Understanding pacemaker rhythms PART 3 : Nursing2020 Critical Care (2024)

The previous two articles discussed the basics of pacemakers and their rhythms, from the normal ones to those indicating potentially serious pacemaker malfunctions. This article, the last in the series, covers "ugly" rhythms, which represent normal pacemaker function despite their bizarre appearance, and in some cases actually protect the patient.

Minimize pacing rhythm, maximize patient rhythms

As the Dual Chamber and VVI Implantable Defibrillator (DAVID) and Mode Selection Trial (MOST) trials demonstrated, paced rhythms aren't without risks to the patient. Atrial fibrillation (AF) can occur from single- or dual-chamber pacing, and ventricular remodeling can occur from right ventricular pacing.^1,2 To minimize these risks, minimize the use of pacing.

We already do that by using pacing modes that sense the patient's intrinsic rhythm and inhibit pacing when the patient's rhythm is faster than the preprogrammed minimum pacemaker rate. However, another way to reduce pacemaker use is to accept a slightly lower rate.

If a patient has a VVI pacemaker with a minimum rate of 80 beats/minute, cardiac output (CO) is decreased by up to 25% from the loss of atrial kick, compared to a patient in normal sinus rhythm at 80 beats/minute. However, the CO from ventricular pacing at 80 beats/minute is also probably lower than normal sinus rhythm at 65 beats/minute. Why? If you take 25% from 80 beats/minute, you find that VVI pacing at 80 beats/minute has about the same CO as normal sinus rhythm (with its atrial kick intact) at 60 beats/minute. Suppose the patient needs VVI pacing at 80 beats/minute for hemodynamic stability. If we turn the pacemaker off and the patient's normal sinus rhythm has a rate of 70 beats/minute, the patient should still be hemodynamically stable. The problem is that the pacemaker needs to have a minimum rate faster than 70 beats/minute. How can we know if the patient would be in normal sinus rhythm at a slower rate if we stopped pacing? Simple...stop pacing!

That is, stop pacing for a short period of time. Increase the timeout interval for one to three beats and watch for the patient's intrinsic rhythm. (See A refresher on some pacing terms.) This technique is known as hysteresis and simply means "to delay." If the pacemaker simply delays its output for a fraction of a second for a few beats in a row, the patient shouldn't suffer any consequence: If the heart's intrinsic rhythm is just a few beats per minute less than the pacemaker minimum rate, the intrinsic rhythm will take over.

There are two types of hysteresis:

• In search hysteresis, after set intervals of continuous pacing, the pacemaker will stop pacing for a few beats and "search" for an intrinsic normal sinus rhythm above the hysteresis rate. If it senses such a rate, it will inhibit firing until the rhythm drops below the hysteresis rate.^3,4
• In normal hysteresis, if the patient is in normal sinus rhythm above the pacemaker minimum rate and the rate begins to decline slowly (for example, as the patient falls asleep), the pacemaker won't fire until the heart rate drops below the hysteresis rate.^3,4

Consider a waveform in which the first seven beats are a ventricular paced rhythm at 75 beats/minute with an associated peak systolic BP (a clinical index of afterload, which determines stroke volume and thus CO) of about 110 mm Hg (see A closer look at hysteresis). The pacemaker stops pacing, performs a search hysteresis, and an intrinsic normal sinus rhythm takes over at a rate of about 70 beats/minute. The patient's peak systolic BP immediately increases to over 140 mm Hg, a 27% increase from natural atrial kick, which increases CO. In addition, atrioventricular (AV) synchrony (synchronized ventricular contractions) is restored, as indicated by the narrow, intrinsic QRS complexes on the ECG (compared to the wide pacemaker-triggered QRS complexes).

