Drugs Used in Cardiac Arrhythmias Lecture - Konorev Flashcards
which cells have fast action potential
ventricular contractile cardiomyocytes
atrial cardiomyocytes
purkinje fibers
which cels have slow (pacemaker AP)
SA node cells
AV node cells
class 1a drugs
quinidine
procainamide
disopyramide
class 1B drugs
lidocaine
mexiletine
class 1C drugs
flecainide
propafenone
class 2 drugs- beta blockers
esmolol
propranolol
class 3 drugs
potassium channel blocking drugs
amiodarone dronedarone sotalol dofetilide ibutilide
class 4 drugs
cardioactive CCB
verapamil
diltiazem
miscelaneous agents
adenosine
class 1 drugs sodium channel blocker -state dependent block
most useful drugs block open activated or inactivated Na+ channels, with very little affinity towards channels in a resting state
class 1A drugs and channels
block sodium channels, slow impulse conduction, reduce automatism of ectopic pacepaker
-use dependent block- preferentiallhy bind to open sodium channels (ectopics with faster rhythms targeted)
- block postassium channels
- prolong AP duration, prolong QRS and QT
class 1A drugs kinetics
dissociate with intermediate kinetics
class 1B drugs and channels
block sodium channels - bind to inactivated sodium channels (preferentially bind to depolarized cells)
-do not block potassium channels, no prolonged AP, QT, or ARS
class 1B drugs and kinetics
dissociate from channel with fast kinetics
-may shorten AP
class 1C drugs and channels
block sodium channels, slow impulse conduction (bind open/activated channels)
block certain potassium channels but not ones responsible for repol
- no proloned AP, or QT
- prolong QRS interval duration
class 1C drugs and kinetics
dissociate from channel with slow kinetics
class 2 drugs effects
slow action potential
SA node decrease HR, increase RR
- AV node - decrease AV conducatance (increase PR)
- ventricular myocardium - decrease Ca2+ overload, prevent delayed afterdepol
class 2 drug effects on ecg
decreased slope due to effects on If and T type ca chanels
increased threshold due to effect on L type Ca channels
class 3 drugs
potassium channel blockers
inwardly rectifying K+ channels are open in resting state
no current in these channels
-limit frequency of AP (regulate duration of refractory period)
-prolong AP duration and QT
class 4 drugs
block both activated and inactivated L type calcium channels
decrease slope of phase 0 depol
slow SA node depol
prolong AP duration and refractory period in AV node
prolong AV node conducation time
-may be effective in DAD-incuded ventricular arrhythmias