Right AtriAL Catheter

A fixed-tip, 5 or 6 Fr quadripolar electrode catheter is typically used. The RA may be entered from the IVC or SVC. The femoral veins are the usual entry sites. Most commonly, stimulation and recording from the RA is performed by placing the RA catheter tip at the high posterolateral wall at the SVC-RA junction in the region of the sinus node or in the RA appendage (Fig. 4-7).

FIGURE 4-7 Fluoroscopic views of catheters in study for supraventricular tachycardia (superoparaseptal bypass tract ablation). Catheters are labeled HRA (high right atrium), right ventricle (RV), and coronary sinus (CS); the CS catheter was inserted from a jugular venous approach.

Right VentricULAR Catheter

A fixed-tip, 5 or 6 Fr quadripolar electrode catheter is typically used. All sites in the RV are accessible from any venous approach. The RV apex is most commonly chosen for stimulation and recording because of stability and reproducibility (see Fig. 4-7).

His Bundle Catheter

A fixed- or deflectable-tip, 6 Fr quadripolar electrode catheter is typically used. The catheter is passed via the femoral vein into the RA and across the tricuspid annulus until it is clearly in the RV (under fluoroscopic monitoring, using the right anterior oblique [RAO] view; see Fig. 4-7). It is then withdrawn across the tricuspid orifice while maintaining a slight clockwise torque for good contact with the septum until a His potential is recorded. Initially, a large ventricular electrogram can be observed, then, as the catheter is withdrawn, the right bundle branch (RB) potential can appear (manifesting as a narrow spike less than 30 milliseconds before the ventricular electrogram). When the catheter is further withdrawn, the atrial electrogram appears and grows larger. The His potential usually appears once the atrial and ventricular electrograms are approximately equal in size and is manifest as a biphasic or triphasic deflection interposed between the local atrial and ventricular electrograms. If the first pass was unsuccessful, the catheter should be passed again into the RV and withdrawn with a slightly different rotation. If, after several attempts, a His potential cannot be recorded using a fixed-tip catheter, the catheter should be withdrawn and reshaped, or it may be exchanged with a deflectable-tip catheter. Once the catheter is in place, a stable recording can usually be obtained. Occasionally, continued clockwise torque on the catheter shaft is required to obtain a stable HB recording, which can be accomplished by looping the catheter shaft remaining outside the body and fixing the loop by placing a couple of towels on it, or by twisting the connection cable in the opposite direction so that it maintains a gentle torque on the catheter.

When the access is from the SVC, it is more difficult to record the His potential because the catheter does not lie across the superior margin of the tricuspid annulus. In this case, a deflectable-tip catheter is typically used, advanced into the RV, positioned near the HB region by deflecting the tip superiorly to form a J shape, and then withdrawing the catheter so that it lies across the superior margin of the tricuspid annulus. Alternatively, the catheter can be looped in the RA (“figure-of-6” position); then the body of the loop is advanced into the RV so that the tip of the catheter is pointing toward the RA and lying on the septal aspect of the RA. Gently withdrawing the catheter can increase the size of the loop and allow the catheter tip to rest on the HB location.

Recording of the HB electrogram can also be obtained via the retrograde arterial approach. Using this approach, the catheter tip is positioned in the noncoronary sinus of Valsalva (just above the aortic valve) or in the LV outflow tract (LVOT), along the interventricular septum (just below the aortic valve).

Coronary Sinus Catheter

A femoral, internal jugular, or subclavian vein may be used. It is easier to cannulate the CS using the right internal jugular or left subclavian vein versus the femoral vein because the CS valve is oriented anterosuperiorly and, when prominent, can prevent easy access to the CS from the femoral venous approach. A fixed-tip, 6 Fr decapolar electrode catheter is typically used for access from the SVC, whereas a deflectable-tip catheter is preferred for CS access from the femoral veins.

The standardized RAO and left anterior oblique (LAO) fluoroscopic views are used to guide placement of catheters in the CS. Although the CS cannot be directly visualized with standard fluoroscopy, the epicardial fat found in the posteroseptal space just posterior to the CS os can be visualized as a characteristic radiolucency on cine fluoroscopy in the RAO projection, where the cardiac and diaphragmatic silhouettes meet.⁷

When cannulating the CS from the SVC approach, the LAO view is used, the catheter tip is directed to the left of the patient, and the catheter is advanced with some clockwise torque to engage the CS os; electrodes should resemble rectangles rather than ovals when the catheter tip is properly oriented to advance into the CS. Once the CS os is engaged, the catheter is further advanced gently into the CS, so that the most proximal electrodes lie at the CS os (see Fig. 4-7).

During cannulation of the CS from the IVC approach, the tip of the catheter is first placed into the RV, in the RAO fluoroscopy view, and flexed downward toward the RV inferior wall (Video 2 ). Subsequently, the catheter is withdrawn until it lies at the inferoseptal aspect of the tricuspid annulus. In the LAO or RAO view, the catheter is then withdrawn gently with clockwise rotation until the tip of the catheter drops into the CS os. Afterward, the catheter is advanced into the CS concomitantly with gradual release of the catheter curve (Fig. 4-8). Alternatively, the tip of the catheter is directed toward the posterolateral RA wall and advanced with a tight curve to form a loop in the RA, in the LAO view, with the tip directed toward the inferomedial RA. The tip is then advanced with gentle up-down, right-left manipulation using the LAO and RAO views to cannulate the CS. In the RAO view, the atrioventricular (AV) fat pad (containing the CS) appears as more radiolucent than surrounding heart tissue.

FIGURE 4-8 Right anterior oblique (RAO) and left anterior oblique (LAO) fluoroscopic views of catheters in a study of typical atrial flutter. A 20-pole Halo catheter is positioned along the tricuspid annulus. The coronary sinus (CS) catheter was introduced from a femoral venous approach. The ablation catheter (Abl) is at the cavotricuspid isthmus.

When attempting CS cannulation, the catheter can enter the RV, and premature ventricular complexes (PVCs) or VT can be observed. Catheter position in the RV outflow tract (RVOT) can be misleading and simulate a CS position. Confirming appropriate catheter positioning in the CS can be achieved by fluoroscopy and recorded electrograms. In the LAO view, further advancement in the CS directs the catheter toward the left heart border, where it curves toward the left shoulder. Conversely, advancement of a catheter lying in the RVOT leads to an upward direction of the catheter toward the pulmonary artery. In the RAO view, the CS catheter is directed posteriorly, posterior to the AV sulcus, whereas the RVOT position is directed anteriorly. Recording from the CS catheter shows simultaneous atrial and ventricular electrograms, with the atrial electrogram falling in the later part of the P wave, whereas a catheter lying in the RVOT records only a ventricular electrogram. The catheter can also pass into the LA via a patent foramen ovale, in which case it takes a straight course toward the left shoulder, and all recordings are atrial.

If used, the CS catheter should be placed first, because its positioning can be impeded by the presence of other catheters. It is also recommended that the CS catheter sheath be sutured to the skin to prevent displacement of the catheter during the course of the EP study.

Fluoroscopy-Guided Transseptal Catheterization

Equipment required for atrial septal puncture includes the following: a 62-cm, 8 Fr transseptal sheath for LA cannulation (e.g., SR0, SL1, Mullins, or Agilis NxT Steerable sheath, St. Jude Medical, Minnetonka, Minn.), a 0.035-inch J guidewire, a 71-cm Brockenbrough needle (e.g., BRK, St. Jude Medical, Minnetonka, Minn.), and a 190-cm, 0.014-inch guidewire.

Venous access is obtained via the femoral vein, preferably the right femoral vein because it is closer to the operator. The sheath, dilator, and guidewires are flushed with heparinized saline. The transseptal sheath and dilator are advanced over a 0.035-inch J guidewire under fluoroscopy guidance into the SVC. The guidewire is then withdrawn, thus leaving the sheath and its dilator locked in place. The dilator within the sheath is flushed and attached to a syringe to avoid introduction of air into the RA.

Attention is then directed to preparing the transseptal needle. The Brockenbrough needle comes prepackaged with an inner stylet, which may be left in place to protect it as it is advanced within the sheath. Alternatively, the inner stylet may be removed and the needle connected to a pressure transducer line (pressure monitoring through the Brockenbrough needle will be required during the transseptal puncture); continuous flushing through the Brockenbrough needle is used while advancing the needle into the dilator. A third approach, when the use of contrast injection is planned, is to attach the Brockenbrough needle to a standard three-way stopcock via a freely rotating adapter. A 10-mL syringe filled with radiopaque contrast is attached to the other end of the stopcock while a pressure transducer line is attached to the third stopcock valve for continuous pressure monitoring. The entire apparatus should be vigorously flushed to ensure that no air bubbles are present within the circuit.

The Brockenbrough needle is advanced into the dilator until the needle tip is within 1 to 2 cm of the dilator tip. The needle tip must be kept within the dilator at all times, except during actual septal puncture. The curves of the dilator, sheath, and needle should be aligned so that they are all in agreement and not contradicting each other. The sheath, dilator, and needle assembly is then rotated leftward and posteriorly (usually with the Brockenbrough needle arrow pointing at the 3 to 6 o’clock position relative to its shaft) and retracted caudally as a single unit (while maintaining the relative positions of its components) to engage the tip of the dilator into the fossa ovalis. Under fluoroscopy monitoring (30-degree LAO view), the dilator tip moves slightly leftward on entering the RA and then leftward again while descending below the aortic root. A third abrupt leftward movement (“jump”) below the aortic root indicates passage over the limbus into the fossa ovalis (Fig. 4-10). This jump generally occurs at the level of the HB region (marked by an EP catheter recording the HB potential). If the sheath and dilator assembly is pulled back farther than intended (i.e., below the level of the fossa and HB region), the needle should be withdrawn and the guidewire placed through the dilator into the SVC. The sheath and dilator assembly is then advanced over the guidewire into the SVC and repositioning attempted, as described earlier. The sheath and dilator assembly should never be advanced without the guidewire at any point during the procedure.

