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Lecture notes

Anti arrhythmic agents

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These notes explain anti-arrhythmic drugs using the Vaughan Williams classification, linking ion channel modulation to changes in cardiac action potentials, ECG findings, clinical uses, and adverse effects, supported by diagrams and colour-coded highlights.

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learning objectives



·
different types of arrhythmia

· cellular mechanisms leading to arrhythmia formation

· how arrhythmia can be maintained by circular and re-entrant electrical paths

· common classes of anti arrhythmic agents

· mechanism of action for these drugs

· know some examples




action potential generated in nodal cells






through gap junctions to
propagate myocytes




activation and inactivation of sodium channels = upstroke


↓ effective refractory period

Balance of calcium and potassium channels =
plateau





Repolarisation and sodium channels available normal 'smooth and coordinated
processes




cyclical excitation 68


Aberrant process disordered and chaotic
otherareasoing
as a pacemaker

maintains
/
the excitation



SAN is unstable since it has less I channels


causes




·
acute myocardial infarction ·
hypokalemia (especially in anorexia
nervosa)

· heart failure · autonomic dysfunction

therapeutic fever
· le .

g
.
digitals) and abase
drugs a




· Inherited mutations of cardiac ion channels


·
hyperthyroidism

, Arrhythmia types



bradycardia - slow HR



tachycardia >
-

fast HR



non-maintained skipped beat
blood clots a lot and can travel

atrial(a.k. a supra ventricular ( ↑

ventricular arrhythmia




cardiac arrhythmias are generated by abnormal impulse formation or impulse propagation




1 in the
changes repetitive SAN activity , depending on its pacemaker currents



AUN
2 creation of subsidiary pacemaker formation in specialised conducting or
purkinje fibres

s ectopic activity in
normally non-automatic atrial and ventricular cardiomyocytes when they are depolarized by some
pathological processes.




usually as a
consequence of defective ion channels , exchangers or ion
handling



Altered
causes automality




exaggeration of normal cellular capacity to fire
Y
funnyent
cations coming depolarisation
Increase in current faster SAN
funny =




in
may occur in a region outside of SAN




Altered automaticity block




first degree >
-
slowed conduction between AVN and ventricle



second degree- > intermittent failure of transmission from atria to ventricle


third degree or complete >
-

complete loss of transmission - uncoordinated atria and ventricle

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Uploaded on
February 5, 2026
Number of pages
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Written in
2024/2025
Type
Lecture notes
Professor(s)
Ian greenwood
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