Cram The Pance - S1E51 AV Blocks (1st, 2nd, and 3rd Degree)

Episode Date: June 20, 2023

High Yield Atrioventricular Block Review. Review for your PANCE, PANRE, Eor's and other Physician Assistant exams. TrueLearn PANCE/PANRE SmartBank:https://truelearn.referralrock.com/l/CRAMTHEPANCE/Discount code for 15% off: CRAMTHEPANCE Included in review: First Degree AV block, Second Degree AV block (Mobitz 1 Wenckebach & Mobitz 2), 2:1 AV Block and Third Degree AV block, ECG findings, av nodal blocking medications, treatment options including atropine, pacemaker, dopamine, dobutamine, clinical manifestations, etiology including lyme disease, cardiomyopathies, myocardial infarction, beta blockers, calcium channel blockers.Become a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so today we're going to be going over AV blocks. As always, a big thank you to everybody who supported the channel. All of the really nice comments. I truly do appreciate it. So thank you so thank you to today's sponsor of the podcast, True Learn. All right, so AV blocks, they are a super high yield topic. They always come up on exams. If you're going to get a disrhythmia 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 yield info you need to know, as well as sharing some pneumonics 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 a V 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 S.A node, which is located in the right atrium. The SA 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 Percinji 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 S-A-B-B-P, S stands for S-A-node, A stands for A-V-Node, B stands for bundle of hiss, second B stands for bundle branches, and the P stands for P-Kingy Fibers. So that's the 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 120 to 200 milliseconds. 200 milliseconds is five little boxes on an ECG or one large box. 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. We'll go over today. You have a first degree A.V. Block. A second degree A.V. Block, which is further classified into a Mobitz type 1,

aka Wankybach, and a Mobitz type 2. 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 a v block so first degree a v block 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 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 avon

although it can affect the HIS-Perkinji 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 40 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 tabloat. blame. There's a number of medications that can cause an AV block. Essentially, any drug that impairs or slows avonotal conduction can cause a first-degree heart block. The ones you need to know, your AV-nodotalking drugs include digoxin, beta blockers, some calcium channel blockers, specifically your non-dihydroperidine agents like verapamil or deltisem. They can all cause A. V blocks. So on your exam, if they ask you and 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,

Remember the common avidotal blocking drugs, you can remember AB, C, D. A, B, C, D, your main avidotal blocking drugs start with A, B, C, or D. A, standing for adenosine, B, standing for beta blockers, C, standing for calcium channel blockers, your non-dihydropyridine specifically, and then finally, D for digoxin. 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, et cetera. For the exam, you absolutely have to remember Lyme 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 Lyme carditis, 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 heart block in the question, make sure you're looking for Lyme disease and the answer choices. And then another one, is a myocardial infarction. This is another potential cause. Often an inferior wall, MI, as the AV 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 dystrophies, Lev disease. But for the exam, focus on your meds, your beta blockers, calcium

channel blockers, et cetera, Lyme disease, MI, and your normal variant, as those are the ones most likely to come up. All right, what about clinical manifestations next? The main thing is, the thing you need to know for clinical manifestations is asymptomatic. Asimptomatic is what you need to know because patients with the 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 degree 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? Well, 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 200 milliseconds. or one large box. On a first degree AV block, there's a traffic jam.

And while the signal is still getting through the ventricles, it's taking a lot longer than it's supposed to. And this leads to a prolonged PR interval, specifically a PR interval over 200 milliseconds. That's all you need to know for a first degree block, PR interval over 200 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 200 milliseconds. So there's a lot of mnemonics for heart 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 widened PR interval over 200 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. 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 YQRS complex in conjunction with prolongation of the PR interval, patients with something known as pseudopacemaker 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 degree heart block. This is a cardiac condition characterized by slow conduction from the atrium 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 200 milliseconds. Most of the time you'll just observe. pacemaker only in some rare cases. That's a first degree heart block. Moving on to our second degree AV block. Remember this is broken into two subtypes, Mobitz type 1 and Mobitz type 2. Let's start with Mobitz type 1, aka Winkybach, named after the Dutch physician Carl Frederick Winkiebach. 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 Mobitz 1, 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 to reach the ventricles, and you have a dropped beat. So again, Mobits type 1, aka WinkyBock, 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 koress complex following it. One important thing to know about Mobits type 1 Winkybach is it usually occurs within the AV node. Mobits 1 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, Mobits type 2, 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 a Mobits 1, which affects the AV node, we see this progressive PR lengthening, where in a Mobit's 2, we generally do not. And we'll go over more detail about that once we talk about Mobits 2. Let's talk about etiology next. As far as your etiology, they're for the most part the same as in a first-degree heart block. Once again, this can be a normal finding in patients like athletes with no underlying cardiac pathology.