Search hysteresis (also called sinus preference pacing) serves a twofold purpose; first, the pacemaker will have a longer battery life as it's discharging less frequently, and second, because the heart depolarizes and contracts in a more normal way with the intrinsic beats, the patient will undergo fewer changes in heart size, geometry, and function (known as ventricular remodeling) that can worsen cardiac function over time.^1,2

On the ECG, hysteresis looks like a sudden onset of failure to pace. The pacemaker is firing at the minimum rate, then suddenly stops, letting the heart's intrinsic rhythm take over at a rate that's lower than the pacemaker's programmed minimum rate. The pacemaker doesn't fire because the intrinsic rate is above a second, slower rate, called the hysteresis rate. This second rate, determined by the practitioner as the rate below which CO from normal sinus rhythm is less than the CO from ventricular pacing, is a safety feature; if the intrinsic rate ever falls below the hysteresis rate (60 beats/minute in our example), the pacemaker would resume pacing at its higher minimum rate.

You may find it concerning to see a pacemaker suddenly stop firing despite a heart rate lower than the preprogrammed minimum, or to see long intervals of a heart rate lower than the pacemaker minimum rate, but remember, the goal is a hemodynamically stable patient. Assess the patient, and you'll frequently find that the heart rate and cardiac function are adequate.

Changing AV interval

The AV interval in a pacemaker rhythm is the equivalent to the PR interval in sinus rhythms—that is, the delay from atrial depolarization to ventricular depolarization. Normally, this interval is kept constant, but it can be programmed to change based on heart rate (similar to what happens in intrinsic cardiac rhythms, where faster rhythms have shorter PR intervals). However, the AV interval in most pacemakers is fixed.

AV hysteresis, also known as PV hysteresis (or time from the intrinsic P wave to the ventricular paced beat), works similarly to search hysteresis as described earlier. However, it only involves searching for a ventricular depolarization. With this feature, a baseline AV interval is programmed, but at set intervals, the pacemaker extends the AV interval by a small amount (hundredths of a second).^3,4 If an intrinsic QRS complex is sensed during this extended period, the pacemaker will use this longer AV interval, allowing natural conduction through the bundle branches and Purkinje fibers, thus minimizing ventricular pacing.^3,4 If the AV conduction deteriorates further, and no intrinsic QRS complex is sensed during the extended AV interval, the pacemaker will return to the shorter programmed AV interval until the next time to check for intrinsic QRS complexes.^3,4

AV hysteresis will appear on the ECG as sudden onset of an abnormally long AV interval with natural QRS complexes, perhaps bizarre in appearance from a natural bundle-branch block. But again, we need to appreciate the effect on the patient–minimizing the asynchronous contraction of the ventricles from right ventricular pacing.

Fusion beats

Imagine you're carpooling to a party with a friend. You're punctual, so you tell your friend that you're leaving precisely at 2000 hours. At 2000 hours, you leave, unaware that your friend was on his way and would have arrived at 2002 hours had you waited. You pass him on the road. You both stop, get into one car, and finish driving to the party from that point forward. This is analogous to fusion beats.

Sophisticated as pacemakers are, they can't see the future. If conduction of an intrinsic P wave takes too long to get to the ventricular pacemaker sensor, the pacemaker discharges via the ventricular lead, and the two signals (one intrinsic, one pacemaker-initiated) both begin to depolarize the ventricles.⁴ The resulting waveform is a fusion of the intrinsic and pacemaker QRS complexes.⁴ (Although atrial fusion beats occur, they're difficult to identify on the ECG, frequently aren't appreciated as fusion beats, and are less likely to be mistaken for pacemaker malfunction.)

If you look at A closer look at fusion beats, you'll see three different QRS complexes, the third, fourth, and fifth beats. The QRS of the third beat is formed from only the pacemaker stimulus. The fifth QRS complex is formed from only the intrinsic depolarization of the ventricles without any contribution from the pacemaker. The fourth QRS complex represents a combination of the intrinsic QRS and the pacemaker QRS complex.

Notice that the fourth QRS complex, the one representing a fusion or combination of intrinsic and pacemaker-initiated ventricular depolarizations start out like an intrinsic QRS complex, positively deflected (pointing upward). The pacemaker-initiated QRS complex is completely negatively deflected (pointing downward), and when the intrinsic and pacemaker-initiated complexes combine you simply add the positive deflection of the intrinsic QRS complex to the negative deflection of the pacemaker-initiated QRS complex. The result can vary depending on how much of the ventricular tissue is depolarized naturally before the pacemaker discharges.

