Overview
Anti-arrhythmics are used to manage arrhythmias, these can be ventricular or supraventricular (in the atria or the AV node). The arrhythmias can be caudes by defects in impulse generation in the SA node or defects in impulse conduction and propagation, leading to dropped beats or heart block.
There are various different causes for arrhythmias and each one needs different drugs. There is a classification system called the vaughan williams classification which is used in this teaching.
It is good to review cardiac electrical properties to gain a thorough understanding of this class, if you feel like it is a bit hard to remember.
Vaughan williams classification and MoAs of drugs
This classifies drugs into classes 1-4 based on what ionic current it alters, as well as ß-adrenergic activation. Lots dont fit into this classification however.
Class I - Na+ blockers
These have 3 sub classes Ia Ib and Ic
These bind to and disable Na+ channels, which means it slows conduction velocity. There is the unwanted effect of slower conduction leading to the induction of arrhythmias.
Uses:
Lignocaine (aka Lidocaine) may be used for polymorphic VT, and flecinide may be used for chemical cardioversion.
Class II - Autonomic modulators
Beta-blockers work reduce the effects of adrenaline and noradrenaline in the heart, where they reduce the rate of the funny current depolarisation in the cardiac conductilecells, reducing automaticity.
It can abolish ß-receptors firing at the SA node, it slows conduction velocity, especially around the AV node and may prevent reentrant tachycardia at this av site.
Examples:
- Metoprolol
- propranolol
Uses:
- Rate control in atrial fibrillation
- Treatment of SVTs and VTs precipitated by sympathetic signalling like stress and exercise
- prevent recurrent tachycardias
- decreasing mortality post MI
Adverse effects:
- Bronchospasm in asthmatics
- bradycardia and decreased inotrophy
- AV node block
Class III - K+ blockers
These block K+ channels which are involved in repolarisation of membrane potential. This means that they will prolong the duration of the action potential.
A note on amiodarone is that it can alter a number of other lipid membrane potential and effect both Na+ flux and well as Ca2+ ion channels. It is effective against a wide range of arrhythmias and is also used for refractory ventricular fibrillation after adrenaline or shock. amiodarine has lots and lots of adrs and also reduces warfarin and digoxin clearance.
Uses:
Adverse effects:
Examples:
Class IV - Ca2+ blockers
Cardioselective CCBs reduce Ca2+ entry into nodal cell and cardiomyocytes. This means that conduction is slowed and refractory period is lengthened at the AV node. It decreases the rate of discharge at the SA node so rate reduction.
In ventricular cardiomyocytes CCbs depress myocardial contraction.
Therefore this class decreases inotropy and chronotropy
Uses
It is used for rate control in supraventricular arrhythmias.
ADRs
There are quite a few, including:
- Nausea, headache, fatigue, constipation
- Hypotension
- Bradycardia and heart block
Examples
- Verapamil
- Diltiazem
Misc
Some drugs which do not fit into the vaughan williams classification to highlight are:
- Digoxin (It is a positive inotrope and an antiarrhythmic by way of increased vagal activity)
- Adenosine
- Atropine
Information about what to learn from the lecture
Learn the drugs:
- Metoprolol
- Amiodarone (not amlodipine)
- Diltiazem
- Digoxin
Learn AF treatment pathways:
- Rate control
- Pharmacological
- ß-blockers
- Ca2+ blockers
- Digoxin
- Amiodarone (in HF)
- non-pharmacological
- Ablate and pace
- Pharmacological
- Sinus Rhythm (SR) maintainance
- Pharmacological
- Class Ia
- Class Ib
- Class III
- ß-blockers
- Amiodarone
- non-pharmacological
- Cathether ablation
- Pacing
- Surgery
- Implantable devices
- Pharmacological
- Stroke prevention
- Pharmacological
- DOACs
- Dabigatran
- Rivaroxaban
- VKAs
- Warfarin
- DOACs
- non-pharmacological
- Sugrical isolation of LA
- Pharmacological