Ventricular fibrillation definition

Ventricular fibrillation is by definition hemodynamically unstable, due to the absence of pulse and blood pressure. Initial management includes provision of basic life support, including calling for help and initiation of cardiopulmonary I resuscitation (CPR).48 Oxygen should be administered as soon... 

The common ventricular arrhythmias include (1) premature ventricular complexes (PVCs), (2) ventricular tachycardia, and (3) ventricular fibrillation. Again, these arrhythmias may result in a wide variety of symptoms. PVCs often cause no symptoms or only mild palpitations. Ventricular tachycardia may be a life-threatening situation associated with hemodynamic collapse or be totally asymptomatic. Ventricular fibrillation, by definition, is an acute medical emergency necessitating cardiopulmonary resuscitation (CPR). 

Human Toxicity Moderate exposures can cause symptoms similar to alcohol inebriation. Higher concns can have narcotic effect. Deaths occurring after heavy exposure have been attributed to ventricular fibrillation. Liver injury is not definitely established in occupational exposures. Found to induce hepatocellular carcinomas in National Cancer Institute tests on mice Chem. < Eng. News 54, 4 (Apr- 5, 197b). 

Inappropriate therapy is the most common adverse event associated with ICDs (53). With the first generation of ICDs (Ventak 1500,1550, inappropriate shocks ranged from 15-25%. Unfortunately, the frequency of inappropriate therapy with the latest generation of devices is probably similar (5). In the Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation (DEFINITE) Trial, that evaluated the use of ICDs in patients with nonischemic cardiomyopathy, inappropriate therapy was more likely than appropriate therapy (22 versus 18%) (78). A case of an inappropriate shock due to noise oversensing inducing ventricular fibrillation and subsequent death in a patient has been reported (79). Finally it is important to confirm from the device that therapies were in fact delivered phantom shocks are not uncommon, occurring in approximately 6-7% of people (80). 

Flecainide slows conduction in all cardiac cells including the anomalous pathways responsible for the Wolff-Parkinson-White (WPW) syndrome. Together with encainide and moricizine, it underwent clinical trials to establish if suppression of asymptomatic premature beats with antiarrhythmic drugs would reduce the risk of death from arrhythmia after myocardial infarction. The study was terminated after preliminary analysis of 1727 patients revealed that mortality in the groups treated with flecainide or encainide was 7.7% compared with 3.0% in controls. The most likely explanation for the result was the induction of lethal ventricular arrhythmias possibly due to ischaemia by flecainide and encainide, i.e. a proarrhythmic effect. In the light of these findings the indications for flecainide are restricted to patients with no evidence of structural heart disease. The most common indication, indeed where it is the drug of choice, is atrioventricular re-entrant tachycardia, such as AV nodal tachycardia or in the tachycardias associated with the WPW syndrome or similar conditions with anomalous pathways. This should be as a prelude to definitive treatment with radiofrequency ablation. Flecainide may also be useful in patients with paroxysmal atrial fibrillation. 

The beneficial effects were related to these plasma concentrations, as were the time to the first bout of atrial fibrillation, the frequency of bouts of atrial fibrillation, and the time between episodes. However, when atrial fibrillation occurred there was no difference in the ventricular rate in the different groups. Adverse effects necessitated drug withdrawal in four patients one had heart failure and two had gastrointestinal symptoms. These effects were not dose-related, although there were too few occurrences for a definitive conclusion. The authors suggested that this stepwise approach, with increasing doses of propafenone and increasing doses of quinidine could be beneficial in the treatment of paroxysmal atrial fibrillation. 

Some individuals exhibit an impaired heart rate response to increased metabolic demand. Patients in sinus rhythm may have sinus node dysfunction, leading to decreased maximal sinus rates with exertion. Patients in chronic atrial fibrillation may have a slow ventricular response that does not increase adequately with exertion. In both these cases, the heart rate response to exertion may be blunted, a condition termed chronotropic incompetence. The definitions of chronic incompetence are varied It is sometimes defined as failure to achieve 75% of the maximal predicted heart rate. Relative chronic incompetence refers to a blunted heart rate response at lower levels of exertion and is more difficult to define. 

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