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Tachyarrhythmias, Diagnosis and Management

Tachyarrhythmias, Diagnosis and Management Laurent Lewkowiez, MD Assistant Professor Denver Health and Hospitals University of Colorado Health Sciences Mechanisms of Arrhythmia Abnormal automaticity automatic impulse generation from unusual site or overtakes sinus node

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Tachyarrhythmias, Diagnosis and Management

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  1. Tachyarrhythmias, Diagnosis and Management Laurent Lewkowiez, MD Assistant Professor Denver Health and Hospitals University of Colorado Health Sciences

  2. Mechanisms of Arrhythmia • Abnormal automaticity • automatic impulse generation from unusual site or overtakes sinus node • Triggered activity • secondary depolarization during or after repolarization • Dig toxicity, Torsades de Pointes • Reentry • 90 % of arrhythmias

  3. Reentry • Most common mechanism • Requires two separate paths of conduction • Requires an area of slow conduction • Requires unidirectional block

  4. Supraventricular TachycardiasDiagnosis • ECG is cornerstone • Observe zones of transition for clues as to mechanism: • onset • termination • slowing, AV nodal block • bundle branch block

  5. Regular SVT in adults • 90% reentrant 10 % not reentrant • 60% AV nodal reentrant tachycardia (AVNRT) • 30% orthodromic reciprocating tachycardia (ORT) • 10% Atrial tachycardia • 2 to 5% involve WPW syndrome

  6. Differential Dx of Regular SVT • Short RP tachycardia • AV nodal reentrant tachycardia • ORT( Orthodromic reciprocating tachycardia) • atrial tachycardia when associated with slow AV nodal conduction Short RP interval

  7. AV Nodal Reentrant Tachycardia Slow pathway • 2 pathways within or limited to perinodal tissue • anterograde conduction down fast pathway blocks with conduction down slow pathway, with retrograde conduction up fast pathway. • May have very short RP interval with retrograde P wave visible as an R’ in lead V1 or psuedo-S wave in inferior leads in 1/3 of cases . No p wave seen in 2/3 Fast pathway

  8. AV Nodal Reentrant Tachycardia • Responds to vagal maneuvers in 1/3 cases • Very responsive to AV nodal blocking agents such as beta blockers, CA channel blockers, adenosine. • Recurrences are the norm on medical therapy • Catheter ablation 95% successful with 1% major complication rate

  9. Ablation AVNRT His bundle Ablation area

  10. Orthodromic Reciprocating Tachycardia • Anterograde over AV node and retrograde conduction of an accessory pathway. • RP interval short but longer than AVNRT due to required conduction through ventricle prior to conduction up accessory pathway • Frequently presents in patients with WPW patients as narrow complex tachycardia Conduction down AVnode Up accessory pathway

  11. ORT • Amenable to AV nodal blocking agents in absence of WPW syndrome (anterograde conduction of pathway) • Amenable to catheter ablation with 95% success and 1% rate major complication Conduction down AVnode Up accessory pathway

  12. Differential Dx of Regular SVT Long RP interval • Long RP tachycardia • Atrial tachycardia • Sinus node reentry • Sinus tachycardia • Atypical AV nodal reentrant tachycardia • Permanent form of junctional reciprocating tachycardia

  13. Atrial Tachycardia • Atrial rate between 150 and 250 bpm • Does not require AV nodal or infranodal conduction • P wave morphology different than sinus • P-R interval > 120 msec differentiating from junctional tachycardia • Origin inferred from P wave morphology.

  14. Atrial tachycardia • P wave upright lead V1 and negative in aVL consistent with left atrial focus. • P wave negative in V1 and upright in aVL consistent with right atrial focus. • Adenosine may help with diagnosis if AV block occurs and continued arrhythmia likely atrial tachycardia • 70-80% will also terminate with adenosine.

