Beta blockers atrial fibrillation

As with other Class I agents, patients treated with flecainide for atrial flutter have been reported with 1 1 atrioventricular conduction due to slowing the atrial rate. A paradoxical increase in the ventricular rate also may occur in patients with atrial fibrillation who receive flecainide. Concomitant negative chronotropic therapy such as digoxin or beta-blockers may lower the risk of this complication. 

Contraindications Atrial fibrillation or flutter associated with accessory conduction pathways, cardiogenic shock, CHF, second- or third-degree heart block, severe hypotension, sinus bradycardia, ventricular tachycardia, within several hours of IV beta-blocker therapy... 

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. 

Kuhlkamp V, Bosch R, Mewis C, Seipel L. Use of beta-blockers in atrial fibrillation. Am J Cardiovasc Drugs. 2002 2 37-42. 

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 two options are rate control or rhythm control. Rate control is the most appropriate in this patient as he is over 65 years. Atrial fibrillation appears to be of long standing and may have been present two months ago when the patient experienced a similar episode. His lisinopril should be stopped as he will get blood pressure control with the beta-blocker. 

The effect of a beta-blocker (metoprolol 30-40 mg/day or bisoprolol 2.5-5.0 mg/day for 1 month) on the change in QT interval, QT dispersion, and transmural dispersion of repolarization caused by bepridil has been studied in 10 patients with paroxysmal atrial fibrillation resistant to various antidysrhythmic drugs (17). Bepridil significantly prolonged the QTc interval from 0.42 to 0.50 seconds, QT dispersion from 0.07 to 0.14 seconds, and transmural dispersion of repolarization from 0.10 to 0.16 seconds. The addition of a beta-blocker shortened the QTc interval from 0.50 to 0.47 seconds, QTc dispersion from 0.14 to... 

It produced a small reduction in hospitalizations due to heart failure (nine per 1000 patients-years) balanced by a significant increase in deaths from presumed dysrhythmias. Digitalis is therefore indicated for a small number of patients who have severe heart failure associated with sinus rhythm after treatment with diuretics, vasodilators, beta-blockers, and spironolactone. It remains the drug of first choice in patients with heart failure accompanied by fast atrial fibrillation, especially if due to myocardial or mitral valve disease. A trial of withdrawal of digitalis therapy can be considered in some cases (as noted in point 3 above). 

C Diltiazem. Quinidine can be used to maintain normal sinus rhythm (NSR) after cardioversion of atrial fibrillation. Metoprolol is commonly used to control ventricular rate before conversion to NSR. However, this patient has two contraindications (COPD and diabetes) for beta-blocker use. Unlike diltiazem, amlodipine and nimodipine do not block AV nodal conduction therefore, they would be ineffective at rate control. 

Kim MH, Rachwal W, McHale C, Bruckman D, Decena BF, Rushan P, MoratfyF, Eagle KA. Effect of amiodarone diltiazem beta blocker on frequency of atrial fibrill on, length of ho italization, and hospital costs after coronary artery bypass graftii. Am J Carrol (2002) 89,1126-28... 

On the basis of this report, and on reports of studies in animals and from the known risks associated with the concurrent use of beta blockers (see Disopyramide -i- Beta blockers , p.252), the UK manufacturer warns about combining disopyramide and other drugs [such as verapamil] that may have additive negative inotropic effects. However, they do point out that in some specific circumstances combinations of antiarrhythmie drugs (they specifically name digoxin, beta blockers and verapamil for the control of atrial fibrillation) may be beneficial. They note that severe hypotension caused by disopyramide has usually been associated with cardiomyopathy or uncompensated congestive heart failure. However, the US manufacturer advises that until more data is available, disopyramide should not be given within 48 hours before or 24 hours after verapamil. ... 

Observational studies In a retrospective study of oral quinidine for termination of atrial fibrillation in 501 consecutive patients (mean age 66 years, 32% women), quinidine 200-400 mg was given every 6 hours until cardioversion or for a maximum of 48 hours [87 ]. Quinidine did not have to be withdrawn because of adverse drug reactions and there was no significant QT interval prolongation and no life-threatening ventricular dysrhythmias. The mean total dose of quinidine was 617 mg and 92% of the patients received verapamil or a beta-blocker to slow the ventricular rate to below 100/minute. Cardioversion was successful in 84%. All adverse drug... 

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