Atrial Fibrillation Definition
Atrial Fibrillation Definition
The atria contribute to 25% of the stroke volume, and the 'atrial kick' is lost with the onset of atrial fibrillation. In addition, the ventricles contract irregularly and often at a rapid rate. As ventricular filling is an important determinant of stroke volume, rapid and irregular ventricular contraction impairs the cardiac output. The severity of the haemodynamic compromise is dependent on the contractility of the ventricle. Patients with normal ventricles can tolerate atrial fibrillation and rapid ventricular rates without any appreciable haemodynamic consequence. However, if the ventricles are severely impaired, the onset of atrial fibrillation can result in circulatory shock.Loss of atrial contraction predisposes to stasis and thrombus formation, greatly increasing the risk of stroke.
The precipitating factors of atrial fibrillation are hypoxia, pneumonia, pericarditis, excessive intake of alcohol, myocardial infarction and pulmonary embolism. The risk factors of atrial fibrillation are Hypertensive heart disease, thyrotoxicosis, heart failure, ischemic heart disease, pulmonary disease, diabetes and valvular heart disease.
Atrial fibrillation is caused by haphazard conduction of electrical activity in atria that are enlarged or diseased. This results in irregular uncoordinated atrial contraction at a rate of 300-600/min, detected as a saw tooth baseline on the ECG. Some impulses are carried by the conduction tissue, producing irregularly timed QRS complexes and ventricular contraction.
Atrial fibrillation is usually asymptomatic. Occasionally, patients may complain of palpitations, dyspnoea, fatigue or chest pains (atrial fibrillation can exacerbate angina) or present with the complication of stroke . Patients may have a past medical history of ischaemic heart disease (angina, myocardial infarction) or hypertension ).
On examination, the pulse rate is irregularly irregular, both in rate and volume. The ventricular rate cannot be assessed from the pulse, as irregular ventricular contractions may not produce sufficient pulse pressure for all contractions to be detected. The ventricular rate is assessed by auscultating the apex: the discrepancy between apex and pulse rate is an indicator of rate control (the wider the discrepancy, the poorer the control). Evidence of underlying disease states that predispose to atrial fibrillation includes hypertension and the murmur of mitral valve disease.
On assessment, it is important to ascertain any acute precipitating factors and underlying risk factors and to assess the severity of disease (blood pressure, apex rate). Approximately a third will have no underlying cause: these are labelled as 'lone' atrial fibrillation.
The prevalence of atrial fibrillation is age related: it is present in 1% of patients under the age of 60, rising to 6% of patients over the age of 80.1 It is 1.5 times more common in men.
The most important investigation method is ECG ( electrocardiogram).ECG of atrial fibrillation may reveal the irregularly irregular QRS complexes that occur in the setting of a sawtooth baseline of uncoordinated atrial activity. Besides that, atrial fibrillation is confirmed by the absence of p-waves, an irregular sawtooth baseline and an irregular ventricular rate. There may also be features of underlying disease such as left ventricular hypertrophy (hypertension, heart valve disease) and previous myocardial infarction (abnormal Q waves). 24-hour ECG monitoring ( Holter monitor) may be required to monitor and diagnose paroxysmal atrial fibrillation in patients who have symptoms suggestive of atrial fibrillation but who remain in sinus rhythm on initial investigations.
Other investigations include, Urea and electrolytes (Chronic disturbances of electrolytes (hypokalaemia) may predispose to atrial fibrillation and have implications for therapy (hypokalaemia predisposes to digoxin toxicity)) and thyroid stimulating hormone( TSH is a useful screen for thyrotoxicosis and should be performed for all patients experiencing their first episode of atrial fibrillation).
Chest X-ray is useful to screen for cardiomegaly, an indicator of underlying heart disease or congestive cardiac failure. Transthoracic echocardiography is able to measure the atrial size and screen for thrombus (sensitivity is low) and valvular heart disease. In addition, ventricular size and function can be quantified. Transoesophageal echocardiography is indicated when there is a suggestion of left atrial thrombus on transthoracic imaging.
Initial management may focus with observing the haemodynamic status.Although the majority of patients will not have clinically apparent haemodynamic compromise, it is important to identify and correct it if present.
This is follow later with Identification and correction of an acute precipitating cause (e.g. oxygen for hypoxia) may correct atrial fibrillation. Identification and correction of the underlying cause is an important aspect of patient management. The onset of atrial fibrillation in severe mitral regurgitation indicates the need for surgery.
The aim of rhythm control is to achieve and sustain sinus rhythm, whereas the aim of rate control is to slow the ventricular rate and prevent stroke by anticoagulation with warfarin. In patients over the age of 65, both treatments produced similar results for survival and risk of stroke.
Rhythm control strategy involve pharmacological cardioversion and electrical cardioversion. Pharmacological cardioversion involved the use of amiodarone. Amiodarone is a commonly used agent that can be given orally, in a decreasing loading dose over 2 weeks. An alternative agent is flecainide.
Electrical cardioversion involved synchronous DC cardioversion. Synchronous DC cardioversion is usually undertaken following 4 weeks of anticoagulation with warfarin to reduce the risk of stroke. Alternatively, transoesophageal echocardiography may be used to screen for thrombus and pre-procedure anticoagulation undertaken only in patients with evidence of thrombus. DC cardioversion is successful in 95%, and the risk of stroke is 0.5% (increasing to 7% if pre-procedure anticoagulation was not undertaken). Post procedure, patients should continue anticoagulation therapy for 4 weeks.Amiodarone, β-blockers or sotalol may be prescribed to maintain sinus rhythm.
Rate control strategy involved pharmacological rate control. Digoxin is a common agent used for rate control. Alternative agents are β-blockers and dihydropyridine calcium antagonists (verapamil and diltiazem). Warfarin should be prescribed for patients at high risk of stroke to maintain an INR of 2.0-3.0; this subset of patients includes the elderly (age more than 75), patients with cardiac failure (or with an ejection fraction of less than 35%) or those with a history of hypertension. Low-risk patients, aged less than 60 years without any of the aforementioned risk factors, may receive 325 mg of aspirin daily instead.
Surgical management may include maze procedure. The maze procedure is currently under evaluation as a curative procedure for atrial fibrillation. The classic maze procedure requires cardiopulmonary bypass to perform multiple cuts on the atrial wall. The scarring resulting from the healing process of each incision acts as an insulator to electrical currents, and multiple cuts with a maze-like appearance prevent haphazard conduction of electrical activity. The atria are then reconstructed using sutures. More recently, radiofrequency probes have been developed that allow the creation of scar tissue by contact with the atria. The maze procedure has a reported success rate of upto 80% in establishing and maintaining sinus rhythm, although this may take up to 8 weeks. Heart block is a common postoperative complication that resolves by 8 weeks.
Atrial fibrillation is not a benign rhythm: approximately 15% of patients die within the first 30 days of diagnosis. The risk of death reduces thereafter: within the age group 55-74, the 1- and 5-year survival is approximately 82% and 60% respectively. The annual incidence of stroke is 1.5% in patients aged between 50 and 59, and this increases to 23.5% in those aged between 80 and 89 years.
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