This article is the fourth in our latest series, The 12 Rhythms of Christmas, where each day we examine a new rhythm disorder. It is a continuation of the theme behind last year’s 12 Leads of Christmas.
An 84 year old male presents with a chief complaint of abdominal pain. The ECG below is performed:
What is the rhythm?
You may think the title of this article gives the answer away but, as we learned in the series’ first post on sinus tachycardia, the obvious can fool you when we’re dealing with ECG’s. Let’s walk through it step by step.
- There are regular P-waves of normal polarity at about 60 bpm
- Though they look like rounded U-waves in several leads (I, II, V5, V5), they are sharply peaked in V1–V4, confirming them as P-waves. U-waves will never come to a point like this.
- There are regular, narrow (suprventricular) QRS complexes at a rate of approximately 60 bpm.
- There is a 1:1 ratio between the P-waves and QRS-complexes.
And that’s all we know for certain at this point. The first step to dissecting tricky rhythms is to accept as fact only those things that we can state objectively. Never assume a relationship between complexes unless there is convincing evidence for it.
Why is that important? At this point in our analysis the large distance between the P-waves and QRS-compelxes raises doubts that the two are even connected! That leaves us three major rhythm diagnoses in play:
- Sinus rhythm with marked first degree AV-block
- Sinus rhythm with an long-cycle type I AV-block (also called an”atypical Wenckebach”)
- Isorhythmic AV-dissociation with normal sinus rhythm and an accelerated junctional rhythm occurring at almost exactly the same rate.
Those last two might be a new concept for some readers, but we’ll discuss them in the articles on AV-dissociation and type I AV-block later in this series. All you need to know is that for isorhythmic AV-dissociation, the atria and ventricles are beating independently of one-another but not communicating (like we see with complete heart block, but there are other causes!).
With a long-cycle type I AV-block, it’s just like any other Wenckebach, but instead of the 3:2 or 5:4 conduction ratios we usually see, they are longer—like 15:14 or more. That means you could see upwards of 15 or 20 P-waves conducting with prolonged PR-intervals before a dropped beat occurs. The reason that’s a concern here is that we only see ten P-waves in Fig. 1, so there’s a possibility we could be in the middle of a Wenckebach cycle and just not seeing the dropped P-wave that happens sometime after the paper ends.
Let’s talk about the subject of this article, however:
First Degree AV-Block
A first degree AV-block is said to be present when the PR-interval is greater than 200 ms in the setting of a sinus rhythm.
The prolonged PR-interval is caused by a delay in conduction, usually within the AV-node but sometimes slightly above it in the atrial tissue or slightly below it in the bundle of His. The location of the delay cannot be determined from the surface ECG.
While there are potentially serious causes of acute first degree AV-blocks (i.e. inferior STEMI), outside of those otherwise apparent instances it is almost always a benign finding. It’s presence may signal age-related degeneration of the conduction system, or it could just be a normal variant, but unless there are other signs of serious conduction disease (bifascicular block, type II AV-block), a first degree AV-block is of no concern.
Most of the time they are barely even worth remarking upon, and it’s not uncommon for young, healthy people to exhibit to PR-intervals slightly over 200 ms.
In those cases it’s usually because we define “normal” as the middle chunk of a bell-shape curve, which always leaves a certain percentage of healthy outliers who get falsely labelled “abnormal” on either end.While we designate a normal PR-interval as 120–200 ms, that definition is somewhat arbitrary and based on ease of measurement just as much as it is physiology (earlier this week we harped on the same theme when we discussed the “normal” heart rate). Note how those values correspond perfectly to the width of three to five small boxes, respectively—the body shouldn’t care about the size or speed of our EKG paper.
Most folks outside those bounds, with PR-intervals of 110 or 210 ms, are also usually “normal” and exhibit no discernible conduction abnormalities except that their numbers do not match our chosen ideal. The same goes for patients with PR-intervals of 100 or 220 ms. The further away you get from the mean, however, the more you move into zones of “abnormality” and pathology.
Still, we had to choose some sort of numbers to define normal, and 120–200 ms usually works well. That said, more important than the actual value of a PR-interval is the company it keeps. Below is an ECG from a healthy 36 year old male:
With a PR-interval of 212 ms and no major healthy history, his “first degree AV-block” is almost certainly just a normal variant and does not indicate any cardiac disease. Compare that with the ECG below:
While Fig. 5 and Fig. 6 share the same exact computerized PR-interval, the latter ECG was performed on a 79 year old male with a history of hypertension and coronary artery disease. Additionally, while Fig. 5’s ECG was otherwise normal, the tracing in Fig. 6 also demonstrates a non-specific intraventricular conduction abnormality with a leftward QRS axis. Our 79 year old’s first degree AV-block is much more likely to be due to true disease of the conduction system, but that inference is based more on the patient’s history and other ECG findings than the actual presence of the AV-block.