FIGURE 4-10 Right anterior oblique (RAO; left) and left anterior oblique (LAO; right) fluoroscopic views during transseptal catheterization. A, Initially, the transseptal sheath-dilator assembly is advanced into the superior vena cava. B, The transseptal assembly is withdrawn into the high right atrium. C, With further withdrawal, the dilator tip abruptly moves leftward, indicating passage over the limbus into the fossa ovalis at the level of the His bundle catheter. At the fossa ovalis, the dilator tip has an anteroposterior orientation in the RAO view and a leftward orientation in the LAO view. D, The transseptal assembly is advanced across the atrial septum. CS = coronary sinus.

Several fluoroscopic markers are used to confirm the position of the dilator tip at the fossa ovalis. As noted, an abrupt leftward movement (jump) of the dilator tip below the aortic knob is observed as the tip passes under the muscular atrial septum onto the fossa ovalis (see Video 4 ). In addition, the posterior extent of the aortic root can be marked by a pigtail catheter positioned through the femoral artery in the noncoronary cusp or by the HB catheter (recording a stable proximal HB potential), which lies at the level of the fibrous trigone opposite and caudal to the noncoronary aortic cusp. When the dilator tip lies against the fossa ovalis, it is directed posteroinferiorly to the proximal HB electrode (or pigtail catheter) in the RAO view and to the left of the proximal HB electrode (or pigtail catheter) in the LAO view (see Fig. 4-10). Another method that can be used to ensure that the tip is against the fossa ovalis is injection of 3 to 5 mL of radiopaque contrast through the Brockenbrough needle to visualize the interatrial septum. The needle tip then can be seen tenting the fossa ovalis membrane with small movements of the entire transseptal apparatus. Typically, septal staining remains visible after contrast injection, which allows for real-time septal visualization while monitoring the pressure during transseptal puncture.

Once the position of the dilator tip is confirmed at the fossa ovalis, the needle, dilator, and sheath assembly is pushed slightly against the interatrial septum, and the needle is then briskly advanced to protrude outside the dilator in the LAO view during continuous pressure monitoring. If excessive force is applied without a palpable “pop” to the fossa, then the Brockenbrough needle likely is not in proper position. After passage through the fossa ovale and before advancing the dilator and sheath, an intraatrial position of the needle tip within the LA, rather than the ascending aorta or posteriorly into the pericardial space, needs to be confirmed. Recording an LA pressure waveform from the needle tip confirms an intraatrial location (Fig. 4-11). An arterial pressure waveform indicates intraaortic position of the needle. Absence of a pressure wave recording can indicate needle passage into the pericardial space or sliding up and not puncturing through the atrial septum. A second method is injection of contrast through the needle to assess the position of the needle tip. Opacification of the LA (rather than the pericardium or the aorta) verifies the successful transseptal access. Alternatively, passing a 0.014-inch floppy guidewire through the Brockenbrough needle into a left-sided PV (beyond the cardiac silhouette in the LAO fluoroscopy view) helps verify that needle tip position is within the LA (see Video 4 ). If the guidewire cannot be advanced beyond the fluoroscopic border of the heart, pericardial puncture should be suspected. In addition, aortic puncture should be suspected if the guidewire seems to follow the course of the aorta. In these situations, contrast should be injected to assess the position of the Brockenbrough needle before advancing the transseptal dilator. Sometimes, the guidewire enters the LA appendage rather than a PV; in this setting, a clockwise torque of the sheath and dilator assembly can help direct the guidewire posteriorly toward the ostium of the left superior or left inferior PV.

FIGURE 4-11 Left anterior oblique (LAO) fluoroscopic views and simultaneous electrical and pressure (P) recordings during transseptal catheterization. Left, The transseptal assembly is in the right atrium (RA), indicated by typical A and V waves of right-heart pressure tracing. Middle, The pressure waveform is dampened somewhat as the catheter tip abuts the septum. Right, The needle is across the atrial septum, and characteristic waves (V larger than A) are seen. CSdist = distal coronary sinus; CSprox = proximal coronary sinus; LA = left atrium.

Once the position of the needle tip is confirmed to be in the LA, both the sheath and dilator are advanced as a single unit over the needle by using one hand while fixing the Brockenbrough needle in position with the other hand (to prevent any further advancement of the needle). Preferably, the sheath and dilator assembly is advanced into the LA over a guidewire placed distally into a left-sided PV, which helps direct the path of the assembly as it enters the LA and minimize the risk of inadvertent puncture of the lateral LA wall. Once the dilator tip is advanced into the LA over the needle tip, the needle and dilator are firmly stabilized as a unit—to prevent any further advancement of the needle and dilator—and the sheath is advanced over the dilator into the LA. Once the transseptal sheath tip is within the LA, the dilator and needle are withdrawn slowly during continuous flushing through the needle or while suction is maintained through a syringe placed on the sheath side port to minimize the risk of air embolism and while fixing the sheath with the other hand to prevent dislodgment outside the LA. The sheath should be aspirated until blood appears without further bubbles; this usually requires aspiration of approximately 5 mL. The sheath is then flushed with heparinized saline at a flow rate of 3 mL/min during the entire procedure.

The mapping-ablation catheter is advanced through the sheath into the LA. Flexing the catheter tip and applying clockwise and counterclockwise torque to the sheath help confirm free movement of the catheter tip within the LA, rather than possibly in the pericardium. It is important to recognize that merely recording atrial electrograms does not confirm an LA catheter location because an LA recording can be obtained from the epicardial surface of the LA, from the RA, or even the aortic root.

When two transseptal accesses are required, the second access can be obtained through a separate transseptal puncture performed in a fashion similar to that described for the first puncture. Alternatively, the first transseptal puncture can be used for the second sheath. This technique entails passing a guidewire or thin catheter through the first transseptal sheath into the LA, preferably into the left inferior or superior PV, and then the sheath is pulled back into the RA. Subsequently, a deflectable tip catheter is used through the second long sheath to interrogate the fossa ovalis and to try to access the LA through the initial puncture site. Once this is accomplished, the first sheath is advanced back into the LA, and the guidewire is replaced with the mapping catheter. Alternatively, instead of using a deflectable catheter, the needle, dilator, and sheath assembly is advanced into the SVC and pulled back and positioned at the fossa ovalis (as described earlier for the first transseptal puncture). Once the tip of the dilator falls into the fossa ovalis, gentle manipulation of the assembly under biplane fluoroscopy guidance is performed until the dilator tip passes along the guidewire through the existing transseptal puncture, without advancing the needle through the dilator. The assembly is then advanced as a single unit into the LA.

An intravenous heparin bolus is administered just before or immediately after puncturing the atrial septum, followed by intermittent boluses or continuous heparin infusion to maintain an elevated ACT (more than 250 to 300 seconds).

Intracardiac Echocardiography–Guided Transseptal Catheterization

The intent of ICE-guided transseptal catheterization is to image intracardiac anatomy and identify the exact position of the distal aspect of the transseptal dilator along the atrial septum—in particular, to assess for tenting of the fossa ovalis with the dilator tip.

Two types of ICE imaging systems are currently available, the electronic phased-array ultrasound catheter and the mechanical ultrasound catheter.⁸ The electronic phased-array ultrasound catheter sector imaging system (AcuNav, Siemens Medical Solutions, Malvern, Pa.) uses an 8 or 10 Fr catheter that has a forward-facing 64-element vector phased-array transducer scanning in the longitudinal plane. The catheter has a four-way steerable tip (160-degree anteroposterior or left-right deflections). The catheter images a sector field oriented in the plane of the catheter. The mechanical ultrasound catheter radial imaging system (Ultra ICE, EP Technologies, Boston Scientific, San Jose, Calif.) uses a 9-MHz catheter-based ultrasound transducer contained within a 9 Fr (110-cm length) catheter shaft. It has a single rotating crystal ultrasound transducer that images circumferentially for 360 degrees in the horizontal plane. The catheter is not freely deflectable.

When using the mechanical radial ICE imaging system, a 9 Fr sheath, preferably a long, preshaped sheath, for the ICE catheter is advanced via a femoral venous access. To enhance image quality, all air must be eliminated from the distal tip of the ICE catheter by flushing vigorously with 5 to 10 mL of sterile water. The catheter then is connected to the ultrasound console and advanced until the tip of the rotary ICE catheter images the fossa ovalis. Satisfactory imaging of the fossa ovalis for guiding transseptal puncture is viewed from the mid-RA (Fig. 4-12).⁸

FIGURE 4-12 Intracardiac echocardiography (ICE)-guided transseptal puncture using the Ultra-ICE catheter. These ICE images, with the transducer placed in the right atrium (RA), show (A) the RA, fossa ovalis (arrowheads), left atrium (LA), and aorta (AO). B, The transseptal needle is properly positioned, with tenting (yellow arrow) against the midinteratrial septum at the fossa ovalis. RV= right ventricle.

The AcuNav ICE catheter is introduced under fluoroscopy guidance through a 23-cm femoral venous sheath. Once the catheter is advanced into the mid-RA with the catheter tension controls in neutral position (the ultrasound transducer oriented anteriorly and to the left), the RA, tricuspid valve, and RV are viewed. This is called the home view (Fig. 4-13A; see Video 5 ). Gradual clockwise rotation of a straight catheter from the home view allows sequential visualization of the aortic root and the pulmonary artery (see Fig. 4-13B), followed by the CS, the mitral valve, the LA appendage orifice, and a cross-sectional view of the fossa ovalis (see Fig. 4-13C and D). The mitral valve and interatrial septum are usually seen in the same plane as the LA appendage. Posterior deflection or right-left steering of the imaging tip in the RA, or both, is occasionally required to optimize visualization of the fossa ovalis; the tension knob (lock function) can then be used to hold the catheter tip in position. Further clockwise rotation beyond this location demonstrates images of the left PV ostia (see Fig. 4-13E). The optimal ICE image to guide transseptal puncture demonstrates adequate space behind the interatrial septum on the LA side and clearly identify adjacent structures, but it does not include the aortic root because it would be too anterior for the interatrial septum to be punctured safely. In patients with an enlarged LA, a cross-sectional view that includes the LA appendage is also optimal if adequate space exists behind the atrial septum on the LA side.⁸

FIGURE 4-13 Phased-array intracardiac echocardiography (ICE) AcuNav serial images with the transducer placed in the middle right atrium (RA) demonstrate serial changes in tomographic imaging views following clockwise rotation of the transducer. Each view displays a left-right (L-R) orientation marker to the operator’s left side (i.e., craniocaudal axis projects from image right to left). A, Starting from the home view, the RA, tricuspid valve (yellow arrowheads), and right ventricle (RV) are visualized. B, Clockwise rotation brings the aorta (AO) into view. PA = pulmonary artery. C, Further rotation allows visualization of the interatrial septum (green arrows), left atrium (LA), coronary sinus (CS), left ventricle (LV), and mitral valve (red arrowheads). D, Subsequently, the left atrium appendage (LAA) becomes visible. E, The ostia of the left superior pulmonary vein (LSPV) and left inferior PV (LIPV) can be visualized with further clockwise rotation.

