71 year old male with “seizures” that prove to be ICD shocks

EMS is called to the residence of a 71 year old male for “seizures.”

On arrival the patient’s spouse meets the ambulance outside and hurries the paramedics along saying “Come quickly! Please help him!”

The paramedics arrive at the patient’s side just in time to see him receive an ICD shock.

They ask how long this had been going on.

“That was my 15th shock!”

The patient states that he “felt himself going faint” just prior to the first shock.

The cardiac monitor is attached and the following rhythm strips are recorded.


The patient appears anxious. His skin is pink, warm, and moist.

Numerous skin tears are noted to the patient’s arms which the spouse states are related to convulsions induced by the ICD shocks.

Vital signs are assessed.

  • RR: 20
  • HR: 60
  • NIBP: 108/72
  • SpO2: 98% on room air

Past medical history:

The EMS crew learns that this patient survived two sudden cardiac arrests prior to receiving his first ICD in 1992. The device was replaced in 2008. The patient does not have his device ID card but knows that it was made by St. Jude Medical.


The patient states he takes several medications but he can only remember one of them: Coumadin.

The EMS crew contacts Online Medical Control and receives permission to apply a ring magnet to the device. The magnet is applied and taped in place. The tape doesn’t hold and a FF is assigned to hold the magnet over the device.

A 12-lead ECG is obtained.


And another.


A bigeminal rhythm is noted on the monitor.


The patient is loaded for transport.

IV access is achieved.

En route the the hospital serial 12-lead ECGs are obtained.



Vital signs are re-assessed.

  • RR: 18
  • HR: 76
  • NIBP: 102/70
  • SpO2: 99% on room air

The patient feels much calmer and says, “Please don’t let that thing shock me again.”

A final 12-lead ECG is captured on arrival at the hospital.


What do you think the patient would say was the most important thing the EMS crew did for him?

For a full discussion of inappropriate or ineffective ICD shocks, including when and how to apply a ring magnet, see the following links.

Inappropriate or ineffective ICD shocks: Part 1

Inappropriate or ineffective ICD shocks: Part 2

Inappropriate or ineffective ICD shocks: Part 3

Updated 01/06/2016

90 year old female with abdominal pain and wide complex tachycardia

EMS is called to the residence of a 90 year old female who awoke to an “uncontrolled bowel movement” that corresponded with sudden onset abdominal pain.

On EMS arrival, the patient is alert and oriented to person, place, time, and event. She has a grimace on her face and appears acutely ill.

When asked the exact location of her pain she points to the epigastric area.

Past medical history: “Cardiac problems”

Medications: Numerous (but list unavailable)

Vital signs are assessed.

  • RR: 18 shallow
  • HR: Too rapid to count
  • NIBP: 118/60
  • SpO2: 96% on room air

The cardiac monitor is attached.

A wide complex tachycardia is noted with a rate of 194.


The patient is immediately loaded on the gurney and relocated to the back of the ambulance where she is placed on oxygen, an IV is established, and the combo-pads are placed.

Breath sounds are clear bilaterally.

A pacemaker is noted in the upper-left chest.

A 12-lead ECG is captured.

Atypical RBBB morphology in lead V1 (left bunny ear taller than right bunny ear) with QS complex in lead V6 and right axis deviation.


wellensWellens’ Criteria

Wide and fast rhythms should be considered VT until proven otherwise. Regardless, in this case the morphology strongly favors VT over SVT with aberrancy.

See also: 60-Second Soapbox: Wide Complex Tachycardia at Academic Life in Emergency Medicine.

At this point the patient’s skin appears grayish, pasty, and moist. Her level of consciousness is diminished and she stops responding to verbal stimuli.

Synchronized cardioversion is performed at 100 J.


The patient is successfully converted to sinus rhythm and immediately becomes more responsive.


Another 12-lead ECG is obtained on arrival at the hospital.


Sinus rhythm with demand pacing at a rate of 70.

The patient was given amiodarone and admitted to the ICU.


Wellens HJ, Bar FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med 1978;64:27-33.

The 12 Rhythms of Christmas: High-Grade AV-Block

This article is the eighth in our latest series, The 12 Rhythms of Christmas, where each day we examine a new rhythm disorder. It’s a continuation of the theme behind last year’s 12 Leads of Christmas.

In our recent articles we’ve discussed three different types of AV-block that cause dropped P-waves: type I, type II, and 2:1 AV-block. Consider the prototypical tracings from each article:

Type I AV-block (Wenckebach)

Figure 1. Type I AV-block.

Type II AV-block

Figure 2. Type II AV-block.

