Ventricular arrhythmias premature complexes

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. 

Moricizine is indicated for the treatment of documented ventricular arrhythmias, particularly sustained ventricular tachycardia. Moricizine was evaluated in the CAST II clinical trial for the prevention of postinfarction ventricular premature complexes. It was ineffective and found to be proarrhythmic. Patients in the moricizine arm of the trial exhibited a greater incidence of sudden cardiac death than did controls. 

One of the more serious complications of magnesium deficiency is cardiac arrhythmias. Premature atrial complexes, atrial tachycardia and fibrillation, ventricular premature complexes, ventricular tachycardia, and ventricular fibrillation may be associated with magnesium deficiency. These effects maybe partly caused by the hypokalemia, renal wasting, and intracellular depletion of potassium caused by hypomagnesemia. 

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). 

Flecainide is absorbed well, has a long half-hfe of 3 to 5 days, is metabolized to -O-deaUcylated flecainide (active antiarrhythmic agent with less potency than flecainide) and to -0-deaUcylated lactam of flecainide, which is an inactive metabolite. A portion of flecainide is excreted unchanged. Flecainide, like other antiarrhythmic agents, can cause new or worsen supraventricular or ventricular arrhythmias. Ventricular proarrhythmic effects range from an increase in frequency of premature ventricular complexes (PVCs) to the development of more severe ventricular tachycardia, e.g., tachycardia that is more sustained or more resistant to conversion to sinus rhythm, with potentially fatal consequences. 

On the basis of two large randomized trials aimed at suppressing premature ventricular complexes after MI, so-called warning arrhythmias, it was discovered that many common antiarrhythmic medications actually increase the risk of mortality [20, 21]. Amiodarone also has been shown to have no definitive effect on mortality in patients after an MI, including in the recent SCD-HeFT trial [22-24]. In fact, of all antiarrhythmic medications, only beta blockers have been clearly shown to prevent SCD after MI [25], particularly among those with depressed LV function [11]. 

Endogenous norepinephrine stimulates cardiac beta receptors. Receptor-linked cAMP-dependent protein kinases phosphorylate calcium channels to increase intracellular calcium. Elevated intracellular calcium increases conduction velocity (phase 0) and decreases the threshold potential in normal SA and AV node cells (see Figure 12.13). Beta blockers slow spontaneous conduction velocity in the SA node by approximately 10-20 percent. In addition, beta blockers can slow conduction velocity while increasing the refractory period of the AV node. These effects control the ventricular rate in atrial fibrillation or flutter and terminate paroxysmal supraventricular tachycardias. They are also safer, although somewhat less effective, than other drugs for suppression of premature ventricular complexes (PVCs). Drugs in this class approved by the FDA for treatment of various arrhythmias include propranolol, acebutolol, and esmolol. Problems with the beta blockers include drowsiness, fatigue, impotence, and depressed ventricular performance. 

The side-effects are associated with vagal effects on the gastrointestinal tract (anorexia, abdominal discomfort/pain, vomiting and diarrhoea), while cardiotoxic effects include premature ventricular depolarizations, nodal rhythms and AV dissociation, Toxicity is enhanced by hypokalaemia, and this may predispose to more complex arrhythmias. 

Because of the results of the Cardiac Arrhythmia Suppression Trials and other trials, antiarrhythmic drugs (except /3-blockers) should not be used routinely in patients with prior myocardial infarction (Ml) or left ventricular (LV) dysfunction and minor ventricular rhythm disturbances (e.g., premature ventricular complexs). 

Despite the discouraging results of the CAST, post-MI patients with complex ventricular ectopy remain at risk for death. Other drugs besides type Ic drugs have been studied, including sotalol. Sotalol is marketed as a racemic mixture of a D- and L-isomer both are type in potassium blockers, but the L-isomer has /3-blocking actions. Chronic therapy with D-sotalol was studied in patients with remote MI complicated by complex ectopy in the Survival With Oral D-Sotalol (SWORD) trial. Unlike in the CAST, D-sotalol treatment was not designed to cause PVC suppression, yet (as in the CAST) the trial was halted prematurely because of excessive mortality in the treatment arm. Again, the presumed reason for this observation was D-sotalol-related pro arrhythmia. Currently, only two antiarrhythmic... 

Premature ventricular complexes and life-threatening arrhythmias. 

Used to assess QRS-complex arrhythmias, monitor premature ventricular beats and P-wave changes, distinguish different types of tachycardia (ventricular, supraventricular) and bundle-branch defects, and confirm pacemaker wire placement. 

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