Invasive Electrophysiology
Abbreviations
0-9
3D
three dimensional
A
ACT
activated clotting time
AD
afterdepolarization
AF
atrial fibrillation
AICD
automated implantable cardioverter defibrillator
AP
accessory pathway
ASD
atrial septal defect
ATP
antitachycardia pacing
AV
atrioventricular
AVN
atrioventricular node
AVNERP
atrioventricular nodal effective refractory period
AVNRT
atrioventicular node re-entrant tachycardia
AVRT
atrioventricular re-entrant tachycardia
AWCL
anterograde Wenckenbach cycle length
B
BBB
bundle branch block
BP
blood pressure
C
CFAE
complex and fractionated atrial electrogram
CS
coronary sinus
CT
computed tomography
D
DVT
deep vein thrombosis
E
ECG
electrocardiogram
EP
electrophysiology
ERP
effective refractory period
F
FAT
focal atrial tachycardia
FFP
fresh frozen plasma
H
HCM
hypertrophic cardiomyopathy
HRA
high right atrium
HSVPB
His syndrome ventricular premature beat
I
IAP
incremental atrial pacing
ICD
implantable cardiac defibrillator
ICegram
intracardiac electrogram
IVC
inferior vena cava
IVP
incremental ventricular pacing
L
LA
left atrium
LAA
left atrial appendage
LAO
left anterior oblique
LBBB
left bundle branch block
LIPV
left inferior pulmonary vein
LSPV
left superior pulmonary vein
LV
left ventricle
M
MI
myocardial infarction
MRI
magnetic resonance imaging
MV
mitral valve
N
NYHA
New York Heart Association
P
PE
pulmonary embolism
PV
pulmonary vein
R
RAO
right anterior oblique
RF
radiofrequency
RSPV
right superior pulmonary vein
RVA
right ventricular apex
RVOT
right ventricular outflow tract
RWCL
right Wenckenbach cycle length
S
SA
sinoatrial
SAN
sinoatrial node
SCD
sudden cardiac death
SR
sinus rhythm
SVC
superior vena cava
SVT
supraventricular tachycardia
T
TIA
transient ischaemic attack
TOE
transoesophageal echocardiography
TV
tricuspid valve
V
VERP
ventricular effective refractory period
VF
ventricular fibrillation
V/Q
ventilation-perfusion
VT
ventricular tachycardia
W
WCL
Wenckenbach cycle length
WPW
Wolff-Parkinson-White (syndrome)
Mechanism of tachycardias
Knowledge of how arrhythmias are initiated and perpetuated is fundamental to understanding the techniques described in this chapter.
The electrical wavefront
The excitable impulse is generated at the cell membrane by the action potential. As one cell depolarizes, it causes a reduction in negativity of the resting potential in the adjacent cell such that it this cell also reaches the threshold potential and depolarizes. The shape, orientation, and presence of gap junctions between myocardial cells allow rapid progression of this depolarization, which can be described as an electrical wavefront. After a cell has depolarized, it cannot depolarize again until a fixed period of recovery time has passed, the refractory period. Cells that are able to depolarize are excitable and those that cannot are refractory.
In sinus rhythm (SR), the source of these wavefronts is the sinoatrial node (SAN), and they may be modulated between the atrium and ventricle by the atrioventricualar (AV) node. They are initiated (and therefore the heart rate is controlled) by regulation from the autonomic nervous system and circulating cathecholamines. This control is lost in tachyarrhythmia, and heart rates are inappropriate.
Conduction block
A wavefront will propagate as long as there are excitable cells in its path. Anatomical barriers such as the mitral valve annulus, vena cava, aorta, etc. do not contain myocardial cells and therefore the progression of wavefronts is halted there. This is described as fixed conduction block, as block is always present. Dead cells are another important source of fixed conduction block e.g. the left ventricular scar of a myocardial infarction (MI).
