I. General concepts; intracardiac electrograms

Four main catheters are used: RA catheter, RV catheter, His catheter, and coronary sinus (CS) catheter. These catheters record electrograms (EGMs) and may also be used for pacing. The His and CS catheters typically have multiple recording electrodes (e.g., proximal, mid, and distal). The His catheter is placed just across the tricuspid valve, unto the high membranous ventricular septum, where the His bundle lies.

• RA recording is characterized by A wave (atrial activity).
  
• RV recording is characterized by V wave (ventricular activity).
  
• His recording is characterized by three waves: A, H (His activity), and V (Figures 15.1, 15.2). The A wave on His recording normally occurs slightly later than the A wave on RA recording, due to the delayed transmission of the atrial activity to the His catheter. The His spike is typically narrower and of smaller amplitude than the A and V waves, and looks like a narrow bar.
  
• CS recording mainly shows A wave; it may show a far-field, low-amplitude V wave (Figure 15.2).

In order to identify the deflections on any channel, always correlate them with the surface ECG. This should always be the first step in analyzing intracardiac EGMs. The A wave coincides with the P wave, the V wave coincides with the QRS complex (~superimposed with QRS), and H is between A and V. Regardless of the channel, V waves line up with the QRS complexes.

The AH interval corresponds to AV nodal conduction, while the HV interval corresponds to His+infra-His conduction. AH is measured from the onset of A on His recording to the onset of H, while HV is measured from the onset of H to the onset of the earliest ventricular activation, which is usually the onset of QRS on the ECG. The HV interval is the only interval where the surface ECG is needed not just for identification but for measurement as well; in fact, the electrocardiographic QRS often starts earlier than the His V wave, and is closer to the RV V wave, as the ventricular stimulation starts at the mid-ventricular wall then spreads up to His. The normal AH interval is 60–120 ms, while the normal HV interval is 35–55 ms; HV is severely increased if >100 ms.

In the EP lab, programmed stimulation may be performed using two pacing techniques: (i) extrastimulus, where a progressively more premature extrastimulus S2 is introduced after a baseline pacing sequence S1 (~8-beat train S1, at a fixed cycle length); (ii) incremental pacing , where a steady pacing sequence, faster than the baseline rate, is introduced; progressively faster pacing sequences are then introduced.

II. AV conduction abnormalities

AH prolongation or, worse, A wave that is not followed by H and V waves, indicates AV block at the nodal level.

HV prolongation, or A wave that is followed by H but not V wave, indicates infranodal AV block and thus is more ominous and more readily dictates pacemaker placement, in a symptomatic or even asymptomatic patient (Figure 15.3). The block may be intra- or infra-Hisian; H wave may be prolonged, fragmented or split in intra-Hisian block.

In the EP lab, the AV conduction may be stressed using the incremental pacing or the extrastimulus technique or drugs (procainamide).

Incremental pacing. The AV node is characterized by decremental conduction and longer refractory period with faster atrial pacing, which is opposite to the myocardial tissue. With progressively faster atrial pacing trains, the AH interval normally increases, and a conduction block may normally be seen at the AV nodal level, which manifests as a drop of both H and V complexes in a Wenckebach pattern. The pacing interval at which this occurs is the Wenckebach cycle length, normally ≤ 450 ms (≥130 bpm). Wenckebach AV block occurring at a slower rate implies AV nodal disease. The HV interval should not change with pacing; an increase in HV interval (especially >100 ms) or a drop of V wave with fast atrial pacing indicates infranodal AV block.

Extrastimulus technique. Progressively more premature atrial extrastimuli are inserted until A fails to conduct to His. The earliest A–A interval at which A stops leading to H complex is the AV nodal effective refractory period. On the other hand, the earliest interval at which the premature extrastimulus does not lead to A complex is the atrial effective refractory period. Beside having slower conduction than the atrial and ventricular tissues, the AV node normally has a longer refractory period. An AV node effective refractory period >425 ms is abnormal.

III. Sinus node assessment

During fast overdrive atrial pacing (~30 seconds), and similarly to atrial fibrillation, the sinus node activity is inhibited. Upon cessation of atrial pacing, the sinus node needs time to recover its electrical activity. The duration of the pause between the last paced A complex and the recovery A complex is called the sinus node recovery time (SNRT). A diseased sinus node has a prolonged SNRT. The corrected SNRT is equal to SNRT minus basic cycle length, basic cycle length being the A–A interval prior to atrial pacing (e.g., SNRT 1100 ms, basic cycle length 700 ms, corrected SNRT =400 ms). The corrected SNRT is normally <550 ms.

Also, a blunted sinus node response to atropine + propranolol (i.e., to the removal of the autonomic tone) implies sinus node disease.

Note, however, that rhythm monitoring (e.g., event monitor), which correlates symptoms with paroxysmal conduction blocks/sinus pauses, has the highest yield in establishing that conduction blocks are the cause of the patient’s symptoms. Invasive EP evaluation of the AV or sinus node does not have a high sensitivity or specificity for conduction abnormalities. For example, the presence of sinus nodal disease or AV nodal block does not imply that the conduction abnormality underlies the patient’s symptoms. Only the finding of HV infranodal block (a drop of V wave or HV interval >100 ms) is highly specific for a serious conduction disorder and usually mandates pacemaker placement regardless of symptoms.

