonged pr interval, but it didn't get progressively
longer, and most importantly, there was never a dropped beat. All P
waves were followed by a QRS complex. All right, So that's the typical
ECG findings. Pretty simple. I have another rhyme for you, so a
mobits type one aka Winkiebok. The pr interval gets longer, longer, longer,
until eventually it a beat. So for Winki Bok, remember the rhyme
longer, longer, longer drop. Then you have a Winkie Bok longer,
longer, longer drop than you have a Winkie Bok because remember, the pr
interval gets longer and longer until it drops. Another way I've heard of remembering
it is by remembering the W and Winkie box stands for warning because the pr
interval progressively getting longer warns you of the impending drop. Le suck about treatment
next. So the treatment goes like this. If they're asymptomatic, they're stable
in most cases they don't require any treatment. If they're symptomatic and most importantly
hemodynamically unstable hemodynamically unstable meaning they're hypotensive, they have altered mental status, chest
pain, etc. You give them atropine. So why atropine will Atropine speeds
up conduction through the AV node, which in a patient with an AV block
with slow conduction through the AV node, that would obviously be ideal Atropine achieves
this by blocking the parasympathetic influences on the heart, specifically the effects of acetal
colline. So that's why we use atropine first line for these unstable patients.
Now, if atropine is ineffective, you can use temporary cardiac pacing and then
finally as a last resort option, in patients that have symptomatic braided cardia with
no reversible etiology, no mads to discontinue that may be causing it, no
electrol disturbances that can be fixed. Then in those patients they need a pacemaker.
So a quick recap of a Mobitz type one aka Winkie block second degree
AV block. This is a progressive delay and a transmission of electrical signals from
the A tree to the ventricles, occasionally resulting in a non conducted impulse block
is going to be at the level of the AV node. In most cases
etiology remember blocks, bloc ks, beta blockers, lime disease, ordinary calcium
channel blockers, k increase STEMI. Most patients will be asymptomatic on ECG.
You're looking for longer, longer, longer drop than you have. A Winkie
bock treatment asymptomatic, just observed symptomatic and unstable atropine. And then finally last
line, definitive option pacemaker. All right, let's talk about a Mobits type
two second degree a V block next. So I want you to recognize a
shift once we get to ambits two and beyond, and that shift is once
you cross the threshold of a Mobitz two, it's getting more serious. You'll
notice we're not really going to see this in our young, healthy athletes anymore.
The treatment is going to be more aggressive. So just kind of be
aware of that shift once we get to that level. So Mobitz two is
a disease of the cardiac conduction system leading to occasional dropped beats with a pr
interval that is fixed and consistent, so you'll still have the non conducted beat
and the mobitz too. But the big difference between a Mobitz one and ambits
too, and what you should really focus on is that a Mobitz too,
the pr interval remains constant. You do not have that progressive prolongation like we
saw in a moobits type one block. That's the main difference between the two.
Mobitz one was longer, longer, longer drop Mobitz two is same,
same, same drop that's the idea fixed pr interval. So why does a
Moobitz too have a fixed pr interval with drop beats and a Mobitz one had
progressive prolonged gation with drop beats well su to the area of the heart where
the block occurs. And a Mobitz type two block almost always results from a
block below the level of the AV node. The block is at the bundle
of HISS and approximately twenty percent of cases and need the bundle branches in the
remainder. This is different than an emobits type one as we discussed before,
that almost exclusively occurs at the level of the AV node. So Mobitz type
one the block was at the AV node. Mobitz type two the block is
below the level of the AV node. And because of this one small difference,
your ECG findings are going to be different and your treatment options will change.
And we'll go over more about that in a minute. As far as
eteology, there's not a lot new to know here compared to amobits type one,
so I won't bore you with the details. Med's myocardial infarction myocardide is
from lime disease, hyperkalemia, et cetera. The key difference though, in
what I want you to remember is we are no longer going to see this
in our young, healthy, athletic patient. Mobitz type two block is rarely
seen in patients without underlying heart disease, So this is no longer going to
be a normal variant like we saw in the first couple of VV blocks we
went over. Patients with the mobits too generally has something else going on,
some type of structural heart disease to get to this point, myocarditis, myocardio,
schemia, fibrosis, etc. That's the main takeaway here for eteology and
what differentiates it from a type one and a first degree block. So the
neumonic we went over before still applies. Just subtract that over ordinary as this
is rare to occur in normal, ordinary patients without underlying heart disease. Remember
that shift, as I talked about before. Once we get to amobits,
two things are getting more serious at this point. Now. Clinical manifestations,
they can widely vary, and I don't think you need to memorize each individual
symptom, but you do need to know is that patients with the Mobits type
two second degree AV block will present with some form of symptoms. It can
be mild fatigue, dispnea all the way to syncope and sudden cardiac arrest.
