Supraventricular Arrhythmias

Dr. Arun Srinivas Chief Cardiologist Vikram Hospital, Mysore

‡ Rapid heart rhythm during which the electrical impulse propagates down the normal His Purkinje system similar to normal sinus rhythm ‡ Distinct from ventricular tachycardia which only originates in the ventricles

Mechanisms of Arrhythmia
‡ Automaticity
± Enhanced automaticity ± Abnormal automaticity

Mechanisms of Arrhythmia
‡ Triggered Activity ± early or late after depolarizations

Mechanisms of Arrhythmia ‡ Reentry-most common mechanism ± Short circuit that forms between two ³pathways´ that are either anatomically or functionally distinct ± Typically: ‡ Path 1: Slow conduction. long refractory period . short refractory period ‡ Path 2: Rapid conduction.

Panel C: Potential to have reentry back up the previously refractory pathway Panel D: Reentry then can persist. due to longer refractoriness in one pathway. Panel B: Unidirectional block.Reentry Panel A: Most impulses conduct down both pathways. .

Supraventricular Arrhythmias ‡ Atrial arrhythmias (AT. AFL and AF) ‡ Atrioventricular nodal reentrant tachycardia (AVNRT) and junctional ectopic tachycardia (JET) ‡ Atrioventricular reentrant tachycardia (AVRT) Wolf-Parkinson-White Syndrome ± Orthodromic AVRT ± Antidromic AVRT .

neck pounding Weakness/malaise Dyspnea Chest pain Lightheadedness Near syncope/syncope ‡ Symptoms usually abrupt in onset and termination ‡ May have history of symptoms since childhood or have a positive FHx .SVT: Symptoms ‡ May be variable ± ± ± ± ± ± Palpitations. chest pounding.

SVT: Physical Exam ‡ In absence of tachycardia. . usually normal ‡ Rapid heart rate (150-250) ± May be irregular or regular (mechanism) ‡ BP may be low or with narrow pulse pressure ‡ Neck veins may reveal cannon waves.

Sinus Rhythm ‡ Originates in sinus node (automaticity) ‡ 50-100 bpm resting ‡ Up to 200 bpm ‡ Conduction through normal AV axis ‡ P wave morphology reflects site of onset .

Atrial Tachycardia ‡ Ectopic atrial focus ± Reentrant. automatic or triggered ‡ ‡ ‡ ‡ 150-250 bpm 1:1 AV conduction Paroxysmal or ³warm up´ P wave morphology variable .

Focal Atrial Tachycardia RAA SN * * * LAA CT RAFW CSO IVC PV LAFW .

20 yr woman with post-partum congestive heart failure postI II III aVR aVL aVF V1 V2 V3 V4 V5 V6 .

Adenosine Injection I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 .

Adenosine Injection I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 .PostPost.

Catheter location : Right atrial appendage LAO RAO CT MAP CS His CT MAP CS His .

Earliest Atrial Activation : Right Atrial Appendage I II III aVL MAP dist MAP prox CT 1.23 msec .8 CT 9.10 CT 11.14 CT 15.6 CT 7.16 CS dist CS prox .4 CT 5.2 CT 3.12 CT 13.

12 CT 13.16 CT 17.14 CT 15.Atrial Tachycardia I II III aVL MAP dist MAP prox CT 1.8 CT 9.6 CT 7.4 CT 5.18 CT 19.10 CT 11.9 sec .2 CT 3.20 CS dist CS prox Sinus Rhythm RF on 1.

Atrial Flutter ‡ Reentrant circuit localized to the RA ‡ 250-350 bpm ‡ 2:1 or variable AV block ‡ Classic ³saw-tooth´ P waves .

14 TA 17.18 TA 19.2 TA 3.Activation on Halo Catheter Typical = Counterclockwise V1 II aVF TA 19.2 .20 TA 9.4 TA 5.20 CS Os TA 1.8 CS Os TA 9.12 TA 13.10 TA 1.10 TA 11.6 TA 7.

18 19.2 .Activation on Halo Catheter Atypical = Clockwise V1 II aVF TA 19.2 TA 3.12 TA 13.6 TA 7.10 TA 1.4 TA 5.20 CS Os TA 1.20 TA 9.14 TA 17.10 TA 11.8 CS Os TA 9.

CMP.. metabolic dz.. valvular dz.Atrial Fibrillation ‡ Chaotic atrial rhythm due to multiple reentrant wavelets ‡ 350-500 bpm ‡ Ventricular rate irregular and rapid due to variable AV block ‡ HTN. EtOH .

catheter ablation. surgical Maze) . ASA) ± Decreasing the ventricular rate (beta-blockers.Atrial Fibrillation ‡ The rapid atrial activity results in: ± Increased risk of thrombus formation and stroke ± Rapid and irregular ventricular rate ‡ The treatment is aimed at: ± Decreasing the risk of stroke (coumadin. calcium channel blockers. digoxin) ± Restoring the rhythm to sinus (drug therapy.