Remember, the pacemaker stimulus doesn't use the fast track of the natural conduction system; it has to travel cell to cell, a much slower process. This means that even if the pacemaker discharges as soon as the atrial signal reaches the bundle branches, the result will be a fusion beat. Also, remember that the ECG doesn't show a deflection when the signal travels through the bundle bran ches, only the results of the signal traveling through the bundle branches—that is which parts of the ventricles depolarize in what order.

Pseudofusion beats

The ECG can play tricks on our eyes. We can see a pacemaker spike directly in front of a QRS complex, but that doesn't mean that the pacemaker contributed to the QRS complex at all. In A closer look at pseudofusion beats, the first beat is a pacemaker-triggered QRS complex. The next three beats are each preceded by pacemaker spikes, but these are intrinsic QRS complexes. To confirm this, look at the fifth QRS complex, the only one without a pacemaker spike. It looks identical to the three previous QRS complexes, except for the pacemaker spike. This shows that they all originated in the same location and followed the same conduction pathway. Because we know the fifth QRS originated in the AV node and followed the normal bundle-branch pathway to the ventricles (because there's no pacemaker spike), the other three must have done the same thing. As a comparison, the last beat on the strip is a fusion beat—a combination of the negatively deflected, pacemaker-triggered QRS complex and the positively deflected, intrinsic QRS complex.

Anytime the pacemaker spike falls just before or even in the QRS complex, the pacemaker impulse may not contribute to the depolarization of the ventricles. If the pacemaker fires just as the intrinsic stimulus reaches the pacemaker lead, the natural stimulus may have already depolarized all the tissue surrounding the pacemaker lead. When this happens, you'll still see the pacemaker spike, but the pacemaker hasn't depolarized any ventricular tissue of consequence because the tissue was refractory.

Pseudo-pseudofusion beats

You may not see this category in any books on cardiac rhythms, but it's important in completely understanding the ugly pacemaker rhythms that you may see. This tracing can only be produced in patients with dual-chamber AV pacemakers.⁵ If the patient has a natural premature ventricular beat (PVC) just as the atrial pacemaker lead fires, you'll see a pacemaker spike at the beginning of a wide QRS complex.

Although this QRS complex looks exactly like a pacemaker-generated QRS complex, the atrial lead has depolarized the atria, not the ventricles. In A closer look at pseudo-pseudofusion beats, you see two spikes in one complex (the first and third asterisks)—one at the beginning of the QRS complex and one at the peak of the T wave. If you measure carefully, you'll find that the two spikes are the same distance apart as the atrial and ventricular pacemaker spikes in the paced beats. This proves that the spike preceding the beat in question is an atrial spike that couldn't depolarize the ventricles; the second spike is the ventricular lead firing after the QRS, when ventricular depolarization is complete. In the other two beats (marked by the second and fourth asterisks), the atrial lead fired when the PVC occurred, but the ventricular lead sensed the PVC, suppressed the ventricular stimulus, and left a beat that looks like a ventricular paced beat.

As long as the ventricular pacemaker stimulus occurs before the relative refractory period of the QRS complex (usually before the peak of the T wave), all the variations of pacemaker spikes and QRS complexes represent normal, albeit ugly, pacemaker behavior.

ECG artifact

The ECG strip doesn't include all the electrical signals received from the ECG electrodes. In an effort to reduce artifact and make the ECG easier to interpret, the monitoring equipment uses filters. At the bottom of a 12-lead ECG, you'll see two numbers that represent a range, in hertz (the unit of measure of electricity) or cycles per second that the machine is programmed to measure. Anything outside this range is considered artifact and is ignored.

Most bedside cardiac monitoring equipment has a setting called "Filter," with choices such as "monitor mode" and "diagnostic mode." Monitor mode may filter out some true signals from the heart in the interest of simple rhythm identification. Diagnostic mode keeps more signals, but may generate more artifact in active patients.

