Cardiac Electrophysiology Procedures

Cardiac Electrophysiology Procedures

Susan Blancher

The use of cardiac electrophysiology (EP) procedures includes diagnostic testing and interventional treatment procedures. In general, diagnostic EP studies are performed to determine an arrhythmia diagnosis or EP mechanism of a known arrhythmia. Interventional or therapeutic EP studies consist of endocardial catheter ablation of supraventricular and ventricular arrhythmias. The placement of implantable cardioverter defibrillators (ICDs) for the management of ventricular tachycardia (VT) and ventricular fibrillation (VF) is also an interventional EP procedure and is discussed in Chapter 32. Knowledge of electrocardiography (see Chapter 15), normal cardiac activation (see Chapter 1), and cardiac activation during arrhythmias (see Chapter 16) is needed to understand EP studies.


Before an EP study, a patient needs to be prepared for the procedure. This preparation and the techniques, complications, and indications of EP studies are presented here.

Patient Preparation

Preparation for EP procedures is similar to that for cardiac catheterization (see Chapter 20). Patients are kept fasting and usually sedated during EP studies. The degree of sedation depends on the type of study being performed and the preferences of the center performing the procedures. A peripheral intravenous line is required for administration of medicine. Systemic anticoagulation may be used during EP studies to decrease the incidence of thromboembolic complications.1 Appropriate emergency and resuscitation equipment is required for all EP procedures.


During invasive EP testing, spontaneous and pacing-induced intracardiac and surface electrical signals are recorded. The normal timing and sequence of electrical activation can be observed and measured during a normal or baseline rhythm. Abnormal timing and electrical activation sequences are recorded and studied during tachyarrhythmias. Programmed electrical stimulation may also be used to induce and analyze paroxysmal arrhythmias that are the same as or similar to a patient’s clinical arrhythmia.2

Flexible catheters with at least 2 and up to 10 electrodes are introduced percutaneously. The catheters are advanced using fluoroscopy into the heart. The right and left femoral, subclavian, internal jugular, and median cephalic veins are the most commonly used venous access sites. One to several catheters may be placed depending on the type of study to be performed (Fig. 18-1). The usual intracardiac recording sites include the high right atrium, right atrial appendage, right ventricular apex, right ventricular outflow tract, coronary sinus, the His bundle region, and occasionally the left atrium. In addition, a roving catheter can be used to map intracardiac electrograms arising from different regions of the heart during tachycardia. Occasionally, the left ventricle is used during a diagnostic study for programmed electrical stimulation if VT cannot be induced from the right ventricle.

After the catheters are in place and connected to the physiologic recording equipment, intervals are measured from both the 12-lead electrocardiogram (ECG) and the intracardiac electrograms in the baseline state (Fig. 18-2). The AH interval is a measurement of conduction time from the low right atrium through the atrioventricular (AV) node to the His bundle and is an approximation of AV node conduction time. The AH interval can vary a great deal depending on the patient’s autonomic state and measures approximately 55 to 120 milliseconds.2 The HV interval represents conduction time from the onset of His bundle depolarization to the onset of ventricular activity. The normal HV interval measurement is 35 to 55 milliseconds.3 After baseline recordings, various pacing techniques may be performed to assess the patient’s electrical conduction system. Refractory periods for the atrium, AV node, and ventricle are recorded. The presence of retrograde or ventricular-atrial conduction is noted, as is the activation sequence. Attempts to induce and document the arrhythmia using the introduction of extrastimuli in either the atrium or the ventricle are then made. Intravenous isoproterenol or epinephrine may be used to help induce arrhythmias or reveal accessory pathway (AP) or slow pathway conduction.

The patient must be adequately prepared before the study and should understand that arrhythmia induction is often one of the primary goals of the study. The electrophysiologist attempts to gather as much information as possible depending on the type of arrhythmia induced and how well it is hemodynamically tolerated. Special physiologic recording equipment is able to document simultaneously every beat in 12-lead ECG and intracardiac electrogram format. Induced arrhythmias can then be reviewed and analyzed after they are terminated. It is important to note the method of arrhythmia termination. Tachycardias may be self-terminating or require antitachycardia pacing to stop them. Occasionally, it is necessary to cardiovert or defibrillate the patient to stop the arrhythmia. It is usually necessary to wait until the patient loses consciousness before defibrillation to prevent painful shock in an awake state.

If the patient is hemodynamically stable during a ventricular arrhythmia, attempts to map its origin can be performed, particularly if ablation is planned (see the section titled “Interventional EP and Catheter Ablation”). Atrial arrhythmias are usually well tolerated and allow for extensive mapping. Recordings are made at various locations in the heart and compared with a reference signal, either a surface ECG lead or a stable intracardiac electrogram. The site of earliest activation is closest to the site where the arrhythmia originates. Occasionally, the clinical arrhythmia cannot be induced or is not sustained long enough for adequate mapping.