Functional conduction block describes the situation when block is only present under certain conditions. An example is myocardial ischaemia, which may alter the electrical properties of myocytes so that they do not conduct. It is also functional block that prevents a wavefront turning back on itself, as the cells behind the leading edge are temporarily refractory and force the wavefront to continue in one direction. Other causes of functional block are: cyanosis, myocardial stretch, rate of wavefront, and direction of wavefront.
Arrhythmia mechanism
Three distinct mechanisms are described:
enhanced automaticity
re-entry
triggered activity.
The first two account for nearly all clinical tachycardias, and their characteristics are compared in Table 11.1.
Table 11.1 Characteristics of automatic and re-entry tachycardiasa | |||||||||||||||||||||||||||
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Mechanism of arrhythmias
Enhanced automacity
If a nidus of myocardial cells depolarizes faster (rapid phase 4 of the action potential) than the SAN, they will act as the source of wavefronts that conduct through the heart. They may be atrial or ventricular, but if they occur in the atria they will override the SAN. As they occur from a single site they are often termed focal. Common sites are where myocardial cells suddenly change shape/size or those under abnormal pressures such as; the junction of veins/atrium (superior vena vava (SVC), pulmonary veins (PVs)), crista terminalis, coronary sinus (CS), AV node area, mitral/tricuspid ring, ventricular outflow tracts.
Re-entry
Re-entry accounts for >75% of clinical arrhythmias. It is caused by a perpetually propagating wavefront that it is constantly meeting excitable myocardium. For re-entry to occur, at least two distinct pathways must exist around an area of conduction block. This is best described using the example of VT due to re-entry around a LV myocardial scar (see Fig. 11.1).
A myocardial scar acts as an area of block, around which a normal sinus wavefront passes via normal myocardium (A) and slowly through it via diseased myocardium (B)—hence there are two distinct pathways.
The sinus beat is followed closely by a ventricular ectopic, which is conducted around A normally but is blocked in B, which is still refractory following the last sinus beat.
The distal end of B, however, is now excitable and the wavefront passes backwards up B, which has had time to fully recover by the time it reaches the proximal end. Conduction is sufficiently slow up B that now A is excitable again and the wavefront can pass down A.
Thus, a re-entry wavefront has been formed that is constantly meeting excitable myocardium.
Triggered activity
This has features of both the above mechanisms. They are caused by spontaneous (hence automatic) afterdepolarizations (ADs) occurring late in phase 3 (early ADs) or in phase 4 (delayed ADs) of the action potential. These ADs, however, are often triggered by premature beats and are therefore inducible (like re-entry). If these ADs reach the threshold level, then a single or burst of action potentials is set off. The ADs can be induced experimentally by ischaemia, QT-prolonging drugs, cell injury, or low potassium. This mechanism underlies torsades de pointes and arrhythmias due to digoxin toxicity.
 Fig. 11.1 Re-entry as a mechanism of tachycardia. 1. Normal sinus beat passing around and through scar 2. Ectopic beat passing around but blocked through scar 3. Re-entry circuit of tachycardia (Dark grey represents scar, light grey normal myocardium, and white arrows electrical wavefronts.) |
The electrophysiology study
The electrophysiology (EP) study is most useful for the diagnosis of tachycardia. When this has already been documented or is strongly suspected, then it is usually the first part of a combined procedure with catheter ablation to cure the arrhythmia. Note that in EP it is usual to discuss cycle lengths (in ms) rather than heart rates e.g. 60/min = 1000 ms, 100/min = 600 ms, 150/min = 400 ms.
Mapping electrical activity in the heart
EP is wrongly considered to be complex. Fundamentally, it is just recording of the heart’s electrical signals either during sinus rhythm, arrhythmia, or in response to pacing at specific sites. The electrocardiogram (ECG) provides a great deal of this information and so a full 12-lead ECG is recorded throughout the procedure.
The intracardiac electrogram (ICegram)
The ECG summates the entire cardiac activation. By placing 2 mm electrodes directly on the heart’s endocardial surface, the electrical activity at precise locations is known. The ICegram is therefore much narrower than the ECG and is best appreciated at a sweep speed of 100 m/ms, four times faster than a standard ECG recording.
