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
Clinical use of calcium channel blockers
supraventricular tachycardias
control of ventricular rate in AF
Adverse effects of calcium channel blockers
side effects due to smooth muscle relaxation:
- hypotension + dizziness
- ankle oedema
- constipation
unwanted cardiac actions:
- heart block
- bradycardia
Half-life of adenosine
10 seconds
Adenosine MOA
ADP receptor agonist
activates G protein-coupled adenosine (A1 receptors)
inhibits calcium ion channel open whilst increasing potassium channel opening
negative chronotropic effect on SA node with slowed AV conduction
Adenosine administration route
IV
Clinical use of adenosine
termination of paroxysmal SVT
slowing of AV conduction to enable more precise diagnosis of SVTs
Adverse effects of adenosine
flushing
chest pain
dyspnoea
bronchospasm
transient because rapid elimination of adenosine
Actions of Digoxin
slows heart
slows AV conduction
prolongs AV node refractory period
increased force of contraction in failing heart
Digoxin MOA
inhibits sodium/potassium ATPase in plasma membrane
increased intracellular sodium ions reduces calcium ion extrusion thus increasing intracellular calcium
