Atrial Fibrillation: An Irregular Heart Rhythm

Atrial fibrillation is a common heart rhythm disorder in which the upper chambers activate chaotically rather than contracting in an organised way. It can cause palpitations, breathlessness or fatigue, but may produce no symptoms. The main preventable danger is stroke, so diagnosis and stroke risk assessment remain important even when the rhythm feels harmless.

What atrial fibrillation is Atrial fibrillation is usually shortened to AF. It is an abnormal heart rhythm beginning in the atria, which are the two upper heart chambers. Electrical activity becomes rapid and disorganised instead of following one coordinated signal. The atria then quiver rather than producing an effective, organised contraction. Normal electrical rhythm A normal heartbeat usually begins in the sinoatrial node within the right atrium. The electrical signal spreads across both atria and then reaches the atrioventricular node. It continues through specialised pathways that activate the ventricles in a coordinated sequence. This regular pattern is called sinus rhythm. Electrical activity during AF During AF, many small electrical wavefronts move through the atria at the same time. Some episodes are triggered by rapidly firing cells near the pulmonary veins. The atrioventricular node blocks many impulses but allows others to reach the ventricles. Because the impulses arrive unpredictably, the ventricular rhythm becomes irregular. An irregularly irregular pulse The pulse in AF is typically irregularly irregular. This means that the gaps between beats vary without a repeating pattern. The heart rate can be fast, normal or occasionally slow. A regular pulse does not completely exclude intermittent AF, and an irregular pulse does not prove AF. A 12 lead ECG is needed to confirm the rhythm. Loss of organised atrial contraction The atria normally provide a final contribution to ventricular filling before each ventricular contraction. This contribution is sometimes called the atrial kick. Losing it may have little noticeable effect in a healthy heart. It can matter more when the ventricles are stiff, the heart rate is rapid or valve disease is present. AF is not the same as atrial flutter Atrial flutter is another rhythm arising in the atria. Its electrical activity usually follows a more organised circuit than AF. The pulse can be regular or irregular depending on conduction to the ventricles. Atrial flutter still carries thromboembolic risk and is assessed using the same NICE stroke risk framework. Paroxysmal AF Paroxysmal AF consists of episodes that stop without treatment within seven days. Most stop within 48 hours. Episodes may last minutes, hours or several days. A person can feel every episode, some episodes or none of them. Paroxysmal AF still carries stroke risk according to the person's clinical risk factors. Persistent AF Persistent AF continues beyond seven days or requires cardioversion to restore sinus rhythm. The term describes duration and treatment history rather than severity. Persistent AF may cause few symptoms, while short paroxysms can feel very distressing. Long standing persistent AF Long standing persistent AF has continued for at least 12 months when a rhythm control strategy is still being considered. The longer AF continues, the more the atria can remodel electrically and structurally. Restoring and maintaining sinus rhythm can then become more difficult. This category does not mean that rhythm control is impossible. Permanent AF Permanent AF means that the person and clinical team accept the ongoing rhythm. No further attempt to restore sinus rhythm is currently planned. Treatment focuses on ventricular rate, stroke prevention, symptoms and associated conditions. Permanent does not mean untreatable or inevitably worsening. AF categories are not stages Paroxysmal, persistent and permanent AF describe rhythm patterns and management decisions. They are not stages through which everyone must progress. Some people remain paroxysmal for many years. Others present for the first time with persistent or permanent AF. AF can be newly diagnosed without being newly started A first ECG diagnosis does not always show when the rhythm began. AF may have been present silently for days, months or longer. This uncertainty matters when cardioversion is considered because a clot may already have formed. Common causes and risk factors AF becomes more common with increasing age. High blood pressure, coronary disease, heart failure and valve disease are frequent contributors. Diabetes, chronic kidney disease, obesity and sleep apnoea also increase risk. Several factors often coexist and gradually alter atrial structure. High blood pressure Longstanding hypertension increases pressure within the left ventricle and left atrium. The atrium can enlarge and develop fibrosis. These changes make disorganised electrical activity more likely to begin and persist. Treating blood pressure helps reduce wider cardiovascular risk and may reduce AF progression. Coronary heart disease and heart attack Coronary disease can damage heart muscle and alter chamber pressure. A myocardial infarction can trigger AF during the acute illness. AF can also occur later because of scarring, heart failure or atrial enlargement. Heart valve disease Mitral valve disease has a particularly close association