But the key takeaway is unlike the other two AV blocks we talked about previously,
where most patients were asymptomatic, that's not the case at the MOBITS two.
They will usually present with some degree of symptoms. Remember that shift.
All right, let's talk about our ECG finding next. What are we going
to find on an ECG in a patience with a MOBITS type two. So
in a MOBITS two, you're going to have pr intervals that are the same
no progressive prolongation that will be followed by a P wave that fails to conduct
to the ventricles, so a sudden dropped beat no qors complex. So you're
looking at your ECG, try to visualize this in your head. You see
your P wave followed by a QRS complex as expected, next beat pwave pr
interval the same as the last, no prolongation aka no warning like we saw
on MOBITS one. Then all of a sudden dropped beat no qors complex.
That's the pattern to look for. Unchanging pr interval. Then suddenly a p
wave that fails to conduct to the ventricles. The big difference as you can
see between this type of second degree harp block compared to ambits type one.
As we've discussed before and as I keep saying, is that there is no
lengthening of the pr interval with each beat. So the pr interval that's the
key here to help differentiate. So the pr interval, it can be prolonged
usually it's going to be normal though, But however long or short the pr
interval is, it ain't changing. The length will remain the same, and
the reason why it remains consistent in amobits two and progressively prolonged in ambits one
all pertains to the area where the block is occurring. And we touched on
this before, but just to give a little more info. So remember a
moobits one, generally the block is at the AV node. Mobits two,
the block is below the level of the AV node. When amobits one that
affects the AV node. Those av nodal cells, they're pretty resilient and even
though they're facing an increased resistance with each beat, taking a little longer to
conductive beat with each interval, they can tough it out for a period of
time and still carry that beat through until eventually they just can't take it anymore
and they just collapse and drop the beat and amobits two though the block is
below the level of the AV node in his Perkinjee system. And these guys
they're all or nothing. They either give it they're all and conduct the beat,
or they don't do crap and they just drop it. There is no
progressive lengthening of the PR. It's the same. The beat is either conducted
or it's not. They don't play no games. So it's usually fairly easy
to distinguish between a mobits one and amobits two on ECG. Just look at
the PR interval. If it remains constant with occasional drop beats, it's ambits
too. If it progressively prolongs and leads to a drop beat. Mobits one
nice and simple, unless you have a two to one block that is which
I'll go over shortly. So how do you remember amobits to ECG finding what's
the rhyme for this one? So remember the rhyme. If some pas don't
get through, then you have a moobitz too. If some pas don't get
through, then you have amobitz too. Remember that rhyme. All right,
let's talk about treatment next. Treatment it's a bit different compared to ambits one,
So mobits two it's a slippery, unstable beast. You can never let
it out of your sight. So even in a stable patient, you're gonna
watch them closely, and you're gonna throw some transcutaneous pacing pads on them to
be ready in the event things go south quickly. You can't just send these
patients home and call it a day. That's because ambits two can frequently progress
to a third degree av block, which we'll talk about next, and eventually,
even your stable patients will likely require a pacemaker unless a treatable underlying cause
is found. Now, if they're unstable, hemodynamically unstable, hypotensive, altered
mental status, signs of shock, et cetera, they're going to get a
beta adrenergic agonist like dopamine, dopamine epinephrine, as long as there's no signs
of mild cardio schemia. And in addition, these patients will often also receive
temporary cardiac pacing. Now you may be asking yourself hemodynamically unstable patients in amobits
one. We gave them atropine. Why don't we give them atropine and amobits
too. I'll give you a second to think about that. Think back to
where the level of the block is. So the effect of atropine, as
we discussed before, is mainly on the AV node. Remember, atropine decreases
the refractory time and speeds up conduction through the AV node. And that was
great in a mobits one. That mainly affects the AV node. But what
area of the heart is affected in ambits too. That's right below the level
of the AV node infranodal. So we don't use atropine and ambits two blocked
in fact it and actually worsen the block in some cases. So stick to
your beta adrenergic agonis, dopamine, domine, etc. Finally, unless there
is a reversible underlying cause found most patients with a mobitz too hart block,
they're going to get a pacemaker. Remember back to that shift I keep talking
about. I want you to recognize this up until now, in a first
degree heart block in a mobits one, if the patient was asymptomatic, they
didn't need a pacemaker most of the time. But once we get to a
Mobitz two. Because of how unstable this type of hart block is. Everyone's
getting a pacemaker unless there is some underlying treatable cause found. So just remember
that when it comes to treatment, once you hit a Mobits two or above,
most patients are going to get a pacemaker. So a quick recap of
a Mobits type two second degree AV block. It's a disease of the cardiac
conduction system leading to occasional drop beats with a constant, constant pr interval,
the block is going to be below the level of the AV node. In
almost all cases, most patients will have some form of underlying heart disease.
