The 12 Rhythms of Christmas: First Degree AV-Block

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:

Sinus rhythm with first degree AV-block

Figure 1. What is the rhythm?

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.

First degree AV-block

Figure 2. Sinus rhythm with first degree AV-block in a 16yo M s/p seizure.

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.

First degree AV-block

Figure 3. Mild first degree AV-block in a healthy 21yo M.

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.

Figure 4. Normal distribution curve. [Source]

Figure 4. Normal distribution curve. “Normal” is a arbitrary chunk of the blue part. [Source]

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:

First degree AV-block

Figure 5. Normal variant PR-elongation in a healthy 36yo M.

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:

First degree AV-block, non-specific intraventricular conduction abnormality

Figure 6. First degree AV-block in a patient with an extensive cardiac history.

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.

Bifascicular block (RBBB + LAFB) and first degree AV-block

Figure 7. Prolonged PR-interval in a patient with bifascicular block (RBBB + LAFB)

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.

Figure 8. Conduction system of the heart. [Source]

Figure 8. Conduction system of the heart. [Source]

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).

Figure 9. PR (blue) and RP intervals from Fig. 1.

Figure 9. PR (blue) and RP intervals from Fig. 1.

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…

Figure 10.

Figure 10.

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.

Figure 11.

Figure 11.

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?

The 12 Rhythms of Christmas: Atrial Flutter

This article is the third 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.

This is a new edit of the first article I ever published on my personal blog, so it may seem familiar to some readers.

Finally, if you were curious about the mystery rhythm in Fig. 16 of the first post on sinus tachycardia, you might be surprised to know that it shows atrial flutter with 2:1 conduction. The same tracing pops up in Fig. 23 of this article.

Atrial Flutter

Have you slammed adenosine to cure a patient’s SVT with a fluorish?

Atrial flutter with 2:1 conduction

Figure 1. Pre-adenosine.

*PUSH* – *FLUSH* – “You’re gonna feel funny.”

Atrial flutter during adenosine bolus

Figure 2. A few seconds after the adenosine push.

…only to see the saw-tooth waves of atrial flutter marching across the monitor?

While you may have performed a successful diagnostic test, your unsuspecting patient has just been given a sneak peek of the day their heart quits beating with no relief from the arrhythmia actually causing their symptoms.

Atrial flutter with variable conduction

Figure 3. s/p adenosine.

Well, you need-not make that mistake again, because I’ve put together a rough list of (almost) every tip out there for diagnosing subtle atrial-flutter with 2:1 conduction. In the end you’ll be talented enough to recognize this arrhythmia with your monitor upside-down (hint)!


There’s three things you need to understand about the physiology of atrial flutter:

  1. Most flutter is caused by a re-entrant circuit that travels around the annulus of the mitral valve. The best way to visualize the mechanism is to watch the animation in the “Atrial Flutter” section of this tutorial (but it’s worth your time to run through all the other chapters).
  2. Because the flutter circuit does not utilize the AV-node, adenosine almost never has an effect on the atrial portion of the arrhythmia; it just temporarily interrupts conduction to the ventricles (and bothers the patient).
  3. New-onset or untreated atrial flutter most often presents with 2:1 conduction ratios, with two flutter waves occurring for every QRS complex.

Flutter isn’t always easy to spot

Basic dysrhythmia classes make it seem like atrial flutter is a simple arrhythmia to identify—just look for prominent saw-tooth waves.

Clockwise atrial flutter with variable conduction

Figure 4. This clockwise atrial flutter is almost suspiciously easy to spot.

That isn’t always the case. Here’s an extraordinarily subtle case of of atrial flutter with 2:1 conduction.

Subtle atrial flutter with 2:1 conduction

Figure 5. Extremely subtle atrial flutter with 2:1 conduction

Consider 2:1 flutter in anyone with a heart rate of 100–200 bpm

2:1 atrial flutter

Figure 6. 2:1 Flutter with an atrial rate of 336 /min and a ventricular rate of 168 bpm.