with AF. Mitral stenosis raises pressure within the left atrium and can cause major atrial enlargement. Mitral regurgitation can create volume overload. Other valve disorders can contribute through pressure changes and heart failure. Heart failure and cardiomyopathy AF can cause or worsen heart failure when the rate remains too fast or filling becomes inefficient. Heart failure can also promote AF through raised atrial pressure and enlargement. Cardiomyopathies may provide structural or inherited substrates for the rhythm. The relationship often operates in both directions. Hyperthyroidism Excess thyroid hormone increases heart rate and electrical excitability. Hyperthyroidism can trigger new AF or make rate control difficult. A thyroid blood test is therefore commonly included during assessment. Treating the thyroid disorder may allow the rhythm to settle, but stroke risk still requires review. Obesity Obesity is associated with atrial enlargement, inflammation and higher blood pressure. It also increases the likelihood of diabetes and sleep apnoea. Sustained weight management can reduce AF symptoms and recurrence in some people. The goal is long term cardiovascular health rather than rapid restrictive dieting. Sleep apnoea Obstructive sleep apnoea repeatedly interrupts breathing during sleep. It causes oxygen changes, pressure swings and surges in stress hormones. Untreated sleep apnoea is associated with AF recurrence and poorer rhythm control outcomes. Loud snoring, witnessed pauses and daytime sleepiness can prompt assessment. Alcohol Alcohol can trigger an AF episode, particularly after heavy or binge drinking. Regular excess intake also increases blood pressure and long term AF risk. Some people notice episodes after smaller amounts. Reducing alcohol is more reliable than trying to identify a universally safe trigger threshold. Infection and acute illness Pneumonia, sepsis and other infections can trigger AF through inflammation, fever and physiological stress. Dehydration and electrolyte disturbance can contribute. New AF during illness may settle after recovery. It still requires stroke risk assessment because recurrence can occur later. Surgery AF is common after cardiac surgery and can also follow major non cardiac operations. Pain, inflammation, fluid shifts and stress hormone release can contribute. Postoperative AF may resolve, but treatment and anticoagulation decisions still require individual assessment. Medicines and stimulants Some medicines can increase heart rate or provoke palpitations. Examples include excessive thyroid replacement and some stimulant or bronchodilator medicines. Cocaine and other recreational stimulants can trigger dangerous arrhythmias. A medicine should not be stopped without checking with the prescriber. Endurance exercise Regular moderate exercise protects cardiovascular health. Very high lifetime volumes of endurance exercise are associated with AF in some people. This does not mean that ordinary exercise causes AF. Activity advice should reflect symptoms, fitness and the person's wider health. Idiopathic or lone AF Sometimes no clear cause is found after appropriate assessment. This has traditionally been called lone or idiopathic AF. The label does not mean that the rhythm is harmless. Risk factors can be subtle, emerge later or remain unidentified, so follow up remains important. Symptoms of AF Palpitations are a common symptom. People may describe pounding, fluttering, racing, skipping or an uneven heartbeat. Breathlessness, fatigue, reduced exercise capacity, dizziness and chest discomfort can occur. Symptoms depend partly on heart rate, ventricular function and how abruptly the rhythm begins. Palpitations Palpitations describe awareness of the heartbeat rather than one diagnosis. AF palpitations often feel irregular, but other rhythms and extra beats can feel similar. Anxiety, caffeine, anaemia and thyroid disease can also cause palpitations. An ECG recording during symptoms provides more useful information than the sensation alone. Breathlessness A rapid irregular rhythm can reduce filling and cardiac output. Raised atrial pressure can worsen congestion in someone with heart failure. Breathlessness has many other causes, including lung disease, anaemia and infection. Severe or sudden breathlessness with an irregular pulse requires urgent assessment. Fatigue and exercise intolerance AF can reduce efficient cardiac performance. A persistently fast rate can make ordinary activity exhausting. Medicines used for rate control can also contribute to tiredness when the heart becomes too slow or blood pressure falls. The symptom should be interpreted with rate, rhythm and other health conditions. Dizziness and fainting AF can cause light headedness when the ventricular rate is very fast or occasionally very slow. Fainting is not a routine benign AF symptom. It raises concern about low blood pressure, another arrhythmia, valve disease or another serious condition. Chest discomfort AF can increase the heart's oxygen demand, particularly when the rate is rapid. It can provoke angina in someone with coronary disease. Chest pressure may also indicate acute coronary syndrome rather than AF alone. A fast irregular rhythm with chest pain requires emergency assessment. AF can cause no symptoms Some people have no awareness of AF. It may be found