This is an atrial rhythm which is ineffective, chaotic and irregular, usually of around 300-600 bpm.
50% of paroxysmal (as in, episodic) and 15-20% of chronic AF are idiopathic. Secondary AF is caused by dilatation, increased muscle mass or inflammation, infiltration and fibrosis.
AF is generally associated with left atrium hypertrophy. The ineffective contractions result in blood stasis (getting stuck) in the atria. This predisposes to thrombus formation - from the left atrium, this can mean a CVA; in the right atrium, this can mean PEs.
There are three types of AF:
- Acute AF - associated with systemic disease, often precipated by electrolyte disturbance or hypoxia, resolves with treatment of underlying pathology
- Paroxysmal AF - recurrent episodes of AF lasting less than 48 hours which can progress to:
- Chronic AF - aka permanent AF. It's permanent - go figure.
- Heart disease such as coronary artery occlusion, cardiac valve disease, pericarditis, congenital heart disease, etc - pretty much any heart problems make it more likely.
- Lung diseases especially pneumonia, lung cancer, and PE
- Drinking too much - alcohol can cause it, commonly seen in binge drinking.
- Carbon monoxide poisoning
Before it gets to the stage of chronic AF, really the only signs are vague - namely fatigue and dyspnoea. Pretty unhelpful really.
Chronic phase has some other
- Irregular pulse (some of the impulses from the atria reach the ventricle, throwing it out of sinus rhythm). The force of contraction will also be irregular
- deterioration with exercise
- absent 'a' waves in JVP
- insensitivity to carotid massage
- thromboembolic events - CVA and PE. This will probably become more obvious as the patient might die.
In chronic AF, you can just take an ECG but in other forms, you may needs a 24h ECG (aka 24h tape).
- No P waves
- irregular QRS complexes (though they are sometimes normal)
- transient flutter waves in V1
- Echocardiography - size of left atrium, left ventricular function, may require transoesophageal echo for assessment of thrombus formation.
The aim of management should be a return to sinus rhythm. This may not always be possible - control of ventricular rate and thromboembolism prevention are what you aim for in lieu of this.
Avoid alcohol and caffeine. Correct underlying pathologies - usually electrolyte disturbance or hypoxia.
Cardioversion and pacing are explained above. Others are:
- Surgery - using strips of myocardium: creating connections between the SAN and the AVN (corridor procedure) or channeling depolariation across the atria (maze procedure).
- Percuatneous radiofrequency ablation - stick a catheter up the femoral vein to the heart with radiological guidance. Do tests and ablate some stuff to stop the AF.
- Acute onset - this is only an issue if haemodynamicaly unstable. You do: emergency cardioversion if it's life-threatening; hasty cardioversion if not life-threatening - with IV amiodarone (a class III antiarrhythmic) if there's a delay.
- Paroxysmal - treatment only required if symptomatic. Use beta-blockers 1st-line; class Ic antiarrhythmics second-line (e.g. flecanide); sotalol (class III) with CAD where beta-blocker fails; amiodarone in poor left ventricular function where beta-blockers fail.
- Rate-control strategy- digoxin + rate-limiting calcium-channel blocker/beta blocker. If this fails, consider pacemaker + ablation. Patient should be: <65 years old; symptomatic; presenting for the 1st time; lone AF; or congestive heart failure.
- Rhythm-control strategy - chemical cardioversion (amiodarone), beta-blocker if necessary. 2nd-line: class Ic (e.g. flecanide) or sotalol (class III), amiodarone in structural heart disease. Patietns should be: >65 years old; coronary heart disease; contraindications to antiarrhythmics or cardioversion; no congestive heart failure.
Use warfarin - it reduces the incidence of stroke by 70%. If you can't, use aspirin.