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1. CARDIOVASCULAR DISEASES ARRYTHMIA

2. MECHANISMS OF CARDIAC ARRYTHMAI Alterations in Impulse Initiation: Automaticity Afterdepolarizations and Triggered Automaticity Abnormal Impulse Conduction: Reentry

3. AUTOMATICITY Spontaneous (phase 4) diastolic depolarization underlies the property of automaticity (pacemaking) The rate of phase 4 depolarization and, therefore, the firing rate of pacemaker cells are dynamically regulated Normal or enhanced automaticity of subsidiary latent pacemakers produces escape rhythms in the setting of failure of more dominant pacemakers

4. AUTOMATICITY

5. A FTERDEPOLARIZATIONS AND TRIGGERED AUTOMATICITY

6. REENTERY D efined as a continuous repetitive propagation of an excitatory wave traveling in a circular path, returning to its site of origin to reactivate that site It is the electrophysiologic mechanism responsible for most of the clinically important arrhythmias

7. REQUIREMENTS FOR THE DEVELOPMENT OF REENTERANCE TACHYCARDIS The one event crucial to the development of a reentrant tachycardia is the failure of a group of fibers to activate during a depolarization wave Adjacent tissue or pathways must have different electrophysiologic properties (conduction and refractoriness) and be joined proximally and distally, forming a circuit Each involved pathway of the circuit must be capable of conducting an impulse in an antegrade and retrograde direction

8. REQUIREMENTS FOR THE DEVELOPMENT OF REENTERANCE TACHYCARDIS Conduction velocity in the normal unblocked pathway must be slow enough relative to the refractoriness of the blocked pathway to allow recovery of the previously blocked pathway Retrograde conduction in this previously blocked pathway must be slow enough to allow the normal pathway to recover, and again be capable of being excited

9. Schematic diagram of reentry

10. THERAPY OF ARRYTHMIA Antiarrythmic drugs Catheter ablation Pacemakers External Defibirilators ICDs (Intracardiac Defibrilators)

11. Antiarrhythmic Drug Therapy The interaction of antiarrhythmic drugs with cardiac tissues and the resulting electrophysiologic changes are complex T he structural similarity of target ion channels R egional differences in the levels of expression of channels and transporters, which change with disease T ime and voltage dependence of drug action T he effect of these drugs on targets other than ion channels

12. The Vaughan-Williams classification of antiarrhythmic action C lass I : local anesthetic effect due to blockade of Na + current C lass II : interference with the action of catecholamines at the adrenergic receptor C lass III : delay of repolarization due to inhibition of K + current or activation of depolarizing current C lass IV : interference with calcium conductance

13. The Vaughan-Williams classification of antiarrhythmic action

14. CATHETER ABLATION

15. ARRYTHMIA BRADYARRYTHMIAS

16. BRADYCARDIA Failure of impulse initiation (SA node dysfunction) Failure of impulse conduction (AV conduction block)

17. B RADYARRYTHMIA S A NODE DYSFUNCTION

18. ETIOLOGIES OF SA NODE DYSFUNCTION EXTRENSIC INTERINSIC Autonomic dysfunction Drugs Hypothyrodism Sleep apnea Hypoxia Endotracheal suctioning Hypothermia Increased ICP Sick Sinus Syndrome (SSS) Coronary artery disease Inflammatory Senile amyloidosis Congenital heart disease Iatrogenic Chest trauma Familial and heriditary diseases

19. CLINICAL MANIFESTATIONS OF SA NODE DYSFUNCTION Asymptomatic Hypotension Syncope Presyncope Fatigue and weakness In many cases, symptoms associated with SA node dysfunction are the result of concomitant cardiovascular disease A significant minority of patients with SSS will develop signs and symptoms of heart failure that may be related to slow or fast heart rates One-third to one-half of patients with SA node dysfunction develop supraventricular tachycardia, usually atrial fibrillation or atrial flutter. The incidence of persistent atrial fibrillation in patients with SA node dysfunction increases with advanced age, hypertension, diabetes mellitus, left ventricular dilation, valvular heart disease, and ventricular pacing. Up to one-quarter of patients with SA node disease will have concurrent AV conduction disease