Atrial Fibrillation ‡ Advantages of rhythm control: ± Abolition of symptoms ± Halting atrial enlargement ± Improvement in left ventricular function and exercise capacity ‡ Disadvantages of rhythm control: ± Subjecting patients to drug therapy and/or procedure that might be associated with complications .

Atrial Fibrillation Catheter Ablation Ablate PV potentials PV Isolation Pappone (circumferential LA ablation) .

AV Nodal Reentrant Tachycardia Morphology and location of P wave relative to QRS distinct .

27 y.o with palpitations .

Pseudo R¶ in V1 during tachycardia NSR AVNRT .

Junctional Ectopic Tachycardia .

Normal sinus rhythm Junctional tachycardia .

Wolff-Parkinson-White Syndrome ‡ Second electrical connection exists between the atria and ventricles (accessory pathway) ± Resemble atrial tissue ± Results in a short PR and ± Delta wave (pre-excitation) ‡ Some AP conducts only retrograde (concealed) .

Arrythmias in WPW ‡ The most common arrhythmia is orthodromic AV reentrant tachycardia (narrow QRS) ‡ Less common are pre-excited tachcyardias (wide QRS) ± ± ± ± Antidromic AV reentrant tachycardia Atrial tachycardia/flutter with pre-excitation AVNRT with pre-excitation Atrial fibrillation with pre-excitation (most life threatening due to rapid ventricular response) .

Orthodromic AVRT Conduction down AV axis during tachycardia gives NARROW QRS complex .

Pre-excited Tachycardia Mechanisms AVRT AT AVNRT Conduction down AP during tachycardia gives WIDE QRS complex .

Atrial Fibrillation .

RF Ablation in WPW .

SUMMARY Mechanisms of SVT SP FP Atrial Tachycardia AVNRT AVRT .

Differential Diagnosis of NCT ‡ Short RP ± AVRT ± AT ± Slow-Slow AVNRT ‡ Long RP ± AT ± Atypical AVNRT ± PJRT ‡ P buried in QRS ± Typical AVNRT ± AT ± JET .

Ventricular Arrhythmias .

‡ Life is good ‡ Death is not so good .

Sudden Death ‡ Sudden cardiac death remains a major public health problem ‡ Several hundred thousand victims succumb each year to primary ventricular fibrillation during periods of acute ischemia .

Ventricular Arrhythmias: Treatment ‡ The goal of treatment is to prevent lifethreatening hemodynamic compromise or sudden death and not to ³stamp out PVC¶s´ ‡ Treatment is justified only if there is evidence that the arrhythmia in question represents an independent risk factor for these events .

Decreased Incidence of Arrhythmic Deaths in Patients with CHD ‡ ‡ ‡ ‡ ‡ ‡ Thrombolytic therapy PTCA CABG ACE inhibitors Lipid-lowering agents Beta blockers .

Vaughan Williams Classification ‡ Class I agents: block fast-sodium channels ‡ Class II agents: block adrenergic influences ‡ Class III agents: lengthen cardiac repolarization ‡ Class IV agents: block the slow-calcium channel .

III agents. ‡ Major focus is shifting away from this class of compounds towards Class II. ‡ This class of drugs can increase mortality because of proarrhythmia.Ventricular Arrhythmias: Chronic Treatment ‡ For many years sodium channel blockers (Class I agents) have been used for controlling cardiac arrhythmias. ‡ Growing use of ICD¶s and catheter ablation procedures .

Proarrhythmia--Torsaides .

.Amiodarone ‡ Has emerged as an agent with the most versatile pharmacodynamic and clinical therapeutic effects. ‡ Very low propensity to induce torsades des pointes. ‡ Improves ventricular function. ‡ Can be combined with beta-blockers to augment its antiarrhythmic effects.

Ventricular Arrhythmias Clinical Situations Ventricular Arrhythimias ormal eart Acute Ischemia ost I Car iomyo athy Su en eath Sur i or .

‡ Ventricular ectopy with no evidence of structural heart disease .

complex. asymptomatic VPC¶s and nonsustained v-tach ‡ No prognostic significance for sudden death in the abscence of organic heart disease . frequent.Ventricular Premature Complexes ‡ Rare.

VPC¶S/NSVT: Evaluation ‡ In the absence of structural heart disease/ECG abnormalities the patient is not at increased risk of sudden arrhythmic death. .

