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Supra ventricular tachycardia

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Supra ventricular tachycardia

  1. 1. DR.TAMIL MANI V
  2. 2. Supraventricular TachycardiasSupraventricular - a rhythm process in which the ventricles are activated from the atria or AV node/His bundle region.
  3. 3. SVT Sinus Tachycardia and Sinus Node Reentry Atrial flutter Atrial Fibrillation Atrial Tachycardia AV nodal reentry tachycardia AV reentry tachycardia - the WPW(Wolff-Parkinson White) Syndrome
  4. 4. EPIDEMIOLOGY AF is the most common arrhythmia treated in clinical practice. The most common arrhythmia for which patients are hospitalized; Approximately 33% of arrhythmia-related hospitalizations are for AF.
  5. 5. MECHANISM Two electrophysiological mechanism of AF: AUTOMATIC FOCUS{DRIVERS}: These focus discharge impulses at rapid rates which travel at rapid speed throughout atria causing to fibrillate. MULTIPLE RE-ENTRANT CIRCUITS: These wander throughout the atria
  6. 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. 7. AF
  8. 8. Atrial fibrillation
  9. 9. CAUSES CARDIAC CAUSES: Hypertensive heart disease Ischemic heart disease Mitral valve disease Cardiomyopathies{ hypertropied/dilated} Severe pulmonary hypertension NON CARDIAC CAUSES: ENDOCRINAL: Thyrotoxicosis,pheochromocytoma IATROGENIC: Ionotrophic drugs,post-operative OTHERS: obesity,excessive alcohol intake,obstructive sleep apnea.
  10. 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. 11. DIAGNOSTIC EVALUATION History Clinical features Investigation
  12. 12. History and physical examination Presence and nature of symptoms associated with AF. Clinical type of AF (first episode, paroxysmal, persistent, or permanent) Onset of the first symptomatic attack or date of discovery of AF Frequency, duration, precipitating factors, and modes of termination of AF Response to any pharmacological agents that have been administered Presence of any underlying heart disease or other reversible conditions (eg, hyperthyroidism or alcohol consumption)
  13. 13. CLINICAL FEATURES Clinical 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. 14.  SYMPTOMATIC AF: palpitations fatigue dyspnea effort intolerance lightheadedness Post palpatory-Polyuria{ANP induced}
  15. 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 in conjunction with antiarrhythmic drug therapy
  16. 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. 17.  Blood tests of thyroid, renal, and hepatic function. Holter monitoring or event recording. Transesophageal echocardiography. Chest radiograph.
  18. 18.  All patients with AF (paroxysmal, persistent or permanent), should be stratified using a predictive index for stroke (e.g. CHADS2) and for the risk of bleeding (e.g. HAS-BLED), and that most patients should receive antithrombotic therapy.
  19. 19. CHADS2 Score Risk Factor Score CHF 1 Hypertension 1 Age > 75 years 1 Diabetes 1 Stroke/TIA 2
  20. 20. CHADS2 Score and CVA Risk
  21. 21. CHADS2 VASc Score Risk Factor Score CHF 1 Hypertension 1 Age > 75 1 Diabetes 1 Stroke/TIA 2 Vascular disease 1 (MI,PVD) Age 65-74 1 Sex Category Female 1
  22. 22. CHADS2 VASc Stroke Rate
  23. 23. Predicting Bleeding RiskHAS-BLED Score Hypertension (>160 mmHg systolic 1 Abnormal Renal/Hepatic function 1-2 Stroke 1 Bleeding history or anemia 1 Labile INR (TTR < 60%) 1 Elderly (age > 75 years) 1 Drugs/Alcohol (antiplatelet/NSAIDs) 1-2 High Risk (>4%/year) >4 Moderate Risk (2-4%/year) 2-3 Low Risk (<2%/year) 0-1
  24. 24. Anticoagulation in Atrial Fibrillation Risk Category Recommended Therapy No risk factors Aspirin, 81-325 mg/d CHADS2 = 0 One Moderate Risk Aspirin, 81 mg-325 mg/d Factor or Warfarin – target INR CHADS2 = 1 2.5 CHADS2 > 2 or mitral Warfarin – target INR 2.5 stenosis Prosthetic valve Warfarin – target INR 3.0
  25. 25. INR
  26. 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. 27. RR = 0.91, P<0.001, non-inf RR = 0.66, P<0.001 sup mo. RE-LY Trial. Stroke or Systemic Embolism
  28. 28. Afib -OAC Contraindicated Pt In patients in whom OAC therapy is contraindicated, combination of Clopidogrel and Aspirin is recommended to reduce risk of thromboembolic complications.