20. Electrocardiography of SA Node Disease Sinus bradycardia: b y definition sinus bradycardia is a rhythm driven by the SA node with a rate of <60 beats/min; sinus bradycardia is very common and typically benign . Resting heart rates of <60 beats/min are very common in young healthy individuals and physically conditioned subjects. A sinus rate of <40 beats/min in the awake state in the absence of physical conditioning is generally considered abnormal Sinus pause and sinus arrest : s inus pauses of up to 3 s are common in the awake athlete, and pauses of this duration or longer may be observed in asymptomatic elderly subjects Sinus exit block Tachycardia (in SSS) Chronotropic incompitance

21. Diagnostic Testing Resting ECG Holter and event monitors Implantable ECG monitors (12 to 18 months) Exercise testing ( failure to reach 85% of predicted maximal heart rate at peak exercise, or failure to achieve a heart rate > 100 beats/min with exercise or a maximal heart rate with exercise less than two standard deviations below that of an age-matched control population ) Autonomic nervous system Electrophysiologic testing

22. Therapy of Sinoatrial Node Dysfunction Since SA node dysfunction is not associated with increased mortality, the aim of therapy is alleviation of symptoms Chronic pharmacologic therapy for sinus bradyarrhythmias h as limited value (atropin, theophylin and i soproterenol ) Pace maker implantation

23. Summary of Guidelines for Pacemaker Implantation in SA Node Dysfunction

24. BRADYARRYTHMIA ATRIOVENTRICULAR CONDUCTION DISEASE

25. Etiologies of Atrioventricular Block Autonomic dysfunction Metabolic/Endocrine disorders Drug-related Infectious Heritable/Congenital Inflammatory Infiltrative Neoplastic/Traumatic Degenerative Coronary Artery Disease

26. CLASSIFICATION AV BLOCK 1 AV block 2 AV block Mobitz type 1 or Wenckebach Mobitz type 2 3 AV block

27. FIRST DEGREE AV BLOCK Atrioventricular impulse transmission is delayed in first degree AV block, resulting in a PR interval longer than 200 msec (>210 msec at slow heart rates) The PR interval includes activation of the atrium, AV node, His bundle, bundle branches and fascicles, and terminal Purkinje fibers

28. SECOND DEGREE AV BLOCK Mobitz type 1: progressive PR interval prolongation preceded a nonconducted P wave Mobitz type 2: the PR interval remained unchanged prior to the P wave that suddenly failed to conduct to the ventricles

29. THIRD DEGREE AV BLOCK

30. Guideline Summary for Pacemaker Implantation in Acquired AV Block

31. ARRYTHMIA TACHYARRYTHMIAS

32. CLASSIFICATION OF TACHYARRYTHMIAS SVT = supraventricular tachycardia; CSM = carotid sinus massage; AV = atrioventricular; AVNRT = AV nodal reentrant tachycardia; AVRT = AV reciprocating tachycardia; AT = atrial tachycardia; SANRT = sinoatrial nodal reentry tachycardia; AP = accessory pathway

33. Classification of narrow QRS complex tachycardias by structures required for initiation and maintenance

34. PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA The term paroxysmal supraventricular tachycardia (PSVT) is applied to intermittent SVTs other than AF, atrial flutter, and MAT

35. CAUSES OF WIDE QRS COMPLEX TACHYCARDIA

36. TACHYARRYTHMIA SINUS TACHYCARDIA

37. CLASSIFICATION OF SINUS TACHYCARDIA PHYSIOLOGIC INAPPROPRIATE Hyperthyroidism Fever Effective volume depletion Anxiety Pheochromocytoma Sepsis Anemia Hypotension and shock Pulmonary embolism Acute coronary ischemia and myocardial infarction Heart failure Chronic pulmonary disease Hypoxia Exposure to stimulants (nicotine, caffeine) or illicit drugs Inappropriate sinus tachycardia (IST) is an unusual condition that occurs in individuals without apparent heart disease or other cause for sinus tachycardia, such as hyperthyroidism or fever Affected patients have an elevated resting heart rate and/or an exaggerated heart rate response to exercise; many patients have both

