Transcutaneous Pacing (TCP): The Problem of False Capture
Updated: Aug 14
Transcutaneous pacing (TCP) is perhaps the most underutilized and misunderstood intervention in all of ACLS. Why? Simple. Because it’s impossible to simulate during training.
From the 2010 AHA ECC Guidelines – Part 8:3: Management of Symptomatic Bradycardia and Tachycardia
“It is reasonable for healthcare providers to initiate TCP in unstable patients who do not respond to atropine (Class IIa, LOE B). Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available (Class IIb, LOE C). If the patient does not respond to drugs or TCP, transvenous pacing is probably indicated (Class IIa, LOE C).”
Be honest. In paramedic school, when you went through the bradycardia station, and you were given a scenario with a patient who was experiencing hemodynamically unstable bradycardia, what happened when you told the instructor that you wanted to immediately attempt transcutaneous pacing?
If you’re like hundreds of other paramedic students all over the country (and for all I know, the world) you were told: “the pacer is broken.” That was your cue to say, “Okay, then I’d give 0.5 mg atropine rapid IV push.”
Is it any wonder that so many paramedics (and to be fair, other health care providers) perform this skill poorly or not at all?
Let’s look at a case study.
This was an elderly male that the treating paramedic found supine on the floor with an altered level of consciousness. Radial pulses were present, but slow and irregular. The cardiac monitor was attached and the following ECG was obtained.
I don’t remember any other details about the history or clinical presentation, but it’s irrelevant to the central point of this case study.
The treating paramedic elected to perform immediate transcutaneous pacing (TCP). The combi-pads were attached and the pacer was turned on.
As you can see in the ECG strip below, the computer began tracking QRS complexes and the pacer was set for 60 PPM.
I would also like to point out that this particular LP12’s pacer had a default setting of “non-demand mode”. This is somewhat unusual, but it turns out to be the key to solving this case.
The treating paramedic increased the current to 40 mA.
At this point, the paramedic reported radial pulses that corresponded to the pacer and an improved level of consciousness. The rate was changed from 60 to 70 PPM.
Does the paramedic have capture? Be honest! It looks like it, right?
Unfortunately, no. The paramedic does not have capture.
Then what in the Wide World of Sports are the QRS complexes after the pacer spikes?
The answer is that the monitor is showing phantom QRS complexes or false capture.
Don’t believe it? Let me prove it to you.
Here is the same rhythm strip. The underlying rhythm appears to be junctional at approximately 40 beats/min.
In the next strip, you can see the underlying rhythm marching through the absolute refractory period of a (presumed to be) paced QRS complex. That’s not scientifically possible!
In the next strip, you can see a (presumed to be) paced QRS complex in the absolute refractory period of a QRS complex from the underlying rhythm. That’s also impossible!
Finally, you will note that the SpO2 monitor is counting the pulse rate at 42 BPM, not 70 BPM.
Whatever these complexes are that follow the pacer spikes, they do not represent ventricular depolarization.
So what are they?
What kind of artifact?
Let’s look at a side-by-side comparison of the phantom QRS complexes as the current was dialed up.
As you can see, the QRS complexes look essentially the same (QS complexes with an almost vertical downstroke and slightly curved upstroke back to the isoelectric line, non-distinct ST segment, and a virtually absent T-wave). The only difference is the size. As the current was dialed up, the complexes got larger.
As you can see in the following graph, there’s an almost linear relationship between the amount of current and the amplitude (or depth) of the phantom QRS complexes.
Where does this electrical artifact come from? Why didn’t anyone tell us it would be there?
I discussed this case at length with a Sr. Clinical Specialist from Physio-Control. He told me that the LP12 essentially closes its eyes for approximately 40 ms (one small block) after each pacer spike (a pacer spike is nothing more than a graphic representation that an electrical current is about to be sent between the combi-pads).
To understand why the LP12 “closes its eyes” when it delivers an electrical impulse, you need only ask yourself one simple question. What does an ECG monitor measure?
If it didn’t “close its eyes” so to speak, the ECG recording would go right off the paper! So the idea is that the monitor closes its eyes while the current is delivered, and then “opens them” in time to see the QRS complex it creates.
Do you see where this is going?
If the monitor opens its eyes too soon, the electrical signal has not yet returned to baseline. The result is a phantom QRS complex on the ECG.
It certainly doesn’t help that the ACLS textbook has shown the exact same rhythm strips for transcutaneous pacing for as long as I’ve been a paramedic!
Let’s take a look.
The first strip shows sinus bradycardia. The second strip shows sinus bradycardia and pacer spikes without capture. The third strip shows a beautifully paced rhythm!
If only it was this simple in the real world!
I know what you’re thinking. Why did the paramedic report pulses that corresponded with the pacer?
Think about it!
The patient has an underlying rhythm, so some pulse waves are going to be felt. In addition, do not underestimate the combination of skeletal muscle twitching and wishful thinking! You are being visually stimulated with every pacer spike, and it’s impressive!
Ever heard of cough-CPR? I am convinced that the contraction of pectoral muscles, intracostal muscles, and other intrathoracic structures produces some type of arterial pulse wave.
But you said the paramedic also reported an improved level of consciousness!
That’s true, but something tells me you’d be more alert, too, if someone started to shock you once a second for a couple of minutes! Your blood pressure might even go up.
Here are some clinical pearls to get you through the procedure.
The most common cause of failure with transcutaneous pacing (TCP) is poor pad placement combined with insufficient milliamperes! Remember, the pacer goes up to 200 mA! If you lose your nerve at between 70-90 mA, there’s a good chance you’re not going to achieve capture. Consider anterior/posterior pad placement to “sandwich” the left ventricle between the pads and reduce transthoracic resistance.
Look for a tall, broad T-wave that is the telltale sign of true electrical capture.
Perform, but do not rely solely on a manual pulse check. Consider using an instrument like an SpO2 monitor, doppler, or bedside 2D echo (for in-hospital patients) to verify mechanical capture.
Run a continuous rhythm strip that shows the transition from false capture to true electrical capture. Be able to document the exact milliamperes that capture is gained, and capture is lost. One of the quirks of the human heart is that once you gain capture it is harder to lose (a manifestation of the Wedensky effect). In other words, you might achieve capture at 120 mA, but then you might have to dial it back down to 90 mA to lose it again. Many protocols state that you should add 10 mA as a safety margin once capture is achieved. In my experience this is unnecessary.
Finally, you can consider placing the pacer in non-demand mode and examine the absolute refractory periods of the underlying rhythm and the (presumed to be) paced rhythm. If the paced rhythm and the underlying rhythm are marching through each others’ absolute refractory periods, you don’t have true electrical capture.