This occurs as the peri- cardium is relatively fixed to the spine and the sternum and therefore fluid in the pericardial space is more likely to accumulate posterolaterally followed by antero- laterally. The accu- mulation of a small pericardial effusion detected on ICE during an AF ablation may indicate an increase in the risk of a late post procedure pericardial effusion while no evidence of effusion on ICE indicates a very low post procedural risk. All EP laboratories should have equipment for emergency pericardiocentesis including rapid access to echocardiography.
In order to keep this as simple as possible the needle used to access the femoral vein and a 0. After confirmation that the wire is within the pericardial space by pushing it as far as possible and ensuring that it is not within one or more cardiac chambers a short sheath and a pigtail catheter can be used to rapidly drain the effusion.
Phrenic Nerve Injury The right phrenic nerve runs alongside the SVC and passes laterally along the RA running anteriorly to the right pulmonary veins passing more closely to the superior than the inferior right pulmonary vein Fig. The left phrenic nerve runs over the fibrous pericardium with a variable course over the LA and LV and terminates in the left hemidiaphragm.
The incidence of phrenic nerve palsy following an AF ablation is approximately 0. This generally occurs with isolation of the right superior pulmonary vein or the superior vena cava. Left phrenic nerve palsy is less common but may occur in left atrial appendage ablation. Various techniques may be used to help map the location of the phrenic nerve before or during catheter ablation.
Pacing at high output may be performed in order to assess for phrenic nerve capture. The vagus nerve is also seen in both images prior to performing this maneuver as muscle relaxants are often administered which will inhibit the effects of pacing on the phrenic nerve.
Additionally the diaphragm can be monitored using fluoroscopy during ablation in the absence of nerve para- lytic agents. More novel techniques such as recording electromyograms from the diaphragm have been described in which either a catheter is positioned in the hepatic vein or modified surface electrodes are positioned over the diaphragm with pacing performed from either subclavian vein. Phrenic nerve palsy is generally noted on CXR as an elevated hemidiaphragm and may be associated with dyspnea, a cough or hiccups.
The majority of phrenic nerve palsy recovery within 9 months. In this lateral image the ascending aorta Ao is anterior to the left atrium LA. The oesophagus Oe is posterior to the left atrial wall.
Also seen in this image is the descending aorta DAo posterior wall of the LA and the anterior portion of the esophagus is variable but may be as little as 5 mm [23].
The location of the esophagus may run either central to the posterior wall of the left atrium, towards the left pulmonary veins or towards the right pulmonary veins as is generally closer at the atrial pulmonary vein junction and in more inferior locations.
Although the esophagus can be clearly visualized on a pre-ablation CT scan the esophagus is a mobile structure and therefore the loca- tion may change during the procedure. Esophageal injury occurs predominantly as a result of direct thermal injury from catheter ablation along the posterior wall of the LA.
Other contributing factors may include damage to the arterial flow to the esophagus as well as to the vagus nerve and plexus. This may result in mucosal erythema, esophagitis or atrioesophageal fistula. Discrete mucosal changes have been noted to be present in approximately half of all patients who undergo catheter ablation for AF with almost one fifth devel- oping esophageal ulceration [24].
The incidence of fistula formation between the left atrium and the esophagus as a result of catheter ablation for AF ranges from 0. Symptoms relating to atrio-esophageal fistula may occur from 3 days to 6 weeks post ablation and are often non specific.
The most common is a pyrexia fol- lowed by neurological symptoms relating to thrombo-embolism. Other symptoms include chest pain and dysphagia.
The white cell count is generally elevated. Management depends on acute recognition of the condition followed by surgical repair. Although the esophagus can be visualized pre-procedure this is generally unreli- able due to intra-procedural movement. The esophagus can be visualized during ablation using fluoroscopy with a marker such as a naso-gastric tube, a temperature probe or barium paste. Esophageal temperature monitoring is performed by some operators using a tem- perature probe.
Evidence for the efficacy in preventing esophageal injury is limited and conflicting and overall there is no general consensus as to whether luminal esophageal temperature is a good predictor of mucosal injury. It is generally considered reasonable to limit maximum power to 25—30 W and to spend no longer than 30 s on one region when ablating along the posterior wall of the left atrium.
It is also common to prescrive proton pump inhibitors post ablation in order to reduce the effects of acid reflux on the esophagus. Coronary Artery Injury This may occur if ablation is performed in close proximity to a coronary artery such as the aortic cusps.
Other regions where ablation may be in close proximity to a coronary artery or one of its branches include the coronary sinus as shown in Fig. Endocardial ablation of accessory pathways along the mitral and tricuspid annu- lus carries a low risk of coronary artery stenosis.