2:1 atrial flutter

Figure 7. 2:1 flutter with an atrial rate of 224 /min and a ventricular rate of 112 bpm.

It’s going out on a limb, but I’m going to boldly state that you’re unlikely to come to the correct diagnosis unless you think of it first. Atrial flutter is said to be fairly uncommon, but my personal experience begs to differ. It is indeed less prevalent than atrial fibrillation, but I see an example almost every day in my emergency department, so it’s still very common in its own right. It may seem like overkill to think about it almost every time you encounter a tachycardic patient, but I guarantee it’s an easy habit to pick up and you’ll look like a rock-star picking up flutter that otherwise would have been missed. Now, a lot of things can cause a rate in that range, including sinus tach and a-fib, so that brings us to the next sign…

The heart rate in 2:1 flutter is extremely stable

HR trend in 2:1 flutter

Figure 8. Stable HR trend in a patient with 2:1 atrial flutter.

Atrial fibrillation is usually fairly easy to identify because it is truly irregularly-irregular, but both a-flutter with uniform conduction and sinus tach are described as being regularly-regular. While this may be true if you’re feeling a manual pulse, watch the heart rate generated by the monitor and sinus tachycardia will almost always show at least some variation over the course of a few minutes. In atrial flutter with fixed conduction, while the rate displayed may occasionally vary by a beat or two, it will hardly move (Fig. 8). Sinus tach won’t do that. Every rule has an exception, however, and there are plenty of times when the rate will vary with a-flutter, leading to our next tip…

Look for breaks in the regular rhythm

2:! atrial flutter with PVC

Figure 9. 2:1 atrial flutter with a single PVC

Atrial flutter

Figure 10. Atrial flutter with 2:1 conduction and brief periods of 3:1 conduction.

Occasionally even untreated flutter may waver from 2:1 conduction for a beat or two, and those moments should be used to scrutinize the strip for signs of atrial activity. PVC’s in particular can provide a brief glimpse of the underlying rhythm. Vagal maneuvers are an option but aren’t always successful. Additionally, flutter tends to crop up in elderly patients—a population famous for passing out if they bear-down too hard—so maybe having them Valsalva is not the slickest choice. On the other hand, if the only other route is adenosine, vagal maneuvers may be easier to tolerate. Unfortunately, vagal maneuvers often fail or are not a option, and cases where the rhythm shows gaps without provocation are pretty uncommon, so knowledge and experience really are the key to identification.

Scrutinize every lead

Atrial flutter best seen in V1

Figure 11. Atrial flutter, with F-waves only visible in V1.

The standard ECG has 12-leads so quit relying on just monitoring lead II for arrhythmia identification! While flutter waves typically show up well in lead II, they tend to show up best in III and aVF. Also, we’re not talking about easy cases here, so use all of the information available to you. V1 is an excellent lead for detecting atrial activity, especially flutter waves (or the “Lewis lead” if you’re monitoring), and don’t discount less common views of the heart like aVR. Flutter waves usually appear upright in V1 and aVR, sometimes making them easier to spot than the inverted F-waves in II, III, and aVF.

2:1 atrial flutter

Figure 12. 2:1 atrial flutter with F-waves best visible in leads I, aVR, and V1.

The Bix rule

2:1 atrial flutter Bix rule

Figure 13. 2:1 atrial flutter demonstrating the Bix rule.

Harold Bix, a cardiologist from Vienna, noted that if a P-wave is located halfway between two QRS complexes, there’s a good chance there is also a P-wave buried inside the QRS as well. Since flutter waves tend to be somewhat wide and rarely fall perfectly inside a narrow QRS complex, you can often find signs of buried waves as slurring in the upstroke or downstroke of the QRS. In the EKG above there is a slight “notch” or “slur” at the tail end of each QRS complex, confirming that there is indeed atrial activity hidden there.

Bix atrial flutter

Figure 14. “Bix” F-waves.

Not all tracings are going to give you a hint of the buried activity. In those instances all you can rely on is Bix’s suggestion, your clinical suspicion, and the other tips presented here.