38. SYMPTOMS OF SINUS TACHYCARDIA Sinus tachycardia is often asymptomatic, although the patient may complain of a rapid heart beat Underlying cardiac disease Decrease the cardiac output by shortening ventricular filling time Exacerbate coexisting myocardial and/or valvular heart disease Increase myocardial oxygen consumption Reduce coronary blood flow

39. TREATMENT OF SINUS TACHYCARDIA Treatment of physiologic sinus tachycardia is directed at the underlying condition causing the tachycardia response. Uncommonly, beta blockers are used to minimize the tachycardia response if it is determined to be potentially harmful, as may occur in a patient with ischemic heart disease and rate-related anginal symptoms. Pharmacotherapy with beta blockers or catheter ablation can be used for symptomatic patients with IST

40. TACHYARRYTHMIA ATRIAL FIBRILLATION

41. GENERAL REMARKS ABOUT AF AF is the most common sustained arrhythmia Atrial fibrillation (AF) is characterized by rapid and irregular atrial fibrillatory waves at a rate of 350 to 600 impulses/minute and, in the presence of normal atrioventricular (AV) nodal conduction, by an irregularly irregular ventricular response of 90 up to 140 to 170 beats/min, but it may be higher in some patients

42. EPIDEMIOLOGY OF AF

43. EPIDEMIOLOGY OF AF

44. CLASSIFICATION OF AF Paroxysmal (i.e., self-terminating) — AF is classified as paroxysmal if episodes terminate spontaneously in less than seven days, usually less than 24 hours. Persistent AF — AF is classified as persistent if it fails to self-terminate within seven days. Episodes may eventually terminate spontaneously, or they can be terminated by cardioversion. A patient who has had an episode of persistent AF can have later episodes of AF that classify as paroxysmal (i.e., self-terminating in less than seven days). Permanent AF — Permanent AF is considered to be present if the arrhythmia lasts for more than one year and cardioversion either has not been attempted or has failed. "Lone" AF — "Lone" AF describes paroxysmal, persistent, or permanent AF in individuals without structural heart disease

45. ETIOLOGIES OF AF Valvular heart disease Hypertensive heart disease Coronary heart disease H eart failure (10-30%) HCMP (10-28%) Congenital heart disease Other types of cardiopulmonary disease Obesity Hyperthyrodism Surgery Inflammation and infection Autonomic dysfunction Other supraventricular tachyarrhythmias Diet Medications Genetics

46. VALVULAR HEART DISEASE AND AF MS ,MR, and TR — 70 percent MS and MR — 52 percent Isolated MS — 29 percent Isolated MR — 16 percent Isolated AS-1%

47. CLINICAL MANIFESTATIONS OF AF Asymptomatic Symptoms of underlying disease Symptoms directly related to AF(mechanisms) T he loss of atrial contractility T he inappropriate fast ventricular response T he loss of atrial appendage contractility and emptying leading to the risk of clot formation and subsequent thromboembolic events

48. ECG FINDINGS OF AF

49. GENERAL TREATMENT ISSUES Rate control Rhythm control Rate Vs Rhythm control Prevention of systemic embolization Nonpharmacologic therapy

50. FACTORS TO BE CONSIDERED UPON DECIDING A TREATMENT PLAN FOR AF Is the patient hemodynamically stable Is left ventricular function normal or impaired? Does the patient have WPW? Is the duration of AF less than or more than 48 hours? Is anticoagulation indicated? Can the patient undergo electrical cardioversion safely? Is the ventricular rate too high?

