Introduction To Electrophysiology


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General introduction to electrophysiology concepts and procedures.

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  • Great overview for those interested in the field of EP!
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  • 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).
  • Posterior, anterior, lateral internodal pathways + Bachmann's bundle
  • 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.
  • Introduction To Electrophysiology

    1. 1. Introduction to ELECTROPHYSIOLOGY<br />What Are They DOING Over There?!<br />
    2. 2. Basic Principles<br />Electrophysiology: the study of electrical activity in the body<br />Three main activities in the EP lab:<br />EP Studies<br />Device Implants<br />Catheter Ablation<br />
    3. 3. Basic Principles<br />Anatomy of the Cardiac Electrical System<br />SA Node<br />AV Node<br />His Bundle<br />Bundle Branches<br />Purkinje Fibers<br />*Remember: The heart has several levels of backup pacing in place.<br />
    4. 4. Basic Principles<br />
    5. 5. Basic Principles<br />Normal path of conduction<br />SA Node AV Node His Bundle Bundle Branches Purkinje Fibers<br />
    6. 6. Basic Principles<br />Cardiac Action Potential<br />
    7. 7. Basic Principles<br />Cardiac Action Potential<br />
    8. 8. Basic Principles<br />Abnormal Heart Rhythms<br />Bradycardia<br />Failure to generate impulse<br />Failure to propagate impulse<br />Tachycardia<br />Automatic- seen in acutely ill patients<br />Reentry Circuits- most common (SVTs, VT)<br />Triggered<br />
    9. 9. Basic Principles<br />Treatment of Arrhythmias<br />Drug Therapy<br />Class I through 5 Antiarrhythmics<br />Watch out for proarrhythmia!<br />Drug toxicity<br />***Only use antiarrhythmic drugs for patients with significant symptoms or life threatening arrhythmias.<br />
    10. 10. Basic Principles<br />Non-pharmacologic Therapies<br />Reverse underlying cause<br />Example: hypokalemia<br />Surgery<br />PCI/CAB for ischemia<br />Devices<br />Pacemaker for bradycardia<br />Ablation<br />Can cure certain tachycardias<br />
    11. 11. EP Studies<br />INTRODUCTION TO EP STUDIES<br />An EP study is performed by doing two things:<br />Recording<br />Pacing<br />That’s it! Diagnosis depends on speed of conduction through the system, direction of impulses, and any arrhythmias induced.<br />
    12. 12. EP Studies<br />Indications for EP Study<br />Syncope<br />Palpitations<br />Documented tachycardia<br />Suspected SA or AV node disease<br />Risk assessment for Sudden Cardiac Death (SCD)<br />
    13. 13. EP Studies<br />Electrode Catheters <br />Can use femoral, subclavian, or IJ access<br />Typically use 5.5 and 6 French sheaths for diagnostic studies<br />Similar to temporary pacing catheters, but with more electrodes near the tip<br />Different shapes for different areas of the heart<br />
    14. 14. EP Studies<br />
    15. 15. EP Studies<br />Electrode Catheters<br />A basic study will use two. <br />More complex studies (SVT studies) will use more.<br />***Multiple catheters in multiple locations can track the speed and direction of electrical impulses across the heart.<br />
    16. 16. EP Studies<br />ECG versus EGM<br />Surface ECG is a total of all the electrical activity across the heart<br />EGM = IntracardiacElectrogram<br />Records only the activity of a localized area, i.e. between electrodes on the catheters<br />Faster sweep speed used (typically 100mm/sec)<br />
    17. 17. EP Studies<br />IntracardiacElectrograms (EGMs)<br />
    18. 18. EP Studies<br /><ul><li>IntracardiacElectrograms
    19. 19. These deflections represent rapid myocardial depolarization only.
    20. 20. Therefore, we do not see the slower conduction through the SA and AV nodes.