during a pulse check, blood pressure measurement, preoperative assessment or unrelated ECG. Asymptomatic AF is not automatically low risk. Stroke prevention depends on clinical risk factors rather than symptom intensity. AF can be intermittent and missed A short ECG records only a brief period. Paroxysmal AF may have stopped before the person reaches a clinic. Repeated symptoms with a normal resting ECG therefore do not exclude the rhythm. Longer monitoring is selected according to how often episodes occur. Manual pulse assessment NICE recommends manual pulse feeling when AF is suspected. Relevant presentations include palpitations, breathlessness, dizziness, syncope, chest discomfort, stroke or TIA. The clinician assesses regularity and rate. Pulse feeling identifies a clue rather than providing the final diagnosis. Twelve lead ECG A 12 lead electrocardiogram confirms AF when the rhythm is present. It usually shows no consistent P waves and irregular ventricular activation. The ECG also assesses rate, conduction, previous infarction and other rhythm abnormalities. It records electrical activity rather than the strength of cardiac contraction. Ambulatory ECG monitoring A portable ECG can record rhythm during ordinary activity. NICE recommends a 24 hour monitor when episodes occur less than 24 hours apart or silent episodes are suspected. Longer event monitoring is used when symptomatic episodes are more widely separated. The goal is to capture an ECG during the suspected rhythm. Consumer watches and handheld devices A smartwatch or handheld ECG can identify an irregular rhythm or produce a short tracing. This information can support further assessment. Automated labels can be wrong because of movement, extra beats or poor contact. A device alert should not be treated as a complete clinical diagnosis or ignored when symptoms are serious. Echocardiography An echocardiogram assesses heart structure and function. It can show atrial enlargement, ventricular dysfunction and important valve disease. It is particularly relevant when baseline imaging will influence long term management or rhythm control is considered. An echocardiogram is not required solely to calculate stroke risk once anticoagulation criteria are already clear. Blood tests Blood tests commonly assess thyroid function, kidney function, liver function, electrolytes and blood count. They can identify triggers, treatment contraindications and anticoagulant dosing factors. No blood test confirms AF without an ECG rhythm recording. The central concern is stroke AF can allow blood to become relatively static within the left atrium. Stasis is most important within the left atrial appendage, a small muscular pouch. A thrombus can form and later travel through the arterial circulation. If it blocks an artery in the brain, an ischaemic stroke results. AF related stroke can be the first recognised presentation AF may be silent or intermittent. A person can therefore experience a stroke before the rhythm has been diagnosed. Longer ECG monitoring is sometimes used after an unexplained stroke to look for intermittent AF. Earlier detection allows appropriate anticoagulation to reduce preventable embolic events. Symptoms do not predict stroke risk reliably A person with distressing daily palpitations may have few stroke risk factors. Another person with silent intermittent AF may have a high clinical risk. The duration and burden of AF may provide additional information in specialist settings. Current NICE anticoagulation decisions use formal clinical risk assessment across AF patterns. CHA2DS2 VASc NICE recommends the CHA2DS2 VASc score for people with symptomatic or asymptomatic AF. It is used for paroxysmal, persistent and permanent AF and for atrial flutter. It also applies when AF may recur after cardioversion or ablation. The score estimates thromboembolic risk rather than diagnosing AF. What the letters represent C represents heart failure or left ventricular dysfunction. H represents hypertension. A2 represents age 75 or older and contributes two points. D represents diabetes. S2 represents previous stroke, TIA or systemic embolism and contributes two points. The remaining components V represents vascular disease such as previous myocardial infarction or peripheral arterial disease. A represents age from 65 to 74. Sc represents the sex category component recorded as female. Age cannot be counted in both age categories. The score must be calculated from verified clinical information. Sex category within the score The female sex category point acts mainly as a risk modifier alongside other factors. NICE does not recommend anticoagulation for someone under 65 whose only point is sex. This avoids treating sex alone as sufficient stroke risk. The score is a professional decision aid rather than a public self prescribing tool. NICE anticoagulation thresholds NICE offers a direct acting oral anticoagulant for a CHA2DS2 VASc score of 2 or above when suitable. Anticoagulation is considered for men with a score of 1. People under 65 with no risk factor other than sex are not offered anticoagulation for AF stroke prevention. Stroke and bleeding risks are reviewed because age and health conditions change. Paroxysmal AF still counts Anticoagulation decisions are not based simply on whether AF comes and goes. A person with paroxysmal AF can form an