1. Principles of electrophysiology(His bundle,Mapping techniques)

2. History
Equipment
Catheter positions
Basic electrophysiology study
Mapping techniques
Complications

3. History Sherlag et al-1968-His bundle electrogram
Durrer et al,Coumel et al-programmed electrical stimulation of heart
Wellens et al-combined both techniques
Josephson et al-endocardial catheter mapping of VT
Huang et al,1985-radiofrequency catheter ablation

4. Equipment Flouroscopy Electrode catheters Junction box
Recording apparatus
Stimulator
Cardioverter/defibrillator

5. Electrode catheters Woven dacron catheters/polyurethane
Composed of thin wires attached to electrodes located at the tip and more proximal rings insulated by plastic
Electrograms are usually recorded from two adjacent electrodes,electrode number is even
Diagnostic catheters used in the atrium, His bundle, and ventricle are quadripolar (4 electrodes)
Catheters used in the Coronary Sinus are usually decapolar
Electrodes numbered from distal to proximal
Distal electrodes used for pacing(in contact with endocardium)
Preformed shapes-Josephson,Cournand

6. Cournand
Josephson

7. Lasso catheter-pul.vein activation sequencing
Halo catheter-Rt.atrial activation sequencing

8. Inter electrode distance
May range from 1 mm to 10 mm
Narrow inter electrode distance-
precise timing of electrical activity
compromise width of EGM and components of a multicomponent EGM
2mm or 5mm usual

9. Signal acquisition Unipolar Vs bipolar
Unipolar-only one electrode within heart;anode can be Wilson central terminal or another pole cm from the tip
Bipolar-sum of unipolar signals from two intracardiac electrodes
Unipolar –
broad lower-amplitude signal
Polarity &morphology of signal preserved
important role during ablation
Bipolar-
More specific for local activity
far field ventricular signal “cancels out”-
effects of depolarization in a smaller region of tissue

12. Junction box Pairs of multiple pole switches
Matched for each recording and stimulation channel
Permits ready selection of any pair of electrodes for stimulation or recording

13. Recording apparatus
Recording systems record signals from all intracardiac electrodes that have been placed
Signal processor-amplification and filtering
split screen viewing, sweep speed changes and case tracking software
Amplification
Physiological signals< 10 mV
Avoidance of extraneous signals at input of amplifier

14. Filtering High pass filters
Eliminate components below a particular frequency
Surface ECG 0.05 Hz
Preserve T wave
Eliminate baseline drift
Unipolar EGM-0.05 Hz
Polarity &signal morphology important
Bipolar EGM-30 to 50 Hz
Timing of signal more important,not morphology

15. Low pass filters Notch filters
Eliminate components above a particular frequency
To eliminate noise at higher frequencies
ECG-100 to 200 Hz
EGM- 500 Hz
Notch filters
Eliminate a particular frequency
Usually to eliminate AC interference-50 Hz

16. 0.05-400 Hz-low frequency components obscure others
High pass 30 Hz-ECG unacceptable
ECG-0.05 to 200,EGM-30 to 500 Hz

17. Stimulator Stimulator is used to define pacing rates and protocols
Output is usually set at twice the diastolic treshold for a particular site
Different modes
Rapid pacing
Single or multiple extrastimuli following a sensed beat
Extra stimulus after a paced drive train

19. Catheter positions High RA RV apex His bundle
Quadripolar catheter,5mm spacing
SVC/RA junction in posterolateral wall or RAA
RV apex
Quadripolar catheter 5 or 10 mm spacing
His bundle
Curved tip or steerable quadripolar;2mm spacing
Placed in the region of His bundle, straddling RA&RV with catheter tip just past the tricuspid valve.
Confirmed by HBE, with atrial and ventricular potentials approx.equal size and HB potentials seen b/w them

20. Coronary sinus Decapolar catheter with 2-8-2 spacing
Subclavian or jugular approach.femoral if steerable catheter available
Catheter advanced until prox.pole over lateral border of spine in PA view
EGM from LA and LV

23. RAO view

24. LAO view

25. Basic electrophysiology study
Signals are evaluated at faster sweep speeds:100 mm/second or higher
Always look at simultaneous surface ECG
Heart rate in bpm=60000/cycle length in ms

26. Measurement of basic intervals
PA interval
Time interval from earliest atrial activation in the region of sinus node and atrial activation in the AV node region
Measured as interval from earliest atrial activity(p onset in ECG or deflection in atrial electrogram) to earliest reproducible rapid deflection of atrial signal recorded in HB catheter
25-55 ms normal

27. First atrial electrogram before the onset of the P wave in RA catheter
First atrial electrogram before the onset of the P wave in RA catheter.RA activation is complete when atrial signal recorded in His catheter. LA activation occurs after RA activation latest atrial signal recorded in distal CS(CS 1,2)

28. AH interval
Time taken by the cardiac impulse to travel from low right atrium at IAS,over AV node,to the His bundle
Measured from the earliest reproducible rapid deflection of atrial signal in electrogram recorded by His cather to the onset of His deflection(earliest deflection from baseline) in HBE
ms considered normal
Affected by autonomic tone

29. HV interval
Time taken for conduction from proximal His bundle to the ventricular myocardium
Measured from the onset of His deflection in HBE to the earliest onset of ventricular activity recorded from multiple surface ECG leads or ventricular EGM in His bundle recording
35-55 ms normal.

