Anti-arrhythmic drugs Flashcards
Flecainide MOA
block of open sodium channels
causes increase in effective refractory period and slowed AV conduction
How is Flecainide given and how is it excreted?
oral or IV
mostly excreted in urine
Clinical use of Flecainide
prevention of AF and ventricular tachyarrhythmias
cardioversion of acute onset AF
Adverse effects and cautions with Flecainide
suitable only for patients without ischaemic or structural heart disease
increases likelihood of dysrhythmia
may increase mortality due to ventricular fibrillation post-infarction
Beta blocker actions
antidysrhythmic, antihypertensive and antianginal
blocks actions of catecholamines on beta adrenoceptors
Beta blockers MOA
beta-adrenoceptor antagonist
block sympathetic drive , reducing pacemaker activity and increasing AV conduction time
Beta blockers examples
bisoprolol
propranolol (has additional class 1 action)
Clinical use of beta blockers
atrial fibrillation
supraventricular and ventricular tachyarrhythmias
reduction of mortality after infarct
Adverse effects of beta blockers
bronchoconstriction in asthma
bradycardia and heart block
Class 3 (amiodarone, sotalol etc) MOA
potassium channel blockers
increases refractory period
amiodarone also blocks sodium channels and beta adrenoceptors
sotalol is a beta adrenoceptor antagonist with class 2 actions
Clinical use of amiodarone and sotalol
atrial fibrillation and flutter
ventricular tachyarrhythmias
Amiodarone adverse effects
serious toxicity: pulmonary fibrosis, liver damage, photosensitive skin rashes and thyroid malfunction
Sotalol adverse effects
Torsades de pointes
less likely with amiodarone
Calcium channel blocker examples
Verapamil
Diltiazem
Calcium channel blocker MOA
blocks L-type voltage-gated calcium ion channels which are important in the action potential plateau
decreases automaticity and slows AV conduction