atrial clot and experience embolic stroke. A brief or symptom free pattern does not cancel clinical risk factors. Anticoagulation after cardioversion or ablation Restoring sinus rhythm does not prove that AF will never recur. Recurrences may be silent. NICE advises against stopping anticoagulation solely because AF is no longer detectable. The decision is based on reassessed stroke risk, bleeding risk and the person's preferences. Bleeding risk assessment Anticoagulants reduce stroke risk but increase bleeding risk. NICE recommends the ORBIT score when starting or reviewing anticoagulation. The score estimates bleeding probability and supports informed discussion. It is not intended as an automatic cut off denying anticoagulation. Modifiable bleeding risks Uncontrolled high blood pressure increases intracranial bleeding risk. Anaemia should be investigated and reversible causes treated. Alcohol excess and interacting medicines can increase bleeding. NSAIDs, antiplatelets and some antidepressants require medication review. Age and falls Age increases both stroke and bleeding risk. NICE advises not withholding anticoagulation solely because someone is older or at risk of falls. The team should reduce preventable falls, review medicines and discuss the overall balance of benefit and harm. Direct acting oral anticoagulants Direct acting oral anticoagulants are usually shortened to DOACs. NICE recommends apixaban, dabigatran, edoxaban or rivaroxaban as options when anticoagulation is indicated and the medicine is suitable. They are preferred over warfarin for most eligible people with AF. Choice depends on kidney function, interactions, dosing schedule, bleeding profile and preference. DOACs are not interchangeable household medicines Each DOAC has its own dose rules and contraindications. Kidney function, age, weight and interacting medicines can alter the prescribed dose. Taking a lower unapproved dose may reduce stroke protection without safely removing bleeding risk. The medicine must be taken exactly as prescribed. Missed DOAC doses matter DOAC effects wear off relatively quickly. Repeated missed doses can leave someone without adequate stroke protection. The correct response to a missed dose depends on the particular medicine and timing. The person should follow the supplied instructions or contact a pharmacist or anticoagulation service rather than guessing or doubling doses. Warfarin Warfarin is a vitamin K antagonist. It remains appropriate when a DOAC is contraindicated, not tolerated or unsuitable. It is used for people with mechanical heart valves and commonly for AF with moderate or severe rheumatic mitral stenosis. Regular INR testing is required because food, illness and medicines can alter its effect. INR and time in therapeutic range The international normalised ratio is usually shortened to INR. It measures the anticoagulant effect of warfarin through part of the clotting system. The target range depends on the indication. Time in therapeutic range shows how consistently results remain within the intended range. Aspirin is not an alternative to anticoagulation Aspirin affects platelets rather than providing adequate anticoagulation for AF related stroke prevention. NICE advises against aspirin monotherapy solely for this purpose. Aspirin may still be prescribed for a separate coronary or vascular indication. Combining antiplatelet and anticoagulant treatment increases bleeding and needs a clear clinical reason. Anticoagulant monitoring DOACs do not require routine INR testing. They still require review of kidney function, liver function, blood count, adherence and interactions. Warfarin requires INR monitoring and dose adjustment. All anticoagulants need at least annual review, with more frequent assessment when health changes. Bleeding while anticoagulated Easy bruising and prolonged bleeding from small cuts can occur. Blood in urine, black stool, vomiting blood or uncontrolled bleeding requires urgent assessment. A sudden severe headache, neurological deficit or collapse can indicate intracranial bleeding. Anticoagulant treatment should not be stopped independently for minor bruising. Left atrial appendage occlusion A device can close the left atrial appendage in selected people. NICE considers this when anticoagulation is contraindicated or not tolerated. It is not a routine alternative for someone who can take anticoagulation safely. The procedure has its own risks and does not treat the electrical rhythm itself. Stroke prevention and symptom control are separate decisions Anticoagulation reduces thromboembolic risk. Rate or rhythm treatment aims to improve symptoms, cardiac function or both. Restoring sinus rhythm does not automatically remove the need for anticoagulation. A person may need anticoagulation even when no rate or rhythm medicine is required. Rate control Rate control accepts the atrial rhythm but limits how quickly impulses reach the ventricles. NICE recommends it as the usual first line strategy outside several important exceptions. The goal is symptom control and safe ventricular function rather than making the pulse perfectly regular. When rhythm control may be preferred earlier Rhythm control may be more suitable when AF has a reversible cause. It can be considered in new onset AF or when AF is thought to be causing heart failure. It may also be selected