Invasive diagnostic cardiac electrophysiology studies

INTRODUCTION — Invasive cardiac electrophysiology (EP) is a collection of clinical techniques for the investigation and treatment of cardiac rhythm disorders. These techniques permit a detailed analysis of the mechanism(s) underlying the cardiac arrhythmia, precise location of the site of origin, and, when applicable, definitive treatment via catheter-based ablation techniques.

An overview of invasive cardiac EP studies will be presented here. Issues related to its use in the evaluation of specific arrhythmias are discussed separately. (See "Overview of catheter ablation of cardiac arrhythmias" and "Catheter ablation for the treatment of atrial fibrillation: Technical considerations for non-electrophysiologists" and "Atrial fibrillation: Catheter ablation".)

INDICATIONS AND CONTRAINDICATIONS

Indications — Broadly speaking, the indications for invasive EP studies can be broken down to two categories: diagnosis and risk stratification [1]. EP studies suffer from limited sensitivity and specificity. The significance of the findings is often determined by the underlying cardiac disease and the patient's clinical presentation.

Diagnosis — EP studies can be helpful to diagnose the etiology of syncope, sudden cardiac death, wide complex tachyarrhythmia, and atrioventricular conduction delay or disease.

●Syncope – In many cases of syncope, an EP study can serve as a useful diagnostic test. Specific scenarios are described below:

•Syncope and ischemic or other structural heart disease – The concurrent diagnosis of cardiac disease can be based on history, physical examination, electrocardiography, and/or echocardiography. The aim of an EP study for such patients would be to determine if sustained ventricular arrhythmias (or atrial tachyarrhythmias in the case of adults with congenital heart disease such as transposition of the great arteries with atrial switch) or bradyarrhythmias may be the underlying cause of heart disease [2-4]. If a patient with syncope undergoes an EP study and is induced into a clinically relevant and hemodynamically significant sustained ventricular tachycardia (VT) or ventricular fibrillation (VF), the implantation of an implantable cardioverter-defibrillator (ICD) is indicated.

•Syncope with suspected sinus node dysfunction – Often, this is suspected based on inappropriate sinus bradycardia. The detection of a prolonged corrected sinus node recovery time may predict future recurrence of syncope [3].

•Syncope in patients with bifascicular block – This includes patients who have syncope with left bundle branch block, or right bundle branch block with a fascicular block when noninvasive evaluation has been unrevealing [3]. The causes of syncope in patients with bifascicular block can be multifactorial. An EP study can help delineate the cause, define the prognosis, and determine the therapy [5]. The induction of infra-Hisian block in patients with bifascicular block can predict future adverse cardiovascular events [6].

•Syncope in patients who are employed in high-risk occupations (eg, airline pilots, school bus drivers, police officers) – An EP study can be helpful when all other noninvasive diagnostic tools have failed to arrive at a cause for syncope.

•Syncope immediately following palpitations [3].

•Unexplained syncope [7].

●Other diagnostic indications

•Sudden cardiac death (SCD) with no established cause – In this case, an EP study is considered a step in the diagnostic cascade recommended to try to establish a diagnosis [2,8].

•Patients with wide complex tachyarrhythmias – In patients in whom a diagnosis cannot be established by noninvasive means or who are suspected of harboring a life-threatening arrhythmia, an EP study can define the mechanism of the arrhythmia to help determine therapy and prognosis [9].

•Abnormal atrioventricular (AV) conduction – An EP study in such patients can help determine the site of block when clinical and electrocardiographic information fail to help localize the site of block. Rare cases of AV conduction abnormalities may be due to concealed junctional beats that can only be demonstrated through an invasive EP study [4,10].

•Patients with documented tachyarrhythmias who are undergoing catheter ablation – These patients will automatically undergo a diagnostic EP study, usually directed at the putative tachyarrhythmia, before catheter ablation is performed. The purpose of this EP study is to define the diagnosis and localize the pathway responsible for the arrhythmia. In the pediatric population, the role of programmed electrical stimulation is limited and is not expected to confer value beyond what has already been collected noninvasively. While a diagnostic EP study is employed in conjunction with a preplanned catheter ablation for a documented arrhythmia, it is rarely used to risk stratify patients with nonsustained polymorphic ventricular arrhythmias or to define endocardial scar [11].

Risk stratification — EP studies may be helpful to risk stratify in the following conditions.