The potential difference between either two closely spaced electrodes (a bipolar electrogram) or one electrode and infinity (a unipolar electrogram) can be recorded. The unipolar electrogram is more accurate regarding direction and location of electrical activity; however, it is subject to much greater interference. Note that a pacing current can be passed through any of these electrodes. Standard catheter location is shown in Fig. 11.2.
Pacing protocols
Pacing in the EP study is done in a predefined manner, termed programmed stimulation. This has three forms:
incremental pacing: the pacing interval is started just below the sinus interval and lowered in 10 ms steps until block occurs or a predetermined lower limit (often 300 ms) is reached
extrastimulus pacing: following a train of 8 paced beats at a fixed cycle length, a further paced beat (the extra stimulus) is introduced at a shorter coupling interval (the time between the last stimulus of the drive and the first extrastimulus). The stimuli of the drive train are conventionally termed S1, the first extra stimulus S2, the second extrastimulus S3, and so on. Extra stimuli can also be introduced after sensed heart beats (‘sensed extras’)
burst pacing: pacing at a fixed cycle length for a predetermined time.
 Fig. 11.2 Standard positions of catheters in the EP study and intracardiac electrograms at those sites. Catheters have been passed up into the right heart from sheaths in the femoral veins under fluoroscopic guidance. These images from the right anterior oblique (above) and left anterior oblique (below) demonstrate the standard positions at the high right atrium (HRA) close to the SAN, on the His bundle (HIS), at the RV apex (RVA) and a catheter passed through the os of the coronary sinus (CS), which wraps around the left posterior atrioventricular groove. From this position, ICegrams are recorded from the left atrium and ventricle. This catheter is often inserted via the left or right subclavian veins. The ICegrams are conventionally ordered HRA, HIS, CS, and RV (not displayed here), with an ECG lead at the bottom. On each catheter, bipoles are then ordered proximal to distal. In SR then activation is seen to start at the HRA, pass across the His bundle, and then along the CS catheter proximally to distally. Earliest ventricular activation is at the RVA (where the Purkinje fibres insert). Normal sinus intervals are PA = 25-55 ms, AH = 50-105 ms, HV 35-55 ms, QRS <120 ms, corrected QT <440 ms men, <460 ms women. |
Uses of the electrophysiology study
Sinus node function
The corrected sinus node recovery time and sinoatrial conduction time are both measures of SAN function. Unfortunately, however, they are unreliable tests as SAN function is greatly influenced by autonomic tone, drugs and observer error. SAN dysfunction is best assessed with ambulatory monitoring and exercise testing. It is very rare that invasive EP testing would contribute to the decision to give a patient a permanent pacemaker and therefore it is not part of our routine procedure.
AV conduction
Heart block: The degree of heart block is assessed via the ECG, which can also indicate the level (i.e. either at the AV node itself or in the His Purkinje system, infra nodal. The level of block is ascertained easily in the EP study. The AH time is prolonged in nodal and the HV time in infranodal block. The AH (but not the HV) time may be shortened by exercise, isoprenaline or atropine and prolonged by vagal manoeuvres.
AV nodal function: This is assessed both anterogradely (A to V) and retrogradely (V to A), using both incremental and extrastimulus pacing. By incremental pacing at the HRA, conduction is observed in the His bundle and RVA until block occurs. The longest pacing interval at which block occurs is the anterograde Wenckebach cycle length (WCL). Normal values are <500 ms; however, this increases with age and autonomic influences. The retrograde WCL is also measured; however, absent VA conduction can be normal. From the HRA, extrastimulus pacing is performed. As the coupling interval between S1 and S2 is reduced, AV conduction is observed. The longest S1-S2 interval at which AV block occurs is the anterograde atrioventricular node (AVN) effective refractory period (ERP). This is measured at drive trains of 600 and 400 ms. If VA conduction is present, the retrograde atrioventricular nodal effective refractory period (AVNERP) is measured.