Speaking of intraventricular conduction abnormalities, let’s talk about bifascicular blocks for a second.
The term bifascicular block is used when there is a conduction abnormality in the right bundle branch (RBBB) and one of the two major divisions of the left bundle branch: the left anterior fascicle (LAFB) or the left posterior fascicle (LAFB) [note: fans of Dr. Tawara are constantly disappointed that the septal fascicle gets no respect]. Because the left posterior fascicle is much bulkier and more diffuse (fan-like) in its structure—and thus harder to damage—bifascicular block typically manifests as RBBB + LAFB.Bifascicular block is important because its presence suggests that conduction from the atria to the ventricles is only occurring via the one remaining patent fascicle. If conduction were to fail in that last fascicle as well, complete heart block would result.
That’s fine. What irks me to no end is when the term “trifascicular” block gets applied to an ECG like we see in Fig. 7. The idea is that, when we see a prolonged PR-interval with a bifascicular block, there must be a significant conduction abnormality in that last remaining fascicle delaying the activation of the ventricles. There is a huge problem with that line of thinking, however, and it is the implicit assumption that there is no AV-block present. Patients with bifascicular block are just as likely, if not more, to have a delay in the AV-node, so the only way to differentiate incomplete block in the last fascicle from block in the AV-node is to perform an invasive electrophysiological study with a His bundle recording.
Unless proven in the EP lab, the term trifascicular block should be reserved for cases of RBBB plus alternating LAFB and LPFB. In that situation we know there is true disease of all three fascicles because we can see a fixed block in the right bundle and intermittent blocks in the LAF and LPF. Use of the term in other situations is imprecise and alarmist, often making the patient sound sicker than they really are.
I very much prefer to describe Fig. 7 as showing a “bifascicular block with a prolonged PR-interval,” but even calling it a “bifascicular block with first degree AV-block” is alright. Anything except “trifascicular block,” please.
Back to the case
With that digression out of the way (I’m allowed two or three per article, right?), let’s get back to the ECG in Fig. 1.
The most important thing we can do is map out the PR and RP intervals. Everyone knows the PR-interval, but folks are less familiar with the RP-interval. It is the measurement from the QRS complex to P-wave that follows it. I’m not sure if you’re supposed to measure from the beginning of the QRS or the end (maybe one of my rhythm buddies can tell me), but it doesn’t really matter. When we talk of the RP-interval we’re usually using it in rough terms like “long” (more than half the RR-interval) or “short” (less than half the RR-interval), so exact timing isn’t a huge concern. In this case we’re going to actually measure the distance, but as long as we’re consistent across the entire tracing it doesn’t matter which point we use.
Here are the PR and RP intervals mapped out (in milliseconds).
Note that the PR-intervals in blue are exceedingly stable—wavering by only 10 ms across the tracing. This variation could be due to measurement error, but even a normal PR-interval isn’t perfectly fixed so there is also some natural fluctuation (especially when it is so prolonged).
Compare that with the RP-intervals in red. While they are fairly similar, and certainly appear constant at first glance, they vary a greater amount: 40 ms across the strip.
This suggests that the PR-interval must be fairly fixed and the RP-interval more variable. That is the relationship we expect when AV-conduction is intact and the P-waves are dictating the response of the QRS complexes.
For further confirmation we can also map out the PP-intervals…
Recall that the sinus node does not care what is going on in the AV-node or ventricles. The rate at which the sinus node discharges varies slightly from beat to beat, especially over the respiratory cycle (physiologic sinus arrhythmia). As a result, we expect a slight up-and-down variation of the PP-intervals (in green), which is what we see above.
Now note, as you walk from left to right across Fig. 11, that as the PP-interval increases, so does the corresponding RP-interval. Likewise, when the PP-interval shrinks, so does the RP-intervals. This is further proof that the atria and ventricles are communicating.
That rules out AV-dissociation as a cause for the prolonged PR-interval. We cannot being seeing the “isorhythmic AV-dissociation” we mentioned earlier in the differential.
What about an atypical (long-cycle) Wenckebach? That is still a posibility, but prolonged monitoring of the patient showed no dropped complexes.
The ECG we are looking at must show sinus rhythm with marked first degree AV-block and a PR-interval of about 495 ms.
So there you go! You probably didn’t think there could be so much to say about a topic as seemingly simple as first degree AV-block.
What’s the longest PR-interval you’ve ever seen with first degree AV-block?