2:1 AV-block

Figure 3. 2:1 AV-block of uncertain mechanism.

Each shows different conduction ratios—ranging from 2:1 to 3:2 to 4:3—but they don’t demonstrate something like 3:1 conduction, where two P-waves in a row would be blocked before the third one conducts.

That’s because we classify that with another distinct term:

High-Grade AV-Block

High-grade AV-block (sometimes called advanced AV-block) is how we describe a form of pathological AV-block where two or more consecutive P-waves fail to conduct to the ventricles.

High-grade AV-block

Figure 4. High-grade AV-block with 3:1 conduction. There are 3 P’s for every 1 QRS.

Why don’t we just call the tracing in Fig. 4 type II AV-block? Think back to the basis of our article on 2:1 AV-block: Since we never see two P-waves in a row that conduct, we cannot assess whether the PR-interval is progressively increasing (as in type I AV-block) or fixed (as in type II AV-block). You might think  that all high-grade AV-blocks must be due to a type II mechanism because the conduction defect looks so severe, but even type I AV-blocks can exhibit the sort of behavior we see above. In fact, based on subsequent tracings (not shown here), there’s a pretty decent chance both the patients whose rhythms we’re going to examine in this post were experiencing high-grade AV-block due to an underlying type I mechanism.

So, just like 2:1 AV-block, high-grade AV-block can have an underlying conduction defect that is either type I or type II in mechanism, but since we usually cannot tell which it is from the surface ECG, we have to use a different name and reserve those latter two terms for cases where we can prove (or at least highly suspect) the actual pathology at play.

High-grade AV-block does not include physiological AV-nodal activity, like we see sometimes with ectopic atrial tachycardia or atrial flutter, where it’s possible to see two consecutive non-sinus P-waves dropped as a matter of normal physiology. As a result, to be diagnosed as “high-grade AV-block” the atrial rate should be reasonable (Marriott proposed less than 135 /min[1]) and regular. Excessive atrial rates, like the 300 /min we see with atrial flutter, can display 3:1 or 4:1 conduction as a normal finding—especially if the patient is on an AV-nodal blocking medication.

Atrial flutter with 4:1 conduction

Figure 5. Atrial flutter with 4:1 conduction. This is NOT high-grade AV-block.

It also does not include complete heart block, where no sinus P-waves are conducted to the ventricles.

Complete AV-block

Figure 6. Complete AV-block. This is NOT high-grade AV-block either.

Importantly, high-grade AV-block is not synonymous with high-degree AV-block. The latter is a non-specific term sometimes used to designate more malignant conduction disturbances—like type II and complete AV-block—from first degree AV-block (and sometimes type I), but I’ve never seen a consensus for its definition and its use is not encouraged.

Most resources do not give much consideration to high-grade AV-block, which is a shame because it can present some pretty interesting rhythms. Let’s look at a few, starting with the 12-lead from Fig. 4.

High-grade AV-block

Figure 7. Contrary to the cardiologist’s interpretation, this is high-grade AV-block.

I would not fault most folks for wanting to call the rhythm in Fig. 7 complete AV-block—every single provider involved in the patient’s care did—but it’s not. The first clue here is the fixed PR-intervals:

High-grade AV-block

Figure 8. Fixed PR-intervals, measured in milliseconds.

That could just be a fluke of timing that is sometimes seen with complete heart block, so let’s also look at the RR-intervals.

High-grade AV-block

Figure 9. Slightly varying RR-intervals, measured in milliseconds.

Now that’s an important finding; there is subtle but significant variation in the RR-intervals. In order for the PR-intervals to be perfectly fixed with a fluctuating ventricular rate, there must be a corresponding rise and fall in the atrial rate as well. For those two things to occur independently—and with the exact same magnitude—pushes this beyond the realm of coincidence.

There must be communication between the atria and ventricles, and we can say with certainty that we are looking at high-grade AV-block.

Here’s a more complicated (and interesting) example:

High-grade AV-block

Figure 10. A trickier example of high-grade AV-block.

The first clue is that we’re not dealing with complete AV-block is that the ventricular rate is again irregular—this time markedly so.

High-grade AV-block

Figure 11. Varying RR-intervals in high-grade AV-block.

Most examples of complete AV-block display an unwavering ventricular rate since the ventricles are under the sole control of an isolated junctional or ventricular escape pacemaker, which are both typically very regular (see Fig. 6). Even if an observant reader notes the irregularity in the above rhythm, their next step is often to mistakenly attribute it to PVC’s. While the early complexes are indeed wide (I peg them right around 125 ms), they do not display a morphology really consistent with ventricular ectopy. I’d describe them more as resembling a left anterior fascicular block with non-specific QRS widening.