Decremental conduction: This is the key physiological property of the AV node. As the interval between successive impulses passing through the AV node decreases, the conduction velocity within the AV node also decreases. In AV conduction, this is manifest as a prolongation of the AH (and AV) interval, as the atrial pacing interval decreases. This phenomenon can be observed during incremental and extrastimulus pacing. During extrastimus pacing, if the AH interval is plotted against the S1-S2(=A1-A2), then an anterograde conduction curve can be plotted.
Dual AV nodal physiology: It is possible in many patients (but not all) to identify two electrical connections between the atrial myocardium surrounding the compact AV node and the node itself, which have different conduction properties. The slow pathway has slower conduction velocity but a shorter ERP than the fast pathway. This is observed by plotting an anterograde conduction curve. For longer A1-A2 intervals, AV conduction is preferentially via the fast pathway; however, once the fast-pathway ERP is reached, conduction is via the slow pathway and consequently the AH time suddenly prolongs. This is called an AH interval jump and is defined as a lengthening of the AH by >50 ms, following reduction in the A1-A2 interval of 10 ms. Dual AV nodal pathways are the substrate for AVNRT.
Table 11.2 A standard basic electrophysiology study | ||||||||||||||||||||||||||||||
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Indications for electrophysiology study
Diagnose the mechanism of documented symptomatic tachycardia (usually proceed immediately to ablation)
Diagnose the mechanism of tachycardia in a patient with palpitations and suspected arrhythmia (may proceed immediately to ablation)
Determine electrical properties of the accessory pathway (Wolff-Parkinson-White (WPW))—stratify the risk of sudden cardiac death (SCD) and need for ablation
Risk stratification of SCD in patient with impaired left ventricular (LV) function or inherited arrhythmia, e.g. Brugada syndrome and need for implantable cardiac defibrillator (ICD)
Diagnose the mechanism of syncope—when arrhythmia is strongly suspected
Look for evidence of AV nodal conduction disease (measure HV interval) and need for pacemaker.
Identifying abnormal AV connections
In normal hearts there is only one connection between the atrium and ventricle, the AV node. Activation of the atrium (during V pacing) or ventricle (during A pacing or SR) should therefore start at the AV node. Accessory pathways (APs) do not decrement. Their presence can be identified by both abnormal activation patterns and conduction physiology using incremental and extrastimulus pacing.
Atrial pacing: As the AV node decrements, a greater proportion of ventricular activation will occur via the AP. Thus, non-decremental AV conduction times and broadening of the QRS complex will be observed as the pacing interval shortens. Note: If the ERP of the AP is shorter than the ERP of the AV node, then the QRS will suddenly narrow and the AV time suddenly prolong when the AP blocks.
Ventricular pacing: The normal order of atrial activation is His then CS (proximal to distal) and finally the HRA, termed concentric activation. If the atrium is activating via an AP, an eccentric activation pattern is observed. The site of the earliest atrial activation will localize the AP. Non-decremental VA conduction is also seen.
Induction of arrhythmia
The presence of an AP, dual AVN physiology or a known ventricular scar provides the substrate for a tachycardia but does not necessarily imply it will occur. A diagnosis can only be confirmed by inducing the tachycardia.
In addition to the pacing techniques described, burst pacing, extrastimulus pacing with multiple extrastimuli, and sensed extras are deployed. If this fails, pacing manoeuvres can be repeated during an isoprenaline infusion (1-4 mcg/min) or boluses (1-3 mcg). This is particularly important for tachycardias with an enhanced automaticity mechanism. ‘Aggressive’ induction protocols increase the likelihood of inducing an unwanted arrhythmia such as AF or VF (ventricular fibrillation).
Once a tachycardia is initiated, it is useful to compare it with a 12-lead ECG recorded during symptoms to ensure this is the clinical arrhythmia. How individual tachycardias are diagnosed and treated is considered in subsequent chapters.
