The basic EP study is performed to evaluate the components of the conduction system in order to determine physiologic and pathologic properties, assess possible AV connections that may exist, and determine the presence of any accessory pathways. In addition, the study may be an attempt to elicit the original arrhythmia(s) that have brought the patient to the lab.
The basic EP study consists of 5 distinct parts: measurement of baseline intervals, decremental ventricular pacing, decremental atrial pacing, atrial extrastimulus testing, and ventricular extrastimulus testing. This article will briefly review the purpose of each of these components and then focus on measurement of baseline intervals. Subsequent articles will cover the remaining components. This material has been adapted from the Order and Disorder EP Training Program content.
Overview of Components
Measurement of baseline intervals is the first activity during the study, while the patient is in sinus rhythm. The measurements made include sinus cycle length (SCL), AH interval (AH), HV interval (HV), and QRS duration (QRS).
Decremental ventricular pacing (DVP) is continuous pacing from the right ventricular apex (or RVOT) with progressively shorter cycle lengths, or at a faster rate, until AV block occurs. This is retrograde AV block as the pacing is initiated in the ventricle. This step allows for assessment of retrograde AV function plus the identification of alternative pathways for an impulse to enter the atria from the ventricle.
Decremental atrial pacing (DAP) is pacing in the atria with progressively shorter cycle lengths or with a progressively faster rate until AV block occurs. This allows for assessment of antegrade AV function and unmasks potential alternative AV pathways that may exist.
Atrial extrastimulus testing (AET) also assesses antegrade AV nodal function and any alternative available pathways. In addition, the refractory periods of the available routes can be determined.
Ventricular extrastimulus testing (VET) is performed to induce ventricular tachycardias. Single, double, or triple impulses are delivered.
Next, we will focus on baseline intervals.
Measuring the intervals
The normal findings for an electrogram are the following:
Sinus cycle length SCL (600-1200 msec)
AH interval AH (50-140 msec)
HV interval HV (35-55 msec)
QRS duration QRS (80-110 msec)
Where are you supposed to start and stop an interval measurement? There are two possibilities, either of which is correct as long as you use the same reference point from start to finish. The onset of an electrogram is a reasonable reference point for the beginning and the end of an interval measurement, and is shown in Figure 1 on the left for a typical AH interval. It reflects the timing of the approaching wavefront as it arrives very close to the electrode pair. The biggest problem with this approach is slurring of the upstroke, making it difficult to tell the “onset of the onset.” This is made worse with wide-spaced recordings, wherein some slurring can consume up to as much as 20-30 msec of time. Generally, the onset of the upstroke is easier to identify when it is the product of close-spaced electrodes.
The other method for interval measurement is shown in Figure 1 on the right. The zero-crossover point may be a better alternative to the onset method because it represents the exact moment when the leading edge of the wavefront passes beneath a point halfway between the two electrodes. If your electrodes are close spaced, the halfway point essentially is the electrode pair for all practical purposes. Again, recordings from wide-spaced electrodes will really make the measurement difficult, because the breadth of the electrogram is large and often fractionated. On the other hand, some tissue already may naturally have that fractionated look and a zero-crossover is impossible to find.
With respect to the HV interval, the measurement ends with the onset of the surface QRS complex, not the onset of the ventricular electrogram in the His lead, as is illustrated in Figure 2. In fact, you’re looking for the earliest evidence of QRS onset. This means that you need to look in all three surface leads to find the best (earliest) one, in this case V1.
Figure 3 illustrates the measurements for SCL, AH, HV, and QRS intervals. In this example, the His atrial electrogram is better seen in the proximal recording, while the His potential is more easily seen on the distal recording pair. Although it is not the preferred approach, it’s alright for the A and the His electrograms to come from different electrode pairs when you measure the AH interval. Ideally, the measurement should start and stop in the same electrode recording, but this isn’t always what you get.
When you see a His bundle recording in which only the His and V potentials are visible, most likely that His spike is really the right bundle branch potential.
Note that in this example, there are only two recordings for the His lead (i.e., two electrode pairs in a quadripolar catheter). The reason one might use a hexapolar — or, better yet, an octapolar as a His catheter — is to optimize the opportunity to get a stable and readily visible His potential. The more electrode pairs on the catheter, the greater the likelihood of getting a His on at least one recording. Moreover, if one uses a deflectable tipped octapolar, getting all the electrograms to appear is much easier.
Note that the end of the HV interval is always measured from the surface ECG onset of the QRS complex — not from the V potential of the intracardiac His recording, as might seem intuitive. The reason for this is because the surface ECG provides the best estimate of the onset of ventricular muscle activation during a sinus conducted impulse. The only way an intracardiac recording could tell us when the true onset of ventricular activation occurred is to have an electrode catheter located at that site — usually somewhere on the middle and left sides of the interventricular septum.
