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Tachydysrrhythmias Lisa Campfens MD, FRCPC, FACEP Generation of Dysrrhythmias Two fundamental causes Disturbances of automaticity Disturbances of conduction AV block Reentry Presentation Multiple symptoms: Fatigue Dyspnea Presyncope Chest pain Dizziness Palpitations Patients can be symptomatic even with single premature beats or non-sustained atrial arrhythmias Complications SVTs common but persistent Rarely life-threatening but present sig problems in patient management A fib/A flutter: Stroke 2°to embolization Persistence of tachycardia : Dilated cardiomyopathy CHF Referral All patients with wide complex tachycardia of unknown origin Resistant/intolerant to pharmacological therapy WPW Syndrome Classification of Antidysrrhythmic Drugs Vaughan Williams classification Class I: Na channel blockers Class II: B blockers Class III: K channel blockers Class IV: Ca channel blockers Other: adenosine, digoxin, and ibutilide Class I: Na Channel Blockers Class IA Class IB Class IC Quinidine, Procainamide Lidocaine, Phenytoin, Mexilitine Flecainide, Propafenone Procainamide Therapeutic use Ventricular tachycardia SVT with aberrancy Pre-excitation Syndromes Class II: Beta Blockers Metoprolol, Atenolol, Esmolol Therapeutic use Slow ventricular rate (A fib/ A flutter) Terminate SVT caused by an AV nodal reentrant circuit Class II: Beta Blockers (cont’d) Adverse effects Heart block Heart failure AV block Sinus arrest Hypotension Bronchospasm (asthma/COPD) Class III: K Channel Blockers Amiodarone Therapeutic use Life-threatening ventricular dysrrhythmias SVT with aberrancy Pre-excitation Syndromes Class IV: Ca Channel Blockers Verapamil, Diltiazem Therapeutic use Slow ventricular rate (A fib/ A flutter) Terminate SVT caused by an AV nodal reentrant circuit . Other Antidysrhythmic Drugs Adenosine Half-life few seconds Intense but transient AV block thereby terminating tachycardia Safe in patients with heart disease Contraindications: asthma/COPD Therapeutic use termination of PSVT PSVTs A Fibrillation A Flutter AVNRT AVRT (ORT) Reentry Most common mechanism Requires two separate paths of conduction Requires an area of slow conduction Requires unidirectional block Regular SVT in Adults 90% reentrant 60% AVNRT 30% AVRT (ORT) 10% Atrial tachycardia 2 to 5% involve WPW syndrome AV Nodal Reentrant Tachycardia Slow pathway Re-entrant circuit is small and is in or closely related to the AV node Fast pathway AV Nodal Reentrant Tachycardia 3o % respond to vagal maneuvers Very responsive to AVN blocking agents: B blockers, CA channel blockers, adenosine. Recurrences are the norm on medical therapy Catheter ablation 95% successful with 1% major complication rate Orthodromic Reciprocating Tachycardia Anterograde over AV node and retrograde conduction of an accessory pathway. Frequently presents in patients with WPW as narrow complex tachycardia Conduction down AVnode Up accessory pathway 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 Atrial Tachycardia Atrial rate 150-250 bpm Does not require AVN or infranodal conduction P wave morphology different PR interval > 120 ms differentiating from junctional tachycardia Atrial Tachycardia Left atrial focus- P wave upright V1/negative in aVL Right atrial focus-P wave negative V1/upright in aVL Adenosine may help with diagnosis 70-80% will also terminate with Adenosine. Atrial Tachycardia Most are due to abn automaticity and have right atrial focus May be reentry in patients with prev atriotomy scar, such as CABG or congenital repair patients Atrial Tachycardia Therapy Antiarrhythmics Class 1 : procainamide, quinidine, flecainide Patients without structural heart disease. Class III : sotalol, amiodarone, dofetilide AVN blocking agents for rate control Catheter ablation effective in 70-80% 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 Atrial Flutter and Risk of Stroke Although risk of stroke historically thought to be low, multiple instances of stroke with cardioversion lead to similar indication for anticoagulation as AF 42 year old smoker presents to the ED with palpitations. BP 100/60. A. Emergent