The posterolateral branch of the RCA or the circumflex coronary artery often run closely to this location and this may be a closer to the anterior and inferior walls of the Fig. The RCA originates in the right coronary cusp of the aortic root and courses along the right atrioventricular grove anteriorly and inferiorly where it eventually courses towards the proximal coronary sinus CS.
In this region there is close proximity to the CS. If ablation is being performed in this location a coronary angiogram should be considered and a minimum distance of 5 mm should be maintained between the site of ablation and the coronary artery. Epicardial ablation is now increasingly performed particularly for non-ischemic VT and to a lesser degree ischemic VT. Coronary CT or angiography should be performed in these cases prior to ablation.
One gray is defined as the absorp- tion of 1 J of ionizing radiation by 1 Kg of matter. The equivalent dose Sievert is the absorbed dose in Gy multiplied by the radiation weighting factor which varies according to the source of radiation and is 1 for X-rays.
This can be further modi- fied in order to calculate the effective dose when the radiation is predominantly exposed to certain regions of the body. This can be achieved by reducing the frame rate to as low as possible, minimizing the duration of time performing fluo- roscopy and not taking cine images. The development of 3 D mapping systems has had a significant impact on reducing the need for fluoroscopy particularly in com- plex ablations.
Administration of Sedation and Anesthesia The requirements for sedation and anesthesia vary according to the precise proce- dure being performed. For EP studies minimal doses of sedation are given for anx- iolytic effects as larger doses may reduce the inducibility of the arrhythmia particularly in adrenaline sensitive focal atrial tachycardia and outflow tract tachy- cardia. Moderate doses of sedation are often required for ablation and in particular for performing anatomical lesions such as a cavotricuspid isthmus ablation.
Ablation for AF and complex VT may be performed with moderate to deep sedation or gen- eral anesthesia. There are several potential advantages to the use of general anesthe- sia in such procedures such as minimizing patient discomfort and movement thus facilitating 3D mapping as well as allowing the use of TEE visualization.
Care must be taken in order to minimize the doses of paralytic agents when assessing for phrenic nerve capture. Benzodiazepines and opioids are used in the EP laboratory for their anxiolytic and partial amnesic effects. All patients undergoing any procedure involving the administra- tion of intravenous sedation should have a history and rapid airway assessment prior to starting the procedure. Ideally there should be involvement of an anes- thesiologist.
All patients should be closely monitored post procedure until their vital parameters have returned to normal limits. The most common benzodiazepines used in the EP laboratory are midazolam and diazepam. Although either of these agents can be used midazolam tends to have a shorter duration of action particularly in the elderly or in those with reduced car- diac output, respiratory depression, hepatic and renal impairment.
Midazolam can be administered at a dose of 0. Generally no more than 10 mg is needed for the entire procedure. Midazolam tends to have less effect on suppression of induction of supraven- tricular tachycardia compared to diazepam. Routine administration of the benzodi- azepine antagonist flumazenil should not be performed and this should be reserved only for cases of significant over sedation.
A dose of 0. The patient should be monitored closely for 2 h in order to ensure that there are no further sedative effects as the drug effects wear off. Fentanyl is a useful opioid which can be administered at the start of the case at a dose of 0.
The overall duration of action is approxi- mately 30—60 min. If used in conjunction with a benzodiazepine fentanyl may result in respiratory depression and therefore monitoring is required. The effects of fentanyl can be partially reversed by naloxone at a dose of 0. Propofol is frequently used in the EP laboratory. The individual responsibility for this depends on the country where the procedure is performed. Propofol is gen- erally administered at a dose of 0.
Further doses may be administered in 5 mg boluses if required. It has no significant electrophysi- ological effects on arrhythmia induction. Very occasionally propofol infusion syndrome may occur particularly at higher doses and for longer periods of time.
This may occur as a result of mito- chondrial respiratory chain inhibition or impaired fatty acid metabolism and results in acute refractory bradycardia leading to asystole with either metabolic acidosis, rhabdomyolysis, hyperlipidaemia, and or fatty liver. The only effective treatment for this condition is haemodialysis or haemoperfusion with cardiorespiratory support. Peri-procedural Anticoagulation For the majority of right sided ablations anticoagulation is not required although some operators choose to give low dose heparin in order to try to lower the potential risk of deep venous thrombosis and pulmonary embolism.
For left sided ablations intravenous heparin is administered aiming for an Activated Clotting Time ACT of greater than s. In patients who are already taking oral anticoagulation the decision to continue, discontinue or bridge with heparin depends on the risks of thrombo-embolism compared to the risk of bleeding.