31. Structures involved in basic interval measurement

32. Validation of His bundle potential
In sinus rhythm,apparent His deflection with H-V interval <30 ms- RBB potential or preexcitation
Most proximal his bundle deflection a/w largest atrial electrogram
Pace His bundle-if morphology similar to sinus rhythm ECG &stimulus to V interval identical to H-V interval in sinus rhythm
His bundle deflection can be recorded in aorta from non coronary cusp and compared.
Advancement of Lt.catheter to LV can record LBB potential.if coinciding with potential recorded from His catheter it is RBB potential

33. Tests of sinus node function
SNRT-sinus node recovery time
Time taken by the sinus rhythm to resume after a period of overdrive atrial pacing(conventional 30 s)
Defined as the interval measured in HRA from the last paced complex to first spontaneous complex after cessation of pacing
Pacing at several cycle lengths done and longest values taken
Normal<1500
Corrected SNRT-
SNRT –basic sinus cycle length
Normal<550 ms
Total recovery time (TRT)
interval b/w cessation of pacing and return to basic sinus cycle length
Normal <5s

36. Atrial extrastimulus testing
Drivetrain of 8 paced beats at a fixed cycle length f/b an extrastimulus at same site
Drive train is repeated while coupling interval of extrastimulus decreased progressively until atria no longer captured.
Uses
Refractory periods
Dual AV nodal physiology
Presence of accessory pathways
Arrhythmia induction

37. Concept of refractoriness
Extrastimulus is more closely coupled-first
a subnormal phase 0 upstroke occurs (relative
refractoriness) –less Na+ channels available
Extrastimulus does not produce a phase 0
upstroke (absolute refractoriness)-no Na+channel available for activation

38. RRP-longest coupling interval of a premature impulse that result in prolonged conduction of premature impulse compared to basic drive
ERP- longest coupling interval of a premature impulse that fails to propagate through the tissue
FRP-minimum interval b/w two consecutively conducted impulses through the tissue
Determination of ERP of a tissue requires that FRP of proximal tissue should be less than that

39. AVNRRP- longest A1A2 at A2H2 prolongation-380ms
AVNFRP-shortest H1H2 interval-370ms
AVNERP-longest A1A2 not conducted-280ms

40. S1 –S2 380 ms. slight prolongation of A-H interval. H-V remain same
S1 –S2 380 ms.slight prolongation of A-H interval.H-V remain same.pattern of activation in CS electrogram is different.

41. S1-S2 320 ms.atrial electrogram with no His potential recording.
AVNERP-A1-A2 interval 330 ms.
S2-A2>S1-A1 interval-atrial RRP

42. S1-S2 280 ms.no atrial capture-atrial ERP

43. AVNERP cannot be calculated by this method if FRP of atria longer than ERP of AV node
Earlier coupling intervals decrease refractoriness.multiple extrastimuli given-first one conditions atrial tissue to shorten refractory period so that a second closely coupled stimulus can be used to measure AVNERP

44. Atrial refractory period reached at 260 ms before AVN refractoriness could be calculated

45. In order to evaluate the properties of the AV node in the same patient, two atrial
extrastimuli are delivered.First (S2) with a coupling interval of 280 ms and the second (S3) at 220 ms(S2 S3 interval gradually decreased until blocked).No conduction through the AV node a/w S3.AVNERP can now be calculated at 220 ms.

46. Dual AV node physiology
An increase in the AH interval ≥50 ms caused by a decrease in the coupling interval of an atrial extrastimulus by 10 ms
ERP of fast pathway has reached and conduction over the AV node has shifted from the usual fast pathway to a slow pathway
Dual AV nodal physiology can be inferred from discontinuity in antegrade conduction curve of AV node
More than one discontinuity suggest presence of multiple AV nodal pathways

51. Gap phenomenon
Conduction of an impulse may be blocked at a certain S1S2 interval and reappear at a lower S1S2 interval
Impulse conducted over two structures in sequence first having a shorter ERP
Delay in proximal structure causes the impulse to arrive at second structure with an increased coupling interval

54. Incremental atrial pacing
Incremental pacing (e.g. in the atrium) begins at a stable cycle length slightly below that of the sinus rhythm
pacing cycle length is then shortened by 10
to 50 ms, a few beats are observed at the new pacing cycle length and the cycle length is again decreased by the same amount.
AH interval increases due to decremental conduction property of the AV node(depolarisation due to slow inward Ca2+ current).
HV interval and the QRS complex remain same(depolarisation due to fast inward Na+channel)

