Atrial Fibrillation


Atrial fibrillation (AF) is the most common sustained dysrhythmia and is characterised by disorganised atrial electrical activity and contraction resulting in an “irregularly irregular” ventricular response (“fibrillation waves”)

  • AF may be acute, transient, paroxysmal, or chronic and may or may not be rate-controlled
  • Patients with AF may be stable or unstable
  • AF has multiple possible underlying causes
  • The incidence and prevalence of AF is increasing, with a lifetime risk for people over the age of 40 years of ~25%
  • AF prevalence increases with age
  • AF is a common occurrence post cardiac surgery (10-40%, typically day 2 to 3)


The classification below is according to pathophysiological mechanism

  • Alternatively, can causes can be classified according to a ‘surgical sieve’ (e.g. vascular, inflammatory, trauma, etc)

Catecholamine excess or increased sensitivity

  • Exogenous (eg. adrenaline infusion, hydrocarbon exposure)
  • Endogenous
    • Subarachnoid haemorrhage
    • Stress
    • Phaeochromocytoma
    • Thyrotoxicosis

Atrial distension

  • Pulmonary hypertension
    • primary
    • secondary, such as OSA, PE, pulmonary fibrosis
  • Septal defects
  • Valvular disease (e.g. mitral stenosis), including infective endocarditis

Abnormality of conducting system

  • Congenital cardiac disease, eg. septal defect
  • Infiltrative cardiac disease, eg. amyloidosis, sarcoidosis
  • Ischaemic heart disease
  • Age-related fibrotic changes
  • Haemochromatosis/iron overload
  • Hypothermia

Increased atrial automaticity / irritation

  • Alcohol (“holiday heart”)
  • Caffeine
  • Catecholamines
  • Electrolyte derangement (hypokalaemia, hypomagnesaemia)
  • Myocarditis


Adverse effects on haemodynamics:

  • loss of atrial systole (aka “atrial kick”) (normally responsible for about 20% of ventricular filling)
  • Decreased diastolic filling time due to tachycardia
  • Rate-related cardiomyopathy (can occur over weeks)

Atrial thrombus formation

  • Systemic embolism, especially stroke
  • Pulmonary embolism

Annual risk of embolic stroke from AF

  • The CHA2DS2-VASc scoring system is recommended for estimating the risk of stroke (Lip et al, 2002; January et al, 2014)
  • There are 3 categories:
    • score 0: negligible risk of stroke (~ 0%/y) (very few patients!)
    • score 1: 1.3%/y risk of stroke
    • score >1 (2 or more): >2.2% risk of stroke (high risk category)
  • The maximum score of 9 predicts a 15.2%/y risk of stroke
  • A CHA2DS2VASC calculator is available on MDCalc
C Congestive heart failure (or Left ventricular systolic dysfunction) 1
HHypertension: blood pressure consistently above 140/90 mmHg (or treated hypertension on medication) 1
A2Age ≥75 years2
DDiabetes Mellitus1
S2Prior Stroke or TIA or thromboembolism2
VVascular disease (e.g. peripheral artery disease, myocardial infarction, aortic plaque)1
AAge 65–74 years1
ScSex category (female sex score 1 point)1



  • 12 lead ECG
  • blood gas (e.g. hypokalaemia)


  • UEC (e.g. hypokalaemia)
  • CaMgPO4 (e.g. hypomagnesemia)
  • FBC (e.g. anaemia)
  • TFTs (e.g. hyperthyroidism)


  • CXR (e.g. cardiomegaly, atrial dilation, pulmonary odema, other lung disease)
  • Echocardiography (e.g. structural heart disease, TOE to exclude atrial thrombus)



  • address life threats, determine if stable or unstable
  • Unstable features (if significant and attributable to AF)
    • chest pain
    • dyspnoea
    • heart failure
    • hypotension
  • Electrical cardioversion
    • start at 100J (synhronised), then increased to 150J (ALS guidelines, in practice 50J may be successful)
    • provide procedural sedation

Specific treatments for stable AF patients (see below)

  • rate control versus rhythm control
  • anticoagulation

Seek and treat underlying cause and complications

  • replace electrolytes (e.g. K > 4 mmol/L, Mg > 0.9 mmol/L)
  • treat cause (e.g. ischaemia, sepsis, thyroid function)

Ablation therapy is indicated if:

  • permanent AF where ventricular rate difficult to control and persistent symptoms/LV dysfunction
  • rate-related cardiomyopathy due to refractory AF
  • refractory symptomatic paroxysmal AF


  • stable patients may be discharged with outpatient follow up following cardioversion or rate-control
  • cardiology referral for patients requiring specialist follow-up
  • patients with a significant underlying cause or comorbidities require admission to hospital
    • some require cardiac monitoring
    • those with critical illness require HDU/ ICU