If this is 0 then anticoagulation is generally not required pre-ablation however in all other cases therapeutic anticoagu- lation is recommended for a minimum period of 4 weeks [2] Table 2. This occurs as a result of endothelial injury as well as potential mechanical dysfunction of the left atrium post ablation. It is therefore necessary to administer heparin for left sided ablations aiming for an activated clotting time ACT of s [2] even in patients who are receiving warfa- rin.
In patients who are allergic to heparin bivalirudin may be considered. It is recommended that oral anticoagulation is continued for at least 8 weeks post ablation in these patients and long-term in patients with a higher risk of thromboem- bolism [2]. The choice of whether to continue with oral anticoagulation compared with heparin bridging is largely dependent on individual operator and center experi- ence.
Continuation of warfarin during catheter ablation for AF is likely superior to bridging with heparin with reported lower rates of thrombo-embolism, pericar- dial effusion and major bleeding [27]. Although there is limited data regarding the use of uninterrupted direct oral anticoagulants in AF catheter ablation given the shorter half life of the direct oral anticoagulants minimal interruption can be performed pre-ablation and appears to be effective particularly if a pre-procedure Table 2.
In general provided the patient has normal renal function the last dose of oral anticoagulant can be admin- istered 24 h pre ablation with the first dose post procedure administered 4 h after sheath removal. EP Laboratory Set-Up The EP lab is composed of an EP recording system, a stimulator, a RF generator with the potential for irrigation and an electroanatomic mapping EAM system as well as a cryoablation system and the cables and interfaces which connect these systems.
Additional to this is resuscitation at least one defibrillator with rapid access to a second and ventilation equipment and fluoroscopic equipment for image acquisition Fig. EAM electroana- tomic mapping system How Electrograms Are Derived: Amplification and Filtering Electrograms recorded in the heart are generally less than 5 mV in amplitude and often as small as 0.
In order to display these signals they must be amplified and filtered. Signals may be amplified up to 10, times prior to being filtered. The amplified signal then passes through a high pass filter. This allows higher frequency signals to pass through while removing signals below a designated fre- quency. On the surface ECG this is set very low at 0. For bipolar intracardiac signals this is set higher at 30 Hz which therefore filters out a larger range of low frequen- cies that may occur as a result of catheter movement, electrical farfield or respira- tory variability.
For unipolar intracardiac signals where the morphology of the signal is more relevant the setting is similar to the surface ECG at 0. This signal then passes through an isolation amplifier which isolates the current from the patient and is subsequently transmitted through a low pass filter. This is generally set at Hz for bipolar intracardiac electrograms and filtered and unfiltered unipolar electrograms and Hz for surface ECG sig- nals Fig.
Additionally most EP systems have a notch filter, which removes signals at a specific frequency range generally in the range of electrical frequency. This is often set at 50 Hz in Europe and 60 Hz in North America and is designed to reject interference outside of the range around this. This also has several potential disadvantages including a reduction in the amplitude of certain electrograms such as pulmonary vein potentials as well as the potential to add interference.
For unipolar electrograms the low pass is either minimized or switched off in order to reduce artifact on the signal. If the standard settings are kept on for unipolar signals often an artefactual R wave may appear on the signal. Despite filtering of signals the best policy is to minimize noise in the first place.
This can be due to direct electrical interference from other devices in the lab, leak- age current from other devices as well as electrical cables which may be closely coupled with cables transmitting electrograms. It is therefore important when designing the EP laboratory in the first place that electrical cables are not positioned beside cables used for transmitted electrocardiograms. This cumulative current also may result in considerable elec- trical interference which must be filtered.
Noise which occurs specifically during ablation may often be due to the fact that the pacing function is enabled at the distal electrode at the same time as the ablation function. This is the result of a slight difference in the current between the distal and proximal poles which exists even when pacing is not being performed. Other potential causes include problems with the ablation catheter or cable, issues with the grounding pad and inadequate gel on the back patch.
Electrogram Signals: Unipolar and Bipolar Electrogram signals occur as a result of voltage gradients which occur between myocytes at different phases of the cardiac AP. This therefore records both near and farfield, the latter of which may distort the local signal. Bipolar signals are amplified signals recorded from two closely spaced uni- poles.
In general the distal pole is negative while the proximal pole is positive. Bipolar recordings are affected by the direction of the wave front with respect to the electrode orientation, electrode spacing and configuration and are generally consid- ered more useful in clinical practice. Both types of signal can be used in cardiac mapping for example in exit site and accessory pathway localization where a deep Q wave with no R wave may indicate proximity to the activation site in unipolar electrograms [29].