when symptoms continue despite adequate rate control. AF duration, atrial size, comorbidities and personal priorities influence the decision. Beta blockers A standard beta blocker can slow conduction through the atrioventricular node. Examples include bisoprolol and atenolol. The choice and dose depend on symptoms, heart rate, blood pressure and associated conditions. Possible effects include fatigue, low blood pressure, bradycardia and worsening of some airway symptoms. Rate limiting calcium channel blockers Diltiazem and verapamil can slow the ventricular response. They are options for people without contraindicating heart failure patterns. They can cause low blood pressure, ankle swelling, constipation or excessive slowing. They are generally avoided in HFrEF because they can worsen systolic function. Digoxin Digoxin increases vagal slowing through the atrioventricular node. NICE considers it as initial monotherapy for non paroxysmal AF in people who do little physical activity or cannot use other options. It controls resting rate less reliably during physical activity. Kidney function and medicine interactions affect toxicity risk. Combination rate control One medicine may not control symptoms sufficiently. NICE allows selected combinations involving a beta blocker, diltiazem or digoxin. Combining rate slowing medicines can cause bradycardia or heart block. Specialist or experienced clinical review is therefore important. Amiodarone is not routine long term rate control Amiodarone can slow the heart and maintain rhythm. Long term exposure can damage the thyroid, lungs, liver, eyes, skin and nerves. NICE advises against using it as ordinary long term rate control treatment. It has selected rhythm control and short term roles. Rhythm control Rhythm control aims to restore and maintain sinus rhythm. It can involve cardioversion, antiarrhythmic medicines or catheter ablation. Successful rhythm control may improve symptoms and ventricular function. AF can recur even after an initially successful treatment. Electrical cardioversion Electrical cardioversion delivers a synchronised electrical shock under sedation or anaesthesia. It resets atrial electrical activity and can restore sinus rhythm. It does not remove the underlying atrial tendency to develop AF. Recurrence is more likely when AF has lasted longer or structural disease remains. Pharmacological cardioversion Selected antiarrhythmic medicines can restore sinus rhythm without an electrical shock. The medicine depends on structural heart disease, ventricular function and the acute situation. Flecainide is unsuitable in known ischaemic or significant structural heart disease. Amiodarone has selected uses but substantial long term toxicity. Why AF duration matters before cardioversion Atrial clot risk increases when AF has continued beyond 48 hours or the start time is uncertain. Restoring atrial contraction can dislodge an existing clot. NICE therefore delays elective cardioversion until at least three weeks of therapeutic anticoagulation in this situation. A transoesophageal echocardiogram guided strategy can be considered in selected services. Cardioversion after recent onset AF When AF definitely began less than 48 hours earlier and the person is stable, rate or rhythm control can be considered. The decision depends on symptoms, recurrence risk, comorbidities and anticoagulation assessment. The 48 hour distinction must be applied clinically and is not a safe home timing rule. Emergency cardioversion Life threatening haemodynamic instability caused by new onset AF requires emergency electrical cardioversion. Treatment is not delayed to achieve prior anticoagulation. Features can include shock, severe ongoing ischaemia or critical pulmonary oedema. This is a hospital resuscitation decision. Long term antiarrhythmic medicines Antiarrhythmic medicines modify electrical conduction or recovery. Their safety depends on ventricular function, coronary disease, kidney function and other ECG findings. They can sometimes provoke a different dangerous arrhythmia. Selection and monitoring belong within an experienced clinical pathway. Pill in the pocket treatment Some people with infrequent symptomatic paroxysmal AF can take a prescribed antiarrhythmic when an episode begins. This is called a pill in the pocket strategy. It is reserved for carefully selected people without important structural or ischaemic heart disease. The medicine and first dose safety plan must be established by the clinical team. Catheter ablation Catheter ablation aims to isolate or destroy small areas supporting AF. Most procedures target electrical connections around the pulmonary veins. Heat, freezing or another specialised energy source can create controlled lesions. It is considered when drug treatment is unsuccessful, unsuitable or not tolerated in symptomatic paroxysmal or persistent AF. What ablation can and cannot do Ablation can reduce AF episodes and improve quality of life. It is not always successful, and repeat procedures may be required. Complications can include bleeding, vascular injury, cardiac perforation, stroke and damage to nearby structures. Anticoagulation decisions continue to depend on stroke risk rather than the apparent procedural success alone. Pulmonary vein isolation Pulmonary vein isolation creates an electrical barrier around the