Antiarrhythmic drugs Flashcards
list the 5 categories of the vaughn Williams classification of antiarrhythmic drugs
- Na+ channel blockers
- Beta blockers
- K+ channel blockers
- Calcium channel blockers
- Miscellaneous Drugs
what are the 3 miscellaneous drugs in the vaughn Williams classification of antiarrhythmics
Adenosine, Digoxin, magnesium sulfate
what is phase 0 of the non-pacemaker action potential curve
activated Na+ channels open, Na+ ions inward
what is phase 1 of the non-pacemaker action potential curve
Na+ channels are inactivated, K+ outward
what is phase 2 of the non-pacemaker action potential curve
Plateau phase; Ca++ ions inward are balanced by K+ ions outward
what is phase 3 of non-pacemaker action potential curve
repolarization due to K+ ions outward and inactivation of Ca++ channels
what is phase 4 of non-pacemaker action potential curve
RMP by Na+/K+ ATPase pump
what is phase 0 of the pacemaker action potential curve
activation of L-type Ca++ channels
what is phase 3 of the pacemaker action potential curve
K+ ions outward
what is phase 4 of the pacemaker action potential curve
pacemaker current made of inward Na+/Ca++ ions and Outward K+
what is responsible for the depolarization of the action potential of pacemaker cells
Ca++
what maintains the RMP of non-pacemaker cells
K+
define effective refractory period (ERP)
impossible to produce a response regardless of the stimulus
define relative refractory period
period during which a strong impulse may elicit a response
define refractoriness
ERP/APD (as ERP decreases, you run a greater risk of the formation of premature impulses)
what are the 3 states the sodium channel toggles between
resting, active, and refractory (inactivated)
what class do quinidine, procainamide, and disopyramide belong to
Class 1a (Na+ channel blockers)
list the class 1a Na+ channel blockers
quinidine, procainamide and disopyramide
what is the MOA of class 1a Na+ channel blockers
decrease Vmax and prolong APD
(decrease rate of depolarization)
what is the clinical significance of prolonging the action potential duration (extend the refractory period)
it reduces the likelihood of arrhythmias
which of the class 1a drugs is most anticholinergic
disopyramide
what are the adverse effects of quinidine
tinnitus, GI upset, diplopia, increase QT interval (torsades de pointes); displaces digoxin from tissue binding sites
which class 1a drug doesnt have alpha blocking activity
procainamide
what are the adverse side effects of procainamide
agranulocytosis and SLE like syndrome in slow acetylators
how do class 1b drugs differ from class 1a na+ channel blockers
they have no effect on Vmax and they have a preference for ischemic tissue bc they only work on inactivated Na+ channels, and they increase the threshold for V fib
what class of drugs do lidocaine, tocainide, and mexiletine belong to?
class 1b Na+ channel blockers
what is lidocaine indicated for?
vtac after MI
what is the most notable adverse effect of lidocaine
convulsions (be careful with dose)
what two class 1b na+ channel blockers are given orally
mexiletine and tocainide
what are the three class 1b Na+ channel blockers
lidocaine, tocainide, and mexiletine
what are the three class 1c Na+ channel blockers
flecainide, propafenone, and moricizine
what class of drugs do flecainide, propafenone, and moricizine belong to
class 1c Na+ channel blockers
what is the MOA of class 1c Na+ channel blockers
decrease Vmax significantly but no effect on APD
what is the main difference between class 1a, 1b and 1c Na+ channel blockers with regard to MOA
1a. decrease Vmax and APD
1b. no effect on Vmax and only effective at inactive Na+ channels
1c. no effect on APD
What are the clinical uses for flecainide, propafenone and moricizine (Na+ channel blockers)
life-threatening Vtac and Vfib
what are the adverse effects of the class 1c Na+ channel blockers
proarrhythmic effect
risk of sudden death and cardiac arrest
decrease in LV function after MI
what are the class 2 beta blockers used to treat arrhythmias
metoprolol, propranolol, acebutolol and Esmolol
what is the MOA of class 2 beta blockers
decrease SA and AV nodal conduction and decrease the slope of phase 4
what are the clinical uses of the class 2 beta blockers: metoprolol, propranolol, acebutolol, and esmolol
prophylaxis for ventricular arrhythmias post MI
what are the adverse effects of class 2 beta blockers
proarrhythmic: can cause AV block
what is esmolol indicated for
emergency rx of SVT
what beta blocker is used in an emergency rx of SVT
esmolol
what are the 5 class 3 K+ channel blocker drugs
amiodarone, dofetilide, ibutilide, sotalol, and dronaderone
what is the MOA of class 3 K+ channel blockers
increase APD, and ERP; prolong repolarization and lengthen phase 2
what class of antiarrhythmic drugs do amiodarone, dofetilide, ibutilide, sotalol, and dronaderone belng to?