Rate control with anticoagulation is the strategy of choice, rather than rhythm control, for most patients

  • Prior to the 2000s, rhythm control was preferred due to theoretical benefits from preventing cardiac remodelling due to chronic AF
  • However, rate control was supported by a number of studies from the early 2000s (AFFRIM, RACE, STAF, and PIAF)
  • A subsequent meta-analysis of 8 high-quality studies (n=7499) by Caldeira et al, 2012 found:
    • no clear survival benefit for rate control over rhythm control
    • composite endpoint (death, stroke and recurrent hospitalisation) favours rate-control

Rate control strategies

  • Recommendations based on the 2014 AHA guideline:
    • β-blocker or calcium channel blocker for paroxysmal AF
      • can be given IV if hemodynamically stable (CCBs preferred in COPD patients)
    • IV amiodarone for critically ill patients
    • AV nodal blockade (e.g. BB, CCB, amiodarone) is not recommended in patients with pre-excitation (e.g. Wolff-Parkinson-White) – procainamide (not widely available in Australia) or electrical cardioversion is the better choice
    • avoid calcium channel blockers in decompensated heart failure (digoxin or amiodarone are preferred). Combination of digoxin and a β-blocker recommended for long-term management of compensated heart failure patients.
    • target a rate of 80 as the endpoint, however, higher rates (e.g. ~110/min) are acceptable in stable patients with preserved LV function
  • Digoxin is slow acting and ineffective in patients with increased sympathetic tone (most critically ill patients)

Rhythm control strategies

  • DC cardioversion
    • essential in unstable patients
    • is also an effective strategy when performed electively using procedural sedation within 48 hours of AF onset or later following adequate anticoagulation and TOE
  • Pharmacological options for cardioversion can be used in hemodynamically stable patients
    • amiodarone
    • flecanide (only an option in structurally normal hearts, as associated with sudden cardiac death in structurally abnormal hearts)
    • propafenone
    • vernakalant
  • Options for maintenance of sinus rhythm inlcude:
    • amiodarone
    • disopyramide
    • flecanide
    • sotolol


2014 AHA recommendations for anticoagulation:

  • No anticoagulation is reasonable choice if the AF <48 hours and the CHA2DS2-VASc score is 0
    • risk of stroke is 0.2% pa
    • If AF <48 hours and the score is >0, therapeutic anticoagulation (e.g. IV heparin, enoxaparin)
  • If AF >48 hours: therapeutic anticoagulation (e.g. IV heparin, enoxaparin)
  • Anticoagulation should continue for at least 3 weeks before and 4 weeks after TOE-cardioversion
    • aspirin is an option if CHA2DS2-VASc score =1
    • Warfarin (INR 2-3) or equivalent if CHA2DS2-VASc score >1 (e.g. all patients >75-years-old)

The effectiveness of different anticoagulation therapies for stroke prevention per year:

  • Warfarin: RRR 62%; ARR 2.8%
  • Aspirin: RRR 22%; ARR 1.5%
  • Warfarin plus aspirin: no additional benefit over warfarin alone
  • Dabigatran: RRR 35% compared to warfarin

Benefits of anticoagulation should always be weighed against the harms (e.g. falls risk, coexistent bleeding diathesis)

  • No anticoagulation is also reasonable if there is increased bleeding risk and/or AF is likely transient (e.g. post-cardiac surgery, many ICU patients)


Most textbooks and literature focus on the management of AF in the ward, emergency department, or outpatient setting.

Differences in the ICU include:

  • AF is often transient (only about 15% of patients with AF in ICU will still be in AF at the time of ICU discharge (Artucio et al, 1990).
  • AF is usually caused by reversible, non-cardiac underlying illnesses (Kanji et al, 2012), such as hypoxia, electrolyte abnormalities, and sepsis
  • implications for patient outcomes are different for ICU patients with AF
    • unclear if AF is a cause of, or secondary marker of, greater illness severity in ICU patients overall
    • death from stroke is less likely
    • multi-organ dysfunction is more likely (e.g. worsening shock state)
  • a standardised approach to pharmacotherapy is lacking (Kanjii et al, 2008)
    • Amiodarone is commonly used but has a relatively poor cardioversion success rate (40-76% at 12 h)
    • Cardioversion success rate at 12h for other options:
      • Esmolol and flecainide: 60-100%
      • Magnesium: 51-93%
  • many ICU patients with AF have a higher risk of bleeding (e.g. post-cardiac surgery), so anticoagulation for persistent AF is typically delayed


If AF with slow ventricular response, suspect:

FOAM and web resources

Journal articles


CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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