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 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 13/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate 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 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 14/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate (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. Use of UpToDate is subject to the Terms of Use. REFERENCES https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 15/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate 1. Muresan L, Cismaru G, Martins RP, et al. Recommendations for the use of electrophysiological study: Update 2018. Hellenic J Cardiol 2019; 60:82. 2. Khairy P, Van Hare GF, Balaji S, et al. PACES/HRS Expert Consensus Statement on the Recognition and Management of Arrhythmias in Adult Congenital Heart Disease: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology (ACC), the American Heart Association (AHA), the European Heart Rhythm Association (EHRA), the Canadian Heart Rhythm Society (CHRS), and the International Society for Adult Congenital Heart Disease (ISACHD). Heart Rhythm 2014; 11:e102. 3. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J 2018; 39:1883. 4. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2019; 74:e51. 5. Ezri M, Lerman BB, Marchlinski FE, et al. Electrophysiologic evaluation of syncope in patients with bifascicular block. Am Heart J 1983; 106:693. 6. Dhingra RC, Wyndham C, Bauernfeind R, et al. Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block. Circulation 1979; 60:1455. 7. Krol RB, Morady F, Flaker GC, et al. Electrophysiologic testing in patients with unexplained syncope: clinical and noninvasive predictors of outcome. J Am Coll Cardiol 1987; 10:358. 8. Priori SG, Wilde AA, Horie M, et al. HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart Rhythm 2013; 10:1932. 9. Pedersen CT, Kay GN, Kalman J, et al. EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Heart Rhythm 2014; 11:e166. 10. Josephson MD. Chapter 4: Atrioventricular Conduction. In: Clinical Cardiac Electrophysiolog y: Techniques and Interpretations, 4, Lippincott Williams & Wilkins, Philadelphia 2008. p.107. 11. Crosson JE, Callans DJ, Bradley DJ, et al. PACES/HRS expert consensus statement on the evaluation and management of ventricular arrhythmias in the child with a structurally normal heart. Heart Rhythm 2014; 11:e55. https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 16/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate 12. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2018; 72:e91. 13. Buxton AE, Lee KL, Fisher JD, et al. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators. N Engl J Med 1999; 341:1882. 14. Zipes DP. Second-degree atrioventricular block. Circulation 1979; 60:465. 15. Pediatric and Congenital Electrophysiology Society (PACES), Heart Rhythm Society (HRS), American College of Cardiology Foundation (ACCF), et al. PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson- White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS). Heart Rhythm 2012; 9:1006. 16. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Heart Rhythm 2016; 13:e136. 17. Birnie DH, Sauer WH, Bogun F, et al. HRS expert consensus statement on the diagnosis and management of arrhythmias associated with cardiac sarcoidosis. Heart Rhythm 2014; 11:1305. 18. Saguner AM, Medeiros-Domingo A, Schwyzer MA, et al. Usefulness of inducible ventricular tachycardia to predict long-term adverse outcomes in arrhythmogenic right ventricular cardiomyopathy. Am J Cardiol 2013; 111:250. 19. Sroubek J, Probst V, Mazzanti A, et al. Programmed Ventricular Stimulation for Risk Stratification in the Brugada Syndrome: A Pooled Analysis. Circulation 2016; 133:622. 20. Zipes DP, Calkins H, Daubert JP, et al. 2015 ACC/AHA/HRS Advanced Training Statement on Clinical Cardiac Electrophysiology (A Revision of the ACC/AHA 2006 Update of the Clinical Competence Statement on Invasive Electrophysiology Studies, Catheter Ablation, and Cardioversion). J Am Coll Cardiol 2015; 66:2767. https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 17/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate 21. Narula OS, Cohen LS, Samet P, et al. Localization of A-V conduction defects in man by recording of the His bundle electrogram. Am J Cardiol 1970; 25:228. 22. Castellanos A Jr, Castillo CA, Agha AS. Symposium on Electophysiologic Correlates of Clinical Arrhythmias. 