An approach to arrhythmia

  • fast or slow?
  • ventricular or supraventricular?
  • compromised or not?
  • does arrhythmia need management?
  • what is underlying substrate predisposition?
  • what is trigger?
  • will arrhythmia recur?


  • blocks and bradycardia are caused by impaired automaticity or conduction
  • if one pacemaker fails another generally takes over at a lower rate



  • reentrancy
  • automaticity (increased/abnormal)
  • triggered activity


  • impulse reaches a point where it can go two ways (A or B) -> if A is blocked then impulse can only go down B.
  • however, when impulse reaches a point where A and B re-join -> impulse may be retrogradely conducted up path A until it reaches the beginning and travels down path A creating a reentry loop.
  • the block that leads to rentry is often transient and timing dependent.
  • sometimes they do not even occupy a fixed anatomical location (ie. some forms of AF)


  • increased: normal spontaneous depolarisation is increased for some reason (adrenergic stimulation)
  • abnormal: local ischaemia, hypokalaemia, drugs

Trigger Activity

  • = ‘after depolarisation’ where normal action potential suddenly swings positive again allowing another depolarisation to occur abnormally.
  • early after depolarisations: occur before repolarisation has finished (partial blockade of Ik)
  • delayed after depolarisations: occur after membrane potential has returned to normal (from raised intracellular Ca2+)



  • MI
  • hypertrophy
  • myopathic ventricle
  • ischaemia
  • congenital defects


  • hypoxia
  • acidosis
  • electrolytes
  • catecholamines


  • catecholamines
  • proarrhythmic drugs
  • anti-arrhythmics in certain situations:
    • -> toxicity (increased dose or reduced clearance)
    • -> severe LVF -> digoxin
    • -> brachycardia


  • Simple, but problematic as many drugs fall into multiple classes

Class 1 – inhibit fast Na+ channels

  • inhibit fast voltage sensitive sodium channels during depolarisation (phase 0) of cardiac action potential -> decreased depolarization & conduction velocity. -> membrane stabilisers

1a – Prolonged AP duration

  • decrease rate of phase 0 depolarisation -> reducing the excitability of the non-nodal regions in the heart which are important for propagation of the action potential.
  • lengthen duration of action potential
  • ie. quinidine, procainamdie

1b – Shortened AP duration

  • decrease rate of spontaneous phase 4 outside the atria -> decreases automaticity
  • ie. lignocaine, phenytoin

1c – No change in AP duration

  • potent Na+ channel blockers -> decrease in rate of phase 0 depolarisation and speed of conduction of cardiac impulses.
  • little effect on the duration of cardiac action potential & effective refractory period in ventricular myocardial cells
  • shortens the duration of the action potential in Purkinje fibres.
  • ie. flecanide, encainide

Class II – decrease rate of depolarisation (beta blockers)

  • beta-adrenoceptor antagonists
  • increase effective refractory period of AV node & decreased automaticity, decreased QT duration -> decrease HR & O2 consumption
  • ie. metoprolol, esmolol, propanolol

Class III – inhibit K+ ion channels

  • prolong the refractory period block K+ channel -> prolong cardiac depolarisation, action potential duration & effective refractory period. -> decrease the time in which the cardiac muscle cells are excitable.
  • ie. amiodarone, sotalol, bretylium
  • amiodarone has some class I ( Na channel), II (beta-blocker), III (K+ channel) & IV effects (Ca2+ channel)

Class IV – inhibit slow Ca2+ channels

  • inhibit inward slow calcium ion currents that may contribute to development of VT
  • block L type Ca2+ channels -> impair SA node pacemaker activity.
  • decrease duration of action potential but no effect on automaticity
  • ie. verapamil, diltiazem, nifedipine


Mannik MD’s medical rap for learning about anti-arrhythmic drugs


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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