1 / 64

Approaches for Arrhythmias

Approaches for Arrhythmias. Seoul National University Hospital Department of Thoracic & Cardiovascular Surgery. Mechanisms of Arrhythmias. Cellular Physiology of Conduction. Cardiac electrical activity is determined by transmembrane potentials

derron
Download Presentation

Approaches for Arrhythmias

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Approaches for Arrhythmias Seoul National University Hospital Department of Thoracic & Cardiovascular Surgery

  2. Mechanisms of Arrhythmias

  3. Cellular Physiology of Conduction • Cardiac electrical activity is determined by transmembrane potentials • Normally intracellular compartment has more negative than positive ions • Each membrane channel is selective for its particular ions (Na,K,Ca) • Resting membrane potential for most cells is determined by potassium current • Following depolarization, resting potential is resorted by an energy-dependent Na-K exchange pump • The cell regains full capacity to depolarize once refractory period is over

  4. Normal Cardiac Electrical Activity • Transmembrane potential ;Voltage difference (polarized, 70-85mV); more negative in intracellular, more positive in extracellular • Changes of membrane potential ;Flow of positively charged ion from ECF (Na, K, Ca) into intracellular through membrane channel, or gap junction between the cardiac cells • Action potential Phase 0 ; rapid upstroke by Na current at beginning of AP Phase 1 ; top of action potential (depolarized) Phase 2 ; Ca influx slightly later& last longer, plateau of AP Phase 3 ; K efflux from cell, leading to repolarization Phase 4 ; back to membrane potential

  5. Action Potentials of Normal Automatic Cells

  6. Cardiac Conduction Anatomy

  7. Embryology of Conduction TissuesThe position of primodial sinus node is located in the sinoatrial groove between the sinus venosus and primitive atriun

  8. Embryology of Conduction Tissues • Conduction tissue development in normal septation of heart

  9. Anatomy of the Right Atrium

  10. Boundaries of Triangle Koch

  11. Boundaries of Triangle Koch

  12. Posterior Septum & Coronary Sinus

  13. Human Atrial Pacemaker Complex

  14. Normal Sinus Node & Atrium • Heart beat from cells of 5x15mm teardrop-shaped , ability to depolarize spontaneously (phase 4 depolarization). • Impulses spread from SA node over atria, completing atrial depolarization in about 80-100ms. • Although bundles of atrial tissue with some enhanced conduction properties ( Bachman’s bundle, Thorel’s tract ), there are no specialized interatrial tract. • The crista terminalis (particular arrangement of atrial cells) facilitate impulse transmission along their long axis. • Blood supply is from RCA in 55% & circumflex in 45% • Richly innervated by both sympathetic & parasympathetic fibers and responds depending on the balance.

  15. Normal Atrio-ventricular Node • Special cells transmit impulses very slowly, requiring 60 to 130ms to traverse about 1 cm of node. • Slowing of impulse facilitates optimal filling of ventricles afforded by atrial contraction & also protect from racing in response to rapid atrial arrhythmias by not allowing all impulse through. • AV node has rich innervation from both autonomic nervous system. • Blood supply is from RCA in 90% and left circumflex in 10%. • AV node cells have no capacity to depolarize spontaneously, so-called nodal rhythms are in fact generated in the infranodal portion of conduction.

  16. His-Purkinje System & Ventricles • Rapid impulse spread through ventricle is mediated by cells of His-Purkinje system • This network is situated just beneath the endocardial surface • Entire mass of ventricular myocardium is depolarized in about 80-100ms, the same as in the atria. • Blood supply to His and main bundles is from LAD ; the very proximal His may have variable right coronary artery supply. • Cells within the HPS are capable of spontaneous depolarization at rates of from 30 to 50 beats depending on autonomic tone.