Figure 18-1 Diagram of intracardiac placement of catheters. 1, right atrial recording catheter; 2, right ventricular recording catheter; 3, His recording catheter; 4, coronary sinus catheter.


Horowitz reviewed the experience of his EP laboratory and the laboratories of five others. During a 4-year period, 8,545 EP studies were performed on 4,015 patients. Five deaths (0.12%) occurred, all caused by intractable VF. The complications that occurred most frequently after EP studies were cardiac perforation (0.5%) and major venous thrombosis (0.5%). Cardiac perforation and pericardial effusion resolved without treatment in most patients; five patients required pericardial drainage or open repair. The femoral catheter site was the location of thrombosis for 95% of the 20 patients with venous thrombosis. Pulmonary emboli followed venous thrombosis in nine patients (0.2%).1 A slightly higher incidence of venous thrombosis (1.1%) and pulmonary emboli (1.6%) was found in a study by DiMarco et al. including 359 patients during 1,062 EP studies.4 They reported a 10% incidence of the use of countershock to terminate unstable VT; all patients returned to their original rhythms without complications. Systemic or catheter site infections were reported in 1.7% of patients in the study by DiMarco et al. but were not reported in Horowitz’s study. Major hemorrhage and arterial injury are uncommon complications of EP studies and are substantially less than those with standard cardiac catheterization. In general, the actual risk of death from electrophysiological study procedures approaches zero because reentrant VT or fibrillation induced under controlled conditions can be quickly terminated.5


A list of indications for EP testing is provided in Display 18-1. Specific clinical indications are discussed in the subsequent sections. Indications for testing supraventricular tachyarrhythmias are discussed in the section titled “Interventional EP and Catheter Ablation.”

Cardiac Arrest Survivors

People who survive a cardiac arrest not associated with an acute transmural myocardial infarction are at high risk for recurrence. The 2-year recurrence rate has been reported at 47%.6 VF was the rhythm most commonly found at the time of cardiac arrest.7,8 VT and VF were induced during EP testing in a baseline, antiarrhythmic, drug-free state in 70% to 80% of patients resuscitated from cardiac arrest.9,10 A full discussion of sudden cardiac death can be found in Chapter 27.

Serial, EP-guided, antiarrhythmic drug testing was once common practice in EP laboratories. The goal was to identify a drug that was effective in suppressing inducible VT or VF and subsequent recurrent cardiac arrest. VT or VF suppression with EP-guided antiarrhythmic drug therapy has been reported in 26% to 80% of cardiac arrest survivors.9,10 Antiarrhythmic medications may also provoke or exacerbate arrhythmias; this situation is referred to as proarrhythmic effect.

In recent years, several studies have shown ICD therapy as superior to EP-guided antiarrhythmic drugs in reducing all-cause mortality.11, 12, 13, 14, 15, 16 Therefore, ICD therapy is usually recommended as first-line therapy for patients with inducible VT or survivors of cardiac arrest.

EP testing is often recommended for patients who receive nonpharmacologic drug therapy. Implantation of combination antitachycardia pacemakers and ICDs usually requires a baseline EP test and may require testing after implantation to allow for correct
programming of the device. Knowledge of baseline conduction and the presence of concurrent atrial arrhythmias are also helpful for appropriate device selection (see Chapter 28). Patients with ischemic or nonischemic cardiomyopathy and reduced left ventricular function may be eligible to undergo prophylactic ICD implantation for primary prevention of cardiac arrest without undergoing prior EP evaluation.16,17

Figure 18-2 Basic intervals. Channel 1-I is lead I; channel 2-II is lead II; channel 4-V1 is lead V1; channel 6-RV is a right ventricular tracing (V); channel 7-RA is a right atrial tracing (A); channel 8-HIS PROX is a tracing from the proximal portion of the His bundle; channel 9-HIS MID is a tracing from the middle portion of the His bundle; channel 10-HIS DIST is a tracing from the distal portion of the His bundle. On channel 8-HIS PROX, the first waveform represents atrial depolarization (A) and occurs slightly later than the P wave on lead II. The next waveform is the His bundle deflection (H). The last waveform represents ventricular depolarization (V), corresponding to the QRS complex. Atrial and ventricular tracings are also recorded on channels 11-15-CS and reflect proximal to distal coronary sinus electrograms.

Wide-Complex Tachycardias

Wide-complex tachycardias can be caused by VT, supraventricular tachycardia with aberration, or preexcitation syndromes such as antidromic reciprocating tachycardia, in which an accessory bypass tract is the antegrade limb and the AV node is the retrograde limb of the tachycardia. Although guidelines and criteria have been established to help practitioners diagnose wide-complex tachycardias using the 12-lead ECG, necessary criteria may be difficult to identify, and the diagnosis may not be certain.18,19 In these cases, EP studies are necessary to confirm or establish a diagnosis so that proper safe treatment can be initiated.20

During invasive EP testing for wide-complex arrhythmias, the timing and sequence of atrial activation in relation to ventricular activation are recorded. Although it may be difficult to distinguish the various preexcitation syndromes from VT, the presence of AV dissociation favors a diagnosis of VT.