 Fig. 11.3 AV nodal jump demonstrated during anterograde conduction curve. In both panels, 5 ICegrams are shown; top to bottom: high right atrium (HRA), 3 bipolar recordings from the bundle of His (His), right ventricular apex (RVA) and lead 1 of the ECG are displayed. 8 paced beats (drive train) have been delivered through the HRA at 600 ms and then a single extra stimulus. Only the final two beats of the drive train and the extra stimulus are shown. The coupling interval of the extra stimulus is 380 ms and 320 ms in the top and bottom panels respectively. Despite only a slight shortening of the coupling interval, there is dramatic lengthening of the AH (and AV) time, suggesting dual AVN physiology. |
Programmed ventricular stimulation
An EP study focusing on induction of ventricular arrhythmias (the VT stimulation study) has previously been used to risk stratify for SCD, and to decide on the effectiveness of antiarrhythmic drugs in suppressing VT, and the need for an ICD. Evidence has now accumulated, however, that it is of little predictive value, and that decisions regarding ICD prescription should be based on other risk factors, particularly LV function. The EP study can be useful prior to ICD implant for other reasons:
to aid programming of the device:
is VT well tolerated haemodynamically?
is it easily terminated with overdrive pacing?
is there VA conduction? During V pacing or VT?
are other arrhythmias present and easily induced?
Programmed ventricular stimulation is performed using the protocol devised by Wellen, or a modification thereof (see below).
Protocol for programmed ventricular stimulation
From the RV apex, extrastimulus pacing, reduce the coupling interval until refractory:
1 extrastimulus during SR
2 extrastimuli during SR
1 extrastimulus following 8 paced beats at 600 ms
2 extrastimuli following 8 paced beats at 600 ms
1 extrastimulus following 8 paced beats at 400 ms
2 extrastimuli following 8 paced beats at 400 ms
3 extrastimuli during SR
2 extrastimuli following 8 paced beats at 600 ms
3 extrastimuli following 8 paced beats at 400 ms
If no ventricular arrhythmia is induced, repeat from RV outflow tract.
Thus, the pacing protocol becomes gradually more aggressive. The more aggressive the induction protocol, the less specific the result. The most useful result is induction of a sustained monomorphic VT with one or two extrastimuli. This indicates a potential substrate for ventricular arrhythmias. Non-sustained VT, polymorphic VT, and VF are all non-specific results.
New technologies
Non-fluoroscopic three-dimensional mapping
EP procedures have become increasingly complex (e.g. ablation of AF or atrial tachycardia in congenital heart disease), leading to longer procedures with greater X-ray exposure. Non-fluoroscopic electroanatomical mapping systems help overcome these challenges by generating a threedimensional (3D) image as the ablation catheter is moved around the cardiac chamber being mapped. Two systems are commonly used; Carto (Biosense Webster) and Navx (St Jude Medical), which locate the catheters using magnetic and electrical fields respectively.
These maps can be used as anatomical guides, and can display the timings (activation maps) or voltages of ICegrams represented by colours. The maps can be viewed in any orientation or from internally. Points of interest or labels, e.g. ablation lesions, can be marked, which gives memory of where the catheter has been. This is particularly useful in ablation of AF where a series of ablation points need to be delivered to from continuous circular or linear ablation lines. The identification of areas of scar (voltage mapping) is essential in VT ablation, as these are critical to its re-entrant mechanism.
Non-contact mapping (Ensite Array, St Jude Medical), allows simultaneous collection of ICegrams from the entire endocardial surface of the chamber in which the catheter is placed. An array of 64 unipolar electrodes, mounted on a balloon, records the signals from the endocardium conducted through the blood. The ‘virtual’ ICegrams are reconstructed and displayed on a map of the chamber. The mechanism of a regular tachycardia can be determined from a single ectopic beat.