3. Contribution of His bundle recordings to the understanding of clinical arrhythmias. Am J Cardiol 1971; 28:499. 23. Benditt DG, Klein GJ, Kriett JM, et al. Enhanced atrioventricular nodal conduction in man: electrophysiologic effects of pharmacologic autonomic blockade. Circulation 1984; 69:1088. 24. Amat-y-Leon F, Dhingra R, Denes P, et al. The clinical spectrum of chronic His bundle block. Chest 1976; 70:747. 25. Bharati S, Lev M, Wu D, et al. Pathophysiologic correlations in two cases of split His bundle potentials. Circulation 1974; 49:615. 26. Kupersmith J, Krongrad E, Waldo AL. Conduction intervals and conduction velocity in the human cardiac conduction system. Studies during open-heart surgery. Circulation 1973; 47:776. 27. Dhingra RC, Palileo E, Strasberg B, et al. Significance of the HV interval in 517 patients with chronic bifascicular block. Circulation 1981; 64:1265. 28. Scheinman MM, Peters RW, Suav MJ, et al. Value of the H-Q interval in patients with bundle branch block and the role of prophylactic permanent pacing. Am J Cardiol 1982; 50:1316. 29. Josephson ME. Intraventricular Conduction Disturbances. In: Clinical Cardiac Electrophysiolo gy. Techniques and Interpretations, 3rd ed, Josephson ME (Ed), Lippincott, Philadelphia 200 2. p.110. 30. McAnulty JH, Rahimtoola SH, Murphy E, et al. Natural history of "high-risk" bundle-branch block: final report of a prospective study. N Engl J Med 1982; 307:137. 31. Strauss HC, Bigger JT, Saroff AL, Giardina EG. Electrophysiologic evaluation of sinus node function in patients with sinus node dysfunction. Circulation 1976; 53:763. 32. Narula OS, Shantha N, Vasquez M, et al. A new method for measurement of sinoatrial conduction time. Circulation 1978; 58:706. 33. Cramer M, Hariman RJ, Boxer R, Hoffman BF. Electrograms from the canine sinoatrial pacemaker recorded in vitro and in situ. Am J Cardiol 1978; 42:939. 34. Cramer M, Siegal M, Bigger JT Jr, Hoffman BF. Characteristics of extracellular potentials recorded from the sinoatrial pacemaker of the rabbit. Circ Res 1977; 41:292. 35. Gomes JA, Kang PS, El-Sherif N. The sinus node electrogram in patients with and without sick sinus syndrome: techniques and correlation between directly measured and indirectly estimated sinoatrial conduction time. Circulation 1982; 66:864. https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 18/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate 36. Hariman RJ, Krongrad E, Boxer RA, et al. Method for recording electrical activity of the sinoatrial node and automatic atrial foci during cardiac catheterization in human subjects. Am J Cardiol 1980; 45:775. 37. Reiffel JA, Bigger JT Jr. Current status of direct recordings of the sinus node electrogram in man. Pacing Clin Electrophysiol 1983; 6:1143. 38. Reiffel JA, Gang E, Gliklich J, et al. The human sinus node electrogram: a transvenous catheter technique and a comparison of directly measured and indirectly estimated sinoatrial conduction time in adults. Circulation 1980; 62:1324. 39. Dhingra RC, Wyndham C, Amat-Y-Leon, et al. Sinus nodal responses to atrial extrastimuli in patients without apparent sinus node disease. Am J Cardiol 1975; 36:445. 40. Strauss HC, Saroff AL, Bigger JT Jr, Giardina EG. Premature atrial stimulation as a key to the understanding of sinoatrial conduction in man. Presentation of data and critical review of the literature. Circulation 1973; 47:86. 41. Rakovec P, Jakopin J, Rode P, et al. Clinical comparison of indirectly and directly determined sinoatrial conduction time. Am Heart J 1981; 102:292. 42. Heddle, W, Dorveaux, et al. Use of rapid atrial pacing to assess sinus node function. Clin Prog Electrophysiol Pacing 1985; 3:299. 43. Josephson ME. Sinus Node Dysfunction. In: Clinical Cardiac Electrophysiology. Techniques an d Interpretations, 3rd ed, Josephson ME (Ed), Lippincott, Philadelphia 2002. p.68. 44. Wellens HJ, Brugada P, B r FW. Indications for use of intracardiac electrophysiologic studies for the diagnosis of site of origin and mechanism of tachycardias. Circulation 1987; 75:III110. 45. Brugada P, Farr J, Green M, et al. Observations in patients with supraventricular tachycardia having a P-R interval shorter than the R-P interval: differentiation between atrial tachycardia and reciprocating atrioventricular tachycardia using an accessory pathway with long conduction times. Am Heart J 1984; 107:556. 