16 arrhythmias2009


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  • Insert Process Fig. 20.13 with verbiage, Insert Animation: Conducting System of the Heart.exe
  • Sinoatrial node located at junction of superior vena cava and the right atrium.
  • 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)
  • 1 no p waves 2. irregular baseline 3.irregular QRS comeplex 4.depressed ST segment 5. normal T waves
  • 16 arrhythmias2009

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