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Basic EP Study
- 1. Electrophysiology Study (EPS) Maruli Butarbutar, MD
- 2. Definition & Indications • Electrophysiology study (EPS) involves the placement of multipolar electrode catheters in specific locations in the heart in order to: • Assess the conduction system of the heart, including SA node, AV node and HPS • Determine the location and characteristics of arrhythmias and the type of therapy required • Evaluate the efficacy of therapies involving antiarrhythmic drugs and devices. • Indications: • Supraventricular tachycardia (SVT): Narrow QRS complex SVT, Wide QRS complex SVT • Ventricular tachycardia (VT): Non-sustained VT, Sustained monomorphic VT, Polymorphic VT, PVC • Sinus node dysfunction: Sinus bradycardia, Sinoatrial block, Sinus arrest, Chronotropic incompetence, Sinus pause. • Conduction abnormalities: AV block, Bundle branch block/bi-, tri- fascicular block, intraventricular conduction disease • Evaluation of syncope: the most common indication of EPS; may be caused by AV block or SND • Other indications
- 3. Patient Preparations • Informed consent: • Vascular complications: bruising with palpable hematomas, venous thrombosis, arterial occlusion, formation of fistulae or false aneurysm • Major but treatable conditions: pneumothorax, cardiac tamponade • Specific complications: AV nodal damage, arrhythmia induction • Thromboembolic complications • Radiation exposure • Patient preparations: • Antiarrhythmic drugs should be discontinued for at least four half lives (2-3 days) • Fasting at least 6 hours, and usually overnight • IV access and 12-leads ECG should be obtained before procedure
- 6. Minimum Protocol for Diagnostic EPS • Basic intervals • Measurement: rhythm, cycle length (CL), PA int., AH int., HV int., QRS dur. & morph., QTc int. • SA node function • Assessment of SNRT at basic CLs of 800, 600, 500, 400 and 350 ms • Measurement: CSRNT • Atrial extra stimulus pacing • Assessment of refractoriness at CLs of 600 and 400 ms • Measurements: AVN ERP, AVN FRP, AERP • It can also assess dual AV nodal physiology, ventricular pre-excitation dan may induce atrial arrhythmia • Atrial incremental pacing • Incremental atrial pacing from slightly faster than sinus rhythm down to AV Wenckebach point, or a minimum CL of 300 ms • Measurement: AV WCL • Ventricular extra stimulus pacing • Assessment of refractoriness at CLs of 600 and 400 ms • Measurement: VERP, retrograde AVN ERP • It can also assess retrograde conduction and atrial activation and may induce VT • Ventricular incremental pacing • Incremental atrial pacing from slightly faster than sinus rhythm down to VA Wenckebach point, or a minimum CL of 300 ms • Measurement: VA WCL (only if VA conduction is present)
- 7. Variations on the Minimum Protocols • Suspected sinus node disease • Measurement of SACT • Suspected ventricular tachycardia • Programmed ventricular stimulation using multiple extra stimuli (short- long-short induction sequences) • Suspected AV nodal reentry or atrial arrhythmias • Intravenous isoproterenol and/or atropine • Atrial extra stimulus testing at different cycle lengths, using double, triple or more atrial extra stimuli • Suspected accessory pathway • Intravenous isoproterenol and/or atropine may facilitate tachycardia induction, usually by improving conduction over the AVN • Pacing at sites other than HRA or RVA may demonstrate the presence of APs • Pacing and drug administration during tachycardia
- 11. SA Node Function: SNRT & CSNRT
- 13. SA Node Function: SACT
- 14. Refractory Periods: ERP, RRP, FRP • The refractoriness of a cardiac tissue can be defined by the response of that tissue to the introduction of premature stimuli. • Refractoriness is generally expressed in terms of three measurements • Effective refractory period (ERP) • Relative refractory period (RRP) • Functional refractory period (FRP)
- 18. Antegrade & Retrograde Refractory Periods ERP of the atrium: the longest S1-S2 interval that fails to result in atrial depolarization ERP of the AVN: the longest A1-A2 interval measured in the His bundle electrogram that fails to propagate to the His bundle ERP of the HPS: the longest H1-H2 interval that fails to result in ventricular depolarization RRP of the atrium: the longest S1-S2 interval at which the S2-A2 interval exceeds the S1-A1 interval (latency) RRP of the AVN: the longest A1-A2 interval at which the A2-H2 interval exceeds the A1-H1 interval RRP of the HPS: the longest H1-H2 interval at which the H2-V2 interval exceeds the H1-V1 interval or results in an aberrant QRS complex FRP of the atrium: the shortest A1-A2 interval in response to any S1-S2 interval FRP of the AV node: the shortest H1-H2 interval