●Selected patients with ischemic cardiomyopathy and nonsustained VT – Among patients with an ischemic cardiomyopathy due to a prior myocardial infarction or revascularization and who have left ventricular ejection fraction (LVEF) <40 percent with nonsustained VT on ambulatory cardiac rhythm monitoring, the induction of sustained VT or VF constitutes a class I indication for the implantation of an ICD [12]. The MUSTT trial enrolled patients with recent myocardial infarction or revascularization, LVEF <40 percent, and asymptomatic nonsustained VT [13]. All patients underwent an EP study. Patients in whom sustained ventricular tachyarrhythmias were induced by programmed stimulation were randomly assigned to receive either antiarrhythmic therapy, including drugs and implantable defibrillators, as indicated by the results of EP testing, or no antiarrhythmic therapy. The patients who were assigned an ICD had a lower risk of sudden cardiac death.

●Asymptomatic second-degree AV block, if the site of block cannot be determined reliably – AV conduction abnormalities below the level of the AV node may progress to complete AV block with catastrophic consequences [14]. The site of block in patients with Mobitz type II second degree AV block is infranodal (intra- or infra-Hisian), and this constitutes an indication for pacing even if the patient is asymptomatic. An EP study is indicated if the site of block cannot be determined reliably in an asymptomatic individual with second degree AV block. If the site is infranodal, pacing is indicated [4].

●Asymptomatic young (8 to 21 years) patients with electrocardiographic evidence of preexcitation – Such patients may be at high risk of SCD due to atrial fibrillation progressing to VF. These patients are advised to undergo exercise stress testing. The clear and sudden loss of preexcitation with exercise stress testing predicts a favorable prognosis. If clear loss of preexcitation is not seen or the data are uninterpretable, invasive risk stratification via transesophageal pacing or EP studies is recommended [15]. Programmed electrical stimulation for risk stratification of a manifest accessory bypass tract is a class I indication in a symptomatic patient and a class IIa indication in an asymptomatic patient if the noninvasive measures described cannot be met [16]. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Risk stratification of asymptomatic patients with WPW pattern'.)

●Cardiac sarcoidosis – In patients with cardiac sarcoidosis and an LVEF >35 percent despite optimal medical therapy and immunosuppression, an EP study can be helpful. In such patients, programmed electrical stimulation can be considered to help risk stratify sudden cardiac death [12,17].

●Arrhythmogenic right ventricular cardiomyopathy – In patients who are asymptomatic, programmed electrical stimulation is occasionally used to help risk stratify them [12,18]. (See "Arrhythmogenic right ventricular cardiomyopathy: Diagnostic evaluation and diagnosis", section on 'Electrophysiologic testing and electroanatomic mapping'.)

●Tetralogy of Fallot – EP studies are used for risk stratification of adults with tetralogy of Fallot with high-risk factors for sudden cardiac death, such as left ventricular systolic and diastolic dysfunction, QRS ≥180 milliseconds, extensive right ventricular scarring, pulmonary regurgitation or stenosis, and nonsustained VT (class IIa indication). EP studies should not be used as a screening test on patients with tetralogy of Fallot who do not have high-risk factors or in patients with repaired tetralogy of Fallot [2]. Adult patients with congenital heart disease of moderate to severe complexity who display high-risk features such as syncope and ventricular arrhythmias should undergo invasive EP studies to determine if they are at risk for sudden cardiac death and may benefit from an ICD (class IIa indication) [12].

●Brugada syndrome – The role of EP studies in Brugada syndrome is controversial. Patients with Brugada syndrome who have had a history of syncope or have survived sudden cardiac death are more likely to be inducible. However, the role of EP studies in predicting future events is controversial [8]. The implantation of an ICD may be considered in a patient with Brugada syndrome who is induced into VF. One study analyzed the role of clinical factors and programmed ventricular stimulation in determining the risk of arrhythmic events in patients with Brugada syndrome. The investigators concluded that clinical factors such as syncope and spontaneous type 1 Brugada pattern and the induction of ventricular arrhythmias by programmed ventricular stimulation all portend a higher risk of events. The value of programmed ventricular stimulation was greater if ventricular arrhythmias were induced with single or double extrastimuli. A negative study did not predict arrhythmia-free survival [19]. Professional society guidelines allow the use of invasive programmed electrical stimulation with one to two premature ventricular extrastimuli for risk stratification of asymptomatic patients with class I Brugada pattern (class IIb) [12]. (See "Brugada syndrome or pattern: Management and approach to screening of relatives".)