46. Denes P, Wu D, Amat-y-Leon F, et al. The determinants of atrioventricular nodal re-entrance with premature atrial stimulation in patients with dual A-V nodal pathways. Circulation 1977; 56:253. 47. Yu WC, Chen SA, Chiang CE, et al. Effects of isoproterenol in facilitating induction of slow- fast atrioventricular nodal reentrant tachycardia. Am J Cardiol 1996; 78:1299. 48. Josephson ME, Caracta AR, Ricciutti MA, et al. Electrophysiologic properties of procainamide in man. Am J Cardiol 1974; 33:596. https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 19/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate 49. Tonkin AM, Heddle WF, Tornos P. Intermittent atrioventricular block: procainamide administration as a provocative test. Aust N Z J Med 1978; 8:594. 50. Akhtar M, Damato AN, Caracta AR, et al. Electrophysiologic effects of atropine on atrioventricular conduction studied by His bundle electrogram. Am J Cardiol 1974; 33:333. 51. Dimarco JP, Garan H, Ruskin JN. Complications in patients undergoing cardiac electrophysiologic procedures. Ann Intern Med 1982; 97:490. 52. Horowitz LN, Kay HR, Kutalek SP, et al. Risks and complications of clinical cardiac electrophysiologic studies: a prospective analysis of 1,000 consecutive patients. J Am Coll Cardiol 1987; 9:1261. 53. Haines DE, Beheiry S, Akar JG, et al. Heart Rythm Society expert consensus statement on electrophysiology laboratory standards: process, protocols, equipment, personnel, and safety. Heart Rhythm 2014; 11:e9. Topic 980 Version 32.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 20/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate GRAPHICS Revised (2018) Vaughan Williams classification of antiarrhythmic drugs abridged table Class 0 (HCN channel blockers) Ivabradine Class I (voltage-gated Na+ channel blockers) Class Ia (intermediate dissociation): Quinidine, ajmaline, disopyramide, procainamide Class Ib (rapid dissociation): Lidocaine, mexilitine Class Ic (slow dissociation): Propafenone, flecainide Class Id (late current): Ranolazine Class II (autonomic inhibitors and activators) Class IIa (beta blockers): Nonselective: carvedilol, propranolol, nadolol Selective: atenolol, bisoprolol, betaxolol, celiprolol, esmolol, metoprolol Class IIb (nonselective beta agonists): Isoproterenol Class IIc (muscarinic M2 receptor inhibitors): Atropine, anisodamine, hyoscine, scopolamine Class IId (muscarinic M2 receptor activators): Carbachol, pilocarpine, methacholine, digoxin Class IIe (adenosine A1 receptor activators): Adenosine Class III (K+ channel blockers and openers) Class IIIa (voltage dependent K+ channel blockers): https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 21/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Ambasilide, amiodarone, dronedarone, dofetilide, ibutilide, sotalol, vernakalant Class IIIb (metabolically dependent K+ channel openers): Nicorandil, pinacidil Class IV (Ca++ handling modulators) Class IVa (surface membrane Ca++ channel blockers): Bepridil, diltiazem, verapamil Class IVb (intracellular Ca++ channel blockers): Flecainide, propafenone Class V (mechanosensitive channel blockers): No approved medications Class VI (gap junction channel blockers) No approved medications Class VII (upstream target modulators) Angiotensin converting enzyme inhibitors Angiotensin receptor blockers Omega-3 fatty acids Statins HCN: hyperpolarization-activated cyclic nucleotide-gated; Na: sodium; K: potassium; Ca: calcium. Graphic 120433 Version 3.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 22/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Options for hands-free pacemaker/defibrillator pad positioning Positioning options for hands-free pacemaker/defibrillator pads showing anterior/lateral positioning (left) and anterior/posterior positioning (right). Graphic 103268 Version 2.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 23/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Normal intracardiac electrograms obtained during invasive electrophysiologic study (EPS) The normal intracardiac electrograms, during sinus rhythm, obtained during an electrophysiologic study are shown. Three surface electrocardiogram (ECG) leads are monitored (I, aVF, and V1); intracardiac electrograms are obtained from the high right atrium (HRA); the proximal (p), mid (m), and distal (d) bundle of His (HBE); the p, m, and d coronary sinus (CS); and right ventricular apex (RVA). For an ablation procedure, an exploratory catheter (exp) is also used for more extensive mapping. The electrogram obtained includes those from the atrium (A), bundle of His (H), and ventricle (V). Graphic 64875 Version 4.