Atrial fibrillation (AF) is a cardiac arrhythmia characterized by disorganized electrical activity within the atria, which leads to ineffective atrial contraction and irregular ventricular contraction.
AF is the most common cardiac arrhythmia in adults. Its prevalence increases significantly with age, so that 10% of those over 85 have atrial fibrillation.
AF can be classified as paroxysmal, persistent or permanent:
To better understand the pathophysiology of AF, it is firstly important to understand the normal cardiac conduction system.
Cardiac electrical impulses are first generated in the sinoatrial node (SAN) which is found in the right atrium. The rate at which these impulses are generated is controlled by the autonomic nervous system. The sympathetic branch of the nervous system increases the rate of impulse generation, while the parasympathetic branch decreases the rate.
The electrical impulse then travels through the atria causing atrial contraction, and to the atrioventricular node (AVN) which lies between the atria and ventricles. The AVN slightly delays the impulse before it is sent through the Bundle of His, down the left and right bundle branches, and finally to the Purkinje fibres, resulting in ventricular contraction.
Atrial fibrillation (AF) is a type of supraventricular cardiac arrhythmia meaning the origin of the arrhythmia arises from above the ventricles. It often originates from left atrial myocytes which extend as sleeves around the pulmonary veins. Atrial ectopics from the pulmonary veins trigger micro re-entry circuits in the atria causing chaotic electrical activity and sustained AF.
Conditions including hypertension or mitral regurgitation cause the atria to stretch which changes their electrical properties, increasing the substrate for AF. This combination increases the likelihood of an atrial ectopic triggering AF and the atria sustaining it. AF begets AF as AF causes the atria to dilate and increases AF substrate.
This chaotic electrical activity is intermittently conducted through the AVN, giving rise to the characteristic irregularly irregular ventricular rate seen in AF. The ventricular rate is very variable and depends on the speed of AVN conduction. Young patients with slick AV nodes are often very symptomatic and tachycardic.
In addition, AF causes ineffective atrial contraction, leading to blood stasis within the atria, increasing the chance of thrombosis (Virchow's triad) and subsequently embolic complications such as transient ischaemic attacks (TIA), stroke and systemic embolisation.
Numerous conditions/risk factors can increase the substrate and or triggers for AF. These typically cause the atria to stretch. It is important to address these conditions/risk factors to improve prognosis and maintenance of sinus rhythm if a rhythm control strategy is intended.
AF is most commonly associated with hypertension, obesity and alcohol. Other causes of AF can be split into cardiac and non-cardiac causes.
Cardiac causes include heart failure, structural pathology, congenital heart disease, atrial or ventricular dilation, atrial or ventricular hypertrophy, pre-excitation syndromes, sick sinus syndrome, inflammatory conditions and infiltrative conditions.
Non-cardiac causes include acute infection and electrolyte imbalances.
Atrial fibrillation (AF) is a common arrhythmia affecting approximately 1-2% of the population. It is associated with increased morbidity and mortality, so it is important for clinical practitioners to have a good understanding of its aetiology, risk factors, clinical features, differential diagnoses and investigations.
There are several potential causes of AF, including:
As well as the causes of AF discussed above, the following risk factors are associated with an increased likelihood of developing AF:
Caffeine intake is not typically a risk factor although it is often blamed for palpitations.
In some patients, AF can be asymptomatic, even when causing tachycardia and therefore may be an incidental finding during a clinical examination or when performing a 12-lead electrocardiogram (ECG). Increasingly, AF is identified via patient-initiated monitoring (e.g. Apple watches).
Typical symptoms of AF include:
It is also important to remember that a transient ischaemic attack or stroke can be the presenting feature of AF. For this reason, it is essential that patients presenting with symptoms or signs of a TIA or stroke are also asked about the features of AF.
Other important areas to cover in the history include:
In the context of suspected AF, a thorough cardiovascular examination is necessary.
Typical clinical findings in atrial fibrillation include:
Some patients may have co-existing heart failure. Typical clinical findings of heart failure include:
Possible differential diagnoses in the context of suspected AF include:
Relevant bedside investigations in the context of suspected AF include:
A 12-lead ECG is the diagnostic investigation for Atrial Fibrillation (AF). Typical features of AF on an ECG include tachycardia (particularly in new-onset; as aforementioned heart rate depends on the rate of AVN conduction), irregularly irregular rhythm, absent P-waves, fibrillation waves (best seen in lead II and V1 and often confused with atrial flutter waves) and a chaotic (noisy) baseline.
Paroxysmal AF can be captured for diagnostic purposes using an Ambulatory ECG. It consists of 24-hour ECG monitor, a cardiac event recorder, a 7-day Holter monitor or an implantable loop recorder for patients with infrequent symptoms.
Relevant laboratory investigations in the context of suspected AF include:
Relevant imaging investigations in the context of suspected AF include:
The National Institute for Health and Care Excellence recommends an echocardiogram only if the result is likely to alter management, such as when atrial fibrillation (AF) is the presenting feature of a cardiac condition like a cardiomyopathy or valvular pathology.
A Chest X-ray can show changes associated with heart failure, such as alveolar oedema, Kerley B-lines, cardiomegaly, upper lobe diversion, pleural effusion, and fluid in the lung fissures.
The European Society of Cardiology states that the following criteria must be met for a diagnosis of AF:
The first step is to perform an ABCDE assessment to identify any adverse features. Adverse features defined by the Resuscitation Council include any symptoms or signs of shock, syncope, myocardial ischaemia, or heart failure. If any of these features are present, synchronised direct current cardioversion should be delivered.
For further information, please consult the guide to the acute management of atrial fibrillation.
