Ventricular fibrillation primary

In contrast, patients who have ventricular fibrillation associated with acute MI (i.e., during the first 24 hours after symptom appearance) usually have little risk of recurrence. Of all patients who die from an acute MI, approximately 50% die suddenly prior to hospitalization. Ventricular fibrillation associated with acute MI can be subdivided into two types primary ventricular fibrillation and complicated or secondary ventricular fibrillation. Primary ventricular fibrillation occurs in an uncomplicated MI not associated with heart failure secondary ventricular fibrillation occurs in an MI complicated by heart failure. The time course, incidence, mechanisms, treatment, and com-... 

The patients who have the best chance of surviving cardiac arrest are those with primary ventricular flbrillation after myocardial infarction patients with electromechanical dissociation or asystole fare worst. Even in those in the most favourable group, with witnessed ventricular fibrillation in hospital, the best that can be hoped for is a survival rate till discharge of about 20%. 

Lie KI, Wellens HJ, van Capelle FJ, Durrer D. Lidocaine in the prevention of primary ventricular fibrillation A double-blind, randomized study of 212 consecutive patients. N Engl J Med 1974 291 1324-6. 

Wyman MG, W5unan RM, Cannom DS, Criley JM. Prevention of primary ventricular fibrillation in acute myocardial infarction with prophylactic lidocaine. Am J Cardiol 2004 94 545-51. 

It has been argued that drug combinations that contain a beta-adrenoceptor antagonist in combination with a thiazide diuretic minimize the hypokalemic effect of the latter however, marked hypokalemia in the absence of primary hyperaldosteronism has been reported in a patient taking Sotazide (a combination of hydrochlorothiazide and the non-selective drug sotalol) (204). The use of a combination formulation of chlortaUdone and atenolol has also produced hypokalemia (205), in one case complicated by ventricular fibrillation after myocardial infarction (206). 

The primary toxicities observed with procainamide are cardiovascular in nature. Initially, a tachycardia may occur due to procainamide s anticholinergic properties or as a reflex response to vasodilation. Cardiac conduction disturbances may occur. On the ECG, these may be displayed as prolongation of the QRS and/or QTc duration. Heart block, bradycardia, and asystole have been reported. Procainamide can also cause ventricular tachycardia, ventricular fibrillation, and Torsades de Pointes. Severe hypotension due to decreases in cardiac output and/or vasodilation may be seen. Altered mental status and seizure activity can occur in procainamide toxicity. 

Figure 8.31 (A) A patient with an acute myocardial infarction with evident ST-segment elevation and frequent, polymorphic, repetitive, PVC that triggers VF (asterisk) that was resolved with cardioversion. (B) Primary ventricular fibrillation in a patient with acute Ml. VF appears suddenly, without previous PVC and without evident ST-segment elevation. However, the underlying sinus rhythm is fast, which can often be present in cases of primary ventricular fibrillation and express the sympathetic overdrive that is usually present in acute phase of Ml (see p. 252). The electric cardioversion resolved the problem.

Figure 8.32 Final arrhythmias in case of sudden death in different clinical situations. (A) In the acute phase of an ischaemic heart disease (Adgey et at, 1982). In the majority of cases final arrhythmia was primary ventricular fibrillation and only in few cases it was sustained ventricular tachycardia, which developed in fibrillation. (B) In ambulatory patients the most frequent final arrhythmia was sustained VT leading to VF (Bayes de Luna, Coumel and Leclercq, 1989).

Lie KI, Wellens HJ, Downar E, Durrer D. Observations on patients with primary ventricular fibrillation complicating acute myocardial infarction. Circulation 1975 52 755. 

The indications for implantation of an ICD have expanded considerably (Table 17-7). Initially, its efficacy was evaluated in patients who had already suffered a documented episode of ventricular tachycardia or ventricular fibrillation (secondary prevention), but now primary prevention trials have been published or are being planned. These results will help clinicians in choosing the proper therapy for patients with life-threatening arrhythmias. For instance, the Sudden Cardiac Death in Heart Failure Trial (SCD-Heft) is a primary prevention trial that evaluated survival in patients withLV dysfunction... 