  15. Atrial Tachycardia • Most are due to abnormal automaticity and have right atrial focus • May be reentry particularly in patients with previous atriotomy scar, such as CABG or congenital repair patients

  16. Atrial Tachycardia Therapy • Frequently treated with antiarrhythmics • Class 1 agents procainamide, quinidine, flecainide may be used in patients without structural heart disease. • Class III agents sotalol, amiodarone, dofetilide may be used with caution according to specific side effects • AV Nodal blocking agents for rate control. • Catheter ablation effective in 70-80%

  17. Sinus node reentrant abrupt onset and offset P wave complex same as sinus Amenable to calcium channel blockers, much less responsive to beta blockers Amenable to catheter ablation Syndrome of inappropriate sinus tachycardia typical sinus tachycardia with lowest rate on Holter of 130 bpm Treated with high dose beta blockers Poor results with catheter ablation Other Long RP tachycardias

  18. Atrial Flutter • Rate 250 to 350 bpm • Rotates counter-clockwise around right atrium using a protected isthmus • Negative saw-tooth pattern leads II , III, AVF and positive in lead V1 • Treatment similar to atrial tachycardia but rate control more difficult

  19. Atrial Flutter

  20. Atrial Flutter and Risk of Stroke • Although risk of stroke historically has been thought to be low, multiple instances of stroke with cardioversion lead to similar indication for anticoagulation as atrial fibrillation.

  21. A 32 year old female is treated in the emergency room for palpitations. The first ECG is tachycardia and the second is after adensosine.What is the arrhythmia? • A. AVNRT • B. ORT • C. Atrial tachycardia • D. Atrial fibrillation

  22. Answer: AVNRT (A) • A small R’ is seen is lead V1 with pseudo-S waves in the inferior leads that are absent after termination of the arrhythmia. These represent retrograde atrial activation with a very short RP interval.

  23. WPW syndrome • Accelerated AV conduction PR <120 msec • Prolonged QRS > 120 msec • Abnormal slurred upstroke of QRS ( delta wave) • Abnormal depolarization and repolarization may lead to pseudoinfarction pattern

  24. WPW pathophysiology The result isfusionof both normal and accessory conduction • Short AV conduction • early excitation of ventricle at site of accessory pathway • Bizarre upstroke of QRS • abnormal initial site of depolarization • Wide QRS • early initiation of ventricular depolarization No conduction delay AV node Accessory pathway

  25. WPW epidemiology ORT(orthodromic reciprocating tachycardia • Present in 0.3% of the population • Risk of sudden death 1 per 1000 patient-years • Sudden death due to atrial fibrillation with rapid ventricular conduction • Atrial fibrillation often induced from rapid ORT

  26. Atrial Fibrillation and WPW • AV nodal blocking agents may paradoxically increase conduction over accessory pathway by removing concealed retrograde penetration into accessory pathway. Concealed penetration into the pathway causes intermittent block of pathway conduction

  27. Management of Atrial Fibrillation with WPW • Avoid AV nodal blockers • IV procainamide to slow accessory pathway conduction • Amiodarone if decreased LVEF • DC cardioversion if symptomatic with hypotension

  28. Management of Patients with WPW • All patients with symptomatic AF & WPW should be evaluated with EPS • Accessory pathways capable of conducting faster than 240 BPM should be ablated • Patients with inducible arrhythmias involving pathway should be ablated • WPW patients in high risk professions should be ablated.

  29. A 42 year old smoker presents to the ED with palpitations. His blood pressure is 100/60. The following rhythm strip is obtained . What is the next appropriate step? • A. Emergent cardioversion for polymorphic VT. • B. I.V. procainamide • C. I.V. lidocaine • D. diltiazem drip to obtain rate control.

  30. Answer B • This patient has WPW with atrial fibrillation and a rapid ventricular response. He is stable, thus I.V. procainamide is indicated to slow conduction down the accessory pathway. Diltiazem is contraindicated. Lidocaine will have no effect, as this is not VT .

  31. Atrial Fibrillation Epidemiology • Affects 2 to 4% of population • Increases to 5 to 10 % of patients over 80 • Associated with 2-fold increased risk of death • Risk of thromboembolism is approximately 5% per year but may be as high as 20% in high risk groups not anticoagulated

  32. Mechanism of Atrial Fibrillation • Multiple reentrant wavelets moving between right and left atrium • May be initiated by rapidly firing automatic foci found commonly in pulmonary veins, SVC, and coronary sinus. • Factors that shorten atrial refractoriness and slow conduction velocity perpetuate atrial fibrillation • Factors that lengthen atrial refractoriness (antiarrhythmic drugs ) aid in termination

  33. Management of Atrial Fibrillation • Aimed at symptom relief by rate and rhythm control • Aimed at reducing risk of thromboembolism by anticoagulation • Preventing tachycardia mediated cardiomyopathy (a progressive, reversible rate-induced form of LV dysfunction)

  34. Acute Management of Atrial Fibrillation • Focuses on Rate control • Patient with atrial fibrillation may undergo DC cardioversion or pharmacologic conversion if less than 48 hours duration or following TEE on Heparin without evidence of left atrial thrombus. Stroke rate .8% • Following cardioversion the patient should be kept anticoagulated for 4 weeks with goal INR of 2 to 3 until atrial function normalizes.