And actually, up to 10% of long-distance runners have been found to have a Mobits type 1 second-degree block, which I found was pretty interesting. Moving on to your meds, of course, your AV-nodal blocking medications like we went over before, Didge, beta blockers, non-dihadhyraryngal calcium channel blockers can all cause a mobits one. Don't forget your myocarditis from Lyme disease, myocardial infarction, as well as some other underlying heart diseases. And then hyperkillemia, which is the only one I didn't mention for first-degree block, as this is much more common in second and third-degree blocks. So those are the ones to know.

There's, of course, many others. Iotrogenic causes like post-cardiac surgery. cardiomyopathy. 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. B-L-O-C-S as in A-V-Blocks. The B stands for beta blockers. The L stands for Lyme disease. O as in ordinary, as in your normal variant in young healthy athletic patients. C stands for calcium channel blockers, non-dihydroperiodine agent specifically. K stands for K-increase as in hyperkillemia. Remember the element symbol for potassium is K. And then finally, the S stands for Stemi as an ST elevation MI to help you remember

your myocardial infarction. So again, remember blocks for your etiologies, beta blockers, Lyme disease, ordinary calcium channel blockers, K increase, and Stemi. Moving on to clinical manifestations 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 hypopurfusion, 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 you'll thing to know. So 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 Mobits type 1, aka Winkiebok, 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 KORS complex. And then once this happens, it starts all over again, PR interval longer, 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, etc. So comparing this to a first-degree block, remember, a patient with a first-degree 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 Mobitz type 1, aka WinkyBock, the PR interval gets longer, longer, longer, longer, until eventually it drops a beat. So for WinkyBock, remember the rhyme, longer, longer, longer, longer, drop, then you have a WinkyBock. Longer, longer, longer drop, then you have a WinkyBock. 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&W in WinkyBoc stands for WN.

because the PR interval progressively getting longer warns you of the impending drop. Let's talk 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, hemodynamics unstable, hemodynamicly unstable, meaning they're hypotensive, they have altered mental status, chest pain, etc. You give them atropine.

So why atropine? Well, 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 acetylcholine. 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 bradycardia with

no reversible etiology, no meds to discontinue that may be causing it, no electrolyte disturbances that can be fixed, then in those patients, they need a pacemaker. So a quick recap of a Mobits type 1, aka Wankybach, second degree AV block. This is a progressive delay in a transmission of electrical signals from the atrial 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. Etyology, remember blocks, B-L-O-C-S, beta blockers, Lyme disease, ordinary calcium channel blockers, K-increase, Stemi.

Most patients will be asymptomatic. on ECG you're looking for longer, longer, longer, drop. Then you have a WinkyBock. Treatment, asymptomatic, just observe, symptomatic and unstable, atropine, and then finally, last line, definitive option, pacemaker. All right, let's talk about a Mobitz type 2 second degree AV block next. So I want you to recognize a shift once we get to a Mobits 2 and beyond. And that shift is once you cross the threshold of a Mobits 2, 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 Mobits 2 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 in the Mobits 2, but the big difference between Amobits 1 and Amobits 2, and what you should really focus on is that a Mobits 2, the PR interval remains constant. You do not have that progressive prolongation like we saw in a Mobits type 1 block. That's the main difference between the two. Mobits 1 was longer, longer, longer, longer drop. Mobits 2 is same, same, same drop. That's the idea, fixed PR interval. So why does a Mobits 2 have a fixed PR interval with drop beats? And a Mobits 1 had progressive prolongation with drop beats. Well, suit of the area of the heart where the block occurs and a Mobits type 2 block almost

always results from a block below the level of the AV node. The block is at the bundle of hiss and approximately 20% of cases and the bundle branches in the remainder. This is different than an amobits type 1, as we discussed before, that almost exclusively occurs at the level of the AV node. So Mobitz type 1, the block was at the AV node. Mobits type 2, 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 etiology, there's not a lot new to know here compared to a Mobits type 1. So I won't bore you with the details, meds, myocardial infarction, myocarditis from Lyme disease, hyperculemia, etc. The key difference, though, and what I want

you to remember is we are no longer going to see this in our young, healthy, athletic patient. Mobitz type 2 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 2 generally has something else going on. Some type of structural heart disease to get to this point, myocarditis, myocardioschemia, fibrosis, etc. That's the main takeaway here for etiology and what differentiates it from amobics type 1 and a first degree block. So the nomadic we went over before still applies. Just subtract that O for 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 2, 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 what you do need to know is that patients with the Mobits type 2, second degree AV block, will present with some form of symptoms. It can be mild fatigue, dyspnea, 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 with the Mobits 2. 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 and a patients