Symptoms are variable anywhere from plain old fatigue all the way to sudden cardiac arrest.
ECG shows a constant pr interval followed by one or more dropped beats treatment.
Most patients will get a pacemaker unless there is an underlying treatable condition avoid
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the show. Now, before we move on to the last topic, which
is a third degree AV block, I wanted to quickly go over one other
variation, which is the dreaded two to one block. So it understand what
a two to one block is. We first need to understand something called AV
conduction ratio. So with second degree heart blocks, these type of blocks,
when consistent, can be named by the ratio of P waves to QRS complexes.
So look at your ECG. You count up all the pwaves and then
count up all the QS complexes until the first drop beat, and then the
ratio is based on the number of each So if there's four p waves three
QRS complexes, that's a four to three ratio. So an example, you're
reading your ECG, there's a P wave QS complex, pwave QRS complex,
p wave drop beat, no QS complex. This type of block would be
a three to two block because there was three p waves and only two QS
complexes. So now that we understand AV conduction ratio, let's talk about a
two to one block. So two to one block means every other pwave is
blocked, every other pwave is not followed by a QRS complex one conduction and
then no conduction, one conduction and no conduction. So the reason this is
so important or so frustrating is if you have a two to one second degree
AV block, there is no way to assess for PR lengthening, so you
cannot determine if this is a Mobitz type one or a Mobitz type two.
It never goes long enough to see if there is that progressive pr lengthening to
say, okay, this is a Mobitz type one. It just keeps dropping
the beat right away. So this is really the only instance where you can't
determine a Mobitz one from a Mobits two on ECG, and there is some
strategies to help with this. You can obtain a long rhythm strip PREVOUCCG,
certain vegeal maneuvers like Herod Sinus massage you can do in certain patients. Also,
if the PR interval is very long over three hundred milliseconds, or the
QRS complex is narrow, this is more consistent with a Mobits type one.
These aren't things I think you need to memorize, and I only mention this
type of block, not be because I think you'll get it on an exam
question, because that just wouldn't be fair. But I want you to be
ready when you're out there practicing or in clinicals to be familiar with this as
it's something you may see. All right, let's move on to the last
topic, a third degree av block, which is a defect in the cardiac
conduction system in which all atrial impulses fail to reach the ventricles, leading to
complete dissociation of the atria and ventricles. So you can see why this one
is so serious. Before we either had delays in the impulse or occasional drop
beats, but in this case it's no longer an occasional occurrence. There is
a complete, persistent loss of conduction from the atria to the ventricles. No
atrial impulses are reaching the ventricles, which is why this is sometimes known as
a complete heartblock, because nothing's getting through anymore. As far as etiologies,
the main ones are pretty much the same as the other av blocks. We
already went over your av noodal blocking, med's miocardial in farction, miocardias from
lime disease, hypergalimia. List of course doesn't include every etiology, but those
are the main ones. To focus on clinical manifestations, just as an immobids
two. The clinical manifestations can widely vary depending on a number of factors,
anywhere from fatigue, dyspnea and chess pain to syncope and sudden cardiac arrest.