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 24/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Electrophysiologic study (EPS) in advanced conduction disease showing intra-Hisian block The tracing, obtained during an electophysiologic study, records three surface electrocardiogram (ECG) leads (1, 2, and V1) and the bundle of His electrogram (HBE). The first two sinus beats (SB) are conducted normally from the atrium to the ventricle, but the HBE manifests a split bundle of His electrograms (H and H'). The proximal component (H) is present following a nonconducted P wave (P*), but the distal bundle of His (H') is not activated. The level of atrioventricular block is sharply defined as being intra-Hisian, indicating advanced conduction system disease. A: atrial electrogam; V: ventricular electrogram. Graphic 80538 Version 7.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 25/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Electrophysiology study (EPS) tracings used in the determination of the corrected sinus node recovery time (SNRT) This tracing is from a 76-year-old male with paroxysmal atrial fibrillation and recurrent near syncope associated with palpitations. Surface leads represented are I, II, III, V1, and V6. Intracardiac tracings shown are the high right atrium (HRA d), the proximal His bundle electrogram (HIS p), the mid His bundle electrogram (HIS m), the distal His bundle electrogram (HIS d), and the right ventricular apex (RVa d). High right atrial pacing at 400 milliseconds (150 beats per minute) is performed for 30 seconds. Upon termination of pacing, a sinus node recovery time of 2150 milliseconds is observed (arrow). The basal sinus cycle length was 1200 milliseconds, giving a corrected sinus node recovery time of 950 milliseconds, consistent with severe sinus node dysfunction. Note the significant secondary pause extending beyond the end of the tracing providing additional evidence of sinus node dysfunction. ms: milliseconds. Courtesy of Joseph J Germano, DO. Graphic 58763 Version 5.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 26/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Initiation and termination of an atrioventricular reentrant tachycardia captured during invasive electrophysiology studies (EPS) During atrial pacing (S1), a premature atrial beat (S2) is blocked antegradely in the accessory pathway and conducts through the atrioventricular node with a long delay (A2H2 interval), which allows for the recovery of the accessory pathway before retrograde conduction (panel A). The mechanism is an orthodromic atrioventricular reentrant tachycardia (AVRT) using a left- sided pathway, suggested by the atrial activation sequence; earliest retrograde atrial activation during the first echo beat of AVRT (Ae) is in the https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 27/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate mid coronary sinus (CSm). A single ventricular premature beat (VPB) terminates the AVRT (panel B). The VPB conducts to the left atrium but encounters the refractory period of the AV node and is blocked, interrupting conduction in the antegrade limb and terminating the arrhythmia. V: ventricular electrogram; A: atrial electrogram; NSR: normal sinus rhythm; d: distal; p: proximal. Graphic 81938 Version 7.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 28/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Electrophysiology study (EPS) tracing during mapping of atrial tachycardia Shown are three surface electrocardiogram (ECG) leads (I, aVF, V1) and intracardiac recordings from the high posterior right atrium (HRA); posterior left atrium (USER1 and USER 3); proximal, mid, and distal coronary sinuses (CS9-10, CS5-6, CS1-2); and right ventricular apex (RVA). The patient had an incessant atrial tachycardia and dilated cardiomyopathy (left ventricular ejection fraction 9 percent) referred for cardiac transplant evaluation. The P wave (*) falls at the end of the T wave in the surface ECG; its onset is difficult to discern. However, the intracardiac electrograms demonstrate obvious atrial (A) and ventricular (V) activity. Activation mapping involves positioning the mapping catheters in the right (HRA) and left atria (USER) to record earliest electrical activity during the tachycardia. The left atrial catheter records earlier electrical activity (arrow) than the right atrial catheter, but the timing with respect to the surface P wave is obscured because of the T wave of the preceding QRS complex. Graphic 58120 Version 7.