Revision of the cardiac action potential and conduction. Potential mechanisms of arrhythmias. Drugs used in the treatment of arrhythmias will be examined at a cellular and systems level.
Categories of Disturbances in Cardiac Rhythm
Delayed after-depolarisation
Re-entry
Abnormal pacemaker activity
heart block
Classification of Anti-Arrhythmic Drugs (Vaughn-
Williams Classification)
Class I → sodium (Na+) channel blockers
→ membrane - stabalising agents
How it works
Binds to Na+ channels → prevent conduction of ions
The more the heart is used the more the drug binds
binds preferentially to open channel state (use dependant)
3 sub classes
Class IA
Moderate blocker
moderately depress phase 0 of
cardiac AP → prolonged
depolarisation by limiting excitation
↓ slope of phase 4 depolarisation →
shift threshold voltage towards 0
↑ fibrillation threshold in atria
and ventricles
Cardiac Arrhythmias 1
, harder to have a heart rhythm
→ harder to fibrilate
↓ or block AV node conduction
used to treat atrial fibrillation (AF)
↑ effective refractory period (ERP)
Example
Quinidine
Procainamide
Disopyramide
It inhibits the fast sodium
channels
Class IB
Weak blocker
minimal phase 0 depression →
slows conduction
shortens repolarisation
used to treat ventricular arrhythmias
↓ ERP → little effect on refractoriness /
responsiveness
Example
Lignocaine (Lidocaine)
local anaesthetic
stabilising the neuronal
membrane by inhibiting the
ionic fluxes required for the
initiation and conduction of
impulses, thereby effecting local
anaesthetic action
acts on sodium ion channels
located on the internal surface
of nerve cell membranes
Cardiac Arrhythmias 2
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