(Courtesy of AcuNav, Siemens Medical Solutions, Malvern, Pa.)

The sheath, dilator, and needle assembly is introduced into the RA, and the dilator tip is positioned against the fossa ovale, as described earlier. Before advancing the Brockenbrough needle, continuous ICE imaging should direct further adjustments in the dilator tip position until ICE confirms that the tip is in intimate contact with the middle of the fossa, confirms proper lateral movement of the dilator toward the fossa, and excludes inadvertent superior displacement toward the muscular septum and aortic valve. With further advancement of the dilator, ICE demonstrates tenting of the fossa (Fig. 4-14 and see Fig. 4-12). If the distance from the tented fossa to the LA free wall is small, minor adjustments in the dilator tip position can be made to maximize the space. The Brockenbrough needle is then advanced. With successful transseptal puncture, a palpable pop is felt, and sudden collapse of the tented fossa is observed (see Fig. 4-14). Advancement of the needle is then immediately stopped. Saline infusion through the needle is visualized on ICE as bubbles in the LA, thus confirming successful septal puncture (see Video 6 ). With no change in position of the Brockenbrough needle, the transseptal dilator and sheath are advanced over the guidewire into the LA, as described earlier.

FIGURE 4-14 Phased-array intracardiac echocardiography (ICE)-guided transseptal puncture. A, These ICE images, with the transducer placed in the right atrium (RA), show a transseptal dilator tip (yellow arrowhead) lying against the interatrial septum (green arrows). B, With further advancement of the dilator, ICE demonstrates tenting of the interatrial septum at the fossa ovalis. C, Advancement of the transseptal needle is then performed, with the needle tip visualized in the left atrium (LA), and tenting of the interatrial septum is lost.

Alternative Methods for Difficult Transseptal Catheterization

In some cases, the conventional approach using a Brockenbrough needle sheath fails to pierce the septum because of the presence of a small fossa area, a thick interatrial septum, fibrosis and scarring of the septum from previous interventions, or an aneurysmal septum with excessive laxity. Applying excessive force to the needle, dilator, and sheath assembly against a resistant septum (which can be seen as bending and buckling of the assembly in the RA) can lead to building pressure of the needle tip on the septum, which can potentially lead to an uncontrolled sudden jump of the assembly once across the stiff or fibrotic fossa ovalis, thus perforating the opposing lateral LA wall. Similarly, excessive tenting of the interatrial septum (beyond halfway into the LA) can bring it in close proximity to the lateral LA wall, so that the needle can potentially puncture the lateral LA wall once across the septum. Some of these difficulties can sometimes be overcome by manual reshaping of the curvature of the Brockenbrough needle tip, applying slight rotation on the needle and sheath assembly to puncture a different point on the fossa ovalis, using a sharper transseptal needle type (BRK-1 extra sharp), or utilizing a 0.014-inch, sharp-tipped, J-shaped transseptal guidewire (Safe Sept, Pressure Products, Inc., San Pedro, Calif.).^9–13

Other techniques to facilitate transseptal puncture include radiofrequency (RF) perforation of the fossa ovalis and the application of pulses of electrosurgical cautery or RF energy to the proximal end of the Brockenbrough needle. Once the position of the dilator tip is confirmed at the fossa ovalis (under ICE guidance), the needle is advanced beyond the tip of the dilator in contact with the septum until resistance is met. RF energy (5 to 30 W for 1 to 11 seconds) can be applied through a conventional ablation catheter electrode brought manually in contact with the proximal hub of the transseptal needle. Typically, the fossa is punctured almost instantaneously (within 1 to 2 seconds) following RF application. Alternatively, electrosurgical cautery (set to 15 to 20 W for a 1- to 2-second pulse of cut-mode cautery) is applied to the proximal hub of the needle as its tip is advanced out of the dilator. Importantly, the cautery should be initiated on the needle handle prior to pushing the needle tip beyond the dilator tip to help minimize the power needed to puncture the septum, and it should be stopped as soon as the needle is pushed out fully.^14–16

Additionally, a specialized, electrically insulated RF-powered needle (Baylis Medical Company, Inc., Montreal) has been developed to facilitate transseptal puncture. The needle is connected to a proprietary RF generator (RFP-100 RF Puncture Generator, Baylis Medical), which delivers RF energy to the rounded, closed tip of the needle positioned at the interatrial septum. Once septal tenting is visualized on the ICE, RF energy is applied at 10 W for 2 seconds. The RF perforation generators apply a higher voltage for short durations, resulting in a high-energy electric field and an almost instantaneous temperature rise to 100°C, leading to steam popping and septal perforation with minimal collateral tissue damage. In contrast, conventional RF generators deliver a higher power with a lower voltage and impedance range for longer periods of time, with resulting thermal destruction of the local tissue around the needle tip, rather than perforation.^17,18

These methods help minimize pressure application to the needle as it crosses the septum and tenting of the septum, which can potentially reduce the chances of sudden advancement through the lateral LA as the needle crosses the septum. Nonetheless, the powered needle can potentially be more traumatic at the puncture site than a standard needle, and it is possible that the transseptal puncture site created with a powered needle is less likely to close spontaneously. Similarly, inadvertent cardiac perforation occurring in the setting of powered needles can potentially be associated with greater consequences. Whether RF is more likely to cause a thrombus at the puncture site compared with a standard needle is unknown.^17–19

Complications of Atrial Transseptal Puncture

Injury to cardiac and extracardiac structures is the most feared complication. Because of its stiffness and large caliber, the transseptal dilator should never be advanced until the position of the Brockenbrough needle is confirmed with confidence. Advancing the dilator into an improper position can be fatal. Therefore, many operators recommend the use of ICE-guided transseptal puncture, especially for patients with normal atrial size.¹⁹

When the aorta is advertently punctured by the Brockenbrough needle—an arterial waveform is recorded from the needle tip and dye injected through the needle is carried away from the heart—the needle should be withdrawn back into the dilator. If the patient remains stable for 15 minutes and echocardiography shows no pericardial effusion, another attempt at LA access can be made. Advancing the dilator and sheath assembly into the aorta can lead to catastrophic consequences.

It is important to recognize that successful atrial septal puncture is a painless procedure for the patient. If the patient experiences significant discomfort, careful assessment should be made of the catheter and sheath locations (pericardial space, aorta).

Another potential complication is embolism of thrombus or air. To avoid air embolism, catheters must be advanced and withdrawn slowly so as not to introduce air into the assembly. Sheaths must be aspirated with a syringe on a stopcock to the amount of their volume (e.g., an 8 Fr sheath contains 5 mL when filled) to remove any retained air. Thromboembolic complications can be avoided by flushing all sheaths and guidewire with heparinized saline and maintaining the ACT at longer than 300 seconds. In addition, a guidewire should not be left in the LA for more than 1 minute, especially if no systemic heparin has been administered. Administration of heparin before, rather than after, the atrial septal puncture can also help reduce thromboembolism.¹⁹

Occasionally, ST segment elevation in the inferior ECG leads (with or without transient bradycardia or AV block) can occur following transseptal catheterization, potentially secondary to air embolism in coronary arteries, although a Bezold-Jarisch–like reflex mechanism can also be implicated.

Importantly, the presence of an LA thrombus is an absolute contraindication for transseptal catheterization. Additionally, caution should be used in the setting of the presence cardiac or thoracic malformation (e.g., congenital heart disease, kyphoscoliosis).

Transseptal catheterization is feasible and safe in most patients with atrial septal defect or patent foramen ovale repair. Nonetheless, because of the altered anatomical landmarks after repair, fluoroscopic guidance for transseptal puncture can be unreliable, and the procedure can be challenging. In these patients, an understanding of the method of repair and utilization of ICE guidance are essential.

In patients with atrial septal defect closure devices, puncture is preferably performed at the portion of the septum located inferior and posterior to the closure device and not through the device itself. In patients with a septal stitch or pericardial or Dacron patch, puncture can be achieved through the thickened septum or the patch. However, transseptal access is typically not achievable through a Gore-Tex patch (W.L. Gore & Associates, Flagstaff, Ariz.) because of its resistant texture; instead, puncture can be performed directly through neighboring native interatrial tissue. When the patch is wide, sufficient free septal tissue for transseptal puncture may not be available, in which setting transseptal access to the LA may not be feasible.^19,20

Analog Versus Digital Recordings

Intracardiac electrograms are recorded with amplifiers that have high-input impedances (more than 1010 Ω), to decrease unwanted electrical interference and ensure high-quality recordings.²¹ Analog recording systems directly amplify the potential from the recording electrodes, plot the potential on a display oscilloscope, and write it to recording paper or store it on magnetic tape, or both. Analog systems have largely been replaced by digital recording systems that use an analog to digital (A/D) converter that converts the amplitude of the potential recorded at each point in time to a number that is stored.

The quality of digital data is influenced by the sampling frequency and precision of the amplitude measurement.²¹ The most common digital recording systems sample the signal approximately every 1 millisecond (i.e., 1000 Hz), which is generally adequate for practical purposes of activation mapping. However, higher sampling frequencies can be required for high-quality recording of high-frequency, rapid potentials that can originate from the Purkinje system or areas of infarction. The faster sampling places greater demands on the computer processor and increases the size of the stored data files.