It turns out the early complexes we see above are actually capture beats from occasional sinus impulses managing to make it through the AV-node. Since some sinus discharges are making it through, it cannot be complete AV-block.

High-grade AV-block

Figure 12. Escape (E) and capture (C) complexes labelled in the tracing from Fig.7.

Proof that the early beats really are due to sinus capture can be found in the PR-intervals (again).

High-grade AV-block

Figure 13. While the fixed red PR-invervals are indicative of capture, the varying blue PRi’s are not actually representative of atrio-ventricular communication.

You will note that the early capture beats display a fixed PR-interval of 425 ms (shown in red). I attempted to measure a possible PR-interval for the late QRS complexes but: 1) it doesn’t make sense for them to show a longer PR-interval than the early QRS’s (the immediately adjacent P-waves produce too-short a PRi to be viable options), and 2) there is a bit of variance. This variance is pretty small and wouldn’t be a big issue if not for one final scrap of evidence: Looking back at Fig. 11, the escape complexes share the exact same “escape interval” (a term I think I just made up) of 1730 ms. If the late complexes were actually sinus is origin it be highly unlikely for this perfect coincidence to occur, especially since there is some minor irregularity in the atrial rate.

It might seem counter-intuitive for the escape complexes to appear more narrow than the capture beats, but that is because they arise from the His-Purkinje system below the level of the block, while the capture beats—which have to traverse the block—also experience a certain degree of non-specific aberrancy en route to the ventricles.


Here’s an even more subtle example of the same phenomenon, but hopefully it will reinforce the concepts we just discussed. It’s actually from the same patient as Fig. 7, just from two days before during her initial presentation to the ED.

High-grade AV-block

Figure 14. Another example of high-grade AV-block.

The ventricular rate appears more regular in this example, but pay close attention to the shape of the QRS complexes in lead II. They appear to alternate in morphology!

Alternating morphology in high-grade AV-block

Figure 15. Alternating morphology in high-grade AV-block.

This subtle change in QRS morphology prompts us to look for more clues…

High-grade AV-block

Figure 16. Subtle alternations in the RR-intervals.

As in the last case, the longer RR-intervals are perfectly fixed while there is a minor variation in the shorter RR-interval. What are the PR-intervals up to?

High-grade AV-block

Figure 17.

Again, the slightly early complexes all share the same exact PR-interval while there are subtle variations when you attempt to couple P-waves to the late-arriving QRS complexes. It seems we are again seeing high-grade AV-block with alternating escape and capture beats. This subtle form of alternating long and short RR-intervals due to alternating escape and capture beats (respectively) can be termed, appropriately enough, escape-capture bigeminy.

High-grade AV-block

Figure 18. High-grade AV-block with escape-capture bigeminy.

Tomorrow we’ll discuss the dramatic situation we see below, where most of the time the patient is in a normal sinus rhythm with no significant AV-block but then he or she suddenly drops several P-waves in a row before just as suddenly resuming normal conduction.

Paroxysmal AV-block

Figure 19. Despite the consecutive dropped P-waves (hard to see but present) this is not high-grade AV-block.

Further Reading

For more on high-grade AV-block and to see more tracings from the patient featured in Fig. 7 and Fig. 14, please check out CCT Jason Roediger’s post and ladder diagrams walking through why we see the patterns we do with high-grade AV-block; they are phenomenal! Here’s a link, and make sure you check out the comments at the bottom.

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: 2:1 AV-Block

This article is the seventh in our latest series, The 12 Rhythms of Christmas, where each day we examine a new rhythm disorder. It’s a continuation of the theme behind last year’s 12 Leads of Christmas.

Our last two posts have examined type I and type II AV-block, so it’s only fitting that we continue our theme with a topic that combines the two:

2:1 AV-Block

While most everyone has heard of first degree, type I, type II, and complete AV-block, comparatively few people recognize 2:1 AV-block as a valid rhythm diagnosis in its own right. That’s a shame, because 2:1 AV-block is a rather interesting finding. To understand why, consider the following dilemma:

  • Type I AV-block presents with progressively increasing PR-intervals until a P-wave is blocked
    Type I AV-block (Wenckebach) PR-intervals

    Figure 1. Increasing PR-intervals in the setting of type I AV-block. Measurements are in milliseconds.

  • Type II AV-block presents with fixed PR-intervals until a P-wave is blocked
    Fixed PR-intervals in type II AV-block

    Figure 2. Fixed PR-intervals with type II AV-block. Measurements are in milliseconds.