Syncope is defined as a sudden, transient loss of consciousness accompanied by loss of postural tone (Display 18-2).21 It is a common medical problem that is frequently benign, but has a high rate of mortality in patients with underlying heart disease, transient myocardial ischemia, and other cardiac abnormalities. The 1-year mortality rate for presumed cardiac causes of syncope has been reported to be 20% to 30%.22 Therefore, the principal objective when evaluating a patient with syncope, is to rule out any life-threatening etiology.

Although patients are routinely referred to EP centers for syncope evaluation, invasive EP testing is not always indicated. A thorough history, physical examination, and noninvasive testing can frequently uncover the mechanism and direct treatment. The
most common cause of syncope is vasodepressor syncope (otherwise known as neurally mediated syncope (NMS), neurocardiogenic syncope, or vasovagal syncope) followed by primary arrhythmias.

The history, including observers’ statements describing the onset and recovery can provide clues for the cause. For example, sudden onset of syncope without any warning signs or symptoms suggests a cardiac arrhythmia. Recovery from syncope caused by a cardiac event is usually rapid, without neurologic sequelae, whereas recovery from a seizure is usually associated with a period of drowsiness and confusion. Transient ischemic attacks rarely result in syncope. Syncope precipitated by neck turning may be due to carotid sinus hypersensitivity. Medications taken that may be associated with proarrhythmia or orthostasis should be identified. Finally, a family history of unexpected sudden cardiac death should be ascertained.23

The physical examination should include orthostatic vital signs and carotid sinus pressure in patients who do not have cerebrovascular disease or carotid bruits.24 Orthostatic vital signs can reveal a dehydrated patient. The presence of carotid bruits suggest impaired cerebral blood flow and underlying coronary artery disease. A positive carotid sinus test is documented by recording a pause of 3 seconds or longer or a blood pressure decrease greater than 50 mm Hg without symptoms. A blood pressure decrease of 30 mm Hg with symptoms is also considered an abnormal test result.25 Reproduction of symptoms may suggest the cause of syncope, especially if other causes are ruled out. Assessment for abnormalities of visual fields, motor strength, sensation, tremor, cognition and speech, and gait disturbance may point to a neurological etiology.

Once the practitioner determines that a cardiac cause is most likely, a series of noninvasive tests may be indicated. The 12-lead ECG should be evaluated for arrhythmias, long QT syndrome, Brugada syndrome, left ventricular hypertrophy, preexcitation, conduction abnormalities, and ischemia or infarction. An echocardiogram helps to rule out or confirm the presence of structural heart disease, including valvular or obstructive disease and to evaluate left ventricular function. EP study outcomes suggest that an arrhythmia is more likely to be the cause of syncope in patients who have structural heart disease and reduced left ventricular
function. Therefore, when ventricular arrhythmias are suspected, hospitalization with immediate EP testing is indicated because these patients are presumed to be at high risk for sudden cardiac death until proven otherwise.5 Ambulatory monitoring for 24 to 48 hours may be helpful if the patient is having frequent symptoms and is not considered to be at high risk for ventricular arrhythmias. If symptoms are not frequent enough, patient-activated transtelephonic event recorder26 or a subcutaneously implanted loop recorder system (Medtronic, Bedford, NH) may be helpful in documenting the presence or absence of arrhythmia during symptoms of presyncope or syncope.27

Noninvasive risk stratification tools such as the signal-averaged ECG, T-wave alternans, heart rate variability, and baroreceptor sensitivity may prove helpful in identifying candidates with syncope at risk for VT events or sudden cardiac death. The signal-averaged ECG involves recording, amplifying, and filtering the surface ECG. Low-amplitude, high-frequency signals called late potentials are detected at the terminal portion of the QRS.28,29 Delayed myocardial activation in areas of scar tissue represented by late potentials is thought to be the cause of ventricular arrhythmias. While the signal-averaged ECG is most accurate in patients with cardiomyopathy or previous myocardial infarction, it is associated with a low positive predictive value.30 Microvolt T-wave alternans is a test where high-resolution chest electrodes detect tiny beat-to-beat changes in the ECG T-wave morphology during a period of controlled exercise. Spectral analysis, a mathematical method of measuring and comparing time and the electrical signals, is then used to calculate minute voltage changes. The presence of these changes has been associated with an increased risk of ventricular arrhythmias in patients with a history of myocardial infarction or cardiomyopathy. Studies show that the test has good positive and negative predictive accuracy.31

There is a growing body of evidence that supports T-wave alternans as the more powerful predictor for future arrhythmic
events when compared with the signal-averaged ECG.31,32 However, to date, no prospective clinical trials have demonstrated enough evidence to support the widespread use of any of these tests for high-risk screening and further research is still needed.30,33

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Jan 10, 2021 | Posted by in NURSING | Comments Off on Cardiac Electrophysiology Procedures
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