ExploreCME: Diving deep into PANCE Prep!
Daily podcast covering topics geared towards PANCE sucess.
ExploreCME: Diving deep into PANCE Prep!
Heart Blocks, Made Clear
Welcome back to the deep dive. So if you need to quickly and uh thoroughly master one of the most fundamental yet high-stakes topics in cardiology, the heart blocks, you are definitely in the right place. Today we are taking a deep dive into atrioventricular or AV heart blocks. This is where that electrical highway between the atria and the ventricles gets interrupted. Our mission today is to really break down the critical diagnostic differences and the management paths that you need, not just to pass your exams, but to confidently handle these patients in a clinical setting.
SPEAKER_01:Exactly. And to start, let's just lay down the scientific foundation. An AV block is essentially a delay or complete failure of that conduction system. Specifically, it's the signal's ability to pass through the AV node and down the bundle of his to trigger the ventricles to contract. What makes this so clinically crucial is how we classify them. It's not just about how bad the delay is for second or third degree. Critically, it's about where the physical interruption is located.
SPEAKER_00:Aaron Powell And that anatomical location, that's what changes everything, right? The patient's prognosis, the treatment they need, all of it.
SPEAKER_01:Absolutely. You have two main categories. And honestly, understanding this split is probably the most high-yield fact of this entire deep dive. First up, we have what's called a nodal block. The issue here is right inside the AV node itself. This group includes first-degree AV block and uh second degree Mobitz type I, which you'll also hear called Wenkebach. And what's fascinating about these is that they're often physiologic. We can see them in perfectly healthy people, like, say, a highly conditioned athlete with strong vagal tone, or sometimes just during sleep. They're generally considered benign.
SPEAKER_00:Okay, but hold on. If a Mobitz type I can be seen in a healthy athlete, how do we get confident ruling out structural damage and deciding, you know, not to intervene?
SPEAKER_01:Aaron Powell That is the core challenge, and it brings us right to the second and much more dangerous group, the infranodal block. This block happens below the AV node in the bundle of his or the Purkinje system. This category includes Mobitz type 2 and third degree, or complete, AV block. And unlike the nodal types, these are almost always pathologic. They signal irreversible, structural damage, think fibrosis, calcification, real conduction system disease. They demand urgent attention.
SPEAKER_00:Let's use those analogies from our source material here because I think they really capture the prognostic difference perfectly. Mobitz type I and the benign nodal block is the tired tollbooth operator. The operator, you know, representing the AV node gets progressively slower with each car. That's the PR interval getting longer, until they just take a break and drop a beat, but then they resume feeling refreshed. It's functional fatigue, it self-corrects.
SPEAKER_01:Now compare that to Mobitz type 2. It's the complete opposite. This is the structurally unsound bridge. Conduction seems totally normal, the PR interval is constant. And then with absolutely no warning, no progressive worsening, the bridge just fails. A beat is dropped. This represents unpredictable underlying structural damage, and it carries this constant risk of just complete collapse into a third-degree AV block.
SPEAKER_00:Aaron Powell That unstable structural nature explains why Mobitz II is just always considered high risk. And if we're going deeper on structure, we also have to talk about the anatomy beyond just the main bundle.
SPEAKER_01:Aaron Powell Correct. We have to talk about the fascicular blocks. So once the bundle of his splits, you have three paths, the right bundle branch, and then the two fascicles of the left bundle branch. If you have a bifascicular block, that means two of those three paths are blocked. A classic example would be a right bundle branch block plus a left anterior fascicular block. And then when we talk about trifascicular block, this implies there's disease in all three paths, even if they aren't all fully blocked at the same time. It might show up as, say, a right bundle branch block with alternating left hemiblock or a bifascicular block with a really long his ventricular interval that you'd confirm with an EP study. These patients are, structurally speaking, walking a tightrope. They're at a very high risk for progressing to complete heart block.
SPEAKER_00:So we know ischemia and aging, fibrosis, those are common causes. What other pathologic causes should we be looking for when we're reviewing a patient's history?
SPEAKER_01:Well, besides the obvious ones like an acute MI, you have to think beyond the usual suspects. For instance, uh inflammatory processes like myocarditis. This can be from an infection like Lyme disease, and it can severely inflame and damage the node or the bundles. Then you have infiltrative diseases like cardiac sarcoidosis or amyloidosis, which physically crowd out and destroy that conductive tissue. And of course, a huge cause is iatrogenic. Sometimes the block is a complication from cardiac surgery, or very commonly, it's caused by medications.
SPEAKER_00:Let's move right into patient assessment then, because separating those benign nodal blocks from the really dangerous high-grade blocks, it all starts with the history and physical. When you talk to the patient, the ones with first degree and Mobitz ride are usually asymptomatic, but the red flags, they go way up when we see Mobitz type 2 or third degree. These patients show up with clear signs of poor cardiac output. So we're asking about profound fatigue, shortness of breath on exertion, pre-syncopy, and of course the ultimate danger sign. Syncope.