Contraindications — Absolute contraindications to EP study include [20]:

●Unstable angina

●Bacteremia or septicemia

●Acute decompensated congestive heart failure not caused by the arrhythmia

●Major bleeding diathesis

●Acute lower extremity venous thrombosis if femoral vein cannulation is desired

PREPROCEDURAL EVALUATION — In all patients undergoing invasive EP study, the preprocedure evaluation includes a thorough history and physical examination and review of the available electrocardiograms (ECGs), both at baseline and, if available, during the tachycardia. The history should focus on the appropriateness of invasive EP study for the particular patient and screen for any potential contraindications to the procedure. Additional evaluation prior to the procedure in select patients may include:

●Event monitoring for up to four weeks in an effort to document the tachycardia. Event monitoring for longer periods is typically more useful than short-term (24 to 48 hours) Holter monitoring in documenting the tachycardia. (See "Ambulatory ECG monitoring".)

●Transthoracic echocardiography to assess for structural heart disease. Cardiac magnetic resonance imaging may also be considered for special situations (eg, suspicion of arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy, etc).

●Exercise testing, if there is a history of exercise-induced arrhythmia.

●Cardiac catheterization and coronary angiography, if indicated by the patient's clinical presentation and symptoms suggesting coronary heart disease. If the clinical presentation is prehospital cardiac arrest or ventricular tachycardia causing hemodynamic collapse, coronary angiography and an assessment of ventricular function (eg, echocardiography, ventriculography) should usually be obtained prior to invasive EP studies with programmed cardiac stimulation.

In most patients, all atrioventricular (AV) nodal blocking agents, including beta blockers, calcium blockers, digoxin, and class I and III antiarrhythmic drugs (table 1) are discontinued several days prior to the scheduled procedure. In general, beta blockers should be gradually tapered and discontinued, while other agents can be discontinued without tapering.

Because radiation exposure is a necessary component of an invasive EP study, it is reasonable to obtain a pregnancy test on all women of childbearing capacity on the morning of the procedure. (See 'Fluoroscopy' below.)

PREPARATION AND MONITORING — Invasive EP studies are typically performed in a dedicated EP laboratory [20]. In addition to the electrophysiologist, several other staff members are required. Intravenous conscious sedation is typically used to ensure patient comfort, although in some situations (ie, prolonged catheter ablation procedures) general anesthesia can be used. Standard electrocardiogram (ECG) leads are applied to the patient, as well as "hands-off" defibrillation pads. Arterial pressure may be monitored invasively or noninvasively, depending upon the complexity of the procedure. Oxygen saturation, as well as in some cases end-tidal CO₂, is monitored.

The following are considered part of the routine preparation and monitoring involved in invasive EP studies:

●Patients should be fasting after midnight on the day of the procedure, except for oral medications with sips of water.

●Patients should hold their normal cardiovascular medications, particularly medications which affect atrioventricular (AV) node conduction (ie, beta blockers, dihydropyridine calcium channel blockers, and digoxin) and antiarrhythmic medications (table 1). (See 'Preprocedural evaluation' above.)

●Standard cardiorespiratory monitoring should include blood pressure (noninvasively or via arterial monitoring), pulse, oxygen saturation, and cardiac telemetry.

●Defibrillation pads should be placed on the patient prior to beginning the procedure (figure 1).

●Intravenous access is required for administration of sedation and for management of any rhythm-related complications (ie, ventricular fibrillation, sinus bradycardia, etc).

●Supplemental oxygen, a suction device, and intubation equipment should be immediately available for management of respiratory complications (though supplemental oxygen should be removed prior to delivery of any electrical shocks). (See "Cardioversion for specific arrhythmias", section on 'Supplemental oxygen'.)

●A code cart with medications used in advanced cardiac life support should be immediately available in the event of life-threatening arrhythmias that do not respond to defibrillation. (See "Advanced cardiac life support (ACLS) in adults".)

While many cardiologists are trained in the administration of procedural sedation, sedation may also be administered by an anesthesiologist who can immediately assist in the management of respiratory complications should any develop. (See "Procedural sedation in adults in the emergency department: General considerations, preparation, monitoring, and mitigating complications", section on 'Anticipating and mitigating Complications'.)

