1. DR.TAMIL MANI V

2. Supraventricular TachycardiasSupraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle region. 3. SVT Sinus Tachycardia and Sinus Node Reentry Atrial flutter Atrial Fibrillation Atrial Tachycardia AV nodal reentry tachycardia AV reentry tachycardia - the WPW(Wolff-ParkinsonWhite) Syndrome 4. EPIDEMIOLOGY AF is the most common arrhythmia treated in clinicalpractice. The most common arrhythmia for which patients arehospitalized; Approximately 33% of arrhythmia-related hospitalizationsare for AF. 5. MECHANISM Two electrophysiological mechanism of AF: AUTOMATIC FOCUS{DRIVERS}:These focus discharge impulses at rapidrates which travel at rapid speedthroughout atria causing to fibrillate. MULTIPLE RE-ENTRANT CIRCUITS: These wander throughout the atria 6. The focal point remains the PULMONARYVEIN esp. in cases of paroxysmal AF. Thus isolation of pulmonary vein causesabolition of paroxysmal AF, than permanent AF. 7. AF 8. Atrial fibrillation 9. CAUSES CARDIAC CAUSES:Hypertensive heart diseaseIschemic heart diseaseMitral valve diseaseCardiomyopathies{ hypertropied/dilated}Severe pulmonary hypertension NON CARDIAC CAUSES:ENDOCRINAL:Thyrotoxicosis,pheochromocytoma IATROGENIC: Ionotrophic drugs,post-operativeOTHERS:obesity,excessive alcohol intake,obstructive sleep apnea. 10. CLASSIFICATIONOF AF PAROXYSMAL < 7 days PERSISTANT>7 days LONGLASTING >1 YR PERMENANT - Cardioversion failed LONE AF: usually seen in elderly persons{>60 years} who do not have hypertension or heart disease. 11. DIAGNOSTIC EVALUATION History Clinical features Investigation 12. History and physical examination Presence and nature of symptoms associated with AF. Clinical type of AF (first episode, paroxysmal, persistent, orpermanent) Onset of the first symptomatic attack or date of discovery of AF Frequency, duration, precipitating factors, and modes of terminationof AF Response to any pharmacological agents that have been administered Presence of any underlying heart disease or other reversibleconditions (eg, hyperthyroidism or alcohol consumption) 13. CLINICAL FEATURESClinical features of AF varies from being totally asymptomatic to being hemodynamic unstable,thus explaining the two end spectrum of it. ASYMPTOMATIC AF:25% of patients with AF are asymptomatic, more commonly elderly patients and patients with persistent AF. 14. SYMPTOMATIC AF:palpitationsfatiguedyspneaeffort intolerancelightheadednessPost palpatory-Polyuria{ANP induced} 15. Investigations-Electrocardiogram Rhythm (verify AF) LV hypertrophy P-wave duration and morphology or fibrillatory waves Preexcitation Bundle-branch block Prior MI Other atrial arrhythmias To measure and follow the R-R, QRS, and QT intervals inconjunction with antiarrhythmic drug therapy 16. Transthoracic echocardiogram Valvular heart disease LA and RA size LV size and function Peak RV pressure (pulmonary hypertension) LV hypertrophy LA thrombus (low sensitivity) Pericardial disease 17. Blood tests of thyroid, renal, and hepatic function. Holter monitoring or event recording. Transesophageal echocardiography. Chest radiograph. 18. All patients with AF (paroxysmal, persistent orpermanent), should be stratified using a predictive indexfor stroke (e.g. CHADS2) and for the risk of bleeding (e.g.HAS-BLED), and that most patients should receiveantithrombotic therapy. 19. CHADS2 Score Risk Factor ScoreCHF 1Hypertension1Age > 75 years1Diabetes1Stroke/TIA2 20. CHADS2 Score and CVA Risk 21. CHADS2 VASc Score Risk FactorScoreCHF 1Hypertension1Age > 751Diabetes1 Stroke/TIA 2Vascular disease1(MI,PVD) Age 65-74 1Sex Category Female1 22. CHADS2 VASc Stroke Rate 23. Predicting Bleeding RiskHAS-BLED Score Hypertension (>160 mmHg systolic 1Abnormal Renal/Hepatic function1-2 Stroke 1 Bleeding history or anemia 1Labile INR (TTR < 60%)1Elderly (age > 75 years)1 Drugs/Alcohol (antiplatelet/NSAIDs) 1-2High Risk (>4%/year) >4 Moderate Risk (2-4%/year) 2-3Low Risk ( 2 or mitral Warfarin target INR 2.5 stenosis Prosthetic valve Warfarin target INR 3.0 25. INR 26. Warfarin vs dabigatran When OAC therapy is indicated, dabigatran in preference to warfarin. In general, the dose of dabigatran 150 mg po bid is preferable to 27. RR = 0.91, P65 yrs taking diuretics 40. RATE VS RHYTHM Favors Rate Control Favors Rhythm Control Persistent AFParoxysmal AFNewly Detected AF Less Symptomatic More Symptomatic >65 years of age < 65 years of age Hypertension No Hypertension No History of Congestive Congestive Heart FailureHeart Failure clearly exacerbated by AF Previous AntiarrhythmicNo Previous AntiarrhythmicDrug Failure Drug Failure 41. AFFIRM 42. Rhythm Control of AF Strategy of rhythm control has never been shown to reducemortality compared to rate control (AFFIRM, RACE, PIAFtrials, AF CHF) Therefore, goals of rhythm control should focus on improvingquality of life Rhythm control does not necessitate elimination of all AF 43. AAD Patients with AF or AFL who remain symptomaticwith rate control therapy. Improvement in patient symptoms and clinicaloutcomes, and not necessarily the elimination ofall AF. Maintenance oral antiarrhythmic therapy as first-line therapy for patients with recurrent AF inwhom long-term rhythm control is desired 44. AtrialFlutter 45. AFL Atrial flutter is generally used to describe atrialarrhythmias with large reentrant circuits. Atrial rate is usually 240 to 340 beats/min. 46. TYPES Typical atrial flutter reentrant rhythm in the right atriumconstrained anteriorly by the tricuspid annulus andposteriorly by the crista terminalis and eustachian ridge. The flutter can circulate in a counterclockwise directionaround the tricuspid annulus in the frontal plane (typicalflutter, counterclockwise flutter). Clockwise direction (atypical, clockwise, or reverseflutter). 47. CAUSES OF AFL COPD Atrial dilation from septal defects Pulmonary emboli Mitral or tricuspid valve stenosis or regurgitation Chronic ventricular failure Prior extensive atrial ablation Aging Toxic and metabolic - thyrotoxicosis, alcoholism, andpericarditis Surgical repair for congenital heart disease. 48. counterclockwise 49. CARDIOVERSION Cardioversion - the initial treatment of choice. DC -- 50 J. If the electrical shock results in atrialfibrillation, a second shock at a higher energy level isused to restore sinus rhythm. Ibutilide - IV. successfully cardiovert- 60% to 90%. prolongs the QT interval, torsades de pointes Other medications- procainamide 50. Ablation Highly effective for typical flutterStable patients who do not require immediatecardioversion. Success rate of 90% to 100% 51. Anticoagulation Indications for anticoagulation in patients with atrialflutter are similar to those with atrial fibrillation 52. AT Rapid (usually PR AV reentrant (Example slower than more common rate SVT 150-250 beats per min) 54. AT 55. Treatment of AT Catheter ablation is the primary therapy regardless ofthe underlying mechanism. Antiarrhythmic drug choices are similar to that in AF 56. MAT 57. Multifocal AtrialTachycardia 58. Multifocal Atrial TachycardiaECG Characteristics: Discrete P waves with at least 3differentmorphologies.Absence of one dominant atrial pacemakerAtrial rate > 100 bpm.The PP, PR, and RR intervals all vary. 59. MAT Signature tachycardia of patients with significant pulmonarydisease. The atrial rhythm is characterized by at least three distinct P-wave morphologies and often at least three different PRintervals.Atrial and ventricular rates are typically between 100 and 150beats per minute.The presence of an isoelectric baseline distinguishes thisarrhythmia from AF. The absence of any intervening sinus rhythm distinguishesMAT from normal sinus rhythm with frequent multifocalAPCs. 60. TREATMENT Correction of the underlying pulmonary problem. Cardioversion is ineffective. Calcium channel blockers- limited success. In selected patients, -blockers may have a role- use islimited by bronchospasm. 61. Sinus tachycardia Heart rate faster than 100 beats/min that is caused byrapid impulse formation from the sinoatrial node. It occurs with fever, exercise, emotion, pain, anemia,heart failure, shock, thyrotoxicosis, or in response to manydrugs 62. AVNRT Patients may be asymptomatic except for awareness of rapid heart action, but some experience mild chest pain or shortness of breath. 63. AV NODAL REENTRANT TACHYCARDIA 64. AVNRT Presence of a narrow complex tachycardia with regular R-Rintervals and no visible p waves. P waves are retrograde and are inverted in leads II,III,avf. P waves are buried in the QRS complexes simultaneousactivation of atria and ventricles most common presentation ofAVNRT 66%. If not synchronous pseudo s wave in inferior leads ,pseudo rwave in lead V1---30% cases . P wave may be farther away from QRS complex distorting theST segment ---AVNRT ,mostly AVRT. 65. Vagotonic Maneuvers Carotid sinus massage Valsalva maneuver (bearing down) Facial ice pack. Mueller maneuvers, gagging. 