Getting back to basics with permanent pacemakers, part II

Nursing, Nov 2004 by Geiter, Henry B Jr

Learn about complications and how they affect ECG interpretation.

In my previous article (October 2004), I described basic functions of permanent cardiac pacemakers. Here, I'll discuss complications of pacemakers and their implications for electrocardiogram (ECG) interpretation.

A patients natural heart rate and rhythm are determined by a complex interaction of many factors and can change from minute to minute. Although permanent pacemakers are incredible lifesaving devices, they can't really replace a properly functioning cardiac conduction system, and in some cases, they can cause dangerous rhythms and rates. Let's look at some examples.

Pacemaker-mediated tachycardia (PMT)

This dangerous acceleration in heart rate occurs only with dual-chamber pacemakers and is due to intact retrograde atrioventricular (AV) node conduction. PMT can be triggered by a premature ventricular contraction (PVC) that triggers atrial depolarization. The pacemaker senses an atrial impulse and waits for a coordinated ventricular impulse-which doesn't happen because the AV node has just been depolarized. The pacemaker finally discharges to maintain an appropriate PR interval. This sequence of events is repeated in rapid succession, causing tachycardia. (See Recognising Pacemaker-Mediated Tachycardia.)

Today's pacemakers can be programmed to recognize and terminate this self-created tachycardia. The pacemaker monitors the order of the impulses and can recognize that a PVC followed closely by a P wave is out of the normal order. Then the pacemaker can use one of two techniques to break the cycle:

* The pacemaker can switch modes, so it's no longer tracking the atria. This stops the PMT because the pacemaker won't recognize retrograde conduction when the atria depolarize and won't trigger ventricular depolarization.

* The pacemaker can terminate PMT by changing the ventriculoatrial blanking period (also known as the post-ventricle atrial refractory period). This is the time after a ventricular beat when the pacemaker is blind to atrial activity. Atrial depolarization caused by retrograde AV node conduction falls into this blind period, and the pacemaker won't respond. This stops PMTs or terminates one that has begun.

Finally, medications that affect AV nodal conduction, such as adenosine, verapamil, or beta-blockers, can block retrograde conduction and terminate PMT.

Pacemaker syndrome

This common complication of cardiac pacing is usually associated with single-chamber pacemakers, but also can occur with dual-chamber pacemakers. Loss of AV synchrony or too-rapid atrial or ventricular pacing can result in decreased cardiac output (CO). The patient's signs and symptoms may mimic heart failure or coronary artery disease.

In VVI pacemakers (which pace and sense the ventricles and inhibit responses to a sensed event), a ventricular discharge may be conducted retrograde through the AV node, causing atrial contraction against closed AV valves during ventricular contraction. The increased pressure created when the atria can't empty causes release of atrial natriuretic peptide. This hormone causes the kidneys to excrete more sodium and water, decreasing preload and causing a further drop in CO beyond that caused by the loss of atrial kick.

Pacemaker syndrome also can occur in patients with VVI pacemakers who are in sinus rhythm. The patients natural atrial contractions aren't sensed by this type of pacemaker, and an atrial contraction can occur during a pacemaker-induced ventricular contraction. The results are the same as if the asynchrony was caused by retrograde AV conduction.

Signs and symptoms of pacemaker syndrome are related to reduced CO and mimic heart failure: shortness of breath, hypotension, chest pain, fatigue, and confusion. If retrograde AV conduction is the cause, you may notice increased jugular vein distension or cannon A waves in the patient's neck. On the ECG, you may see evidence of ventricular pacing with the QRS complexes followed too closely by P waves or intrinsic P waves and paced QRS complexes with apparent third-degree AV block.

Treatment focuses on improving AV synchrony. The method used depends on the patient; options include upgrading to a dual-chamber pacemaker, changing the AV interval, or changing to a mode that tracks the atria, such as VDD.

Pacer-induced Wenckebach phenomenon

Altering the ventriculoatrial blanking period can stop PMTs, but can cause pacemaker-induced Wenckebach phenomenon if the patient's natural atrial rate is slightly faster than the pacemaker's maximum tracking rate.

When an atrial discharge is sensed by the pacemaker but not followed by a natural QRS, the pacemaker (after the programmed AV delay) causes a ventricular discharge to maintain atrial kick. However, the atrial tissue is discharging faster than the pacemaker is programmed, so the next natural discharge occurs before the pacemaker is allowed to fire. (If it were to fire, the ventricular rate would be greater than the maximum programmed heart rate.) The pacemaker therefore delays the ventricular discharge until the appropriate amount of time has passed since the last ventricular event. This causes a prolonged PR interval because of the delayed response to the sensed atrial event.