This is not perfect for localization of the focus. Despite this the electrogram is not significantly earlier than the surface QRS. Although this was the earliest unipolar and bipolar electro- gram on the endocardium this focus was found to be located on the epicardial surface.
The bipolar and unipolar electrograms are on time with the onset of the surface QRS. The unipolar electrogram has no R wave and a deep Q wave.
Although this indicated activating moving away from the catheter the fact that the signal is not early indicated that this was not the focal site of the PVC.
This was mapped to the epicardial surface of the inferior wall of the LV where the local signal was 20 ms ahead. As a result of the difference in the surface area between the tip of the ablation catheter and the dispersive elec- trode pad the maximum zone of resistive heating, which is directly related to current density is generally within 2 mm of the catheter tip. The majority of this is lost in the blood flow as blood has a lower resistance than myocardium.
The rest of the lesion, which is in fact the majority, is formed by conductive heat. The size of the lesion increases as the temperature increases. The actual impedance during RF ablation is dependent on the tissue in contact with the catheter, the temperature, body characteristics, catheter properties, cables and reference patch.
A sudden rise in the impedance as shown in Fig. A thermocouple incorporated into the tip of the ablation catheter measures the temperature. In temperature guided ablation the temperature of the ablation elec- trode is set at the start of the ablation and automatically adjusts power output to Fig.
There is a sudden rise in impedance and temperature at the interface between the catheter and the endocardium. Ablation can also be set at a power limit so that RF is delivered until a certain power is achieved. Lesion sizes are usually 5 mm in diameter but can be increased by the use of a larger diameter ablation catheter or with the addition of irrigation, which flushes the tip of the catheter. Cryoablation Cryoablation has been used in the ablation of slow and accessory pathways ana- tomically close to the compact AV node as well as in pulmonary vein isolation PVI.
There are several potential benefits in the use of this modality. This confers the potential advantage in the case of ablation of a nodal or accessory pathway that is close to the compact AV node where the risk of AV block is considered to be significant. During the application of cryoablation the catheter tends to remain stuck to the tissue which results in increased catheter stability. The concept relies on localised hypothermia at the catheter endocardial surface. There are three biophysical phases to this process.
Freezing — thawing phase This occurs acutely during delivery of cryoablation. During the first few minutes this may be reversible. As a result of this there is an increase in ion concentrations in the extracellular space which becomes hypertonic resulting in a shift of fluid from the intracellular space to the extracellular space. This results in a reduction in intracellular pH causing mitochondrial damage.
There is progressive microcirculatory vasoconstriction resulting in further localised dam- age to the local tissue. Following the completion of localised freezing passive rewarming occurs knowing as thawing. This results in fusion of the ice crystals with further cellular damage as well as resulting in microvascular occlusion as a result of platelet aggregation and microthrombi formation. Hemorrhagic — inflammatory phase As thawing continues the changes in the microvasculature result in regional hyperemia and tissue edema with microscopic hemorrhagic changes and inflam- mation.
This tends to occur within 48 h of the thawing process and may continue for up to 1 week. Replacement — fibrosis phase Replacement fibrosis and apoptosis of cells near the periphery of the lesion occurs within the first week and up to 3 months after the delivery of the lesion. Neovascularisation and collagen remodelling occurs until finally a fibrotic scar forms. Ablation Catheters Ablation catheters in their simplest form delivery energy to the myocardium while providing feedback in terms of tissue temperature and impedance.
They vary in the size of the tip electrode as well as ability to delivery irrigation. Some catheters also provide feedback in terms of contact force data. The majority of available catheters tend to have a platinum tip. Other materials such as gold have also been studied and also appear to be efficacious. Ablation Catheter Size Larger electrode sizes have a larger percentage of surface area exposed to blood rather than endocardium. A higher power is therefore required in order to achieve the target temperature which results in a larger lesion.
Smaller electrodes have a better electrogram resolution. Larger tip catheters have been shown to be more effective with a reduced number of RF applications and reduced fluoroscopy time in atrial flutter ablation [31]. The temperature measured at the tip of the catheter is not a good estimate of the tissue temperature. Irrigation In open loop irrigation saline is flushed through the ablation catheter resulting in cooling of the catheter tip with lowering of the catheter tip temperature resulting in the ability to create deeper lesions, with less focal hot spots and a reduced risk of thrombus formation.
Using the same power and electrode size a catheter with irrigation tends to result in a larger lesion Fig. Temperature feedback is not reliable and therefore abla- tion is limited by power. Although lesion sizes are larger using irrigation they tend to grow beyond 60 s and therefore a longer application should be considered. The rate of irrigation should be altered according to the power delivered.
