Atrial Fibrillation Management
Atrial fibrillation (AFib) is an irregular and often very rapid heart rhythm. An irregular heart rhythm is called an arrhythmia. AFib can lead to blood clots in the heart. The condition also increases the risk of stroke, heart failure and other heart-related complications. During atrial fibrillation, the heart’s upper chambers — called the atria — beat chaotically and irregularly. They beat out of sync with the lower heart chambers, called the ventricles. For many people, AFib may have no symptoms. But AFib may cause a fast, pounding heartbeat, shortness of breath or light-headedness. Episodes of atrial fibrillation may come and go, or they may be persistent. AFib itself usually isn’t life-threatening. But it’s a serious medical condition that needs proper treatment to prevent stroke. Treatment for atrial fibrillation may include medicines, therapy to shock the heart back to a regular rhythm and procedures to block faulty heart signals. A person with atrial fibrillation also may have a related heart rhythm problem called atrial flutter. The treatments for AFib and atrial flutter are similar.
Symptoms of AFib
Atrial Fibrillation (AFib) is a heart condition characterized by an irregular and often rapid heartbeat. Symptoms can vary among individuals and may include:
- Heart palpitations: Feeling like your heart is fluttering, pounding, racing, or skipping beats.
- Fatigue: Feeling unusually tired or weak, even with normal activity.
- Shortness of breath: Difficulty breathing or catching your breath, especially during physical exertion.
- Dizziness or lightheadedness: Feeling faint or dizzy, sometimes leading to loss of consciousness.
- Chest discomfort: Some people may experience chest pain or discomfort, although this is less common than with other heart conditions.
- Weakness: Feeling generally weak or experiencing a decrease in exercise tolerance.
- Anxiety: Feeling anxious or on edge due to the irregular heartbeat.
- Sweating: Experiencing sudden sweating, especially during periods of increased heart rate.
Risk Factors for AFib
Even people committed to healthy lifestyles and who have no other medical problems can develop AFib. The most common risk factors include:
- Age over 60
- High blood pressure
- Coronary artery disease
- Heart failure
- Heart valve disease
- Untreated atrial flutter (another type of abnormal heart rhythm)
- Prior open-heart surgery
- Sleep apnea
- Thyroid disease
- Diabetes
- Chronic lung disease
- Excessive alcohol or stimulant use
- Serious illness or infection
Complex Arrythmia a.k.a. Ventricular Tachycardia
Sustained ventricular tachycardia (VT) may lead to hemodynamic collapse. Consequently, these patients require urgent conversion to sinus rhythm. The strategy for conversion depends on hemodynamic stability.
Unstable patients have signs or symptoms of insufficient oxygen delivery to vital organs as a result of the tachycardia. Such manifestations may include the following:
- Chest pain
- Dyspnea
- Hypotension
- Altered level of consciousness
Unstable patients with monomorphic VT should be immediately treated with synchronized direct current (DC) cardioversion. Unstable polymorphic VT is treated with immediate defibrillation. Stable patients have adequate vital end-organ perfusion and thus do not experience signs or symptoms of hemodynamic compromise. Treatment depends on whether the VT is monomorphic or polymorphic and whether left ventricular function is normal or impaired (e.g. reduced left ventricular ejection fraction [LVEF] or heart failure).
In stable patients with monomorphic VT and normal left ventricular function, restoration of sinus rhythm is typically achieved with intravenous (IV) procainamide or sotalol. Lidocaine may also be used.
A 12-lead electrocardiogram (ECG) should be obtained for all patients of VT before conversion. It helps to further plan the long term management of these patients.
If left ventricular function is impaired, amiodarone (or lidocaine) is preferred to procainamide for pharmacologic conversion because procainamide exacerbarates heart failure. However, evidence indicates that amiodarone should not be the first-line antiarrhythmic for stable VT, because its effects on myocardial conduction and refractoriness. If medical therapy is unsuccessful, synchronized cardioversion (50-200 J monophasic) following sedation is appropriate.
Polymorphic VT in stable patients typically terminates on its own. However, it tends to recur. After sinus rhythm returns, the ECG should be analyzed to determine whether the QT interval is normal or prolonged. Polymorphic VT in patients with a normal QT interval is treated in the same manner as monomorphic VT.
If the patient has runs of polymorphic VT punctuated by sinus rhythm with QT prolongation, treatment is with magnesium sulfate, isoproterenol, pacing, or a combination thereof. Phenytoin and lidocaine may also help by shortening the QT interval in this setting, but procainamide and amiodarone are contraindicated because of their QT-prolonging effects. Magnesium is unlikely to be effective in patients with a normal QT interval.
In patients with electrolyte imbalances (eg, hypokalemia or hypomagnesemia from diuretic use), correction of the abnormality may be necessary for successful cardioversion. In patients with severe digitalis toxicity (eg, with sustained ventricular arrhythmias, advanced atrioventricular AV block, or asystole), treatment with antidigitalis antibody may be indicated.
After conversion of VT, the clinical emphasis shifts to determining the severity of heart disease, assessing the prognosis, and formulating the best long-term management plan. Options, depending on the severity of symptoms and degree of structural heart disease, include the following:
- Antiarrhythmic medications
- Implantable cardioverter-defibrillator (ICD)
- Catheter ablation
Combinations of these therapies are often used when structural heart disease is present.
Antiarrhythmic drugs have traditionally been the mainstays of treatment for clinically stable patients with VT. However, some patients experience unacceptable side effects or frequent recurrence of VT with drug therapy. As a result, cardiologists are increasingly making use of devices and procedures designed to abort VT or to remove the arrhythmogenic foci in the heart. In patients with idiopathic VT (associated with structurally normal hearts), medications are often avoided entirely through the use of curative catheter-based ablation.
Congenital long QT syndrome and catecholamine polymorphic VT has been linked to sudden cardiac death. Patients with these disorders are managed with a combination of genetic typing, beta blockers, lifestyle modification, and, in selected cases, ICD placement.
In the 1980s, several centers explored ventricular arrhythmia surgery, using excision and cryoablation of infarct zones to prevent recurrent VT. This strategy has been essentially abandoned as a consequence of the high mortality and the advent of ICDs and ablative therapies.
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