Monitor mode on bedside equipment filters out as artifact any large signal that's very short in duration. The rationale is that the human heart isn't capable of such extreme depolarizations. However, this is exactly what the pacemaker artifact looks like to the ECG equipment. The solution is a pacemaker setting, which can be used in patients with artificial pacemakers. The equipment will still heavily filter the ECG signal to reduce noise, but will display the short, large-energy pacemaker spikes. Look at strip 1 in A closer look at ECG artifact, which is 100% ventricular paced rhythms. The first four beats appear to be a sinus rhythm with a bundle-branch block (as well as a first-degree AV block) until the pacemaker mode was selected on the monitor. The last four beats of the strip show the pacemaker spikes representative of a pacemaker rhythm that the natural filters previously discarded.

Conversely, the ECG may see artifact as pacemaker spikes. In strip 2, you see pacemaker spikes, but they're irregularly spaced and occur at a very high rate. This may be mistaken for a pacemaker malfunction known as runaway pacemaker rhythm, in which the pacemaker discharges at extremely fast rates (up to 400 paces/minute) that can be lethal.⁴ In reality, it's artifact, possibly from a loose patch or patient motion. The machine was told to display any signal that was short in duration and high in energy level as a pacemaker spike ... so it did! This pacemaker is functioning normally, but the recording equipment is getting it wrong. Note that there are numerous spikes before each of the normal, natural QRS complexes. This is a clear sign that the spikes aren't real.

Rate modulation

Pacemakers are the heart's backup should something go wrong with the patient's intrinsic rhythm. Originally, pacemakers were designed to ensure that the patient's heart rate never dropped below the programmed minimum rate. Newer pacemakers address situations other than bradycardia, but can cause a confusing ECG.

For example, at the beginning of the shift, your patient's rhythm was 100% ventricular paced at a rate of 60 beats/minute. You get him out of bed and into the chair and now his rhythm is 100% ventricular paced at 72 beats/minute. Finally, just after lunch, you ambulate your patient in the hall and the telemetry monitor shows him in a 100% ventricularly paced rhythm at a rate of 90 beats/minute.

The pacemaker isn't malfunctioning. This patient's pacemaker has an "R" in the fourth letter location of the NBG generic pacemaker code (see Reviewing pacer codes). In this case, the patient appears to have a VVIR pacemaker. The "R" means that his device is capable of modulating, or adjusting, its minimum heart rate parameter.^3–5 The pacemaker has sensors and can adjust its minimum acceptable rate depending on the patient's needs. These sensors include:

• mixed venous oxygen saturation sensors, which use right ventricle oxygen saturation levels to estimate the patient's oxygen use and whether higher or lower pacing rates are needed.⁴
• piezoelectricsensors, which sense increased muscle activity.⁴ The pacemaker measures the vibrations caused by these sensors and uses an algorithm to determine the needed pacing rate; for example, prompting the pacemaker to increase the minimum rate in response to the patient's increased need for oxygen delivery.
• pH level sensors, which sense when the blood has become more acidotic, and increase the pacemaker's minimum rate to deliver more oxygen and remove more carbon dioxide.⁴

Rate modulation, also called rate responsive pacing, although beneficial to the patient, can result in a 100% paced rhythm that's irregular and at a higher rate than you might expect.

Another form this rate modulation can take is a function known as rate-stepping or rate drop response. This feature, which can be turned off, saves the patient from sudden large changes in heart rate. For example if your patient has sick sinus syndrome (abnormalities in the sinoatrial node that cause slow or irregular heart rates), the cardiologist implants a pacemaker and programs a minimum ventricular rate of 60 so the patient will maintain a minimum heart rate of 60 beats/minute. However, when the patient is active, the patient's intrinsic heart rate may be 90 or 100 beats/minute due to increased demand for oxygen—but the sick sinus syndrome means that the intrinsic heart rate can vary greatly, from 100 to 60 beats/minute in the blink of an eye.

These variations in heart rate would be catastrophic, cutting CO in half in a matter of seconds and causing signs and symptoms such as dizziness, presyncope, or syncope, all potentially life-threatening if the patient is driving, for example.

A pacemaker with rate-stepping enabled won't let this happen. Instead, the pacemaker will prevent the heart rate from declining more than a preset amount (for example, 5%) from beat to beat.³ If the heart rate is naturally 100 beats/minute, the time between natural beats is 600 ms. The pacemaker with rate-stepping enabled at 5% would wait 630 ms before firing, which creates a rate of 97 beats/minute. The next time, the pacemaker will wait no more than 662 ms before it fires, for a heart rate of 91 beats/minute.

