1. The Diagnosis and Management of Cardiac Dysrhythmias - Atrial tachycardia. Pharmacologic treatment 8/19/09

2. Narrow–QRS-complex (SVT) tachycardias (QRS 0.12second) in order of frequency Sinus tachycardia Atrial fibrillation Atrial flutter AV nodal reentry Accessory pathway–mediated tachycardia Atrial tachycardia (ectopic and reentrant) Multifocal atrial tachycardia (MAT) Junctional tachycardia

3. Initial Evaluation Primary Survey Is patient stable or unstable? – stable: determine rhythm, treat accordingly – unstable chest pain, dyspnea, decreased level of conciousness, low BP, CHF, Acute MI If HR is cause of symptom (almost always HR>150): cardiovert Secondary Survey Specific Rhythms – Atrial fib/flutter – Narrow-Complex (Supraventricular) Tachycardia – Wide-Complex Tachycardia, Unknown Type

4. Differential diagnosis for narrow QRS tachycardia.

5. Questions to answer in order to identify an unknown arrhythmia: 1. Is the rate fast (>100 bpm)? Suggest increased/abnormal automaticity or reentry 2. Is the rhythm irregular? Irregular  Suggests atrial fibrillation, 2 nd degree AV block, multifocal atrial tachycardia, or atrial flutter with variable AV block 3. Is the QRS complex narrow or wide? Narrow  Rhythm must originate from the AV node or above Wide  Rhythm may originate from anywhere

6. Questions to answer in order to identify an unknown arrhythmia: 4. Are there P waves? Absent P waves  Suggests atrial fibrillation, ventricular tachycardia, or rhythms originating from the AV node 5. What is the relationship between the P waves and QRS complexes? More P waves than QRS complexes  Suggests 2 nd or 3 rd degree AV block More QRS complexes than P waves  Suggests an accelerated junctional or ventricular rhythm 6. Is the onset/termination of the rhythm abrupt or gradual? Abrupt  Suggests reentrant rhythm Gradual  Suggests altered automaticity

7. PulseMost likely diagnosisECG to rule out Regular and slow (~60 bpm)Sinus rhythm Junctional rhythmComplete heart block Regular and fast (~150 bpm)Atrial flutter with 2:1 AV blockVentricular tachycardia Regular and fast (>150 bpm)AV node re-entrant tachycardiaVentricular tachycardia Irregular and fastAtrial fibrillation with rapid ventricular response Ventricular tachycardia Irregular and slowAtrial fibrillation with controlled ventricular response Ventricular tachycardia Most Likely

8. Four Major Classes of Supraventricular Tachyarrhythmia Sinus tachycardia Paroxysmal supraventricular tachycardia (PSVT) Atrial Fibrillation Atrial flutter

9. Class Antiarrhythmic Drugs Class I Sodium Channel blocker Class II Beta blockers Class III Potassium channel blockers Class IV Calcium channel blockers

10. Sinus Tachycardia

12. Rate: Greater than or equal to 100. Rhythm: Regular. P waves: Upright, consistent, and normal in morphology (if no atrial disease) P–R interval: Between 0.12–0.20 seconds and shortens with increasing heart rate QRS complex: Less than 0.12 seconds, consistent, and normal in morphology

13. Sinus tachycardia ACC/AHA/ESC criteria 1. The presence of a persistent sinus tachycardia (heart rate more than 100 bpm) during the day with excessive rate increase in response to activity and nocturnal normalization of rate as confirmed by a 24-hour Holter recording 2. The tachycardia (and symptoms) is nonparoxysmal 3. P-wave morphology and endocardial activation identical to sinus rhythm 4. Exclusion of a secondary systemic cause (eg, hyperthyroidism, pheochromocytoma, physical deconditioning)

14. Recommendations for Treatment of Inappropriate Sinus Tachycardia The treatment of inappropriate sinus tachycardia is predominantly symptom driven ACC/AHA/ESC Guidelines

15. Paroxysmal Supraventricular Tachycardia

16. Paroxysmal supraventricular tachycardia (PVST) PSVT suspected when a rhythm strip shows a rapid and typically very regular nonsinus rate at about 140 to 220 beats/min (range: 100 to 250 beats/min).

