This article is the ninth in our latest series, The 12 Rhythms of Christmas, where we examine a different rhythm disorder with each new post. It’s a continuation of the theme behind last year’s 12 Leads of Christmas. And, just like last year’s series, I’m rather late getting the final articles out, but the end is in sight.
Hope you had a good Valentine’s Day—let’s talk about some heart stuff. Today I want to discuss a form of AV-block that many providers don’t even realize is its own unique entity:
What differentiates this arrhythmia from the other AV-blocks is that it occurs in discrete, self-limited episodes—or “paroxysms.” You patient will be hanging out, minding their own business, when out of nowhere they suddenly drop two or three or forty QRS complexes in a row until the AV-node just as suddenly recovers. It tends to give you a pretty good wake-up.
The strip above was run on an 80 year old male who was being treated for pneumonia when he unexpectedly appeared to have a short seizure. It wasn’t a seizure—it was syncope—and this strip is our proof.
Most folks would call the above rhythm “Mobitz II AV-block” because there are dropped QRS complexes without an apparent increase in the PR-interval preceding them, but as we discussed in our article on high grade AV-block, we shouldn’t really be labeling something a type II AV-block if two or more consecutive QRS complexes are dropped.
Well, then it must surely be “high-grade AV-block?”
Not quite. That term implies a fairly fixed conduction disturbance. A true high-grade AV-block will typically last somewhere on the time span of hours to forever, whereas the conduction disturbance we see in Fig. 1 lasted only 20 seconds or so and is—you guessed it—paroxysmal.
The patient never showed any dropped QRS complexes in the two hours before that spell, and he didn’t show any more over the next two days until he received a permanent pacemaker. In hindsight he recalled experiencing two unexplained “falls” in the days preceding his admission, so based on his inability to recall how or why he fell, it seems likely that similar paroxysms of AV-block had struck him then as well.
That’s the interesting and scary thing about paroxysmal AV-block—it can strike without warning in patients whose resting 12-leads are fairly unremarkable.
How about at some more cases?
Similar to the last patient, Fig. 4 is from an 80 year old female who fell at home and may or may not have experienced syncope; she was unable to recall.
Also similar to the last patient, she has a left anterior fascicular block (LAFB) on her 12-lead, but this time there is the addition of a right bundle branch block (RBBB); together they produce a bifascicular block.
While a bifascicular block usually isn’t an acute issue, in the patient presenting with syncope it can be a major red flag that he or she has extensive conduction disease and could be experiencing paroxysms of AV-block.
Our patient was asymptomatic in the ED… That is, until she experienced another episode of syncope while in bed.
She had an uneventful night in the hospital and received an implanted pacemaker the next day. Are you noticing a pattern?
This next patient is an 84 year old male who was brought to the ED because his family claimed that he had experienced a couple of brief “staring episodes.” They said that while he never fell or “passed out,” on a couple of occasions over the past two days he had stopped responding for about 10 seconds and just stared into the distance. Fig. 6 is his 12-lead on arrival in the ED.
Much to the annoyance of his family and staff, the bedside monitor seemed to have trouble tracking his QRS complexes and occasionally set off a crisis alarm of ASYSTOLE even though the patient, under constant watch of his loved ones, was fine.
While I have changed many details of the case, this next part really happened…
So, being the guy who troubleshoots all the monitors, I got called back to figure out why it kept alarming indiscriminately. My first step was to see what kind of events it was alarming for and I pulled up the following strip:
Turns out it wasn’t a false alarm. Then, literally, while I was looking at that strip, I heard the machine crisis alarm again and looked up to see the following rhythm:
Turns out the patient had experienced a couple of short, asymptomatic paroxysms of AV-block while in the ED that were setting off the monitor’s alarm but were not immediately noticed. Of course, we all picked up on that last episode.
If your monitor alarms for VT, VF, or asystole, always look for a reason!
Sometimes even fatal arrhythmias are transient and self-resolve before you can look up or the patient can even become symptomatic, and it’s kind of important to know if your patient had a brief period of ventricular standstill while you weren’t looking. What appears to be V-tach at the end of the strip is actually artifact from seizure-like activity he exhibited as the AV-block subsided—a new development for our patient. Have I mentioned that syncope and cardiac arrest are often mistaken for seizures? I feel like I have…
While he experienced several more short and long spells of paroxysmal AV-block in the ED, he responded well to transcutaneous pacing and went on to receive an implanted pacemaker the next day without further issue.
With that, I leave you for today; go forth and call paroxysmal AV-block by its proper name.
Check out the rest of The 12 Rhythms of Christmas! (updated as new posts come out):
The 12 Rhythms of Christmas: Sinus Tachycardia
The 12 Rhythms of Christmas: Sinus Bradycardia
The 12 Rhythms of Christmas: Atrial Flutter
The 12 Rhythms of Christmas: First Degree AV-Block
The 12 Rhythms of Christmas: Type I AV-Block
The 12 Rhythms of Christmas: Type II AV-Block
The 12 Rhythms of Christmas: 2:1 AV-Block
The 12 Rhythms of Christmas: High-Grade AV-Block
You’re still here?
Well, if you’re still around, you must be interested in some of the gritty details of paroxysmal AV-block. You know, minor stuff like, “What even triggers paroxysmal AV-block?” Let’s dive in.
