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Cardiology > Electrophysiology Procedures
Diagnostic Programmed Electrical Stimulation
Article Last Updated: Aug 9, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 8  
Author: Chirag M Sandesara, MD, Fellow, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics
Chirag M Sandesara is a member of the following medical societies: American College of Cardiology, American College of Physicians-American Society of Internal Medicine, American Heart Association, and American Medical Association
Coauthor(s):
Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine;
Noel G Boyle, MB, BCh, MD, PhD, Co-Director of Cardiac Electrophysiology, Assistant Professor, Department of Internal Medicine, Division of Cardiology, University of California at Los Angeles School of Medicine
Editors: Justin D Pearlman, MD, PhD, ME, MA, Director of Dartmouth Advanced Imaging Center, Professor of Medicine, Professor of Radiology, Adjunct Professor, Thayer Bioengineering and Computer Science, Dartmouth-Hitchcock Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Steven J Compton, MD, FACC, FACP, Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals; Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital; Leonard Ganz, MD, Associate Professor of Medicine, Temple University School of Medicine; Cardiac Electrophysiologist, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Cent, West Penn Hospital
Author and Editor Disclosure
Synonyms and related keywords:
diagnostic programmed electrical stimulation, programmed stimulation, electrophysiology studies, premature stimulation, electrophysiology, EP, intracardiac electrogram recordings, radiofrequency catheter ablation
Intracardiac electrogram recordings were measured first in the 1960s, and the methods of diagnostic programmed electrical cardiac stimulation were introduced in the 1970s. These procedures are safe when performed under the carefully controlled conditions of the electrophysiology (EP) laboratory. Typically, a number of catheters (wires) are placed in the heart under x-ray fluoroscopic guidance, and electrograms are recorded from various sites, most frequently the high right atrium, His bundle (ie, atrioventricular [AV]) junction), coronary sinus, and right ventricle.
In addition to recording the electrograms from these sites, pacing the heart is also possible using an external stimulator. This setup provides the ability to assess the conduction properties of the heart, as well as the ability to induce and terminate cardiac arrhythmias using various pacing protocols. Analysis of the electrogram patterns and the patient's response to pacing interventions and drugs provides an accurate diagnosis of the mechanisms and circuits for most arrhythmias. The introduction of radiofrequency catheter ablation in the 1980s provided the option for therapeutic interventions during the EP study. This has revolutionized the treatment of cardiac arrhythmias and has high success rates, particularly for reentrant supraventricular arrhythmias.
Indications for programmed electrical stimulation
- Risk stratification (regarding ventricular arrhythmias) in patients with structural heart disease
- Risk assessment in patients with Wolff-Parkinson-White (WPW) syndrome
- Evaluation of patients with syncope
- Characterization of AV conduction
- Determining the mechanism of supraventricular tachycardia
- Assessment of efficacy of catheter ablation
METHODS OF PROGRAMMED ELECTRICAL STIMULATION OF THE HEART
The following types of pacing protocols are used during EP testing:
- Burst pacing or continuous pacing: The atrium or ventricle is paced at a faster fixed rate than the underlying sinus rate, for example, during measurement of sinus node function (see Image 1).
- Decremental pacing is burst pacing but with a continuous increase in the pacing rate and hence a decrease in the cycle length (CL), for example, as in the measurement of the Wenckebach CL or the rate at which the AV node blocks a beat in conduction from the atrium to the ventricle (see Image 2 and Image 5).
- Extrastimuli: Typically, 6-8 beats are delivered at a fixed rate (drive train), followed by 1-3 additional premature beats at a shorter CL or faster rate, for example, used particularly for induction of reentrant supraventricular or ventricular arrhythmias (see Images 6-7, and Image 10).
- Extrastimuli during tachycardias: Premature atrial or ventricular beats may be introduced during tachycardia to help differentiate the circuit and mechanism of the arrhythmia. In addition, accelerating the rate of tachycardia by pacing at a faster rate with a catheter in or near the circuit is possible; this is called entrainment.
- Pace termination: Pacing at a faster rate (shorter CL) near the circuit can frequently terminate reentrant tachycardias (see Image 8 and Image 11).
Note: A heart rate (HR) of 60 beats per minute (bpm) corresponds to a CL of 1000 milliseconds (1 second); thus, CL (in milliseconds) equals 60,000/HR.
