21-31 - Antiarrhythmic Drugs Flashcards
four ways of decreasing spontaneous activity
- decrease slope of phase 4
- increase threshold
- increase maximum diastolic potential
- increase action potential duration
two ways of increasing refractoriness
- sodium channel blocker
- action potential prolonging durg
sicilian gambit: class 1 MOA
block fast inward sodium channels to varying degrees in conductive tissues of the heart
how do class I drugs effect maximum depolarization rate (vmax of phase 0)?
decrease
class I drugs _________ automaticity and _____ conduction
reduce
delay
how do class I drugs effect the ERP?
prolonged
do class I drugs completely block the sodium channel?
no - moderate binding to Na channel also block the potassium channel
–> prolonged QRS and QT
do class I drugs block the calcium channel?
only at high doses
review the sicilian gambit table
page 10 of handout –> look for patterns
quinidine MOA
block rapid inward sodium channel –> slows conduction
is quinidine used clinically?
no
only in refractory pts to convert afib or aflutter, prevent reoccurrance of afib and to treat ventricular arrhythmias
adverse effects quinidine
- diarrhea
- cinchonism
- hypotension
- torsades de pointes (proarrhythmic)
cinchonism is what? it is an adverse effect of what drug?
= tinnitus, hearing loss, blurred vision
quinidine intoxication
MOA procainamide
block rapid inward Na channel –> slows stuff down
what is the effect of procainamide on APD and refractoriness?
blocks K channels –> prolongs APD and refractoriness
quinidine v. procainamide
procainamide has little vagolytic activity and does not prolong the QT interval to as great an extent
clinical use of procainamide
ventricular arrhythmias
acute treatment of reentrant SVT, afib, aflutter with WPW sydnrome
ventricular tachycardia following an Mi presents to your ER: why don’t you treat with procianamide?
although this drug can be used to treat ventricular arrhythmias, it takes too long (20 min IV loading)
observe SLE-like syndrome in a pt: what drug are they taking?
this is an adverse effect of procainamide
class Ib general MOA
weak binding of Na channels
due to rapid on off kinetics
how do class Ib drugs effect action potential
accelerated phase 3 repolarization
indications for class Ib drugs
digitalis and MI induced arrhythmia
lidocaine MOA
blocks open and inactivated sodium channels –> reduces vmac and shortens AP (When unnaturally long)
would you use lidocaine in an infranodal block?
no - potentiates infranodal blocks
indications for lidocaine
second choice for ventricular arrhythmias
can lidocaine be used for atrial issues?
no - ineffective in atrial tissue
first choice drug for immediately life threatening/symptomatic arrhythmias
amiodarone
storngest binding class to sodium channels
class Ic
because slow on/off kinetics
MOA propafenone
strong inhibitor of Na channel
indications for propafenone
treat atrial arrhythmias, PSVT, and ventricular arrhythmias **in pt with no or minimal heart disease and preserved ventricular function
MOA flecainide
potent NA channel blocker –> slows intraventricular conduction
clinical use of flecainide
only refractory ectopic ventricular arrhythmia
**not first line because can cause fatal proarrhythmic effects
beta-adrenergic antagonists =
class II agents
indications for beta-adrenergic antagonists
supraventricular arrhythmias due to excessive sympathetic activity
only antiarrhythmic drus found to be clearly effective in preventing sudden cardiac death in pt wit hprior MI
b adrenergic antagonist
main MOA of class III agents
potassium blockers
but really block all the channels to some extent
main effect of class III agents
prolong phase 3 repolarization , increase QT interval
amiodarone half life
after IV: 5-68 hrs
after saturation in tissue (lipophilic) = 13-103 days
most dangerous complication of amiodarone
lethal interstitial pneumonitis
could also see hypotension and hypothyroidism
MOA class IV agents
calcium channel blockers
–> depressed SA nodal automaticity, AV nodal conduction, decreased ventricular contractility
major cardiovascular site of action for calcium channel blockers
- vascular smooth muscle cells
- cardiac myocytes
- SA and AV nodal cells
do calcium channel blockers completely block the pore?
no - blockade is incomplete
no CCB binds to all pores
calcium channel blocker which effects mainly the vasculature
dihydropyridines
ex: nifedipine
calcium channel blockers with effects mainly in the heart
non-dihydopyridines
ex: verapamil and diltiazem
do calcium channel blockers effect smooth muscle? uterine muscle? skeletal muscle?
NO
YES - relaxes, can be used for preterm contractions
NO
4 main clinical applications for calcium channel blockers
- HTN
- angina pectoris
- SVT supraventricular tachycardia
- post-infarct protection
MOA verapamil
blocks slow Ca channels in nodal tissue –> decreased HR and increased PR interval, cardiac depression
is verapamil a good drug for ventricular arrhythmias?
no - ineffective on ventricular arrhythmia
indications for verampamil
- SVT
- rate control in afib
- angina pectoris
- HTN
adverse effects of verapamil
constipation and exacerbate CHF
contraindications for verapamil
- WPW with afib
- ventricular tachycardia
what type of drug is diltiazem?
type IV calcium channel blocker like verapamil
MOA adenosine
A1 receptor in SA and A nodes –> decrease firing rate
also does vasodilation and stimulates pulmonary stretch receptors
treatment for paroxysmal supraventricular tachycardia caused by reentry involving accessory bypass pathways
adenosine - rapid acting
half life adenosine
10-15 sec
adverse effects of adneosine
hypotension
flusing
complete heart block
management for bradycardia (3 things)
- atropine
- isoproterenol
- pacemaker
non-pharmacological management for sinus tachycardia, PSVT
vagal stimulation through caroid sinus massage or valsalva maneuver
AV nodal reentry tachycardia: drug of choice to treat
adenosine - rapidly reduces HR
ventricular tachycardia - drug of choice to treat?
amiodarone or lidocaine