17. PVST The three major types of PSVT Atrial tachycardia (AT) Often MAT Atrioventricular nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT) involving a bypass tract of the type seen in the Wolff- Parkinson-White (WPW) syndrome

18. PSVT A Normal B Atrial tachycardia (MAT) C atrioventricular nodal reentrant tachycardia (AVNRT) D AV reentrant tachycardia (AVRT) involving a bypass tract of the type seen in the Wolff- Parkinson-White (WPW) syndrome

19. AV nodal reentrant tachycardia (AVNRT) Distinct arrhythmia caused by a rapidly circulating impulse in the AV node area. The cardiac impulse literally spins around and around and appears to “chase its own tail.” Reentry can occur in virtually any part of the heart. AVNRT produces a very rapid and regular supraventricular rhythm with rates typically between 140 and 250 beats/min This arrhythmia may occur with otherwise normal hearts or with underlying heart disease. Runs of AVNRT are generally initiated by an APB

20. Tachycardia due to a rapidly circulating impulse in the atrioventricular (AV) node (junction) AV nodal reentrant tachycardia Marked regularity of rhythm rate of about 170 beats/min. No P waves are visible AV nodal reentrant tachycardia

21. Pseudo r in V1 (arrow) and accentuated S waves in 2, 3, aVF (arrow) are pathognomonic for AVNRT. ECG pattern of typical atrioventricular nodal reciprocating tachycardia (AVNRT)

22. Recommendations for Long-Term Treatment of Patients With Recurrent AVNRT

23. Bypass tract (accessory pathway, WPW syndrome ), an abnormal tract of cardiac muscle that connects the atria and ventricles, circumventing the AV node. Tachycardia caused the impulse travels down the normal conduction system (AV node and His bundle) into the ventricles, recycles rapidly up into the atria via the bypass tract, and then goes down the AV node again. Repetition of this large reentrant circuit leads to atrioventricular reentrant (bypass tract) tachycardia (AVRT), a type of PSVT ATRIOVENTRICULAR REENTRANT (AVRT) TACHYCARDIA

24. Accessory Pathways Causing PSVT. Accessory pathways (Wolff- Parkinson-White syndrome) among other bypass types. In Wolff-Parkinson-White syndrome, a shortened PR interval and a slurred upstrike to the QRS complex “delta wave” on the resting ECG indicate the presence of an accessory pathway ATRIOVENTRICULAR REENTRANT (AVRT) TACHYCARDIA

25. Recommendations for Long-Term Therapy of Accessory Pathway–Mediated Arrhythmias

26. Atrial tachycardia (AT) Three or more consecutive Atrial Premature beats (APB) Most episodes involve an ectopic (nonsinus) pacemaker located in either the left or right atrium that fires off “automatically” in a rapid way. AT has been observed in patients without apparent structural cardiac abnormality as well as in those with virtually any type of heart disease. The atrial rate with AT may be as high as 200 beats per minute or faster (usual range: 100 to 250 beats/min). A sustained episode that lasts 30 seconds or longer in individuals with limited reserve, can induce angina or congestive heart failure (CHF).

27. Atrial tachycardia terminating with resumption of sinus rhythm. The P waves of the tachycardia (rate: about 150 beats/min) are superimposed on the preceding T waves. Atrial tachycardia (AT)

28. MULTIFOCAL ATRIAL TACHYCARDIA Tachyarrhythmia with multiple ectopic foci stimulating the atria. Three or more (nonsinus) P waves with different shapes at a rate of 100 or more per minute. The PR intervals often vary. MAT is usually seen in patients with chronic lung disease. Ventricular rate is irregular and rapid, making this arrhythmia likely to be mistaken for AF.

29. Rapidly occurring P waves showing variable shapes and variable PR intervals

30. MAT Increased Automaticity Causing PSVT Increased automaticity usually occurs when the atrium is enlarged, as in patients with chronic lung disease, congestive heart failure, or electrolyte and acid-base disturbances. Usually, the stretched atria fire irregularly, producing multiple premature beats that emanate from different areas of the atria. Because the foci for the ectopic beats are in multiple sites, the P waves vary in morphology “multifocal atrial tachycardia.”

31. MAT Treatment is directed at correcting the underlying cause. Antiarrhythmic drugs are usually not helpful.

32. Younger patients and individuals without significant underlying cardiovascular disease may tolerate heart rates up to 250 beats/min with complaints of only palpitations or light- headedness. In patients with limited cardiac reserve, however, a heart rate above 160 beats/min (or even less) may result hypotension, stroke myocardial ischemia/ infarction may occur, CHF Treatment Options for Supraventricular Tachycardias

33. Electrical cardioversion should be performed urgently if PSVT is sustained and there is Angina Shortness of breath Decreased level of consciousness Hypotension Congestive heart failure

34. Treatment Options for Supraventricular Tachycardias If the symptoms are restricted to discomfort (e.g., palpitations and anxiety), conservative measures should be applied. Conservative management of PSVT can include both nonpharmacologic and pharmacologic measures

35. Treatment Options for Supraventricular Tachycardias

37. The goal of pharmacologic management is to slow or block atrioventricular nodal conduction. Agents used for this purpose include Adenosine Calcium channel blockers Beta blockers.