MEASUREMENTS DURING ELECTROPHYSIOLOGY TESTING
Conduction intervals The AH interval is defined as the time from the onset of the atrial signal to the His bundle deflection, measured in the His catheter electrograms. It represents the conduction time through the AV node and is usually less than 150 milliseconds. The AH interval varies tremendously, depending on the patient's autonomic tone. The HV interval is defined as the time from the His bundle deflection to the earliest ventricular signal, measured in any intracardiac or surface recording. It represents the conduction time through the His Purkinje system and is typically 35-55 milliseconds (see Image 1). Sinus node assessment The sinus node recovery time is measured by pacing the high right atrium at a rate faster than the sinus rate for up to 1 minute and then measuring the interval from the last paced beat to the first sinus beat. The normal range is less than 1500 milliseconds. Patients with sick sinus syndrome have prolonged sinus node recovery times (see Image 1). AV node assessment The function of the AV node is to control the rate of impulse conduction from the atria to the ventricles. When the atrial rate increases above a certain rate (typically 150-200 bpm), the AV node initially causes AV block in a Wenckebach pattern and then generates higher degrees of block if the atrial rate increases further, thus controlling the ventricular rate and preserving cardiac output.
- Two measurements of AV nodal function are as follows:
- Wenckebach CL uses decremental pacing to measure the lowest rate (longest CL) at which a dropped ventricular beat occurs (see Image 2).
- The AV nodal effective refractory period (ERP) is measured by introducing a single extrastimulus (S2) after a drive train of 8 stimuli at a fixed rate (all S1), at which time the S1-S2 interval is decreased until the S2 impulse does not conduct to the ventricle. This interval defines the AV nodal ERP (see Images 3-4).
Decremental pacing of the ventricle, as previously described for antegrade (A->V) conduction, assesses retrograde (V->A) conduction (see Image 5). Extrastimulus pacing in the ventricle, in a method similar to that previously described for the AV node, measures ventricular refractory periods. The ventricular ERP is defined as the longest S1-S2 interval in which S2 fails to capture the ventricle.
Most arrhythmias encountered during EP testing are reentrant in nature and are therefore amenable to induction by the methods of extrastimuli. A reentrant arrhythmia requires a circuit with different limbs that have different refractory periods. When conduction blocks in one limb, the electrical impulse may travel down the other limb and then return (reenter) via the limb that was blocked. For example, in typical AV nodal reentrant tachycardia (AVNRT), the impulse initially blocks in the fast pathway, conducts antegrade (A->V) over the slow pathway, and is then able to enter retrograde (V->A) over the fast pathway, which has recovered conduction. When the impulse continues to travel around this circuit, a reentrant arrhythmia is generated, yielding a supraventricular tachycardia (see Images 9-10). Other examples of reentrant tachycardias are (1) AV reentrant tachycardia (AVRT), in which antegrade conduction over the AV node and retrograde conduction over a bypass tract occur; (2) atrial flutter, which is a reentrant circuit, usually in the right atrium; and (3) scar-related ventricular tachycardia of coronary artery disease, in which the impulse travels through or around the area of scar tissue. A typical stimulation protocol for induction of reentrant arrhythmias uses a drive train of 8 paced beats (S1 beats) at a fixed CL (eg, 500 milliseconds) with a premature beat (S2) added to the end of the drive train. The S2 stimulus is brought into atrial or ventricular refractoriness in intervals of 10 milliseconds. When S2 no longer captures, this defines the ERP of the tissue. A second extrastimulus, S3, is then added, with S2 set at a coupling interval 20 milliseconds above the ERP. The S2-S3 interval is also decremented until refractoriness is reached. If no arrhythmia is induced, the pacing sequences may be repeated using a third extrastimulus, ie, S4 (see Image 6). By convention, drive CLs (S1) of 500 and 400 milliseconds are used in ventricular pacing protocols. Arrhythmias with a reentrant mechanism are most often induced with this method. Another type of pacing sequence is the continuous (or straight) burst pacing sequence, in which the atrium or ventricle is paced at a fixed rate (S1) for up to 10 seconds. In arrhythmias that have mechanisms other than reentry, this method is more likely to induce such triggered activity (see Image 6). In addition, burst pacing at a rate faster than the arrhythmia CL often terminates reentrant arrhythmias (see Image 8 and Image 11).