Bix rule 2:1 flutter

Figure 15. Believe it or not, and despite the cardiologist’s official interpretation at the top, this is actually 2:1 atrial flutter (proven after giving diltiazem). The only hint that there might be hidden atrial activity on this tracing is the Bix rule. This is from the same patient as the ECG in Fig. 11.

ST or T-wave abnormalities are the norm

Atrial flutter false-positive STEMI

Figure 16. Atrial flutter triggering a false-positive STEMI interpretation.

Atrial flutter is excellent at mimicking ST-depression and ST-elevation. It can also leave the T-wave totally unidentifiable in some leads. This is because flutter waves are relentless and will barrel through everything on a tracing. QRS complexes are relatively large deflections and not easily affected, but ST-segments and T-waves end up being fairly susceptible to distortion. Because of the timing and slope of the F-waves in 2:1 flutter, this most often manifests as apparent ST-depression in the inferior leads. Any unusual ST-depression, T-wave shapes, or unexpectedly biphasic T-waves should tip you off to search for signs of more buried deflections approximately 200 ms later (1 large box, corresponding to the usual atrial rate of 300 bpm).

The presence of atrial flutter should also make you question the diagnosis of STEMI. The two can be present at the same time but it is a pretty rare occurrence and most computer-generated statements of STEMI in the setting of flutter are false-positives. Acute MI can sometimes trigger atrial fibrillation but it’s rather unusual for it to present with new-onset flutter. That said, flutter + STEMI is not impossible, especially if the patient has a history of the former, and if the EKG shows a clear STEMI then it’s a STEMI.

Never trust the computerized interpretation

2:1 atrial flutter, misdiagnosed as sinus tach by the GE Marquette algorithm.

Figure 17. 2:1 atrial flutter, misdiagnosed as sinus tach by the GE Marquette algorithm.

2:1 atrial flutter, misdiagnosed as "SVT" by the Mortara VERITAS algorithm.

Figure 18. 2:1 atrial flutter, misdiagnosed as “SVT” by the Mortara VERITAS algorithm.

It’s fairly well-known that the GE Marquette 12-lead algorithm is a poor diagnostician of rhythm abnormalities, but when it comes to 2:1 atrial flutter it is especially flawed. In my experience an incorrect interpretation is the norm. The Mortara VERITAS algorithm is much better at considering the possibility of flutter (though it has plenty of other flaws), but it’s still not perfect.

It just doesn’t look right

This funny-looking-tachycardia is actually 2:1 atrial flutter.

Figure 19. This funny-looking-tachycardia is actually 2:1 atrial flutter.

When it comes to odd-looking rhythms with very wide complexes, hyperkalemia should always pop into your mind. In the same vein, if you see a tachycardia that just doesn’t look like a typical sinus tach, AVNRT, or AVRT (“SVT” if you prefer the vernacular for the latter two), consider atrial flutter.

Turn the beat around

This is probably my favorite trick of the bunch so I’m not sure why it’s buried so far down the list.

Most people don’t realize this, but disco singer Vicki Sue Robinson was not an actual electrophysiologist. Lacking an MD or DO, her rendition of the hit song “Turn the Beat Around,” which instructed cardiologists to, “turn the beat around, turn it upside-down,” still managed to make waves in the diagnosis of atrial flutter.

Flutter waves tend to show up best as negative deflections in the inferior leads (II, III, aVF), so if you’re considering the diagnosis, flip the ECG upside down and look at these leads. You’ll be amazed how much easier it is to identify the regular F-waves of flutter once they’re upright. It also makes it easier to see how those ST and T-wave distortions mentioned in #6 really are the predictable result of atrial activity.

It looks like an ectopic atrial rhythm, but the Bix Rule tells us to consider buried atrial activity here...

Figure 20. It looks like an ectopic atrial rhythm, but the Bix Rule tells us to consider buried atrial activity here…

Zooming in on the leads with the most clear atrial activity…

Those S-waves look a little wide, but not markedly abnormal...

