INVASIVE ELECTROPHYSIOLOGY 543 LV MI MRI MV NYHA PE PV RAO RF RSPV RVA RVOT RWCL SA SAN SCD SR SVC SVT TIA TOE TV VERP VF V/Q VT WCL WPW left ventricle myocardial infarction magnetic resonance imaging mitral valve New York Heart Association pulmonary embolism pulmonary vein right anterior oblique radiofrequency right superior pulmonary vein right ventricular apex right ventricular out \202 ow tract right W enckenbach cycle length sinoatrial sinoatrial node sudden cardiac death sinus rhythm superi or vena cava supraventricular tachycardia transient ischaemic attack transoesophageal echoc ardiography tricuspid valve ventricular effective refractory period ventricular \201 bril lation ventilation \200\223perfusion ventricular tachycardia Wenckenbach cycle length Wolff \200\223Parkinson \200\223White (syndrome) 544 CHAPTER 11 Invasive electrophysiology Mechanism of tachycardias Knowledge of how arrhythmias are initiated and perpetuated is fun damental to understanding the techniques described in this chapter. The electrical wavefront The excitable impulse is generated at the cell membrane by the act ion 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 pres- ence of gap junctions between myocardial cells allow rapid progression of this depolarization, which can be described as an electri cal wavefront . After a cell has depolarized, it cannot depolarize again until a \201 xed period of recovery time has passed, the refractory period . Cells that are able to depolar ize 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 autonomi c 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 pat h. Anatomical barriers such as the mitral valve annulus, vena cava, aorta, etc. do not cont ain myocardial cells and therefore the progression of wave- fronts is halted there. This is described as \201 xed conduction block , as block is always present. Dead cells are anot her important source of \201 xed conduction block e.g. the left ventricular scar of a myo cardial infarction (MI). Functional conduction block describes the situation when block is only present under certai n 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 wavef ront turning back on itself, as the cells behind the leading edge are temporarily refractor y and force the wavefront to continue in one direction. Other causes of functional block ar e: cyanosis, myocardial stretch, rate of wavefront, and direction of wavefront. Arrhythmia mechanism Three distinct mechanisms are described: \200 enhanced automaticity \200 re-entry \200 triggered activity. The \201 rst two account for nearly all clinic al tachycardias, and their charac- teristics are compared in Table 11.1 . MECHANISM OF TACHYCARDIAS 545 Table 11.1 Characteristics of automatic and re-entry tachycardiasa Re-entrya Automatic Autonomic sensitivity? (e.g. to exercise, emotion) Often Unusual No Yes Reproducible induction and termination by programmed pacing? Entrainment of the tachycardia by pacing (p)? No Yes Induced by atropine/isoprenaline infusion? Yes May augment induction by pacing a Related to metabolic causes Often Unusual Onset/offset May be gradual (warm up and down) Sudden Macroreentrant atrial tachycardia, AVNRT, AVRT, VT Speci \201 c tachycardias caused Focal atrial tachycardia, RVOT VT a The conduction properties of, e.g. the AV node, are in \202 uenced by autonomic tone. Sp ontaneous or drug-induced changes in this may then in \202 uence the development of re-ent ry tachycardias such as AV-nodal re-entry tachycardia (AVNRT); AF (atrial \201 brillation ); AVRT (atrioventricular re-entrant tachycardia); RVOT (right ventricular out \202 ow tra ct); VT (ventricular tachycardia). 546 CHAPTER 11 Invasive electrophysiology Mechanism of arrhythmias Enhanced automacity If a nidus of myocardial cells depolarizes fas ter (rapid phase 4 of the action potential) than the SAN, they will act as the source of wa vefronts that conduct through the heart. They may be atrial or ventricular, but if they occ ur 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/tricus pid ring, ventricular out \202 ow tracts. Re-entry Re-entry accounts for > 75 % of clinical arrhythmias. It is caused by a perpetu- a lly propagating wavefront that it is constantly meeting excitable myocar- dium. For re-entr y to occur, at least two distinct pathways must exist around an area of conduction block. T his is best described using the example of VT due to re-entry around a LV myocardial scar ( see Fig. 11.1). 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 ) \200\224 hence there are two distinct pathways. 