Main takeaway, nearly all patients with a third degree block will present with some
degree of symptoms. It's uncommon for these patients to be asymptomatic. All right,
let's talk about your ECG finding next. What does a third degree block
look like on ECG? This is obviously the most important thing to know.
And I'm going to go over a few things to look out for on ECG
in a third degree block, but this first one, this is by far
the most important. There will be complete dissociation between the P waves and QS
complexes. This means that the atria and ventricles are beating independent of one another
in a normal ECG, in a normal, healthy patient, we expect to
see a P wave than a QRS complex, P wave then QS complex.
That's not happening anymore. The atria and the ventricles they no longer have a
line of communication. They're no longer on speaking terms. And because of this,
you'll see P waves marching right on through the QS complexes. And that's
the best way to think of this. They no longer have any perception of
where the QS complex is, so you're going to see them popping up right
next to a Q complex. They're going to be far from it. They're
going to be right in the middle of a T wave. There's no pattern
to it. Anymore like we're used to. They're just marching straight on through,
which is really helpful to identify this type of av block. And if
we're thinking on the terms of a pr interval, or at least the appearance
of one, it would be completely variable, prolonged, shorten or even absent.
Now you might ask yourself, since we have a complete block, the
atria can't get through the ventricles to send a signal to tell them to contract
anymore, how do we still even have QRS complexes? How are the ventricles
still contracting? So the heart actually has a backup system, so there is
a pacemaker in the ventricles as well as other places throughout the heart, but
they're usually suppressed by the normal and faster superoventricular rhythm. But when that superoventricular
rhythm is no longer sensed because of this block, the backup system kicks in
and the lower conduction system of the heart takes over and generates its own electrical
impulses. These are called escape rhythms. And while these escape rhythms they can
be slower and at times unreliable, they're essentially the only thing keeping the patient
alive and preventing a sudden cardiac arrest. All right, So that's the first
thing and the most important thing to be aware of on ECG, that AV
dissociation, no relationship between P waves and QS complexes. Next thing to look
out for an n ECG is that the P wave is going to be greater
than the qrs rate. So an ECG you'll notice there's more P waves than
QS complexes and why is that happening? So the atria is going to maintain
its regular rhythm and continue to generate electrical impulses at the normal atrial rate,
which is generally between sixty to one hundred beats per minute. In contrast,
the ventricles are now generating these escape rhythms as we discussed before, and these
escape rhythms have a much slower rate. How slow depends on the level of
the block, but in general, junctional escape rhythms tend to have a rate
between forty to sixty beats per minuted, and ventricular escape rhythms typically have rates
of forty beats per minute or less. So remember on ECG, in a
complete Hart block, you'll see more pwaves than QR complexes. And then finally
a last note, be aware that in a third degree block, you'll usually
have a regular P to P and regular R to our interval. Despite the
Atrian ventricles no longer communicating with each other and working in tandem, the rhythms
will still remain consistent. That means that the P wave will still occur at
the same interval, and each QRS complex will also occur at the same interval.
They'll have absolutely nothing to do with one another, but they'll still pop
up as expected with normal intervals, and this regularity can sometimes help identify a
hidden P wave that might be buried, maybe in a T wave or a
QS complex. So third degree AV block, remember P waves and QS complexes
are going to be independent of each other. They're both doing their own thing
no longer on speaking terms, Remember the P wave rate is going to be
greater than the QRS rate, and finally, remember to look for a regular
P top and regular R to our interval. Most important one to remember though,
is that AV dissociation. The atrion ventricles are beating independent of each other.
So how do you remember this for the exam? You remember the rhyme.
If qes and p's don't agree, then you have a third degree.
If QUES and PAS don't agree, then you have a third degree. This
will help you remember the avid association, which is the most important finding on
ECG for a third degree block and wrap this up. Let's finish up with
treatment. So hemodynamically stable patients do not require immediate treatment with atropine or temporary
cardiac pacing, but you need to be ready for these patients to crash at
any point. As I discussed before, those escape rhythms they're keeping the patients
alive, but they're unreliable and they're unstable, so you want to have transcutaneous
pacing pads in place for the event these patients start to crash, which can
happen very quickly. In addition, you want to be actively looking and treating
any reversible causes now. If they're unstable. Hemodynamically unstable, these patients are
going to be urgently treated with atropine, your beta adrenergic agoness we discussed before,
dopamine, etc. And temporary cardiac pacing. Usually start with atropine.