IV. Ventricular vs. supraventricular tachycardia

AV dissociation is easily characterized on EGM. Identify V deflections, which line up with QRS complexes on the ECG; then identify the other deflections, seen on the atrial and His channels, which correspond to the A deflections. VT is diagnosed if V deflections are more numerous than A deflections. SVT is diagnosed if A deflections are more numerous than V deflections. If A deflections are equal in number to V deflections, the tachycardia could be SVT or VT with 1:1 VA conduction. Assess the onset of the tachycardia (V or A) and which interval changes first (A–A or V–V). In VT, the tachycardia starts with a V deflection and the A–A interval’s length tracks the V–V interval’s length, meaning a change in A–A interval follows, rather than precedes, a similar change in V–V interval.

In VT, V deflections are typically more numerous than A deflections and are dissociated from them. However, V and A could be associated in a 1:1 fashion (1:1 VA conduction), or a 2:1 or 3:1 fashion (2:1 or 3:1 VA conduction). In VT with AV dissociation, His spikes are typically absent. In VT with AV association, His spikes may result from retrograde VA conduction.

V. Dual AV nodal pathways

Normally, after a premature atrial extrastimulus, the AV nodal conduction slows and AH interval increases (relative refractory period). With progressively more premature atrial extrastimuli, AH interval progressively increases, and at some point H and V may drop. If, however, with a small decrement of A–A interval (e.g., 340 ms to 330 ms), AH interval disproportionately increases, by >50 ms (as opposed to a slight increase or a block), it is implied that the AV node has a fast and a slow pathway. While the fast pathway conducts the normal, sinus-initiated beats and the atrial extrastimuli, a very early extrastimulus falls in the absolute refractory period of the fast pathway and fails to conduct through it. Subsequently, this extrastimulus conducts over the slow pathway, leading to an AH jump (Figure 15.4). The slow pathway has a slower conduction but a shorter refractory period, hence the slow pathway conducts when the fast pathway is blocked. This may initiate AVNRT, if the fast pathway recovers quickly enough to allow retrograde conduction (slow–fast reentry).

VI. AVNRT

During AVNRT, A conducts down the AV node’s slow pathway, which then conducts to V and A quickly and almost simultaneously (Figures 15.5, 15.6). The conduction to A occurs retrogradely through the fast pathway. A tachycardia with almost simultaneous V and A deflections is usually AVNRT.

VII. Accessory pathway, orthodromic AVRT, antidromic AVRT

An accessory pathway connects the A and the V. The accessory pathway may conduct from the atrium all the way to the ventricle at baseline (manifest pathway = WPW pattern), or may only partially conduct and not reach the ventricle (concealed pathway).

The accessory pathway has a faster conduction than the AV node but a longer refractory period. Thus, a PAC is more likely to conduct through the AV node than the accessory pathway. By the time the electrical activity reaches the ventricle, the accessory pathway may have recovered, and thus fast retrograde conduction may occur and lead to orthodromic AVRT (= AVRT with retrograde conduction through the accessory pathway). In this case, A conducts to V through His, then V rapidly conducts to A retrogradely through the fast-conducting accessory pathway (Figure 15.7). In contrast to AVNRT, A and V activities are not as close.

Antidromic AVRT is a reentrant AV tachycardia which conducts antegradely over the accessory pathway. It is unusual for a PAC to initiate antidromic AVRT, as it blocks through the accessory pathway before it blocks through the AV node (the accessory pathway has a longer refractory period than the AV node). Antidromic AVRT may occur in rare cases where the accessory pathway has a shorter refractory period than the AV node. In this case, A conducts to V through the accessory pathway, then V conducts back to A through His (Figure 15.7).

A CS catheter helps further differentiate AVNRT from AVRT and localizes the site of the accessory pathway (Figure 15.8). Analyze the His, CS, and RA channels and see the site of earliest A activity during the tachycardia: in AVNRT the earliest A activity is in His, followed by the proximal part of the CS catheter, whereas in AVRT the earliest A activity is in the distal CS catheter (left-sided pathway), proximal CS catheter (posteroseptal pathway), or the RA (right-sided pathway). The site of earliest A activity in the CS (proximal, mid, or distal) allows the localization of the accessory pathway site.

During a baseline study, before arrhythmia induction, the accessory pathway may be diagnosed and localized through ventricular pacing and mapping of the retrograde atrial activation. Normally, retrograde atrial activation spreads through the AV node and the earliest atrial activation is in the His, followed by concentric spread to both atria (concentric atrial activation through His). If an accessory pathway is present, retrograde atrial activation will spread through this pathway into one of the atria first, then spread contralaterally (eccentric atrial activation). The earliest atrial activation is right, left, or posteroseptal (coronary sinus). Occasionally, the retrograde activation may appear normal if the pathway is anteroseptal.