- Atrial Fibrillation (AF) is the most common sustained arrhythmia.
- The incidence and prevalence of AF is increasing.
- Lifetime risk over the age of 40 years is ~25%.
- Complications of AF include haemodynamic instability, cardiomyopathy, cardiac failure, and embolic events such as stroke.
- Characterised by disorganised atrial electrical activity and contraction.
Mechanism of Atrial Fibrillation
The mechanisms underlying AF are not fully understood but it requires an initiating event (focal atrial activity / PACs) and substrate for maintenance (i.e. dilated left atrium).
Some proposed mechanisms are:
- Focal activation – In which AF originates from an area of focal activity. This activity may be triggered, due to increased automaticity, or from micro re-entry. Often located in the pulmonary veins.
- Multiple wavelet mechanism – In which multiple small wandering wavelets are formed. The fibrillation is maintained by re-entry circuits formed by some of the wavelets. This process is potentiated in the presence of a dilated LA — the larger surface area facilitates continuous waveform propagation.
Causes of Atrial Fibrillation
There are multiple causes of AF, including:
- Ischaemic heart disease
- Valvular heart disease (esp. mitral stenosis / regurgitation)
- Acute infections
- Electrolyte disturbance (hypokalaemia, hypomagnesaemia)
- Drugs (e.g. sympathomimetics)
- Pulmonary embolus
- Pericardial disease
- Acid-base disturbance
- Pre-excitation syndromes
- Cardiomyopathies: dilated, hypertrophic.
ECG Features of Atrial Fibrillation
- Irregularly irregular rhythm.
- No P waves.
- Absence of an isoelectric baseline.
- Variable ventricular rate.
- QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction.
- Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm).
- Fibrillatory waves may mimic P waves leading to misdiagnosis.
- Ashman’s Phenomenon – presences of aberrantly conducted beats, usually of RBBB morphology, due a long refractory period as determined by the preceding R-R interval.
- The ventricular response and thus ventricular rate in AF is dependent on several factors including vagal tone, other pacemaker foci, AV node function, refractory period, and medications.
- Commonly AF is associated with a ventricular rate ~ 110 – 160.
- AF is often described as having ‘rapid ventricular response’ once the ventricular rate is > 100 bpm.
- ‘Slow’ AF is a term often used to describe AF with a ventricular rate < 60 bpm.
- Causes of ‘slow’ AF include hypothermia, digoxin toxicity, medications, and sinus node dysfunction.
Classification of Atrial Fibrillation
Classification is dependent on the presentation and duration of atrial fibrillation as below:
- First episode – initial detection of AF regardless of symptoms or duration
- Recurrent AF – More than 2 episodes of AF
- Paroxysmal AF – Self terminating episode < 7 days
- Persistent AF – Not self terminating, duration > 7 days
- Long-standing persistent AF – > 1 year
- Permanent (Accepted) AF – Duration > 1 yr in which rhythm control interventions are not pursued or are unsuccessful
Note paroxysmal AF of > 48 hr duration is unlikely to spontaneously revert to sinus rhythm and anticoagulation must be considered.
Management of Atrial Fibrillation
Management of atrial fibrillation is complex depending on duration of atrial fibrillation, co-morbidities, underlying cause, symptoms, and age.
Management of atrial fibrillation can be considered in a step-wise manner:
- Diagnosis of atrial fibrillation.
- Assessment of duration.
- Assessment for anticoagulation.
- Rate or rhythm control.
- Treatment of underlying / associated diseases.
Guidelines for the Management of Atrial Fibrillation
A number of national and international guidelines exist for the management of AF including:
- European Society of Cardiology Guidelines 2010
- American College of Cardiology Foundation / American Heart Association / Heart Rhythm Society Guidelines 2011 Update
- American College of Cardiology Foundation / American Heart Association / Heart Rhythm Society 2006 Guideline
- Canadian Cardiovascular Society Guidelines 2010
- NICE Guideline 2006 – currently under review.
Risk of Stroke and Anticoagulation
- Atrial fibrillation is associated with disorganised atrial contraction and stasis within the left atrial appendage with associated thrombus formation and risk of embolic stroke.
- AF associated with valvular disease has a particularly high risk of stroke.
- Guideline recommendations for stroke prevention and anticoagulation also include atrial flutter due to the high likelihood of these patients developing AF.
- Anticoagulation strategies may include warfarin, aspirin, clopidogrel and newer agents such as dabigatran.
- Anticoagulation guidelines are based on risk of stroke vs. risk of bleeding.
- Stroke risk stratification requires either an assessment of risk factors or application of a risk score e.g. CHADS2 or CHA2DS2VASc.
- CHADS2 is a commonly used risk score and is shown below.
|Congestive heart failure||1 point|
|Age > 75yrs||1 point|
|Stroke / TIA||2 points|
Low risk = 0 Points, Moderate Risk = 1 Point, High Risk = 2 Points
Atrial Fibrillation in WPW
ECG features of Atrial Fibrillation in WPW are:
- Rate > 200 bpm
- Irregular rhythm
- Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway
- QRS Complexes change in shape and morphology
- Axis remains stable unlike Polymorphic VT
- Treatment with AV nodal blocking drugs e.g. adenosine, calcium-channel blockers, beta-blockers may increase conduction via the accessory pathway with a resultant increase in ventricular rate and possible degeneration into VT or VF
- In a haemodynamically unstable patient urgent synchronised DC cardioversion is required.
- Medical treatment options in a stable patient include procainamide or ibutilide, although DC cardioversion may be preferred.
Read more about WPW here.
- Irregular ventricular response .
- Coarse fibrillatory waves are visible in V1.
- “Sagging” ST segment depression is visible in V6, II, III and aVF, suggestive of digoxin effect.
- Irregular ventricular response.
- Coarse fibrillatory waves are visible in V1.
- Irregular ventricular response.
- No evidence of organised atrial activity.
- Fine fibrillatory waves seen in V1.
AF with rapid ventricular response
- Irregular narrow-complex tachycardia at ~135 bpm.
- Coarse fibrillatory waves in V1.
AF with slow ventricular response
- Irregular heart rate with no evidence of organised atrial activity.
- Fine fibrillatory waves in V1.
- ST depression / T wave inversion in the lateral leads could represent ischaemia or digoxin effect.
- The slow ventricular rate suggests that the patient is being treated with an AV-nodal blocking drug (e.g. beta-blocker, verapamil/diltiazem, digoxin). Another cause of slow AF is hypothermia.
- Atrial fibrillation is diagnosed based on the irregular ventricular rate and presence of fibrillatory waves in V1.
- The third QRS complex is aberrantly conducted: it is broad with a different axis and morphology and occurs following a long RR / short RR cycle (= Ashman aberrancy).
- There are two aberrantly conducted complexes — each follows a long RR / short RR cycle (= Ashman aberrancy).
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