If that's ineffective, you work your way down to the other treatment options temporary
cardiac pacing, etc. Once you stabilize them, it's back to the hunt
again looking for any underlying cause that can be treated to reverse the block.
But ultimately, any patient that has a third degree block where you cannot identify
a reversable etiology, they're going to get a pacemaker. Most patients with a
third degree block will get a pacemaker unless a treatable underlying etiology is found,
and that's your treatment for a third degree block. So a quick recap of
a third degree av block. This is a defect in the cardiac conduction system
or a complete block leads to zero atrial impulses reaching the ventricles, you're going
to have complete dissociation of the atria and ventricles. Causes are similar to the
other types of heart blocks. Med's milecardial infarction milecardiais due to lime disease.
Symptoms will widely vary anywhere from fatigue and dispnea to sudden cardiac arrest diagnosed with
ECG, which will display complete dissociation between the P waves and QS complexes.
Definitive treatment will be with a pacemaker unless a treatable underlying cause is found,
and that's your third degree heart block. Before we move on to a few
questions to test your knowledge, I want to do a quick review of the
four types of HART blocks we went over, highlighting only the highest yield info
from each. So starting with a first degree AV block, remember your pr
interval is going to be over two hundred milliseconds, more than one big box.
That's the key. All impulses are still getting through, which will separate
it from other AV blocks. No frills, nothing fancy, nice and simple,
just a pr interval over two hundred milliseconds. Remember this is often a
normal variant, and remember the rhyme. If the R is far from the
P, then you have a first degree to remember that prolonged pr interval.
Second degree mobits one aka Winkie box usually occurs within the AV node, which
is why atropine is used in a Mobitz one and not often used any mobits
two, which usually occurs below the level of the AV node. Just like
in a first degree block, Remember this can be a normal variant, and
then the highest heel piece of info is to remember your ECG findings. The
pr interval will progressively prolong with each beat until eventually a P wave will fail
to conduct to the ventricles, leading to a dropped beat, and you,
of course remember this by remembering longer, longer, longer drop than you have
a Winkie block. Second degree av block MOBITS type two infra noodal is the
most common area this is going to occur. This block almost always results from
conduction system disease below the level of the AV note so at the bundle of
hiss or at the bundle branches. Remember, because of this, atropine is
generally avoided. And then on ECG, remember you're looking for PR intervals that
are generally the same no progressive prolongation like we saw in ambits one, and
they will be followed by one or more P waves that fail to conduct to
the ventricles, so a sudden dropped beat no qures complex. Remember if some
p's don't get through, then you have amobits two. And remember once you
hit the level of emobits two, we're getting a lot more generous with our
pacemakers. At this level and higher, everyone's getting a pacemaker unless a underlying
treatable cause is found. This is different than ambits one and first degree block
ray Symptomatic patients could just be monitored. To remember that shift in treatment at
this level. Finally, a third degree block, you have to remember on
ECG to look for the P waves to be marched right on through those QRS
complexes. They will be completely out of rhythm, complete AV dissociation. That's
the key. Remember, if qs and ps don't agree, then you have
a third degree. And then, just as in amobids two, most patients
will get a pacemaker unless there is some underlying treatable cause. All right,
let's wrap it up with five quick questions. Question one, Mister Jacobs,
a sixty three year old mail presents to the office complaining of episodes of dizziness
and intermittent syncope. Mister Jacobs has no significant medical history, is not currently
on any prescription medication, and his family history is negative for any cardiac conditions.
ECG is obtained which reveals a constant PR interval without progressive prolongation followed by
sudden failure of conduction. Laboratory tests including a CBC CMP cardiac enzymes are all
within normal limits. Imaging studies reveal no abnormalities. Considering the likely diagnosis,
what would be the most appropriate definitive treatment for mister Jacob's condition? So that
is going to be a pacemaker. So first, what is this patient have?