SPEAKER_01:The most crucial historical question, especially if it's a new diagnosis or the patient is asymptomatic, is always about identifying reversible factors. We need to know: did the patient recently start or increase a dose of an AV nodal blocker? This is where your class II beta blockers, your class 4 calcium channel blockers like verapamil and diltiasm and degoxin become critical points of focus. These drugs directly depress conduction, and often just stopping them can resolve the block.
SPEAKER_00:Okay, let's talk about the physical exam. What signs on exams specifically scream AV dissociation and third-degree block at us?
SPEAKER_01:You're looking for two key things, and they're both caused by the atria and ventricles contracting independently. First, obvious and severe bradycardia is the hallmark, usually an escape rhythm below 50 beats per minute. And a critical sign, the rate is fixed. It won't increase with exercise because the atria are no longer in control of the ventricles. Second, you're looking for evidence of that atrial kick hitting a closed valve. That's where you see canon venous pulsations, this visible, intermittent bounding pulse in the jugular veins. The atrium tries to contract, but the tricuspid valve is already shut, so blood gets sent backward.
SPEAKER_00:And that mechanical disconnect also changes what we hear with the stethoscope, right?
SPEAKER_01:Precisely. If you listen closely, you'll hear a variable intensity of the first heart sound, S1. S1 happens when the AV valves close. But since the PR interval is constantly changing, the valves are in a different position each time the ventricle fires. Sometimes they're wide open, sometimes almost shut. This creates an S1 that sounds soft one beat, then loud the next. It's a dead giveaway for AV dissociation. You might also notice a fluctuating systolic blood pressure and a wide pulse pressure.
SPEAKER_00:So once we have the history and exam, the diagnosis really comes down to the ECG. We have to know these four patterns cold. First degree is easy PR interval, is long, over 200 milliseconds, but it's still one-to-one conduction.
SPEAKER_01:Then you have your second degree types. Type I, Wankebok, that's the progressive PR lengthening until you drop a QRS. Type two is the drop beat without any preceding PR lengthening. The PR is fixed on the conducted beats. And finally, third degree or complete block. P waves and QRS complexes are just marching to their own completely independent rhythms, total AV dissociation.
SPEAKER_00:When we talk about high yield clinical differentiation, the ECG helps us actually localize the block, which is so important for determining urgency. How do we use the QRS width to do that?
SPEAKER_01:This is a huge differentiator. Especially in those tricky cases like a two to one block, where you can't just tell by counting if it's MOBIT's 100 or 2. You look at the width of the QRS complex on the beats that do get through. If the QRS is narrow, less than 120 milliseconds, it strongly suggests the block is nodal. So a type I. Why? Because the escape rhythm, if one is needed, is firing from high up above the bundle of his. So the signal travels normally down both bundles, and you get a narrow, efficient QRS. And if it's wide, if that QRS complex is wide, 120 milliseconds or more, that points straight to an infranodal block, a type two or third degree. And this is critical because it means the escape rhythm is originating way down low in the ventricles or the distal perkinjee system. A ventricular escape is much slower, often below 40 beats per minute, and critically it's far less reliable. It has a much higher risk of just failing completely and leading to a systole. So that with difference alone tells you if you're dealing with a functional fatigue issue or a structural catastrophe waiting to happen.
SPEAKER_00:Okay, so given that sporadic symptoms like syncope are so common, when do we need to move past that standard 12 lead ECG?
SPEAKER_01:If the symptoms are intermittent, yeah, you absolutely need ambulatory monitoring, something like a halter monitor or a loop recorder. You have to correlate the patient's symptoms, the dizziness, the presyncopy, with the actual rhythm disturbance. You have to prove causality. Electrophysiologic, or EP testing, is usually reserved for recurrent, unexplained syncope when the non-invasive tests fail, especially if the patient has an underlying bundle branch block. EP testing directly measures the conduction time through the HIS bundle, giving us a definitive answer. And don't forget the labs, always check digoxin levels and consider titers for things like Lyme disease, since those are treatable causes.
SPEAKER_00:Before we jump into treatment, let's just quickly clarify a common pitfall, distinguishing true heart block from simple AV dissociation.
SPEAKER_01:It's a subtle but vital point. AV dissociation just means the atria and ventricles are contracting independently. But that can happen when a faster ventricular rhythm, like VT, or an accelerated idioventricular rhythm, starts firing faster than the sinus node. So the ventricles are driving the heart, not a block. We have to be sure we're not trying to manage VT when we think we're managing a block. Also, remember that high-risk patient with syncope and a known bifascicular or trifascicular block, if they come in and stabilize, you have to keep a very high suspicion for a cult complete heart block. Their structural damage means they're just prone to sudden total failure. And finally, if everything points away from structural heart disease, you might consider autonomic testing, like a tilt table test, to rule out neurocardiogenic syncope, which is managed very, very differently.