2. 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. 3. 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 suf \201 ciently 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 spont aneous (hence automatic) afterdepolarizations (ADs) occurring late in phase 3 ( early ADs) or in phase 4 ( delayed ADs) of the action poten- tial. These ADs, however, are often trigg ered 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 in duced experimentally by ischaemia, QT-prolonging drugs, cell injury, or low potassium. This mechanism underlies torsades de pointes and arrhythmias due to digoxin toxicity. MECHANISM OF ARRHYTHMIAS 547 Fig. 11.1 Re-entry as a mechanism of tachycardia. 1. Normal sinus beat passing around and t hrough scar 2. Ectopic beat passing around but blocked through scar 3. Re-entry circuit of tachycardia (Dark gray represents scar, light gray normal myocardium, and white arrows elec - trical wavefronts.) 548 CHAPTER 11 Invasive electrophysiology The electrophysiology study The electrophysiology (EP) study is most useful for the diagnos is of tachycardia. When this has already been documented or is strongly suspected, then it is usually the \201 rst part of a combined procedure with catheter ablation to cure the a rrhythmia. Note that in EP it is usual to discuss cycle lengths (in ms) rather than heart r ates 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. Fundamenta lly, it is just recording of the heart \200\231s electrical signals either during sinus rhy thm, arrhythmia, or in response to pacing at speci \201 c sites. The electrocardiogram (EC G) provides a great deal of this information and so a full 12-lead ECG is recorded througho ut the procedure. The intracardiac electrogram (ICegram) The ECG summates the entire cardiac activation. By p lacing 2 mm elec- trodes directly on the heart \200\231s endocardial surface, the electrica l activity at precise locations is known. The ICegram is therefore much narrower than the E CG 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 electrogra m) or one electrode and in \201 nity (a unipolar electrogram) can be recorded. The unipola r electrogram is more accurate regarding direction and location of electrical activity; how ever, 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 prede \201 ned manner, termed program med stimulation . This has three forms: \200 incremental pacing: the pacing interval is s tarted just below the sinus interval and lowered in 10 ms steps until block occurs or a predetermined lower limit (ofte n 300 ms) is reached extrastimulus pacing : following a train of 8 paced beats at a \201 xed 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 \201 rst extrastimulus ). The stimuli of the drive train are conventionally termed S 1 , the \201 rst extra stim ulus S 2 , the second extrastimulus S 3 , and so on. Extra stimuli can also be introduced a fter sensed heart beats ( \200\230sensed extras \200\231) burst pacing: pacing at a \201 xed cycle length for a predetermined time. THE ELECTROPHYSIOLOGY STUDY 549 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 \202 uoroscopic guidance. These images from the right anterior oblique (abov e) and left anterior oblique (below) demonstrate the standard positions at the high right a trium (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 atr ioventricular groove. From this position, ICegrams are recorded from the left atrium and ve ntricle. 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 S R then activation is seen to start at the HRA, pass across the His bundle, and then along t he CS catheter proximally to distally. Earliest ventricular activation is at the RVA (where the Purkinje \201 bres insert). Normal sinus intervals are PA = 25 \200\22355 ms, AH = 50 \200\223105 ms, HV 35 \200\22355 ms, QRS <120 ms, corrected QT <440 ms men, <460 ms women. 550 CHAPTER 11 Invasive electrophysiology Uses of the electrophysiology study Sinus node function The corrected sinus node recovery t ime and sinoatrial conduction time are both measures of SAN function. Unfortunately, howeve r, they are unreli- able tests as SAN function is greatly in \202 uenced 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 decisio n to give a patient a permanent pacemaker and therefore it is not part of our routine proce dure. AV conduction Heart block: The degree of heart block is assessed via the ECG, which can als o indicate the level (i.e. either at the AV node itself or in the His Purkinje system, infr a 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 shortene d by exercise, isoprenaline or atropine and prolonged by vagal maneuvers. 