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Management of Atrial Fibrillation

20 February 2013

1 minute read

Management of Atrial Fibrillation

Atrial fibrillation is one of the most common arrthymia encountered. It presents as a totally irregularly irregular rhythm. Causes of AF are-

  1. Thyrotoxicosis
  2. Mitral valvular heart disease
  3. Chest infection
  4. COPD
  5. Hypertension
  6. Ischemic heart disease
  7. Constrictive pericarditis
  8. A SD-secundum.


Basic cardiac physiology required to understand AF better. 1) Atrial contraction contributes 20 % of cardiac output. Thus with onset of AF, there is loss of 20% of left ventricular systolic function which may result in cardiac failure in patients with pre-existing compromised LVF. 2) Left ventricular filling occurs during diastole. The duration of diastole is inversely proportional to ventricular rate, thus in AF with rapid ventricular rate, the diastolic phase is short and LV filling is impaired. One cardiac cycle may not fill enough to generate a radial pulse. It may require 2 or 3 consecutive cardiac cycles to give a radial pulse. This explains the concept of pulse deficit, whereby in AF the apex beat, is more than the radial pulse. 3) Ventricular rate in AF is reflected clinically by the apex beat and not the radial pulse.

AF manifests as palpitations, giddiness, cardiac failure and thromboembolic phenomenon like stroke.AF may be classified as paroxysmal, persistent or permanent. As the intention is to discuss basic principles of management, the various classes would not be elaborated on. The dispute over rate control over rhythm control is ongoing. Previously, it was thought that everyone with AF should be given one chance for cardioversion (Quote Prof Chu Pak Lau of Hong Kong University). Following the result of AFFIRM (AF follow up investigation of rhythm management), it was shown that rate control or rhythm control have no difference in outcome. The benefit of restoring sinus rhythm is nullified by the adverse effect of antiarrthymic drugs. It is therefore acceptable to leave AF alone and focus on ventricular rate control and thrombophylaxis.Cardioversion is still needed for symptom control if persist despite well controlled ventricular rate.

Acute management of AF depends on time of presentation and haemodynamic state. If patient is haemodynamically unstable like hypotensive with very rapid ventricular response, there is no dispute that immediate electrical cardioversion is mandatory. If presentation is less than 48 hours of onset, if one feels cardioversion is needed, it can be done safely without fear of thromboembolism.However if presentation is more than 48 hours; option is limited for cardioversion then must be done electively with prior anticoagulation for at least 1 month. Alternatively, a transoesophageal echo may be done to rule out LAA (left atrial appendage) thrombus prior to cardioversion.

Ventricular rate control may be by beta- blockers, digoxin or nondihydropyridine calcium blockers like verapamil or diltiazem.My preference is beta blockers to digoxin as beta-blocker can control exercise induced tachycardia whereas digoxin is only good for resting tachycardia.

Thrombophylaxis is traditionally with vitamin K antagonist, warfarin.The thromboembolic risk is determined by CHADS2 score which include factors of age(>75 years), diabetes mellitus, hypertension, cardiac failure and history of ischaemic stroke. Those with CHADS2 score of 2 or more are advised anticoagulation.Warfarin is notorious for having a narrow therapeutic window and requires regular monitoring of INR.Interaction with other drugs and food restrictions must be considered. New anticoagulants are available like dabigatran which is a direct thrombin inhibitor and rivaroxaban which is a factor Xa inhibitor. These new agents are convenient in that it requires no blood monitoring. The drawback is that we are unable to track compliance.

Other invasive interventions like RF ablation restores sinus rhythm in AF patient (MANTRA-PAF trial).AV nodal ablation prevent the atrial impulse from reaching the ventricles. After AV node is ablated, the ventricle will beat at a slow rate and a permanent pacemaker has to be inserted.

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