Unipolar Recordings

A unipolar electrogram is the voltage difference recorded between an intracardiac electrode in close association with cardiac tissue and a distant indifferent (reference) electrode patch applied to the body surface (so that the indifferent electrode has little or no cardiac signal). The precordial ECG leads, for example, are unipolar recordings that use an indifferent electrode created by connecting the arms and left leg electrodes through high-impedance resistors.²²

By convention, the exploring electrode in contact with the cardiac tissue is connected to the positive input of the recording amplifier. In this configuration, an approaching wavefront creates a positive deflection that quickly reverses itself as the wavefront passes directly under the electrode, thus generating an RS complex. In normal homogeneous tissue, the maximum negative slope (dV/dt) of the signal coincides with the arrival of the depolarization wavefront directly beneath the electrode, because the maximal negative dV/dt corresponds to the maximum sodium (Na⁺) channel conductance; Fig. 4-15). This is true for filtered and unfiltered unipolar electrograms.^21,23

FIGURE 4-15 Unipolar and bipolar recordings. Two complexes from different sites are shown in a patient with Wolff-Parkinson-White syndrome. The dashed line denotes onset of the delta wave. In site A, the unfiltered unipolar recording shows a somewhat blunted “QS” complex and small atrial component, but the filtered (30- to 300-Hz) bipolar signal shows a very large atrial signal and very small ventricular signal (arrow), suggesting a poor choice for ablation site. Site B shows a sharper “QS” in the unipolar signal, with a larger ventricular than atrial electrogram, and the initial nadir of bipolar recording coincides with the maximal negative dV/dt of the unipolar recording. Ablation at this site was successful. Abl_dist = distal ablation; Abl_uni = unipolar ablation; CS_dist = distal coronary sinus; His_dist = distal His bundle; HRA = high right atrium; RVA = right ventricular apex.

The unfiltered unipolar recordings provide information about the direction of impulse propagation; positive deflections (R waves) are generated by propagation toward the recording electrode, and negative deflections (QS complexes) are generated by propagation away from the electrode. Therefore, a wavefront of depolarization traveling past a unipolar electrode results in a biphasic electrogram (positive then negative) representing the approach and recession of the activation wavefront.²²

Unipolar recordings also allow pacing and recording at the same location while eliminating a possible anodal contribution to depolarization that is sometimes seen with bipolar pacing at high output.²¹ However, one of the disadvantages of unipolar recording is the inability to record an undisturbed electrogram during or immediately after pacing.

The major disadvantage of unipolar recordings is that they contain substantial far-field signals generated by depolarization of tissue remote from the recording electrode, because the unipolar electrode records a potential difference between widely spaced electrodes.²³ Noise can be reduced by using an indifferent electrode in the IVC. The unipolar electrograms are generally unfiltered (0.05 to 300 Hz or more), but are usually filtered at settings comparable to those of bipolar electrograms (10 to 40 to 300 Hz or more) when an abnormal tissue (scars or infarct areas) is studied, where local electrograms can have very low amplitude and can be masked by larger far-field signals. Filtering the unipolar electrograms can help eliminate far-field signals; however, the filtered unipolar recordings lose the ability to provide directional information.

Bipolar Recordings

Bipolar recordings are obtained by connecting two electrodes that are exploring the area of interest to the recording amplifier. At each point in time, the potential generated is the sum of the potential from the positive input and the potential at the negative input. The potential at the negative input is inverted; this is subtracted from the potential at the positive input so that the final recording is the difference between the two.²¹

Unlike unipolar recordings, bipolar electrodes with short interpolar distances are relatively unaffected by far-field events. The bipolar electrogram is simply the difference between the two unipolar electrograms recorded at the two poles. Because the far-field signal is similar at each instant in time, it is largely subtracted out, thus leaving the local signal. Therefore, compared with unipolar recordings, bipolar recordings provide an improved signal-to-noise ratio, and high-frequency components are more accurately seen.^6,23

Although local activation is less precisely defined, in a homogeneous sheet of tissue the initial peak (or nadir) of a filtered (10 to 40 to 300 Hz or more) bipolar recording coincides with depolarization beneath the recording electrode and corresponds to the maximal negative dV/dt of the unipolar recording (see Fig. 4-15).

Several factors can affect bipolar electrogram amplitude and width, including conduction velocity (the greater the velocity, the higher the peak amplitude of the filtered bipolar electrogram), the mass of the activated tissue, the distance between the electrode and the propagating wavefront, the direction of propagation relative to the bipoles, the interelectrode distance, the amplifier gain, and other signal-processing techniques that can introduce artifacts. To acquire true local electrical activity, a bipolar electrogram with an interelectrode distance of less than 1 cm is desirable.²³

The direction of wavefront propagation cannot be reliably inferred from the morphology of the bipolar signal. Moreover, bipolar recordings do not allow simultaneous pacing and recording from the same location. To pace and record simultaneously in bipolar fashion at endocardial sites as close together as possible, electrodes 1 and 3 of the quadripolar mapping catheter are used for bipolar pacing, and electrodes 2 and 4 are used for recording.²³

The differences in unipolar and bipolar recordings can be used to assist in mapping by simultaneously recording bipolar and unipolar signals from the mapping catheter.²¹ Although bipolar recordings provide sufficient information for most mapping purposes in clinical EP laboratories, simultaneous unipolar recordings can provide an indication of the direction of wavefront propagation and a more precise measure of the timing of local activation.²³

Signal Filtering

The surface ECG is usually filtered at 0.1 to 100.0 Hz. The bulk of the energy is in the 0.1- to 20.0-Hz range. Because of interference from alternating current (AC), muscle twitches, and similar relatively high-frequency interference, it is sometimes necessary to record the surface ECG over a lower frequency range or to use notch filters.⁶

Amplifiers are also used to filter the low- and high-frequency content of the intracardiac electrograms. Intracardiac electrograms are usually filtered to eliminate far-field noise, typically at 30 to 500 Hz. The range of frequencies not filtered out is frequently called the bandpass. The high-pass filter allows frequencies higher than a certain limit to remain in the signal (i.e., it filters out lower frequencies), and the low-pass filter filters out frequencies higher than a certain limit.

Timing of Local Events

As noted, with an unfiltered unipolar electrogram, a wavefront of depolarization that is propagating toward the exploring electrode generates a positive deflection (an R wave). As the wavefront reaches the electrode and propagates away, the deflection sweeps steeply negative. This rapid reversal constitutes the intrinsic deflection of the electrogram and represents the timing of the most local event (i.e., at the site of the electrode). The maximum negative slope (dV/dt) of the signal coincides with the arrival of the depolarization wavefront directly beneath the electrode (see Fig. 4-15).²²

Filtering the unipolar signal does not affect its usefulness as a measure of the local activation time. The slew rate or dV/dt of the filtered electrogram is so rapid in normal heart tissue that the difference between the peak and the nadir of the deflection is 5 milliseconds or less. Identification of the local event is therefore easy with filtered or unfiltered electrograms in normal tissue. On the other hand, diseased myocardium can conduct very slowly with fractionated electrograms, and this makes local events harder to identify.

To acquire true local electrical activity, a bipolar electrogram with an interelectrode distance of less than 1 cm is preferable. Smaller interelectrode distances record increasingly local events. In normal homogeneous tissue, the initial peak of a filtered (30 to 300 Hz or more) bipolar recording coincides with depolarization beneath the recording electrode and corresponds to the maximal negative dV/dt of the unipolar recording (see Fig. 4-15). However, in the setting of complex multicomponent bipolar electrograms, such as those with marked fractionation and prolonged duration seen in regions with complex conduction patterns, determination of local activation time becomes problematic.⁶

When the intracardiac electrogram of interest is small relative to the size of surrounding electrograms (e.g., His deflection), and the gain must be markedly increased to produce a measurable deflection, clipping the signals can help eliminate the highly amplified surrounding signals to allow concentration on the deflection of interest (Fig. 4-16). It is important to recognize, however, that clippers eliminate the ability to determine the amplitude and timing of the intrinsic deflection (local timing) of the signals being clipped.⁵

FIGURE 4-16 Effect of electronic clipping on recordings. The same two complexes are shown in both panels. Left, Both His and coronary sinus (CS) recordings are electronically attenuated (clipped) to reduce excursions on the display. The CS atrial and ventricular signals appear to have equal amplitude, and the ventricular electrogram in the His recording is small. Right, Without clipping, the true signal amplitudes are seen, showing a very large ventricular signal in the His recording and a larger atrial than ventricular signal in the CS recording. Abl_dist = distal ablation; Abl_uni = unipolar ablation; CS_dist = distal coronary sinus; His_dist = distal His bundle; HRA = high right atrium; RVA = right ventricular apex.

Choices of Surface and Intracardiac Signals

Baseline recordings obtained during a typical EP study include several surface ECG leads and several intracardiac electrograms, all of which are recorded simultaneously. Timing of events with respect to onset of the QRS complex or P wave on the surface ECG is often important during the EP study, but it is cumbersome to display all 12 leads of the regular surface ECG. It is more common to use leads I, II, III, V₁, and V₆, which provide most of the information required to determine the frontal plane axis, presence and type of intraventricular conduction abnormalities, and P wave morphology.

Intracardiac leads can be placed strategically at various locations within the cardiac chambers to record local events in the region of the lead. A classic display would include three to five surface ECG leads, high RA recording, HB recording, CS recording, and RV apex recording (Fig. 4-17). Depending on the type of study and information sought, stimulation and recording from other sites can be appropriate and can include RB recording, LV recording, transseptal LA recording, and atrial and ventricular mapping catheter tracings for EP mapping and ablation.²¹

FIGURE 4-17 A classic display of surface ECG and intracardiac recordings during an electrophysiology study of supraventricular tachycardia. Included are four surface ECG leads, high right atrium (HRA) recording, two His bundle recordings (proximal and distal His [His_prox and His_dist]), five coronary sinus (CS) recordings (in a proximal-to-distal sequence), and a right ventricular apex (RVA) recording. The relative amplitudes of atrial and ventricular electrograms in CS recordings are also shown. Right, The back of the heart is shown with a CS catheter in position. The distal portion of the CS (CS_dist) is closer to the ventricle (originating as the great cardiac vein on the anterior wall); the CS crosses the atrioventricular groove at the lateral margin and becomes an entirely atrial structure as it empties into the right atrium. Left, Thus, proximal CS (CS_prox) recordings show large atrial and small ventricular signals, whereas more distal recordings show small atrial, large ventricular signals. IVC = inferior vena cava; PVs = pulmonary veins; SVC = superior vena cava.