TERMINATION OF ARRHYTHMIAS
Programmed stimulation can also be used to terminate reentrant cardiac arrhythmias. In ventricular tachycardia, pacing at a rate faster than the tachycardia rate (overdrive pacing) can capture part of the tissue in the circuit and render it refractory, thus terminating the tachycardia. This is used clinically in the methods of overdrive pacing or antitachycardia pacing used in implantable cardioverter-defibrillator (ICD) devices (see Image 8). Overdrive pacing in the right atrium can terminate atrial flutter, and either atrial or ventricular pacing can terminate AVNRT and AVRT (see Image 11). Pacing methods are not successful in treatment of atrial or ventricular fibrillation because these arrhythmias comprise multiple small reentrant circuits or breakdown of spiral waves.
| Media file 1:
Measurement of sinus node recovery time (SNRT). Four surface leads are shown from the top, including I, aVF, V1, and V6; 4 intracardiac recordings, including high right atrium (HRA) and 3 His recordings (proximal, mid, and distal); and a marker channel showing that atrial stimulation is in progress. In this example, the right atrium has been paced at a cycle length (CL) of 500 milliseconds (120 beats per minute) for 30 seconds. The last 5 atrial paced beats are shown. The SNRT is defined as the time from the last paced beat to the first intrinsic or sinus beat, and it was measured as 990 milliseconds in this example. The AH and HV intervals for the final paced beat also are shown. The SNRT is measured at multiple pacing CLs. The corrected sinus node recovery time (CSNRT) is defined as the maximum SNRT minus the sinus CL. The CSNRT is a better indicator of sinus node function than SNRT. |
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Atrial pacing showing AV nodal Wenckebach. Four surface leads are shown from the top, including I, aVF, V1, and V6; 4 intracardiac recordings, including high right atrium (HRA) and 3 His recordings (proximal, mid, and distal); and a marker channel showing that atrial stimulation is in progress. The right atrium is being paced at a cycle length (CL) of 380 milliseconds (158 beats per minute) when a dropped beat occurs. Note that the fourth atrial paced beat does not conduct to the ventricle. The AH intervals are prolonged for the first 3 conducted beats in a typical Wenckebach fashion and then shorten again after the nonconducted beat. |
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Atrial pacing with extrastimuli. Four surface leads are shown from the top, including I, aVF, V1, and V6; 4 intracardiac recordings, including high right atrium (HRA) and 3 His recordings (proximal, mid, and distal); and a marker channel showing that atrial stimulation is in progress. The last 2 beats (S1) of an 8-beat drive train at 600 milliseconds (100 beats per minute) are shown, followed by an atrial extrastimulus (S2) at a coupling interval of 400 milliseconds. This beat conducts to the ventricle; the His catheter electrogram recordings show atrial (A), His (H), and ventricular (V) electrograms. |
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Measurement of atrioventricular (AV) nodal effective refractory period (ERP). Four surface leads are shown from the top, including I, aVF, V1, and V6; 4 intracardiac recordings, including high right atrium (HRA) and 3 His recordings (proximal, mid, and distal); and a marker channel showing that atrial stimulation is in progress. As in Image 3, the atrium is paced at a cycle length (CL) of 600 milliseconds for 8 beats (S1), of which the last 2 beats are shown, followed by an extrastimulus at 340 milliseconds (S2). Note that now the S2 beat blocks in the AV node and does not conduct to the His or ventricle (no H or V electrograms are observed after S2). The AV nodal ERP is defined by the longest S1-S2 interval for which S2 fails to conduct. |
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Ventricular pacing to evaluate retrograde (V->A) conduction. Four surface leads are shown from the top, including I, aVF, V1, and V6; 2 intracardiac recordings, including high right atrium (HRA) and right ventricular apex (RVA); and a marker channel showing that ventricular stimulation is in progress. The ventricle is paced at increasingly faster rate (shorter cycle length [CL]) until, at 420 milliseconds (143 beats per minute), atrioventricular (AV) dissociation occurs. In this tracing, the first 2 ventricular paced beats conduct to the atrium, while the third beat blocks with onset of ventriculoatrial (VA) dissociation. |
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Four types of ventricular pacing sequences used for induction of ventricular arrhythmias. The top 3 panels show a drive train of 8 beats at a cycle length (CL) of 400 milliseconds (150 beats per minute [bpm], S1), with single (S2), double (S2, S3), and triple (S2, S3, S4) extrastimuli delivered at the right ventricular apex (RVA). The bottom panel shows continuous, or burst, pacing at a CL of 250 milliseconds (240 bpm). |
