Atrial Fibrillation

Atrial fibrillation is one of the most common tachyarythmias. There is paroxysmal or persistent form. Paroxysmal form has spontaneous beginning and spontaneous end of fibrillation. In the opposite, persistent form can be ended only by using special therapy (pharmacotherapy or electrical cardioversion).

It can be presented at normal healthy persons but it is quite frequent in patients with :


 * Atrial Dilatation
 * Mitral Stenosis
 * ICHS
 * Sick sinus syndrome
 * Myocarditis
 * Pericarditis
 * Thyreotoxicosis
 * COPD
 * Pulmonary Embolism

Pathophysiology
This kind of arrhythmia is based on focal source of impulses and reentry phenomenon. Focal source is usually localized in left atrium, or in one of pulmonary veins. It leads to unorganized atrial activity with very high rate (400-800/min ). Atrial contraction becomes uneffective. Ventricular response is irregular, because not every atrial repolarization is conducted to ventricles (concealed conduction). Common ventricular rate in atrial fibrillation is 150-200/min. In result the heart rate of the patient is not based on physical activity. There is tachycardia at rest and bradycardia in enhanced physical activity.

Symptoms

 * palpitations
 * dyspnea
 * tiredness
 * heart failure
 * pulmonary edema
 * or no symptoms…
 * ECG – there is no P wave, in fact P wave is replaced by many F waves with rate 400-800/min, QRS complex is normal but RR distance is irregular (heart rate is irregular).

Complications and Consequences
Typical complication in AF is thromboembolic disease. Thrombus can be formed in left atrium with risk of peripheral embolization, especially stroke. Excessive ventricular rate can cause :
 * systemic hypotension;
 * lung congestion;
 * angina pectoris (shortened diastole leads to shortened perfusion of corronary arteries → myocardial ischemia);
 * tachycardia induced cardiomyopathy.

Therapy
Therapy of AF is based on:
 * 1) therapy of AF paroxysm (sinus rhythm restoring) → pharmacotherapy or electrical cardioversion,
 * 2) prevention of AF paroxysm (with therapy of cause of AF) → antiarrhythmics,
 * 3) ventricle rate modification → β-blockers
 * 4) prevention of thrombembolic disiese.

Pharmacotherapy

 * β-blockers - effect: AV node refractedy period prolongation and conduction slowing, they are prefered if we can not stop AF paroxysm. e.g. metoprolol
 * antiarrhythmics are used for sunus rhythm restoring and new AF paroxysm prevention:
 * propafenone (IC)
 * sotalol (III)
 * amiodarone (III)

Electrical Cardioversion
Cardioversion is one of methods, how to stop AF paroxysm. There are some conditions to performed it:
 * AF paroxysm less than 24(-48) hours;
 * no trombus in left atrium (transesophageal echocardiography);
 * anticoagulant therapy.

Note: Presence of thrombus in left atrium mens high risk of stroke after cardioversion!

Catheter Ablation
Catheter ablation is a method prefered in younger patient resistent on pharmacotherapy with no structural defect in atrial or ventricular myocardium. Then we expect the source of AF in pulmonary veins which will be isolated by catheter ablation.

Prevention of Thrombembolic Disease
The most offten used drug is warfarin, it should be indicated when patient has CHADS2 score 2 and higher. In every new found atrial fibrillation should be performed anticoagulant therapy. Warfarin is definitely prefered, but it can take more than 72 hours for the anticoagulant effect to develop! And there is high possibility off thrombus creation even after 24 hours of atrial fibrillation. We should start with low molecular weight derivatives of heparin (fraxiparine, enoxaparine, ...) for first 5-6 days and together start with warfarin. Every patient on warfarin therapy has to be monitored for INR (it’s level should be 2,0-3,0).

Warfarin can be replaced in special indications (high risk of bleeding) by antiagregants like ASA.

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 * Electrocardiography