Contact Force Catheters The contact force and orientation between the catheter tip and the endocardial sur- face provides valuable information regarding whether delivery of RF energy is hav- ing a significant impact on the tissue rather than the blood pool. It has been shown Irrigated Lesion size Fig. Excessive contact force may result in perforation. There are two commercially available contact force catheters which employ different technologies.
This is an irrigated 7. This is able to transmit data regarding directionality of the electrode tip relative to the shaft of the catheter to the processing unit. In order to measure the force applied there are an additional 3 sensors within the shaft. Although this records a minimum change of 1 g every 50 ms the mean force is displayed every 1 s [34]. Minimum contact force, duration of force as well as catheter stability, power, impedance and temperature changes can all be programmed on in order to set a minimum criteria for display of a lesion using Visitag software on Carto 3.
Given the sensitivity of the electrode tip an introducing tool should be used when advanc- ing the catheter through a sheath. A zero baseline reference should also be obtained after the catheter has been in the blood pool for a minimum of 15 min while the catheter is not in contact with any cardiac structure Fig. The Tacticath catheter St. Jude Medical, Cardiology Division, Inc.
The force time interval FTI can also be displayed and may help to guide ablation. Using the Tacticath a contact force greater than 20 g appears to result in durable pulmonary vein isolation while a contact force less than 10 g tended to be associated with recurrences [32].
A target of 20 g with a minimum greater than 10 g and a minimum force time index greater than g appears to result in a higher likelihood of transmural lesions in the left atrium [33]. Vascular Access Electrophysiology catheters are positioned in the heart by gaining access via the central veins; generally the femoral veins for most catheters and occasionally the internal jugular or subclavian veins for coronary sinus catheter placement.
Femoral Cannulation Femoral vein access is the most commonly used for most EP procedures. The femo- ral artery is palpated and cannulation is performed medial to the femoral artery while maintaining a position inferior to the inguinal ligament.
In generally up to three standard EP catheters can be positioned into a femoral vein provided separate cannulations are performed although this depends on the overall size of the patient. If there is any concerns regarding the potential for vein occlusion then the left femoral vein can also be cannulated. The femoral artery may be used to access the left ventricle and in particular LVOT focal tachycardias.
It is important to maximize the distance between the femoral venous and arterial access points in order to minimize the risk of arteriovenous fis- tula. The relationship of the right femoral vein to the femoral artery is shown on the anatomical images in Fig. The course of the left axillary and subclavian vein are shown on the CT scan in Fig. Following infiltration with local anesthesia the needle is directed towards and very slightly deep to the junction of the medial one third of the clavicle with the remainder of the clavicle.
This should be superficial to the first rib. If fluoros- copy is used this can be achieved. If venous flow is not obtained a slightly deeper approach can be made. Provided the needle does not pass medial to the first rib or deep to the first rib via the second intercostal space then a pneumothorax should not occur. Alternatively a venogram can be performed. The advantage of subcla- vian access over internal jugular is that the vein does not appear to collapse and remains patent due to soft tissue attachments with the costoclavicular ligament and the clavicular periostium.
The axillary vein runs anterior to the first rib towards the clavicle. Medial to this it becomes the subclavian vein which joins the superior vena cava.
Also seen in this image is the ascending aorta. At the subclavian axillary junction the subclavian artery is significantly posterior and slightly superior to the vein. These two structures are separated by the anterior scalene muscle which is 1—1. This muscle is not present laterally however and the risk of arterial punc- ture increases in more lateral positions.
More medial to the juncture of the subcla- vian and axillary juncture the apical pleura of the lung is posterior to the vein. It is therefore important to keep the needle as horizontal as possible with only slight increases in depth if a more medial approach is being made.
More inferior loca- tions are also more likely to puncture the pleura and lung due to the conical shape of the chest. Internal Jugular Vein Cannulation of the internal jugular vein may occasionally facilitate positioning of the coronary sinus catheter.
Infiltration of local anaesthesia following by Seldinger cannulation should be performed at the apex of the triangle of Sedillot. This triangle is formed medially by the sternal head of the sternocleidomastoid, laterally by the clavicular head of the sternocleidomastoid and inferiorly by the medial one third of the clavicle. Transient flexion of the neck should help to accentuate these landmarks in most patients if they are not clear.
The right internal jugular passes anterior to the right subclavian artery and joins the right subclavian vein where the two become in innominate vein. The right brachial plexus is shown in yellow palpation of the trachea can be performed while palpating laterally over the sternal head of the sternocleidomastoid into the recess of the triangle. The carotid pulse can also be palpated prior to but not at the same time as cannulation as this often com- presses the internal jugular vein.