He has a MOBITS two second degree heartblock. This is evident by those
consistent unchanging pr intervals followed by a sudden failure of conduction. Most importantly,
there is no progressive prolongation which helps us roll out a MOBITS one. Next,
he has no underlying treatable conditions, at least that are mentioned in the
vignette. He's not taking any meads that can be to blame. Labs and
imaging studies are normal, so we have no underlying treatable condition that could be
to blame for the av block. And as we discussed before, a patients
with the MOBITS two with no underlying treatable etiology, they need a pacemaker.
Question two. A fifty seven year old female with a history of hypertension is
brought to the emergency department by ambulance. Patient is experiencing chess pain along with
altered mental status. On examination, she appears pale and diapheretic. Blood pressure
is eighty over fifty millimeters of mercury. An ECG is obtained which reveals progressive
lengthening of the pr interval with occasional non conducted p waves. Given the likely
diagnosis, which medication should be promptly started in this patient, so that is
going to be atropine. So we have a patient with the MOBITS one second
degree av block. This is evident as on the ECG we have progressive lengthening
of the pr interval with occasional non conducted p waves. This patient is clearly
hemodynamically unstable. She has altered mental status chess pain, hypotension. So we
know we need to act fast and the first line treatment for an unstable MOBITS
one would be atropine. If the patient remains unstable, transcutaneous pacing is another
option. We can start with atropine which speeds up conduction through the AV node,
and be careful because if I change one small detail and this patient instead
had a MOBITS too, we know we would avoid atropine because we know mobits
too is generally caused by a block below the level of the AV node.
Question three. Miss Smith, a sixty year old female, presents to the
office for her annual physical exam. She has a history of hypertension, hyperlipidemia,
osteoarthritis, and is currently taking verapamil, a tourvistatin, and neproxin.
Additionally, she recently completed a course of amoxicillin for a sinus infection. ECG
is obtained which reveals a first degree heart block characterized by a prolonged PR interval.
What intervention could be pursued to potentially alleviate the first degree block is seen
in this patient? Again, remember she's taking verapamil, torvestatin, aproxin.
She recently had a sinus infection tokamoxyscillin, and an ECG shows a first degree
block. What can we do to improve the first degree block? That would
be to discontinue verapamil. All the other stuff in this vignette, including the
sinus infection and antibiotics, they're all just distractors. It's all about verapamil.
So remember there's a lot of causes for AV blocks, and while you don't
need to memorize all of them, you should be very familiar with your medications.
Remember, any medication that can compare or slow nodal conduction can lead to
an AV block, dijox and beta blockers, and in the case of this
patient, non dihydroperiodin calcium channel blockers, specifically verapamil. Remember it's the non
dihydropuriody in agents like verapamil or deltaism. That are the big issues with AV
blocks because these types of calcium channel blockers slow cardiac contractility and conduction compared to
dihydroperiodins like m low to pene, nifetipine, etc. Which generally don't have
this effect and are predominantly vasodilators. Question four, an ECG is conducted,
revealing a pronounced dissociation between the PE waves and QRS complexes. The QS complexes
appear narrow, indicating a junctional escape rhythm. Notably, both the atrial and
ventricular rates remain steady while the atrial rate is surpassing the ventricular rate. This
pattern corresponds to which classification of a V block, so that is going to
be a third degree AV block. This is a pretty easy one complete dissociation
between the atria and ventricles. Junctional escape rhythm has kicked in. Atrial rate
is faster than the ventricular rate. That is a third degree block all the
way. Question five last question. A forty five year old female presents the
emergency room with complaints of fatigue, arthrologists and a rash. She is employed
as a park ranger and spends most of the day outdoors. She has a
history of type one diabetes hypertension and is currently taking Lantis NovoLog and lescinepril.
An ECG is obtained which reveals a mobits type one second degree AV block.
Taking into account the patient's medical history and symptoms, which of the following diagnostic
tests would be most appropriate to help determine the underlying cause of the AV block.
A chest X ray, B lime disease serology, C cardiac authorization,
D hemoglobe and A one C E toxicology screening, So that would be answer
B lime disease serology. This patient has fatigue, arthrologists, rash works outdoors
as a park ranger, and has an AV block. Lime disease should definitely
be high on your list of differentials as it appears this patient has early disseminated
disease and she is developing limecarditis which is leading to the av block. So
limesterology would be an important diagnostic test to order in this patient as this is
likely the underlying etiology of the AV block. All right, well, I
hope that was helpful. Thank you so much for listening to the podcast.