Atrial Fibrillation

• Atrial fibrillation (AF)


  A cardiac arrhythmia characterised by disorganised electrical activity within the atria, which results in ineffective atrial contraction and irregular ventricular contraction
• AF is the most common cardiac arrhythmia in adults
• Types of AF


  • Paroxysmal: episodes last >30 seconds but <7 days and are self-terminating but recurrent
  • Persistent: episodes last less than or more than seven days but require electrical or chemical cardioversion
  • Permanent: episodes fail to terminate with cardioversion OR a terminated episode that relapses within 24 hours OR long-standing AF (usually >1 year) in which cardioversion has not been indicated or attempted
• Sinoatrial node (SAN)


  The part of the cardiac conduction system that generates the electrical impulses that cause the heart to beat
• Atrioventricular node (AVN)


  The part of the cardiac conduction system that briefly delays the electrical impulse between the atria and ventricles
• Cardiac electrical conduction


  1. Electrical impulses generated in the SAN travel through the atria to the AVN

  2. The impulse is briefly delayed in the AVN

  3. The impulse then travels through the Bundle of His, down the left and right bundle branches, and to the Purkinje fibres, resulting in ventricular contraction
• Supraventricular arrhythmia


  An arrhythmia that originates from above the ventricles
• Micro re-entry circuits


  Chaotic electrical activity in the atria that sustains AF
• Conditions that cause atrial stretch

  Increase the substrate for AF
• AF begets AF


  AF causes the atria to dilate and increases the substrate for AF
• Virchow's triad


  The three factors that increase the risk of thrombosis: blood stasis, endothelial injury, and hypercoagulability
• Cardiac causes of AF

  • Heart failure
  • Structural pathology (e.g. valve stenosis or regurgitation)
  • Congenital heart disease
  • Atrial or ventricular dilation
  • Atrial or ventricular hypertrophy
  • Pre-excitation syndromes
  • Sick sinus syndrome
  • Inflammatory conditions
  • Infiltrative conditions
• Non-cardiac causes of AF

  • Acute infection
  • Electrolyte imbalances
  • Pulmonary embolism
  • Thyrotoxicosis or hypothyroidism
  • Diabetes mellitus
• Risk factors for AF

  • Male sex
  • Caucasian ethnicity
  • Increasing age
  • Alcohol
  • Cigarette smoking
  • Obesity
  • Co-morbidities (e.g. chronic kidney disease and obstructive sleep apnoea)
• Radial-apical deficit


  When each ventricular contraction is not sufficiently strong enough to transmit a pulse to the radial artery, so palpating only the radial artery can miss tachycardia
• Differential diagnoses for AF


  • Other supraventricular tachycardias
  • Ventricular ectopics
• Bedside investigations for suspected AF

  • Basic observations (vital signs)
  • 12-lead ECG
  • Ambulatory ECG
• Laboratory investigations for suspected AF

  • Full blood count
  • Urea & electrolytes
  • Liver function tests
  • Thyroid function tests
  • CRP
  • Clotting screen
  • BNP
• Imaging investigations for suspected AF

  • Echocardiogram
• Hepatic function


  Baseline to be established before giving anticoagulant drugs
• Thyroid function tests


  To assess for thyroid dysfunction. Raised T4 and low TSH levels indicate hyperthyroidism
• CRP


  To assess for a reversible cause such as acute infection. Raised CRP is suggestive of underlying infection
• Clotting screen


  To establish a baseline coagulation status before giving anticoagulant drugs
• BNP


  Can be considered to assess for underlying heart failure but should be interpreted with caution based on the patient's clinical presentation. AF in itself can cause a raised BNP without evidence of heart failure
• Imaging investigations in the context of suspected AF

  1. Echocardiogram: to assess for underlying structural or valvular disease and/or left ventricular systolic dysfunction

  2. Chest X-ray: to assess for changes associated with heart failure
• Diagnosis of AF


  European Society of Cardiology criteria: A standard 12-lead ECG recording or a single-lead ECG recording of ≥30 seconds showing a heart rhythm of no discernible repeating P-waves AND Irregular RR intervals
• Immediate management of AF

  1. ABCDE assessment to identify any adverse features

  2. If adverse features present, synchronised direct current cardioversion should be delivered
• Ongoing management of AF

  1. Anticoagulation is the primary consideration

  2. Rhythm control or rate control strategy based on symptoms and likelihood of maintaining sinus rhythm

  3. Management of modifiable AF risk factors is essential
• New-onset AF


  Rhythm control is an appropriate strategy for patients presenting with new-onset AF (defined as <48 hours)
• Electrical cardioversion


  Sedating/anaesthetising the patient and applying defibrillation pads to the patient's chest and delivering synchronised DC cardioversion
• Flecainide


  A class 1c antiarrhythmic drug that blocks sodium channels within the heart and thereby raises the threshold for depolarisation. Should not be used in patients with evidence of structural or ischaemic heart disease
• Amiodarone


  A class 3 antiarrhythmic drug that blocks potassium channels within the heart and thereby prolongs the refractory period of the myocardium. Can be used in patients with evidence of structural heart disease. May prolong the QT interval and should be avoided in patients with QT prolongation
• Anticoagulation for cardioversion


  Therapeutic anticoagulation is required for 4-6 weeks prior to and 4 weeks post either electrical or pharmacological cardioversion unless the onset of AF is within the last 48 hours, and it is a single isolated episode of AF
• Non-acute AF


  Rhythm control is an appropriate strategy for patients presenting with non-acute AF who have ongoing symptoms despite adequate rate control, or for patients whom a rate control strategy has not been successful
• Electrical cardioversion for non-acute AF


  Should be delayed until the patient has received adequate anticoagulation (i.e. 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 for non-acute AF

  Can be given for 4 weeks prior to electrical cardioversion and continued for 12 months following electrical cardioversion to maintain sinus rhythm
• Transoesophageal echocardiography-guided cardioversion


  Can confirm the absence of a thrombus and deliver cardioversion if waiting for adequate anticoagulation is not appropriate
• Beta-blockers


  The first-line drug for long-term rhythm control
• Amiodarone


  The most effective anti-arrhythmic drug, but it requires regular lung, liver and thyroid monitoring and should only be prescribed by a specialist
• Rate control


  An appropriate strategy for patients presenting with AF onset <48 hours or >48 hours, patients whose AF does not have a reversible cause, patients who do not have heart failure thought to be caused primarily by AF, and patients for whom rhythm control would not be more suitable based on clinical judgment