  29. 29. Management of patients with AF Objectives—1. Rate control,2. Prevention of thromboembolism,3. Rhythm control.
  30. 30. Rate control Primary goal is to improve symptoms and prevent deterioration of cardiac function associated with excessively rapid ventricular rates during AF. Suggested that strict rate control < 80 at rest, < 110 with exercise
  31. 31. Agents for Rate Control Beta-blockers Non-dihydropyridine calcium channel blockers  Diltiazem, Verapamil Digoxin, digitalis  Reserved for sedentary, LV dysfunction, second-line therapy Dronedarone  Second line therapy Amiodarone  Avoid using unless exceptional circumstances
  32. 32. Cardioversion >48 hrs In hemodynamically stable patients with AF of ≥ 48 hr or uncertain duration for whom electrical or pharmacological cardioversion is planned should receive therapeutic OAC therapy (warfarin [INR 2-3] or dabigatran) for 3 weeks before and at least 4 weeks post cardioversion. Following attempted cardioversion:  If AF persists or recurs or if symptoms suggest that the presenting AF ohas been recurrent, the patient should have antithrombotic therapy continued indefinitely using either OAC or aspirin as appropriate.  If sinus rhythm is achieved and sustained for 4 weeks, the need for ongoing antithrombotic therapy should be based upon the risk of stroke.
  33. 33. Cardiovertion <48 hrs In hemodynamically stable patients with AF of known duration < 48 hr may undergo cardioversion without prior or subsequent anticoagulation. However, if the patient is at particularly high risk of stroke (e.g. mechanical valve, rheumatic heart disease, recent stroke or TIA), cardioversion should be delayed and the patient should receive OAC for 3 weeks before and at least 4 weeks post cardioversion. Following attempted cardioversion:  If AF persists, recurs, or if symptoms suggest that the presenting AF has been recurrent, antithrombotic therapy (OAC or aspirin as appropriate) should be commenced and continued indefinitely.  If NSR is achieved and sustained for 4 weeks, the need for ongoing antithrombotic therapy should be based on the risk of stroke according to CHADS2 score.
  34. 34.  That hemodynamically unstable patients with AF who require emergency cardioversion be managed as follows: a) If the AF is of known duration < 48 hr, the patient may generally undergo cardioversion without prior anticoagulation. However, if the patient is at particularly high risk of stroke (e.g. mechanical valve, rheumatic heart disease, recent stroke or TIA), the patient should receive IV UFH or LMWH before cardioversion is possible, or immediately thereafter if even a brief delay is unacceptable, and then be converted to OAC for at least 4 weeks post cardioversion. b) If the AF is of ≥ 48 hr or uncertain duration.the patient receive IV UFH or LMWH before cardioversion if possible, or immediately therafter if even a brief delay is unacceptable. Such a patient should then be converted to OAC for at least 4 weeks post cardioversion.
  35. 35. Amiodarone Inpatient: 5 to 7 mg/kg over 30 to 60 min, then 1.2 to 1.8 g per day continuous IV or in divided oral doses until 10 g total, then 200 to 400 mg per day maintenance for inpatients. Outpatient: 600 to 800 mg per day divided dose until 10 g total, then 200 to 400 mg per day maintenance. Hypotension, bradycardia, QT prolongation, torsades de pointes (rare),GI upset, constipation,phlebitis (IV)
  36. 36. Other drugs Dofetilide Ibutilide Flecainide Propafenone Quinidine
  37. 37. Drug Therapy to Maintain Sinus Rhythm in Patients with Recurrent Paroxysmal or Persistent Atrial Fibrillation Heart Disease No (or minimal) Yes Heart Failure CAD Hypertension Flecainide Propafenone Sotalol Amiodarone Sotalol LVH greater than Dofetilide or equal to 1.4 cm Amiodarone Amiodarone, Dofetilide Dofetilide Yes No Flecainide Disopyramide Propafenone Disopyramide Consider Procainamide Procainamide nonpharmacological Quinidine Quinidine options Amiodarone Dofetilide Amiodarone Sotalol. Disopyramide, Procainamide, Quinidine
  38. 38. Normal Ventricular Function Dronedarone Flecainide* Propafenone* Sotalol Catheter Ablation Amiodarone* Class I agents should be AVOIDED in CAD They should be combined with an AV-nodal blocking agents
  39. 39. Abnormal Left Ventricular Function EF > 35% EF ≤ 35% Amiodarone Amiodarone Catheter Ablation Dronedarone Sotalol** Sotalol should be used with caution with EF 35-40% Contra-indicated in women >65 yrs taking diuretics