The carotid artery runs medial and posterior to the internal jugular although on occasions may only be posterior. Excessive contralat- eral rotation of the head beyond a 45 degree angle pushes the carotid artery more lateral and posterior to the internal jugular vein.
The internal jugular vein generally lies 1—2 cm deep in the skin at the apex of the triangle. The needle should be advanced at a 45 degree angle. Advancing the needle greater than 2 cm increases the risk of a pneumothorax. The use of an ultrasound may be helpful to differentiate between vein and artery.
The artery is in general more medial, deeper, non compressible and has a visible pulsation. The anatomy of the right internal jugular vein is shown on Fig. Electrophysiology Catheters and Positioning Electrophysiology catheters are generally made of platinum coated electrodes with polyurethane coated shafts. They are categorized according to the diameter of the shaft, the number of poles used to record and pace through, the spacing between electrodes and the ability to deflect. Ablation catheters are also categorized accord- ing to the curve, length of the tip of the catheter, ability for irrigation and ability to measure contact force.
Therefore to convert the French size to mm it is simply divided by 3. The majority of diagnostic EP catheters are either 5 Fr or 6 Fr. The number of poles record- ing and pacing can range from 2 up to Commonly quadripolar catheters are posi- tioned in the right atrium, His bundle and right ventricle while a decapolar is positioned in the coronary sinus.
A duodecapolar catheter may be used to map right atrial activa- tion during a cavotricuspid isthmus ablation although this is generally not required. Catheters that are deflectable are easier to position. The high right atrium RA catheter in an EP study is generally positioned in the high posterolateral wall at the junction of the RA with the superior vena cava close to the sinus node.
The catheter can also be positioned in the RA appendage. A non deflectable quadripolar catheter is sufficient for this. The RV catheter is generally best placed along the base or septum. It may be positioned close to the His and used to record the His and ventricular signals. The coronary sinus catheter is initially positioned in the RA and advanced with a clockwise rotation towards the more posterior CS Os in the LAO projection.
Alternatively it can be positioned in the RV and withdrawn with clockwise rotation in the same view. The general locations of EP catheters are shown in Fig. Baseline Measurements Sinus Node Recovery Time SNRT SNRT is measured using the principle of overdrive suppression in which pacing is performed close to the sinus node at a rate faster than the sinus rate and the time taken from the last paced beat to the first intrinsic sinus beat is measured.
This is longer than the baseline sinus rate and generally takes 5 to 6 beats to return to normal after this maneuver is performed. A prolonged sinus node recovery time greater than ms is abnormal. This may not always occur at faster cycle lengths as entry block may intermittently occur in the perinodal cells and therefore not every beat may depolarize the sinus node.
The SNRT is also dependent on the baseline sinus cycle length and is longer for longer baseline cycle lengths and shorter for shorter cycle lengths. This is measured by posi- tioning a catheter close to the sinus node and pacing at a rate slightly faster than the baseline cycle length for a single beat only in order to avoid overdrive suppression.
This is therefore divided by two in order to calculate the SACT. A normal SACT is considered to be to be 50— ms. The normal range is 50— ms. A pro- longed AH interval may occur as a result of intrinsic AV nodal dysfunction, as a result of increased vagal tone or a result of antiarrhythmic drugs. A short AH inter- val can occur spontaneously or under the effect of sympathetic stimulation.
This generally reflects the Fig. The normal range is considered to be between 30 and 55 ms. Intrinsic His dysfunction or antiarrhythmic drugs may prolong the HV interval.
A short HV interval may be seen with accessory pathway conduction which may even be nega- tive. In the presence of accessory pathway conduction the HV does not reflect His- Purkinje conduction but is the result of accessory pathway conduction the true HV interval.
Care must be taken not to confuse the right bundle electrogram as the His elec- trogram as this may artificially lead to what may seem like a short HV interval. This is the longest coupling interval in which the stimulus fails to stimulate the myocardium at twice the diastolic threshold. During decremental atrial extrastimuli the AH interval gradually pro- longs while the HV interval remains the same.
This provides some data on the functional conduction through the AV node. In each case a drive train is performed at a cycle length of ms for 8 beats in order to achieve a steady state. This is followed by a progressively shorter extrastimulus until capture fails to occur. In the case of the atrium and ventricle this is seen as lack of local capture. In most diagnostic EP studies a quadripolar catheter is positioned in the HRA as well as the RV septum and a decapolar catheter is positioned in the coronary sinus.
Pacing is performed from the RV septal catheter at a constant rate faster than the sinus rate. This is to look for the presence of VA conduction, and if present the atrial activation sequence. This generally indicates VA nodal conduction. This is not always the case and it is important not to miss an anteroseptal accessory pathway with decremental retrograde conduction.