in response to any A1-A2 interval FRP of the HPS: the shortest V1-V2 interval in response to any H1-H2 interval ERP of the ventricle: the longest S1-S2 interval that fails to evoke a ventricular response ERP of the HPS: the longest S1-S2 or V1-V2 interval at which S2 or V2 blocks below the bundle of His. ERP of the AVN: the longest S1-H2 or H1-H2 interval at which H2 fails to propagate to the atrium RRP of the ventricle: the longest S1-S2 interval at which the S2-V2 interval exceeds the S1-V1 interval. FRP of the ventricle: the shortest V1-V2 interval as measured on the surface ECG or local ventricular electrogram in response to any S1-S2 interval FRP of the HPS: the shortest S1-H2 or H1-H2 interval in response to any V1-V2 interval FRP of the AVN: the shortest A1-A2 interval in response to any H1-H2 interval Antegrade Refractory Periods Retrograde Refractory Periods
- 19. Atrial Extra Stimulus Pacing: AVN ERP
- 20. Atrial Extra Stimulus Pacing: Dual AV nodal physiology • Dual or multiple AV nodal pathways can be demonstrated in 7% of the population. • Fast pathway is associated with rapid conduction (short AH interval) and a long refractory period. • Slow pathway is associated with a slow conduction (long AH interval) and a shorter refractory period. • Conduction switches (“jump”) to the slow pathway when the fast pathway reaches its refractory period. • With the introduction of premature atrial stimuli, a jump from the fast to the slow pathway is defined by a ≥50 msec increase in the A2-H2 interval in response to a 10 msec decrease in the A1-A2 coupling interval
- 21. Atrial Extra Stimulus Pacing: Ventricular Preexcitation
- 22. Atrial Incremental Pacing: AV WCL
- 23. Ventricular Extra Stimulus Pacing
- 24. Ventricular Extra Stimulus Pacing
- 25. Ventricular Extra Stimulus Pacing
- 26. Ventricular Extra Stimulus Pacing
- 27. Ventricular Extra Stimulus Pacing
- 28. Retrograde Conduction & Atrial Activation
- 29. Ventricular Incremental Pacing: VA WCL
Editor's Notes
- Other indications for EPS include patients with progressive cardiac conduction disease, dilated cardiomyopathy, muscular dystrophies (Duchenne, Becker), post antiarrhythmic surgery, sarcoidosis, congenital heart disease, survivors of cardiac arrest, undocumented palpitations, guiding drug therapy, conduction disorders after transcatheter aortic valve replacement.
- Catheters with multiple (4 to 64) platinum electrodes through which electrical stimuli can be delivered and intracardiac electrograms recorded are advanced through one or more veins (typically the inferior vena cava [IVC] or superior vena cava [SVC]) for mapping RA, RV, LA and LV; or retrogradely through the aorta (transaortic approach) for mapping the LV and mitral annulus (for VT and left-sided BTs); or transeptal approach for mapping and ablation in the LA and has also been increasingly used for accessing the LV.. During a basic diagnostic EP study, catheters are placed in the right atrium (usually right atrial appendage [RAA]), across the tricuspid annulus to record a His bundle electrogram, in the coronary sinus (CS), and in the right ventricle. HRA - SA node (near junction of SVC) His - for recording and marking AV node CS - for recording/pacing; records left atrial activity and activity from the base of the left ventricle. RVA - for recording/pacing
- Measurement of basic intervals establishes whether a long PR interval is due to slow conduction in the AVN or HPS (or both), and may indicate whether a short PR interval is due to ventricular pre-excitation Atrial extra stimulus pacing can also assess dual AV nodal physiology, ventricular pre-excitation dan atrial arrhythmia induction. Eccentric retrograde atrial activation or VA conduction that is non-decremental or shows discontinuity may indicate the presence of an accessory pathway or dual AV nodal physiology.
- Baseline recordings obtained during a typical electrophysiological study include surface electrocardiograms to time events from the body's surface, and intra-cardiac electrograms, all of which are recorded simultaneously. The intracardiac recordings obtained from the electrodes are sharper unlike the waveforms of the surface ECG. Typical electrograms of the high right atrium electrode will show a sharp deflection in the early part of the P wave. Recording from the His electrode shows an A (Atrial) signal, a H (His) signal and a V (Ventricular) signal. As the coronary sinus is in the left AV groove, a coronary sinus catheter records both the left atrial and left ventricular electrograms. Activation of the left atrium at the CS ostium (CSP) electrode is normally earlier than at the CS distal (CSD) electrode. RV catheter records ventricular signals from the right ventricle.