  35. Acute Management of Atrial Fibrillation • 50% of patients with paroxysmal atrial fibrillation will spontaneously convert within 24 hours • Digoxin used heavily in the past for prevention and conversion of atrial fibrillation is ineffective at either and may be profibrillatory as it decreases the atrial refractory period

  36. Acute Management of Atrial Fibrillation • Rate control may be attained with calcium channel blockers or beta blockers in patients with normal L.V. function. • Calcium channel blockers may be used cautiously in patients with depressed LV function but are associated with increased mortality in the long term. • Beta blockers should be avoided in acutely decompensated CHF patients with atrial fibrillation

  37. Atrial Fibrillation and Depressed L.V. Function • Digoxin and amiodarone may be of effective in patients with LV dysfunction and decompensated congestive heart failure to slow ventricular response. • Digoxin alone is rarely effective when the patient is sympathetically driven • Avoid high dose digoxin with amiodarone as digoxin levels increase 2-fold with amiodarone

  38. Chronic Management of Atrial Fibrillation • Patients with atrial fibrillation, paroxysmal or sustained should be anticoagulated if any of the following risk factors for stroke are present: • diabetes – hypertension • valvular disease – congestive heart failure • hyperthyroidism – age greater than 65 • Prior CVA

  39. Rate control with calcium channel blockers, beta blockers or combination with digoxin. Digoxin may be used in bed bound patients but is easily overcome with sympathetic stimulation. Maintenance of sinus is similar with class I and class III drugs approaching 50% recurrence at 1 year Recurrence of atrial fibrillation 80% at 1 year without treatment Chronic Management of Atrial Fibrillation

  40. Class III agents may have improved efficacy Amiodarone pulmonary toxicity thyroid liver Dofetilide Torsades des Pointes Safe in CHF and CAD Limited due to side effect profile Class IC agents safe in absence of structural heart disease. Few side effects Need stress testing Can lead to 1 to 1 ventricular conduction of atrial flutter Use with beta blocker Chronic management of Atrial Fibrillation

  41. Chronic Management of Atrial Fibrillation • Recent large trials reveal no benefit of rhythm control over rate control. • Trend of increased mortality in rhythm arm likely due to proarrhythmia from drugs. • Patients unable to tolerate atrial fibrillation due to symptoms were not enrolled in these studies and are increasingly undergoing ablation , catheter and surgical procedures.

  42. Nonpharmacologic Treatment of Atrial Fibrillation • Maze Procedure • 90% freedom from atrial fibrillation • 2% mortality required thoracotomy • Catheter ablation procedure • only moderate success • long procedures, difficult • selecting population • 60% to 80% effective • Pulmonary vein stenosis,cva,perforation, • esophageal fistula

  43. Nonpharmacologic Treatment of Atrial Fibrillation • AV node ablation with pacemaker implant • recently shown to have no effect on mortality • effective at reducing symptoms • Does not alter need for anticoagulation • Pace at 90 BPM 1 month after procedure to avoid Torsades des Pointes

  44. Wide ComplexTachycardias • Ventricular Tachycardia • SVT with aberrancy (functional bundle branch block) • SVT with underlying bundle branch block • SVT with pre-excitation

  45. Additional Mimimics of Wide Complex Tachycardias • SVT with severe hyperkalemia • SVT with use of antiarrhythmic agents particularly 1C agents • SVT with acute MI

  46. Wide-Complex Tachycardia • Majority are sinus tachycardia with bundle branch block • In higher risk population , previous MI, Decreased Left ventricular dysfunction • Predominantly Ventricular Tachycardia

  47. Differentiating Ventricular Tachycardia from SVT with Aberrancy • Leads to correct initial therapy • Avoids use of Verapamil which may precipitate hemodynamic collapse with V.T. • Cannot use rate or the presence or absence of symptoms as discriminator ! • Use ECG criteria for diagnosis • Use presence of risk factors for V.T. as discriminator

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