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 29/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Electrophysiology study (EPS) tracing showing the effects of procainamide on an abnormal His-Purkinje conduction system These tracings were taken from a 58-year-old male with syncope. The baseline 12-lead electrocardiogram demonstrated sinus rhythm with prolonged atrioventricular (AV) conduction and a left bundle branch block with left axis deviation. Surface leads represented are I, II, III, and V1. Intracardiac tracings shown are the high right atrium (HRA), the distal His bundle electrogram (HIS d), the proximal His bundle electrogram (HIS 2), and the right ventricular apex (RVa). The left side of Panel A shows a baseline HV interval of 68 milliseconds. The right side of Panel A demonstrates prolongation of the HV interval to 100 milliseconds after the administration of procainamide indicating severe His-Purkinje conduction disease. Panel B (same lead schema) demonstrates high right atrial pacing at 400 milliseconds (150 beats per minute) with infra-Hisian block (arrow) after the administration of procainamide, confirming severe His-Purkinje disease. A: atrial depolarization; H: His bundle depolarization; msec: milliseconds; V: ventricular depolarization. Courtesy of Joseph J Germano, DO. Graphic 56786 Version 5.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 30/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Complications of invasive cardiac electrophysiology studies Associated with percutaneous catheterization of veins and arteries Pain Adverse drug reaction Infection/abscess at the catheterization site, sepsis Excessive bleeding, hematoma formation Thrombophlebitis Pulmonary thromboembolism Arterial damage, aortic dissection Systemic thromboembolism Transient ischemic attack/stroke Associated with intracardiac catheters and programmed cardiac stimulation Cardiac chamber or coronary sinus perforation Hemopericardium, cardiac tamponade Atrial fibrillation Ventricular tachycardia/ventricular fibrillation Myocardial infarction Right or left bundle branch block Associated with transcatheter ablation Complete heart block Thromboembolism Vascular access problems (bleeding, infection, hematoma, vascular injury) Cardiac trauma (myocardial perforation, tamponade, valvular damage) Coronary artery thrombosis/myocardial infarction Cardiac arrhythmias Pericarditis Pulmonary vein stenosis Phrenic nerve paralysis Radiation skin burns Possible late malignancy Atrioesophageal fistula https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 31/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Death resulting from one of the above complications Graphic 63157 Version 4.0 https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 32/33 7/5/23, 10:46 AM Invasive diagnostic cardiac electrophysiology studies - UpToDate Contributor Disclosures Munther K Homoud, MD Speaker's Bureau: Abbott [Live heart dissection]. All of the relevant financial relationships listed have been mitigated. Bradley P Knight, MD, FACC Grant/Research/Clinical Trial Support: Abbott [Electrophysiology]; Atricure [Electrophysiology]; Biosense Webster [Electrophysiology]; Biotronik [Electrophysiology]; Boston Scientific [Electrophysiology]; BSCI [Electrophysiology]; MDT [Electrophysiology]; Philips [Electrophysiology]. Consultant/Advisory Boards: Abbott [Electrophysiology]; Atricure [Electrophysiology]; Biosense Webster [Electrophysiology]; Biotronik [Electrophysiology]; Boston Scientific [Electrophysiology]; BSCI [Electrophysiology]; CVRx [Heart failure]; MDT [Electrophysiology]; Philips [Electrophysiology]; Sanofi [Arrhythmias]. Speaker's Bureau: Abbott [Electrophysiology]; Biosense Webster [Electrophysiology]; Biotronik [Electrophysiology]; Boston Scientific [Transeptal catheterization]; BSCI [Electrophysiology]; MDT [Electrophysiology]. All of the relevant financial relationships listed have been mitigated. Nisha Parikh, MD, MPH No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. Conflict of interest policy https://www.uptodate.com/contents/invasive-diagnostic-cardiac-electrophysiology-studies/print 33/33