First off, you may have heard the terms “phase 3” or “phase 4” block used in reference to paroxysmal AV-block—or maybe you haven’t—either way, those are probably misnomers. For a full explanation of why, I highly suggest this paper by El-Sherif and Jalife (I’m not going to re-hash the whole thing). For now just know that I’m going to refer to the former “phase 3 block” as tachycardia-dependent paroxysmal AV-block (TD-PAVB) and the former “phase 4 block” as pause-dependent paroxysmal AV-block (PD-PAVB). They’re big names but the concepts are simple and we’ll look at some examples in a second.
In the most basic sense, TD-PAVB is a paroxysmal AV-block that’s initiated by an early beat or increase in heart rate and constitutes most PAVB’s, while PD-PAVB occurs when a run of paroxysmal AV-block is triggered by the intrinsic heart rate slowing or a pause in the sinus rhythm, and it is comparatively less common. Since nothing is ever that simple or dichotomous, sometimes PAVB strikes without any appreciable change in the sinus rate—in which case we just call it plain old paroxysmal AV-block and try not to think too much about it. There may have been a subtle change in the patient’s physiology that set it off, but at the bedside we can’t even begin to fathom what exactly that might have been.
I haven’t seen a great many papers on this topic and my bookcase of textbooks is not at all helpful, but it seems that the block often occurs at the level of the bundle of His—even in patients with infra-Hisian conduction disturbances (bundle branch blocks). Its mechanism seems most closely related to that of the classic type II AV-block, however I have seen a couple of purported examples of supra-Hisian (AV-nodal) PAVB. I guess what I’m saying is that we should approach this like high-grade and 2:1 AV-block and not make any assumptions whether the underlying mechanism is type I or type II based on the surface 12-lead—leave that to the electrophysiologists with their His-bundle electrocardiograms.
Let’s examine which flavor of PAVB each of our patients above experienced…
Despite being the least common form, it looks like our first patient is experiencing pause-dependent PAVB as evidenced by the longer-than-normal PP-interval (803 ms) that triggers the AV-block. Interestingly, it’s not a huge slowing of the sinus rate that sets off the PAVB—it’s not even the longest PP-interval on this short strip—and while we can’t guarantee cause-and-effect from this solitary episode, that’s the #1 contender for a diagnosis at the moment. I’m about 60% confident it’s really PD-PAVB.
How about the patient from Fig. 5?
It’s rather tough to see exactly what’s going on here because artifact obscures some of the atrial activity, but it looks as though the AV-block is instigated by an acceleration in the sinus rate (PP-interval of 639 ms); so this is likely a tachycardia-dependent PAVB.
Finally, what about that patient with the sneaky pause in Fig. 7? It turns out that I have a bunch of strips from him…
Hopefully I don’t need to march out the PP-intervals this time—it should be apparent that each of these paroxysms of AV-block are precipitated by a PAC. As a result, they are all examples of tachycardia-dependent paroxysmal AV-block. I didn’t post the full strips, but the runs of AV-block that resulted from each PAC lasted anywhere from a couple of seconds to over 20 seconds.
Fascinatingly, just before each PAC that sets off the PAVB, there is a brief spell of artifact. If I posted the longer versions of each of those strips, you would see that there isn’t a hint of artifact in the time leading up to those episodes. Either the patient is somehow able to predict when he’s going to have one of these paroxysms and becomes symptomatic or braces himself, or something related to his movement is actually triggering the PAC’s that in turn set off the PAVB—I have no idea why or how this is happening but if anyone has any insight please let me know in the comments.
Before we conclude for real, I have one more mind teaser for you. The following strip is from the same patient that we saw in Fig. 7–8, and Fig. 11–15, but it looks a bit different from those earlier rhythms.
Is this still paroxysmal AV-block?
That big deflection about 2/3 of the way through the tracing is from the transcutaneous pacer kicking in. While we just established that this patient has been experiencing TD-PAVB, this pause doesn’t seem to be preceded by an apparent premature complex (or any weird movement artifact!). Maybe the PP-intervals are subtly diminishing and the heart rate increasing?
Odd. There’s no significant variation in the PP-intervals… Perhaps it’s just plain old paroxysmal AV-block this time, with no increase or decrease in the atrial rate? The only issue—and it’s a big one—is that I don’t see any P-waves marching out either, so it can’t really be true AV-block…
Maybe something is up with the sinus node? Could this patient have combined SA and AV-nodal dysfunction?
Another interesting finding is that this pause is much shorter than any of the other episodes of PAVB we’ve seen in this patient. Perhaps the transcutaneous pacer kicking in is allowing the heart to recover sooner?
Well, that can’t be the case, because the pacer isn’t capturing! As we see in Fig. 18, there is a native QRS buried in what should be the absolute refractory period following the pacer spike. If the pacer was actually achieving electrical capture, the myocardium would still be refractory at that point and unable to generate a QRS.
So, enough Socratic jabber, what’s really going on?
Don’t forget your basic arrhythmia training!
The most common cause of a pause is a non-conducted PAC—keep that in mind even in patients with wacky AV-blocks! I know it’s super subtle and you should certainly be skeptical of my explanation at this point, but here’s some more examples from the same patient to prove that what we’re seeing this time really is non-conducted PAC’s.
So, it turns out that this patient has conducted PAC’s that are triggering paroxysmal AV-block, and non-conducted PAC’s that are mimicking AV-block or SA-node dysfunction. What a world!
For real, we’re done now.