Ventricular Arrhythmias Claire B. Hunter, M.D.

Objectives To know the implication and management of PVC To know the diagnosis and acute treatment of VT and VF To know the common etiologies of Torsades de pointes To understand the implication of accelerated ventricular rhythm To know the major indications of implantable cardioverter-defibrillators (ICD)

Origin of Ventricular Arrhythmias

Normal Action Potential

Action Potential – ECG Correlation

Mechanisms of Cardiac Arrhythmias Abnormal impulse formation Increased normal automaticity Abnormal automaticity Triggered activity due to early afterdepolarization (EAD) Triggered activity due to delayed afterdepolarization (DAD) Abnormal impulse conduction reentry

Increased Automaticy

Abnormal Automaticity

Early Afterdepolarization (EAD) Stim. Triggered activities Stim.

Delayed Afterdepolarization (DAD) Triggered activities

Reentry Simple reentry Figure of 8 reentry

Premature Ventricular Contraction (PVC): ECG coupling interval Compensatory pause Full compensation (2100 ms) (2100 ms)

PVC Bigeminy v v v v v v v

PVC Trigeminy v v v v

PVC Couplet

Polymorphic PVCs PVC A PVC B

Interpolated PVC

Parasystole

Premature Ventricular Complex (PVC) Prevalence: PVC is the most common cardiac arrhythmia, observed in about 50% of healthy medical students, 60% of healthy adult male, and 80% of patients with previous MI. Mechanism: Probably reentry in majority, increased automaticity in some (parasystole). The role of triggered activities remains uncertain.

PVC: Etiology No identifiable heart diseases in many patients. Some known causes: ischemia, myocarditis, cardiomyopathy, some medications, conditions associated with increased blood catecholamines, alcohol, caffeine, and others.

PVC: Clinical Presentation Most patients have no symptoms. In symptomatic patients, it is mostly reported as “skipped heart beats”, or “irregular heart beats” – palpitation.

PVC: Implications PVC alone may not indicate heart diseases or cause heart damage. Frequent PVCs are associated with an increased mortality in patients with cardiac dysfunction – a risk marker. PVCs may trigger VT or VF in some patients with underlying heart diseases.

PVC: Evaluation Careful history and physical examination are generally sufficient to rule out significant cardiovascular diseases. ECG is important to correlate symptoms with PVCs. PVC frequency may increase or decrease during exercise.

PVC: Treatment Reassurance: the treatment of choice. Drug therapy: only for a few patients with severe symptoms that are persistent after reassurance. Low dose -blocker is the first line drug. Goal of therapy: to improve symptoms, not to eliminate PVCs. Suppression of PVCs by class I antiarrhythmic drugs in patients with MI and LV dysfunction may increase mortality!

CAST (Cardiac Arrhythmia Suppression Trial) Study patients: post MI, left ventricular dysfunction, frequent PVCs that were suppressed by flecainide or encainide. Randomization: flecainide/encainide vs. placebo Result: The flecainide/encainide group had a higher mortality than the placebo group!

Ventricular Tachycardia (VT): Definitions VT: ectopic ventricular rhythm >100 bpm. Monomorphic VT: QRS morphology remains the same. Polymorphic VT: QRS morphology changes. Sustained VT: VT duration  30 sec or requires immediate intervention because of hemodynamic instability. Nonsustained VT: VT from 3 beats to 30 sec.

MonomorphicVT: Etiologies Coronary disease is the most common cause, particularly after MI. Acute ischemia is unlikely the direct cause of monomorphic VT. Any other heart diseases that are associated with myocardial scar or slow conduction (cardiomyopathy, RV dysplasia, valvular disease, congenital heart disease). Idiopathic in a small number of patients w/o structural heart disease (RV outflow tract VT, idiopathic left ventricular VT).

VT mechanism - reentry

Monomorphic VT: Presentation Symptoms are variable, from palpitation to syncope or cardiac arrest. Dizziness and dyspnea are common. Blood pressure can be normal, reduced or un-measurable. Heart rate can vary from 100 to 300 beat/minute.

Monomorphic VT: Diagnosis ECG is very useful. The major challenge is to differentiate VT from SVT with bundle branch block (BBB) or aberrancy. Evidences supporting VT: A-V dissociation or fusion beats Positive or negative concordance on V1 to V6. “Pseudo-delta waves”

VT - AV Dissociation &Negative Concordance

VT - Positive Concordance

VT - Pseudo-delta Waves

MonomorphicVT: Treatment Stable: iv antiarrhythmic drug  DC cardioversion if drug fails. Unstable (hypotension or pulmonary edema): DC cardioversion first  iv antiarrhythmic drug  repeat DC cardioversion if VT recurs.

Example of VT Cardioversion shock Never shock an awake patient!