It should be clear from the two examples above (and the others in this series) that both forms of AV-block can present with various—and actively varying—conduction ratios: 5:4, 4:3, 3:2, etc… That doesn’t affect our ability to diagnose the rhythms, and in fact, it can be helpful to see how the PR-intervals behave with different ratios of P-waves to QRS-complexes.

  • What do you do, however, when every-other P-wave is blocked?
    2:1 AV-block

    Figure 3. 2:1 AV-block of uncertain mechanism.

It’s not a problem you really think about until you first run into it.

At first glance it seems clear that there are constant PR-intervals in Fig. 3, but it is important to note that in order to diagnose type I or type II AV-block, we must be able to see two consecutively conducted P-waves. A constant PR-interval is only meaningful if we see it in consecutively conducted P-waves. While the PR-intervals of the conducted P-waves in Fig. 3 are all the same, we cannot know if they are truly fixed unless we see two P-waves in a row conduct to the ventricles.

I keep repeating that statement because it is so important. If you’re looking at a 2:1 AV-block with a constant conduction ratio (i.e. every-other P-wave is conducting across the entire strip), it’s impossible to differentiate a type I from a type II mechanism.

Think about it: when every second P-wave is blocked you can’t tell if the PR-interval is progressively lengthening (since the AV-node “resets” with each blocked P). As a result, it’s also impossible to determine whether the AV-block we are observing is due to a type I or type II mechanism.

I think I’ve said the same thing about five time but the distinction is important because it can have implications for the patient’s prognosis and management.

What’s a helpless young electrocardiographer to do??

Unless we have strong proof of the underlying mechanism, it is proper etiquette to make no assumptions and simply call the rhythm in Fig. 3 “2:1 AV-block.” Your peers may try to pressure you to pick sides and call it either type I or type II, but the right move is to remain uncommitted and call it what it is: 2:1 AV-block.

For those with a background in physics. it’s almost like the setup for the Schrödinger’s cat thought experiment[1]: If we do not open the box to see if the cat is alive or dead, it may be both at the same time. Likewise, we know it must be of of the two types of AV-blocks governing the 2:1 phenomenon, but since we can’t tell which, we just assume it is both simultaneously. Thankfully, in our case, if we do manage to get a peek at the actual mechanism, there’s not a 50% chance of killing a helpless feline.

Why not guess?

I suppose if you were so inclined you could just assume all 2:1 AV-blocks were due to a type I mechanism and you’d be right more often than not (since type I AV-blocks are more common than type II), but that seems a bit messy for my taste. Plus, if you look at the middle portion of Fig. 2, you’ll note that there is a brief spell of 2:1 AV-block in that proven example of type II AV-block.

Does a bundle branch block help the diagnosis?

Recall that type II AV-blocks are a manifestation of extensive infra-AV-nodal conduction system disease and usually present with a bundle branch block (BBB). So, if you see a 2:1 AV-block with a BBB, does that mean it’s more like to be due to a type II block?


There’s no rule saying type I AV-blocks can’t have a fixed BBB as well. In fact, seeing the two together is quite common, and again, since type I AV-blocks are more common than type II’s, the odds are probably even that a given 2:1 AV-block with a BBB either type I or type II in origin.

In fact, let’s look at the 12-lead from that rhythm strip in Fig. 3.

2:1 AV-block with RBBB.

Figure 4. 12-lead showing 2:1 AV-block with a RBBB.

While there is no bifascicular block, there is a clear RBBB with a prolonged PR-interval on the conducted P-waves. If I was a gambling man I’d be tempted to wager that there was a type II mechanism underlying the 2:1 AV-block.

Good thing I’m not, because I’d be wrong. Here are some more rhythms strip from that same patient showing a clear type I mechanism as the cause of his AV-block (they may seem familiar from our last post on type I AV-block).

Type I AV-block (Wenckebach)

Figure 5.

Type I AV-block (Wenckebach)

Figure 6.

Type I AV-block (Wenckebach)

Figure 7.

Type I AV-block (Wenckebach)

Figure 8.

So there’s no shortcut?

The only way to determine if there’s a type I or type II mechanism is to search for two consecutive P-waves?


Here’s a subtle example that gives away the type I AV-block underlying the 2:1 AV-block. Though the strip appears pretty similar to Fig. 3, there’s one small difference. See if you can spot it.

Type I AV-block (Wenckebach)

Figure 9.

Did you see the two consecutive P-waves that manage to conduct with a lengthening PR-interval?


Figure 10.

Speaking of subtle…

2:1 AV-block can present with astounding subtlety. Here are some examples; would you spot them all?