cardioversion for polymorphicVT B. IV procainamide C. IV lidocaine D. IV diltiazem to obtain rate control. Answer WPW with AF and a rapid ventricular response. He is stable, thus IV procainamide indicated to slow conduction down the accessory pathway Diltiazem contraindicated Lidocaine will have no effect, as is not VT Epidemiology of AF Affects 2-4% of population Increases to 5-10 % >80 yrs 2-fold increased risk of death 15-25% of all strokes in US attributed to AF Risk of thromboembolism approx 5%/yr but may be as high as 20% in high risk groups not anticoagulated Management of Atrial Fibrillation Symptom relief by rate and rhythm control Reduce risk of thromboembolism by anticoagulation Prevent tachycardia-mediated cardiomyopathy Acute Management of AF Focus on rate control DC cardioversion or pharmacologic conversion if <48 hrs or following TEE on Heparin without evidence of left atrial thrombus Following cardioversion anticoagulate for 4 wks with goal INR of 2-3 until atrial fx normalizes** Acute Management of AF 50% spontaneously convert <24 hours Digoxin used heavily in past for prevention/ conversion, ineffective at either May be profibrillatory as decreases atrial refractory period Acute Management of Atrial Fibrillation Rate control: Ca channel blockers or B blockers in patients with normal LV fx Cautious use of Ca channel blockers if depressed LV fx. Associated with increased mortality in long term. Avoid Beta blockers in acutely decompensated CHF patients with AF AF and Depressed LV Fx Digoxin and amiodarone may be effective if LV dysfx and decompensated CHF to slow ventricular response. Digoxin alone rarely effective when patient sympathetically driven Avoid high dose digoxin with amiodarone as digoxin levels increase 2-fold with amiodarone Chronic Management of AF Maintenance of sinus similar with class I and class III drugs-50% recurrence at 1 year Recurrence of AF 80% at 1 year without treatment Chronic Management of AF Recent large trials reveal no benefit of rhythm vs rate control Trend of increased mortality in rhythm arm Patients unable to tolerate AF due to symptoms were not enrolled in these studies and are increasingly undergoing ablation , catheter and surgical procedures. Wide ComplexTachycardias Ventricular Tachycardia SVT with aberrancy (functional bundle branch block) SVT with underlying bundle branch block SVT with pre-excitation Additional Mimimics of Wide Complex Tachycardias SVT with severe hyperkalemia SVT with use of antiarrhythmic agents particularly 1C agents SVT with acute MI Wide-Complex Tachycardia Majority are SVT with BBB In higher risk population VT until proven otherwise Differentiating VT from SVT with Aberrancy Leads to correct initial therapy Verapamil may ppt hemodynamic collapse Hemodynamic status or rate not a clue to mechanism In higher risk population VT until proven otherwise ECG criteria for diagnosis The Brugada Criteria Table I. Diagnosis Of Wide QRS Complex Tachycardia With A Regular Rhythm Step 1. Is there absence of an RS complex in all precordial leads V1 – V6? If yes, then the rhythm is VT. Sens 0.21 Spec 1.0 Step 2. Is the interval from the onset of the R wave to the nadir of the S wave greater than 100 msec in any precordial leads? If yes, then the rhythm is VT. Sens 0.66 Spec 0.98 Step 3. Is there AV dissociation? If yes, then the rhythm is VT. Sens 0.82 Spec 0.98 Step 4. Are morphology criteria for VT present? See Table II. If yes, then the rhythm is VT. Sens 0.99 Spec 0.97 Morphology Criteria for VT Table II. Morphology Criteria for VT Right bundle type requires waveform from both V1 and V6. V1 V6 Monophasic R wave QR or QS RS or QR R/S <1 Left bundle type requires any of the below morphologies. V1or V2 V6 R wave > 30 msec QR or QS Notched downstroke S wave. Greater than 60msec nadir S wave. Adapted from Brugada et al. A new approach to the differential diagnosis of regular tachycardia with a wide QRS complex. Circulation 1991; 83:1649-59. Therapy for VT Stable-chemical or DC cardioversion Unstable-DC cardioversion Amiodarone 150 mg IV over 10 mins, max 2.2 gm/24 hrs class IIA recommendation New ACLS