pulmonary vein openings. This prevents common triggering impulses from reaching the rest of the atrium. It does not physically close the veins or remove them. The procedure treats rhythm triggers rather than atherosclerotic disease. AV node ablation and pacing Atrioventricular node ablation deliberately blocks electrical conduction from atria to ventricles. A permanent pacemaker then controls the ventricular rhythm. This can help selected people with uncontrolled rate and severe symptoms after other treatments fail. It does not remove AF or eliminate atrial stroke risk. Pacemakers A pacemaker treats excessively slow rates or allows selected rate control strategies. It does not usually stop AF within the atria. Some devices record episodes and help quantify rhythm burden. A pacemaker alone is not a substitute for anticoagulation when stroke risk warrants treatment. Acute AF and haemodynamic stability A new rapid AF episode can reduce blood pressure and cardiac output. The team first assesses for shock, chest ischaemia, acute heart failure or loss of consciousness. Unstable AF requires emergency treatment. Stable acute AF allows time to address rate, rhythm, anticoagulation and the underlying trigger. AF with acute decompensated heart failure Rate slowing medicines require particular care during pulmonary oedema or severe ventricular failure. NICE advises senior specialist input before using beta blockers in this setting. Rate limiting calcium channel blockers are avoided because they can worsen cardiac function. Treating reversible contributors Infection, thyroid excess, electrolyte disturbance and acute alcohol effects require direct treatment. Managing the trigger does not replace stroke risk assessment. AF can recur after the apparent cause has resolved. Blood pressure control Hypertension increases AF recurrence, stroke and bleeding risk. Accurate measurement and effective treatment are central to long term care. Blood pressure control can also make anticoagulation safer. Weight and metabolic health Sustained weight reduction can improve AF symptoms in people living with obesity. Diabetes and lipid management reduce wider cardiovascular risk. Treatment should avoid extreme diets and should account for other health conditions. Sleep and sleep apnoea treatment Regular sleep and treatment of obstructive sleep apnoea may reduce rhythm recurrence. Continuous positive airway pressure is used when indicated. Sleep treatment supports, rather than replaces, anticoagulation and rhythm management. Exercise Regular moderate physical activity supports cardiovascular health and weight management. Exercise intensity may need adjustment during symptomatic episodes or uncontrolled rapid AF. A person with chest pain, severe breathlessness, faintness or sustained palpitations during exercise needs assessment. Caffeine Caffeine does not trigger AF in everyone. Some individuals notice a clear association with high intake or energy drinks. A practical approach is to avoid personally reproducible triggers without imposing unnecessary restrictions. Smoking Smoking increases cardiovascular and stroke risk. Stopping smoking benefits blood vessels, lungs and overall AF management. Evidence based cessation support is more effective than relying on willpower alone. Follow up AF care requires periodic review even when symptoms are stable. The team reassesses stroke risk, bleeding risk, ventricular rate and treatment effects. Kidney function can alter DOAC dosing. New heart failure, diabetes, vascular disease or increasing age can change the anticoagulation decision. When treatment is not controlling symptoms Persistent palpitations, breathlessness or exercise limitation require review. The rate may remain too fast, become too slow or vary excessively. Symptoms may also have another cause despite AF being present. NICE advises prompt specialist referral when treatment fails and more specialised management is needed. Living with AF Many people live active lives with AF. Understanding the emergency plan, anticoagulant safety and treatment purpose reduces uncertainty. The rhythm can affect confidence, sleep, exercise and mental wellbeing. Support should address psychological as well as physical effects. Prognosis AF increases the risk of stroke, heart failure and hospital admission. Risk varies greatly according to age and associated disease. Anticoagulation substantially reduces embolic stroke risk when appropriately prescribed. Rate, rhythm and risk factor treatment can improve symptoms and cardiac function. What this lesson should not be used for This lesson cannot diagnose AF from a pulse, smartwatch alert or symptom description. It cannot determine whether an individual should start anticoagulation or undergo cardioversion. Do not use CHA2DS2 VASc or ORBIT as home prescribing or stopping rules. Do not start aspirin as a substitute for anticoagulation. Call 999 for stroke symptoms, chest pain, severe breathlessness, collapse or an unstable fast irregular rhythm.

Atrial fibrillation is disorganised atrial electrical activity that usually produces an irregularly irregular ventricular rhythm. It may be symptomatic or silent. Management separates three questions: preventing stroke with risk based anticoagulation, controlling ventricular rate, and restoring sinus rhythm when symptoms or clinical circumstances justify it.