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Supraventricular Arrhythmia

Supraventricular Arrhythmia. Israel Freeman, MD Associate Professor of Clinical Medicine. Cardiac Arrhythmias-Outline. Supraventricular Arrythmias - Regular: Sinus tachycardia Paroxysmal Atrial Tachycardia AV Reentry Tachycardias

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Supraventricular Arrhythmia

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  1. Supraventricular Arrhythmia Israel Freeman, MD Associate Professor of Clinical Medicine

  2. Cardiac Arrhythmias-Outline • Supraventricular Arrythmias - Regular: Sinus tachycardia Paroxysmal Atrial Tachycardia AV Reentry Tachycardias Atrial Flutter with constant conduction - Irregular: Atrial Fibrillation/ Flutter with irregular conduction Multifocal Atrial Tachycardia • Bradyarrhythmias Sinus bradycardia Sinus Pause AV Block • Ventricular tachyarrhythmias Premature ventricular contraction Ventricular tachycardia Ventricular fibrillation

  3. Introduction • Sustained supraventricular tachyarrhythmias usually permit adequate cardiac output • Sustained ventricular arrhythmias often cause collapse or death

  4. Atrial Fibrillation

  5. Atrial Fibrillation • Rapid, irregular electric waves of depolorization of the atria (f = 400 beat / min) • The disordered electrical activity conducts only part of those impulses through the AV node (decremental conduction) leading to the sporadic ventricular contractions • The disordered atrial activation results in loss of a coordinated atrial contraction • EKG: Absence of visible discreet P waves, or the presence of irregular fibrialltion waves and an irregular ventricular response

  6. ECG Showing Atrial Fibrillation and Normal Sinus Rhythms (a) Electrocardiographic tracing and (b) intracardiac atrial electrographic tracing during AF (left) and NSR (right). In AF, atrial depolarization occurs with multiple wavelets of electrical activation. Conduction to the AVN is irregular and rapid, resulting in irregular conduction to the ventricles and loss of synchronous atrial contraction. In NSR, the sinus node initiates a regular electrical impulse, which is conducted with a uniform depolarization wave through the atria to the AVN.

  7. Atrial Fibrillation

  8. Atrial Fibrillation • Paroxysmal • Chronic (chronic paroxysmal) • Acute (onset within 24 – 48 hrs) • Lone (younger than 60, no HTN no CVD no Pulmonary disease)

  9. Atrial Flutter

  10. Most Common Associated Heart Disease Hypertensive heart diseaseIschemic heart disease Other Associated Conditions Rheumatic valvular diseaseCardiomyopathyNonrheumatic valvular diseaseCongestive heart failureCongenital heart diseasePulmonary embolismThyrotoxicosisChronic lung diseaseWolff-Parkinson-White syndromePericarditisNeoplastic diseasePostoperative stateNormal heart affected by: alcohol, stress, drugs, excessive caffeine, hypoxia, hypokalemia, hypoglycemia, infection Factors Predisposing to Atrial Fibrillation .

  11. Atrial fibrillation accounts for 1/3 of all patient discharges with arrhythmia as principal diagnosis. • 6% PSVT • 6% PVCs • 18% Unspecified • 4% Atrial Flutter • 9% SSS • 34% Atrial Fibrillation • 8% Conduction Disease • 10% VT • 3% SCD 2% VF Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.

  12. Prevalence of Atrial Fibrillation in the U.S. Estimated prevalence of atrial fibrillation in the United States.8

  13. Atrial Fibrillation Morbidity and Mortality • Two fold increase in CV moratality • The most important consequence of AF are thromboembolic events and stroke • AF is one of the most potent risk factors for stroke • 4 – 6 fold increase risk of stroke/15 fold with h/o RHD • Persistent rapid ventricular rate associated with AF may lead to tachycardia induced cardiomyopathy (reversible) • limitation in functional capacity from symptoms of palpitations, fatigue, dyspnea, angina, or CHF

  14. Risk Event Rate CategoriesAge < 65 yearsNo risk factorsOne or more risk factors (95% CI) 1% (0.3-3.1)4.9% (3.0-8.1) Age 65-75 yearsNo risk factorsOne or more risk factors 4.3% (2.7-7.1)5.7% (3.9-8.3) Age > 75 yearsNo risk factorsOne or more risk factors 3.5% (1.6-7.7)8.1% (4.7-13.9) Annual Event Rates per Age Groups and Risk Factors* *Risk factors are history of hypertension, history of diabetes, or history of prior stroke or transient ischemic attacks.