The primary consideration for AF patients is anticoagulation. Following this, the management of AF can be broadly split into rhythm control and rate control. Generally, the choice is based on symptoms and the likelihood of maintaining sinus rhythm. There is no clear benefit to restoring sinus rhythm, however, managing modifiable AF risk factors is essential for overall patient health and increases the chance of maintaining sinus rhythm.
If symptoms are not managed in primary care, the National Institute for Health and Care Excellence recommends a prompt referral to a specialist for invasive treatment.
Rhythm control is an appropriate strategy for patients presenting with new-onset AF (defined as less than 48 hours). Most patients (69%) will spontaneously cardiovert within 48 hours and delayed cardioversion has been shown to be non-inferior to early cardioversion at four weeks.
Electrical cardioversion is achieved by sedating/anaesthetising the patient and applying defibrillation pads to the patient’s chest and delivering synchronised DC cardioversion.
Pharmacological cardioversion is achieved by using either flecainide or amiodarone. Flecainide is a class 1c antiarrhythmic drug that blocks sodium channels within the heart and should not be used in patients with structural or ischaemic heart disease due to the risk of sudden cardiac death. Amiodarone is a class 3 antiarrhythmic drug that blocks potassium channels within the heart and prolongs the refractory period of the myocardium. It should be avoided in patients with QT prolongation and can cause side effects such as life-threatening lung fibrosis, liver failure, photosensitivity, hyper/hypothyroidism, neuropathy, and visual deficits.
Amiodarone can be given orally or intravenously; however, special precautions are needed when given intravenously as extravasation can cause serious skin necrosis.
Therapeutic anticoagulation is required for 4-6 weeks preceding and after either electrical or pharmacological cardioversion, unless the onset of AF is within the past 48 hours and is a single, isolated episode of AF.
Rhythm control is a suitable approach for patients presenting with non-acute AF who have ongoing symptoms despite adequate rate control or for those for whom rate control has not been successful.
Electrical cardioversion is achieved by applying defibrillation pads to the patient’s chest and delivering synchronised DC cardioversion. This should be deferred until the patient has received adequate anticoagulation (for example, from the day the direct-acting oral anticoagulant is started or when INR is 2 if using Warfarin) for at least 4-6 weeks.
Amiodarone can be given for 4 weeks prior to electrical cardioversion and continued for 12 months post electrical cardioversion to maintain sinus rhythm.
If it is not satisfactory to wait for adequate anticoagulation, transoesophageal echocardiography-guided cardioversion can be utilized to verify the lack of a thrombus and deliver cardioversion.
Beta-blockers (e.g. bisoprolol) are the first-line drug for long-term rhythm control.
Amiodarone is the most effective anti-arrhythmic drug, yet it requires regular lung, liver and thyroid monitoring and should only be prescribed by a specialist.
Rate control is an acceptable strategy for the following groups:
Pharmacological options for rate control include:
For patients with paroxysmal AF and minimal symptoms, or if symptoms are caused by a known precipitant (e.g. alcohol), a ‘no drug treatment’ or ‘pill-in-the-pocket strategy’ can be used.
If there is a clear precipitant for the paroxysm then this should be avoided whenever possible.
Class 1c antiarrhythmic drugs are used for the ‘pill-in-the-pocket strategy’ (e.g. flecainide and propafenone). These medications can be taken regularly or as required when a patient experiences a paroxysm of AF.
The risk of structural heart disease increases with age and flecainide should be used with caution/specialist advice in older patients.
The following criteria must be met prior to a patient being started on the ‘pill-in-the-pocket strategy’:
If paroxysmal AF is not managed with the ‘pill-in-the-pocket strategy’, regular flecainide can be considered. Failing this, pulmonary vein ablation or the pace and ablate strategy can be considered.
The risk of thromboembolic complications is higher in patients with AF due to blood stasis within the heart resulting in an increased likelihood of thrombus formation.
For patients with atrial fibrillation (AF), anticoagulation must be considered in order to reduce their risk of TIA and stroke.
The CHA2DS2VASc tool (Table 1) can be used to assess the risk of stroke in AF. It consists of eight components that, when added together, inform the decision to offer anticoagulation therapy.
The total CHA2DS2VASc score can then be used to decide whether to start anticoagulation therapy (Table 2).
If it is decided that a patient should be started on anticoagulation therapy, they should be offered a choice of either a direct-acting oral anticoagulant (DOACs) or a vitamin K antagonist such as warfarin.
DOACs are the first-line option. These drugs inhibit factor Xa within the clotting cascade and thereby prevent thrombus formation. Dabigatran works by inhibiting the action of thrombin and thus thrombus formation.
Warfarin is a vitamin K antagonist. It prevents the activation of clotting factors 10, 9, 7 and 2, which are vitamin K dependent, and therefore inhibits thrombus formation.
The ORBIT tool (recommended by NICE, previously HAS-BLED was used) can be used alongside the CHA2DS2VASc score to help guide decisions regarding anticoagulation. It consists of six components that are used to identify patients at high risk of bleeding (Table 3).
The ORBIT tool is a useful device for assessing a patient's risk of bleeding. Points are awarded depending on the following criteria:
The ORBIT score can be used to categorise whether a patient is at low, medium or high risk of bleeding (Table 4).
Following the restoration of sinus rhythm, there is always a risk of recurrence of AF. The decision to stop anticoagulation, after the minimum 4-week period of post cardioversion anticoagulation, should be based upon a patient's CHA2DS2VASc score, ORBIT score and individual preferences.
Invasive management should be considered when drug treatment has been unsuccessful, unsuitable or not tolerated.
This involves creating small scars within the myocardium of the left atrium to block abnormal electrical signals and restore sinus rhythm.
Left atrial ablation is a complex procedure with the risk of serious complications. However, in significantly symptomatic patients, it can be a life-changing procedure.