- Pacing rate or heart rate (beats per minute) = 60,000/cycle length (msec) QRS complex indicates the duration of ventricular activation. QT interval represents the combination of ventricular activation and repolarization, it depends on HR. QTc can be calculated using Bazett or Frederica formula. The specific intervals measured during sinus rhythm are: 1. PA interval: time for activation to travel into the right atrium between the region of the sinus node and the region of the atrioventricular node. This PA interval is measured between the earliest recorded atrial activity in any channel (either the P-wave onset, or that of the earliest atrial electrogram) and the rapid deflection of the atrial electrogram on the His bundle catheter. The standard value is considered 25-55 ms. A prolonged PA interval indicates delay in intra-atrial conduction, usually due to atrial disease or drugs. 2. AH interval: time for activation to travel over the AVN; is measured between atrial electrogram recorded on His bundle catheter and the beginning of the His electrogram itself. The normal value is 55-125 ms. Causes of prolonged AH interval: increased vagal tone (prolonged AH interval in well sedated patient use atropine to confirm), decreased cycle length (due to its decremental conduction properties related to Ca2+ phase 0 depolarization in AVN), infectious processes such as Lyme disease, antiarrhythmic medications, infarction (inferior myocardial infarction [MI]), or fibrocalcific degeneration. Causes of shortened AH interval: heightened sympathetic tone, conduction over a fast pathway in an individual with dual AV nodal pathways, a bypass tract (BT) between the atrium and His bundle (i.e., atrio-His bypass tract/James fiber). 3. HBE duration: the duration from the beginning to the last component of the His bundle electrogram. It corresponds to the total conduction time through the His Bundle. The standard value is under 30 ms. Conduction delay in His bundle manifests as a notched/fragmented deflection or split HBE with separated early and late components. 4. HV interval: the conduction time over the specialized ventricular conduction system, His-Purkinje system (HPS); it gets measured between the His bundle electrogram and the earliest ventricular activation. The standard value is 35-55 ms. It is not affected with autonomic tone or varied cycle length [HPS does not have decremental conduction properties (due to Na+ dependent phase 0 depolarization)]. Causes of prolonged HV interval: degenerative fibrocalcific disease (Lyme disease, aortic & mitral annular calcification), infiltrative processes, surgery or antiarrhythmic drugs. Causes of shortened HV interval: a bypass tract (BT) between the atrium and ventricle (i.e., atrio-ventricular bypass tract/Bundle of Kent), PVC (a fusion between supraventricular and ventricular impulse).
- Two tests of sinus node function are in common use: the sinus node recovery time (SNRT) & the sino-atrial conduction time (SACT) SNRT is a measure of the recovery of sinus node automaticity following overdrive suppression. The test is performed by pacing the atrium for at least 1 minute (or 30s) at multiple cycle lengths above the intrinsic sinus rate (basic CLs of 800, 600, 500, 400 and 350 ms). The sinus node is suppressed, and once pacing is stopped, the time required for sinus node automaticity to recover is measured. This is the most widely used electrophysiologic measure of sinus node function because it has correlated best with clinical evidence of sinus node dysfunction. The longest values of SNRT and CSNRT obtained are used. Normal values: maximum SNRT <1500 ms and maximum SNRT <550 ms (500-600 ms). However, SNRT varies with the sinus rate, so CNSRT is used. CSNRT = SNRT – SCL (Sinus cycle length). Figure 2.2. The sinus recovery time (SNRT) is the time taken for sinus rhythm (yellow) to resume after a period (conventionally 30s) of overdrive atrial pacing (blue).
