16 arrhythmias2009
- 1. Cardiac Arrhythmias Liu Pin-Ming, M.D., Ph.D. Professor of Medicine Department of Cardiology Sun Yat-sen Memorial Hospital Sun Yat-sen University
- 2. Master the causes, clinical manifestations, ECG characteristics and management principles of common arrhythmias Be familiar with the classification of arrhythmias, and its relevant cardiac electrophysiological mechanisms, and pharmacological treatment of tachyarrhythmias Learning Objectives
- 3. The Cardiac Conduction System
- 4. Normal sinus rhythm Sinoatrial node is cardiac pacemaker Normal sinus rhythm 60-100 beats/min Depolarisation triggers depolarisation of atrial myocardium ( ‘ forest fire ’ ) Conducts more slowly through AV node Conducts rapidly through His bundles and Purkinje fibres
- 5. Arrhythmias Definition: An arrhythmia is an abnormality of rate, regularity, or site of origin of the cardiac impulse or a disturbance in conduction that causes an abnormal sequence of activation. Irregular rhythm Abnormal Rate Conduction abnormality
- 6. Clinical classification of arrhythmias Heart rate (increased/decreased) Heart rhythm (regular/irregular) Site of origin (supraventricular/ventricular) QRS complexes on ECG (narrow/broad)
- 7. Mechanisms Responsible for Arrhythmias Abnormalities of impulse generation A. Alterations of normal automaticity B. Abnormal automaticity C. Triggered activity Early/Delayed afterdepolarization Abnormalities of impulse conduction A. Reentry: 1. Unidirectional block; 2. Anatomic or functional reentrant circuit ; 3. wavelength B. Conduction block Combined abnormalities of impulse generation and conduction
- 8. A: Contractile cell B: Autorhythmic cell: spontaneous depolarization at phase 4 Transmembrane Potentials of Myocardial Cells
- 9. Alterations of normal automaticity Autonomic neurotransmitters
- 10. Triggered activity: Early/Delayed afterdepolarization
- 11. Re-Entry Mechanism Branch 2 has a unidirectional block Impulses can travel retrograde (3 to 2) but not orthograde. An AP will travel down the branch 1, into the common distal path (br 3), then travel retrograde through the unidirectional block in branch 2. When the AP exits the block, if it finds the tissue excitable, it will continue by traveling down (reenter) the branch 1. If it finds the tissue unexcitable (ERP) the AP will die. Timing is critical –AP exiting the block must find excitable tissue to propagate. If it can re-excite the tissue, a circular pathway of high frequency impulses (tachyarrhythmia) will become the source of APs that spread throughout a region of the heart (ventricle) or the entire heart.
- 12. Reentrant Arrhythmias Anatomic or functional reentrant circuit Unidirectional block on one path; Slow conduction on the other path Necessitating 3 requirements
- 13. Diagnostic Approaches to Arrhythmias History and physical examination ECG Ambulatory ECG recording: Holter recording Exercise ECG: treadmill test Trans-esophageal electrophysiological study Invasive electrophysiological study (EPS)
- 14. Management of Arrhythmias Antiarrhythmic drugs Cardiac pacemakers DC cardioversion/defibrillation Implantable cardioverter/defibrillater (ICD) Radiofrequency catheter ablation Surgical operation Non-pharmacological Pharmacological (All antiarrhythmic agents may also be proarrhythmic)
- 15. Vaughan Williams classification of antiarrhythmic drugs Class I : block sodium channels Ia (quinidine, procainamide, disopyramide) AP Ib (lignocaine) AP Ic (flecainide) AP Class II : β -adrenoceptor antagonists (propranolol, sotalol) Class III : prolong action potential and prolong refractory period (suppress re-entrant rhythms) (amiodarone, sotalol) Class IV : Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil, diltiazem) Phase 4 Phase 0 Phase 1 Phase 2 Phase 3 0 mV -80mV II I III IV How about others: adenosine, digoxin?
- 16. Atrial fibrillation: Common Causes Coronary artery disease Hypertensive heart disease Valvular heart disease, mitral stenosis Cardiomyopathy Thyrotoxicosis Occasionally, no structural heart disease, especially paroxysmal atrial fibrillation
- 17. Atrial Fibrillation: ECG Characteristics Absence of P waves Very irregular baseline, f waves, with a rate of 350-600 bpm, best seen in V1, Ⅱ Irregular QRS complex rate, usually normal shape
- 21. Atrial Fibrillation: Auscultation Features Variation in the intensity of S1 Extremely irregular heart rate Pulse deficit (because each contraction is not sufficiently strong to open the aortic valve or transmit an arterial pressure wave through the peripheral arteries)
- 22. Atrial fibrillation: Clinical Considerations Decreased hemodynamic functions —— rapid ventricular rates —— the loss of atrial contraction Risk of systemic embolism 5 to 7 times greater than that in controls
- 23. Atrial fibrillation: Classification and Management Strategies Paroxysmal (<24-48hr): preventing further attacks Persistent: attempting restoration of sinus rhythm Permanent: offering good control of ventricular rate
- 24. Atrial Fibrillation: Treatment Etiological therapy Restoration of sinus rhythm paroxysmal: beta-blocker, propafenone, cedilanid, amiodarone persistent: drugs, DC cardiovertion Control on the ventricular rate digoxin, betablocker Prevention of thromboembolism aspirin or clopidogrel, warfarin
- 25. Atrial flutter: Characteristics Regular sawtooth like wave with a rate of 250-350 bpm Ventricular response may be 1 :1 (300), 2:1 (150), 3:1 (100) or 4:1 (75), etc Severity of the symptoms depends on the ventricular rate Causes are similar to atrial fibrillation