Figure 21. Those S-waves look a little wide, but not markedly abnormal…

When flipped…

Flipping the leads vertically (and horizontally so it still reads left-to-right), those wide S-waves look a bit more like they're hiding something. This was confirmed to be markedly slow atrial flutter in a patient on carvedilol.

Figure 22. Flipping the leads vertically (and horizontally so it still reads left-to-right), those wide S-waves look a bit more like they’re hiding something. This was confirmed to be markedly slow atrial flutter in a patient on carvedilol. Flipping the leads vertically (so it still reads left-to-right), it becomes a bit more suggestive that those wide S-waves are hiding something. With the P-waves now upright, it is easier to see that the terminal portion of the S-waves look very similar to the tail end of the P-waves. This was confirmed to be markedly slow atrial flutter in a patient on carvedilol.

If it’s less than 150 bpm it still might be 2:1 flutter

Many anti-arrhythmic medications (I’ve always thought mostly class I and III, but apparently at least some, if not all beta-blockers as well) can slow down the rate of the circus movement of the atria, consequently slowing down ventricular response. Of note, this can lead to a very dangerous state if the atrial rate slows down enough for the AV node to begin conducting 1:1 rather than the default 2:1. This becomes a big concern with the use of class I antiarrhythmics, which have a tendency to slow down the rate of  the flutter circuit without actually breaking the rhythm. 300 /min is too fast for the AV-node to conduct, but slow the atrial rate to 220 /min without also blocking the AV-node and the patient’s ventricular rate can suddenly jump from a rate of 150 bpm with 2:1 conduction to 220 bpm with 1:1 conduction.

I missed this one but the Mortara VERITAS algorithm somehow picked it up. Very slow 2:1 atrial flutter with an atrial rate of 206 /min.

Figure 23. I missed this one but the Mortara VERITAS algorithm somehow picked it up. Very slow 2:1 atrial flutter with an atrial rate of 206 /min.

3:1 flutter with an atrial rate of 195 /min.

Figure 24. 3:1 flutter with an atrial rate of 195 /min.

Atrial flutter with variable conduction and an atrial rate of 225 /min.

Figure 25. Atrial flutter with variable conduction and an atrial rate of 225 /min.

Atrial flutter with 4:1 conduction and an atrial rate of 186 /min.

Figure 26. Atrial flutter with 4:1 conduction and an atrial rate of 186 /min.

A saw-tooth pattern is not necessary to seal the diagnosis

Very few of the EKG’s I’ve shown so far have demonstrated the clear, classic “saw-tooth” pattern that is touted as being representative of atrial flutter. The F-waves of flutter can take a variety of morphologies, but most often the bulk of the wave is negative in the inferior leads and upright in V1. Also, as the atrial rate slows with the use of medications, there is a loss of F-wave amplitude and the morphology can become incredibly subtle. This makes slow atrial flutter, at rates that often causes us to omit flutter from our differential, very difficult to identify.

There’s no easy way to get around these tough cases and your best tool will be keen observation. Keep an eye open for repeating patterns in the baseline with a consistent relationship to the QRS complexes that could easily be written off as artifact.

CAUTION – MATH! – If there is variable conduction to the ventricles, atrial fibrillation becomes a common misdiagnosis. Measure a bunch of R-R intervals and look for a lowest-common-denominator. For example, if the atria are contracting at 300 bpm, meaning F-waves are 200 ms apart (1 large box), even with variable conduction every RR interval should be a multiple of 200. This means that 2:1 conduction would result in R-waves exactly 2 large boxes apart (400 ms); 3:1 conduction leads to R-waves 3 large boxes apart (600 ms); and 4:1 conduction would exhibit 4 large boxes between R-waves (800 ms). It’s minutiae for a diagnosis that probably won’t change the treatment plan, but who cares about patient outcomes when you can prove to everyone that you’re smarter than them.

F-waves are not exclusive to flutter

If you see what appear to be F-waves at a rate exceeding 350 bpm, they’re probably “f-waves” associated with atrial fibrillation (note the clever use of lower-case in this case). The key to this distinction is that in atrial flutter with regular conduction (be it 2:1, 4:1, or 7:1), the QRS complex will typically appear at a regular interval in relation to the F-waves. In fibrillation the QRS will vary its relationship to the f-waves. The morphology of fibrillatory f-waves will often vary as well, sometimes by a very small degree, though I have also seen cases of very regular appearing fibrillatory waves.