The intracardiac electrograms are generally displayed in the order of normal cardiac activation. The first intracardiac tracing is a recording from the high RA close to the sinus node. The next intracardiac tracing is the HB recording, obtained from a catheter positioned at the HB, which shows low septal RA, HB, and high septal RV depolarizations. One to five recordings may be obtained from the CS, which reflects LA activation, followed by a recording from the RV catheter (see Fig. 4-17).⁶

Coronary Sinus Electrogram

Because the CS lies in the AV groove, in close contact to both the LA and the LV, the CS catheter records both atrial and ventricular electrograms. However, the CS has a variable relationship with the mitral annulus. The CS lies 2 cm superior to the annulus as it crosses from the RA to the LA. More distally, the CS frequently overrides the LV. Consequently, the most proximal CS electrodes (located at the CS os) are closer to the atrium and typically show a local sharp, large atrial electrogram and a smaller, far-field ventricular electrogram. The more distal CS electrodes, lying closer to the LV than the LA, record progressively smaller, less sharp, far-field atrial electrograms and larger, sharper, near-field ventricular electrograms (see Fig. 4-17).

During normal sinus rhythm (NSR), the atrial activation sequence proceeds from the CS os distally. However, if the CS catheter is deeply seated in the CS, so that the most proximal electrodes are distal to the CS os and the most distal electrodes are anterolateral on the mitral annulus, then both proximal and distal electrodes can be activated at the same time (Fig. 4-18).

FIGURE 4-18 Influence of catheter position on coronary sinus (CS) atrial electrograms. Two different CS atrial activation sequences are shown from different patients. A, A proximal-to-distal sequence is shown. B, The latest activation is in the mid-CS electrodes. The diagrams at the bottom show relative positions of the CS catheter in each instance (atrioventricular grooves viewed from above). With more proximal CS position (CS_prox), propagation is proximal-distal, indicating relative distance from the sinus node. With a more distal CS position (CS_dist), the mid-CS electrodes are farthest from the sinus node. His_dist = distal His bundle; His_mid = middle His bundle; His_prox = proximal His bundle; HRA = high right atrium.

His Bundle Electrogram

The HB catheter is positioned at the junction of the RA and RV. Therefore, it records electrograms from local activation of the adjacent atrial, HB, and ventricular tissues (Fig. 4-19). Using a 5- to 10-mm bipolar recording, the His potential appears as a rapid biphasic spike, 15 to 25 milliseconds in duration, interposed between local atrial and ventricular electrograms. The use of a quadripolar catheter allows simultaneous recording of three bipolar pairs.²⁴

FIGURE 4-19 Intracardiac intervals. Shaded areas represent the P wave–atrial (PA) (blue), atrial–His bundle (AH) (pink), and His bundle–ventricular (HV) (yellow) intervals. It is important that the HV interval be measured from the onset of the His potential in the recording showing the most proximal (rather than the most prominent) His potential (His_prox) to the onset of the QRS on the surface ECG (rather than the ventricular electrogram on the His bundle [HB] recording). CS_dist = distal coronary sinus; CS_prox = proximal coronary sinus; His_dist = distal His bundle; HRA = high right atrium; PRI = PR interval; RVA = right ventricular apex. See text for details.

Before measuring conduction intervals within the HB electrogram, it is important to verify that the spike recorded between the atrial and ventricular electrograms on the HB catheter actually represents activation of the most proximal HB and not the distal HB or RB. The most proximal electrodes displaying the His potential should be chosen, and a large atrial electrogram should accompany the proximal His potential. Anatomically, the proximal portion of the HB originates in the atrial side of the tricuspid annulus; thus, the most proximal HB deflection is the one associated with the largest atrial electrogram. Recording of a His potential associated with a small atrial electrogram can reflect recording of the distal HB or RB and therefore would miss important intra-His conduction abnormalities and falsely shorten the measured HB-ventricular (HV) interval (see Fig. 4-19). Even if a large His potential is recorded in association with a small atrial electrogram, the catheter should be withdrawn to obtain a His potential associated with a larger atrial electrogram. Using a multipolar (three or more) electrode catheter to record simultaneously proximal and distal HB electrograms (e.g., a quadripolar catheter records three bipolar electrograms over a 1.5-cm distance) can help evaluate intra-His conduction.⁵

Validation of the HB recording can be accomplished by assessment of the HV interval and establishing the relationship between the His potential and other electrograms.²⁴ The HV interval should be 35 milliseconds or longer (in the absence of preexcitation). In contrast, the RB potential invariably occurs within 30 milliseconds before ventricular activation. Atrial pacing can be necessary to distinguish a true His potential from a multicomponent atrial electrogram. With a true His potential, the atrial-HB (AH) interval should increase with incremental pacing rates. HB pacing can also be a valuable means for validating HB recording. The ability to pace the HB through the recording electrode and obtain HB capture (i.e., QRS identical to that during NSR and stimulus-to-QRS interval identical to the HV interval during NSR) provides the strongest evidence validating the His potential. However, this technique is inconsistent in accomplishing HB capture, especially at low current output. Higher output can result in nonselective HB capture. The use of closely spaced electrodes and the reversal of current polarity (i.e., anodal stimulation) can facilitate HB capture. Failure to capture the HB selectively does not necessarily imply that the recorded potential is from the RB.

Other measures that can be used, although rarely required, to validate the HB recording include recording of pressure simultaneously with a luminal electrode catheter (which should reveal atrial pressure wave when the catheter is at the proximal His electrogram position) and simultaneous left and right recording of the His potential. The His potential can be recorded in the noncoronary sinus of Valsalva (just above the aortic valve) or in the LVOT along the interventricular septum (just below the aortic valve). Because these sites are at the level of the central fibrous body, the proximal penetrating portion of the HB is recorded and can be used to time the His potential recorded via the standard venous route. Recording the HB from the noncoronary cusp (versus the LVOT) is preferred because only a true His potential can be recorded from that site.²⁵

P Wave–Atrial Interval

The P wave–atrial (PA) interval is measured from the first evidence of sinus node depolarization, whether on the intracardiac or surface ECG, to the atrial deflection as recorded in the HB lead. It represents conduction through the RA to the inferoposterior interatrial septum (in the region of the AV node [AVN] and HB; see Fig. 4-19).

The PA interval is a reflection of internodal (sinus node to AVN) conduction; prolonged PA intervals suggest abnormal atrial conduction and can be a clue to the presence of biatrial disease or disease confined to the RA. The normal range of the PA interval is 20 to 60 milliseconds. Rarely, diseased atrial conduction can underlie first-degree AV block, indicated by a prolonged PA interval. A short PA interval suggests an ectopic source of atrial activation.

Interatrial Conduction

Normal atrial activation begins in the high or mid-lateral RA (depending on the sinus rate), spreads from there to the low RA and AV junction, and then spreads to the LA.

Activation of the LA is mediated by three possible routes. Superiorly, activation proceeds through the Bachman bundle; this can be seen in 50% to 70% of patients and can be demonstrated by CS os activation followed by distal CS and then mid-CS activation. Activation also propagates through the mid-atrial septum at the fossa ovalis and at the region of the central fibrous trigone at the apex of the triangle of Koch. The latter provides the most consistent amount of LA activation.

Interatrial conduction is measured by the interval between the atrial electrogram in the high RA lead and that in the CS lead. LA-to-RA activation during LA pacing appears primarily to cross the fossa and low septum and not the Bachman bundle, as reflected by relatively late high RA activation.

Normal retrograde atrial activation proceeds over the AVN. The earliest atrial activation is recorded in the AV junction (HB recording), then in the adjacent RA and CS os, and finally in the high RA and LA. More detailed mapping reveals atrial activation to start at the HB recording, with secondary breakthrough sites in the CS (reflecting activation over the LA extension of the AVN) or the posterior triangle of Koch, or both. At faster ventricular pacing rates, the earliest atrial activation typically shifts to the posterior portion of the triangle of Koch, the CS os, or within the CS itself.

Atrial–His Bundle Interval

The AH interval is measured from the first rapid deflection of the atrial deflection in the HB recording to the first evidence of HB depolarization in the HB recording (see Fig. 4-19). The AH interval is an approximation of the AVN conduction time, because it represents conduction time from the low RA at the interatrial septum through the AVN to the HB.

The AH interval can vary according to the site of atrial pacing. During LA or CS os pacing, the impulse can enter the AVN at a different site that bypasses part of the AVN, or it can just enter the AVN earlier in respect to the atrial deflection in the HB electrogram. Both mechanisms can give rise to a shorter AH interval.

The response of the AH interval to atrial pacing or drugs often provides more meaningful information about AVN function than an isolated measurement of the AH interval. Autonomic blockade with atropine (0.04 mg/kg) and propranolol (0.02 mg/kg) can be used to evaluate AVN function in the absence of autonomic influences. Not enough data, however, are available to define normal responses under these circumstances.²⁴

The AH interval has a wide range in normal subjects (50 to 120 milliseconds) and is markedly influenced by the autonomic nervous system. Short AH intervals can be observed in cases of increased sympathetic tone, reduced vagal tone, enhanced AVN conduction, and preferential LA input into the AVN, as well as unusual forms of preexcitation (atrio-His BTs).

Long AH intervals are usually caused by negative dromotropic drugs (such as digoxin, beta blockers, calcium channel blockers, and antiarrhythmic drugs), enhanced vagal tone, and intrinsic disease of the AVN. Artifactually prolonged AH intervals can result from an improperly positioned catheter or the incorrect identification of an RB potential as a His potential. This situation needs to be distinguished from true AH interval prolongation.

His Potential

His potential duration reflects conduction through the short length of the HB that penetrates the fibrous septum. Disturbances of HB conduction can manifest as fractionation, prolongation (longer than 30 milliseconds), or splitting of the His potential.

