![ELECTRODE CATHETER
PLACEMENT
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).](https://image.slidesharecdn.com/basicsofelectrophysiology-191013202607/85/Basics-of-electrophysiology-20-320.jpg)
Basics of electrophysiology
- 1. BASICS OF ELECTROPHYSIOLOGY PRESENTOR- DR PINKESH PARMAR MODERATOR- DR KAMAL H SHARMA
- 2. INTRODUCTION Invasive cardiac electrophysiology (EP) is a collection of clinical techniques for the investigation and treatment of cardiac rhythm disorders. Electrophysiology (EP) study can accomplish the following goals. • Make a completely accurate diagnosis of an arrhythmia • Establish the etiology for syncope/palpitations • Evaluate prognosis and stratify risk of sudden cardiac death in patients at risk • Guide antiarrhythmic drug therapy • Evaluate the requirement, feasibility or outcome of non pharmacologic therapy (e.g. Pacemaker, radiofrequency ablation, antiarrhythmic surgery, or implantable cardiac defibrillator).
- 3. INDICATIONS The indications for invasive EP studies can be broken down to two categories: diagnostic and risk stratification. Diagnostic indications can be divided into : Bradyarrhydhmias Tachyarrhydhmias Syncope of unknown etiology
- 4. DIAGNOSTIC INDICATIONS Syncope when an individual is suspected of having sick sinus syndrome, based on inappropriate sinus bradycardia. The detection of a prolonged corrected sinus node recovery time may predict future recurrence of syncope Syncope in patients with bifascicular block (left or right bundle branch block and hemifascicular block). The induction of infra-Hisian block in patients with bifascicular block can predict future adverse cardiovascular events. To determine the site of block in patients with abnormal atrioventricular conduction
- 5. DIAGNOSTIC INDICATIONS Patients with wide complex tachyarrhythmias in whom a diagnosis cannot be established by noninvasive means or who are suspected of harboring a life-threatening arrhythmia should undergo EP studies.
- 6. DIAGNOSTIC INDICATIONS Syncope in patients with ischemic heart disease or other structural heart disease. Syncope immediately following palpitations Syncope in patients who are employed in high-risk occupations (eg, airline pilots, school bus drivers, police officers) after failure of all noninvasive diagnostic tools to arrive at a cause. Unexplained syncope In survivors of sudden cardiac death (SCD) with no established cause (idiopathic VF), an EP study is considered a step in the diagnostic cascade recommended to try to establish a diagnosis
- 7. RISK STRATIFICATION In the primary prevention of SCD, patients with an ischemic cardiomyopathy due to a prior myocardial infarction and who have left ventricular ejection fraction (LVEF) <40 percent should undergo ambulatory cardiac rhythm monitoring. EP studies are indicated if they are found to have nonsustained VT. The induction of sustained VT or VF constitutes a class I indication for the implantation of an ICD
- 8. RISK STRATIFICATION Atrioventricular (AV) conduction abnormalities below the level of the AV node may progress to complete AV block with catastrophic consequences. 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
- 9. RISK STRATIFICATION Asymptomatic young (8 to 21 years) patients with electrocardiographic manifestations of preexcitation 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.
- 10. RISK STRATIFICATION The role of EP studies in the Brugada syndrome is controversial. Patients with the Brugada syndrome who have had a history of syncope or have survived SCD are more likely to be inducible. However, the role of EP studies in predicting future events is controversial. The implantation of an ICD may be considered in a patient with Brugada syndrome who is induced into VF.
- 11. RISK STRATIFICATION For purposes of risk stratification for SCD, programmed electrical stimulation can be considered (a class IIa indication) in patients with cardiac sarcoidosis and an LVEF >35 percent despite optimal medical therapy and immunosuppression For purposes of risk stratification for SCD, programmed electrical stimulation is occasionally used in asymptomatic patients with arrhythmogenic right ventricular cardiomyopathy
- 12. RISK STRATIFICATION In the risk stratification of adults with tetralogy of Fallot with risk factors for SCD, such as left ventricular systolic and diastolic dysfunction, QRS ≥180 milliseconds, extensive right ventricular scarring, and nonsustained VT. It 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. 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 of SCD and may benefit from an ICD (class IIa indication)
- 13. CONTRAINDICATIONS Bleeding disorder Unstable angina Uncontrolled congestive heart failure Uncooperative patient Severe peripheral vascular disease Valvular or sub valvular stenosis (LV access) Thrombophlebitis (femoral access) Groin infection Bilateral amputee (femoral access)
- 14. 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. 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.
- 15. PREPROCEDURAL EVALUATION 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.
- 16. PREPARATION AND MONITORING 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. Standard cardiorespiratory monitoring should include blood pressure (noninvasively or via arterial monitoring), pulse, oxygen saturation, and cardiac telemetry.
- 17. PREPARATION AND MONITORING Defibrillation pads should be placed on the patient prior to beginning the procedure. 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).
- 18. VASCULAR ACCESS 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.
- 19. EP EQUIPMENT Programmable stimulator Multichannel lead switching box (junction box) Electrode catheters Ablation system –Generator, Irrigation Pump, Remote Panel, Cables, Tubing 3D Navigational Mapping System
- 20. ELECTRODE CATHETER PLACEMENT 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).
- 21. ELECTRODE CATHETER PLACEMENT 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.
- 22. ELECTRODE CATHETER PLACEMENT 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.
