Atrial arrhythmias control

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. 

Unlabeled Uses Control of hemodynamicallystableventriculartachycardia, control of rapid ventricular rate due to accessory pathway conduction in preexcited atrial arrhythmias, conversion of atrial fibrillation to normal sinus rhythm, in cardiac arrest with persistent ventricular tachycardia or ventricular fibrillation, paroxysmal supraventricular tachycardia, polymorphic ventricular tachycardia or wide complex tachycardia of uncertain origin, prevention of postoperative atrial fibrillation... 

Digitalis is useful in the management of atrial arrhythmias because of its cardioselective parasympathomimetic effects. In atrial flutter and fibrillation, the depressant effect of the drug on atrioventricular conduction helps to control an excessively high ventricular rate. Digitalis has also been used in the control of paroxysmal atrial and atrioventricular nodal tachycardia. At present, calcium channel blockers and adenosine... 

Clinical use Used to improve cardiac output in CHF. Also used in atrial arrhythmias for rate control. 

Most side effects of /3-blockers are an extension of their ability to antagonize /3-adrenoceptors. /3-Blockade in the myocardium can be associated with bradycardia, atrioventricular conduction abnormalities (e.g., second- or third-degree heart block), and the development of acute heart failure. The decreases in heart rate actually may benefit certain patients with atrial arrhythmias (e.g., atrial fibrillation and atrial flutter) and hypertension by both providing rate control and lowering BP. /3-Blockers usually only produce heart failure if... 

Uses Rapid anticoagulation (intensive) for thromboses, emboli, unstable angina, disseminated intravascular coagulation (DIC), open-heart surgery, etc. Longer-term anticoagulation (controlled) for thromboses, emboli, post-MI, heart valve damage, atrial arrhythmias, etc. 

Lau CP, Tai YT, Fong PC, Li IP, Chung EL. Atrial arrhythmia management with sensor controlled atrial refractory period and automatic mode switching in patients with minute ventilation sensing dual chamber rate adaptive pacemakers. Pacing Clin Electrophysiol. 1992 15 1504-1514. 

Wu X, Wang C, Zhu J, Zhang C, Zhang Y, Gao Y. Meta-analysis of randomized controlled trials on magnesium in addition to beta-blocker for prevention of postoperative atrial arrhythmias after coronary artery bypass grafting. BMC Cardiovasc Disord 2013 3 5. 

Verapamil. Verapamil hydrochloride (see Table 1) is a synthetic papaverine [58-74-2] C2qH2 N04, derivative that was originally studied as a smooth muscle relaxant. It was later found to have properties of a new class of dmgs that inhibited transmembrane calcium movements. It is a (+),(—) racemic mixture. The (+)-isomer has local anesthetic properties and may exert effects on the fast sodium channel and slow phase 0 depolarization of the action potential. The (—)-isomer affects the slow calcium channel. Verapamil is an effective antiarrhythmic agent for supraventricular AV nodal reentrant arrhythmias (V1-2) and for controlling the ventricular response to atrial fibrillation (1,2,71—73). 

The prominent depressant action of verapamil and diltiazem at the SA and A-V nodes finds use in specific arrhythmias. They are of proven efficacy in acute control and long-term management of paroxysmal supraventricular tachycardia (see Chapter 16).Their ability to inhibit conduction at the A-V node is employed in protecting ventricles from atrial tachyarrhythmias, often in combination with digitalis or propranolol. 

Mechanism of Action An antiarrhythmicthat slows atrial, AV, His-Purkinje, and intraventricular conduction. Decreases excitability conduction velocity and automaticity. Therapeutic Effect Controls atrial, supraventricular, and ventricular arrhythmias. Pharmacokinetics Almost completely absorbed following PO administration. Protein binding 40%. Metabolized in liver. Excreted in urine. Half-life 19-22 hr. 

Arrhythmias, including prevention of recurrent paroxysmal supraventricular tachycardia and control of ventricular resting rate in chronic atrial fibrillation or flutter (with di-goxin) PO 240-480 mg/day in 3-4 divided doses. 

Diltiazem appears to be similar in efficacy to verapamil in the management of supraventricular arrhythmias, including rate control in atrial fibrillation. An intravenous form of diltiazem is available for the latter indication and causes hypotension or bradyarrhythmias relatively... 

Recent evidence indicates that many patients with atrial fibrillation—a very common arrhythmia in the elderly—do as well with simple control of ventricular rate as with conversion to normal sinus rhythm. Measures (such as anticoagulant drugs) should be taken to reduce the risk of thromboembolism in chronic atrial fibrillation. 

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. 

These agents appear to be similar in efficacy to verapamil in the management of supraventricular arrhythmias, including rate control in atrial fibrillation. An intravenous form of diltiazem is available for the latter indication and causes hypotension or bradyarrhythmias relatively infrequently. Bepridil also has action potential- and QT-prolonging actions that theoretically may make it more useful in some ventricular arrhythmias but also create the risk of torsade de pointes. Bepridil is only rarely used, primarily to control refractory angina. 

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. 

Digoxin (see p. 158) shortens the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in Purkinje fibers. Digoxin is used to control the ventricular response rate in atrial fibrillation and flutter. At toxic concentrations, digoxin causes ectopic ventricular beats that may result in ventricular tachycardia and fibrillation. [Note This arrhythmia is usually treated with lidocaine or phenytoin.]... 

Mrs GG has atrial fibrillation which if not controlled can cause temporary loss of cardiac output resulting in a drop of blood pressure. Mrs GG s description of suddenly going dizzy associated with a jump in the chest suggest that her fall was probably caused by this. Her sudden dizziness is consistent with an arrhythmia and not some other acute cause such as epilepsy. 

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 atrial rate is 120-250/min, and commonly there is AV block. If the patient is taking digoxin, it should be suspected as the possible cause of the arrhythmia, and stopped. If the patient is not taking digoxin, it may be used to control the ventricular rate. These patients should be considered for referral for radiofrequency ablation. 

Digitalis glycosides are positive inotropic agents used in the management of patients with congestive heart failure. They control ventricular rate in supraventricular arrhythmias including atrial fibrillation and atrial flutter. 

The only calcium channel blocking drug to have been licensed for the treatment of cardiac arrhythmias is verapamil. Its main uses are in the treatment of supraventricular tachycardia (SVT) and paroxysmal SVT. Because verapamil lengthens the ERP and FRP of the AV node and prolongs AV nodal conduction time [16], it can be used to control the ventricular rate in atrial fibrillation or atrial flutter and it usually terminates re-entry arrhythmias involving the AV node [208, 209], However, intravenous verapamil should not be given to patients who have the Wolff-Parkinson-White syndrome and atrial... 

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