The pacemaker will continue this stair-step slowing of the heart rate until the pacemaker reaches the minimum programmed rate (in our example, 60 beats/minute or 1,000 ms) or it reaches the patient's intrinsic rate if that rate is greater than 60 beats/minute.

Rate-stepping looks strange indeed on the ECG—a ventricular pacemaker rhythm with progressively longer distances between pacemaker stimuli. But the slow rate of 60 beats/minute isn't the problem—the sudden drop of the intrinsic heart rate by 40% is the problem. Reducing the patient's rate from 100 to 60 beats/minute over the course of a minute or two is better tolerated.

Mode switching

Imagine your patient has a dual-chamber AV pacemaker with a minimum programmed rate of 60 beats/minute. The patient is in normal sinus rhythm at 70 beats/minute with 100% ventricular pacing. The ECG tracing shows an intrinsic P wave followed by a pacemaker spike and a wide, bizarre pacemaker-triggered QRS complex. Suddenly, the patient's ECG shows an irregular ventricular paced rhythm at 110 beats/minute with no discernible P waves. What's going on?

What has occurred is that your patient is now in AF. In normal sinus rhythm, the pacemaker sensed the patient's 70 intrinsic P waves per minute and fired a ventricular stimulus when there was no QRS complex following after the programmed interval. Now AF is generating 300 to 900 mini P waves per minute. They all don't depolarize the entire atria, and the pacemaker doesn't sense them all, but it may sense 150 or more per minute.

However, the pacemaker has a maximum tracking rate parameter that's set when the pacemaker is implanted. This is the maximum rate that ventricular lead will fire regardless of how frequently the atrial lead senses intrinsic atrial activity. So if your patient's pacemaker has a maximum tracking rate of 100 beats/minute, the pacemaker will always wait at least 600 ms after the last sensed or triggered QRS complex before delivering another ventricular stimulus. (To convert heart rate to ms, use the formula beats per minute = 60,000/ms; to convert ms to heart rate, use the formula ms = 60,000/beats per minute.) If the patient's P waves occur every 600 ms (an atrial rate of 100 beats/minute) then all is well. However, if the P waves come every 200 ms (an atrial rate of 300 beats/minute), the pacemaker won't deliver a ventricular stimulus until that 600 ms has elapsed (see About mode switching). This excessive frequency of P waves creates an undesirable situation in which the pacemaker fires at its maximum tracking rate of 100 beats/minute.

With mode switching, the pacemaker will initially respond to this rhythm change by delivering ventricular stimuli at its maximum tracking rate, but only for a limited time. If the patient remains in AF after this preprogrammed time has elapsed, then the pacemaker will change from DDD mode to VVI mode, essentially ignoring the intrinsic atrial activity and converting itself into a single-chamber ventricular only pacemaker.³

Now there is no maximum tracking rate as the pacemaker is no longer tracking atrial activity. The heart rate will be either the minimum programmed rate or the patient's intrinsic rate, whichever is higher.

The pacemaker can still monitor atrial activity and if it senses a conversion back to normal sinus rhythm (as evidenced by a drop in the frequency of sensed atrial signals), it can automatically switch back to DDD mode, improving CO by restoring atrial kick.³

Pacemaker Wenckebach

Anyone familiar with cardiac dysrhythmias has heard the term Wenckebach. This phenomenon is a type of second-degree AV block in which the PR interval gets progressively longer until one P wave isn't conducted.^3,5 The ECG shows a P wave without a QRS complex—a "dropped beat."

In patients without pacemakers, this is considered abnormal, if not pathological, AV nodal behavior. But because the AV node doesn't conduct the signal at all in dual-chamber AV pacing, a Wenckebach rhythm in a patient with a pacemaker has to be caused by something other than a problem with the AV node.