FLUOROSCOPY — Fluoroscopy is required for anatomic orientation throughout the EP study, including vascular access, catheter positioning, etc. Operators should make every effort to minimize radiation exposure to the patient as well as the procedural staff. (See "Radiation-related risks of imaging".)

VASCULAR ACCESS AND ELECTRODE CATHETER PLACEMENT — In nearly all EP studies, venous vascular access is required, often from multiple sites. The Seldinger technique is employed to place multiple venous accesses. The femoral approach is most common, but the subclavian, internal jugular, or brachial approach may be used, most often for placement of a catheter in the coronary sinus.

Multipolar electrode catheters are positioned in the heart. Typical positions include:

●The right atrium (high right atrium [HRA])

●Anterior tricuspid valve annulus to record the bundle of His

●The right ventricle (right ventricular apex [RVA])

A catheter may be placed in the coronary sinus to record left atrial activation, particularly in studies of patients with supraventricular tachycardia (SVT).

When mapping and ablation are performed, electrodes may be placed in the left heart. Left heart access may be obtained via either a transseptal or retrograde aortic approach. Intracardiac recordings and programmed electrical stimulation (PES) are performed via the electrode catheters. Typically, for evaluation of ventricular arrhythmias requiring LV mapping, a retrograde aortic approach is employed, while the transseptal approach is preferred for left-sided SVTs. Either approach may be used for patients with a suspected left-sided accessory pathway.

When catheters are placed into left-sided cardiac chambers, systemic anticoagulation is required to prevent thromboembolic complications. Typically intravenous heparin is initiated at the time of the procedure and continued until the catheters are removed from the left-sided cardiac chambers.

At the conclusion of the procedure, the access sheaths are pulled and hemostasis is achieved using manual or mechanical pressure or a vascular closure device. The patient is generally kept on bed rest for four to six more hours to ensure adequate hemostasis has been achieved. (See "Complications of diagnostic cardiac catheterization", section on 'Hemostasis at the femoral access site' and "Percutaneous arterial access techniques for diagnostic or interventional procedures", section on 'Hemostasis at the access site'.)

ELECTROCARDIOGRAPHIC AND ELECTROPHYSIOLOGIC RECORDINGS

Baseline recordings — Baseline recordings obtained during a typical invasive EP study include several surface electrocardiograms (ECGs) to time events from the body's surface and several intracardiac electrograms, all of which are recorded simultaneously. The intracardiac electrograms are generally displayed in the order of normal cardiac activation (waveform 1).

●The first intracardiac tracing is a recording from the high right atrium (HRA) close to the sinus node. Pacing at this position allows evaluation of sinoatrial node function and atrioventricular (AV) conduction; the addition of premature atrial complex (also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) or burst atrial pacing may result in the induction of supraventricular tachyarrhythmias. Sinus node function is determined by measuring the sinus node recovery time (SNRT), a reflection of the node's automaticity, and the sinoatrial conduction time (SACT), a reflection of peri-sinus node conduction properties. Great care must be exercised in interpreting the findings from EP studies due to limited sensitivity and specificity.

●The next intracardiac tracing is the His bundle recording (HBE), obtained from a catheter positioned at the bundle of His (in the area of the tricuspid annulus).

●One to three recordings may be obtained from the coronary sinus (CS) in patients with supraventricular tachyarrhythmias or preexcitation. Since the coronary sinus runs in the mitral annulus, these recordings reflect left atrial activation.

●The next is a recording from a right ventricular apex (RVA) electrode catheter. The stability and reproducibility of the right ventricle apex position (during a given study as well as from one study to the next) makes it a useful site for adding premature stimuli during programmed ventricular stimulation. (See 'Programmed electrical stimulation' below.)

●Depending upon the particular study, other required recordings may include right bundle branch recording, left ventricular recording, transseptal left-atrial recording, and atrial and ventricular mapping catheter tracings for EP mapping and ablation.

AH interval — The AH interval is measured on the His bundle electrogram and represents the interval from the earliest rapid deflection of the atrial recording (activation of the lowest part of the right atrium) to the earliest onset of the His bundle deflection. This interval approximates AV nodal conduction. More precisely, however, it is the sum of conduction through the low right atrial inputs into the atrioventricular node, the atrioventricular node proper, and the proximal His bundle.

The AH interval has a wide range in normal subjects (50 to 120 milliseconds) and is markedly influenced by the autonomic nervous system [21,22].