55. Atrial pacing at 600 ms-

56. Cycle length 450 ms.AH prolongation.1:1 A-V relation

57. Cycle length 350 ms.A V relation not 1:1.AVBCL reached

58. Cycle length at which the atrial:ventricular relationship is no longer 1:1 is called atrioventricular blocked cycle length or AVBCL
AVBCL provides information on the robustness of atrioventricular conduction.
Devt. of AV Wenckebach block at rapid paced rates is normal.AV block at slow paced rates suggests the presence of AV nodal disease

59. Ventricular extrastimulus testing
V A conduction can be demonstrated in majority either at rest or by using isoproterenol
Earliest part of atria depolarised is near AV node-so earliest atrial activation in His catheter f/b CS from proximal to distal f/b HRA
This sequence –concentric atrial activation
During antegrade conduction (atrial pacing) decremental response occurs mainly in AV node.
During retrograde conduction (ventricular pacing), the decremental conduction can occur in two different structures: the His-Purkinje system and/or the AV node

60. S1S2 600ms.retrograde atrial activation

61. VAERP 580 ms

62. BB reentry a/w ventricular extra.His deflection occurs prior to this

63. premature ventricular extrastimulus blocks retrogradely in RBB,but depolarization travels slowly across IVS and up the LBB. It reenters the right bundle and leads to an additional QRS
Complex of LBBB morphology

64. Incremental ventricular pacing –VABCL can be measured
Cycle length at which 1:1 VA relation disappear is VABCL

66. Mapping
Mapping is used to localise site of origin of abnormal beats or to identify the tachycardia circuit in case of Reentrant arrhythmias
Mapping procedures
Activation Sequence Mapping
Voltage mapping( Substrate / Fractionated electrogram )
Pace Mapping
Entrainment Mapping
Miscellaneous

67. Pace mapping
Manipulation of mapping catheter to region of origin of tachycardia
Pace at this site at same cycle length as tachycardia
Greater the concordance b/w tachycardia and morphology during pacing-closer exit site
Look for 12/12 match
More useful in ventricular tachycardia as QRS morphology is easier to compare
Allows to home in on the region of interest,cannot pinpoint site for ablation
Does not require tachycardia to sustain over a longer time

68. Pace Map 12/12 Match

69. Activation sequence mapping
Required to pinpoint focus of tachycardia
During tachycardia mapping catheter explores the endocardium to identify the site where earliest electrogram relative to a fixed reference is recorded.
Suitable site
Local electrogram precedes any other activity
One from which any movement results in a later electrogram
One at which unipolar electrogram shows a sharp initial negative deflection

71. Entrainment mapping Allows confirmation of Reentry
Allows localisation of circuit and isthmus
Entrainment is a continous resetting of a reentrant circuit by a series of stimuli

72. Criteria for entrainment
Constant fusion during constant overdrive pacing,last paced beat entrained not fused
Progressive fusion during overdrive pacing as pacing rate increases
Localised conduction block to a site for one paced beat a/w interruption of the tachycardia ,followed by activation of that site by next paced beat from a different direction and with a shorter conduction time
During pacing at two different rates during a tachycardia,there is change in conduction time to and EMG morphology at a recording site

73. Entrainment results in a fusion complex
Pacing stopped-last one entrained but goes round the circuit-morphology similar to original rhythm

74. If pacing CL progressively shortened circuit is invaded to a greater extent-fusion increases

75. A premature paced beat collides with head and tail-fails to propagate
Next beat is purely paced and R is activated from a different direction

76. Manifest entrainment-demonstration of resetting with fusion
Cocealed entrainment-failure to demonstrate fusion but PPI equal to tachycardia cycle length.site protected isthmus
PPI equal to TCL (within ms)if pacing site within reentrant circuit
Post pacing interval-interval b/w last pacing stimulus that entrained the tachycardia and the next recorded EGM at the pacing site

78. Manifest Entrainment with Fusion
Premature impulse invade tachycardia circuit.In antidromic direction it collides and extinguishes reentrant wavefront.In orthodromic direction it creates a new wavefront(resets).

79. Concealed Fusion
Antidromic wave front does not contribute much to the morphology of tachycardia beat
Area of slow conduction : Isthmus

80. Concealed Fusion
Post Pacing Interval
If paced from the critical Isthmus PPI = TCL

82. Substrate( Volatage) Mapping
Scarred Myocardium has Low Voltage
0.5 mV or Less : Dense Scar
0.5 – 1.5 mV : Borderline Zone
> 1.5 mv : Normal area

83. Advanced mapping systems
Electroanatomic mapping-CARTO system
Metal coil placed in a magnetic field
Catheter contains a location sensor in tip
A 3D map is created by placing catheter in known anatomic positions
Local electrogram at each point superimposed on anatomical map to give a color coded activation map

85. Non contact mapping-ENSITE
Multi electrode array probe with 64 non contact electrodes
Endocardial boundaries defined with a conventional mapping catheter
3D endocardial potential map is created from a single cardiac cycle
Magnetic navigation system
Ablation catheter can be guided and positioned by magnetic fields to a desired site within cardiac chamber

86. Complications Vascular complications Pneumothorax Cardiac tamponade
AV node damage requiring PPI
Arrhythmia induction
Thromboembolic complication
Pulmonary vein stenosis

87. Thank you