Algorithm VT with Depressed LV Fx Amiodarone drug of choice mortality neutral or beneficial Initial dose 150 mg IV. over 10 mins effective in VF using 300 mg bolus with improved arrival to hospital. DC cardioversion always acceptable option Procainamide contraindicated VT with Preserved LV Fx DC cardioversion Amiodarone 1st line RX according to ACLS Procainamide Lidocaine Avoid use of combination antiarrhythmic agents AVRT Extranodal Accessory Pathways and WPW Syndrome Extremely symptomatic but rarely observed In the presence of AF, VF can occur if the refractory period of the accessory pathway is <250 msec WPW Not an arrhythmia but a clinical syndrome ECG: PR<.12 sec, QRS>.10 sec, delta wave Many types of arrhythmias ‘Is AVN an integral part or an innocent bystander?’ WPW AV Node Integral AVRT-Orthodromic AV blocking diagnostic and therapeutic AVRT-Antidromic Regular AV blocking diagnostic and therapeutic WPW AV Node Innocent Bystander AF Can be serious problem Polymorphic VT Immediate defibrillation IV Lidocaine , Amiodarone Usually result of severe metabolic disturbance or cardiac ischemia. Monomorphic VT in Patients with Normal LV Fx No structural heart disease Present as palpitations, syncope but rarely as sudden death Monomorphic VT in Patients with Normal LV Fx RV outflow tachycardia LBB morphology inferior axis adenosine, Calcium channel , occ beta blockers Amenable to Ablation Idiopathic LV tachycardia RBB superior axis Verapamil and adenosine sensitive Amenable to Ablation Torsades de Pointes Polymorphic VT assoc with long QT Frequently initiated after pause Iatrogenic QTc >440msec , QT > 500 msec hypoK, hypoMg, Hypo Ca, Drugs, Combination Congenital QT Prolonging or Torsadogenic Drugs The following drugs have been shown to prolong the QT interval or have documented clinical Torsades de Pointes reported in the literature Amantadine Quetiapine Aminophylline Quinidine Amiodarone Risperdone Barium Salmeterol Bepridil Thioridazine Chloralhydrate Sparfloxacin Chloroquine Sumatriptan Ciprofloxacin Tacrilimus Cisapride Tamoxifen Sertraline Chlorpromazine Disopyramide Tizanide Dofetilide Trimethorprim Sulfa Doxepine Venlafaxine Droperidol Vistaril Sotalol Flecanide Fluoxetine Foscarnet Fosphentoin Gatifloxin Halofantrine Haloperidol Ibutilide Imipramine Indipamide Isradapine Ketaconazole Levofloxacin Levomethadyl Mesoridazine Moexitine/Hctz Moxifloxicin Naratripan Nicardipine Octreotide Pentamidine Pimozide Probucol Erythromycin Zolmitriptan Felbamate Clarithromycin Terfenadine Desipramine Treatment of Torsades de Pointes Goal to shorten QT Remove offending agent Replete K IV Mg even if normal level Treatment of Torsades de Pointes Overdrive pacing isoproterenol Pacing DC Cardioversion Rarely required May be refractory Sudden Death with Normal LV Fx Brugada Syndrome Incompete RBB ST elevation V1V2 RV Dysplasia Delayed RV activation Epsilon wave , deep precordial Twave inversion Sudden Death with Normal LV FX Hypertrophic Cardiomyopathy Major cause in U.S. in young patients without CAD Risk factors ICD effective 67 yr old male with prior infarct and LV dysfx presents with palpitations and dizziness. BP is 80/40 A. Synchronized cardioversion for VT B. IV Procainamide for AF with WPW syndrome C. Synchronized cardioversion for unstable SVT with aberrancy. D. IV Amiodarone for SVT with aberrancy in a patient with LV dysfx Answer This patient has VT. An RS interval >100 msec clearly visible. In addition, by history this patient is overwhelmingly likely to present with VT with a wide complex rhythm Unstable with relative hypotension requiring immediate cardioversion as opposed to pharmacologic therapy. 46 yr old alcoholic, on methadone, with schizophrenia. She began feeling dizzy after starting a fluoroquinalone for a UTI A. Administer IV Procainamide B. Consult EP for placement of a ICD C. Discontinue antibiotic and antipsychotic, treat with IV Mg, and consider temporary pacing D. Administer IV Amiodarone Answer Torsades de Pointes with classic polymorphic VT and prolonged QT demonstrated on bottom strip. Procainamide or amiodarone would worsen this rhythm. ICD is not indicated .