Electrophysiology is the study of electrical activity in the body. There are three main activities in an EP lab: EP studies to record and pace cardiac electrical activity, device implants like pacemakers and ICDs, and catheter ablation to destroy arrhythmia-causing heart tissue. EP studies help diagnose arrhythmias by evaluating conduction speeds and induced rhythms. Devices like pacemakers, ICDs, and CRT devices are implanted to treat arrhythmias and heart failure. Catheter ablation uses energy to destroy specific areas of heart tissue and can cure certain arrhythmias without medications.
2. Basic Principles Electrophysiology: the study of electrical activity in the body Three main activities in the EP lab: EP Studies Device Implants Catheter Ablation
3. Basic Principles Anatomy of the Cardiac Electrical System SA Node AV Node His Bundle Bundle Branches Purkinje Fibers *Remember: The heart has several levels of backup pacing in place.
8. Basic Principles Abnormal Heart Rhythms Bradycardia Failure to generate impulse Failure to propagate impulse Tachycardia Automatic- seen in acutely ill patients Reentry Circuits- most common (SVTs, VT) Triggered
9. Basic Principles Treatment of Arrhythmias Drug Therapy Class I through 5 Antiarrhythmics Watch out for proarrhythmia! Drug toxicity ***Only use antiarrhythmic drugs for patients with significant symptoms or life threatening arrhythmias.
10. Basic Principles Non-pharmacologic Therapies Reverse underlying cause Example: hypokalemia Surgery PCI/CAB for ischemia Devices Pacemaker for bradycardia Ablation Can cure certain tachycardias
11. EP Studies INTRODUCTION TO EP STUDIES An EP study is performed by doing two things: Recording Pacing That’s it! Diagnosis depends on speed of conduction through the system, direction of impulses, and any arrhythmias induced.
12. EP Studies Indications for EP Study Syncope Palpitations Documented tachycardia Suspected SA or AV node disease Risk assessment for Sudden Cardiac Death (SCD)
13. EP Studies Electrode Catheters Can use femoral, subclavian, or IJ access Typically use 5.5 and 6 French sheaths for diagnostic studies Similar to temporary pacing catheters, but with more electrodes near the tip Different shapes for different areas of the heart
15. EP Studies Electrode Catheters A basic study will use two. More complex studies (SVT studies) will use more. ***Multiple catheters in multiple locations can track the speed and direction of electrical impulses across the heart.
16. EP Studies ECG versus EGM Surface ECG is a total of all the electrical activity across the heart EGM = IntracardiacElectrogram Records only the activity of a localized area, i.e. between electrodes on the catheters Faster sweep speed used (typically 100mm/sec)
20. Therefore, we do not see the slower conduction through the SA and AV nodes.
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22. EP Studies Programmed stimulation can be used to: Measure SA node and AV node function Measure refractory periods of nodes and myocardium Induce and terminate Ventricular Tachycardia This can determine which patients receive an ICD implant.
23. Evaluation of SA Node Sa Node = Pacemaker of the Heart Comma- shaped Located near SVC Has sympathetic (“fight”) and parasympathetic (“flight”) innervation *SA Node disease is the most common cause of bradycardia.
24. Evaluation of SA Node Types of SA Node Disease: Intermittent or sustained bradycardia Sudden SA Node arrest Periods of bradycardia with tachycardia Brady-Tachy Syndrome *If significant symptoms are present, these conditions are termed Sick Sinus Syndrome.
25. Evaluation of SA Node Symptoms of SA Node Disease Lightheadedness Dizziness Presyncope Syncope
26. Evaluation of SA Node Causes of SA Node Disease: Fibrosis SA Nodal artery disease Cardiac Trauma Cardiac inflammatory/infiltrative disease Thyroid disorders
27. Evaluation of SA Node Measurement of SA Node Function in EP Lab Sinus node recovery time (SNRT) Based on overdrive suppression Sino-atrial conduction time (SACT) Exit block
28. Evaluation of AV Node AV Node = Rate Regulator of the Heart Located on interatrial septum, near TV Has mostly parasympathetic innervation *AV Node disease is the second major cause of bradycardia.