VT Treatment: Antiarrhythmic drugs Drugs: lidocaine, procainamide, amiodarone. First choice varies according to patient profile and physician preference but lidocaine is no longer recommended as the first choice. Lidocaine (class Ib): fast action but not very effective. Acute side effects mainly neurological. Procainamide (class Ia): fast action and quite effective. Acute side effects mainly hypotension. Amiodarone (class III): very slow action but very effective. Acute side effects mainly hypotension. Avoid iv verapamil or diatilzem

Ventricular Fibrillation (VF) VF: sustained, rapid (>300 bpm) and irregular ventricular rhythm. Venticular flutter (VFL): sustained, rapid (>300 bpm) and regular ventricular rhythm. VFL and rapid sustained monomorphic VT are arbitrarily defined. Sustained polymorphic VT and VF are also arbitrarily defined. VF is the most important cause of sudden death!

Example of VF

VF: Etiologies Any terminal disease Ischemia, myocarditis, cardiomyopathy. Electrolyte or metabolic disturbances, drugs. Electrocution/trauma. Genetic disorders (Brugada syndrome) Others

VF: Mechanism

Management of VF Shock ASAP! Asynchronized DC shocks CPR (cardiopulmonary resuscitation) while waiting for shocks. Search and treat underlying etiologies after successful defibrillation.

Example of Ventricular Defibrillation Shock

Nonsustained VT with normal QT

Nonsustained VT with Normal QT Presentation: No symptoms Palpitation Dizziness Syncope

Nonsustained VT with Normal QT: Management Search and treat underlying etiology Asymptomatic with LV dysfunction: refer for consideration of implantable cardioverter-defibrillator (ICD) for prevention of sudden death. Asymptomatic with normal LV function: follow-up only. Symptomatic with normal LV function: antiarrhythmic drugs for symptom relief.

Nonsustained VT with QT prolongation (Torsades de pointes) R on T Recorded 10 minutes after iv ibutilide 1 mg for atrial fibrillation conversion.

Nonsustained VT with QT prolongation (Torsades de pointes) 29F, alcoholic, K2.9.

Nonsustained VT with QT prolongation (Torsades de pointes) 90F, sinus node dysfunction.

Treatment of Torsades de pointes Search and treat etiology KCl: only slow iv infusion is allowed, unlikely to see immediate effect. MgSO4: 1 g iv over 2-5 min, may repeat 1 dose, may see immediate effect. Isoproterenol: Start from 1 mcg/patient/min, titrate up (1 mcg increment) until VT suppression, or 5 mcg/patient/min. A HR up to 120 bpm may be necessary to suppress VT. Never use this drug if you are not sure if the VT is true torsade de pointe! Overdrive pacing

Example of torsades de pointes suppression By Overdrive Pacing

Congenital Long QT Syndrome Torsade de pointe

Accelerated Ventricular Rhythm Definition: 3 consecutive ectopic ventricular complexes with rate between 40-100 bpm. Mechanism: possibly increased automaticity from the His-Purkinje fiber. Implication: Most commonly seen after thrombolytic therapy for acute myocardial infarct but can also be observed in patients with other heart diseases or without a heart disease. Evaluation & Treatment: observe only.

Accelerated Ventricular Rhythm

ICD (implantable cardioverter defibrillator)

ICD Today: Small Devices, Long Battery Life, Pectoral Implant, Endocardial Leads Transvenous, single incision Local anesthesia; conscious sedation Short hospital stays and few complications Perioperative mortality < 1% Programmable therapy options Single- or dual-chamber therapy Battery longevity up to 9 years* More than 100,000 implants/year Today’s devices are implanted pectorally, either subcutaneously or submuscularly in most patients. 1998 actual implants (estimates): 45,000 in U.S. 10,000 outside of U.S. 55,000 Worldwide Battery longevity projections for Medtronic devices: GEM 5.0 years – 100% pacing, monthly shocks 6.9 years – 100% pacing, quarterly shocks 9.1 years – 100% sensing, 0% pacing, quarterly shocks GEM DR 5.5 years – 100% pacing, monthly shocks 6.6 years – 100% pacing, quarterly shocks 7.8 years – 0% pacing, monthly shocks 9.6 years – 0% pacing, quarterly shocks Micro Jewel II 4.9 years – 100% pacing, monthly shocks 7.8 years – 100% sensing, 0% pacing, quarterly shocks Jewel AF 5.1 years – 100% pacing, monthly shocks 8.9 years – 0% pacing, quarterly shocks

Example of ICD Antitachycardia Pacing Therapy for VT (ATP) Patient A Patient B

Example of ICD Shock Therapy for VT

Who Needs ICD? VF survivors who have no reversible etiology. Patients with severe cardiac dysfunction (ejection fraction <35%). Patients with sustained VT that is not appropriate for drug or ablation therapy.

Catheter Ablation of VT 1. Patients without apparent heart disease. 2. ICD patients with frequent shocks.

Long-term Drug Therapy of Ventricular Arrhythmias Only beta-blockers (class II) have been shown to reduce symptoms and mortality. Class I and III drugs are used to reduce frequent ICD shocks. Calcium blockers (class IV) are rarely useful for ventricular arrhythmias.

Questions? E-mail to me: chunter@creighton.edu