His Bundle–Ventricular Interval

The HV interval is measured from the onset of the His potential to the onset of the earliest registered surface or intracardiac ventricular activation. It represents conduction time from the proximal HB through the distal His-Purkinje system (HPS) to the ventricular myocardium (see Fig. 4-19).²⁴

The HV interval is not significantly affected by the autonomic tone, and it usually remains stable. The range of HV intervals in normal subjects is narrow, 35 to 55 milliseconds. A prolonged HV interval is consistent with diseased distal conduction in all fascicles or in the HB itself. A validated short HV interval suggests ventricular preexcitation via a BT. A falsely shortened HV interval can occur during sinus rhythm with PVCs or an accelerated idioventricular rhythm that is isorhythmic with the sinus rhythm, or when an RB potential rather than a His potential is inadvertently recorded.

Pacing Output

Stimulation is usually carried out using an isolated constant current source that delivers a rectangular impulse. Pacing output at twice (2×) diastolic threshold is generally used. Pacing threshold is defined as the lowest current required for consistent capture determined in late diastole. The pacing threshold can be influenced by the pacing cycle length (CL); therefore, the threshold should be determined at each pacing CL used. In general, refractory periods are somewhat longer when determined using 2× threshold (as opposed to higher outputs), and this can reduce the incidence of induction of nonclinical tachyarrhythmias.²⁴ Additionally, diastolic excitability can be influenced by drug administration; re-evaluation of the pacing threshold and adjustment of the pacing output (2× threshold) are therefore required in such situations. A pulse duration of 1 or 2 milliseconds is generally used.

High current strength is generally used for determination of strength-interval curves to overcome drug-induced prolongation of refractoriness, assess the presence and mechanism of antiarrhythmic therapy, and overcome the effect of decreased tissue excitability (e.g., pace mapping in scar-related arrhythmias).

Cycle Length

During EP testing, CLs often change from beat to beat, so that these measures are more relevant than an overall rate expressed in beats per minute. The use of rates in beats per minute is retained mostly to facilitate communication with physicians who are more comfortable with this terminology. Pacing rate is determined by dividing 60,000 by the CL (in milliseconds).

Incremental Versus Decremental

The terms incremental and decremental can have opposite meaning, depending on whether one is considering the pacing rate in beats per minute or the pacing CL in milliseconds. The term incremental pacing rate is derived from stimulators controlled by an analog dial. Digitally controlled devices often increase the rate by choosing a sequence of CL decrements, but the term incremental pacing may still be used.

Overdrive Pacing (Straight Pacing)

Pacing stimuli are delivered at a constant pacing rate (or pacing CL) throughout the duration of the stimulation. The pacing rate is faster than the rate of the baseline rhythm to ensure capture of the spontaneous rhythm.

Burst Pacing

Pacing stimuli are delivered at a constant rate for a relatively short duration, but at successively faster rates with each burst until a predetermined maximum rate (or minimum CL) has been reached. This technique is generally used for induction or termination of tachycardias.

Stepwise Rate-Incremental Pacing

After pacing at a given rate for a predetermined number of stimuli or seconds, the rate is increased (with intervening pauses) in a series of steps until predetermined endpoints are reached. It is important to maintain the pacing at any given rate for at least 15 seconds (period of accommodation) before increasing the pacing rate. Otherwise, the initial stimuli at any given rate can produce effects different from those observed several seconds later, because the ability of a tissue to conduct is affected by the baseline rate or CL of the preceding beats. A disadvantage for this technique is the prolonged pacing required at each rate, which is time-consuming.

Ramp Pacing

Ramp pacing implies a smooth change in the interval between successive stimuli, with gradual decrease of the pacing CL every several paced complexes (without intervening pauses). Ramps are often used as an alternative to the stepwise method for assessment of conduction. The pacing rate is slowly increased at 2 to 4 beats/min every several paced beats until block occurs. This method avoids prolonged rapid pacing at each pacing CL and is particularly useful when multiple assessments of conduction are planned (e.g., after therapeutic interventions) and in the assessment of retrograde conduction. Because each successive paced interval differs from its predecessor by only a few milliseconds, the interval at which block occurs can be determined more precisely using the ramp method. However, prolonged episodes of continuous high-rate pacing can provoke significant hypotension, and close monitoring of blood pressure is important while performing these maneuvers.

For tachycardia induction or termination, the ramp is decreased in duration, but the inter-stimulus intervals are decreased more rapidly. Ramp pacing is generally used in antitachycardia pacing algorithms in implantable cardioverter-defibrillators. Programmed rate-incremental ramps are also known as autodecremental pacing.

Extrastimulus Technique

Ultrarapid Train Stimulation

Pacing at very short CLs (10 to 50 milliseconds) is rarely performed, mainly for induction of ventricular fibrillation (VF), to test defibrillation threshold during implantation of a cardioverter-defibrillator.

Conduction

During depolarization, the electrical impulse spreads along each cardiac cell, and rapidly from cell to cell, because each myocyte is connected to its neighbors through low resistance gap junctions. As discussed in Chapter 1, conduction velocity refers to the speed of propagation of an electrical impulse through cardiac tissue, which is dependent on both the active membrane properties of the individual cardiac myocyte that generates the action potential (i.e., electrical excitability or refractoriness, or both) and passive properties governing the flow of current between cardiac cells (cell-to-cell coupling and tissue geometry).^26,27

Conduction can be assessed by observing the propagation of wavefronts during pacing at progressively incremental rates. Rate-incremental pacing is delivered to a selected site in the heart while propagation to a selected distal point is assessed. Conduction velocity is assessed by measuring the time it takes for an impulse to travel from one intracardiac location to another. During tests of conduction, it is usual for capture to be maintained at the site of stimulation and block to occur at a distal point.⁶

Refractoriness

As discussed in Chapter 1, during a cardiac cycle, once an action potential is initiated, the cardiac cell is unexcitable to stimulation (i.e., unable to initiate another action potential in response to a stimulus of threshold intensity) for some duration of time (which is slightly shorter than the “true” action potential duration) until its membrane has repolarized to a certain level.^28–30

There are different levels of refractoriness during the action potential. During the absolute refractory period (which extends over phases 0, 1, 2, and part of phase 3 of the action potential), the tissue is completely unexcitable and a second action potential absolutely cannot be initiated, no matter how large a stimulus is applied, because of inactivation of most Na⁺ channels. After the absolute refractory period, a stimulus may cause some cellular depolarization but does not lead to a propagated action potential. The sum of this period (which includes a short interval of phase 3 of the action potential) and the absolute refractory period is termed the effective refractory period (ERP). The ERP is followed by the relative refractory period (RRP), which extends over the middle and late parts of phase 3 of the action potential. During the RRP, initiation of a second action potential is inhibited but not impossible; a larger-than-normal stimulus can result in activation of the cell and lead to a propagating action potential. However, the upstroke of the new action potential is less steep and of lower amplitude and its conduction velocity slower than normal. Of note, there is a brief period in phase 3 of the action potential, the supernormal period, during which excitation is possible in response to an otherwise subthreshold stimulus; that same stimulus fails to elicit a response earlier or later than the supernormal period (see later).

Measurements of Refractory Periods

Refractoriness (or, more appropriately, excitability) is defined by the response of a tissue to premature stimulation.^31,32 Refractory periods are analyzed by the extrastimulus technique, with progressively premature extrastimuli delivered after a train of 8 to 10 paced beats at a fixed pacing CL to allow for reasonable (more than 95%) stabilization of refractoriness, which is usually accomplished after 3 or 4 paced beats.

Several variables are considered in the assessment of refractory periods, including the stimulus amplitude and the drive rate or CL. Longer CLs are generally associated with longer refractory periods, but refractory periods of different parts of the conducting system do not respond comparably with changes in the drive CLs.³⁰

Additionally, the measured ERP is invariably related to the current used. Thus, standardization of the pacing output is required. In most laboratories, it is arbitrarily standardized at twice the diastolic threshold. A more detailed method of assessing refractoriness is to define the strength-interval curves at these sites. The steep portion of that curve defines the ERP of that tissue. The use of increasing current strengths to 10 mA usually shortens the measured ERP by approximately 30 milliseconds. However, such a method does not offer a useful clinical advantage, except when the effects of antiarrhythmic drugs on ventricular excitability and refractoriness are to be characterized. Moreover, the safety of using high current strengths, especially when multiple extrastimuli are delivered, is questionable, because fibrillation is more likely to occur in such situations.

It is important that measurements of refractory periods be taken at specific sites. Measurements of atrial and ventricular ERP are taken at the site of stimulation. Measurements of AVN ERP and HPS ERP are taken from responses in the HB electrogram.²⁴

Cycle Lengths Responsiveness of Refractory Periods

Normally, refractoriness of the atrial, HPS, and ventricular tissue is directly related to the basic drive CL (i.e., the ERP shortens with decreasing basic drive CL). This phenomenon (termed peeling of refractoriness) results from rate-related shortening of the action potential duration and is most marked in the HPS.³² Abrupt changes in the CL also affect refractoriness of these tissues. A change from a long- to short-drive CL (e.g., with introduction of an extrastimulus [S₂] following a pacing drive [S₁] with a long CL) shortens the ERP of the HPS and atrium, whereas a change from a short to a long drive CL markedly prolongs the HPS ERP but alters the ventricular ERP little, if at all. Refractoriness of the atrial, HPS, and ventricular tissue appears relatively independent of autonomic tone; however, data have shown that increased vagal tone reduces atrial ERP and increases ventricular ERP.³⁰

In contrast, the AVN ERP increases with increasing basic drive CL in response to the fatigue phenomenon, which most likely results because AVN refractoriness is time-dependent and exceeds its action potential duration (unlike HPS refractoriness). Additionally, AVN refractory periods are labile and can be markedly affected by the autonomic tone. On the other hand, the response of AVN FRP to changes in pacing CL is variable, but it tends to decrease with decreasing pacing CL.³² This paradox occurs because the FRP is not a true measure of refractoriness encountered by an atrial extrastimulus (AES; A₂); it is significantly determined by the AVN conduction time of the basic drive beat (A₁-H₁); the longer the A₁-H₁ is, the shorter the calculated FRP will be at any A₂-H₂.³³

Limitations of Tests of Conduction and Refractoriness

It is unusual to be able to collect a complete set of measurements. With refractory period testing, the atrial ERP is often longer than the AVN ERP, so that atrial refractoriness is encountered before AVN refractoriness, thus limiting the ability to assess the latter. Moreover, an AES cannot be used to test the HPS if conduction is blocked at the AVN level. This is a limitation that applies to most patients undergoing conduction or refractory period testing.³¹ On the other hand, it is possible to assess anterograde conduction and refractoriness distal to the AVN by direct pacing of the HB. This is not part of the routine EP evaluation, however, and is reserved for cases in which the information is particularly desired.⁶

It is important to recognize that atrial conduction can materially affect the determination of refractory periods. Therefore, refractory periods should not be timed from the site of stimulation, but from the point in the conduction cascade that is being assessed. For example, if the high RA is stimulated in a patient with a left lateral BT, an early AES can encounter the RRP of the atrium, so that intraatrial conduction time is prolonged. Thus, the timing of the S₁-S₂ stimuli in the high RA would be shorter than the timing of the propagated impulse when it arrives at the region of the BT as the local A₁-A₂ interval.

