Lisa Campfens MD, FRCPC, FACEP Tachydysrrhythmias Lisa Campfens MD, FRCPC, FACEP

Generation of Dysrrhythmias Two fundamental causes Disturbances of automaticity Disturbances of conduction AV block Reentry Abnormal electrical activity in heart Too fast/too slow Supraventricular vs ventricular

Presentation Multiple symptoms: Fatigue Chest pain Dyspnea Dizziness Presyncope Palpitations Patients can be symptomatic even with single premature beats or non-sustained atrial arrhythmias Chest pain usually unrelated to CAD

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 Rapid stimulation of atrial tissue occurs at 100-280bpm> mean of 170bpm Persistence of tachycardia: decreased cardiac output increased CHF increased ischemia Usually takes weeks to months to develop Ventricular dysfx usually reversable

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 Quinidine, Procainamide Class IB Lidocaine, Phenytoin, Mexilitine Class IC Flecainide, Propafenone All class IC agents can exacerbate existing dysrhythmias and create new ones

Procainamide Therapeutic use Ventricular tachycardia SVT with aberrancy Pre-excitation Syndromes Old drug/ now for most part replaced by Amiodarone as first line agent for chemical cardioversion. There has not been any head to head comparison of the two drugs After use of procainamide, in most cases still need to put the patient on a long-term oral agent Both Procainamide and Amiodarone prolong QT- contraindicated in Torsades de pointes Adverse effects: hypotension

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 Meotprolol: 5mg IV for 3 doses q2-5min

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 QRS widening Prolongation of the PR and QT intervals 150mg IV over 10 mins then 1mg/min for 6 hours

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 Ist choice if contraindication to B blocker or if Adenosine terminates PSVT but recurs immediately Diltiazem: 0.25mg/kg IV, may repeat at 0.35mg/kg in 15 mins Verapamil: 5-10mg IV, may repeat to max 15mg .

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 Should also theoretically be avoided in wide QRS tachycardia. If given to WPW with AF could detiorate into VF

PSVTs A Fibrillation A Flutter AVNRT AVRT (ORT) SVT includes all forms of tachycardia that arise above the bifurcation of the bundle of HIS HR at least 100bpm QRS usually narrow Tachys which respond to vagal maneuvers or other cholinergic agents like adenosine are usually due to re-entry and involve the compact region of the AV node SVT that persists even when AV block is achieved by CSM or other interventions are independent of AVN conduction QRS maybe widened /abnormal because of intrinsic conduction disturbance, myocardial disease, or rate-related BBBB. Rate-related BBB: occurs if either right or keft BB reaches its effective refractory period and cannot conduct impulses to match the rapid rate of the tachycardia

Reentry Most common mechanism Requires two separate paths of conduction Requires an area of slow conduction Requires unidirectional block 15

Regular SVT in Adults 90% reentrant 60% AVNRT 30% AVRT (ORT) 10% Atrial tachycardia 2 to 5% involve WPW syndrome 16

AV Nodal Reentrant Tachycardia Slow pathway Re-entrant circuit is small and is in or closely related to the AV node Re-entrant circuit is small and is in or closely related to the AV node Narrow QRS Absent p waves Rate 160-180bpm Fast pathway 17

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 18

Orthodromic Reciprocating Tachycardia Conduction down AVnode Anterograde over AV node and retrograde conduction of an accessory pathway. Frequently presents in patients with WPW as narrow complex tachycardia Up accessory pathway AVRT(ORT): re-entrant circuit large-involves atria, AV node and ventricles QRS narrow 19

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 20

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 Origin inferred from P wave morphology. 21

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. Adenosine may help with diagnosis if AV block occurs and continued arrhythmia likely atrial tachycardia 22

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 23

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% 24

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 Rapid atrial depolarization of 250-350 bpm Block can be variable and appear as irregular Often converts to AF or NSR Re-entrant circuit confined to right atrium Sync cardioversion start at 25J Antiarrhythmic drugs not very successful-50% 25

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 26

42 year old smoker presents to the ED with palpitations. BP 100/60. A. Emergent cardioversion for polymorphic VT B. IV procainamide C. IV lidocaine D. IV diltiazem to obtain rate control. 27

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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 Ca channel blockers block AV node and accelerate conduction down accessory pathway thaT HAS VERY SHORT REFRACTION PERIOD THEREFORE allowing AF to detiorate to VF very quickly. Results in refractory hypotension and refractory to cardioversion 29

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 Most common arrhythmia encountered 15-25% of all strokes in US can be attributed to AF Random chaotic depolarization of atria 400-700bpm but ventricular rate limited by refractory period of AVN so ventricular rate 140-170bpm Irregularly irregular 30

Management of Atrial Fibrillation Symptom relief by rate and rhythm control Reduce risk of thromboembolism by anticoagulation Prevent tachycardia-mediated cardiomyopathy 31

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** . Stroke rate .8% Amiodarone is a lousy rate control agent. Often combine with B blocker to slow rate and then Amiodarone to cardiovert over time Stunning of atria and stasis can occur after cardioversion leading to thrombus formation even though patient in NSR Patients often unaware of short episodes of AF 32

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 33

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 34

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 35

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 36

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. Trend of increased mortality in rhythm arm likely due to pro-arrhythmia from drugs 37

Wide ComplexTachycardias Ventricular Tachycardia SVT with aberrancy (functional bundle branch block) SVT with underlying bundle branch block SVT with pre-excitation 38

Additional Mimimics of Wide Complex Tachycardias SVT with severe hyperkalemia SVT with use of antiarrhythmic agents particularly 1C agents SVT with acute MI 39

Wide-Complex Tachycardia Majority are SVT with BBB In higher risk population VT until proven otherwise :High risk: Most important predictor of VT is prev MI with centricular myocardial scar formation LV dysfx Valvular HD Congenital HD 40