Short PR Interval
The patient from Figure 4 has a PR interval measuring 104 msec, below the usual 120 msec minimum. There is no preexcitation since there is no delta wave or widened QRS complex.
The intracardiac recordings for this patient are seen in Figure 5. Note the AH interval is only 35 msec, less than the 50 msec lower limit. Since the HV interval is within the normal range, the short PR is entirely due to fast AV nodal pathway conduction time. Historically, such a patient was regarded as having Lown-Ganong-Levine syndrome if they also had PSVT. The implication was that they had uncharacteristically rapid AV nodal conduction implying propagation over an AV nodal bypass tract, circumventing normal AV nodal conduction. In fact, the observation is simply due to a more rapid degree of AV nodal conduction than is normally encountered, which is now known to be a variant of normal.
Long PR Interval
The patient from Figure 6 has a PR interval measuring 296 msec, above the usual 200 msec maximum. This patient is 22 years old. Transient increased vagal tone is the most likely cause for preferential impulse conduction over the slow AV nodal pathway and, consequently, the long PR interval. Most likely, this patient exhibits fast AV nodal pathway conduction at other times, but there may be a great degree of variability in conduction over the fast and slow pathways, partially mediated by the autonomic nervous system.
The intracardiac recordings for this patient are seen in Figure 7. This shows that the delay in the PR interval is entirely due to delay in the AV node since the HV interval is a normal 50 msec. The AH interval measures 260 msec, abnormally prolonged and consistent with antegrade slow AV nodal pathway conduction. The normal upper limit for the AH interval is probably around 105-110 msec, but some suggest as high as 140 msec. Also present is complete right bundle branch block (CRBBB), as seen in V1 with an rSR' QRS configuration. A long PR interval in the presence of CRBBB might have raised the suspicion of an underlying prolongation of the HV interval, but this proved not to be the case.
Abnormally Prolonged HV
In Figure 8, the patient’s baseline HV interval measured 75 msec. The normal range is 35-55 msec. Note that complete left bundle branch block (CLBBB) is present, as seen in lead V1, with a wide, completely negative QRS complex. When one is found to have a prolonged HV interval, there is almost always an associated intraventricular conduction defect such as RBBB or LBBB. This is because the conduction delay or block generally begins below the level of the His bundle — involving either of the bundle branches. The conduction impairment may then progress with time if the underlying disease is left unchecked, and may eventually involve the contralateral side. At that point, the HV interval will begin to lengthen.
Not true of the converse: when one is found to have a bundle branch block on their ECG, usually both the AH and HV intervals are normal, hence a normal PR interval. In fact, if the PR interval is lengthened, it is much more common to see a prolonged AH interval as the cause, as Figure 7 shows.
If one has a prolonged HV interval with left bundle branch block, it implies that the right bundle branch also has conduction impairment. As such, a very prolonged HV interval (≥100 msec) is an indication for permanent DDD pacing. This scenario would also imply the need for pacing if infranodal block were to develop at atrial paced rates at or below 120 bpm.
Note that the end of the HV interval is seen best by lead V1, because it is the lead with the earliest onset QRS. Lead I is the worst, with the onset there delayed by 20-30 msec (vertical arrow). Using lead I for the HV interval measurement would have grossly overstated its value at 100 msec.
Abnormally Short HV Interval
The disorder associated with a short HV interval during sinus rhythm is Wolff-Parkinson-White syndrome. In this example, there is a left-sided accessory pathway (AP) connecting atria to ventricles.
During sinus rhythm, the impulse crosses nearly simultaneously into the ventricles over two routes: the normal AV conduction system, and the AP. Because of far less delay in conduction into the ventricles via the AP, ventricular activation is “premature” and initiates the beginning of the QRS prior to the completion of impulse passage through the normal His-Purkinje system (prior to the end of the usual HV interval). Hence, there is “preexcitation” of the ventricles during sinus rhythm, and this produces the ECG triad of a short PR interval, delta wave, and wide QRS.
Note how closely the atrial and ventricular electrograms are to each other in the coronary sinus recordings. When a recording electrode pair is on the annulus in the vicinity of the AP, the shortest conduction time between atria and ventricles will be seen. Contrast this short AV interval with recordings at a site remote from the AP such as the His bundle region (also annular), where the AV interval measures more like 140-150 msec.
We have reviewed the first step in a diagnostic EP study: the measurement of baseline intervals. As can be seen by the examples we have presented, a vast amount of information can be obtained from just this first step. Subsequent articles will cover the additional maneuvers that are performed for a comprehensive analysis.
Disclosure: The authors have no conflicts of interest to report regarding the content herein.