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, conducti on 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 <50 0 ms; however, this increases with age and autonomic in \202 uences. The retrograde WCL is also measured; however, absent VA conduction can be normal. From the HRA, extrastimulus pa cing is performed. As the coupling interval between S 1 and S 2 is reduced, AV conduction i s observed. The longest S 1 \200\223S 2 interval at which AV block occurs is the anterogra de 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 nod al effective refractory period (AVNERP) is measured. Decremental conduction: This is the key physiological property of the AV node. As the inter val between successive impulses passing through the AV node decreases, the conduction veloc ity 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 S 1 \200\223S 2 (=A 1 \200\223A 2 ), then an anterogra de conduction curve can be plotted. Dual AV nodal physiology: It is possible in many patients (but not all) to identify two ele ctrical connections between the atrial myocardium surrounding the compact AV node and the n ode itself, which have different conduction properties. The slow pathway has slower conduct ion velocity but a shorter ERP than the fast pathway . This is observed by plotting an ante rograde conduction curve. For longer A 1 \200\223A 2 intervals, AV conduction is preferent ially via the fast pathway; however, once the fast-pathway ERP is reached, conduction is vi a the slow pathway and consequently the AH time suddenly prolongs. This is called an AH int erval jump and is de \201 ned as a lengthening of the AH by > 50 ms, following reduction i n the A 1 \200\223A 2 interval of 10 ms. Dual AV nodal pathways are the substrate for AVNR T. USES OF THE ELECTROPHYSIOLOGY STUDY 551 Table 11. 2 A standard basic electrophysiology study Pacing protocol Measure Comments Is there AV conduction block? 1. Sinus rhythm Basic sinus intervals (PA, AH, HV, QRS, corrected QT) RWCL Is VA conduction present? If so, is atrial activation normal and decremental? 2. Incremental ventricular pacing (IVP) 3. Incremental atrial AWCL Is AV conduction decremental? Is pre-excitation manifest during pacing? pacing (IAP) Is AV conduction decremental? Is pre-excitation manifest during pacing? Is there dual AV no dal physiology? Anterograde AVNERP at 600 and 400 ms 4. Extrastimulus pacing from atrium at 600 and 400 ms Is VA conduction present? If so, is atrial activation normal and decremental? Retrograde AVNERP at 600 and 400 ms 5. Extrastimulus pacing from ventricle at 600 and 400 ms Note pacing protocol that induces arrhythmia. Is it reproducible? Compare arrhythmia induce d to clinical arrhythmia. 6. Arrhythmia induction from atrium. Use 2 \200\2234 extrastimuli, sensed extra stimuli, bu rst pacing VERP at 600 and 400 ms 7. If VT suspected, perform Wellen \200\231s protocol Essential for tachycardias with enhanced automaticity mechanism. 8. Repeat steps 2 \200\2237 during isoprenaline infusion AVNERP = atrioventricular nodal effective refractory period; AWCL = anterograde Wenckebach cycle length; RWCL = retrograde Wenckebach cycle length; VERP = ventricular effective refra ctory period. Indications for electrophysiology study \200 Diagnose the mechanism of documented symptom atic tachycardia (usually proceed immediately to ablation) Diagnose the mechanism of tachycardia in a patient with palpitations and suspected arrhythm ia (may proceed immediately to ablation) \200 Determine electrical properties of the acce ssory pathway (Wolff \200\223 Parkinson \200\223White (WPW)) \200\224 stratify the risk of sudden cardiac death (SCD) an d need for ablation Risk strati \201 cation of SCD in patient with impaired left ventricular (LV) function or inherited arrhythmia, e.g. Brugada syndrome and need for implantable cardiac de \201 brill ator (ICD) Diagnose the mechanism of syncope \200\224 when arrhythmia is strongly suspected Look for evidence of AV nodal conduction disease (measure HV interval) and need for pacemaker. 