There’s also a rare form of atrial flutter (type II) that can generate flutter waves at 340-440 bpm, but in contrast to a-fib, this should still present with a fairly fixed relationship between the F-waves and QRS complexes.

Confusing things further, if the rate is less than 250 bpm it may be an entity known as “atrial tachycardia.” In A-tach you will see distinct P-waves of abnormal morphology at a rate exceeding the normal physiological rate of sinus rhythm, often with similar conduction ratios to a-flutter, except they don’t have the saw-tooth pattern of flutter waves and are slower. As I stated in #9, there can be some overlap with slow a-flutter and atrial tach, leaving a diagnostic grey-zone. Thankfully they’re still treated the same acutely.

Small fibrillatory waves with a changing morphology in V1 and a irregularly-irregular ventricular response confirms this is atrial fibrillation.

Figure 27. Small fibrillatory waves with a changing morphology in V1 and a irregularly-irregular ventricular response confirms this is atrial fibrillation.

There are large waves in V1 that very closely resemble atrial flutter. There is a slight variation to their morphology and peak-peak interval which, combined with the irregularly-irregular ventricular response confirms atrial fibrillation.

Figure 28. There are large waves in V1 that very closely resemble atrial flutter. There is a slight variation to their morphology and peak-peak interval which, combined with the irregularly-irregular ventricular response confirms this is actually atrial fibrillation.

Again, this looks like atrial flutter at first glance, but there is a changing morphology to the atrial waves and the ventricular rhythm is irregularly-irregular. This is atrial fibrillation.

Figure 29. Again, this looks like atrial flutter at first glance, but there is a changing morphology to the atrial waves and the ventricular rhythm is irregularly-irregular. This is atrial fibrillation.

Ectopic atrial tachycardia with 2:1 conduction—difficult to differentiate from 2:1 flutter.

Figure 30. Ectopic atrial tachycardia with 2:1 conduction—difficult to differentiate from 2:1 flutter.

Read a lot of ECG’s

If you’ve spent any time studying ECGs beyond the simplistic introduction to arrhythmias we all start with, it has probably become apparent that there is a lot of gray surrounding the many distinct electrophysiologic abnormalities recognizable on a 12-lead. This post is not intended to act as a hard framework for making the diagnosis of atrial flutter, but is merely a collection of the thoughts that cross my mind when I’m dissecting a difficult tracing. In these cases there will always be a lot of overlap with atrial fibrillation, AVNRT, atrial tachycardia, and several other dysrhythmias. The best advice I can offer is just to read LOTS of ECGs. There are scores of algorithms and diagnostic criteria to aid in making an electrocardiographic diagnosis, and while they have their place and can be of some utility (e.g. the aVR algorithm for ruling-in V-Tach, or the Sgarbossa criteria for recognizing STEMI w/ LBBB), the most useful tool is a well-trained eye capable of noticing when something on a tracing just doesn’t fit.

The 12 Rhythms of Christmas: Sinus Bradycardia

This article is the second 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 of last year’s 12 Leads of Christmas.

We were almost day behind kicking off the series (a peril of posting around the holidays), so I’m going to interrupt my planned order with an easy post to get things back on schedule. The arrhythmia hinted at near the end of the first post will instead be revealed tomorrow.

Last year I posted a nearly identical article titled Don’t let your bradycardic patient D.I.E., but this is an update focused on sinus bradycardia and with a slightly new mnemonic. Our new post should be called, Don’t let the cause of bradycardia H.I.D.E..

Sinus Bradycardia

I’ve told you before that I’m terrible with mnemonics, but there is one I used to find both memorable and useful: the DIE mnemonic for insidious but reversible causes of bradycardia in the emergency medicine and acute care setting. DIE stands for drugs, ischemia, electrolytes. While I love its simplicity, I no longer rely on that exact mnemonic because it leaves out an important cause of bradycardia you do not want to miss—hypothyroidism.