On the converse lack of decrement does not always exclude VA conduction as rapid ventricular pacing from the RV may result in infrahisian block. The first paced beat on the left propagates from the RV apex retrogradely up the right bundle and activates the His.
Following this there is atrial activation A1 recorded on the HIS d channel followed shortly there- after by the proximal his recording HIS p. In the following beat there is no conduction from the RV acti- vation followed by His activation and no atrial activation As shown in Fig.
Although this may infer that AVRT is not possible it is generally better to repeat pacing during infusion of isoprenaline where VA conduction may become evident. A ventricular extrastimulus test is performed by pacing at a contant cycle length and adding in an extrastimulus at a progressively shorter cycle length.
This pacing mode is used to calculate the VERP and the retrograde conduction properties. Pacing from the HRA is performed in order to calculate sinus node function. In panel A conduction occurs antegradely over the fast pathway.
In panel B a sudden reduction in the atrial extrastimulus by 20 ms results in an increase in the AH interval by more than 50 ms. Antegrade conduction has suddenly shifted from the fast to a slow pathway. A Brandon-Hill recommended title. Interventional Cardiac Electrophysiology is the first and only comprehensive, state-of-the-art textbook written for practitioners in multiple specialties involved in the care of the arrhythmia patient. Encompassing the entire field of interventional therapy for cardiac rhythm management, from basic science to evidence-based medicine to future directions, topics include: Technology and Therapeutic Techniques — EP techniques; imaging and radiologic technology; device and ablation technology; drug therapy.
Interventional Electrophysiologic Procedures — Diagnostic and physiologic EP techniques; mapping in percutaneous catheter and surgical EP procedures; catheter and surgical ablation; device implantation and management.
New Directions in Interventional Electrophysiology — Hybrid therapy for atrial and ventricular arrhythmias and staged therapy. This book will be essential reading for clinicians and researchers that form the health care team for arrhythmia patients: cardiologists, adult and pediatric clinical electrophysiologists, interventional electrophysiologists, cardiac surgeons practicing arrhythmia surgery, allied health care professionals, pharmacologists, radiologists and anesthesiologists evaluating arrhythmia patients, and basic scientists from the biomedical engineering and experimental physiology disciplines.
Professor Sanjeev Saksena has been involved in this arena for over three decades and has brought his experience to this textbook, assembling editorial leadership from medical and surgical cardiology to provide a global perspective on fundamentals of medical practice, evidence-based therapeutic practices, and emerging research in this field.
This book includes 95 videos. The Essential Visual Guide to Basic Cardiac Electrophysiology Cardiac Electrophysiology: A Visual Guide for Nurses, Techs, and Fellows fulfills the need of allied health personnel and new fellows for a practical, hands-on pictorial guide that clearly illustrates the essential concepts of clinical cardiac electrophysiology. Authored by a team of experts, Cardiac Electrophysiology: A Visual Guide for Nurses, Techs, and Fellows is an invaluable resource for a complex technology, providing superb guidance in acclimating new trainees and personnel to the EP laboratory and empowering them with the knowledge and skills needed to practice clinical electrophysiology.
In the fast paced world of clinical training, students are often inundated with the what of electrophysiology without the why. This new text is designed to tell the story of electrophysiology so that the seemingly disparate myriad observations of clinical practice come into focus as a cohesive and predictable whole.
Presents a unique, conceptually-guided approach to understanding the movement of electrical current through the heart, the impact of various disease states and the positive effect of treatment Reviews electrophysiologic principles and the analytic tools which, when combined with a firm grasp of EP mechanisms, allow the reader to think through any situation Presents the mathematics necessary for the practice of cardiac electrophysiology in an accessible and understandable manner Contains accompanying video clips, including computer simulations showing the flow of electrical current through the heart, which help explain and visualise concepts discussed in the text Includes helpful chapter summaries and full color illustrations aid comprehension.
Effective identification of patients at increased risk of malignant cardiac arrhythmia presently represents a clinically important unmet need. Existing guidelines for the selection of candidates for the prophylactic implantation of cardioverters-defibrillators ICD are based solely on the reduction of ventricular haemodynamic performance.
Although this guidance is based on statistical results of previously conducted randomized clinical trials, available experience shows that it does not serve clinical needs efficiently. The majority of patients who are implanted with ICDs for prophylactic reasons never utilize the device during its technical longevity whilst, at the same time, many patients who succumb to sudden cardiac death do not have ventricular haemodynamic performance particularly compromised.