- 24. ELECTROCARDIOGRAPHIC AND ELECTROPHYSIOLOGIC 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
- 25. ELECTROCARDIOGRAPHIC AND ELECTROPHYSIOLOGIC RECORDINGS 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 stimulation 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.
- 26. ELECTROCARDIOGRAPHIC AND ELECTROPHYSIOLOGIC RECORDINGS 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.
- 27. ELECTROCARDIOGRAPHIC AND ELECTROPHYSIOLOGIC RECORDINGS The next is a recording from a right ventricular apex (RVA) electrode catheter. 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.
- 29. 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
- 30. AH INTERVAL Short AH intervals 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 interval 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
- 31. 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
- 32. 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)
- 33. HV INTERVAL A prolonged HV interval is consistent with diseased distal conduction in all fascicles. 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. 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.
- 35. 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.
- 36. SINOATRIAL CONDUCTION TIME Sinus nodal (SN) function is assessed by sinoatrial conduction time and sinus nodal recovery time. Measuring Sino-atrial conduction time (SACT) involves placement of a catheter near the sinus node from which progressively premature atrial extra stimuli are introduced after every eighth to tenth beat of either a stable sinus rhythm (Strauss method) , or atrial pacing for 8 beats is done at a rate just lower than the sinus rate (Narula method). The difference of time of the recovery beat post pacing versus that of the sinus cycle length gives us 2 times the SACT value. Interval of upto 250 msec is considered normal.
- 37. SINOATRIAL CONDUCTION TIME Due to the limitations of indirect methods in assessing the SACT, techniques for direct recording of the sinus electrogram (EGM) have been developed. 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. Studies have shown a good correlation between indirect and direct methods of measuring SACT. However, SACT is a relatively insensitive test for SA node dysfunction.
- 38. 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. It is important to wait at least one minute between pacing sequences to allow full recovery of the SN.
- 39. SINUS NODE RECOVERY TIME 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. A total recovery time (TRT) can also be calculated, which is the time required to return to the basal sinus rate.
- 40. SINUS NODE RECOVERY TIME Normal values have generally been estimated as follows: 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.
- 42. PES 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.
- 43. VENTRICULAR PACING Normally during ventricular pacing the impulse travels retrograde into the atrium through the AV node. VA dissociation is referred when while pacing the ventricle, no impulse travels back to the atrium. Ventricular pacing is then done at decreasing cycle length till VA conduction is blocked. Thereafter ventricular extra stimuli (single or multiple) are given at decreasing interval till a VA block is obtained (Figure 5 b). During ventricular pacing atrial activation pattern whether central (His A is earliest) or eccentric (His A is later that A in either RA or LA recording catheter) is seen.
- 44. VENTRICULAR PACING Lengthening of VA interval with decrement in the stimulus interval suggests decremental conduction. Central and decremental conduction generally suggests conduction through the nodal tissue (Figure 5a). Eccentric and non-decremental conduction suggests presence of a retrograde conducting accessory pathway (Figure 5c). Multiple (3 to 5) ventricular extrastimuli may be needed to induce ventricular arrhythmia sometimes.
- 48. ATRIAL PACING Atrial pacing from either the right atrium or the left atrium as clinically indicated is done to see for antegrade conduction characteristics through the AV node. In presence of WPW syndrome, there can be eccentric activation with increasing preexcitation which can be easily appreciated on a 12 lead electrocardiogram during the study. Atrial extra-stimuli are then given (single and if required multiple).
- 49. ATRIAL PACING Atrial extra stimuli may show an AH jump (wherein there is AH prolongation of more than 50 msec with a decrement of 10 msec on atrial extra-stimuli interval), induce a tachycardia or bring out preexcitation with or without decremental antegrade conduction with a preexcited QRS complex.
- 50. TACHYCARDIA STUDY Once tachycardia is induced relationship of the atrium and ventricular signals are noted. 1:1 AV activation generally suggests AVNRT (Figure 7a), AVRT (Figure 7b) and atrial tachycardia but rarely ventricular tachycardia (VT). A>V suggests atrial tachycardia and rarely AVNRT but never an AVRT or VT. V>A suggests ventricular tachycardia (Figure 7c). During SVT atrial activation patterns helps to diagnose the nature of tachycardia (Figure 7a and b).
- 56. PACING MANEUVERS DURING TACHYCARDIA Continuous pacing at a slightly faster than that of the tachycardia (Figure 8a) or programmed single extra-stimuli when the His is refractory (Figure 8b), can be used to differentiate the mechanism of arrhythmia.
- 59. MAPPING FOR LOCALIZING SITE OF ABLATION In many cases, catheter ablation immediately follows the diagnostic electrophysiologic study. 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.
- 60. MAPPING FOR LOCALIZING SITE OF ABLATION Activation mapping: - Where the activation signal in the mapping catheter shows earlier signals as compared to the surface P/QRS (Figure 9a) suggests the area to be near the origin of the arrhythmia and suggests an appropriate site for treatment. Pace-mapping: - In a patient especially with ventricular tachycardia, pacing at the same cycle length as the tachycardia from the mapping catheter and comparing the 12 lead ECG obtained during pacing with that of tachycardia is called pace-mapping. If there is a 12/12 match it suggests the origin of the tachycardia to be nearby (Figure 9b) and is especially helpful for treatment of idiopathic ventricular outflow tachycardias.
- 63. COMPLICATIONS reported complication rates of approximately 2 percent 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
- 64. THANK