66. Carotid Sinus Massage Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes 67. Termination of SVT byVagotonic Maneuver (Carotid SinusMassage) 68. Treatment:Many episodes of Supraventricular Tachycardia (SVT) soon stop and notreatment Is needed. If an episode of SVT does last a long time or issevere admitted to a hospital to stop it.Medicines which are given by injection into a vein will usually stop anSVT. [Adenosine is commonly used] Adenosine works by blockingVerapamil is an alternative if adenosine is not advised. [People with asthma electrical impulses of the heart.cannot have adenosine]Electric Shock treatment is rarely needed to stop anepisode of SVT. 69. Prevention Drugs that slow conduction in the antegrade slowpathway, such as digitalis, beta blockers, and calciumchannel blockers. History of exercise-precipitated AVNRT, the use ofbeta blockers . Patients who do not respond to drug therapy directedat the antegrade slow pathway, treatment with class IAor IC agents directed at altering conduction of the fastpathway may be considered. 70. Pill in the pocket approach In whom recurrences are infrequent. But sustained.well tolerated hemodynamically. Patients who have had only a single episode of SVT.. 100-200mg of flecainide at the onset of SVT is a reasonableapproachuntil he reaches the hospital. 40-160 mg verapamil without preexcitation, Betablockers Propafenone 150-450 mg. 80% cases interrupted with a combination of CCBand BB in 2hrs 71. Catheter ablation Directed at elimination or modification of slowpathway conduction, is very effective in permanentlyeliminating AVNRT. Patients with recurrent AVNRT that producessignificant symptoms or heart rates >200 beats/minand patients reluctant to take chronic drug therapyshould be considered for ablative therapy. Cure >95% of patients 72. Catheter Ablation of Cardiac Arrhythmias. 73. CLINICAL FEATURES Preexcitation occurs in the general population at afrequency of around 1.5 per 1000. Of these, 50% to 60% of patients becomesymptomatic. Symptoms range from palpitations to syncope. Episodes of tachycardia may be associated withdyspnea, chest pain, decreased exercise tolerance,anxiety, dizziness, or syncope. 74. AV REENTRANT TACHYCARDIA 75. WPW syndrome Two typesOrthodromic Antidromic Antidromic is wide complex tachycardia In NSR detected by delta wave. Can ppt into AF and VF on use of AV nodal blockers CONCEALED WPW syndrome no delta wave .lessrisk of AF 76. Manifest vs Concealed 77. Accessory Pathway with Ventricular Preexcitation(Wolff-Parkinson-WhiteSinusSyndrome)HybridbeatDelta WaveQRS shapePR < .12 sAPFusion activation QRS .12 sof the ventricles 78. AVRT Typical RP interval < PR interval RP interval > 80 milli sec Atypical RP interval > PR interval 79. Orthodromic AV ReentrantTachycardiaNSR withV Preex NoteSVT: retrogradeV PreexP wavesgone in the ST segment 80. Orthodromic AVRT 81. Catheter Ablation of AccessoryPathways Catheter ablation of APs is performed in conjunctionwith a diagnostic EPS.(TOC) Success of catheter ablation in curing APs was 93%. Asymptomatic RR cycle length < 220 ms, a shortrefractory period is present. These individuals are athighest risk for sudden death, and prophylacticablation is indicated. 82. Pharmacologic Therapy Narrow-complex reentry rhythms involving a bypass tract can bemanaged as discussed for AVNRT. AF and AFL with antegrade conduction- digoxin, calciumchannel blockers, and even -blockers may decrease therefractoriness of the accessory pathway or increase that of the AVnode, often leading to faster ventricular rates. Therefore, theseagents should be avoided. The class Ia(procainamide), classIc(flecainide,propafenone), and class III antiarrhythmic agentswill increase the refractoriness of the bypass tract and are thedrugs of choice for wide-complex tachycardias involvingaccessory pathways. If hemodynamic compromise is present, electrical cardioversionis warranted. 83. P wave present but not of same morphology assinus rhythmPseudo rPseudo SPwave wave inwave on lead II ST-T changes V1Positive inNegative inAVNRTAVNRTinferior leads lead I AVRTAVRT Right posteroseptalLeft sidedaccessory Accessory pathway pathway