with a Mobits type 2. So in a Mobits 2, 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 QRS 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, P wave, PR interval the same as the last, no prolongation, a.k.k.a. no warning like we saw in Mobits 1. then all of a sudden, dropped beat, no QRS 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 heart block compared to a mobobics type 1, 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 a Mobits 2 and progressively prolonged in a Mobitz 1, 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, amobits 1 generally the block is at the AV node. Mobits 2, the block is below the level of the AV node. When a Mobits 1 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 conduct a 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. In a Mobits 2, though, the block is below the level of the AV node in his Percinji system. And these guys, they're all or nothing. They either give it their 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 MoBets 1 and a MoBets 2 on ECG. Just look at the PR interval. If it remains constant with occasional drop beats, it's a MoBets 2. If it progressively prolongs and leads to a drop beat, Moabits 1. Nice and simple. Unless you have a two to one block that is, which I'll go over shortly. So how do you remember a Moabits 2-E-Bitch 2? What's the rhyme for this one? So remember the rhyme, if some P's don't get through, then you have a Mobits 2. If some peas don't get through, then you have a Mobits 2. Remember that rhyme. All right, let's talk about treatment next. Treatment, it's a bit different compared to a Mobits 1. So Mobits 2, it's a slippery, unstable beast. You can never let it out of your sight. So even in a stable patient, you're going to watch them closely and you're going to 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 a Mobits 2 can frequently progress to a third degree AV block, which will 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, etc., they're going to get a beta adrenergic agonist like dopamine, dopamine, dopamine, epinephine, as long as there's no signs of myocardioschemia. And in addition, these patients will often also receive temporary cardiac pacing. Now, you may be asking yourself, hemodynamics unstable patients in a Mobits 1,

we gave them atropine. Why don't we give them atropine in a Mobits 2? Well, 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 1 that mainly affects the AV node, but what area of the heart is affected in a Mobits 2? That's right, below the level of the AV node, So we don't use atropine in a Mobits 2 block. In fact, it can actually worsen the block in some cases. So stick to your beta adrenergic agonist, dopamine, dopamine, et cetera. Finally, unless there is a reversible underlying cause found, most patients with a Mobits 2 heart 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 Mobitz 1. If the patient was asymptomatic, they didn't need a pacemaker most of the time. But once we get to a Mobits 2, because of how unstable this type of heart 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 amobits 2 or above, most patients are going to get a pacemaker.

So a quick recap of a Mobitz type 2 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 planal 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 atropine, and that's a mobits too.

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You can visit trulearn.com to sign up or click the link in the show notes and make sure to use the code, cram the pants when signing up to save 20% off subscriptions of 90 days or more. Now, back to 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 2 to 1 block. So to understand what a 2 to 1 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 P waves, then count up all the QRS 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, QRS complex, P wave, QRS complex, P wave, drop beat, no QRS complex.

This type of block would be a three to two block, because there was three P waves and only two QRS complex. So now that we understand AV conduction ratio, let's talk about a 2 to 1 block. So a 2 to 1 block means every other P wave is blocked. Every other P wave 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 2 to 1 second degree AV block, there is no way to assess for PR lengthening, so you cannot determine if this

is a Mobitz type 1 or a mobits type 2. It never goes long enough to see if there is that progressive PR lengthening to say, okay, this is a Mobitz type 1. It just keeps dropping the beat right away. So this is really the only instance where you can't determine a Mobitz 1 from a Mobitz 2 on ECG. And there is some strategies to help with this. You can obtain a long rhythm strip, a previous ECG, certain vagal maneuvers like carotid sinus massage you can do in certain patients.

Also, if the PR interval is very long, over 300 milliseconds, or the QRS complex is narrow, This is more consistent with amobics type 1. These aren't things I think you need to memorize, and I only mention this type of block, not 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 heart block, because nothing is 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 avidotal blocking meds, myocardiain, myocarditis from Lyme disease, hypercalemia. This, of course, doesn't include every etiology, but those are the main ones to focus on. Clinical manifestations, just as in a mobits too, the clinical manifestations can widely vary depending on a number of factors, anywhere from fatigue, dyspnea, and chest 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 is 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 QRS complexes. This means that the atria and ventricles are beating independent of one another. In a normal ECG and a normal healthy patient, we expect to see a P wave

than a QRS complex. P wave than QRS complex. That's not happening anymore. The atria and the 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 QS 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, prolong, 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 superventricular rhythm. But when that superventricular 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 QRS complexes. Next thing to look out for in ECG is that the P wave is going to be greater than the QRS rate. So on ECG, you'll notice there's more P waves than QRS 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 60 to 100 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 40 to 60 beats per minute, and ventricular escape rhythms typically have rates of 40 beats per minute or less. So remember on ECG in a complete heart block, you'll see more P waves than QS 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 R interval. Despite the atrium 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 QRS complex.

