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 bradycardias are caused by impaired automaticity or conduction
- if one pacemaker fails another generally takes over at a lower rate
- 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
- = ‘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+)
FACTORS CONTRIBUTING TO ARRHYTHMOGENESIS
- myopathic ventricle
- congenital defects
- proarrhythmic drugs
- anti-arrhythmics in certain situations:
-> toxicity (increased dose or reduced clearance)
-> severe LVF
VAUGHAN-WILLIAMS CLASSIFICATION OF ANTI-ARRHYTHMICS
- 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