2:1 AV-block

Figure 11. 2:1 AV-block of uncertain mechanism.

2:1 AV-block

Figure 12. 2:1 AV-block later proven to be due to type II AV-block.

2:1 AV-block

Figure 13. Can you spot the hidden 2:1 AV-block?

2:1 AV-block

Figure 14. This is actually the same patient as Fig. 13, but now the 2:1 AV-block is more apparent.

Subtle 2:1 AV-block

Figure 15. I actually had this categorized as “sinus brady with first degree AV-block” in my collection, but when I pondering its use for some of the other articles in this series something caught my eye… There is actually extremely subtle 2:1 AV-block!


Thanks for following the series, and be sure to catch up below on any of the other rhythms you may have missed!

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


  1. I’m sorry to anyone who actually knows some physics out there; I realize it’s not a great analogy and a disservice to the great thought experiment. If I recall correct, Schrödinger was also proposing the experiment to demonstrate a perceived fallacy underlying quantum mechanics, not to support it.

The 12 Rhythms of Christmas: Type II AV-Block

This article is the sixth in our latest series, The 12 Rhythms of Christmas, where each day we examine a new rhythm disorder. It’s a continuation of the theme behind last year’s 12 Leads of Christmas.

Type II AV-Block

Except for first degree,  type II is probably the simplest of the AV-blocks to identify. There’s really only two major criteria:

  1. P-wave suddenly and unexpectedly fail to conduct to the ventricles.
  2. The PR-intervals of the P-waves that do conduct are fixed and equal.

Let’s examine the ECG below, which exhibits both of those findings. The computer, however, disagrees and suggests and alternate diagnosis. Which of us is right?

Mobitz II AV-block

Figure 1. This ECG has P-waves that don’t conduct; is it type II AV-block?

The first step in our rhythm analysis is to examine the atrial rate for regularity. Why is that important? Because:

The most common cause of a pause is a non-conducted PAC.

Non-conducted PAC’s

Let’s digress for a moment and examine an ECG that the computer interprets as actually showing type II AV-block. It was obtained on a 33 year old male with a chief complaint of pleuritic chest pain x 3 weeks.

Non-conducted PAC's

Figure 2. Sinus rhythm with frequent non-conducted PAC’s interpreted as type II AV-block by the computer.

The first thing you’ll notice on the above ECG is that there are several pauses in the regular sinus rhythm. Close inspection, however, reveals the culprit…

Non-conducted PAC's

Figure 3. Non-conducted PAC’s.

There are P-waves buried in the T-waves preceding each pause! Not only are they P-waves, but they arrive markedly early, confirming their identity as PAC’s. But why aren’t they followed by QRS complexes?

Recall that the existence of the absolute refractory period in the heart. The myocardium works in such a way that it cannot depolarize a second time immediately after it has already depolarizated. The AV-node exhibits that same trait, but to a greater degree in that it takes a longer time to “recharge” than the myocardium. Not only does that allow ample time for the ventricular cells to fully repolarize before the next impulse can discharge them, it’s also a protective mechanism that discourages excessive heart rates by limiting the rate at which atrial impulses can traverse the AV-node and cause the ventricles can contract.

If the AV-node didn’t protect the ventricles, everyone in atrial fibrillation (with atrial rates of 400–600 bpm) would also be in ventricular fibrillation because every atrial depolarization would be transmitted to the ventricles.

The PAC’s above simply arrive so early following the preceding P-waves that the AV-node fails to conduct them. If the AV-node didn’t prevent their conduction, the patient would be at risk of an R-on-T phenomenon and V-fib or V-tach. The AV-node saves the day!

Here’s some more examples from the same patient of the AV-node doing it’s thing.

Non-conductec PAC's

Figure 4. Sinus rhythm with non-conducted PAC’s. This is the same patient as Fig. 2.

Non-conducted PAC's

Figure 5. Non-conducted PAC’s from Fig. 4 are highlighted.

Non-conducted PAC

Figure 6. A single non-conducted PAC. This is the same patient as Fig. 2 and Fig. 4.

Blocked or Non-conducted?

Note that in the discussion above I refer to the PAC’s as “non-conducted,” but you might have seen them referred to as “blocked” PAC’s” in other sources. That is a conscious choice I make to avoid confusion regarding whether the failure to conduct the P-waves is pathological or not.

In Fig. 2 thru Fig. 6, the AV-node is behaving normally and doing it’s job of filtering out overly premature atrial discharges from reaching the ventricles. Contrast that with the cases in our last article on type I AV-block, where the AV-node was behaving abnormally, progressively delaying conduction until a P-wave was eventually blocked.