- Four possibilities of atrial extrastimulus pacing to SA node: (i) No reset: a late coupled atrial extrastimulus (long A1A2) collides with a sinus impulse outside the SA node, and does not affect the timing of the next sinus beat (A3). Thus, the return cycle length (A2A3) is a full compensatory pause, such that A1A2 + A2A3 = 2 x A1A1 (SCL) (ii) Reset: an earlier coupled atrial extrastimulus (shorter A1A2) and resets the SA node. The next sinus beat originates one SCL later, and is conducted out to the atrium. Thus, A1A2 + A2A3 < 2x A1A1 and A2A3 = A1A1 + 2 x SACT. Therefore, SACT can be calculated (Reset is a must!) (iii) Interpolation: if its conduction into SA node is blocked, the SA node is not reset, and the next sinus impulse emerges on time. This extrastimulus is said to “interpolated” between sinus beats. Thus, A1A2 + A2A3 ~ A1A1 (iv) Echo: The extrastimulus may give rise to local “reentry”, resulting in a very premature A3. Thus, A1A2 + A2A3 < A1A1
- SACT is a test of sinus node function, which is performed with the introduction of premature atrial stimuli during sinus rhythm following an 8- to 10-beat stable drive train at a cycle length just shorter than sinus. This test assumes that the time required to enter the sinus node is equal to the conduction time out of the sinus node and back to the recording/stimulating catheter (may not be true). It is calculated by subtracting the baseline SCL or A1-A1 from the time it takes for the sinus node to recover from the premature stimulus (A2-A3) divided by two for the time in and out of the sinus node. SACT = [(A2−A3)−(A1−A1)]/2. Normal SACT value is between 50-115 ms “Reset” and “No Reset” criteria: (i) No reset: A1A2 + A2A3 = 2 x A1A1 (ii) Reset: A1A2 + A2A3 < 2x A1A1
- The refractoriness of a cardiac tissue can be defined by the response of that tissue to the introduction of premature stimuli. In clinical electrophysiology, refractoriness is generally expressed in terms of three measurements: effective, relative and functional. The refractory periods of the cardiac chambers and the components of the AV conduction system are evaluated by the technique of premature stimulation. Refractoriness is influenced by several factors including the intensity of the extrastimuli and the cycle length of the spontaneous or paced rate at which the refractory period is measured. There is a basic difference in the responses of myocardium and nodal tissue to increasing rate or increasing prematurity: in atrial or ventricular muscle there is a decrease in the refractory periods, in contrast to the AV node where there is an increase in refractory intervals and conduction time (decremental conduction). Refractory periods: 1. Effective refractory period (ERP) of a cardiac tissue is the longest coupling interval between the basic drive and the premature impulse that fails to propagate/be conducted through that tissue. The effective refractory period (ERP) of a tissue or structure is the longest coupling interval that fails to capture the tissue or be conducted over the structure. 2. Relative refractory period (RRP) is the longest coupling interval of a premature impulse that results in prolonged conduction of the premature impulse relative to that of the basic drive. The relative refractory period (RRP) is the ‘input’ interval to a tissue or structure at which the ‘output’ interval just begins to differ from the ‘input’ interval. 3. Functional refractory period (FRP) of a cardiac tissue is the minimum interval between two consecutively conducted impulses through that tissue. The functional refractory period (FRP) of a tissue or structure is the shortest ‘output’ coupling interval that can be elicited from a tissue or structure by any ‘input’ interval.
- By convention, the notation used is as follows: S1 is the basic stimulus and S2 is the first premature stimulus; S1-S1 is the paced cycle length; S1 –S2 is the coupling interval between the last complex of the paced cycle and the premature stimulus S2. The corresponding notations for the atrial, His-bundle, and ventricular electrograms are A1-A1 and A1-A2, H1-H1 and H1-H2, and V1-V1 and V1-V2, respectively.
- Decremental conduction of AVN is due Ca2+ dependent phase 0 depolarization (L-type Ca2+ ion channel is voltage-operated; activated by depolarization. Long-lasting activation. Inactivation is time-dependent and Ca2+-dependent).
- In patients with dual AV nodal pathways, conduction in the basal state occurs over the fast pathway in most circumstances (short or normal PR interval). Conduction switches to the slow pathway when the refractory period of the fast pathway is reached and a “jump” to the slow pathway results.
- Patient with a posteroseptal accessory pathway. During drive train (S1S1), there is pre-excitation with a slurred upstroke of the QRS complex. With the extrastimulus (S2), a greater degree of pre-excitation is seen due to delayed conduction of the AV node (Increased AH interval). Note that, stimulus-to-delta interval is unchanged.
- Wenckebach CL (WCL) is the cycle length at which 1:1 conduction over the AV node ceases. At CL 340 ms, there is prolongation of AH interval followed by a blocked cycle (*). Therefore AV WCL is 340 ms
- VERP and retrograde AVN ERP can be calculated Latency is a delay occur between the extrastimulus and the electrogram generated by the tissue because the extrastimulus is impinging on the refractory period of the adjacent myocardium.
- VERP and retrograde AVN ERP can be calculated Latency is a delay occur between the extrastimulus and the electrogram generated by the tissue because the extrastimulus is impinging on the refractory period of the adjacent myocardium.
- VERP and retrograde AVN ERP can be calculated Latency is a delay occur between the extrastimulus and the electrogram generated by the tissue because the extrastimulus is impinging on the refractory period of the adjacent myocardium.
- VERP and retrograde AVN ERP can be calculated Latency is a delay occur between the extrastimulus and the electrogram generated by the tissue because the extrastimulus is impinging on the refractory period of the adjacent myocardium.
- 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. 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).
- At CL 320 ms, there is 1:1 VA conduction. However, at CL 300 ms there is intermittent VA block (*). Therefore, VA WCL is 300 ms