Ventricular fibrillation is electrical anarchy of the ventricle resulting in no cardiac output and cardiovascular collapse. Death wiU ensue rapidly if effective treatment measures are not taken. Patients who die abruptly (within 1 hour of initial symptoms) and unexpectedly (i.e., sudden death) usually have ventricular fibrillation recorded at the time of death. Sudden cardiac death accounts for about 400,000 deaths per year or 1000 deaths per day in the United States. Sudden cardiac death occurs most commonly in patients with ischemic heart disease and primary myocardial disease associated with LV dysfunction, less commonly in those with WPW syndrome and mitral valve prolapse, and occasionally, in those without associated heart disease (e.g., Brugada syndrome). Patients who have sudden cardiac death (not associated with acute MI) but survive because of appropriate CPR often have inducible sustained ventricular tachycardia and/or ventricular fibrillation during electrophysiologic studies. These individuals are at high risk for the recurrence of ventricular tachycardia and/or ventricular fibrillation. 

Dekker LR, Bezzina CR, Henriques JP, et al. Familial sudden death is an important risk factor for primary ventricular fibrillation a case-control study in acute myocardial infarction patients. Circulation 2006 114(11) 1140—5. 

Bethanidine is being investigated as an orphan drug to be used in treatment of primary ventricular fibrillation and to treat or prevent the recurrence of primary ventricular fibrillation. 

The primary efficacy endpoint of FINESSE is the composite of all-cause mortality and post-MI complications within 90 days of randomization. Complications included in the endpoint are resuscitated ventricular fibrillation occurring >48 hours after randomization, rehospitalization or emergency department visit for congestive heart failure, and cardiogenic shock. This composite endpoint was chosen to reflect the physiological hypothesis that combination medical therapy prior to PCI will result in earlier and improved reperfusion, leading to improved myocardial salvage and, hence, decreased infarct size-dependent complications. 

A 21-year-old man who had taken chloroquine 250 mg/day for primary hemosiderosis since the age of 8, suddenly collapsed with ventricular fibrillation and had no spontaneous circulation. A single shock was delivered and he regained... 

The primary intent of the study using the canine carotid arterial thrombosis model was to determine if the recombinant enzyme could achieve thrombolysis in an experimental animal model in which a platelet-rich, occlusive arterial thrombus, develops in response to deep arterial wall injury. We found that fibrolase produced rapid thrombolysis. The experimental model is similar to one originally developed by Lucchesi in the coronary artery (30) and subsequently adapted to the carotid artery to minimize experimental loss due to ventricular fibrillation (31). The use of the carotid has the additional advantage of greater yield of experimental data, and when necessary allows the animal to serve as its own internal control, thereby facilitating the interpretation of results and simplifying statistical evaluation. This was an important consideration in the present study where r-fibrolase was in limited supply thus accounting for the need to employ relatively small animals and to administer the enzyme by local injection immediately proximal to the occlusive platelet-rich arterial thrombus. 

Primary indications for the use of quinidine include (1) abolition of premature complexes that have an atrial, A-V junctional, or ventricular origin (2) restoration of normal sinus rhythm in atrial flutter and atrial fibrillation after controlling the ventricular rate with digitahs (3) maintenance of normal sinus rhythm after electrical conversion of atrial arrhythmias (4) prophylaxis against arrhythmias associated with electrical countershock (5) termination of ventricular tachycardia and (6) suppression of repetitive tachycardia associated with Wolff-Parkinson-White (WPW) syndrome. 

Low doses (100-200 mg/d) of amiodarone are effective in maintaining normal sinus rhythm in patients with atrial fibrillation. The drug is effective in the prevention of recurrent ventricular tachycardia. It is not associated with an increase in mortality in patients with coronary artery disease or heart failure. In many centers, the implanted cardioverter-defibrillator (ICD) has succeeded drug therapy as the primary treatment modality for ventricular tachycardia, but amiodarone may be used for ventricular tachycardia as adjuvant therapy to decrease the frequency of uncomfortable cardioverter-defibrillator discharges. The drug increases the pacing and defibrillation threshold and these devices require retesting after a maintenance dose has been achieved. 

Patients with chronic atrial fibrillation—a common supraventricular arrhythmia—routinely receive warfarin to prevent the development of blood clots in the poorly contracting atrium and to decrease the risk of embolism of such clots to the brain or other tissues. Such patients are also often treated with anti arrhythmic drugs. The primary goals of antiarrhythmic treatment are to slow the atrial rate and, most importantly, control the ventricular rate. 

Although rate is the primary method that ICDs use to detect malignant ventricular arrhythmias, other arrhythmias, such as atrial fibrillation, atrial flutter, or sinus tachycardia may be associated with ventricular rates that would fall within the rate-detection criteria. Manufacturers have developed additional... 

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