- 26. Atrial flutter: ECG
- 27. Atrial flutter: ECG
- 28. Atrial flutter: ECG
- 29. Paroxysmal SVT —— AVNRT & AVRT: ECG Features Sudden initiation and termination Fixed relationship between p wave and QRS complex, with p often superimposed in ORS-T Regular rate of 150-250 bpm Narrow QRS complexes unless there is an aberrant ventricular conduction or pre-existing bundle branch block
- 30. Paroxysmal SVT —— AVNRT & AVRT: ECG Features
- 31. Mechanism Responsible for AVNRT
- 32. Pre-excitation syndrome Abnormal connection between the atrium and the ventricle
- 33. Pre-excitation syndrome ECG Features Short PR interval Slurred upstroke of QRS complexes (the delta wave) broad QRS complexes Secondary ST-T abnormalities (reflecting modified ventricular repolarization secondary to abnormal depolariozation 11111
- 34. Mechanism Responsible for AVRT
- 36. Paroxysmal SVT: Treatment Vagal maneuvers: Valsalva maneuver or carotid sinus massage First choice of drugs: adenosine 6-12 mg iv, or verapamil 5 mg iv Preferred choice of drugs: propafenone 70 mg iv; cedilanid 0.4-0.6 mg iv S ynchronized DC cardioversion ( shock delivery that is timed with in the QRS complex Radiofrequency catheter ablation
- 37. Radiofrequency Catheter Ablation
- 38. Radiofrequency Catheter Ablation
- 39. Premature Beats Atrial AV junctional Ventricular Clinical considerations ECG features Management strategies
- 40. Normal AP Conduction in Ventricles Initiation site Normal conduction VPB conduction
- 46. Ventricular Tachycardia ECG : ≥3 VPBs in succession at a rate of 100-250 bpm; suggesting VT: ventricular captures, fusion complexes Clinical : coronary heart disease, AMI; dilated cardiomyopathy; signifying myocardial damage Treatment : drugs (lidocaine, amiodarone) DC cardioversion (synchronized)
- 47. Ventricular Tachycardia ECG : ≥3 VPBs in succession at a rate of 100-250 bpm; Non-sustained VT ( ＜ 30 sec), sustained VT suggesting VT: ventricular captures, fusion complexes
- 48. Ventricular Tachycardia A wide QRS tachycardia is VT until proven otherwise. Features suggesting VT include: evidence of AV dissociation independent P waves (shown by arrows here) capture or fusion beats beat to beat variability of the QRS morphology very wide complexes (> 140 ms) same morphology in tachycardia as in ventricular ectopics history of ischaemic heart disease absence of any rS, RS or Rs complexes in the chest leads concordance (chest leads all positive or negative)
- 49. Ventricular Tachycardia A54 year-old woman collapsed 24 hours post MI
- 50. Torsades de Pointes (TDP) ECG : an irregular rapid ventricular rhythm with a periodic twisting axis seen on ECG; long QT interval Etiology : congenital long QT syndrome; acquired long QT syndrome, as antiarrhythmic drugs (ClassⅠa, ClassⅢ); hypokalamia, hypomagnesemia
- 51. Torsades de Pointes (TDP)
- 52. Torsades de Pointes (TDP)
- 53. Torsades de Pointes Management Identifying and treating any precipitating factors MgSO 4 , IV; avoidance of drugs lengthening APD Atropine, isoprenaline infusion or ventricular pacing to increase heart rate Beat-blocker for congenital long QT sydrome
- 54. Ventricular Flutter / Fibrillation Irregular rapid ventricular depolarization No organized ventricular contractions, no pulse, loss of consciousness Most common cause: AMI, drug toxicity, electrolyte disturbances, electric shock, end stage of many disease processes Management: non-synchronized DC defibrillation, cardiopulmonary resuscitation
- 55. Ventricular Fibrillation Chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump.
- 59. DC Defibrillation Defibrillator: used to "shock" the heart from an abnormal rhythm pattern back into a normal rhythm
- 62. Sick Sinus Syndrome (SSS) Definition:characterized by intrinsic inadequacy of sinus node pacemaking and /or conduction failure between sinus node and the rest of the atrium Etiology: coronary heart disease, degenerative process, cardiomyopathy Clinical manifestations: insufficiency of blood supply to important organs
- 63. Sick Sinus Syndrome (SSS) ECG Features Marked sinus bradycardia < 50 bpm measured as SNRT, SACT and IHR Sinus arrest / sinoatrial block Holter recording Bradycardia-tachycardia syndrome atrial tachyarrhythmias Probable coexistence with atrioventricular block
- 64. Sick Sinus Syndrome (SSS)
- 65. Sick Sinus Syndrome (SSS)
- 68. Pacemaker Implantation Failure to generate enough impulses on time Pauses may last for several seconds and cause syncope Definitive therapy for symptomatic bradyarrhythmias requires pacemaker implantation .
- 69. Cardiac Arrhythmias Questions? What are the common causes, ECG features, auscultation characteristics and management strategies of atrial fibrillation? Please list the management protocols of paroxysmal supraventricular tachycardia Please list the concept and ECG findings of sick sinus syndrome Please consider the differential diagnosis of wide QRS tachycardia
- 70. Cardiac Arrhythmias Thank you!
Editor's Notes
- #4: Insert Process Fig. 20.13 with verbiage, Insert Animation: Conducting System of the Heart.exe
- #5: Sinoatrial node located at junction of superior vena cava and the right atrium.
- #7: Narrow originate in atria or AV node Broad originate from ventricles or from atria or AV node wirh aberrant concuction to the ventricles (LBBB or RBBB)
- #18: 1 no p waves 2. irregular baseline 3.irregular QRS comeplex 4.depressed ST segment 5. normal T waves