552 CHAPTER 11 Invasive electrophysiology Identifying abnormal AV connections In normal hearts there is only one connection between t he atrium and ven- tricle, the AV node. Activation of the atrium (during V pacing) or ventr icle (during A pacing or SR) should therefore start at the AV node. Accessory pathways (APs ) do not decrement. Their presence can be identi \201 ed by both abnormal activation patte rns and conduction physiology using incre- mental and extrastimulus pacing. Atrial pacing: As the AV node decrements, a greater proportion of ventricular activation wi ll occur via the AP. Thus, non-decremental AV conduction times and broadening of the QRS co mplex will be observed as the pacing interval shortens. Note: If the ERP of the AP is short er 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 dista l) and \201 nally 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 activat ion 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 s car provides the substrate for a tachycardia but does not necessarily imply it will occur. A diagnosis can only be con \201 rmed by inducing the tachycardia. In addition to the paci ng techniques described, burst pacing, extra- stimulus pacing with multiple extrastimuli, a nd sensed extras are deployed. If this fails, pacing maneuvers can be repeated during an is oprenaline infusion (1 \200\2234 mcg/min) or boluses (1 \200\2233 mcg). This is particularl y important for tachycardias with an enhanced automaticity mechanism. \200\230Aggressive \200\231 induction protocols increase the likelihood of inducing an unwanted arrhythmia suc h as AF or VF (ventricular \201 brillation). Once a tachycardia is initiated, it is useful to compare it with a 12-lead ECG recorded dur ing symptoms to ensure this is the clinical arrhythmia. How individual tachycardias are dia gnosed and treated is considered in subsequent chapters. USES OF THE ELECTROPHYSIOLOGY STUDY 553 600 380 HRA His A H V His His RVA Lead I 320 600 H V A 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 pa ced beats (drive train) have been delivered through the HRA at 600 ms and then a single ext ra stimulus. Only the \201 nal two beats of the drive train and the extra stimulus are sh own. 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 d ramatic lengthening of the AH (and AV) time, suggesting dual AVN physiology. 554 CHAPTER 11 Invasive electrophysiology Programmed ventricular stimulation An EP study focusing on induction of ventricular arrhyth mias (the VT stimulation study) has previously been used to risk stratify for SCD, and to d ecide on the effectiveness of antiarrhythmic drugs in suppressing VT, and the need for an I CD. 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: \200 to aid programming of the device: is VT well tolerated haemodynamically? \200 is it easily terminated with overdrive pacing ? \200 is there VA conduction? During V pacing or VT? to assess suitability for VT ablation (e.g. bundle branch VT) \200 are other arrhythmias present and easily induced? Programmed ventricular stimulation is performed using the proto col devised by Wellen, or a modi \201 cation thereof (see below). Protocol for programmed ventricular stimulation \200 From the RV apex, extrastimulus paci ng, reduce the coupling interval until refractory: \200 1 extrastimulus during SR \200 2 extrastimuli during SR \200 1 extrastimulus following 8 paced beats at 600 ms \200 2 extrastimuli following 8 paced be ats at 600 ms \200 1 extrastimulus following 8 paced beats at 400 ms \200 2 extrastimul i following 8 paced beats at 400 ms \200 3 extrastimuli during SR \200 2 extrastimuli f ollowing 8 paced beats at 600 ms \200 3 extrastimuli following 8 paced beats at 400 ms If no ventricular arrhythmia is induced, repeat from RV out \202 ow tract. Thus, the pacing protocol becomes gradually more aggressive. The more aggressive the induct ion protocol, the less speci \201 c the result. The most useful result is induction of a s ustained 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-speci \201 c results. This page intentionally left blank 556 CHAPTER 11 Invasive electrophysiology New technologies Non- \202 uoroscopic three-dimensional mapping EP procedures have become increasingly complex (e.g. ablation of AF or atrial tachycardia in congenital heart disease ), leading to longer proce- dures with greater X-ray exposure. Non- \202 uoroscopic electr oanatomical mapping systems help overcome these challenges by generating a three- dimension al (3D) image as the ablation catheter is moved around the cardiac chamber being mapped. Tw o systems are commonly used; Carto (Biosense Webster) and Navx (St Jude Medical), which loc ate the cath- eters using magnetic and electrical \201 elds respectively. These maps can be used as anatomical guides, and can display the timings (activation maps) or voltages of ICegrams represented by colors. 