    21. 21. Remember the different action potentials of muscles cells versus nodal cells.</li></li></ul><li>EP Studies<br />By manipulating the electrode catheters, pacing can be performed from virtually any area of the heart.<br />Premature impulses are delivered by the EP MD with precise timing and patterns.<br />This is called Programmed Stimulation.<br />A stimulator computer program is used to create the patterns for pacing.<br />
    22. 22. EP Studies<br />Programmed stimulation can be used to:<br />Measure SA node and AV node function<br />Measure refractory periods of nodes and myocardium<br />Induce and terminate Ventricular Tachycardia<br />This can determine which patients receive an ICD implant.<br />
    23. 23. Evaluation of SA Node<br />Sa Node = Pacemaker of the Heart<br />Comma- shaped<br />Located near SVC<br />Has sympathetic (“fight”) and parasympathetic (“flight”) innervation<br />*SA Node disease is the most common cause of bradycardia.<br />
    24. 24. Evaluation of SA Node<br />Types of SA Node Disease:<br />Intermittent or sustained bradycardia<br />Sudden SA Node arrest<br />Periods of bradycardia with tachycardia<br />Brady-Tachy Syndrome<br />*If significant symptoms are present, these conditions are termed Sick Sinus Syndrome.<br />
    25. 25. Evaluation of SA Node<br />Symptoms of SA Node Disease<br />Lightheadedness<br />Dizziness<br />Presyncope<br />Syncope<br />
    26. 26. Evaluation of SA Node<br />Causes of SA Node Disease:<br />Fibrosis<br />SA Nodal artery disease<br />Cardiac Trauma<br />Cardiac inflammatory/infiltrative disease<br />Thyroid disorders<br />
    27. 27. Evaluation of SA Node<br />Measurement of SA Node Function in EP Lab<br />Sinus node recovery time (SNRT)<br />Based on overdrive suppression<br />Sino-atrial conduction time (SACT) <br />Exit block<br />
    28. 28. Evaluation of AV Node<br />AV Node = Rate Regulator of the Heart<br />Located on interatrial septum, near TV<br />Has mostly parasympathetic innervation<br />*AV Node disease is the second major cause of bradycardia.<br />
    29. 29. Evaluation of AV Node<br />The major question with AV Node disease is: “Does the patient need a pacemaker?”<br />This depends on:<br />Symptoms<br />Site of conduction block<br />Degree of conduction block<br />
    30. 30. Evaluation of AV Node<br />Symptoms are the same as SA Node disease:<br />Lightheadedness<br />Dizziness<br />Presyncope<br />Syncope<br />
    31. 31. Evaluation of AV Node<br />Site of AV Block:<br />General Rule:<br />Block located in AV Node = no PPM<br />Block located below AV Node = PPM<br />
    32. 32. Evaluation of AV Node<br />Degree of AV Block<br />General Rule:<br />If 1st Degree = no PPM<br />If 2nd Degree = maybe PPM<br />If 3rd Degree = PPM<br />
    33. 33. HIS Bundle<br />His Bundle = Conductor to Ventricles<br />Compact bundle of Purkinje fibers arising after AV node<br />Rapid conduction through the fibrous AV skeleton<br />Divides into Right and Left Bundle branches<br />If patient has disease in His Bundle, a PPM may be indicated.<br />
    34. 34. Bundle Branches<br />Bundle Branches = Coordinators of Ventricular Contraction<br />Left Bundle Branch divides into two: anterior and posterior<br />All end as Purkinje fibers, which rapidly spread the impulse to all ventricular muscle<br />Order of contraction: septum apex lateral walls base<br />
    35. 35. Bundle Branches<br />Any delay in impulse conduction in or below the bundle branches = Interventricular Conduction Delay (ICVD)<br />Can disrupt normal ventricular contraction<br />ICVD leads to wide QRS on surface ECG<br />If delay is significant and leads to heart failure, Cardiac Resynchronization Therapy (CRT) may be indicated.<br />
    36. 36. Bundle Branches<br />Take Note:<br />If performing a right heart cath on a patient, be prepared if they have existing LBBB:<br />Swan catheters may hit the Right Bundle Branch, causing Right Bundle Branch Block.<br />Patient would then have complete heart block and need a temporary pacing wire.<br />
    37. 37. Device Therapy<br />Three kinds of implants in the EP Lab:<br />Permanent pacemakers (PPM)<br />Implantable Cardioverter-Defibrillators (ICDs)<br />Cardiac Resynchronization Therapy (CRT) devices<br />
    38. 38. Device Therapy<br />Implanted Devices<br />Most are implanted in the pectoral region<br />Can have one, two, or three leads<br />Can be programmed in a variety of ways, to suit each individual patient<br />