Unlike ischemia, hypothyroidism is not a major concern from a prehospital perspective, and unlike hyperkalemia, it’s not quickly reversible, but given its importance in the trajectory of a patient’s care and how easily it can be overlooked, I think it still deserves a spot in my favorite memory aid.


Yes, there are other causes of bradycardia that should be on your differential, but what makes this list special is that all four have specific emergency treatments, the standard ACLS trio of pacing, atropine, and dopamine/norepi does little or nothing to address them, and, if missed, patients are unlikely to get better with only supportive care.

It’s okay to miss Lev’s disease in the emergency setting because the definitive treatment is contained in the usual ACLS algorithm: pacing. If you don’t recognize that your patient is hyperkalemic, however, then all the atropine and transcutaneous pacing in the world isn’t going to lower her potassium.

You don’t even need to have heard of sick sinus syndrome to properly treat it, again with pacing. If you miss ischemia though, and don’t transport/transfer the patient to a PCI center, there could be serious mobidity or even mortality down the line.

I don’t think you need the EKG to diagnose hypothermia and start warming, but you’d better be considering medication effects in every significantly bradycardic EKG you see. Beta blockers and calcium channel blockers can easily sneak past your differential, while the QT-prolonging effects of other anti-arrhythmics can be magnified by a slow heart rate and pose an extra threat of sudden death that must be considered.

While the Cushing reflex is an important cause of bradycardia and its care is mostly supportive, the underlying issue (increased ICP) is usually clear. If a patient is unresponsive with decompensated hypothyroidism (myxedema coma), however, supportive care will get them nowhere unless someone decides to check their thyroid function. Since the majority of patients we see with a decreased level of consciousness are experiencing neurological events, sepsis, and/or drug/alcohol intoxication, it requires a high level of suspicion to pick up the more subtle signs of serious hypothyoidism.


While decidedly less common than the other three entities, as discussed above, it is no less important. If hypothyroidism is not suspected as the cause of a patient’s bradycardia during the patient’s initial presentation, it is unlikely it will be picked up down the line. Certainly not all patients with hypothyroidism are bradycardic, but it’s certainly worth considering when the finding is present.

We don’t have time to delve deeper into the diagnosis of severe hypothyroidism and myxedema coma, but the linked articles over at Medscape are a good starting point.

Sinus bradycardia, T-wave inversions, hypothyroidism

Figure 1. This ECG was performed on a patient with severe hypothyroidism whose TSH was 60.12 mcIU/mL (ref 0.36–3.74) and Free T4 0.19 ng/dL (ref 0.76–1.46).



Despite its relatively high prevalence, ischemia is probably (hopefully?) the least missed of the four topics discussed here. Still, even though most STEMI’s present with normal heart rates, subtle ischemia is common and can be accompanied by bradycardia, so it’s good to force yourself to at least consider the possibility in any patient with a low heart rate. Though brady-dysrhythmias (i.e. SA node dysfunction, AV-blocks) are often associated with inferior MI’s due involvement of the SA and AV-nodes, standard sinus bradycardia can be see with STEMI’s of any distribution.

Acute inferior STEMI with sinus bradycardia

Figure 2. Acute inferior STEMI with sinus bradycardia

Acute anterior STEMI with sinus bradycardia

Figure 3. Acute anterior STEMI with sinus bradycardia

Early acute anterior STEMI with sinus bradycardia

Figure 4. Early acute anterior STEMI with sinus bradycardia

Acute inferior STEMI with sinus bradycardia

Figure 5. Acute inferior STEMI with sinus bradycardia

Inferior STEMI with sinus bradycardia and a PAC

Figure 6. Late inferior STEMI with sinus bradycardia and a PAC

Figure 7. Acute inferior STEMI with sinus bradycardia

Figure 7. Acute inferior STEMI with sinus bradycardia

Acute anterior STEMI with marked sinus bradycardia

Figure 8. Acute anterior STEMI with marked sinus bradycardia



I’m going to throw around the terms “drugs” and “overdose,” but what we’re really talking about is any supratherapeutic levels of an illicit drug or prescribed medication the patient may have taken. The overdose can be intentional or accidental, and things like decreased renal function can lead to the latter without the patient even taking a single extra pill. The culprits I worry about most in the undifferentiated bradycardic patient are calcium channel blockers, beta blockers, and digoxin, but there’s a whole host of medications—lots of them anti-arrhythmics—that cause marked bradycardia in excessive doses.