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 V tach: repetetive firing of an irritable ventricular ectopic focus at 140-180bpm V fib: electricaL CHAOS IN VENTRICLES Avoids use of Verapamil which may precipitate hemodynamic collapse refractory hypotension/refractory to cardioversion 41

The Brugada Criteria Clinical signs of AV dissociation: Cannon a waves Irregular pulse Varying intensity of S1 Beat to beat change in SBP ECG signs of Av dissociation: Pathopneumonic for V tach but only seen in 25% Independent P waves Capture/fusion beats Capture: when sinus impulse conducted to ventricle during VT Fusion: sinus impulse activates the ventricle at the same time as a VPC (leads to narrower QRS complexes) Indeterminate axis/ extreme right axis Uniform concordance In V1-V6 either positive or negative 42

Morphology Criteria for VT 43

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 44

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 46

VT with Preserved LV Fx DC cardioversion Amiodarone 1st line RX according to ACLS Procainamide Lidocaine Avoid use of combination antiarrhythmic agents Lidocaine: Reduced to 3rd line therapy due to relative little effectiveness in non ischemic VT. 47

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 syndrome is reserved for those persons who have a combination of the WPW pattern and SVT.

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?’ Syndrome: predilection for dysrrythmias abn ECG symptoms Pre-excitation: implies early depolarization of ventricle represented as delta wave Delta wave- dec PR in association with slurring of upstroke of QRS. PR is short because ventricle being prematurely activated through accessory path QRS wide because ventricle activated from abn location Sinus impulse travels to ventricle via both AV node and accessory pathways. Results in fusion of ventricular activity via both conventional His-Purkinje system and the accessory path Because AV nodal conduction is decremental and relatively slow, the 1st part of the QRS is slurres. Anterograde accessory pathway conduction reaches ventricle 1st forming delta wave. This slurring persists until AV node conduction propagates into ventricle, activating ventricle rapidly and resulting in terminal QRS that is closer to normal in morphology Abn ECG not always present(depends on tone of AVN, location of accessory path, site of atrial impulse, size of atria, etc)

WPW AV Node Integral AVRT-Orthodromic AVRT-Antidromic AV blocking diagnostic and therapeutic AVRT-Antidromic Regular AVRT-Orthodromic Most common type PAC conducts down AVN and up accessory path Narrow QRS, regular, occ neg P AVRT-Antidromic Conduction down accessory path and retrograde through AVN Wide QRS

WPW AV Node Innocent Bystander AF Can be serious problem Normal AVN protects ventricle from fast atrial rate in AF. If refractory period of accessory path is short, may allow rapid activation of ventricle (300-500bpm) ie VF

Polymorphic VT Immediate defibrillation IV Lidocaine , Amiodarone Usually result of severe metabolic disturbance or cardiac ischemia. Important to differentiate polymorphic VT form Torsades. Normal QT Important implications for treatment 52

Monomorphic VT in Patients with Normal LV Fx No structural heart disease Present as palpitations, syncope but rarely as sudden death 53

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

Torsades de Pointes Polymorphic VT assoc with long QT QTc >440msec , QT > 500 msec Frequently initiated after pause Iatrogenic hypoK, hypoMg, Hypo Ca, Drugs, Combination Congenital V rate >200bpm Undulating axis- polarity of complexes shift about baseline Usually short episodes<20secs but sustained runs can be seen Prolonged QT during sinus rhythm Electrophysiologic mechs not well understood. Current research has focused on ‘early after-depolarizations’ Iatrogenic- Drugs: Anti-arhrythmics-Class 1a,1c III Anti-psychotics-phenothiazines, haloperidol Anti-depressants-TCAs Antibiotics Anti-histamines Combo of Quinidine, Digoxn and hypo K well documented Metabolic: hypoK,Mg,Ca CNS: SAH, ICH, tumor CARDIAC: ischemia myocarditis severe bradyarrhythmias TOXINS: organophosphates HYPOTHYROIDISM 55

Drug-induced Torsades is an idiosyncratic response unrelated to drug level. Usually seen within 7 days of initiation of therapy. Can occur without reliable warning signs Anti-arhrythmics-Class 1a,1c III Anti-psychotics-phenothiazines, haloperidol Anti-depressants-TCAs Antibiotics Anti-histamines Combo of Quinidine, Digoxn and hypo K well documented 56

Treatment of Torsades de Pointes Goal to shorten QT Remove offending agent Replete K IV Mg even if normal level Mg tx of choice. Mech of action unclear. Does not shorten QT. Mg levels often normal pre-initiation 2g bolus over 15-20mins and repeat prn twice. IV drip 3-20mg/min Treat Congenital with B blockers and Pacing or ICD 57

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 Brugada Syndrome Incompete RBB ST elevation V1V2 No structural heart disease Genetic Normal QTc exacerbated by Procainamide and Flecainide ICD implantation Prone to develop Torsades and VF leading to sudden cardiac death RV Dysplasia Delayed RV activation Epsilon wave , deep precordial Twave inversion fatty infiltration RV, MRI, RV gram 59

Sudden Death with Normal LV FX Hypertrophic Cardiomyopathy Major cause in U.S. in young patients without CAD Risk factors ICD effective Risk factors- extreme hypertrophy(>3.0 cm) exertional hypotension, nonsustained VT, syncope, family history sudden death ICD effective but appropriate selection for primary prevention problematic 60

A. Synchronized cardioversion for VT 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 61

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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. 63

A. Administer IV Procainamide B. Consult EP for placement of a ICD 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 64

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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 . Antipsychotics, hypoMg, quinolones, all may predispose to this arrhythmia. 66