Ventricular Fibrillation

Bioelectric and Biomagnetic Signal Analysis

Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam in Introduction to Computational Health Informatics, 2019

Thickening of the muscles also deforms the valves and makes them inflexible. This deformity in the valve(s) causes blood to leak continuously. In dilated cardiomyopathy, one of the four chambers gets enlarged. Ventricular enlargement is common. The enlargement causes heart-muscles to get weaker and cause heart failure or heart-valve problems. In restrictive cardiomyopathy, the muscles neither thicken nor enlarge, but they lose flexibility causing the heart to exert more pressure on muscles to pump the blood. Since stiff muscles do not relax, it pumps less blood to flow in the body. The fibrillation of heart-muscles stiffens them, and the corresponding tissues develop ectopic-nodes. Fibrillation in atria is called supraventricular fibrillation, and fibrillation in a ventricle is ventricular fibrillation. This fibrillation leads to irregular and low amplitude heartbeats. Ventricular fibrillation is very serious and may lead to sudden cardiac death. 

Electrocardiogram

Burt B. Hamrell in Cardiovascular Physiology, 2018

In ventricular fibrillation (Figure 7.30), ventricular electrical activity is random and chaotic. There is no organized, sequential wave of depolarization. There is no direct information from the ECG about function, but there is no effective organized ventricular contraction and no effective pumping of blood by the heart in ventricular fibrillation. Obviously, ventricular fibrillation results in death within minutes. Fibrillation waves, giving the appearance of an undulating baseline (Figure 7.30), can be fine or coarse, just as in atrial fibrillation. 

The electrocardiogram in ischaemic heart disease

John Edward Boland, David W. M. Muller in Interventional Cardiology and Cardiac Catheterisation, 2019

Prevention of death from dysrrhythmia is one of the major aims in acute coronary care. Ventricular fibrillation is often induced by electrolyte abnormalities and is more common the more extensive the myocardial infarction. The incidence decreases from 5% to −7% of patients with acute myocardial infarction in the early 1970s to <2% in the late 1980s. This is partly due to use of beta-blockers in acute myocardial infarction, and more vigorous and effective treatment of cardiac failure and correction of electrolyte imbalances. Clinical trials have shown that ventricular premature beats are unreliable predictors of the development of ventricular fibrillation. 

Sustained Ventricular Fibrillation in an Alert Patient: Preserved Hemodynamics with a Left Ventricular Assist Device

Published in Prehospital Emergency Care, 2011

Poonam Patel, Jefferson G. Williams, Jane H. Brice

Emergency medical services (EMS) encountered an alert patient with sustained ventricular fibrillation with preserved hemodynamics via a left ventricular assist device (LVAD). Multiple firings of the patient's implantable defibrillator were the only sign that this patient was experiencing the usually fatal ventricular arrhythmia. Initial attempts at rhythm conversion with amiodarone and 200-J biphasic shocks were unsuccessful. The patient was finally defibrillated to normal sinus rhythm after a 360-J biphasic shock. This case conference highlights the increasing prevalence of LVADs. These devices are used not only as a bridge to cardiac transplantation, but also as definitive therapy for patients in end-stage cardiac failure. Ventricular fibrillation has been shown to be well tolerated in patients with LVADs, and we discuss a standard of care for these patients. The occurrence of sustained ventricular fibrillation in patients with ventricular assist devices represents a challenging situation for EMS and emergency department providers and one that will be increasingly encountered in the future.

Successful Resuscitation from Refractory Ventricular Fibrillation by BLS Providers Employing Double Sequential External Defibrillation: A Case Report

Published in Prehospital Emergency Care, 2020

John Laird, Cesar Costa-Arbulu, Melissa Marighetto, Anna Grochal, Ian R. Drennan, Sheldon Cheskes

Double sequential external defibrillation (DSED) is a novel treatment option for cardiac arrest patients in refractory ventricular fibrillation (VF). There is limited research, however, examining the efficacy of this treatment in clinical practice. Previous research is further confounded by the use of other treatments such as advanced cardiac life support medications. We present the case of the successful use of DSED for refractory out-of-hospital cardiac arrest without the use of advanced life support care.

Ischemic QRS prolongation as a predictor of ventricular fibrillation in a canine model

Published in Scandinavian Cardiovascular Journal, 2018

Jakob Almer, Robert B. Jennings, Michael Ringborn, Henrik Engblom

Objectives. An acute coronary occlusion and its possible subsequent complications is one of the most common causes of death. One such complication is ventricular fibrillation (VF) due to myocardial ischemia. The severity of ischemia is related to the amount of coronary arterial collateral flow. In dog studies collateral flow has also been shown to be associated with QRS prolongation. The aim of this study was to investigate whether ischemic QRS prolongation (IQP) is associated with impending VF in an experimental acute ischemia dog model. Methods. Degree of IQP and occurrence of VF were measured in dogs (n = 21) during coronary occlusion for 15 min and also during subsequent reperfusion (experiments conducted in 1984). Results. There was a significant difference in absolute IQP between dogs which developed VF during reperfusion (47 ± 29 ms, mean ± SD) and those which did not (12 ± 10 ms; p = .001). Conclusions. IQP during acute coronary occlusion is associated with reperfusion VF in an experimental dog model and might therefore be a potential predictor of malignant arrhythmias in patients with acute coronary syndrome.