With the number of patients receiving permanent pacemakers (PPMs) and implantable cardioverter-defibrillators (ICDs) increasing each year, we’ll see more of these devices in our respective clinical settings. With this post, I’ll try to simplify pacemaker nomenclature and discuss some of the considerations surrounding magnets and device settings.
All ICDs have a pacemaker function but NOT all pacemakers are ICDs. Most patients should carry cards with information about their device, but when it’s 2 AM and your patient is found down, a chest x-ray can help you determine the type of device (PPM vs AICD) based on where the pacer leads are located and the presence of a thicker defibrillating lead only found in ICDs. It’s important to know the patient’s underlying rhythm (ie, what do they do without their pacer) and the indication for the PPM/ICD in the first place. Also, all pacers have a minimum backup rate which is the threshold heart rate at which the pacer will kick in.
When in doubt or confused, call your friends in electrophysiology!
Pacemaker nomenclature is most often written as a series of three letters (ie, VVI) but can be as much as five (DDDRO). I’m going to keep things simple! In order, the 3 or 5-letter nomenclature stands for:
- Chamber Paced: A (atrium), V (ventricle), D (dual)
- Chamber Sensed: A (atrium), V (ventricle), D (dual)
- Response to Sensed Beat: I (inhibit), T (trigger), D (dual), O (none)
- Rate Responsiveness: R (rate-responsive), O (none)
- Automatically increases the pacing (and cardiac output) to meet an increase in exertion
- Multisite Pacing: O (none), A (atrium), V (ventricle), D (dual)
For most of us, only the first three characters matter.
A single electrode is fed into either the right atrium (“A wire”) or right ventricle (“V wire”). Now let’s consider some basic nomenclature using the aforementioned patterns.
- AAI: The atrium is paced and sensed. If an intrinsic beat is detected (ie, the patient’s SA node fires), the pacemaker will inhibit itself. This makes sense in conditions like sick sinus syndrome (SSS) where the AV node is working fine and cardiac output can be maintained as long as the atria are firing at an appropriate rate.
- VVI: The ventricle is paced and sensed. If an intrinsic beat is detected (ie, conduction carried down through AV node into the ventricle), the pacemaker will inhibit itself. One can imagine that if the pacer has to constantly fire on the ventricle, some of the signal can be conducted retrograde into the atria during systole causing contraction against the closed tricuspid/mitral valves. Also, ventricular pacing causes the “atrial kick” to disappear which can have severe consequences in patients with poorly compliant ventricles requiring higher filling pressures.
A wire is fed into the right atrium AND right ventricle. DDD is the most common mode I work with. In this setting, the pacemaker can independently sense and pace one or both of the chambers. Because of this, the patient’s EKG can show several rhythms:
- Sinus rhythm: The patient’s native heart rate is faster than the backup rate of the pacemaker. There is normal atrioventricular conduction.
- A sensed, V paced
- A paced, V sensed
- AV pacing: both chambers are paced
Now let’s briefly discuss pacemaker mode switching. If a patient with a DDD dual chamber pacemaker suddenly develops an atrial tachyarrhythmia (atrial rates can exceed 500 bpm), it doesn’t make sense for the pacemaker to fire the ventricle at that rate. Instead, it’ll detect the fast atrial activity and “switch” into a safer mode (like VVI) to basically ignore atrial activity.
The purpose of temporary pacemakers is to sense intrinsic electrical activity and pace the myocardium from the inside (ie, transvenous wires) or outside (epicardial wires). Following cardiac surgery, surgeons often place bipolar leads on the right ventricle (RV) for ventricular sensing/pacing +/- right atrial (RA) leads for synchronized atrioventricular pacing. A current is delivered between the two bipolar leads and “captured” by the myocardium resulting in depolarization.
There are three major settings for pacers:
- Rate: the number of impulses/minute
- Output (mA): the current needed for the myocardium to “capture” the paced signal. In other words, how energy much are you jolting the heart with. Atrial output and ventricular output range from 0.1 – 20 mA and 0.1 – 25 mA, respectively.
- Sensitivity (mV): the point at which the pacing device interprets a native myocardial signal as a pulse. The greater the millivolts, the less sensitive the device is to native cardiac activity which can lead to undersensing and overpacing potentially causing the pacer to fire on a native heartbeat (R-on-T phenomenon). At higher sensitivities (lower millivolts), any – little – signal (including breathing, patient movement, etc.) will be interpreted as a native beat (oversensing).
To “test” a pacer, I select a mode (typically DDD for A-V pacing wires and VVI for only V pacing). I’ll start with the default output and sensitivity settings and increase the pacer rate to something above the patient’s native heart rate. Then I’ll watch the continuous EKG to ensure that the signal is indeed captured at the preset rate while dialing down the output.
If a pacer loses its ability to capture, one must consider possible changes in sensitivity thresholds, electrolyte changes, damaged lead(s), battery depletion, or faulty cables. If I seem to have competition between the pacer and the patient’s native heart rate, I’ll adjust the sensitivity to avoid the aforementioned scenarios of over/undersensing.
Implantable cardioverter-defibrillators (ICDs) are placed for a myriad of reasons ranging from low ejection fraction states and sustained ventricular tachycardia/fibrillation to prior cardiac arrest from channelopathies or structural heart issues like hypertrophic cardiomyopathy. Remember, ALL ICDs have an intrinsic pacemaker function. The question is whether or not the patient is truly “pacer dependent.” This is where recent interrogation reports are important.
Keeping it simple: a magnet will reprogram a regular pacemaker into an asynchronous mode (AOO, VOO, DOO) at a manufacturer-defined heart rate. By contrast, a magnet will deactivate an ICD’s “shock” function; however, the pacemaker portion of the ICD will not be changed.
This is the question I’m often asked as a cardiothoracic anesthesiologist and intensivist.
“Rishi, I have a patient with (insert device name here)… do I need to put a magnet on?”
My first questions are:
- Why does the patient have the device?
- Is the patient “pacer dependent?”
- What’s the surgery? Is electrocautery involved? Are the surgeons working near the chest?
In my specialty, the most common situation I run into is a patient with an ICD coming in for cardiothoracic surgery. The device is located in the surgical field and, oftentimes, will be explanted (ie, at the end of a heart transplant). As mentioned above, a sterile magnet will disable the ICD’s shock function but not affect the pacemaker function. If the patient is also pacer dependent, electrocautery in the field can be misinterpreted as intrinsic cardiac conduction system activity. The pacemaker portion will think the patient’s heart is firing on its own (when in reality, it’s the electrocautery), and the device will therefore inhibit itself. Now the patient’s true heart rate will become apparent which can significantly drop the cardiac output leading to bradycardia/bradyarrhythmias and hypotension.
If you feel like this is a potential scenario in your situation, the safest option is to have the electrophysiology team come reprogram the device to an asynchronous mode prior to surgery. Although I usually also place external defibrillator pads on these patients, remember that if they go into a “shockable rhythm” intraoperatively (ie, VFib), just remove the magnet and let the ICD function kick in.
Lots of information covered in this post – please drop me a comment below with questions!