  17. Anatomic Principles for AblationThis diagram demonstrates the boundaries of each of four anatomic areas where accessory pathways can occur in WPW syndrome

  18. Ablation for Ventricular Arrhythmias • Nonischemic ventricular tachycardia Cardiomyopathy Prior cardiac surgery for CHD Cardiac tumor Arrhythmogenic RV dysplasia • Ischemic ventricular tachycardias Fibrous scar Presence of aneurysm

  19. Abnormalities of Cardiac Rhythm • Bradyarrhythmias 1. Abnormal impulse formation 2. Abnormal impulse transmission • Tachyarrhythmias 1. Automaticity 2. Reentry 3. Triggered activity

  20. Mechanisms of Bradyarrhythmias • Abnormal impulse formation • Sinus node dysfunction 1. Inappropriate sinus bradycardia 2. Brady-tachy syndrome • Abnormal impulse conduction 1. Atrioventricular block 2. Sinus nodal exit block 3. Bundle branch block

  21. Mechanisms of Tachyarrhythmias • Automaticity 1. Normal automaticity 2. Enhanced normal automaticity 3. Abnormal automaticity • Reentry 1. Anatomic reentry 2. Functional reentry 3. Anisotropic reentry 4. Reflected reentry • Triggered activity 1. Early afterdepolarization 2. Delayed afterdepolarization

  22. Types of Automaticity

  23. Abnormal Automaticity • Rate of firing of SA node or His-Purkinje cells can be increased by catecholamine or sympathetic stimuli • Factors suppressing normal automaticity 1. Hyperkalemia 2. Hypoxemia 3. Acidosis 4. Some anti-arrhythmic drugs • Abnormal automaticity has been observed in cellular preparations of diseased human myocardium • Abnormal automatic arrhythmias usually have rates < 200 bpm

  24. Reentry • Most frequent mechanism of arrhythmias in humans, supraventricular or ventricular • Essential elements of reentrant arrhythmias 1. Presence of a closed loop of electrically excitable tissue 2. Heterogeneity of electrophysiologic properties (conduction velocity & refractoriness) 3. An initiator to begin the reentrant process

  25. Types of Reentry • Anatomic reentry ; in which the impulse circulates around a fixed, anatomically determined path • Functional reentry ; in which the impulse circulates within a circuit whose size is determined by refractory periods of the particular cells • Anisotropic reentry ; in which both anatomic and functional properties participate in determining the path taken by the circulating wavefront • Reflected reentry ; in which the impulse retraces its steps along a linear path to return to or reflect on its point of origin

  26. Reentry Once reentry is established, it continues in the same path and direction until one or more required conditions is no longer satisfied.

  27. Arrhythmias due to Reentry • Supraventricular arrhythmias Orthodromic tachycardia Antidromic reentry in WPW AV nodal reentry, Some cases of atrial tachycardia, Atrial flutter, Atrial fibrillation • Ventricular arrhythmias Uniform-morphology VT Some cases of polymorphic VT Ventricular fibrillation

  28. Reentry in WPW Syndrome

  29. Triggered Activity (1) • Depolarization occurs after normal depolarization • "Triggered" by preceding impulses • Early afterdepolarization (EAD) • At phase 2-3 of action potential • Due to increased inward current (hypoxia, injury) • Decreased repolarization outward current (K+) • Present in high catecholamine state, drugs, long QT, torsade de Pointes • Delayed afterdepolarization (DAD) • At phase 4 of action potential • Due to transient inward current from Calcium overload, ? Na+ current • Frequently show overdrive acceleration • Classically in digitalis intoxication

  30. Triggered Activity (2)

  31. Common Types of Arrhythmias • SVT in patients with WPW syndrome /concealed bypass tracts • AV nodal reentry • Atrial flutter • Automatic atrial tachycardia • Postinfarction uniform VT • Bundle branch reentrant VT

