cardio: arrhythmias Flashcards
antiarrythmic drugs: class 1a
sodium channel blockers - moderate:
procainamide, quinidine, disopyramide
antiarrythmic drugs: class 1b
sodium channel blockers - weak:
lidocaine, mexiletine
antiarrythmic drugs: class 1c
sodium channel blockers - strong:
flecainide, propafenone
antiarrythmic drugs: class 2
beta blockers, block sympathetic autonomic effects:
metoprolol
antiarrythmic drugs: class 3
potassium channel blockers, prolong effective refractory period:
amiodarone, sotalol
antiarrythmic drugs: class 4
ccb:
verapamil, diltiazem
antiarrythmic drugs: class 5
other MOA:
digoxin, adenosine, magnesium
normal cardiac rhythm
originates in SA node (frequency: 60-100bpm) -> spreads through the atria and enters the AV node -> AV conduction is low (~0.15s) -> impulse propagates through His-Purkinje system -> ventricular activation complete in <0.1s
arrhythmia
any cardiac depolarisation that deviates from normal rhythm
- abnormality in: site of origin of impulse, rate, regularity, conduction
likely triggers of arrhythmia
ischaemia, hypoxia, acidosis, alkalosis, electrolyte abnormalities, excessive catecholamine, autonomic influence, toxicity eg. digitalis, cardiac fibre overstretch, scarred/disease tissue
all arrhythmias result from disturbance in:
impulse formation/conduction, or both
amiodarone primarily class3, but shares
class 1,2,4 properties and additional actions
sotalol primarily class 3, but also
class 2
aim of antiarrhythmics pharmacology
- reduce ectopic pacemaker activity
- modify conduction/refractoriness in re-entry circuits to disable circus activity
MOA of sodium channel blockers
- local anesthesia action blocking sodium channels
- reduce sodium current, slows upstroke of action potential, hence slows conduction