Session 7: Antiarrhythmics Flashcards
(81 cards)
Where might you find arrhythmias in the heart?
When there is something wrong with either AV or SA node.
When there is a contraction impulse induction issue of the cardiac tissue.
A combination of the two.
When an abnormal impulse is generated in arrhythmias, what are the two types of rhythms?
Automatic rhythms such as enhanced normal automaticity where there are more action potentials from SA node, or ectopic foci.
Triggered rhythms where there is either delayed afterdepolarisation or early afterdepolarisation.
An arrhythmia doesn’t have to be due to an abnormal impulse generation but could be instead due to abnormal conduction.
What types of abnormal conductions are there?
Conduction block such as 1st, 2nd or 3rd degree heart block.
Reentry loops such as circus movements or reflections.
Explain the pathology in wolff-parkinson-white syndrome.
There is an accessory pathway in the heart called the bundle of kent. Here the impulse can re-enter the atrium and reach the AV node again.

Give another example of a cause of a re-entry loop.
An area of an infarct.
This can cause re-entry in the scar.
What part of action potential do you aim to target in the case of an abnormal impulse generation?
Decreasing phase 4 slope in the pacemaker cells.
or
Raising the threshold of action potential.

What part of the action potential do you aim to target in the case of an abnormal conduction?
Decreasing the conduction velocity in phase 0.
or
Increasing the effective refractory period so the cell won’t be re-excited again.
So why do arrhythmias occur?
Automatic or triggered activity
Re-entry due to scar, or WPW syndrome.
What are the broad functions of antiarrhythmic drugs?
Decrease conduction velocity
Change the duration of ERP
Suppress abnormal automaticity
Give examples of class 1A agents.
Procainamide
Quinide
Disopyramide
How are class 1A drugs administered?
Oral or IV
Actions of class 1A drugs?
Decreased conduction by decreasing phase 0.
Increasing refractory period by prolonging action potential duration and NA inactivation.
Target automaticity by decreasing the slope of phase 4 in fast potentials.
Increase the threshold.
Special properties of quinidine.
Anticholinergic to speed AV conduction used with digitalis, beta-blockers or CCBs.
Class 1A effects on ECG.
Increased QRS
Increased PR
Increased QT
Uses of class 1A drugs.
Quinidine: atrial fibrilliation, atrial flutter and preent recurrence. Also for Brugada syndrome.
Procainamide: acute IV treatment of supraventricular and ventricular arrhythmias.
Side effects of class 1A drugs.
Hypotension
Pro-arrhythmic like Torsades de Points
Dizziness, confusion, insomnia, seizures
GI effects
Lupus-like syndrome.
Give examples of class 1B drugs.
Lidocaine
Mexiletine
Administration of lidocaine and mexiletine.
Lidocaine is IV only
Mexiletine is oral.
Effects on cardiac activity by class 1B drugs.
No change in phase 0 in normal tissue
APD will slightly decrease
Increased threshold of action potential
Decrease in phase 0 conduction in fast beating or ischaemic tissue.
Effects on ECG of class 1B drugs.
No changes in normal tissue.
In fast beating or ischaemic tissue there will be an increase in QRS.
Uses of class 1B drugs.
Acute ventricular tachycardia
Not used in atrial arrhythmias or AV junctional arrhythmias
Side effects of class 1B drugs.
Proarrhythmic but less so than class 1A.
CNS effects such as dizziness or drowsiness
GI problems.
Give examples of class 1C drugs.
Flecainide
Propafenone
Administration of flecainide and propafenone.
Oral or IV