Image integration (Fig. 11.4)
A computed tomography (CT) or magnetic resonance imaging (MRI) scan of the patient’s thorax can be segmented to provide a 3D image of the patients own LA (or other chamber). This is then registered with the mapping system (Carto or NavX) by moving the mapping catheter to at least four anatomical points (e.g. junction of a pulmonary vein and the LA) and simultaneously marking them on the image and mapping system. The reconstruction of the LA is then locked into the mapping system, so that the operator can navigate around the complex unique anatomy of a patient’s LA without the need for X-ray.
Remote navigation of ablation catheters
Robotic technologies have been a great success in urological and cardiac surgery. In order to overcome difficulties with manual catheter manipulation in complex procedures, these have been applied in EP—with the operator seated in the lab control room rather than standing by the patient. Proposed advantages are: improved catheter stability and reach, better ablation lesion formation, and reduced operator X-ray exposure and fatigue, which may translate into better clinical outcomes.
Niobe (Stereotaxsis) is a magnetic navigation system in which a lowintensity magnetic field is created by two large magnets permanently housed either side of the cathlab table. A purpose-built mapping catheter contains three magnets that align themselves within the magnetic field. Movement of the catheter is achieved by shifting the magnetic field around,
controlled by a computer mouse on a desktop. Sensei (Hansen Medical) is a robotic navigation system in which a steerable sheath is controlled by a robotic arm attached to the table. This responds to manipulation of a 3D joystick at a purpose-built workstation. The sheath can house any ablation catheter and therefore is compatible with any other mapping system.
controlled by a computer mouse on a desktop. Sensei (Hansen Medical) is a robotic navigation system in which a steerable sheath is controlled by a robotic arm attached to the table. This responds to manipulation of a 3D joystick at a purpose-built workstation. The sheath can house any ablation catheter and therefore is compatible with any other mapping system.
 Fig. 11.4 Image integration. The top image of a LA from the PA perspective reconstructed from an MR scan of the heart taken pre-procedure. The image is registered with the 3D mapping system. The bottom image is the LA viewed from within at a left lateral projection so that the ablation lesions that have been delivered around the right pulmonary veins are visible. |
Catheter ablation
In medical terms, ablation is the removal of tissue. As many tachycardias depend on discrete foci or pathways to be sustained, they are amenable to cure by destruction of these areas.
Energy sources for ablation
Radiofrequency (RF) energy
Cells are destroyed by heating >50°C. The RF generator delivers an alternating current of 500-750 KHz between the active catheter electrode and a large indifferent electrode placed on the patient’s skin. The ions within cells immediately adjacent to the catheter are agitated and generate heat (resistive heating). The heating power generated in this way dramatically decreases as the distance form the catheter increases. The remaining heat is conducted away to the surrounding tissue. A lesion of ˜5 mm depth is formed after 30-60 s, which is sufficient to destroy the full thickness of atrial myocardium. Catheters are 7 Fr, with tip electrodes of 4 mm length as standard or 8 mm where longer lesions are needed.
If the temperature approaches 100°C, boiling of cell water occurs, generating steam that escapes either by exploding through the endocardium causing a large lesion (cavitation) or through the pericardium (perforation ± tamponade). Temperature is monitored at the tip of the catheter, and power delivery is automatically limited to prevent such overheating. The generator allows the power, temperature, and duration of each RF delivery to be adjusted.
Irrigated RF
The tip of the catheter is cooled during RF by the flow of blood, so the hottest part of an RF lesion is 1 mm beneath the surface. Stasis of flow occurs as the lesion is formed; hence the temperature rises, limiting the amount of power that is delivered and therefore size of the lesion. Heparinized saline, passed through a multiple lumen in the tip of the catheter at a rate of 10-30 ml/h, continuously cools the catheter allowing higher powers and larger lesions to be formed. This is needed where the myocardium is thick, e.g. left ventricle (VT) or Eustachian ridge (typical atrial flutter). Low-flow (2 ml/h) RF ablation is useful to keep the tip of the catheter free of thrombus, reducing stroke risk during RF in the LA or LV.
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