SPEAKER_00:That transition brings us straight into patient management and intervention. As we've established, the first step for any degree of block is always managing those pharmacological causes.
SPEAKER_01:Yes. First thing you do, you stop or dramatically reduce any medication that depresses conduction, the beta blockers, the calcium channel blockers, digoxin. This simple step can resolve first degree and Mobitz type I blocks completely.
SPEAKER_00:Now, for the acute intervention, when do we need to step in with drugs and pacing?
SPEAKER_01:If the patient is symptomatic, so we're talking signs of poor perfusion, shock, chest pain, active syncope, or if they have an asymptomatic high-grade block like a Mobitz II or third degree, you must intervene immediately. Your first pharmacologic move is atropine, starting at 0.5 milligrams 40. Atropine works by reducing vagal tone, and since Mobitz type I blocks are often vagually mediated, it can work beautifully for those nurtal blocks. However, you have to be cautious with Mobitz type 2. If the block is infranatal, atropine might speed up the atria, causing more P waves to hit that damaged system, which can actually make the block worse. It could even precipitate a systole.
SPEAKER_00:So atropine is really just buying you time while you prepare for what?
SPEAKER_01:While you prepare for electrical pacing. If atropine fails or while you're getting the pacer ready, you might use a beta-edgenergic agonist infusion, isoproterinol, dopamine, or epinephrine, to temporarily speed up that ventricular escape rhythm. But these are truly temporary bridges. The next step is temporary pacing. You start with transcutaneous pads, followed by transvenous pacing if the wait for a permanent solution is going to be prolonged.
SPEAKER_00:And the definitive treatment for symptomatic high-grade blocks is permanent pacemaker implantation. So what drives the decision making for choosing the device type?
SPEAKER_01:The main goal for anyone who is in sinus rhythm is to preserve AV synchrony. You want the atrium to contract just before the ventricle to maximize your cardiac output. We call that the atrial kick. That 20% boost to cardiac output is really significant. Therefore, the gold standard is a dual chamber pacemaker, often coded as DDD. The D stands for dual. It paces the atrium and ventricle, it senses in both, and it can trigger a response in both. It's the most physiologic choice by far.
SPEAKER_00:And what happens if we only pace the ventricle?
SPEAKER_01:If you only use a single chamber, VVI pacemaker, you lose that atrial pick. The atria and ventricles are no longer coordinated, and this can lead to something called pacemaker syndrome. That's where patients get symptoms of low cardiac output fatigue, presyncopy, even though their pacemakers are working perfectly. We do have specialized options too. We sometimes use leadless pacemakers for certain patients, say someone in permanent AFib who just needs ventricular pacing. And for those with complete heart block plus LV systolic dysfunction, we might choose a specialized system like cardiac resynchronization therapy, CRT, or even his bundle pacing.
SPEAKER_00:Okay, finally, let's wrap this all up with health maintenance and patient education. What's the long-term outlook and what do we tell patients about living with this?
SPEAKER_01:For asymptomatic patients who are found to have, say, a bifascicular block, the prognosis is generally pretty good. But you have to be honest about the risk. The rate of progression to complete heart block is low, about 1% per year, but it's not zero. And that's why we monitor them.
SPEAKER_00:And education is just critical for prevention.
SPEAKER_01:Absolutely. The number one preventive measure for a patient with identified conduction disease is strict education about avoiding those offending rate controlling medications, unless they are absolutely necessary and prescribed by a specialist who knows their full condition.
SPEAKER_00:And for patients who have had a permanent pacemaker implanted.
SPEAKER_01:Our focus shifts to long-term surveillance. We educate them on symptoms that require an immediate follow-up and we monitor closely for complications: infection, hematoma at pocket site, cardiac perforation, pneumothorax during insertion, and lead dislodgement. Those are the risks they need to know about and that we have to watch for. So if we synthesize everything, the single most critical distinction you need to make is between the functional delay of MOBIS type I in the node and the structural pathological damage of MOBIS type II below the node, functionality versus structure. That drives your entire clinical triage.
SPEAKER_00:That is the principle you build your clinical practice on. Now, let's leave you with this final thought to consider. Think about that high-risk patient, the one with a known bifascicular block, who comes into your emergency department after a single sudden episode of syncope. But they stabilize immediately. Heart rate is 65. Based on this concept of occult, complete heart block and that underlying structural vulnerability, how fundamentally does this diagnosis change your triage priorities? Specifically, what are the immediate clinical risks they face? And how quickly should you move toward temporary pacing, even if they look stable right now? Think about the fragility of that one remaining conduction pathway. Thanks for diving deep with us on this critical topic. We'll catch you next time.