A wide range of normal values has been reported for refractory periods (Table 4-2). However, it is difficult to interpret these so-called normal values because they come from pooled data using different standards (different pacing CLs, stimulus strengths, and pulse widths).^24,31,32

Sinus Node Response to Atrial Pacing

The sinus node is the prototype of an automatic focus. Automatic rhythms are characterized by spontaneous depolarization, overdrive suppression, and post-overdrive warm-up to baseline CL. Rapid atrial pacing results in overdrive suppression of the sinus rate, with prolongation of the return sinus CL following termination of the pacing train. Longer pacing trains and faster pacing rates further prolong the return cycle. After cessation of pacing, the sinus rate resumes discharge at a slower rate and gradually speeds up (warms up) to return to the prepacing sinus rate.

Sinus node recovery time is the interval between the end of a period of pacing-induced overdrive suppression of sinus node activity and the return of sinus node function, manifested on the surface ECG by a post-pacing sinus P wave.

Atrioventricular Node Response to Atrial Pacing

The normal AVN response to rate-incremental atrial pacing is for the PR and AH intervals to increase gradually as the pacing CL decreases until AVN Wenckebach block appears (Fig. 4-20). With further decrease in the pacing CL, higher degrees of AV block (2:1 or 3:1) can appear. Infranodal conduction (HV interval) generally remains unaffected.

FIGURE 4-20 Normal atrioventricular node (AVN) response to rate-incremental atrial pacing. A, Fixed-rate high right atrial (HRA) pacing (S) at a cycle length (CL) of 600 milliseconds. B, Decreasing the pacing CL to 500 milliseconds results in prolongation of the atrial–His bundle (AH) interval, as illustrated in the His bundle recording (His). Infranodal conduction (His bundle–ventricular [HV] interval) remains unaffected. C, Further decrement of the pacing CL results in progressive prolongation of the AH interval until block occurs in the AVN (AVB), followed by resumption of conduction, indicating Wenckebach CL. The site of block is in the AVN because no His bundle deflection is present after the nonconducted atrial stimulus. Of note, apparent block of another atrial stimulus is observed (pseudoblock) because of failure of the atrial stimulus to capture (NC), which is confirmed by the absence of an atrial electrogram on the His bundle recording after the stimulus artifact.

Wenckebach block is frequently atypical; that is, the AH interval does not increase gradually in decreasing increments but stabilizes for several beats before the block, or it can show its greatest increment in the last conducted beat. The incidence of atypical Wenckebach block is highest during long Wenckebach cycles (longer than 6.5). It is important to distinguish atypical Wenckebach periodicity from Mobitz II AV block. Additionally, it is important to ensure that the ventricular pauses observed during atrial pacing are not secondary to loss of atrial capture or the occurrence of AVN echo beats (pseudoblock; see Fig. 4-20).

AVN Wenckebach CL is the longest pacing CL at which Wenckebach block in the AVN is observed. Normally, Wenckebach CL is 500 to 350 milliseconds, and it is sensitive to the autonomic tone. There is a correlation between the AH interval during NSR and the Wenckebach CL; patients with a long AH interval during NSR tend to develop Wenckebach block at a longer pacing CL, and vice versa.

At short pacing CLs (less than 350 milliseconds), infranodal block can occasionally occur in patients with a normal baseline HV interval and QRS. This occurs especially when atrial pacing is started during NSR with the first or second paced impulses acting as a long-short sequence. The HPS can also show accommodation following the initiation of pacing. Prolongation of the HV interval or infranodal block at a pacing CL longer than 400 milliseconds is abnormal and indicates infranodal conduction abnormalities.

Atrial Response to Atrial Pacing

It is usually possible to maintain 1:1 atrial capture with rate-incremental pacing techniques to a pacing CL of 200 to 300 milliseconds. Pacing threshold normally tends to increase at faster rates. Rate-incremental pacing can result in prolongation of the intraatrial (PA interval) and interatrial conduction. At rapid pacing rates, induction of AF is not rare and is not necessarily an abnormal response. Vagal tone and medications such as adenosine and edrophonium can slow the sinus rate, but they tend to shorten the atrial ERP, which makes the atrium more vulnerable to induction of AF.

Sinus Node Response to Atrial Extrastimulation

Four zones of response of the sinus node to AES have been identified: the zone of collision, the zone of reset, the zone of interpolation, and the zone of reentry (Fig. 4-21).

FIGURE 4-21 Normal sinus node and atrioventricular node response to atrial extrastimulation. A, Baseline sinus rhythm shown in surface ECG lead II, high right atrium (HRA) recording, and His bundle (His) recording. The shaded area represents two sinus cycle lengths (2× [A₁-A₁]). B, A late coupled atrial extrastimulus (AES) (A₂) collides with the exiting sinus impulse and therefore does not affect (or reset) the sinus pacemaker (zone of collision). The next sinus impulse (A₃) occurs at exactly twice the baseline sinus cycle length. C, An early coupled AES is able to penetrate and reset the sinus node (zone of resetting). D, An even earlier coupled AES reaches refractory tissue around the sinus node and is thus unable to penetrate the sinus node (entrance block); therefore, it does not affect sinus node discharge. The next spontaneous sinus beat (A₃) arrives exactly at the sinus interval (zone of interpolation). The atrial–His bundle (AH) interval progressively prolongs with progressively premature coupling intervals (B to D). In contrast, the His bundle–ventricular (HV) interval remains constant.

Atrioventricular Nodal Response to Atrial Extrasimulation

Progressively premature AES results in prolongation of PR and AH intervals, with inverse relationship between the AES coupling interval (A₁-A₂) and the AH interval (A₂-H₂). The shorter the coupling interval of the AES is, the longer the A₂-H₂ interval will be (see Fig. 4-21). More premature AES can block in the AVN with no conduction to the ventricle (defining AVN ERP). Occasionally, conduction delay and block occur in the HPS, especially when the AES is delivered following long basic drive CLs, because HPS refractoriness frequently exceeds the AVN FRP at long pacing CLs.

The patterns of AV conduction can be expressed by plotting refractory period relating the A₁-A₂ interval to the responses of the AVN and HPS. Plotting the A₁-A₂ interval versus the H₁-H₂ and V₁-V₂ intervals illustrates the functional input-output relationship between the basic drive beat and the AES and provides an assessment of the FRP of the AV conduction system. In contrast, plotting the A₂-H₂ interval (AVN conduction time of the AES) and the H₂-V₂ interval (HPS conduction time of the AES) versus the A₁-A₂ interval (the AES coupling interval) allows determination of the conduction times through the various components of the AV conduction system.³²

Type I Response.

In this type, the progressively premature AES encounters progressive delay in the AVN without any changes in the HPS. Therefore, refractoriness of the AVN determines the FRP of the entire AV conduction, and the ERP of the AV conduction system is determined at the atrial or AVN level. This response is characterized by initial shortening of the H₁-H₂ and V₁-V₂ intervals as the AES coupling interval (A₁-A₂) shortens, whereas AVN conduction (A₂-H₂) and HPS conduction (H₂-V₂) remain stable (Fig. 4-22). With further shortening of the A₁-A₂ interval, the RRP of the AVN is encountered, resulting in progressive delay in AVN conduction (manifesting as progressive prolongation of the A₂-H₂ interval) accompanied by stable HPS conduction (H₂-V₂) and a progressive but identical prolongation of both the H₁-H₂ and V₁-V₂ intervals, until the AES is blocked within the AVN (AVN ERP) or until the atrial ERP is reached. The minimum H₁-H₂ and V₁-V₂ intervals attained define the FRP of the AVN and entire AV conduction system. AVN conduction (A₂-H₂) usually increases by 2 to 3× baseline values before block.²⁴

FIGURE 4-22 A and B, Type I pattern of atrioventricular node response to atrial extrastimulation (AES). C and D, Type II pattern of response to AES. E and F, Type III pattern of response to AES. See text for details. BCL = basic cycle length.

(From Josephson ME: Electrophysiologic investigation: general aspects. In Josephson ME, editor: Clinical cardiac electrophysiology, ed 3, Philadelphia, 2002, Lippincott Williams & Wilkins, pp 19-67.)

Type II Response.

In type II response, conduction delay occurs initially in the AVN; however, with further shortening of the AES coupling interval, progressive delay develops in the HPS. Therefore, refractoriness of the HPS determines the FRP of the entire AV conduction system, and the ERP of the AV conduction system is determined at any level. At longer A₁-A₂ intervals, type II response is similar to type I response; however, as the A₁-A₂ interval shortens, conduction delay develops initially in the AVN (manifesting as progressive prolongation of the A₂-H₂ interval) but then in the HPS (manifesting as aberrant QRS conduction and progressive prolongation of the H₂-V₂ interval) as the RRP of the HPS is encountered. Therefore, in contrast to type I response, both A₂-H₂ and H₂-V₂ intervals prolong in response to progressively shorter A₁-A₂, resulting in divergence in the H₁-H₂ and V₁-V₂ curves until the AES is blocked within the AVN (AVN ERP), in the HPS (HPS ERP), or until the atrial ERP is reached (see Fig. 4-22). Block usually occurs in the AVN, but it can occur in the atrium and occasionally in the HPS (modified type II response). AVN conduction (A₂-H₂) usually increases only modestly (by less than 2× baseline values before block).²⁴

Type III Response.