In my mind (and that of Dr. Henry Marriott, whose texts first taught me about this distinction), a block is something pathological, where the AV-node is failing to transmit atrial discharges that should be conducted.

Non-conducted P-waves, on the other hand, are something decidedly more benign. The AV-node is behaving normally, the atrial complexes just arrive so early that we don’t want them conducting anyway! That is normal physiology, and I don’t want it confused with something pathological. Once you start noticing non-conducted PAC’s (they’re uncommon but certainly not rare), you’ll also notice how folks that don’t understand that distinction over-react to their presence (commonly confusing them with true type II AV-block).

Though the PAC’s might be caused by an underlying issue (we’re not sure if the patient in Fig. 2 thru Fig. 6 was experiencing recurrent pericarditis), their failure to conduct is not the problem.

Back to our first case

So the first thing we want to examine is the PP-intervals to make sure that we’re not missing any PAC’s.

Normal sinus rhythm with tpye II AV-block

Figure 7. The PP-intervals from Fig. 1.

Though there are some minor variations in the PP-intervals, they are acceptable for what we expect with normal sinus rhythm. Additionally, though the PPi’s preceding the second two dropped P-waves appear shorter than the other PPi’s (705 and 710 ms), the last dropped P-wave is preceded by the longest PP-interval on the strip: 750 ms. It’s unlikely that the other P-waves arriving “early” played a role in their failure to conduct.

The next thing we’re worried about is whether there is subtle PR-elongation. Type I AV-block is more common than type II AV-block and can present subtly. The solution is to just compared the PR-intervals.


Fixed PR-intervals in type II AV-block

Figure 8. Fixed PR-intervals from Fig. 1.

All of the conducted P-waves share the same exact PR-interval.

With our two major criteria met, we can say with reasonable confidence that we are truly looking at type II AV-block in Fig. 1.

Icing on the cake

There are some other less important features that also contribute to the diagnosis of type II AV-block in Fig. 1.

First, let’s look at the patient’s age. He’s 84 years old, while the patient in Fig. 2–Fig. 6 was only 33. An 84 year old is much more likely to be experiencing a malignant form of AV-block.

Second, type II AV-block is usually caused by disease of the conduction system below the level of the AV-node, while type I AV-block is typically due to abnormal conduction within the AV-node and non-conducted PAC’s are due to normal AV-nodal behavior. What else is below the AV-node? The bundle branches:

Figure 9. Just the 12-lead from Fig. 1.

Figure 9. Just the 12-lead from Fig. 1.

The 84 year old in our initial case also demonstrates a right bundle branch block. He also shows significant left axis deviation that could be due to a left anterior fascicular block (LAFB), though that is less certain. Since type II AV-block is usually due to significant conduction disturbances in the bundle branches and major Purkinje fibers, it is almost always accompanied by at least some manner of bundle branch block, if not true bifascicular block. There is also a slightly prolonged PR-interval that could be to impaired conduction through the AV-node or in that last conducting posterior fascicle (see our discussion on first degree AV-block)

So, in summary, we have an ECG from an elderly man showing:

  • Normal sinus rhythm
  • No signs of ectopy
  • Fixed PR-intervals
  • Slightly prolonged PR-intervals
  • Right bundle branch block
  • Possible left anterior fascicular block
  • Frequent dropped P-waves

Given the overall picture, we can say with near certainty that what we are looking at is type II AV-block.


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 I AV-Block

This article is the fifth in our latest series, The 12 Rhythms of Christmas, where each day we examine a new rhythm disorder. It’s a continuation of the theme behind last year’s 12 Leads of Christmas.

Before we delve into today’s particular rhythm I’d like to discuss a bit of terminology. My first ECG textbook was the 8th edition of Marriott’s “Practical Electrocardiography,” which I chased with a couple more of  Dr. Marriott’s books. As a result, I tend to describe arrhythmias using the same language he used in his texts.

We should all be aware that there are four main types of atrio-ventricular block:

  • “First degree”
  • “Second degree type I,” also known as “Mobitz type I,” “Mobitz I,” or (commonly) just “Wenckebach”
  • “Second degree type II,” also known as “Mobitz type II,” “Mobitz II,” or (rarely) just “Hay”
  • “Third degree,” also known as “complete AV-block” or “complete heart block”

First and third degree AV-block are pretty straightforward, though I tend to prefer the term “complete AV-block” for the latter in order to avoid confusion over the different “degrees.” The two second degree blocks, however, are as mess[1]. As a result, I find it preferential to refer to them as simply “type I” and “type II,” dropping the bulky eponyms entirely. Additionally, we don’t even need to preface those terms as “second degree” since there are not multiples types of either first degree or complete AV-block, leaving us with:

  • First degree AV-block
  • Type I AV-block
  • Type II AV-block
  • Complete AV-block

As a final point, note that I always try to use the term “AV-block” and not simply “block” when talking about conduction abnormalities of the AV-node. That is because there are other locations where the above blocks can develop (sometimes concurrent with AV-block), such as the sino-atrial node (SA exit block).