38. Adenosine Adenosine works by reducing conductance along the slow antegrade pathway Ultra–short-acting agent that is cleared quickly (half-life of 1 to 6 seconds). Initial dose of 6 mg, followed by or two 12-mg boluses. Side effects include flushing, dyspnea, chest pain and sense of doom. Warn first. Can also decrease the sinus rate transiently and produce a “rebound” sinus tachycardia and should not be used in patients with heart transplants, because such may be highly suseptible

39. Calcium Channel Blockers Disrupt a reentrant pathway. Verapamil can be given in a 5- to 10-mg bolus over 2 minutes, followed by 10 mg in 15 to 30 minutes if the initial dose does not convert the arrhythmia. Diltiazem is also effective. Initial treatment consists of a bolus of 0.25 mg per kg administered over two minutes. A repeat bolus of 0.35 mg per kg given over two minutes can be administered 15 minutes later. Calcium channel blockers should not be used in patients with an undiagnosed wide-complex tachycardia, because of the risk of fatal hypotension or ventricular fibrillation if the arrhythmia is actually ventricular tachycardia and not PSVT.

40. Beta Blockers Esmolol, a short-acting beta blocker given in anintravenous bolus of 0.5 mg per kg over 1 minute or in an infusion at a rate of 0.5 mg per kg per minute after an initial loading dose of 0.5 mg per kg. Short half-life (four to five minutes), compared with the much longer half-lives (three hours or more) of most other beta blockers. Because of a similar depressive effect on left ventricular contractility, esmolol should be used with caution if initial treatment with a calcium channel blocker is not successful.

41. Treatment Options for Supraventricular Tachycardias Other antiarrhythmic drugs, including quinidine, procainamide, flecainide (Tambocor), and amiodarone, may be used in patients if not responsive to initial therapy. Selective radiofrequency ablation is rapidly becoming the treatment of choice in this situation.

42. Summary PSVT EF Normal – Ca-blocker> beta-blocker> digoxin> DC Cardioversion. – Consider procainamide, sotalol, amiodarone. – If unstable proceed to cardioversion EF < 40%, CHF – Digoxin or amiodarone or diltiazem. – If unstable proceed to cardioversion

43. Atrial Fibrillation/Flutter

44. Atrial Fibrillation Atrial fibrillation is caused by numerous wavelets of depolarization spreading throughout the atria simultaneously, leading to an absence of coordinated atrial contraction. Atrial fibrillation is important because it can lead to: Hemodynamic compromise Systemic embolization Symptoms www.uptodate.com

45. Atrial fibrilation Affects 3 to 5 percent of patients more than 60 years The median age of patients with atrial fibrillation is 75 years, and the prevalence of the arrhythmia doubles every 10 years after the age of 55

46. A Fib Risk factors Most risk factors for atrial fibrillation are associated with structural or ischemic heartdisease. Hypertension, Left ventricular hypertrophy Dilated and restrictive cardiomyopathies Coronary artery disease Chronic obstructive pulmonary disease Diabetes in women

47. Afib The annual risk of stroke in patients with atrial fibrillation and normal valve function is about 4.5 percent per year. Anticoagulation with warfarin (Coumadin) reduces the risk by about two thirds.

48. Atrial Fibrillation EKG Characteristics:Absent P waves Presence of fine “fibrillatory” waves which vary in amplitude and morphology Irregularly irregular ventricular response

49. A fib The first step in managing a patient with atrial fibrillation is to decide – If there is a high likelihood of safe conversion to sinus rhythm – Or the patient should be allowed to remain in atrial fibrillation.

50. Restoration of Sinus Rhythm. In General To Convert Within 48 hours of the onset of new atrial fibrillation are candidates for cardioversion with a low risk of embolism. Or Not More than 48 hours or for an undetermined period are more likely to have atrial thrombi and may develop emboli with immediate electrical or medical (pharmacologic) cardioversion.

52. A Fib Conversion Transesophageal echocardiogram to evaluate for thrombi If present anticoagulation is recommended before cardioversion is attempted. Anticoagulation can be accomplished using warfarin, with the dosage adjusted to achieve an International Normalized Ratio (INR) between 2.0 and 3.0 for a minimum of 21 days

53. A Fib Synchronized cardioversion in appropriately selected patients, has a success rate of at least 80 percent. Electrical Cardioversion is preferred in patients with hypotension, angina, heart failure, or other evidence of severe compromise.

55. A Fib Amiodarone therapy is successful in 86 percent of patients who have had atrial fibrillation for less than two years. Treatment is also effective in 40 to 60 percent of patients with long-standing atrial fibrillation that has been resistant to other agents and to electrical cardioversion

56. A Fib Rate Control In patients in whom rhythm conversion is not indicated or those who have new onset atrial fibrillation with a rapid ventricular response, treatment may be needed to control the ventricular rhythm. Excessive ventricular rates may result in diminished cardiac output because of poor filling time, and in ischemia because of increased myocardial oxygen demand.