29. Evaluation of AV Node The major question with AV Node disease is: “Does the patient need a pacemaker?” This depends on: Symptoms Site of conduction block Degree of conduction block
30. Evaluation of AV Node Symptoms are the same as SA Node disease: Lightheadedness Dizziness Presyncope Syncope
31. Evaluation of AV Node Site of AV Block: General Rule: Block located in AV Node = no PPM Block located below AV Node = PPM
32. Evaluation of AV Node Degree of AV Block General Rule: If 1st Degree = no PPM If 2nd Degree = maybe PPM If 3rd Degree = PPM
33. HIS Bundle His Bundle = Conductor to Ventricles Compact bundle of Purkinje fibers arising after AV node Rapid conduction through the fibrous AV skeleton Divides into Right and Left Bundle branches If patient has disease in His Bundle, a PPM may be indicated.
34. Bundle Branches Bundle Branches = Coordinators of Ventricular Contraction Left Bundle Branch divides into two: anterior and posterior All end as Purkinje fibers, which rapidly spread the impulse to all ventricular muscle Order of contraction: septum apex lateral walls base
35. Bundle Branches Any delay in impulse conduction in or below the bundle branches = Interventricular Conduction Delay (ICVD) Can disrupt normal ventricular contraction ICVD leads to wide QRS on surface ECG If delay is significant and leads to heart failure, Cardiac Resynchronization Therapy (CRT) may be indicated.
36. Bundle Branches Take Note: If performing a right heart cath on a patient, be prepared if they have existing LBBB: Swan catheters may hit the Right Bundle Branch, causing Right Bundle Branch Block. Patient would then have complete heart block and need a temporary pacing wire.
37. Device Therapy Three kinds of implants in the EP Lab: Permanent pacemakers (PPM) Implantable Cardioverter-Defibrillators (ICDs) Cardiac Resynchronization Therapy (CRT) devices
38. Device Therapy Implanted Devices Most are implanted in the pectoral region Can have one, two, or three leads Can be programmed in a variety of ways, to suit each individual patient
39. Device Therapy Permanent Pacemakers Indicationsfor use include: Symptomatic Sinus Bradycardia AV Conduction Disease Cardioneurogenic Syncope Bradycardia-induced VT Significant Ventricular Dysfunction with wide QRS
40. Device Therapy Parts of a Pacemaker Generator- contains the circuitry, computer memory, and battery Typical PPM weighs about an ounce (10cc) Leads- usually inserted through venous system to heart Can be active (screwed into heart muscle) or passive (distal tines catch onto heart tissue)
41. Temporary Pacers Settings: Rate mA (current flow) Sensitivity: more sensitivity = less pacing less sensitivity = more pacing asynchronous = pacing regardless of what heart is doing
42. Device Therapy Implantable Cardioverter-Defibrillators Indications for use include: Sustained VT/VF EF < or equal to 35%, Class II/III HF Prior MI with EF < or equal to 30%, Class I HF EF < 40, NSVT, inducible VT Every 3 minutes someone dies from SCA in the USA.
43. Device Therapy Parts of an ICD Generator weighs more that PPM, due to addition of a capacitor Weighs about 3 ounces (36cc) Capacitor stores energy needed for shocks RV lead is designed to deliver shocks to convert VT/VF- looks different from a PPM lead under fluoro
44. Device Therapy Cardiac Resynchronization Therapy Indications for use include: Class III/IV heart failure Dilated or ischemic cardiomyopathy QRS interval > or equal to 120ms EF < or equal to 35% Vast majority of patients fitting this criteria also qualify for ICD therapy. CRT can improve EF up to 10-15%.
45. Device Therapy Parts of a CRT device Generator weighs about Requires placement of an LV lead in coronary sinus Successful transvenous placement in ~95% of patients Other 5% would need surgical placement
46. Cardiac Ablation Ablation: destruction of arrhythmia- causing heart tissue Can be curative, eliminating need for antiarrhytmic drugs or surgery Success rates vary according to arrhythmia, with some over 90%. Major complications occur in about 3% of patients.
47. Cardiac Ablation How it works: Ablation catheter is inserted (usually through femoral vein) to heart, along with electrode catheters for recording. Electrical activity is recorded, and abnormal rhythms are tracked. Ablation catheter is placed at area of arrhythmia, and energy is applied to destroy tissue. Pt is monitored for any further signs of arrhythmia before leaving EP lab.