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Induction of ventricular tachycardia. Four surface leads are shown from the top, including I, aVF, V1, and V6; 2 intracardiac recordings, including high right atrium (HRA) and right ventricular outflow tract (RVOT); and a marker channel showing that ventricular stimulation is in progress. A drive train of 400 milliseconds with triple extrastimuli at 260/200/180 milliseconds is shown pacing the RVOT. This induces a monomorphic ventricular tachycardia, (CL = 240 milliseconds [250 beats per minute]). Note that ventriculoatrial (VA) dissociation is present, confirming that the tachycardia is ventricular. |
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Termination of ventricular tachycardia with overdrive pacing. Four surface leads are shown from the top, including I, aVF, V1, and V6; 2 intracardiac recordings, including high right atrium (HRA) and right ventricular outflow tract (RVOT); and a marker channel showing when ventricular stimulation is in progress. The monomorphic ventricular tachycardia (cycle length [CL] = 240 milliseconds) induced in Image 7 is now subjected to ventricular overdrive pacing from the catheter in the RVOT at a shorter CL of 200 milliseconds and is terminated with cessation of the pacing. The last 3 beats in the tracing show sinus rhythm. Overdrive pacing is also known as antitachycardia pacing (ATP) and is used in the implantable cardioverter-defibrillator (ICD) device in addition to cardioversion/defibrillation for treatment of ventricular tachycardia (VT). |
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Demonstration of dual atrioventricular (AV) node physiology with atrial extrastimuli pacing. Four surface leads are shown from the top, including I, aVF, V1, and V6; 9 intracardiac recordings, including high right atrium (HRA), 3 His electrograms (proximal, mid, and distal), 4 coronary sinus tracings (CS 4 [proximal] to CS [distal]), and a right ventricular apex (RVA); and a marker channel showing when stimulation is in progress. In the left panel, atrial pacing and extrastimuli are delivered from the coronary sinus (CS 3). The premature beat, with a coupling interval of 340 milliseconds conducts over the fast AV nodal pathway (AH = 80 milliseconds). In the panel on the right, when the extrastimulus coupling interval is reduced to 330 milliseconds, the AH interval of the conducted beat prolongs to 164 milliseconds, indicating that conduction over the AV node has now switched to the slow pathway. |
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| Media file 10:
Induction of supraventricular tachycardia with atrial extrastimuli. Four surface leads are shown from the top, including I, aVF, V1, and V6; 10 intracardiac recordings, including high right atrium (HRA), 3 His electrograms (proximal, mid, and distal), 5 coronary sinus tracings (CS 5 [proximal] to CS [distal]), and a right ventricular apex (RVA); and a marker channel showing when stimulation is in progress. The last beat of a drive train at 400 milliseconds with 2 atrial extrastimuli at 200/190 milliseconds is shown.Following the second extrastimulus (S3), conduction over the slow atrioventricular (AV) nodal pathway occurs, followed by retrograde conduction up the fast AV nodal pathway and genesis of an AV nodal reentrant tachycardia (AVNRT). The tachycardia CL = 270 milliseconds (222 beats per minute). Note that during the tachycardia, the atrial and ventricular electrograms line up, which is classic for this type of typical AVNRT, with the ventriculoatrial (VA) interval less than 60 milliseconds. |
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Termination of AV nodal reentrant tachycardia (AVNRT) with ventricular pacing. Four surface leads are shown from the top, including I, aVF, V1, and V6; 11 intracardiac recordings, including 2 ablation catheter electrograms from the low right atrium, 3 His electrograms (proximal, mid, and distal), 5 coronary sinus tracings (CS os [proximal] to CS [distal]), and a right ventricular apex (RVA) electrogram; and a marker channel showing when stimulation is in progress. The tachycardia CL = 350 milliseconds (170 beats per minute); 5 ventricular paced beats are delivered at a shorter CL of 320 milliseconds, which result in termination of the tachycardia by overdrive pacing. The final 2 beats on the right of the tracing are sinus rhythm. Atrial overdrive pacing could also terminate this supraventricular tachycardia. |
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Diagnostic Programmed Electrical Stimulation excerpt Article Last Updated: Aug 9, 2006
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