57. Afib Acute management of ventricular rates can usually be achieved with intravenously administered Calcium channel diltiazem(Cardizem), given in an initial bolus of 15 to 20 mg(0.25 mg per kg) over two minutes Beta blocker such as propranolol (Inderal), given in a dose of 0.5 to 1 mg (up to 3 to 5 mg if needed).

59. A Fib Rate Control Beta blockers are recommended in a consensus by the American and European societies of Cardiology and the North American Society of Pacing and Electrophysiology. Propranolol, metoprolol or atenolol are examples of drugs that have been shown to be effective Side effects including hypotension fatigue depression bronchospasm may prevent use in some

60. A Fib Rate Control Calcium channel blockers are associated with better exercise tolerance, may be preferable to beta blockers. Digoxin is associated with a high degree of exercise intolerance; should be reserved for use in patients who are – relatively immobile – cannot tolerate other treatment options – who have significant ventricular dysfunction.

61. Atrial Flutter

62. Most cases of atrial flutter are caused by a large reentrant circuit in the wall of the right atrium EKG Characteristics:Biphasic “sawtooth” flutter waves at a rate of ~ 300 bpm Flutter waves have constant amplitude, duration, and morphology through the cardiac cycle There is usually either a 2:1 or 4:1 block at the AV node, resulting in ventricular rates of either 150 or 75

63. Unmasking of Flutter Waves In the presence of 2:1 AV block, the flutter waves may not be immediately apparent. These can be brought out by administration of adenosine.

64. Management of atrial flutter

65. Recommendations for Acute Management of Atrial Flutter

66. Cardioversion should be considered only if the patient is anticoagulated (INR equals 2 to 3), the arrhythmia is less than 48 hours in duration, or the TEE shows no atrial clots. Digitalis may be especially useful for rate control in patients with heart failure. Ibutilide should not be taken by patients with reduced LV function. Flecainide, propafenone, and procainamide should not be used unless they are combined with an AV- nodal–blocking agent.

67. Atrial Flutter Atrial flutter is due to a large reentrant circuit usually originating in the right atrium. In the ventricles, reentry may lead to VPBs and sometimes ventricular tachycardia.

68. Recommendations for Long-Term Management of Atrial Flutter

69. Atrial fibrillation/flutter Summary If unstable: proceed more urgently Cardioversion For tachycardia with serious signs and symptoms. Generally not needed for HR<150. If HR>150, prepare for immediate cardioversion. May give brief drug trial. Steps: – Prepare emergency equipment – Medicate if possible – Cardioversion monomorphic VT with pulse, PSVT, A fib, A flutter: 100-200-300-360 J* (Synchronized) – may try 50J first for PSVT or A flutter – may use equivalent biphasic (biphasic 70, 120, 150, and 170 J) – if machine unable to synchronize and patient critical, defibrillate polymorphic VT: use VT/VF algorithm

70. Atrial fibrillation/flutter Summary Management: Control rate, consider rhythm cardioversion and anticoagulate depending on physiologic reserve Normal EF Rate control: Ca-blocker or beta-blocker. Cardiovert: – If onset < 48 hours, consider DC cardioversion OR with one of the following agents: amiodarone, ibutilide, procainamide, (flecainide, propafenone), sotalol. – If onset > 48 hours: avoid drugs that may cardiovert (e.g. amiodarone). Either: Delayed Cardioversion: anticoagulate adequately x 3 weeks, then cardioversion, then anticoagulate x 4 weeks Early Cardioversion: iv heparin, then TEE, then cardioversion within 24 hours, then anticoagulate x 4 weeks Anticoagulate if not contraindicated, if A fib > 48 hrs

71. Atrial fibrillation/flutter Summary Management: Control rate, consider rhythm cardioversion and anticoagulate depending on physiologic reserve EF <40% or CHF Rate control: – digoxin, diltizaem, amiodarone (avoid if onset of AF > 48 hours). – avoid verapamil, beta-blockers, ibutilide, procainamide (and propafenone/flecainide) Cardiovert: Amiodarone. Anticoagulate, if A fib > 48 hr.

72. WPW A Fib Suggested by: delta wave on resting EKG, very young patient, HR>300 Avoid adenosine, beta-blocker, Ca-blocker, or Digoxin If < 48 hour: – If EF normal: one of the following for both rate control and cardioversion: amiodarone, procainamide, propafenone, sotalol, flecainide – If EF abnormal or CHF: amiodarone or cardioversion If > 48 hour – Medication listed above may be associated with risk of emboli – Anticoagulate and DC Cardioversion