  15. Tachycardia - Induced Cardiomyopathy • Chronic tachycardia in otherwise structurally normal heart sole cause of developing ventricular dysfunction • Animal models: Pacing at 240 bpm x 3 weeks  low output CHF • Can follow any chronic cardiac tachyarrhythmia Fenelon G et al. Pacing Clinical Electrophysiol 1996;19:95

  16. Atrial Fibrillation Morbidity and Mortality • Two fold increase in CV moratality • The most important consequence of AF are thromboembolic events and stroke • AF is one of the most potent risk factors for stroke • 4 – 6 fold increase risk of stroke/15 fold with h/o RHD • Persistent rapid ventricular rate associated with AF may lead to tachycardia induced cardiomyopathy (reversible) • limitation in functional capacity from symptoms of palpitations, fatigue, dyspnea, angina, or CHF

  17. Atrial Fibrillation Diagnosis and Clinical Manifestation • Palpitation • Angina • CHF • Diastolic Dysfunction due to rapid rate • Systolic Dysfunction • loss of atrial kick • Loss of AV synchrony • Stock and Thromboembolic events

  18. Atrial Fibrillation Diagnosis • History – precipitating factors Alcohol, Caffeine, sympathomimetic drugs • Laboratory study: Electrolytes, TFT substance abuse • Echocardiogram (VHD, LVF) • Holter (iniciating arrhythmia: SVT, A. Flutter, Bradycardia induced) • EST ( R/O ischemia)

  19. Atrial Fibrillation Management – Ventricular Rate Control Agents that slow AV conduction • Digoxin: less effective in controling paroxysmal, A.F ventricular rates or rates during hyperadrenergic slates (exercise, ICU settings) • Beta Blockers • Calcium Channel Blockers • Sotalol, Amiodarone, flecainide

  20. Adequate Rate Control • At office visits • Apical heart rate (sitting): 80 / min • On 24-hour Holter monitor • Goal: average hourly heart rate  80 / min; no hour  100-100 / min • Exercise testing (if available) • Inadequate:  85% age-predicated maximum heart rate in stage I (Bruce) or 3 min of exercise

  21. Atrial Fibrillation Management Restoring of Sinus Rhythm (Evaluate anticoagulation need) • Synchronized Cardio version • Pharmacological • Procainamide • Ibotilide (Class III) Maintenance of Sinus Rhythm • Often requires antiarrhytmias • Class IA (Quinitine, Procainamide) may enhance AV conduction and ventricular response. QT prolongation 50% success in 1 year. To be started in the hospital • Class IC (Flecainide, Propatenone) CAST contraindicated in patients with CAD and CHF • Class III (Amiodarone, Sotalol), Amiodarone Pulmonary Toxicity – doze dependent

  22. Pharmacologic Cardioversion • Class Ia agents • procainamide (Procanbid) • quinidine (Quinidex, Quinaglute) • disopyramide (Norpace) • Class Ic agents • flecainide (Tambocor) • propafenone (Rhythmol) • Class III agents • amiodarone (Cordarone) - acute efficacy 16%-71% • sotalol (Betapace) • ibutilide - efficacy for flutter (63%), fib (31%) • dofetilide (Tikosyn)

  23. Preference for Acute Cardioversion • i.v. Ibutilide • i.v. Procainamide • Other: • Oral Flecainide • Oral Propafenone • DC Cardioversion

  24. Atrial Fibrillation Non pharmacologic Management • Electric cardioversion – method of choice for the hemodynamically compromised • Evaluate need for anticoagulation • R/O drug toxicity • Anesthesia • Synchronized 50 – 200 joules shock • Control of ventricular rate • AV nodal ablation with PPM • Pulmonary vein ablation (maintenance)

  25. Atrial Fibrillation Management Rate control versus rhythm control • Advantage of maintaining NSR • Adverse effects of antiarrhythmics • After cardioversion even with antiarrhythmic therapy-50% develop recurrent A.F after cardioversion • Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) : Anticoagulation advantageous

  26. AFFIRM • Atrial Fibrillation Follow-up Investigation of Rhythm Management • Hypothesis: Effect on mortality of antiarrhythmic therapy to maintain sinus rhythm vs. ventricular rate control alone, in the presence of anticoagulation • Primary endpoint: Total mortality • Secondary endpoint: Disabling CVA Cost of therapy Quality of life NHLBI AFFIRM Investigators. Am J Cardiol. 1997;79:1198-1202.