  32. Atrial Flutter

  33. Atrial Fibrillation

  34. Automatic Atrial Tachycardia

  35. Intra-atrial Reentrant SVT

  36. AV Nodal Reentry Tachycardia

  37. Orthrodromic SV Tachycardia

  38. Sustained Ventricular Tachycardia

  39. Ventricular Fibrillation

  40. Diagnosis & Treatment

  41. Diagnosis of Cardiac Arrhythmias • Clinical symptoms • Noninvasive methods 1. Resting electrocardiography 2. Ambulatory electrocardiography 3. Event monitoring 4. Exercise testing 5. Signal-averaged electrocardiography • Invasive methods 1. Electrophysiologic study 2. Endocardial mapping

  42. Symptoms of Arrhythmias • A wide variety of symptoms, ranging from a complete absence of awareness of episode to mild palpitation, light-headedness, syncope, sudden cardiac death. • Additional symptoms include chest pain, throat tightness, or dyspnea, any of which may occur alone or in combination with others.

  43. Therapy for Cardiac Arrhythmias • Pharmacologic therapy • Pacemakers • Catheter ablations • Implantable defibrillators • Surgical therapy

  44. Pharmacologic Treatment • Perfect medication Very high efficacy rate Low rates of side effects Low cost Convenient dosing schedule • Bradyarrhythmias Rarely used (anticholinergic; scopolamine patches, sympathetic stimulants; methylxanthines(theophylline), withdrawl of medication • Tachyarrhythmias Complete suppression is ideal but, decrease in frequency & reduction of severity, shortening of duration

  45. Class I Antiarrhythmic Agents • Mechanism ; depression of fast sodium current as a common feature • Class 1A ; procaine amide, quinidine, disopyramide cause marked decrease in conduction velocity as well as an independent prolongation of repolarization used in preventing or slowing the heart rates.(VT, AF, Af, etc) • Class 1B ; lidocaine, mexiletine cause moderate slowing of conduction with minimal effect on repolarization. • Class 1C ; flecainide, propafenone, cause marked decreases in conduction velocity (more than class 1) but minimal effect on repolarization, in treating almost all supraventricular & ventricular arrhythmias.

  46. Class II Antiarrhythmic Agents • Mechanism ; act by antagonizing the effects of epinephrine and norepinephrine at nerve terminals in the heart and elsewhere • These beta-adrenergic blocking drugs are most useful in treating arrhythmias that depend on AV node for perpetuation (SVT), also adjunctively in ventricular arrhythmias • Side effects include sinus bradycardia or AV block, provocation of CHF, peripheral vascular disease, reactive airway disease, and DM.

  47. Class III Antiarrhythmic Agents • Mechanism ; features of blocking intracellular currents (mainly K ion) responsible for repolarization. • Medications including amiodarone, bretylium, sotalol prolong the QT interval, useful in treating almost all types of supraventricular & ventricular arrhythmias, but bretylium generally limited to use in ischemic ventricular arrhythmia. • Side effects ; aggrevation of sinus bradycardia & AV conduction disturbance, heart failure, proarrhythmia. • Amiodarone ; long tissue halh-life(months), & rare side effect of pulmonary fibrosis occasionally can be fatal

  48. Class IV Antiarrhythmic Agents • Mechanism ; These agents, such as verapamil & diltiazem , block the cardiac calcium channels • Used interchangeably with beta blockers in supraventricular arrhythmias because of their actions on the AV node (slowing ventricular rates during atrial flutter or fibrillation, preventing AV nodal reentry, or orthodromic SVT etc.) • Side effects ; heart failure, bradyarrhythmias as is beta blockers or noncardiac side effects

  49. Indications of Pacemakers • Class I : Pacing definitely indicated Complete heart block < 40 beats Symptomatic type I, II heart block Sinus bradycardia less than 40 beats • Class II : Pacing potentially indicated Asymptomatic complete AV block> 40 beats Type II second-degree AV block • Class III : Pacing not indicated Prolonged PR interval & asymptomatic Type I second degree AV block( Wenckebach)

  50. Surgical Principles of Arrhythmia

More Related