51. RATE CONTROL OF AF

52. RATE CONTROL (TARGET HEART RATE) Rest heart rate <= 80 beats/min 24-hour Holter average <= 100 beats/min and no heart rate >110 percent of the age-predicted maximum Heart rate <= 110 beats/min in six minute walk

53. RHYTHM CONTROL S ynchronized external DC cardioversion (75-95%) patients with AF of more than 48 hours duration, of unknown duration, or of less than 48 hours duration in the presence of mitral stenosis or a history of thromboembolism may have atrial thrombi that can embolize. In such patients, cardioversion should be delayed until the patient has been anticoagulated at appropriate levels (INR 2.0 to 3.0) for three to four weeks or shorter term anticoagulation if screening transesophageal echocardiography has excluded atrial and atrial appendage thrombi pharmacologic cardioversion (30-60%)

54. INDICATIONS FOR URGENT CARDIOVERSION Active ischemia Significant hypotension, to which poor LV systolic function, diastolic dysfunction, or associated mitral or aortic valve disease may contribute Severe manifestations of HF The presence of a preexcitation syndrome, which may lead to an extremely rapid ventricular rate

55. PHARMACOLOGIC THERAPY TO MAINTAIN SINUS RHYTHM

56. RATE Vs RHYTHM CONTROL

57. INDICATIONS FOR RHYTHM CONTROL Persistent symptoms (palpitations, dyspnea, lightheadedness, angina, presyncope, and heart failure) despite adequate rate control. An inability to attain adequate rate control Patient preference

58. NONPHARMACOLOGIC APPROACHS Rhythm control  — There are several alternative methods to maintain NSR in patients who are refractory to conventional therapy, including surgery, radiofrequency catheter ablation, and pacemakers   Rate control  — Radiofrequency AV nodal-His bundle ablation with permanent pacemaker placement or AV nodal conduction modification are nonpharmacologic therapies for achieving rate control in patients who do not respond to pharmacologic therapy LAA occlusion or ligation  — Since the vast majority to thrombi in nonvalvular AF arise within or involve the left atrial appendage (LAA), the LAA is occluded at the time of surgery in patients who undergo cardiac surgery for other reasons. Percutaneous approaches have also been evaluated

59. PREVENTION OF SYSTEMIC EMBOLIZATION

60. RISK OF EMBOLIZATION (PAROXYSMAL Vs CHRONIC AF) The stroke risk appears to be equivalent in paroxysmal and chronic AF

61. TACHYARRYTHMIA ATRIAL FLUTTER

62. CLASSIFICATION OF ATRIAL FLUTTER Type I or typical atrial flutter is a macroreentrant arrhythmia , in which a depolarizing stimulus (such as a single atrial ectopic beat) excites an area of the atrium and then travels sufficiently slowly in a pathway that is sufficiently long that there is an "excitable gap," that is, an area behind the wave of depolarization that has recovered its excitability and can be reactivated, thereby forming a circuit. The slowly conducting reentrant circuit is located in the low right atrial isthmus. The isthmus is a path between the orifice of inferior vena cava and the annulus of the tricuspid valve .The reenterant circute may be clockwise or counterclock wise. The flutter rate 240 to 340 beats/min . Type II or true atypical atrial flutter seems to lack an excitable gap, is not isthmus-dependent, and cannot be entrained. It is thought that these characteristics result from an intraatrial reentrant circuit that is very short in contrast to the long isthmus in type I atrial flutter . The flutter rate is 340 to 440 beats/min .