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 line ar ablation lines. The identi \201 cation of areas of scar (voltage mapping) is essential in VT ablation, as these are critical to its re-entrant mechanism. Non-contact mapping (Ens ite Array, St Jude Medical), allows simultanous collection of ICegrams from the entire endo cardial surface of the chamber in which the catheter is placed. An array of 64 unipolar ele ctrodes, mounted on a balloon, records the signals from the endocardium conducted through t he blood. The \200\230virtual \200\231 ICegrams are reconstructed and displayed on a map o f the chamber. The mechanism of a regular tachycardia can be determined from a single ectop ic beat. Image integration (Fig. 11.4 ) A computed tomography (CT) or magnetic resonance imaging (MR I) scan of the patient \200\231s thorax can be segmented to provide a 3D image of the patie nts own LA (or other chamber). This is then registered with the mapping system (Carto or Na vX) by moving the mapping catheter to at least four anatomical points (e.g. junction of a p ulmonary 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 c an navigate around the complex unique anatomy of a patient \200\231s LA without the need fo r X-ray. Remote navigation of ablation catheters Robotic technologies have been a great success in u rological and cardiac surgery. In order to overcome dif \201 culties with manual catheter manipu- lation in complex procedures, these have been applied in EP \200\224 with the oper ator seated in the lab control room rather than standing by the patient. Proposed advantage s 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 low- intensity magnetic \201 eld is created by two large magnets permanently housed either side of the cathlab tabl e. A purpose-built mapping catheter contains three magnets that align themselves within the magnetic \201 eld. Movement of the catheter is achieved by shifting the magnetic \201 eld around, NEW TECHNOLOGIES 557 controlled by a computer mouse on a desktop. Sensei (Hansen Medical) is a robotic navigatio n 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 c an 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 recon- structed from an MR scan of the heart taken pre-procedure. The image is registered with the 3D mappi ng system. The bottom image is the LA viewed from within at a left lateral projection so th at the ablation lesions that have been delivered around the right pulmonary veins are visib le. 558 CHAPTER 11 Invasive electrophysiology 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 destruct ion of these areas. Energy sources for ablation Radiofrequency (RF) energy Cells are destroyed by heating > 50 C. The RF generator delivers an alter- nating current of 500 \200\223750 KHz between the active catheter electrode and a large indifferent electrode placed on the patient \200\231 s skin. The ions within cells immediately adjacent to the catheter are agitated and generat e 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 su rrounding tissue. A lesion of \210 5 mm depth is formed after 30 \200\22360 s, which is su f \201 cient 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 \202 ow of blood, so the hottest part of an RF lesion is 1 mm beneath the surface. Stasis of \202 ow occurs as the lesion is formed; hence the temperature rises, limiting the amount of power that is delive red and therefore size of the lesion. Heparinized saline, passed through a multiple lumen i n the tip of the catheter at a rate of 10 \200\22330 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 \202 utter). Low- \202 ow (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. Cryoablation Completely contained within the specialized ablation catheter, liquid nitrous oxide released into the tip rapidly vaporizes and removes heat from the tissue in contact w ith the catheter. The gas is rapidly recycled back to the catheter console. The tissue temp erature (monitored at the tip of the catheter) falls to \210\222 30 C, at which stage t here is reversible loss of cell function. If an appropriate response is seen (e.g. loss of pre-excitation during AP ablation,) then the tissue is further cooled to \210\222 70 C for 4 minutes to cause permanent destruction. The ice formed adheres the catheter to the ti ssue, making it very stable. If, however, an adverse change is seen (e.g. AVN block) at \210\222 30 C, then the tissue can be rewarmed, theoretically without permanent damage. This page intentionally left blank