Ventricular Fibrillation

Catheter Ablation of Ventricular Fibrillation and Polymorphic Ventricular Tachycardia

Amin Al-Ahmad, Carola Gianni, Andrea Natale

Catheter ablation of ventricular fibrillation and polymorphic ventricular tachycardia Robert Schweikert

Timothy Mahoney, Mauricio Arruda, Andrea Natale, Patrick Tchou

Introduction Catheter ablation of VF: basic principles Catheter ablation of idiopathic VF Catheter ablation of ischemic VF and polymorphic VT Catheter ablation of ventricular fibrillation associated with long QT and Brugada syndrome Summary and conclusions

INTRODUCTION Sudden cardiac death (SCD) remains the leading cause of death in the United States and industrialized world. The majority of sudden cardiac death is caused by ventricular fibrillation (VF) associated with structural and ischemic heart disease. Over the last decade, much time and research has been devoted to the development of implantable cardioverter defibrillators (ICDs). After several multi-center trials demonstrated survival benefit in populations resuscitated from SCD, initial application of this technology centered on secondary prevention.1-3

Indication for ICD implantation expanded further after benefit was demonstrated in populations with ischemic and non-ischemic cardiomyopathy who had ICDs placed for primary prophylaxis.4-6 The recent increase in ICD use has been demonstrated to be cost effective,7 but ICDs remain a large concern from an economic standpoint. Estimates reflect that with current inclusion criteria, approximately 500 000 Medicare beneficiaries now qualify for ICDs.7

Ventricular Arrhythmias in Heart Failure

An Essential Clinical Guide

Antonis S. Manolis, Antonis A. Manolis, Theodora A. Manolis

Ventricular arrhythmias responsible for sudden cardiac death (SCD) have a considerable share in heart failure (HF) mortality and may be related to myocardial ischemia, scar, or fibrosis, neurohumoral activation, worsening congestion, electrolyte abnormalities, proarrhythmic drugs, calcium overload, and genetic susceptibility. Myocardial scar or fibrosis serves as the arrhythmogenic substrate of reentry, the commonest mechanism of sustained monomorphic ventricular tachycardia (VT), which occasionally may degenerate into ventricular fibrillation (VF). However, other mechanisms (abnormal automaticity and triggered activity) may also lead to polymorphic VT and VF. With the possible exception of rapid nonsustained VT (NSVT), asymptomatic complex ventricular arrhythmias, including frequent/multifocal premature ventricular complexes (PVCs) and runs of NSVT, may not predict SCD in HF patients, as these arrhythmias may be a nonspecific manifestation of decompensation. Survivors of malignant ventricular arrhythmias (VT/VF) should be offered an implantable cardioverter defibrillator (ICD) or cardiac resynchronization therapy defibrillator (CRT-D), as appropriate, for secondary prevention of SCD. Patients with potentially malignant ventricular arrhythmias (PVCs/NSVT) may selectively receive ICD/CRT-D for primary prevention if left ventricular ejection fraction is <35% or get further stratified with an electrophysiology study or cardiac magnetic resonance imaging. Catheter ablation is reserved for suspected PVC-induced cardiomyopathy or frequently recurring/incessant VT or electrical storm.

Use of lidocaine for treatment of pulseless ventricular tachycardia after massive cocaine overdose

Published in Toxicology Communications

Jordan A. Woolum, Matthew Travis, Cicero Running Crane, Abby M. Bailey, Regan A. Baum, Peter Akpunonu

A 35-year-old woman presented to the emergency department in cardiac arrest after ingesting large quantities of powdered cocaine. With an initial rhythm of ventricular fibrillation, emergency medical providers were able to achieve return of spontaneous circulation prior to hospital transport. Shortly after emergency department arrival the patient experienced pulseless electric activity arrest. Despite routine advanced cardiac life support, she remained critically ill and intermittently achieved palpable pulses before returning to pulseless ventricular tachycardia. She received intravenous lipid emulsion and dual defibrillation therapies without clinical improvement. After a lidocaine bolus and intravenous infusion, she had a sustained return of spontaneous circulation. The patient was taken to the intensive care unit before withdrawal of care two days later due to a poor prognosis for recovery.

Physician Interpretation and Quantitative Measures of Electrocardiographic Ventricular Fibrillation Waveform

Published in Prehospital Emergency Care

Christopher B. Lightfoot, Thomas J. Sorensen, Michael D. Garfinkel, Lawrence D. Sherman, Clifton W. Callaway, James J. Menegazzi

Objectives. The characteristics of the ventricular fibrillation (VF) waveform may influence treatment decisions and the likelihood of therapeutic success. However, assessment of VF as being fine or coarse and the distinction between fine VF and asystole are largely subjective. The authors sought to determine the level of agreement among physicians for interpretation of varying VF waveforms, and to compare these subjective interpretations with quantitative measures. Methods. Six-second segments of waveform from LIFEPAK 300 units were collected. Fifty segments, including 45 VF and five ventricular tachycardia (VT) distracters, were graphed to simulate rhythm strips. These waveforms were quantitatively described using scaling exponent, root-mean-squared amplitude, and centroid frequency. Thirty-two emergency medicine residents were asked to interpret the arrhythmias as VT, “coarse” VF, “fine” VF, or asystole. Their responses were compared with the qantitative measures. Interphysician agreement was assessed with the kappa statistic. Results. One thousand four hundred forty interpretations were analyzed. There was fair agreement between physicians about the classification of arrhythmias (κ = 0.39). Mean values associated with coarse VF, fine VF, and asystole differed in all three quantitative measure categories. The decision whether to defibrillate was highly correlated with the distinction between VF and asystole (Pearson chi-square = 1,170.40, df = 1, p[two-sided] < 0.001). Conclusions. With only fair agreement on the threshold of fine VF and asystole, defibrillation decisions are largely subjective and caregiver-specific. These data suggest that quantitative measures of the VF waveform could augment the current standard of subjective classification of VF by emergency care providers.

Ventricular tachycardia and ventricular fibrillation

Published in Expert Review of Cardiovascular Therapy

Komandoor Srivathsan, Daniel WC Ng, Farouk Mookadam

Ventricular tachycardia and ventricular fibrillation are the most important causes of sudden cardiac death (SCD), particularly in those with structural heart disease and reduced left ventricular function. It is important to distinguish ventricular tachycardia from supraventricular tachycardia. A wide spectrum of ventricular arrhythmias exists, from those where the heart is structurally normal to those with structural heart disease. Each entity has a distinctive pathophysiology, treatment plan and prognostic outcome. Treatment modalities include simple β-blockade to implantation of implantable cardiac defibrillator and ablative approaches. In general, those ventricular arrhythmias associated with a structurally normal heart are more benign than those associated with structural heart disease.