In type III response, conduction delay occurs initially in the AVN; however, at a critical AES coupling interval, sudden and marked delay develops in the HPS. Therefore, refractoriness of the HPS determines the FRP of the entire AV conduction system, and the ERP of the AV conduction system is determined at any level. However, in contrast to type II response, the HPS is invariably the first site of block. At longer A₁-A₂ intervals, type II response is similar to type I response; however, as the A₁-A₂ interval shortens, progressive delay is noted initially in the AVN (manifest as progressive prolongation in the A₂-H₂ interval), but then a sudden delay of conduction in the HPS occurs (manifesting as aberrant QRS conduction and a sudden jump in the H₂-V₂ interval). This results in a break in the V₁-V₂ curve, which subsequently descends until, at a critical A₁-A₂ interval, the impulse blocks in the AVN or HPS (see Fig. 4–22). The FRP of the HPS occurs just before the marked jump in H₂-V₂. AVN conduction (A₂-H₂) usually increases by less than 2× baseline values before block.²⁴

Type I response is the most common pattern, whereas type III response is the least common. The pattern of AV conduction (type I, II, or III), however, is not fixed in any patient. Drugs (e.g., atropine, isoproterenol) or changes in CL can alter the refractory period relationship among different tissues so that one type of response can be switched to another. For example, atropine can decrease the FRP of the AVN and allow the impulse to reach the HPS during its RRP, changing type I response to type II or III.

The ERP of the atrium is not infrequently reached earlier than that of the AVN, especially when the basic drive is slow (which increases atrial ERP and decreases AVN ERP) or when the patient is agitated, which increases sympathetic tone and decreases AVN ERP. The first site of block is in the AVN in most patients (45%), in the atrium in 40%, and in the HPS in 15%.³¹

Atrial Response to Atrial Extrastimulation

Early AESs can impinge on the atrial RRP, with resulting local latency (i.e., long interval between the pacing artifact and the atrial electrogram on the pacing electrode).³¹ A very early AES delivered during the atrial ERP fails to capture the atrium. The atrial ERP can be longer or shorter than the AVN ERP, especially at long basic drive CLs or in cases of enhanced AVN conduction secondary to autonomic influences.

As with rate-incremental pacing, AES can result in prolongation of intraatrial and interatrial conduction, which is more pronounced in patients with a history of atrial arrhythmias. Development of a fractionated atrial electrogram is more often observed in patients who have a history of AF. Intraatrial block in response to AES is unusual. Occasionally, double or triple AESs induce AF in patients with no history of such arrhythmia. Such episodes usually terminate spontaneously and are not clinically relevant in the absence of a history of known or suspected atrial arrhythmias.

Bundle Branch Reentry Beats

This is the most common response and can occur in up to 50% of normal individuals. In patients with normal hearts, BBR is rarely sustained and is usually self-limiting in one or two complexes. The occurrence of nonsustained BBR in patients with or without structural heart disease is not related to the presence of spontaneous ventricular arrhythmias.

The longest refractory periods in the HPS are found most distally, at or near the Purkinje-myocardial junction. This creates a distal gate that inhibits retrograde conduction of early VES. Thus, when an early VES is delivered to the RV apex, the nearby distal gate of the RB can still be refractory. The results are progressive retrograde conduction delay and block occurring in the distal RB, with subsequent transseptal conduction of the impulse to the LV, leading to retrograde conduction up the LB to the HB (see Fig. 4-27D). At this point, the His potential usually follows the local ventricular electrogram in the HB recording, and retrograde atrial stimulation, if present, follows the His potential. Further decrease in the VES coupling interval produces progressive delay in retrograde HPS conduction. When a critical degree of HPS delay (S₂-H₂) is attained, the impulse can return down the initially blocked RB, thus producing a QRS with a typical LBBB pattern and left-axis deviation, because ventricular activation originates solely from conduction over the RB (see Fig. 4-27E). This beat is called a BBR beat or V₃ phenomenon.²⁴

The HV interval of the BBR beat usually approximates that during anterograde conduction. However, it can be shorter or longer, depending on the site of HB recording relative to the turnaround point and on anterograde conduction delay down the RB.

Ventricular Echo Beats

This is the second most common response and can occur in 15% to 30% of normal individuals. It is caused by reentry in the AVN, and it appears when a critical degree of retrograde AVN delay is achieved. These patients have retrograde dual AVN physiology, and the last paced beat conducts slowly retrogradely up the slow AVN pathway and then anterogradely down the fast pathway to produce the echo beat (Fig. 4-28). In most cases, this delay is achieved before the appearance of a retrograde His potential beyond the local ventricular electrogram. At a critical H₂-A₂ interval (or V₂-A₂ interval, when the His potential cannot be seen), an extra beat with a normal anterograde QRS morphology results. Atrial activity also precedes the His potential before the echo beat.

FIGURE 4-28 Retrograde dual atrioventricular pathways. Fixed-rate ventricular pacing results in retrograde conduction; retrograde His potential is labeled H′. The first three complexes are conducted over a fast atrioventricular nodal (AVN) pathway; with the fourth complex, the fast AVN pathway conduction is blocked and retrograde conduction proceeds up the slow pathway (longer VA interval), followed by a fused QRS complex, partially paced and partially conducted to the His bundle anterogradely over the fast pathway. The two AVN pathways have different earliest atrial activation sites, indicated by colored arrows and dashed lines. CS_dist = distal coronary sinus; CS_prox = proximal coronary sinus; His_dist = distal His bundle; His_prox = proximal His bundle; HRA = high right atrium; RVOT = right ventricular outflow tract.

This phenomenon can occur at long or short coupling intervals and depends only on the degree of retrograde AVN conduction delay. The presence of block within the HPS prevents its occurrence, as does block within the AVN. If a retrograde His potential can be seen throughout the zone of coupling intervals, a reciprocal relationship between the H₂-A₂ and A₂-H₃ intervals can often be noted.

Intraventricular Reentrant Beats

This response usually occurs in the setting of a cardiac pathological condition, especially coronary artery disease with a prior myocardial infarction (MI). It usually occurs at short coupling intervals and can have any morphology, but more often RBBB than LBBB in patients with a prior MI. Such beats occur in fewer than 15% of normal patients with a single VES at 2× diastolic threshold and in 24% with double VESs. In contrast, intraventricular reentrant beats occur following single or double VESs in 70% to 75% of patients with prior VT or VF and cardiac disease. The incidence of this response increases with increasing the number of VESs, basic drive CLs, and stimulation sites used. These responses are usually nonsustained (1 to 30 complexes) and typically polymorphic. In patients without prior clinical arrhythmias, such responses are of no clinical significance.

Ventricular Response During Atrial Fibrillation

Repetitive concealed conduction is the mechanism of a slow ventricular rate during AF and AFL, with varying degrees of penetration into the AVN.^25,35,36 During AF, the irregular ventricular response is caused by the varying depth of penetration of the numerous wavefronts approaching the AVN. Although the AVN would be expected to conduct whenever it recovers excitability after the last conducted atrial impulse, which would then be at regular intervals, the ventricular response is irregularly irregular because some fibrillatory impulses penetrate the AVN incompletely and block, thus leaving it refractory in the presence of subsequent atrial impulses.

Unexpected Prolongation or Failure of Conduction

Prolongation of the PR (and AH) interval or AVN block can occur secondary to a nonconducted premature depolarization of any origin (atrium, ventricle, or HB). The premature impulse incompletely penetrates the AVN (anterogradely or retrogradely), resets its refractoriness, and can make it fully or partially refractory in the presence of the next sinus beat, which may then be blocked or may conduct with longer PR interval (see Fig. 4-26). For example, concealed junctional (HB) impulses can manifest as isolated PR interval prolongation, pseudo–type I AV block, or pseudo–type II AV block. ECG clues to concealed junctional extrasystoles causing such unexpected events include abrupt unexplained prolongation of the PR interval, the presence of apparent type II AV block in the presence of a normal QRS, the presence of types I and II AV block in the same tracing, and the presence of manifest junctional extrasystoles elsewhere in the tracing.

Unexpected Facilitation of Conduction

When a premature impulse penetrates the AV conduction system, it can result in facilitation of AV conduction and normalization of a previously present AV block or BBB by one of two mechanisms: (1) preexciting parts of the conduction system so that its refractory period ends earlier than expected (i.e., peeling back the refractory period of that tissue, thus allowing more time to recover excitability), or (2) causing CL-dependent shortening of refractoriness of tissues (i.e., atria, HPS, and ventricles) by decreasing the CL preceding the subsequent spontaneous impulse.^{25, 35, 36} Abrupt normalization of the aberration by a PVC, the finding of which proves retrograde concealment as the mechanism for perpetuation of aberration, is based on these principles.

Perpetuation of Aberrant Conduction During Supraventricular Tachycardias

The most common mechanism (70%) of perpetuation of aberrant conduction during tachyarrhythmias is retrograde penetration of the blocked bundle branch subsequent to transseptal conduction. For example, a PVC from the LV during an SVT can activate the LB early and then conduct transseptally and later penetrate the RB retrogradely. Subsequently, the LB recovers in time for the next SVT impulse, whereas the RB remains refractory. Therefore, the next SVT impulse travels to the LV over the LB (with an RBBB pattern, phase 3 aberration). Conduction subsequently propagates from the LV across the septum to the RV. By this time, the distal RB has recovered, thereby allowing retrograde penetration of the RB by the transseptal wavefront and rendering the RB refractory to each subsequent SVT impulse. This scenario is repeated and RBBB continues until another, well-timed PVC preexcites the RB (and either peels back or shortens its refractoriness), so that the next impulse from above finds the RB fully recovered and conducts without aberration.