Atrial Fibrillation - Arrhythmias

Arrhythmias

·        For cardiac arrest rhythms (VT, VF, Torsade and asystole)

Atrial Fibrillation

·        = a type of supra-ventricular arrhythmia

·        Mechanism:

o   Wave of depolarisation circulates in atria at much faster rate than the discharge from the SA node. Disorders changing the conduction characteristics of the AV node predispose to AF: ­atrial size, fibrosis, inflammation, thyrotoxicosis, ischaemia, altered autonomic tone, alcohol use, after bypass surgery (30%), after valve replacement surgery (50%)

o   AV node receives irregular impulses at a rate of 250 – 400 per minute. Conducted through the node at a frequency dependent on the pathway‟s refractory period

o   Typical ventricular rate is 120 per minute: but this may ­ if sympathetic stimulation (® ¯refractory period) or alternative conducting path to the AV node (eg Wolf-Parkinson-White syndrome)

·        Epidemiology: most common cardiac arrhythmia.  M > F.  5% of over 70s

·        Causes:

o   IHD: especially post MI

o   Mitral valve disease

o   Alcohol

o   Thyroid disease

o   Idiopathic

·        Potential implications:

o   Thrombo-embolism: Especially cerebral (also mesenteric arteries or lower limbs). If no other risk factors then 1% per year. 5% if one other risk factor (age over 65, ­BP, heart failure, diabetes, IHD, previous embolism, RF). If RF and AF then 20% annual rate

o   Reduced cardiac output: ¯Ventricular filling ® ¯Cardiac output ® heart failure or ¯exercise tolerance. Also high ventricular rate ® ¯filling ® ¯CO

o   Other symptoms: palpitations (25%) and dizziness or syncope (20%)

·        Diagnosis: should always be confirmed by ECG. Ventricular rhythm in AF can be deceptively regular, and not all irregular rhythms are AF (eg variable AV block, ventricular or atrial ectopics)

·        Assessment:

o   Exclude thyrotoxicosis

o   Manage contributing MI, respiratory disease or alcohol abuse

o   Check electrolytes

o   Assess cardiovascular risk factors: eg glucose, lipids

o   Echocardiogram to assess atrial size or abnormal ventricles (eg valvular heart disease). These are harder to cardiovert (also have a higher risk of embolism). Echocardiogram is poor at detecting thrombis (trans-oesophageal echocardiogram is better)

·        Management:

o   Cardioversion: indicated if onset is within 24 – 48 hours and no other risk factors (eg no atrial enlargement or ventricular abnormality). Involves general anaesthetic and synchronised DC shock at 100 then 200J. Successful in about 85%. May need anticoagulation for cardioversion (thrombi may get dislodged if normal rhythm returns).

o   Chemical cardioversion: flecainide and amiodarone – successful in 60 – 90%. (Digoxin does not cardiovert)

o   > 50% revert in one year if no ongoing drug treatment

·        Drug treatment: consider digoxin (increases heart block ® slows ventricle ® improved pump action), flecainide (in those without structural heart disease), Amiodarone (extensive toxicity issues) or Sotalol:

o  Antithrombotic therapy: Reduces annual risk in those at risk from 5% to 1.5% (60% relative risk reduction), with 1% having material anti-coagulant side effects. Use warfarin with a goal of an INR from 2 to 3. Use aspirin if warfarin contra-indicated (only 10 – 15% relative risk reduction)

·        Atrial flutter: probably due to atrial re-entry. Regular atrial saw tooth pattern with ventricular beat every 3:1 or 4:1. If unstable hypotension, synchronised counter-shock at 50J (treat as for AF)