  27. Risk of Stroke in Non –Valvular Atrial Fibrillation • Framingham study (20 yrs flu) • Annual stroke rate 4.2% • HTN RR 3.4 • CAD RR 2.4 • CHF RR 4.3 • A.F RR 4.8 • Risk of stroke related to A.F • 1.5% in the sixth decade • 24% in the ninth decade • Strokes are clustered at the onset of A.F (25%) another 14% within the first year.

  28. Atrial Fibrillation Risk of Stroke Pooled Data from five clinical trials have confirmed 4 predictive stroke risk factors • TIA / previous stroke - RR 2.5 • Diabetes - RR 1.7 • HTN - RR 1.6 • Age 60 and above - RR 1.4 for each decade • In patients with none of the above on ASA or no anticoagulation 1% per year

  29. Risk Event Rate CategoriesAge < 65 yearsNo risk factorsOne or more risk factors (95% CI) 1% (0.3-3.1)4.9% (3.0-8.1) Age 65-75 yearsNo risk factorsOne or more risk factors 4.3% (2.7-7.1)5.7% (3.9-8.3) Age > 75 yearsNo risk factorsOne or more risk factors 3.5% (1.6-7.7)8.1% (4.7-13.9) Annual Event Rates per Age Groups and Risk Factors* *Risk factors are history of hypertension, history of diabetes, or history of prior stroke or transient ischemic attacks.

  30. Risk of Stroke in Atrial Fibriallation LoneAtrial Fibriallation • Lone AF – AF in patients younger than 60 years without: hypertension, Diabetes, h/o TIA or stroke, cardiac disease • The incidence of stroke in Lone AF patients, 1.3% per year ( Mayo Clinic Study)

  31. Paroxysmal Atrial Fibrillation Risk of Stroke • PAF risk of stroke 3.7% a year • The event cluster at the onset of the arrhythmia (68% in the first month)

  32. Atrial Fibrillation Risk of Stroke • Valvular Heart Disease – 15 folds higher than that in an age matched (4.5% per year) • Cardiomyopathies – AF in 20% of DCM and 10 % of HCM. No trials available • Thyrotoxicosis – Occurs in 10 – 30% of patients ( may be higher incidence in some reports)

  33. Atrial FibrillationManagement of the Risk of Stroke • 15 – 20% of ischemic strokes arise afrom emboli in the cardiac chambers and valves • AF accounts for 45% of embolic strokes • Majority of emboli arise in the LAA • Other sources of emboli: LV thrombus Mitral valve disease (including MVP and annular calcification), PFO Atrial septal aneurysm, and complex aortic atheromatous plaques • Corebrovascular disease may also be a cause of stroke

  34. Transesophageal Echocardiogram Showing Thrombus In this transesophageal echocardiogram, a thrombus (arrow) can be seen in the left atrial appendage (LAA).

  35. Echocardiogram of Fibrillating Left Atrium The smokelike echoes, or spontaneous echo contrast, in this transesophageal echocardiogram of a fibrillating left atrium are associated with prethrombotic conditions.

  36. Protruding Atheroma in Descending Aorta Protruding atheroma (arrows) in the descending aorta (DESC AO) is evident in this transesophageal echocardiogram.

  37. Atrial FibrillationManagement of the Risk of Stroke • Anticoagulation with warfarin is twice as effective as with Aspirin • SPAF III: compared warfarin vs. acombination of low doze warfarin and Aspirin, in high risk AF patients the combination was not effective compared to warfarin.