Type I AV-Block

Type I AV-block is a pretty interesting phenomenon, first described in 1899 by Dutch anatomist Karel Wenckebach. It is characterized by progressive lengthening of the PR-intervals that culminates in a dropped (fully blocked) P-wave and a pause in the ventricular rhythm, reseting the AV-node so that the cycle can repeat.

Let’s look at an example:

Type I AV-block (Wenckebach)

Figure 1. Sinus rhythm at 70 bpm with type I AV-block. There are 4:3 and 8:7 conduction ratios.

Even those with limited experience in basic dysrhythmias should be able to identify the increasing PR-intervals…

Type I AV-block (Wenckebach) PR-intervals

Figure 2. Increasing PR-intervals in the setting of type I AV-block. The blue numbers are the PR-intervals in milliseconds.

That, however, is where most folks’ knowledge ends. But I expect most of the folks reading this blog, if they don’t already, would like to understand why this pattern occurs.

Decremental Conduction

It turns out that the healthy AV-node exhibits a normal behavior called “decremental conduction;” where the faster you stimulate the node with impulses, the slower it conducts. In fact, the “refractoriness” of the AV-node can be tested in the EP lab by purposely pacing the atria at increasing rates until the AV-node starts exhibiting slower and slower conduction (with longer and longer PR-intervals). Eventually the conduction slows to such an extent that it fails entirely for a beat, resulting in a blocked P-wave and a brief pause in the ventricular rate. This act “resets” the AV-node and allows it to conduct more rapidly on the next P-wave. The cycle, however, continues as the relentless barrage of atrial impulses slows the AV-node to a greater and greater extent until another P-wave is blocked and the AV-node resets again.

That is an important protective mechanism because it helps control the  ventricular rate in the setting of atrial fibrillation, where the atrial rate can exceed 500 /min. In most patients with type I AV-block, however, this decremental conduction has become pathological to the point that atrial impulses at even normal rates—which should conduct regularly with no signs of decremental conduction—start to exhibit the phenomenon.

To further examine this phenomenon in type I AV-block, let’s start off with a normal sinus rhythm. There is always some minor variation in the sinus rate, but these P-waves march out with fairly regular PP-intervals.

Type I AV-block (Wenckebach)

Figure 3. Regular P-waves. The brown numbers are the PP-intervals in milliseconds.

Now let’s talk about one of the hallmark finding of Wenckebach phenomenon and our sign of decremental conduction on the surface ECG: RP/PR reciprocity.

RP/PR Reciprocity

While everyone should be familiar with the PR-interval, it’s partner the RP-interval is not nearly as well known. Since the PR-interval is the time from a P-wave to the next QRS-complex, the RP-interval is the time from a QRS-complex to the next P-wave.

RP/PR reciprocity in type I AV-block

Figure 4. RP/PR-reciprocity. PR-intervals are shown in blue and RP-intervals in red, both in milliseconds.

One of the most hallmark features of type I AV-block is a reciprocal relationship the PR and RP-intervals: The shorter an RP-interval, the longer the next PR-interval.

Starting at the left side of Fig. 4, we see the first RP-interval (in red) is 520 ms; the PR-interval that follows it is 400 ms. Next, we encounter a shorter RP-interval of 450 ms, followed by a longer PR-interval at 460 ms. The next P-wave arrives with an even shorter RP-interval at about 390 ms (not shown). This RP-interval turns out to be too short to conduct and the P-wave is dropped.

The next P-wave that arrives enjoys a luxurious 1240 ms RP-interval, allowing the AV-node to conduct relatively rapidly with a PR-interval of only 320 ms. The pattern then repeats, although it does not progress as rapidly towards a dropped P-wave the second time around (see Table 1).

Table 1. RP/PR intervals in milliseconds

Table 1. RP/PR intervals in milliseconds

That brings up an exceedingly important feature of type I AV-block…

Grouped Complexes

Because of the patterns that emerge from the Wenckebach phenomenon, you’ll notice that the QRS complexes in the above figures appear to demonstrated two clusters, separated by a relatively long pause after the dropped P-wave.