Recent results also showed that the previous statistical findings of ICD efficacy are not fully reproducible in patients with non-ischemic heart disease and that the reduction of sudden cardiac death after myocardial infarction by external automatic defibrillation vests is lower than expected. Advances in cardiac electrophysiology are needed for better understanding of the mechanisms that are the basis of different arrhythmic abnormalities. Increased understanding of these mechanisms will allow them to be more effectively classified so that optimum therapeutic options can be offered.
Likewise, better understanding of the underlying electrophysiology processes is needed so that novel and more focused randomized clinical trials can be designed. Compared to invasive electrophysiological studies, noninvasive cardiac electrophysiology offers the possibility of screening larger number of patients as well as healthy subjects investigated under different provocations and conditions.
To advance the field, broad spectrum of studies is needed together with meta-analyses and reviews facilitating research interactions.
Skip to content. Author : Douglas P. Handbook of Cardiac Electrophysiology. Author : Francis D. Handbook of Cardiac Electrophysiology Book Review:.
Cardiac Electrophysiology. Author : Andrea Natale,Paul J. Wang,Amin Al-Ahmad,N. Cardiac Electrophysiology Book Review:.
Cardiac Electrophysiology Methods and Models. Author : Daniel C. Sigg,Paul A. Clinical Cardiac Electrophysiology in the Young. Practical Cardiac Electrophysiology. Practical Cardiac Electrophysiology Book Review:.
Frontiers of Cardiac Electrophysiology. Author : M. Rosenbaum,Marcelo V. Frontiers of Cardiac Electrophysiology Book Review:. An Essential Introduction to Cardiac Electrophysiology. Interventional Cardiac Electrophysiology. Author : N. Damiano,Francis E. Interventional Cardiac Electrophysiology Book Review:.
Clinical Cardiac Electrophysiology. Covers anatomic fundamentals of cardiac structures, clinical indications for electrophysiology studies, practicalities and methodology of performing an electrophysiology study, and problems encountered during the procedure. Includes quick clinical summaries and more than illustrations: electrophysiology recordings, ECGs, cardiac anatomy, radiographic images, and electroanatomic maps.
Discusses key topics such as mechanisms of arrhythmias, conventional and electroanatomic mapping systems, fundamentals of cardiac mapping, biophysics of catheter ablation, and much more. Offers real-world guidance on contemporary practice from leading cardiac electrophysiologists Drs. Demosthenes G Katritsis and Fred Morady, with input from a multinational team of electrophysiology fellows and cardiologists.
Ideal as a stand-alone resource or used in conjunction with Dr. Enhanced eBook version included with purchase. Your enhanced eBook allows you to access all of the text, figures, and references from the book on a variety of devices. This new text is designed to tell the story of electrophysiology so that the seemingly disparate myriad observations of clinical practice come into focus as a cohesive and predictable whole.
Presents a unique, conceptually-guided approach to understanding the movement of electrical current through the heart, the impact of various disease states and the positive effect of treatment Reviews electrophysiologic principles and the analytic tools which, when combined with a firm grasp of EP mechanisms, allow the reader to think through any situation Presents the mathematics necessary for the practice of cardiac electrophysiology in an accessible and understandable manner Contains accompanying video clips, including computer simulations showing the flow of electrical current through the heart, which help explain and visualise concepts discussed in the text Includes helpful chapter summaries and full color illustrations aid comprehension.
It represents a compilation of the clinical course, electrophysiologic studies, pharmacological management, and transcatheter ablation therapy in patients from infancy through young adulthood.
Topics include the mechanism, ECG characteristics, electrophysiologic findings, treatment, and prognosis of tachyarrhythmias and bradyarrhythmias; specialized subjects including syncope, cardiac pacemakers, and implantable cardiac defibrillators; pharmacology of antiarrhythmic agents; and the roles of allied healthcare professionals in the management of arrhythmias in the young.
This revised edition includes new or expanded chapters on the molecular biology mechanisms that underlie the structure and function of the cardiac conduction system; new navigation technologies for detecting cardiac arrhythmias while minimizing radiation exposure; genetic disorders of the cardiac impulse; and sudden cardiac death in the young, particularly athletes.
Featuring contributions from practicing clinical cardiac electrophysiologists affiliated with the Michigan Congenital Heart Center at the University of Michigan, Clinical Cardiac Electrophysiology in the Young, Second Edition, is a premier reference for cardiologists, residents, and medical students.
Author : Romeo Vecht,Michael A. In conjunction with a chest X-ray and the echocardiogram it is a fundamental part of the initial investigation of a patient with suspected heart disease. These electrical squiggles have always been difficult for students to understand. In part the problem has been that the formatting of the ECG has only become standard in the last two decades. Some important books have not provided the full twelve-lead ECG.
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