Extreme Bradycardia: a Case-Based Lesson in Pacing

DDD pacer = Dual paced, Dual sensed, Dual response (triggered and inhibited)
Dual means that this occurs in both the atrium and the ventricle.

As you can see from the chart below, a VVI pacer is ventricle only and cannot be triggered by an atrial beat.  It can only be inhibited by an intrinsic ventricular beat.

So a DDD pacer can pace the atrium (if needed), then wait a defined period (e.g., 200 ms, like a PR interval) and pace the ventricle (if needed).  Either or both functions can be inhibited if the atrium or ventricle (or both) fires before the interval passes.

One of the reasons I’m presenting this case is that several residents misunderstood the concept of “failure to sense,” believing it to be a cause of absence of pacing.  This made me realize that pacemaker function is not as well understood as I thought.

However, failure to sense is NOT a reason for absence of pacing.  Failure to sense results in inappropriate pacing: when the pacer is not sensing intrinsic activity that is present (failure to sense), it fails to have its pacing appropriately inhibited.  (If a heart beat comes soon enough, the pacer should sense it and inhibit pacing so that there is no pacing when it’s not needed.)

In fact, when a pacemaker fails to generate an impulse (fails to pace), one reason may be oversensing, not undersensing.  

This is why we use a magnet when there is failure to pace!  To stop oversensing and thus stop inhibtion of pacing.  The magnet turns off the sensing function and the pacer becomes “asynchronous,” meaning it will fire at a regular rate regardless of the intrinsic activity of the heart.  We place the magnet because a failure to pace may be due to oversensing (not undersensing) with inappropriate inhibition of pacing.


A patient called 911 for weakness.

She had recently had a DDD pacemaker placed.

Her prehospital ECG showed failure to pace by the internal pacer.  External pacing was attempted but not tolerated and, because the patient was only mildly hypoperfused, she was transported to the ED without further intervention.

Exam revealed a fresh surgical scar at the area of pacemaker placement with significant swelling due to hematoma at the site of insertion.

Here is the first ED ECG:

What are you seeing?
Try to figure it out before reading the explanation below.

So what is happening here?  Failure to capture.  There may also be failure to sense, but it is not having any effect.

I’ll explain with the arrows:

Black arrows show P-waves marching out regularly at a rate greater than 100.  They are not conducting at all (complete AV block) and thus are not affecting the ventricles at all.  The fact that the sinus node is tachycardic tells us that the sinus node is probably “trying” (teleologically speaking) to compensate for inadequate cardiac output. 

Green arrows show ventricular pacer spikes.  
These spikes come at a fixed interval (200 ms) after every P-wave.  
Therefore, the atrial pacing lead must be sensing the sinus activity and P-wave.  The ventricular pacer is programmed to fire at a fixed time period after the P-wave in order to synchronize atrial and ventricular activity.   If the ventricle had depolarized on its own (had there been no AV block), AND the ventricular sensing function also sensed the depolarization, then there would be no ventricular pacing spike.  

Why are there no atrial pacing spikes in this DDD pacer which has that capacity?  Because they are not needed and are thus inhibited: the sinus node is doing its job; it is firing and resulting in atrial depolarization (P-wave).  The atrial lead would pace if, after a programmed period of time, it did not sense an atrial beat (usually 1 second, corresponding to a rate of 60). For instance, if there were inappropriate sinus bradycardia at less than 60 bpm, the atrial pacer would take over if it is programmed to wait 1 second before firing.  (The atrial pacer would also fire if it failed to sense the atrial activity.)

However, the pacer is clearly not capturing the ventricle (not resulting in depolarization of myocardium, so no QRS).  There are 2 pacer spikes which are missing (between 3rd and 4th arrows and between 6th and 7th).  They may be there and hard to see (hidden); alternatively, they are not there at all.  
If the spikes did not happen at all, that would be a result of the pacer sensing the QRS, resulting in inhibition of pacing [even if it cannot pace (cannot capture)].  This would be unusual, as when the pacer lead is able to sense it is also usually able to pace.
If the spikes are there and just hidden, then the pacer is also not sensing: the escape QRS should inhibit pacing if that beat is sensed.  This latter one is the more likely explanation: that is to say that hidden pacing spikes due to absence of sensing is more likely than sensing + inhibition of pacing.)

Red arrows show escape beats at regular intervals, which in lead II (across the bottom) appear narrow, but if you look up at the leads above, especially at V1 above the 3rd escape beat, you see that it is RBBB morphology and therefore is an escape from the left ventricle (an escape from the junction or bundle of His, along with RBBB, would have the same morphology but at a faster rate).

A couple of these complexes are distorted by coincidental P-waves
The T-wave of the third escape beat is larger than the others because of a coincidentally superimposed P-wave.

The Dark Blue Arrow points to a pacing spike that occurs directly at the onset of a QRS, but that QRS looks exactly like those of the escape beat.  Therefore, it is just a coincidence that it happened at the same time as the onset of the QRS.  It is not capturing and not resulting in a QRS. 

The Light Blue Arrows point to pacing spikes that are followed immediately by wide beats (see brown arrows) that are typical of paced beats and different from the escape beats.  These are beats in which the pacer captured.
The T-waves of both of these beats have, coincidentally, a superimposed P-wave

Clinical course:

The potassium was normal, there was no ischemia or drug toxicity.

She went for emergent pacemaker revision.  It turned out that the hematoma at the “pocket” of the pacemaker had displaced the pacemaker, pulling the ventricular lead out of position.  This was fixed.

Etiologies of Failure to Capture

This was a failure to pace due to Failure to Capture (not due to oversensing, as there were pacer spikes), the differential diagnosis of which is:

–Drug toxicity
–Poor electrode contact (as in this case)
–Fibrosis around electrode tip

Failure to Pace also includes these etiologies, none of which will produce a pacing spike on the surface ECG:

–Broken leads (assess by Chest X-ray)
–Leads detached from generator
–Generator malfunction, including battery depletion and programming error

Emergency Management:

1. Treat hyperkalemia or drug toxicity
2. Treat ischemia (Cath lab)
3. Magnet application if no pacer spikes.
4. External pacing
5. Transvenous pacing
6. Chronotropic support with Isoproterenol, Epinephrine, or Dopamine to increase ventricular escape rate.

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