Treatment of Atrial Fibrillation

Drugs that have antiarrhythmic properties will directly alter the conduction in several ways (1,2). The drug may depress the automatic properties of the abnormal pacemaker cells (1,2). This may be a result of decreasing the slope of phase 4 depolarization or by elevating the threshold potential (1,2). By modifying the rate of spontaneous abnormal impulse generation such that the rate is slower than that of the SA node, normal cardiac rhythm will be restored (1,2). Drugs could also alter the conduction characteristics of the pathways of a reentrant loops (1,2). This can be accomplished by shortening the refractoriness in the area where unidirectional blocks are present, which will allow antegrade conduction to proceed (1,2). On the other hand, the antiarrthymic may depress conduction, which will prolong refractoriness in either area of the unidirectional block in the pathway with the slowed conduction and a relatively shorter refractory period (1,2). If this period of refractoriness is prolonged in the area of unidirection block, retrograde propagation of impulse is not permitted and this will have a bidirectional block. (1,2)

Acute Ventricular Rate Control

The basis for this is slowing the HR, which will allow the ventricles to fill better improving the hemodynamics (1,2). This will reduce the AF symptoms and will reduce emergency treatment and will prevent hospitalization (1,2). The drugs must work in this case to block the AV node. (1,2) The target heart rate depends on the symptoms and if any co-morbid diagnoses are present (1,2). IV agents are used if the patient is symptomatic (1,2). Drugs of this particular class include beta blockers, calcium blockers, digoxin and amiodarone (1,2). The nondihydropyridine calcium channel blockers include verapamil and diltiazem (3,4). This makes up the type IV antiarrhytmic category (3,4). There are two different types of calcium channels that are in use in the SA and AV nodal tissues (1,2). These are the L-type channel and a T-type channel (1,2). L channel blocks, which include verapamil and diltizem will slow down conduction and decrease automaticitiy and prolong the refractoriness in the calcium dependent tissue in the AV and SA nodes (3,4). In afib, these drugs can slow down the ventricular response by slowing the AV nodal conduction (1,2). The dihydropyridine CCBs like nifedipine do not have significant antiarrhythmic acitivty due to a reflex in sympathetic tone that is due to vasodilation that counteracts their direct dromotrophic action (1,2).



Antiarrhythmic; Class IV antiarrhythmic


Inhibition of the calcium ion from entering the slow channels, which are the type L calcium channels (1). This produces a relaxation of the coronary vascular smooth muscle (1). This will decrease the heart rate and prolong AV nodal conduction (1). There are also negative inotropic properties (1).


For the immediate release oral tablets, the onset is 30-60 minutes.

Adverse Effects

The frequency of side effects is related to dose (1). Headache, flushing, dizziness, and edema will occur frequently (1). Sinus bradycardia and AV block will occur frequently as well (1). Cimetidine and propranol will increase the diltizem serum levels. Diltiazem will inhibit CYP3A4 and the metabolism of other drugs that include carbamzepine, cyclosporine and theophylline (1,2). It will also inhibit P-glycoprotein (1,2). There is caution in patients who are on concomitant use of beta blockers that have CHF and those will poor left ventricular function (1,2). Contraindications include second or third degree block or sick sinus syndrome without a pacemaker in the ventricles (1,2). Symptomatic hypotension, severe CHF, acute Mi or pulmonary congestion are contraindications as well (1,2).


There is extensive hepatic first pass metabolism following a single I.V injection (3). This drug is metabolized almost entirely by the liver (1,2). 1-3% is excreted unchanged in the urine (1,2).

Acute Conversion to Normal Sinus Rhythm

By converting to NSR, symptoms may be reduced and cardiac hemodynamics may be improved by restoring the atrial kick (1). The rapid ventricular response will be eliminated (1). Theses drug act on the atrial tissue and prolong the atrial refractory period to convert AF to NSR (1,2). Drugs included are Class IA, IC, and III antiarrhythmic drugs (1,2).



For acute conversion to NSR, Class III Antiarrhythmic agent (1)


Prolongs the effective refractory period of the ventricular and atrial tissue by blocking the conductance of potassium (1). It will decrease the sinus rate and slow the conduction through the AV node through a beta adrenergic blockade (1). The action on afib is due to an interruption of the reentrant substrate or abolition of premature beats that trigger reentry (1).


Oral dosing takes 2 days to 3 weeks. Peak effect is 1 to 5 months (2).

Adverse Effects

Corneal microdeposits occur in all patients (1). This is not a reason to stop treatment (1). Visual disturbances are reported in 5% (1,2). There are neurologic effects which include tremor, ataxia, parathesis, and nightmares (1,2). This is more common during the loading phase. Anorexia, nausea, vomiting and constipation do occur frequently (1,2). Contraindications include sick sinus syndrome, or second or third degree heart block in the absence of a ventricular pacemaker and in patients whom bradycardia has caused syncope (1,2). Amiodarone inhibits CYP 450 enzymes which include CYP1A2, CYP2C9, CYP2D6 and CYP3A4 (3). P-glycoprotein is also inhibited (1,2). Serum levels of cyclosporine, lovastatin, simvastatin, digoxin, flecainide, phenytoin, procainamide, and quinidine will be increased (2). The effects of amiodarone will potentiate the anticoagulant effects of warfarin; reduce the initial dosage of warfarin by one third to one half (2). Metabolism is through hepatic means via CYP2C8 and 3A4 to the active N-desthylamiodarone metabolite (2). There is possible enterohepatic recirculation (2).

Non pharmacological Treatment

The treatment for afib is pharmacological in nature (2). Non pharmacological options would be to reduce the risk factors that would predispose the patient for strokes and atrial fibrillation (2). This includes exercising, losing weight, and controlling hypertension, hypothyroidism, and diabetes. Electrical cardioversion is often used to convert to NSR as well (2).


  1. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, editors. Pharmacotherapy: a pathophysiologic approach. 7th ed. Toronto: McGraw-Hill; 2007. p. 288
  2. Van Norman GA, Quan KJ, Davoudi R. Atrial Fibrillation. MD Consult [online]. Maryland Heights MO: Elsevier Inc. 2011 [cited 2012 Mar 3]. Available from:
  3. Pritchett EL. Management of atrial fibrillation. N Engl J Med. 1992(19); 326:1264
  4. Falk RH. Atrial fibrillation. N Engl J Med. 2001; 344 (14):1067.


This information is presented for informational purposes only and is not meant to be a substitute for advice provided by qualified health care professionals. You should contact your qualified health care provider if you have or suspect any health problems. This article is not intended to provide medical advice for its readers

QR Code
QR Code atrial_fib_treatment (generated for current page)