63. ECG FINDINGS OF ATRIAL FLUTTER

64. ETIOLOGY, CLINICAL MANIFESTATION AND MANAGEMENT Etiology, clinical manifestations and management: similar to AF In all patients, an effort should be made to control the ventricular rate pharmacologically or restore sinus rhythm. Rate control with calcium antagonists (diltiazem or verapamil), beta blockers, and/or digoxin may be difficult. Even higher grade AV slowing, such as a 4:1 AV response, may only be transient and is easily overcome with activity or emotional stress. Owing to the typically faster ventricular rate, AFL tends to be poorly tolerated in comparison to AF

65. TACHYARRYTHMIA WOLFF-PARKINSON-WHITE (WPW) SYNDROME

66. ORTHODROMIC TACHYCARDIA IN WPW SYNDROME

67. ANTIDROMIC TACHYCARDIA IN WPW SYNDROME

68. THERAPY OF WPW SYNDROME Asymptomatic patients does not need therapy Symptomatic patients Ablation (catheter/surgical): best option DC cardioversion Pharmacologic (for patients who are not candidates for ablation)

69. PHARMACOTHERAPY FOR WPW SYNDROME

70. PHARMACOTHERAPY FOR WPW SYNDROME

71. ARRYTHMIA VENTRICULAR TACHYCARDIA

72. CLASSIFICATION Duration Nonsustained VT : three or more consecutive ventricular beats at a rate of greater than 1 00 beats/min with a duration of less than 30 seconds . There is, however, great variability in the literature in the definition of this arrhythmia. Some definitions allow a rate of 1 2 0 beats/min or 140 beats/min Sustained : h emodynamically unstable VT that requires termination before 30 s or VT that is terminated by therapy from an implantable defibrillator is also typically classified as sustained

73. CLASSIFICATION 2. Morphology Monomorphic: a uniform QRS complex morphology during VT Polymorphic: beat to beat change in QRS complex morphology Ventricular flutter : appears as a sine wave on the ECG and has a rate of >250 beats/min Ventricular Fibrilation

74. CLASSIFICATION 3. Hemodynamic stability Stable Unstable

75. ETIOLOGY Structural heart disease (IHD,DCMP,HCMP...) Drugs Electrolyte imbalance Anemia Hypoxia Idiopathic

76. CLINICAL MANIFESTATIONS Ventricular rate Presence and extent of underlying heart disease Function of the left ventricle Presence of atrioventricular (AV) asynchrony Location of the myocardial focus; this is associated with a particular, often abnormal, sequence pattern of left ventricular activation

77. D IFERENTIATING VT FROM SVT WITH ABERRANT CONDUCTIONS History: presence of underlying heart disease Physical examination: features of undelying heart disease and evidence for AV dissociation Maneuvers (carotid sinus pressure and pharmacologic interventions) Baseline ECG: preexcitation and LBBB/RBBB ECG during the attack

78. ECG Clues Supporting the Diagnosis of Ventricular Tachycardia

79. FUSION AND CAPTURE (DRESSLER)BEATS

80. D IFERENTIATING VT FROM SVT WITH ABERRANT CONDUCTIONS(BASED ON QRS MORPHOLOGY)

81. MANAGEMENT OF HEMODYNAMICALLY UNSTABLE PATIENTS

82. MANAGEMENT OF HEMODYNAMICALLY STABLE PATIENTS Urgent or elective cardioversion is usually appropriate. Following appropriate conscious sedation, an initial synchronized shock of 100 to 200 joules (monophasic) or 50 to 100 joules (biphasic) is administered. Repeated shocks at higher energies may be performed as necessary. Class I and III antiarrhythmic drugs are generally reserved for refractory or recurrent arrhythmias. Any associated conditions should be treated, including cardiac ischemia, heart failure, electrolyte abnormalities, or drug toxicities

83. PREVENTION OF RECURRENCE Identify and treat reversible causes ICDs Antiarrythmic drugs C atheter ablation

84. ARRYTHMIA DOSAGE, PRIMARY INDICATIONS AND SIDE EFFECTS OF COMMONLY USED ANTIARRYTHMIC DRUGS

85. Commonly Used Antiarrhythmic Agents—Intravenous Dose Range/Primary Indication

86. Commonly Used Antiarrhythmic Agents—Chronic Oral Dosing/Primary Indications

87. Common Nonarrhythmic Toxicity of Most Frequently Used Antiarrhythmic Agents

88. Proarrhythmic Manifestations of Most Frequently Used Antiarrhythmic Agents