Atrial Fibrillation Basics


Atrial Fibrillation: Background

Atrial Fibrillation – described as a ‘chaotic electric storm’ of the sino-atrial (SA) node is a cardiac dysrhythmia which results in irregular atrial discharges between 300-600/min. The irregular, non-stop arrival of conductance to the AV node leads to uncoordinated contraction (Warning: Real Heart!) between the atria and ventricles – thus leading to decreased stroke volume and arterial pressure, left heart failure and right heart failure – typically in that order.

What is important to note conceptually about AF is that while the ‘fibrillating’ SA node may be discharging electrical activity at rates from 300-600/minute not all of the electrical signals are conducted through the AV node – which permits a physiological maximum of approximately 200/min.


Causes of Atrial Fibrillation

The causes of A.Fib can be divided into 4 categories: anything which can damage the conducting electrical system can cause A.Fib.

  • STARVE – Infarction or Ischaemia (typically old ischaemia – i.e. MI does not commonly present as Atrial Fibrillation)
  • STRETCH – Mitral Regurg, HOCM, CHF, Pulm HTN, P.E., COPD
  • POISON – Acute Alcohol Use (‘Holiday Heart’), Chronic Alcohol Use (Dilated Cardiomyopathy), Caffeine, Thyrotoxicosis
  • INFILTRATION – Haemochromatosis (*Note: Reversible & Common Cause), Sarcoidosis, Endo/Myocarditis, Amyloidosis


Clinical Presentation:

  • Typically an elderly patient (approximately 10 % of individuals > 75yrs)
  • An ‘irregularly irregular’ pulse
  • Evidence of a ‘pulse deficit’ – Clinical maneuver described below:
    • Palpate the radial artery and auscultate the Mitral valve (5th ICS MCL)
    • Due to varying stroke volumes – the ventricular contraction during A.Fib may be too weak to generate enough pressure to open the Aortic valve (>60mmHg) but may be strong enough to open (and therefore close) the mitral valve.
    • This leads to a heart sound on auscultation – without corresponding palpable pulse = +ve Pulse Deficit
  • JVP analysis may reveal an increased JVP without a-waves (particularly in the unstable A.Fib patient)
  • Signs/Symptoms of Congestive Heart Failure


ECG interpretation in AF

The 2 key questions which needs to be asked when assessing a patients rhythm in A.Fib is the following: “Does this ECG have clearly discernable P-waves” and secondly “Is it boringly regular” – if the answer is NO to either of these questions – you should begin thinking about the possibility of A. Fib.

Note: While the terms Fast AF and Slow AF are used commonly in clinical practice – it is important to realise that at a physiological level, all AF is ‘fast’ – with electrical impulses  consistently 300-600/min. Fast vs. Slow AF refer to the ‘ventricular response rate’ – thus the correct term should be AF with either 1. Fast ventricular response or 2. Slow ventricular response. Fast ventricular response can furthermore be divided in either Stable or Unstable AF – depending on vitals such as blood pressure and the clinical symptoms.

Characteristic Findings

  • Absent P-Waves
  • Narrow Q-waves
  • Irregular R-R interval
  • Fibrillatory ‘f’ waves (300-600/min)

A Fib


  1. Rate Control (Beta Blocker/CCB = 1st Line)
  2. Anticoagulate (Warfarin/NOAC)


3. Rhythm control (Young patients, First episode of A.Fib, Caused by ↑↓Electrolytes)

  • D/C Cardioversion (100 joules –> 200 joules –> 360 joules)
  • Chemical Cardioversion (Amiodarone – 300mg x 1hour, followed by 900mg over 23 hrs)


Anti-coagulation in A. Fib

Obviously, the key risk of atrial fibrillation is with regards to stroke. Mean stroke risk in a patient with atrial fibrillation is 4% per year. This risk decreases to ~1% per year with Warfarin (65% Risk Reduction). Anatomically, the left atrial appendage is the site of systemic embolism in >90% of patients.

The CHADsVASc scoring system can be applied to individuals with Atrial Fibrillation to assess need for anticoagulation and yearly stroke risk. Of note, patients with A.Fib and no risk factors (CHADsVASc = 0) do not routinely require anti-coagulation, furthermore, the concomitant use of a HASBLED score – may help determine whether a patients risk of bleeding while on anti-coagulation outweighs the potential benefit of stroke prevention.

The increasing use of Novel Oral Anticoagulants (NOAC’s) has been bred out of wishes for a cleaner alternative to Warfarin. Best studies indicate that patients on Warfarin for A.Fib spend only 60 – 70% of the time within typical therapeutic range (2 – 3 for non-valvular AF/ 3 – 4 for mechanical valves/valvular AF).


Key Anti-Coagulation Trials

1. ACTIVE-W trial (Warfarin vs. Clopidogrel + Aspirin) – Warfarin > Anti-platelets

2. RE-LY trial (Dabigatran) – 150mg of Dabigatran > Warfarin

3. ROCKET-AF trial (Rivoroxaban) – Equivalant to Warfarin with decreased bleeding risk

4. ARISTOTLE/AVERROES trials (APIXABAN) –  Equivalent to Warfarin

  • Renal Clearance w/ NOACs – Dabigatran (80% renal excretion), Rivoroxaban (50% renal excretion), Apixaban (25% excretion)


(Last Updated – April 2016)


3 Comments Add yours

  1. Eoin says:

    Fascinating stuff.


  2. Pingback: Stroke Management

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