  40. 40. RATE VS RHYTHM Favors Rate Control Favors Rhythm Control Persistent AF Paroxysmal AF Newly Detected AF Less Symptomatic More Symptomatic >65 years of age < 65 years of age Hypertension No Hypertension No History of Congestive Congestive Heart Failure Heart Failure clearly exacerbated by AF Previous Antiarrhythmic No Previous Antiarrhythmic Drug Failure Drug Failure
  41. 41. AFFIRM
  42. 42. Rhythm Control of AF Strategy of rhythm control has never been shown to reduce mortality compared to rate control (AFFIRM, RACE, PIAF trials, AF CHF) Therefore, goals of rhythm control should focus on improving quality of life Rhythm control does not necessitate elimination of all AF
  43. 43. AAD Patients with AF or AFL who remain symptomatic with rate control therapy. Improvement in patient symptoms and clinical outcomes, and not necessarily the elimination of all AF. Maintenance oral antiarrhythmic therapy as first- line therapy for patients with recurrent AF in whom long-term rhythm control is desired
  44. 44. AtrialFlutter
  45. 45. AFL Atrial flutter is generally used to describe atrial arrhythmias with large reentrant circuits. Atrial rate is usually 240 to 340 beats/min.
  46. 46. TYPES Typical atrial flutter reentrant rhythm in the right atrium constrained anteriorly by the tricuspid annulus and posteriorly by the crista terminalis and eustachian ridge. The flutter can circulate in a counterclockwise direction around the tricuspid annulus in the frontal plane (typical flutter, counterclockwise flutter). Clockwise direction (atypical, clockwise, or reverse flutter).
  47. 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, and pericarditis Surgical repair for congenital heart disease.
  48. 48. counterclockwise
  49. 49. CARDIOVERSION Cardioversion - the initial treatment of choice. DC -- 50 J. If the electrical shock results in atrial fibrillation, a second shock at a higher energy level is used to restore sinus rhythm. Ibutilide - IV. successfully cardiovert- 60% to 90%. prolongs the QT interval, torsades de pointes Other medications- procainamide
  50. 50. Ablation Highly effective for typical flutter Stable patients who do not require immediate cardioversion. Success rate of 90% to 100%
  51. 51. Anticoagulation Indications for anticoagulation in patients with atrial flutter are similar to those with atrial fibrillation
  52. 52. AT Rapid (usually <250 beats/ min), relatively regular rhythms that originate in the atrial musculature. Mechanisms include abnormal automaticity and triggered activity. Foci are most frequently found in the pulmonary veins in the LA and the crista terminalis in the right atrium. Myocardial infarction, nonischemic heart disease,obstructive lung disease, serum electrolyte disorders, and drug toxicity
  53. 53. Atrial TachycardiaV1 Differs from • RP intervals can be variable AV nodal or • RP often > PR AV reentrant • (Example slower than more common rate SVT 150-250 beats per min)
  54. 54. AT
  55. 55. Treatment of AT Catheter ablation is the primary therapy regardless of the underlying mechanism. Antiarrhythmic drug choices are similar to that in AF
  56. 56. MAT
  57. 57. Multifocal AtrialTachycardia
  58. 58. Multifocal Atrial TachycardiaECG Characteristics: Discrete P waves with at least 3different morphologies. Absence of one dominant atrial pacemaker Atrial rate > 100 bpm. The PP, PR, and RR intervals all vary.
  59. 59. MAT Signature tachycardia of patients with significant pulmonary disease. The atrial rhythm is characterized by at least three distinct P- wave morphologies and often at least three different PR intervals. Atrial and ventricular rates are typically between 100 and 150 beats per minute. The presence of an isoelectric baseline distinguishes this arrhythmia from AF. The absence of any intervening sinus rhythm distinguishes MAT from normal sinus rhythm with frequent multifocal APCs.
  60. 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 is limited by bronchospasm.
  61. 61. Sinus tachycardia Heart rate faster than 100 beats/min that is caused by rapid impulse formation from the sinoatrial node. It occurs with fever, exercise, emotion, pain, anemia, heart failure, shock, thyrotoxicosis, or in response to many drugs
  62. 62. AVNRT Patients may be asymptomatic except for awareness of rapid heart action, but some experience mild chest pain or shortness of breath.