●Short AH intervals may be seen in the following circumstances [23]:

•Increased sympathetic tone

•Enhanced AV nodal conduction, which may be due in some patients to steroid use or pregnancy

•Preferential left-atrial input into the atrioventricular node

●Long AH intervals are most commonly due to:

•Impaired or delayed AV node conduction from drugs such as digoxin, beta blockers, calcium channel blockers, and antiarrhythmic drugs, particularly amiodarone

•Increase parasympathetic (vagal) tone

•Intrinsic disease of the atrioventricular node

Artifactually prolonged AH intervals may result from an improperly positioned catheter and the incorrect identification of a right bundle branch potential as a His bundle potential. This situation needs to be distinguished from true AH prolongation.

His bundle electrogram duration — The His bundle electrogram duration reflects conduction through the short length of compact His bundle that penetrates the fibrous septum. This interval is normally short (15 to 25 milliseconds), with fractionation and prolongation or even splitting of the His bundle potential, seen with disturbances of His bundle conduction (waveform 2) [24,25].

HV interval — The HV interval is measured from the earliest onset of the His bundle deflection to the earliest registered surface or intracardiac ventricular activation anywhere. This measurement reflects conduction time through the distal His-Purkinje system. Unlike the AV node, the His-Purkinje system is far less influenced by the autonomic nervous system, and the range in normal subjects is narrow (35 to 55 milliseconds) [26].

A prolonged HV interval is consistent with diseased distal conduction in all fascicles [27]. In patients with symptoms suggesting a bradyarrhythmia, a prolonged HV interval (>55 milliseconds) warrants pacemaker therapy. In asymptomatic patients with an HV interval >100 milliseconds, a pacemaker is also indicated [28,29]. In asymptomatic patients with an HV interval >70 milliseconds, pacemakers are more controversial [27,28,30].

A validated short HV interval suggests one of two situations:

●Ventricular preexcitation via an AV bypass tract

●Ventricular origin for the beats, such as ventricular premature beats (VPBs) or an accelerated idioventricular rhythm that is isorhythmic with the sinus rhythm

A spurious explanation for a short HV interval is the inadvertent recording of a right bundle branch potential rather than a His potential.

VA conduction — The assessment of ventriculoatrial (VA) conduction is also important in the EP study, particularly for patients with a supraventricular tachycardia (SVT). This is performed by ventricular extrastimulus and incremental ventricular pacing. Absence of VA conduction makes certain SVTs less likely (ie, atrioventricular reciprocating tachycardia and atrioventricular nodal reentrant tachycardia) and suggests an atrial tachycardia (AT), since AT is independent of retrograde VA conduction.

Sinoatrial conduction time — The usual method of calculating sinoatrial conduction time (SACT), which is a measure of sinus node function, is an indirect measure. This approach involves the placement of a catheter in the superior aspect of the right atrium approximating the main intrinsic pacemaker site of the SA node. Progressively premature atrial extrastimuli are introduced by way of that catheter after every 8th to 10th beat of either a stable sinus rhythm (Strauss method) [31] or atrial pacing (Narula method) [32].

Due to the limitations of indirect methods in assessing the SACT, techniques for direct recording of the sinus electrogram (EGM) have been developed [33-38]. Endocardial recordings demonstrate diastolic phase 4 activity followed by a slow upstroke culminating in a rapid atrial EGM. The directly measured SACT was defined as the interval between the local EGM and the rapid atrial deflection.

Normal SACT times generally range from 40 to 150 milliseconds, depending upon the laboratory [39,40]. Studies have shown a good correlation between indirect and direct methods of measuring SACT [35,37,38,41]. However, SACT is a relatively insensitive test for SA node dysfunction.

Sinus node recovery time — The sinus node recovery time (SNRT) is performed by placing a catheter near the SA node and pacing (overdrive suppression) for at least 30 seconds at a fixed cycle length starting slightly faster than the intrinsic sinus rate. This is repeated at progressively shorter cycle lengths. Pacing rates up to 200 beats per minute may be employed for improved sensitivity [42]. It is important to wait at least one minute between pacing sequences to allow full recovery of the SN. Confirmation that the escape beat is sinus by examining P-wave morphology and atrial activation sequence is essential to exclude a shift in pacemaker site [43].

The maximum SNRT is the longest pause from the last pacing stimulus to the first spontaneously occurring sinus beat at any paced cycle length. As the sinus cycle length (SCL) affects the SNRT, it is often normalized or corrected:

●The SNRT is normalized by dividing this value by the SCL.

