Pacemakers and AICDs: Interrogation Reports and Interpretation of EKGs
Pacemakers and AICDs: Interrogation Reports and Interpretation of EKGs
A general practitioner can gain a better understanding of a patient’s underlying cardiac ailments by focusing on the fundamentals of pacemakers and automated implantable cardioverter defibrillators (AICDs).
In the first part of this 3-part article (“Pacemakers and AICDs: The ABCs”), we discussed distinguishing between pacemakers and AICDs. The second part (“Pacemakers and AICDs: Nomenclature and Malfunction”) addressed pacemaker nomenclature and device function, malfunction, and pseudomalfunction. Here we cover interrogation reports and interpretation of EKGs.
A Common Malfunction
The tracing in Figure 1 illustrates a common malfunction, intrinsic atrial activity followed by ventricular pacing. From this we know the patient has a dual chamber system because 1 lead must be in the atrium to sense the intrinsic activity and another in the ventricle to pace, most likely programmed DDD. However, the third P wave has no pacing spike or QRS following.
Here oversensing must be considered in the differential. Although it’s not obviously evident on the EKG, the lead could be oversensing some activity and erroneously classifying it as ventricular activity. As such, the inhibit function is activated and no output from the device is the result, which can be confirmed with interrogation.
Figure 1. EKG demonstrating intrinsic atrial activity followed by ventricular pacing.
Note that oversensing is not the only possibility for the above tracing and this may even represent normal device function. Electrophysiology consult would not be unreasonable in most situations.
A Less Common Abnormality
A less common abnormality is seen in Figure 2. Here there is evidence of high degree heart block. There appears to be sensing of P waves with subsequent ventricular pacing, suggesting a DDD system.
Figure 2. EKG demonstrating high degree heart block.
Toward the right side of the tracing, there are pacing artifacts without QRS complexes following. This represents failure to capture, an emergency in a patient such as this. The device appropriately detects intrinsic activity and attempts to pace but is unable to capture myocardium to effect depolarization. Causes include lead microdislodgement, scar formation, and lead malfunction. Urgent EP consultation is needed to reprogram the device or revise the lead.
Occasionally, pacing spikes fall immediately after a PVC and fail to capture the myocardium. However, this form of failure to capture is physiologic, as the pacing stimulus falls on the refractory period of the ventricle when it is incapable of depolarization. This is a common etiology of pacemaker pseudomalfunction.1
Probably the most common etiology is undercounting of the heart rate by bedside monitors. Because these monitors typically are using only 1 or 2 leads, low amplitude QRS complexes often produced by PVCs will not be counted and the heart rate on the monitor will read an abnormally low number, seeming to violate the lower rate limit of the device, and perhaps suggesting oversensing. However, close inspection of the telemetry strip will show that the device appropriately inhibited in response to a QRS that was not adequately detected by the monitor.2
Whenever an inspection of telemetry strips or the 12-lead ECG does not adequately answer a question of device malfunction, device interrogation is needed to clarify malfunction versus pseudomalfunction. A tremendous amount of information is collected from an interrogation, but a few key points should be emphasized.
First, the pacing mode (VVI, DDD, etc). Second, the device’s lower rate limit and upper tracking limit are listed in the report. The lower rate limit is the lowest heart rate the device will allow before initiating pacing. This limit can never be violated. In many devices, the lower rate limit may be set as low as 40 bpm; thus, not all bradycardic rates in the 50s represent device malfunction.
The upper tracking rate represents the fastest heart rate that a dual or biventricular device will “track,” or trigger, following atrial activation. Patients who have sinus tachycardia and a dual chamber device cannot be “slowed down” by pacemaker reprogramming because the device tracks all atrial activation to the upper tracking rate. Simple lowering of the upper tracking limit would cause Wenckebach or 2:1 AV block, which may not be hemodynamically favorable to sinus tachycardia.
In the case of defibrillators, additional tachycardic therapies are available that usually are programmed in “zones.”3Heart rates above a certain limit, typically higher than the 200 bpm range, are classified as ventricular fibrillation; rates typically between 170 and 200 bpm are classified as ventricular tachycardia. The rates that define these zones are programmable and thus vary widely patient to patient.
The therapies are programmed according to zone and may consist of antitachycardia pacing (ATP), shocks or, usually, some combination. ATP is a useful therapy by which the ICD paces the heart at a rate above the tachycardia rate once it enters this zone. This allows for disruption of the tachycardia circuit and termination of the arrhythmia without using a potentially painful shock. Clearly, this method is useful only for scar-based reentrant arrhythmias.
In addition to achieving a programmed heart rate, the tachycardia must sustain for a programmed interval to trigger therapy. This interval is programmed to a certain number of beats or a length of time. The most common reason for lack of therapy in hospital-monitored patients who have a recorded tachyarrhythmia is lack of fulfilling the rate or time criteria.
The interrogation report should contain any arrhythmias recorded by the device in the log. The specific criteria for recording an arrhythmia are programmable and are similar to the therapy zones. Much of the log is then nonsustained ventricular arrhythmias, or supraventricular arrhythmias.4
Telling Signs With EKG
When physicians review EKGs, a few telling signs may indicate that the patient has had a pacemaker implanted. In atrial pacing, a pacemaker spike is followed by a P wave with morphology dependent upon the location of the atrial pacer lead. The QRS complex appears as if in sinus rhythm. Ventricular pacing appears as a single spike followed by a wide left bundle branch block QRS complex; this is secondary to RV activation prior to that of the LV. Ventricular demand appears as a single pacemaker spike followed by a typical QRS pattern that is representative of a ventricular repolarization. This pattern often is associated with atrial fibrillation.
Dual chamber sequential AV pacing may be identified on an EKG as a pacemaker spike prior to the P wave and QRS complex. If the native atrial beat is faster than the pacemaker, then the native beat spike will appear without a preceding pacemaker complex. The paced complex differs from the native complex in that it resembles a left bundle branch block or a ventricular complex with a wide, bizarre morphology.
Biventricular pacing, also known as cardiac resynchronization therapy, involves pacing leads in the right atrium, RV, and coronary sinus, which collectively conduct impulse to the LV. In contrast to the standard ventricular pacing discussed above, biventricular pacing typically is characterized by a QS complex in leads V5-V6 and a tall R wave in lead VI.5
1. Hayes DL, Vlietstra RE. Pacemaker malfunction. Ann Intern Med. 1993;119:828-835.
2. Gunderson BD, Swerdlow CD, Wilcox JM, et al. Causes of ventricular oversensing in implantable cardioverter-defibrillators: implications for diagnosis of lead fracture. Heart Rhythm. 2010;7:626-633.
3. Barold SS, Stroobandt RX, Sinnaeve AF. Cardiac Pacemakers Step by Step: An Illustrated Guide. Elmsford, NY: Blackwell Publishing. 2004.
4. Hesselson AB. DVI Pacing. In: Simplified Interpretation of Pacemaker ECGs. Oxford, UK: Blackwell Publishing Ltd. 2003. doi: 10.1002/9780470695982.ch15
5. Chow AW, Buxton AE. Implantable Cardiac Pacemakers and Defibrillators: All You Wanted to Know. Blackwell Publishing Ltd. 2006; 47-109.