  38. Recommendations for Anticoagulation in AF • Low risk patient (younger than 65) – do not need anticoagulation • Patients above 65 years who have AF should be anticoagulated. ACCP recommendation – INR 2.0 – 3.0 (reduces risk by 2/3) • Warfarin considered to younger patients with risk factors (previous TIA, HTN, CHF, Diabetes, CAD. MS, Thyrotoxicosis) • Patients, who are high risk for bleeding ASA 325 mg / day • Patients 65 – 75 years with no risk – blance the the low risk of stroke with side effects of therapy • Patients 75 years should receive oral anticoagulant

  39. Atrial FibrillationManagement of the Risk of StrokeContraindications to Anticoagulation • Hemorrhage tendencies • Recent intra-cranial hemorrhage or neurosurgery • Recent hemorrhagic trauma • Recurrent or active bleeding • Diastolic BP>105 Other considerations • Risk of falling • Poor compliance with f/u • Uncontrolled siezure disorder

  40. Atrial Fibrillation Management Cardioversion and the Risk ofThromboembolism • Risk of thromboembolism at cardioversion 0-5.6% • Dislodgement of a preexisting thrombus upon the return of the atrial electrical and mechanical function (up to 4 weeks) • Formation and later dislodgment of newly formed thrombi, when patient returns to NSR but atria in mechanical standstill • 10-15% of patients with acute AF have thrombi on TEE • Most cardioversion related thrombi do not occur at cardioversion, but are delayed for hours or weeks

  41. Atrial Fibrillation Anticoagulation In Patients Undergoing Cardioversion • Those with A.F. longer than 2 days or of unknown duration should receive anticoagulation • Warfarin should be given 3 weeks before cardioversion and 4 weeks after cardioversion • Anticoagulation beyond 4 weeks should be considered in patients with cardiomyopathy h/o previous ambolus or mitral valve disease • TEE role in cardioversion • Useful in r/o thrombus and facilitating early cardioversion by using short term anticoagulation • Acute trial: compared TEE directed approach with brief anticoagulation to conventional

  42. Treatment Protocol in ACUTE Study Treatment protocol used in Assessment of Cardioversion Using TEE (ACUTE) multicenter pilot study. The study involved 126 patients randomized into one of two treatment groups: the TEE guided group (62 patients) and the conventional-treatment group (64 patients).

  43. Atrial Fibrillation: Areas of Research • AFFIRM study • National Heart Institutes atrial fibrillation study • Heart rate control and anticoagulation vs. rhythm control with antiarrhythmic drugs • Patient-activated or automatic atrial defibrillator • Dual-site and biatrial pacing • Atrial pacing therapies for AF prevention • Catheter ablation therapies for AF • Catheter “maze” procedure • Ablation for “focal” AF • Ablation of the Pulmonary Veins

  44. Supraventricular Arrythmias(Regular)

  45. Supraventricular Tachyarrythmias • Two categories: regular cardiac rhythms and irregular rhythms • In general, Supraventricular-tachyarrythmias do not interfere with inter- or intra-ventricular conduction (marrow QRS complex) • The QRS remains narrow in form • Occasionally, atrial arrythmias cause aberrant ventricular conduction with a wide QRS complex.

  46. Atrial Tachycardias • Inter-atrial reentry tachycardia • Automatic atrial tachyardia • Multifocal atrial tachycardia • Sinus node reentry tachcardia

  47. Regular Atrial Tachycardias • 1) Sinus Tachycardia: physiologic or pathologic increase of sinus rate > 100 bpm. • Treat the condition causing the tachycardia, not the tachycardia itself. • However, in cases of acute MI sinus tachycardia must be controlled to prevent myocardial ishemia (beta blockers or Ca-channel blockers) • 2) Paroxysmal Atrial Tachycardia: sudden onset, a normal heart, HR 150-250 bpm. • P waves may be not visible because buried in the QRS complex or the T wave • Therapy: quiet setting and comfort the patient to reduce sympathetic discharge. Increase vagal tone by carotid sinus massage or valsalva maneuver. Medical therapy: Beta-blocker, Ca channel blocker, digoxin, adenosine. If angina, hypotension, or CHF then consider cardioversion.

  48. Supraventricular Tachycardias • Atrial Tachycardia • Atrial Fibrillation/flutter • AV nodal reentry (micro) tachycardia • AV reentry tachycardia (macro) - WPW Syndrome or concealed accessory pathway If the patient is very symptomatic or breaks through drugs, consider catheter ablation

  49. Supraventricular Tachycardias

  50. Supraventricular TachycardiaAtrioventricular Nodal Reentry Tachycardia(AVNRT) • The most common type of paroxsmal SVT (PSVT) • AVNRT accounts for 50 – 60% of PSVT • AVNRT present later than SVT related to accessory pathways (frequently after 20 years of age)

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