Arrhythmias atrioventricular, treatment

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

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. 

Adenosine is the treatment of choice for PSVT. It slows the conduction and interrupts the re-entry pathways through the atrioventricular node, restoring dysrhythmia to NSR. Adenosine is not effective in treating other atrial arrhythmias such as atrial flutter or atrial fibrillation or in treating ventricular arrhythmias. Adenosine is rapidly degraded... 

Propranolol is used in the treatment of arrhythmias of atrial and ventricular origin, angina pectoris, myocardial infarction, and hypertension. It is a nonselective p-blocker with action on cardiac receptors (p,) and on vascular and bronchial smooth muscle receptors ( 2) Propranolol s principal effect is to reduce the heart rate, thus relieving angina, and to slow conduction at the atrioventricular node, reducing tlie ventricular rate in patients with atrial fibrillation. It is included here as representative of other P-blockers, such as acebutalol, prindolol, esmolol, flestolol, metoprolol, nadolol, and sotalol, which are like propranolol. 

Intravenous phenytoin is effective for the treatment of cardiac arrhythmias, but fatal ventricular asystole secondary to i.v. phenytoin has been reported (60 ). Massive overdose from oral Garoin (phenytoin plus phenobarbitone) has produced right bundle branch block (19 ). It has been suggested that the stopping of diphenylhydantoin before anaesthesia for surgery may precipitate atrioventricular or intraventricular conduction defects during the anaesthesia (30 ). 

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