●The corrected sinus node recovery time (CSNRT) is determined by subtracting the SCL from the SNRT (waveform 3).

A total recovery time (TRT) can also be calculated, which is the time required to return to the basal sinus rate.

Normal values have generally been estimated as follows [43]:

●SNRT/SCL <150 percent

●CSNRT <550 milliseconds

●TRT less than five seconds

There are several limitations to the use of overdrive suppression in determining SN function, which include changes in autonomic tone due to the effects of pacing, changes in P-wave morphology or atrial activation suggesting a pacemaker shift, sinoatrial entrance block, and secondary pauses.

PROGRAMMED ELECTRICAL STIMULATION — After baseline measurements are recorded, pacing is performed via the intracardiac electrode catheters. Burst pacing at various fixed cycle lengths as well as programmed electrical stimulation (PES) is administered. With PES, a number of stimuli at a fixed cycle length are delivered (eg, eight beats at a rate of 100 beats per minute), followed by a premature beat. The coupling interval of the premature beat is progressively shortened until the refractory period of the tissue being paced is reached. Multiple premature stimuli can be introduced.

The technique of PES is used to assess the atrioventricular (AV) conducting system and to induce supraventricular and ventricular arrhythmias. Premature beats can be introduced during a tachyarrhythmia to probe the mechanism of the tachycardia.

Programmed atrial stimulation is usually from the high right atrium, although a second atrial site such as coronary sinus pacing is also employed in certain situations (waveform 4A-B) [44,45]. One or sometimes two atrial extrastimuli with progressively shorter coupling intervals are delivered following a train of eight or more drive beats at several cycle lengths until atrial refractoriness is encountered [45,46]. Incremental atrial pacing in steps of 10 milliseconds is also performed until second degree AV block develops.

Programmed atrial extrastimuli can be used to determine the effective refractory period of the His-Purkinje system (HPS), which should be <450 milliseconds. However, the response of refractory periods to pacing may reveal severe HPS disease. As the refractory period of the HPS should shorten with the cycle length, an increasing refractory period with shorter cycle lengths indicates abnormal HPS conduction [29].

MEDICATIONS USED FOR DIAGNOSTIC PURPOSES DURING EPS — Administration of pharmacologic agents may be of help in certain settings. Selective blocking of antegrade atrioventricular (AV) nodal conduction with adenosine, for example, may unmask latent accessory pathway conduction. Atropine or isoproterenol may be used to facilitate the induction of AV nodal reentrant tachycardia (AVNRT) or AV reentrant tachycardia (AVRT) by enhancing ventriculoatrial (VA) conduction in patients with poorer AV nodal conduction characteristics [47] or by widening the tachycardia zone or the section of the cardiac cycle during which extrastimuli cause the necessary block and the critical delay to initiate reentrant activation.

Procainamide normally prolongs the HV interval by 10 to 20 percent [48]. Doubling of the HV interval, an HV interval >100 milliseconds, or the development of infra-Hisian block after administering procainamide represent poor HPS reserve and probably mandates permanent pacing (waveform 5) [29,49].

Evaluation of His-Purkinje system (HPS) conduction can be limited by AV nodal conduction (ie, block in the AV node preventing evaluation of the HPS). In these instances, atropine is often used to shorten the refractory period of the AV node without affecting HPS conduction [50].

MAPPING AND ABLATION — In many cases, catheter ablation immediately follows the diagnostic EP study. Cardiac mapping refers to careful movement of a mapping or ablation catheter in the area of interest, probing for the site at which radiofrequency ablation will be successful at curing the arrhythmia. Cardiac mapping during EP testing identifies the temporal and spatial distributions of electrical potentials generated by the myocardium during normal and abnormal rhythms. This process allows description of the spread of activation from its initiation to its completion within a region of interest and, in its usual application, is focused toward the identification of the site of origin or a critical site of conduction for an arrhythmia. Multiple techniques for mapping have been developed. (See "Overview of catheter ablation of cardiac arrhythmias", section on 'Mapping and localization of the arrhythmia'.)

COMPLICATIONS OF INVASIVE CARDIAC ELECTROPHYSIOLOGY STUDIES — Complications of invasive cardiac EP studies are rare, with reported complication rates of approximately 2 percent [51,52]. Serious complications of these procedures are generally related to the catheterization process itself, including vascular injury, tricuspid valve damage, pulmonary embolism, hemorrhage requiring transfusion therapy, cardiac chamber perforation resulting in pericardial tamponade, sepsis from catheterization site abscess, myocardial infarction, stroke, and death (table 2).