VPC¶s/NSVT ‡ ? Predictive for a more severe arrhythmic event ‡ Presence of syncope indicates a higher probability for sustained v-tach/sudden death .

VPC¶S/NSVT: Treatment ‡ Reassurance ‡ Removal of provocative factors: caffeine. alcohol. tobacco ‡ Rx with beta blockers ‡ Try to avoid traditional anti-arrhythmic agents .

Sustained Ventricular Tachycardia ‡ Usually a marker of severe heart disease ‡ Does not result from pre-existing ventricular arrhythmias .

Monomorphic Ventricular Tachycardia .

‡ Ventricular ectopy in acute ischemic syndromes .

Acute MI: Primary V-Fib ‡ Incidence: 5 to 20% ‡ 75% occurs within first 12 hours ‡ May be associated with increased inhospital mortality ‡ Does not appear to affect long-term mortality .

Ventricular Fibrillation .

hemodynamically unstable v-tach should be treated with prompt electrical cardioversion .MI: Ventricular Arrhythmias ‡ V-fib or sustained.


Acute Ischemic Syndromes: Ventricular Fibrillation ‡ Unsynchronized electrical shock at 200 J ‡ Unsynchronized electrical shock at 200 to 300 J ‡ Unsynchronized electrical shock at 360 J .

Acute Ischemic Syndromes Antiarrhythmic Agents entricular Tachycardia idocaine Amiodarone rocainamide retylium Amiodarone .

Watch for toxicity in patients with hepatic dysfunction.5 mg/kg with supplemental boluses of 0.75 mg/kg every 5 to 10 min ( maximum 3 mg/kg ) ‡ Maintenance Infusion: 2 to 4 mg/min ‡ Precautions: Hepatic clearance.0 to 1.5 to 0.Lidocaine ‡ Loading Bolus: 1. shock. hypotension. . CHF.

V Fib Threshold .

5 mg/min .Amiodarone ‡ Loading Infusion: 150 mg over 10 min ‡ Maintenance Infusion: 1.0 mg/min for 6 hours then 0.

. Administer the loading dose slowly to avoid hypotension.Procainamide ‡ Loading infusion: 20 to 30 mg/min up to 12 to 17 mg/kg ‡ Maintenance infusion: 1 to 4 mg/min ‡ Precautions: Renal clearance. Watch for toxcity in patients with renal impairment.

hypotension .Bretylium ‡ Loading infusion: 5 to 10 mg/kg ‡ Maintenance infusion: 1 to 2 mg/min ‡ Precautions: transient sinus tachycardia.

Acute MI: Warning Arrhythmias ‡ ‡ ‡ ‡ Frequent PVC¶s ( > 6/min ) R on T Multiform PVC¶s Non-sustained v-tach .

R on T .

R on T Phenomenon .

Post MI: Ventricular Arrhythmias ‡ ‡ ‡ ‡ ‡ Beta blockers ACE inhibitors Statin therapy Aspirin Consider EP evaluation with NSVT and LVEF < 35% .

Post MI: Amiodarone
‡ Meta-analysis: confers some benefits of survival ‡ CAMIAT and EMIAT trials found a reduction in arrhythmic deaths but with no effect on total mortality

‡ Ventricular ectopy in patients with congestive heart failure

CHF: Ventricular Arrhythmias Amiodarone
‡ Suppresses ventricular ectopy ‡ Does not increase mortality ‡ May improve survival in patients with advanced Class III-IV CHF

CHF: Ventricular Arrhythmias Amiodarone
‡ No effect on survival in patients with Class II-III CHF ‡ May be a favorable trend in patients with nonischemic CHF ‡ No evidence that suppression of ventricular ectopy is beneficial

Idiopathic Ventricular Tachycardia ‡ Mostly seen in children/young adults ‡ Latent myocardial disease may be present ‡ 70% originate in RV outflow tract ‡ Frequently catecholamines. or adenosine sensitive ‡ Vast majority can be treated with catheter ablation . verapamil.

Sustained V-tach: Implantable Defibrillators ‡ AVID Trial: Patients with previous cardiac arrest/sustained v-tach had lower mortality rates ( 27% ) when treated with AICD vs. amiodarone/sotalol. .

Sustained Ventricular Tachycardia: Implantable Defibrillators ‡ While patients have a low risk of sudden death. total survival of patients with severe heart disease may not be markedly improved .

Sustained Ventricular Tachycardia: Summary of Management ‡ Define underlying heart disease ‡ Address presence of precipitating factors ‡ Severity of ventricular dysfunction is predictive of response to therapy and survival ‡ In most cases an EP evaluation is warranted ‡ Initial Rx options include Amiodarone/ICD .

External Defibrillator .

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