48. Cardiac Ablation Indications for Catheter Ablation: Symptomatic SVT due to AVNRT, WPW, unifocalatrial tachycardia, and atrial flutter. Atrial fib with lifestyle-limiting symptoms, after inefficacy/intolerance of at least one antiarrhythmic drug. Symptomatic VT.
49. Cardiac Ablation Energy Sources: Direct current: in the early days, the ablation catheter was connected to an external defibrillator Greater than 250J could be delivered inside the heart, heating catheter tip to thousands of degrees Celsius Blood was instantly vaporized, causing rise in pressure and flash of light Created lesions up to 4cm2, with ragged edges Only used to ablate His bundle, with 85% success rate (complications were suprisingly low).
50. Cardiac Ablation Radiofrequency (RF) energy: Most commonly used Same as bovie machines in OR Much lower voltage than direct current- no explosions Creates smaller, discrete lesions No muscle or nerve stimulation- no general anesthesia needed
52. Current challenges in EP: Atrial Fib ablation- making it safer and more effective, with less procedure time Optimizing CRT therapy Getting ICD therapy to more patients who qualify
53. References R. Fogoros. Electrophysiologic Testing, 4th ed. Medtronic.com Stiffler, J. The Diagnostic EP Study. Healthworks www.skillstat.com Ellenbogen and Wood. Cardiac Pacing & ICDs, 5th ed. Eprewards.com
Hinweis der Redaktion
Backup pacing: the SA node has an intrinsic rate of 60-100 bpm. If the SA node fails, the AV node can pick up the pacing at a rate of 40-60 bpm. If the AV node fails, the bundle branches can start pacing at 20-40 bpm. The normally functioning SA node wins out over the other areas because of the principle of overdrive suppression (the fastest impulse generator will over-ride and suppress the slower ones).
If you pick up any introductory EP books, they will spend at least one chapter talking about the action potential. I’m not going to force you to listen to all that, but I do want you to notice the different shapes of the action potential in different areas of the heart. This muscle cell and the SA node cell are shaped differently due to their different functions. Muscle cells must conduct the impulse quickly; therefore, the fast upstroke you see at the beginning allows for fast conduction of impulses. The gradual upstroke in the SA node cell is essential for the property of automaticity (automatic generation of an electrical impulse)- there are potassium ions slowly leaking back and forth in phase 4. The membrane potential is slowly increased, until threshold is reached and an impulse is generated. This cycle repeats at a rate between 60-100 times per minute in a normal heart. This same “slow” conduction takes place in the AV node, allowing the impulse to be slowed before it gets to the ventricles. That slowing allows for atrial contraction to complete and fill the ventricles for systole.
Changing the shape of an action potential will change three things: automaticity, conduction velocity, and refractory periods. This is how anti-arrhythmic drugs work- they change the shape of the action potentials, and therefore change heart rhythm.
Failure to generate: SA node is not creating impulses. Failure to propagate: AV node is not passing impulses to the His/BB system.A word about reentry: since reentry is the most common cause of tachycardias, I’ll explain a bit more. It’s not an easy concept to understand, and I needed to read it many times to get a basic grasp of it. But it is essentially this: there is an obstacle in the heart (scar tissue, anatomic structure) that forces the impulse to go around it. There are 2 different paths the impulse can take: a faster path, or a slower path. By nature, the impulse prefers the faster path. However, if a premature contraction occurs in the heart, this early beat can wind up taking the slower path. When it reaches the end of the slower path, the faster path may then conduct the impulse backwards. At the top of the faster path, the impulse may make a circle and go down the slower path– a circuit is formed. This is all dependent of the refractory periods of the two pathways. The trouble comes in when the impulse contracts nearby muscle tissue at high rates, causing SVTs or VT.
Class I: decrease conduction velocity, increase refractory period (procainamide)Class Ib: decrease refractory period (lidocaine)ClassIc: decrease conduction velocity (flecainide)Class II: decrease sympathetic tone (Beta blockers)Class III: increase refractory period (amiodarone)Class IV: direct membrane effect, mainly with SA and AV nodes (cardizem)Class V: increase vagal tone, mainly with SA and AV nodes (digoxin)
SNRT: a catheter in the HRA will pace faster than intrinsic rate, then measure how long SA Node takes to kick back in after pacing is stopped.SACT: sometimes all impulses generated in the SA node do not make it to the atrial tissue to be conducted to the rest of the heart.
Secondaryvs primary prevention- trials in the last 15 years have focused on primary prevention.