It may seem like lengthening PR-intervals are the most prominent feature of type I AV-block, but it turns out that grouped beating is even more important. It can be difficult to follow P-waves or pick up subtle PR-interval elongation or see dropped complexes that are buried, but clumps of QRS complexes are easy to spot.

Type I AV-block

Figure 5. Group beating in type I AV-block

Type I AV-block (Wenckebach)

Figure 6. Atrial tachycardia vs. marked sinus tachycardia with 4:3 conduction and grouped QRS-complexes.

Atrial flutter with Wenckebach

Figure 7. Atrial flutter with paired QRS complexes (3:2 conduction) highly suggestive of Wenckebach phenomenon at the AV-node.

On the topic of grouped complexes, it’s apparent at this point that there is great variability in the patterns that type I AV-block can form. All of the following strips were obtained from the same patient over a short period of time (not continuous):

Type I AV-block (Wenckebach)


Type I AV-block (Wenckebach)

Figure 9

Type I AV-block (Wenckebach)

Figure 10

Type I AV-block (Wenckebach)

Figure 11

Type I AV-block (Wenckebach)

Figure 12

Type I AV-block (Wenckebach)

Figure 13. 2:1 AV-block due to type I AV-block. This will be covered in its own article in two days.

Type I AV-block (Wenckebach)

Figure 14. At first glance this looks like 2:1 AV-block but a single 3:2 ratio with Wenckebach phenomenon is present, confirming the mechanism as type I AV-block.

In this post we’ve seen everything from 8:7 conduction ratios (Fig. 1) all the way down to 2:1 (Fig. 13), and these ratios can be fairly fixed (Fig. 6 and Fig. 7) or quite variable (Fig. 8–14). There are even larger ratios possible, from 14:34 up to 20:19 or more! These longer, more subtle patterns are known as atypical or long-cycle type I AV-block. For more on them check out these posts from our friend Dr. Arnel Carmona over at ECG Rhythms.

There are two more features of Wenckebach phenomenon that come to light after studying its QRS patterns…

The RR-Intervals

With a classic Wenckebach period, due to the timing of the RP/PR reciprocity and the elongation of the PR-intervals, you’ll notice that the RR-intervals decrease progressively across each group of complexes. Let’s look at that first rhythm strip again and measure out the RR-intervals.

Type I AV-block (Wenckebach)

Figure 15. RR-intervals during Wenckebach phenomenon.

Wait! If you’re paying attention, you’ll notice that, while the RR-interval decreases at the beginning of the large group (925 ms, 860 ms, 850 ms), it stabilizes in the middle and actually increases at the end (855 ms, followed by 905 ms).

The key is that I stated progressive RR-shortening occurs in the classic Wenckebach pattern. It turns out that not too many type I AV-blocks fit that ideal (but we love them in spite, or even because of it…).

In fact, it’s pretty common for the last RR-interval in a grouping to be longer than expected; and sometimes it’s even the longest RR in the whole series.

Another classic finding, but one that is more common and we actually see in Fig. 16, is that the longest RR-interval is less than twice the shortest RR-interval.

Figure 16. The long RR-intervals are less than twice the short RR-intervals.

Figure 16. The long RR-intervals are less than twice the short RR-intervals.

Note that the first big RR gap measures 1575 ms, while the shortest cycle preceding it is 910 ms. Since 1575 ms is less than 1820 ms (2*910 ms), that fits with type I AV-block. The same goes for the next series, where 1565 ms is less than 1700 ms (2*850 ms).


The “footprints of Wenckebach” were summarized by Dr. Marriott as:

  • Grouped QRS complexes, especially pairs, and trios (which are easy to miss)
  • Progressive shortening of the RR-intervals across a grouping
  • The longest RR-interval is less than twice the shortest

Keep in mind, however, that many type I AV-blocks do not follow the rules! While there is sometimes no apparent trigger for this rule-breaking, here are some common culprits.

  • Variations in the sinus rate, which affect everything downstream (RP-intervals, PR-intervals, and the ventricular response)
  • Variations in AV-conduction due to fluctuations in the sympathetic and parasympathetic nervous systems
  • Ectopic beats interrupting the process (PAC’s, PVC’s, even concealed PJC’s…), as seen in Fig. 10

We’ll go over some of the common mimics of type I AV-block later this week but for now, while it’s possible that you’re blissfully unaware of them, get out there and spot some Wenckebachs!


  1. Blame it on some interesting history involving Wenckebach, Hay, and Mobitz. In short, Wenckebach first described type I block, Hay first described type II (both without the benefit of electrocardiography!), and Mobitz then named them “type I” and “type II” twenty years later.


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