The issue lies again in the preprogrammed maximum tracking rate. If the pacemaker senses regular atrial activity at a rate of 150 beats/minute (delay of 400 ms), and the pacemaker has a programmed maximum tracking rate of 100 beats/minute (delay of 600 ms), the P waves occur at 0, 400, 800, and 1,200 ms. The pacemaker senses all these P waves and tries to keep up. It triggers the ventricles at 0 ms, but at 400 ms it's too soon to fire, so it waits until 600 ms and then fires. This increases the time from the intrinsic P wave until the pacemaker-triggered QRS, essentially increasing the AV (PR) interval.

The next P wave occurs at 400 ms, but it's only been 200 ms since the pacemaker triggered the ventricle, so the pacemaker waits 400 ms before triggering the ventricles. The next P wave is sensed at 800 ms, but it's only been 200 ms since the pacemaker triggered the ventricles. The pacemaker is programmed to ignore atrial activity this close to the QRS complex, so it ignores or "drops" this P wave. The next P wave is sensed at 1,200 ms. The pacemaker hasn't triggered the ventricles in 600 ms, which is within the maximum tracking rate parameter, so a normal AV (PR) interval is restored. A closer look at pacemaker Wenckebach shows this.

Even though the AV node isn't involved, the pacemaker has parameters that let it act as the AV node, limiting pacemaker-triggered ventricular activity and protecting the patient from excessive ventricular response rates. The dropped beat decreases the heart rate, lets the ventricles fill more completely, and maximizes AV synchrony and atrial kick, thereby maximizing CO.

Many more unusual rhythms can occur when pacemakers correctly follow their programming, but now you're familiar with the most common ones. The key is to not judge pacemaker function by only looking at the ECG, but to judge pacemaker function by assessing your patient and the cardiac rate and rhythm's effect on your patient.

A refresher on some pacing terms

Artifact—on the ECG, an abnormality produced by external action. For example, the pacing spike is an artifact of the pacemaker's electrical pulse. Muscular artifact, on the other hand, consists of electrical signals from the muscles that may be sensed, interfering with pacemaker operation.

AV interval—the period of time, measured in milliseconds, between an atrial event (sensed or paced by a dual-chamber pacemaker) and a scheduled paced ventricular event. This is the pacemaker counterpart to the PR interval.

AV synchrony—The normal activation sequence of the heart, in which the atria and then the ventricles contract. Loss of AV synchrony can hurt hemodynamics. Dual-chamber pacemakers are designed to attempt to maintain AV synchrony.

Fusion beat—a spontaneous cardiac depolarization that occurs coincidentally with a paced depolarization, causing distortion on the ECG.

Hysteresis—a pacing feature that allows a longer timeout interval after a sensed event, giving the heart a greater opportunity to beat on its own.

Pseudofusion beat—pacemaker artifact superimposed on a spontaneous P wave or QRS complex. Because the chamber has already depolarized, the pacing stimulus is ineffective, and the P wave or QRS complex isn't distorted beyond the addition of the pacer spike.

Pseudo-pseudofusion beat—atrial pacing artifact that occurs at the same time as an intrinsic QRS complex. As with a pseudofusion beat, the QRS complex isn't distorted beyond the addition of the atrial pacing spike.

Relative refractory period—the period in the cardiac cycle when the myocardial tissue is partially, but not fully repolarized. Impulses conducting into the myocardium during this time may cause serious dysrhythmias.

Timeout interval—also called the escape interval, it's the time between a paced or sensed cardiac event and the subsequent pacing stimulus from a pulse generator. Usually measured in milliseconds.

Reviewing pacer codes

First letter: Chamber(s) paced

A (atrium)

V (ventricle)

D (dual—atrium and ventricle)

O (none)

Second letter: Chamber(s) sensed

A (atrium)

V (ventricle)

D (dual)

O (none)

Third letter: Response to sensing

I (inhibited)

T (triggered)

D (dual—inhibited and triggered)

O (none)

Fourth letter: Rate modulation

R (rate modulation)

O (none)

Fifth letter: Multisite pacing

A (atrial)

V (ventricle)

D (dual)

Source: Bernstein AD, Daubert J-C, Fletcher, RD, et al. The revised NASPE/ BPEG generic code for antibradycardia, adaptive-rate, and multisite pacing. North American Society of Pacing and Electrophysiology/British Pacing and Electrophysiology Group. Pacing Clin Electrophysiol. 200;25(2):260–264.

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