  63. 63. AV NODAL REENTRANT TACHYCARDIA
  64. 64. AVNRT Presence of a narrow complex tachycardia with regular R-R intervals 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 –simultaneous activation of atria and ventricles – most common presentation of AVNRT –66%. If not synchronous –pseudo s wave in inferior leads ,pseudo r’ wave in lead V1---30% cases . P wave may be farther away from QRS complex distorting the ST segment ---AVNRT ,mostly AVRT.
  65. 65. Vagotonic Maneuvers  Carotid sinus massage  Valsalva maneuver (bearing down)  Facial ice pack.  Mueller maneuvers, gagging.
  66. 66. Carotid Sinus Massage Stimulation of carotid sinus triggers baroreceptor reflex and increased vagal tone, affecting SA and AV nodes
  67. 67. Termination of SVT byVagotonic Maneuver (Carotid SinusMassage)
  68. 68. Treatment: Many episodes of Supraventricular Tachycardia (SVT) soon stop and no treatment Is needed. If an episode of SVT does last a long time or is severe admitted to a hospital to stop it. Medicines which are given by injection into a vein will usually stop an SVT. [Adenosine is commonly used] Adenosine works by blocking Verapamil 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 an episode of SVT.
  69. 69. Prevention Drugs that slow conduction in the antegrade slow pathway, such as digitalis, beta blockers, and calcium channel blockers. History of exercise-precipitated AVNRT, the use of beta blockers . Patients who do not respond to drug therapy directed at the antegrade slow pathway, treatment with class IA or IC agents directed at altering conduction of the fast pathway may be considered.
  70. 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 reasonable approach…until 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 2 hrs…
  71. 71. Catheter ablation Directed at elimination or modification of slow pathway conduction, is very effective in permanently eliminating AVNRT. Patients with recurrent AVNRT that produces significant symptoms or heart rates >200 beats/min and patients reluctant to take chronic drug therapy should be considered for ablative therapy. Cure >95% of patients
  72. 72. Catheter Ablation of Cardiac Arrhythmias.
  73. 73. CLINICAL FEATURES Preexcitation occurs in the general population at a frequency of around 1.5 per 1000. Of these, 50% to 60% of patients become symptomatic. Symptoms range from palpitations to syncope. Episodes of tachycardia may be associated with dyspnea, chest pain, decreased exercise tolerance, anxiety, dizziness, or syncope.
  74. 74. AV REENTRANT TACHYCARDIA
  75. 75. WPW syndrome Two types Orthodromic 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 .less risk of AF
  76. 76. Manifest vs Concealed
  77. 77. Accessory Pathway with Ventricular Preexcitation (Wolff-Parkinson-WhiteSinus Syndrome) Hybridbeat “Delta” Wave QRS shape PR < .12 s AP Fusion activation QRS  .12 s of the ventricles
  78. 78. AVRT Typical – RP interval < PR interval RP interval > 80 milli sec Atypical –RP interval > PR interval
  79. 79. Orthodromic AV Reentrant TachycardiaNSR withV Preex NoteSVT: retrogradeV Preex P wavesgone in the ST segment
  80. 80. Orthodromic AVRT
  81. 81. Catheter Ablation of AccessoryPathways Catheter ablation of APs is performed in conjunction with a diagnostic EPS.(TOC) Success of catheter ablation in curing APs was 93%. Asymptomatic RR cycle length < 220 ms, a short refractory period is present. These individuals are at highest risk for sudden death, and prophylactic ablation is indicated.
  82. 82. Pharmacologic Therapy Narrow-complex reentry rhythms involving a bypass tract can be managed as discussed for AVNRT. AF and AFL with antegrade conduction- digoxin, calcium channel blockers, and even -blockers may decrease the refractoriness of the accessory pathway or increase that of the AV node, often leading to faster ventricular rates. Therefore, these agents should be avoided. The class Ia(procainamide), class Ic(flecainide,propafenone), and class III antiarrhythmic agents will increase the refractoriness of the bypass tract and are the drugs of choice for wide-complex tachycardias involving accessory pathways. If hemodynamic compromise is present, electrical cardioversion is warranted.
  83. 83. P wave present but not of same morphology as sinus rhythmPseudo r’ Pseudo S Pwave wave in wave on lead II ST-T changes V1 Positive in Negative inAVNRT AVNRT inferior leads lead I AVRT AVRT Right posteroseptal Left sided accessory Accessory pathway pathway

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