The induction of serious ventricular tachyarrhythmias occurs frequently during diagnostic EP testing. Such arrhythmias can usually be promptly terminated, either by overdrive pacing or external defibrillation. However, if the arrhythmia is difficult to revert and is of long duration, there may be complications related to the prolonged hypotension and, rarely, sudden death.

Complications with concomitant catheter ablation — Catheter-based radiofrequency (RF) ablation procedures are typically much longer studies with more radiation exposure, administration of higher doses of sedative and analgesic agents, more frequent catheterization of the left heart, and more frequent change of catheters. The duration of some of the RF ablation procedures may raise morbidity from vascular complications, thromboembolic complications, cardiac chamber rupture, or radiation exposure including skin injuries and a possible increased risk for malignancy (table 2). These issues are discussed in detail separately. (See "Overview of catheter ablation of cardiac arrhythmias", section on 'Complications'.)

With the rapid expansion of clinical cardiac EP beginning in the 1990s, the complexity of the procedures performed in the EP laboratory has greatly increased, and, along with the increased complexity, the risks involved have increased. To meet the expanding demands and help provide patients and staff with the safest possible and most productive environment, guidelines concerning the staffing and qualifications of the EP laboratory personnel, as well as the design of the laboratory itself, have been issued [53].

SUMMARY AND RECOMMENDATIONS

●Background – Invasive cardiac electrophysiology (EP) study permits a detailed analysis of the mechanism underlying the cardiac arrhythmia and precise location of the site of origin. (See 'Introduction' above and 'Indications and contraindications' above.)

●Preprocedural evaluation – This occurs prior to catheter ablation and includes a history and physical examination along with an electrocardiogram (ideally during the arrhythmia) or strips from ambulatory monitoring that document the arrhythmia in every patient. Consideration of other testing prior to the ablation should be based on the patient's clinical presentation and symptoms but may include echocardiography, stress testing, cardiac magnetic resonance imaging, or coronary angiography to evaluate for underlying structural heart disease. (See 'Preprocedural evaluation' above.)

●Catheter placement and baseline recordings

•Multipolar electrode catheters are positioned in the heart. Typical positions include the right atrium (high right atrium) and right ventricle (right ventricular apex); a catheter is also positioned across the tricuspid annulus to record a potential from the bundle of His (His). A catheter may be placed in the coronary sinus to record left-atrial activation, particularly in studies of patients with supraventricular tachycardia (SVT). These electrodes allow for the measurement of several intervals with diagnostic implications. (See 'Vascular access and electrode catheter placement' above.)

•Baseline recordings obtained during a typical invasive EP study include several surface electrocardiograms to time events from the body's surface and several intracardiac electrograms, all of which are recorded simultaneously. The intracardiac electrograms are generally displayed in the order of normal cardiac activation (waveform 1). (See 'Electrocardiographic and electrophysiologic recordings' above.)

●Programmed electrical stimulation – After baseline measurements are recorded, pacing is performed via the intracardiac electrode catheters. Burst pacing at various fixed cycle lengths as well as programmed electrical stimulation (PES) is administered. The technique of PES is used to assess the atrioventricular (AV) conducting system and to induce supraventricular and ventricular arrhythmias. Administration of pharmacologic agents may be of help in certain settings. (See 'Programmed electrical stimulation' above and 'Medications used for diagnostic purposes during EPS' above.)

●Mapping and ablation – Cardiac mapping refers to careful movement of a mapping or ablation catheter in the area of interest, probing for the site at which radiofrequency ablation will be successful at curing the arrhythmia. Cardiac mapping during EP testing identifies the temporal and spatial distributions of electrical potentials generated by the myocardium during normal and abnormal rhythms. This process allows description of the spread of activation from its initiation to its completion within a region of interest. Multiple techniques for mapping have been developed. (See 'Mapping and ablation' above.)

●Complications – These are rare but can be potentially life threatening (table 2). (See 'Complications of invasive cardiac electrophysiology studies' above.)

ACKNOWLEDGMENT — The authors and UpToDate thank Dr. Philip Podrid, Dr. Leonard Ganz, Dr. Joseph Germano, Dr. Peter Zimetbaum, and Dr. Brian Olshansky who contributed to earlier versions of this content.