So third degree AV block, remember P waves and QS complexes are going to be indivialiality. 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-to-P and regular R-to-R interval. The most important one to remember, though, is that AV dissociation. The atrium ventricles are beating independent of each other. So how do you remember this for the exam? You remember the rhyme. If Q's and P's don't agree, then you have a third degree. If cues and P's 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 hemodynamics-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 are 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, hemondynamically unstable, these patients are going to be urgently treated with atropine, your beta-adroenergic agonis. We discussed before, dopamine, et cetera, and temporary cardiac pacing. You 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 reversible 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, meds, myocardial infarction, myocarditis due to Lyme disease. Symptoms will widely vary anywhere from fatigue and dyspnea to sudden cardiac arrest. Diagnosed with ECG, which will display complete dissociation between the P waves and QRS 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 heart 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 200 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 200 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 1, aka WinkyBok, usually occurs within the AV node. which is why atropine is used in a Mobits 1 and not often used any Mobits 2, 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 yield 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. You of course remember this by remembering longer, longer, longer drop, then you have a WinkyBock. Second degree AV block, Mobits type 2. Infranodal 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 a Mobits 1. And they will be followed by one or more pee waves that fail to conduct to the ventricles. So I sudden dropped beat, no QRS complex. Remember if some peas don't get through, then you have a Mobits 2.

And remember, once you hit the level of a Mobits 2, 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 a MoBets 1 and first degree block where asymptomatic patients could just be monitored. So 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 marching right on through those QRS. complexes, they will be completely out of rhythm. Complete AV dissociation, that's the key. Remember, if Q's and P's don't agree, then you have a third degree. And then just as in a Mobits 2, 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, Mr. Jacobs, a 63-year-old male presents to the office complaining of episodes of dizziness and intermittent syncope. Mr. 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 Mr. Jacobs' condition?

So that is going to be a pacemaker. So first, what does this patient have? He has a Mobits 2 second degree heart block. 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 1. Next, he has no underlying treatable conditions, at least that are mentioned in the vignette. He's not taking any meds that can be to blame.

Labs and imaging studies are normal. So we have no underlying treatable condition that can be to blame for the AV block. And as we discussed before, a patient's with the Mobits 2 with no underlying treatable etiology, they need a pacemaker. Question 2, a 57-year-old female with a history of hypertension is brought to the emergency department by ambulance. The patient is experiencing chest pain along with altered mental status. On examination, she appears pale and diaphoretic. Blood pressure is 80 over 50 millimeters of mercury. An ECG is obtained, which reveals progressive lengthening of the PR interval with occasional non-conducted pee 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 1 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, chest 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. But you start with atropine, which speeds up conduction through the AV node, and be careful because if I change one small detail, then this patient instead had a Mobitz 2, we know we would avoid atropine because we know Mobot's 2 is generally caused by a block below the level of the AV node. Question 3, Ms. Smith, a 60-year-old female, presents to the office for her annual physical exam. She has a history of hypertension, hyperlipidemia, osteoarthritis, and is currently taking varapamil, atorvastatin, and naproxin. 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 seen in this patient? Again, remember, she's taking varapomilil, a torvastatin naproxin. She recently had a sinus infection, took amoxicillin, and an ECG shows a first-degree block.

What can we do to improve the first-degree block? That would be to discontinue varapamil. All of the other stuff in this vignette, including the sinus infection in antibiotics, they're all just distractors. It's all about verrapamil. 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 impair or slow nodal conduction can lead to an AV block, digoxin, beta blockers, and in the case of this patient, non-dihydropyridine

calcium channel blockers, specifically varapamil. Remember, it's the non-dihydropyridine agents like varapimal or doytopium that are the big issues with AV blocks because these types of calcium channel blockers, slow cardiac contractility and conduction, compared to dihydropyrodines like amlodipine, nipetepine, etc., which generally don't have this effect and are predominantly vasodilators. Question 4, an ECG is conducted, revealing a pronounced dissociation between the P waves and QRS complexes. The QRS 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 45-year-old female presents to the emergency room with complaints of fatigue, arthrologias, and a rash. She is employed as a park ranger and spends most of the day outdoors. She has a history of type 1 diabetes, hypertension, and is currently taking Lantis, Novalog, and Lysinopril. An ECG is obtained, which reveals a Mobits type 1, 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, Lyme disease serology, C, cardiac catheterization, D, hemoglobin A1C, E, toxicology screening. So that would be answer B, Lyme disease serology. This patient has fatigue, arthrologist, rash, works outdoors as a park ranger, and has an AV block. Lyme disease should definitely be high on your list of differentials. As it appears, this patient has early disseminated disease and she is developing Lyme carditis, which is leading to the AV block. So Lyme serology 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.