antiarrhythmic Flashcards
what does class I work on
sodium channels
class I A functions
blocks fast sodium channels, decreases sodium current. preferentially in the open or activated state.
what is the effect of class I A
increases the APD and effective refractory period. this pushes the fast upstroke to the right, taking the cell longer to depolarize
class I A agents
quinidine, procainamide
quinidine blocks what receptors? what is the consequence of this?
muscarinic and alpha-adrenergic. blocking muscarinic causes increased HR and blocking alpha causes vasodilation and reflex tachycardia. this is proarrhythmogenic.
what is quinidine used for
many arrhythmias, A-fib.
what do we have to do first in order to use quinidine
digitalize to slow SA/AV nodal conduction.
what are the adverse effects for quinidine
cinchonism (GI, CNS excitation, tinnitus, ocular dysfunction), hypotension, prolongation of QT and QRS -torsades.
what is cinchonism
the result of the duality of ANS antagonism for the drug.
does quinidine have interactions?
hyperkalemia enhances effect. displaces digoxin from binding sites.
procainamide
class IA antiarrhythmic. has less muscarinic activity than quinidine. metabolized to the active form: NAPA.
side effects of procainamide
one of the three known to cause SLE in 30%. hemotoxicity thrombocytopenia, agranulocytosis. torsades.
class IB mechanism
antiarrhythmic. blocks fast sodium channels in the inactivated state. has a preference for partly depolarized hepatic tissue (ischemic). this results in an increased threshold of excitation and less excitability of hypoxic tissue. there is a decreased APD.
class IB agents
lidocaine (IV), mexiletine (oral)
when is lidocaine used
post-MI and digoxin toxicity. this is the least cardiotoxic of conventionals.
SE of lidocaine
CNS toxic -seizures.
class IC
blocks fast sodium channels especially His-purkinje. these are proarrhythmogenic. there is no effect on APD, no ANS SE.
class IC agents
flecainide
flecainide
last ditch drug, limited due to it s proarrhythmogenicity. there is increased sudden death post-MI.
class II antiarrhythmetics
beta-blockers. they work on the SA/AV node making the PANS more predominant and thus cause bradycardia. EFFECT NODAL CURRENTS. decrease slope of the phase 4 action potential.
what is the primary use for beta blockers
post-MI prophylaxis and SVT.
class III antiarrhythmogenic.
blocks potassium channels. causing a drastic elongation in the time to repolarize. slows potassium current of phase III.
class III agents
amiodarone and sotalol
amiodarone
mimics class I, II, III, IV. increases the APD and ERP in all cardiac tissues. used in many arrhythmias.
what is the biggest problem of amiodarone
half-life of 80 days. loves to bind to proteins increasing its Vd.
SE of amiodarone
pulmonary fibrosis, blue skin, hepatic necrosis. phototoxic, corneal deposits, thyroid dysfunction.
what are the uses of sotalol
V-tach.
class IV antiarrhythmics
calcium channel blockers. blocks slow calcium channels L-type. decreases phase 0, IV. decreases SA and AV nodal activity.
class IV agents.
verapamil and diltiazem.
what are the uses of the class IV.
SVT.
SE of the class IV
well tolerated. constipation, dizziness, flushing, hypotension, AV-block.
what happens if BB or digoxin is taken with CCB
there is the potential for AV-block.
what are the interactions for the CCB
displaces digoxin.
adenosine
activates adenosine receptors causing Gi-coupled decreases i cAMP. this decreases SA and AV nodal arrhythmia.
where else are adenosine receptors found
in the bronchial tree.
what is adenosine used for?
DOC for paroxysmal SVT and AV nodal arrhythmia.
what is the halflife of adenosine
<10 sec
SE of adenosine
flushing, sedation, dyspnea. antagonized by methylxanthines.
magnesium used for?
torsades. it is similar to calcium and impairs its function.
what are the drugs that cause torsades
potassium channel blockers (1A, III)
antipsychotics
TCA