    39. 39. Device Therapy<br />Permanent Pacemakers<br />Indicationsfor use include:<br />Symptomatic Sinus Bradycardia<br />AV Conduction Disease<br />Cardioneurogenic Syncope<br />Bradycardia-induced VT<br />Significant Ventricular Dysfunction with wide QRS<br />
    40. 40. Device Therapy<br />Parts of a Pacemaker<br />Generator- contains the circuitry, computer memory, and battery<br />Typical PPM weighs about an ounce (10cc)<br />Leads- usually inserted through venous system to heart <br />Can be active (screwed into heart muscle) or passive (distal tines catch onto heart tissue)<br />
    41. 41. Temporary Pacers<br />Settings: <br />Rate<br />mA (current flow)<br />Sensitivity: more sensitivity = less pacing<br />less sensitivity = more pacing<br /> asynchronous = pacing regardless of what heart is doing<br />
    42. 42. Device Therapy<br />Implantable Cardioverter-Defibrillators<br />Indications for use include:<br />Sustained VT/VF<br />EF < or equal to 35%, Class II/III HF<br />Prior MI with EF < or equal to 30%, Class I HF<br />EF < 40, NSVT, inducible VT<br />Every 3 minutes someone dies from SCA in the USA.<br />
    43. 43. Device Therapy<br />Parts of an ICD<br />Generator weighs more that PPM, due to addition of a capacitor<br />Weighs about 3 ounces (36cc)<br />Capacitor stores energy needed for shocks<br />RV lead is designed to deliver shocks to convert VT/VF- looks different from a PPM lead under fluoro<br />
    44. 44. Device Therapy<br />Cardiac Resynchronization Therapy<br />Indications for use include:<br />Class III/IV heart failure<br />Dilated or ischemic cardiomyopathy<br />QRS interval > or equal to 120ms<br />EF < or equal to 35%<br />Vast majority of patients fitting this criteria also qualify for ICD therapy.<br />CRT can improve EF up to 10-15%.<br />
    45. 45. Device Therapy<br />Parts of a CRT device<br />Generator weighs about <br />Requires placement of an LV lead in coronary sinus <br />Successful transvenous placement in ~95% of patients<br />Other 5% would need surgical placement<br />
    46. 46. Cardiac Ablation<br />Ablation: destruction of arrhythmia- causing heart tissue<br />Can be curative, eliminating need for antiarrhytmic drugs or surgery<br />Success rates vary according to arrhythmia, with some over 90%.<br />Major complications occur in about 3% of patients.<br />
    47. 47. Cardiac Ablation<br />How it works:<br />Ablation catheter is inserted (usually through femoral vein) to heart, along with electrode catheters for recording.<br />Electrical activity is recorded, and abnormal rhythms are tracked.<br />Ablation catheter is placed at area of arrhythmia, and energy is applied to destroy tissue.<br />Pt is monitored for any further signs of arrhythmia before leaving EP lab.<br />
    48. 48. Cardiac Ablation<br />Indications for Catheter Ablation:<br />Symptomatic SVT due to AVNRT, WPW, unifocalatrial tachycardia, and atrial flutter.<br />Atrial fib with lifestyle-limiting symptoms, after inefficacy/intolerance of at least one antiarrhythmic drug.<br />Symptomatic VT.<br />
    49. 49. Cardiac Ablation<br />Energy Sources:<br />Direct current: in the early days, the ablation catheter was connected to an external defibrillator<br />Greater than 250J could be delivered inside the heart, heating catheter tip to thousands of degrees Celsius<br />Blood was instantly vaporized, causing rise in pressure and flash of light<br />Created lesions up to 4cm2, with ragged edges<br />Only used to ablate His bundle, with 85% success rate (complications were suprisingly low).<br />
    50. 50. Cardiac Ablation<br />Radiofrequency (RF) energy:<br />Most commonly used <br />Same as bovie machines in OR<br />Much lower voltage than direct current- no explosions<br />Creates smaller, discrete lesions<br />No muscle or nerve stimulation- no general anesthesia needed<br />
    51. 51. Cardiac Ablation<br />Complications of Ablation:<br />Complete heart block<br />Cardiac perforation and tamponade<br />Creating MR/TR<br />Embolism/stroke<br />Pulmonary vein stenosis<br />Coronary artery lesions<br />
    52. 52. Current challenges in EP:<br />Atrial Fib ablation- making it safer and more effective, with less procedure time<br />Optimizing CRT therapy<br />Getting ICD therapy to more patients who qualify<br />
    53. 53. References<br />R. Fogoros. Electrophysiologic Testing, 4th ed.<br /><br />Stiffler, J. The Diagnostic EP Study. Healthworks<br /><br />Ellenbogen and Wood. Cardiac Pacing & ICDs, 5th ed.<br /><br />