class 3 K+ channel blockers
what is the significance of amiodarone
is mimics class 1, 2, 3, and 4
binds to Na+ Channel (inactivated)
blocks K+ and Ca++ channels
non-competitive inhibitor of beta receptors
long 1/2 life: 25-60 days
what are the clinical uses of class 3 antiarrhythmic K+ channel blockers
atrial fibrillation and Vtach
what are the adverse effects of amiodarone, dofetilide, ibutilide, sotalol, and dronaderone (K+ channel blockers)
pulmonary fibrosis, hepatotoxicity, smurf skin, hypothyroidism, and hyperthyroidism and notably TdP.
what are the 2 class 3 K+ channel blocker antiarrhythmics that selectively block outward potassium channel called delayed rectifier potassium channel
Ibutilide and deofetilide
what is the significance of ibutilide and deofetilide selectively blocking delayed rectifier potassium channels
it prolongs the ventricular repolarization and increases the QT interval
what are the uses of ibutilide and dofetilide
used for pharmacological cardioversion of atrial fibrillation and flutter
what makes Sotalol unique as an antiarrhythmic drug?
it has properties of both Class 2 and class 3 drugs (beta blocker and a K+ channel blocker)
what are the 2 MOAs of sotalol
decrease heart rate and AV conduction and prolong APD and ERP
what is the clinical use of sotalol
A fib, and life-threatening ventricular arrhythmias
what are the adverse effects of Sotalol
TdP, headache, depression, and impotence
use with caution in asthmatics
what are the class 4 CCB antiarrhythmic drugs
Diltiazem and verapamil
what class of antiarrhythmic drugs wo diltiazem and verapamil belong to
class 4: CCB
what is the MOA of the class 4 CCB drugs, Diltiazem and verapamil
decrease SA and AV conduction and slope of phase 4
what is the clinical use of diltiazem and verapamil
PSVT due to AV nodal re-entry
what are the adverse effects of diltiazem and verapamil
orthostatic hypotension, reduce cardiac output, lower extremity edema, constipation
Verapamil displaces digoxin, increasing its toxicity
Proarrhythmic AV block if used with beta blockers
Caution: Atrial tachycardia due to WPW
what are the miscellaneous antiarrhythmic drugs
Adenosine, Digoxin, and magnesium sulfate
what is the MOA of adenosine
AV nodal blocker
what are the clinical uses of adenosine
drug of choice for PSVT
what is the prophylaxis drug of choice after administration of adenosine for SVT
class 2 (b blocker) or class 4 (ccb)
what drugs increase risk of torsade de pointes
amiodarone, quinidine, sotalol, thioridazine, and TCAs
what is the mechanism behind antiarrhythmics causing torsades de pointes
prolongation of QT intervals
what is the rescue therapy for torsades de pointes
mg sulfate and K+
what is the clinical use of digoxin
heart failure and to control ventricular rates in afib and afluter
what is the antagonist of adenosine
theophylline
what is the antidote for digitalis toxicity
digifab (digibind)
what drugs are proven to decrease mortality in hear failure
ACEI and MRA (i.e. spirinolactone)