Sinus bradycardia, prolonged QT, sotalol overdose

Figure 9. Sinus bradycardia and a prolonged QT-interval in a patient with supratherapeutic sotalol levels

Sinus bradycardia and a prolonged QT-interval in a patient with sotalol overdose, courtesy of Life in the Fast Lane. Click image for source.

Figure 10. Sinus bradycardia and a prolonged QT in a patient with sotalol overdose, courtesy of Life in the Fast Lane. Click image for source.



In terms of overall numbers, I believe that electrolyte disturbances are certainly the most missed cause of bradycardia. It’s unusual to miss ischemia significant enough to cause bradycardia, and drug toxicity and hypothyroidisn are relatively uncommon presentations of bradycardia, but electrolyte abnormalities are an everyday event in most emergency departments.

When we talk about electrolytes in reference to brady-arrhythmias, what we really mean is the serum potassium level, and Hyperkalemia is by far the most common bradycardia-producing electrolyte abnormality. While calcium can affect your ST/T-waves, it is typically not a direct cause of bradycardia. Despite it’s huge role in cardiac action potentials, serum sodium levels actually have little effect on the surface ECG (though sodium channel blockers do…). Similarly, though magnesium plays a role in some arrhythmias, there are no direct EKG signs of hyper/hypo magnesemia. It’s an even less exciting story for the rest of the electrolytes.

While emergency care providers know to look for peaked T-waves and wide QRS complexes, it is constantly sobering just how subtle the signs of hyperkalemia can present on the EKG. Below are just a couple of the subtle hyperkalemia cases I’ve encountered with sinus bradycardia. Importantly, hypokalemia can also present with bradycardia in rare cases, but it is much more often associated with a normal or tachycardic rate. Still, it’s worth keeping in mind.


Figure 11. Sinus bradycardia and mild QRS prolongation in a patient with potassium and a K+ of 6.9 mEq/L.

Subtle hyperkalemia with peaked T-waves

Figure 12. Sinus bradycardia and subtly peaked T-waves in a patient with mild hyperkalemia and a K+ of 5.8 mEq/L.

Severe sinus bradycardia with hyperkalemia

Figure 13. Severe sinus bradycardia in a patient with hyperkalemia and a potassium of 6.5 mEq/L.

Severe sinus bradycardia in hypokalemia

Figure 14. Severe sinus bradycardia in a patient with hypokalemia and a potassium of 1.9 mEq/L.


Let’s discuss rate (again)

While we expounded on the rate bounds of sinus tachycardia yesterday, we should also touch on the definition of sinus bradycardia (in less detail). And, same as before, I don’t agree with most of the published numbers…

Just like we stated that there is no strict upper limit for the rate of sinus tachycardia, there is no lower limit for sinus bradycardia. If the sinus node is firing 10 times a minute, then that is sinus brady all the same (although marked or extreme; see Fig. 13 and Fig. 14).

What about the upper limit for sinus bradycardia? Most folks say it’s 60 bpm; I say it’s 55 bpm. Some people even choose 50 bpm as their definition, but I like 55 because a heart rate of 52 bpm—while likely benign—is still something I believe is worth commenting on. The reason I think 60 bpm is too high is that a lot of patients are on medications to control their heart rates, while those that aren’t tend to be more fit, with the result being that it’s exceedingly common to see rates in the 55-60 bpm range. Additionally, unlike subtle tachycardia—which I find to be very useful in my patient assessments—a heart rate of 57 bpm doesn’t really alert me to anything worthwhile (except in rare cases), so I don’t get anything out of defining it as “abnormal.”