antiarrhythmic

Question 1

what does class I work on

Answer 1

sodium channels

Question 2

class I A functions

Answer 2

blocks fast sodium channels, decreases sodium current. preferentially in the open or activated state.

Question 3

what is the effect of class I A

Answer 3

increases the APD and effective refractory period. this pushes the fast upstroke to the right, taking the cell longer to depolarize

Question 4

class I A agents

Answer 4

quinidine, procainamide

Question 5

quinidine blocks what receptors? what is the consequence of this?

Answer 5

muscarinic and alpha-adrenergic. blocking muscarinic causes increased HR and blocking alpha causes vasodilation and reflex tachycardia. this is proarrhythmogenic.

Question 6

what is quinidine used for

Answer 6

many arrhythmias, A-fib.

Question 7

what do we have to do first in order to use quinidine

Answer 7

digitalize to slow SA/AV nodal conduction.

Question 8

what are the adverse effects for quinidine

Answer 8

cinchonism (GI, CNS excitation, tinnitus, ocular dysfunction), hypotension, prolongation of QT and QRS -torsades.

Question 9

what is cinchonism

Answer 9

the result of the duality of ANS antagonism for the drug.

Question 10

does quinidine have interactions?

Answer 10

hyperkalemia enhances effect. displaces digoxin from binding sites.

Question 11

procainamide

Answer 11

class IA antiarrhythmic. has less muscarinic activity than quinidine. metabolized to the active form: NAPA.

Question 12

side effects of procainamide

Answer 12

one of the three known to cause SLE in 30%. hemotoxicity thrombocytopenia, agranulocytosis. torsades.

Question 13

class IB mechanism

Answer 13

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.

Question 14

class IB agents

Answer 14

lidocaine (IV), mexiletine (oral)

Question 15

when is lidocaine used

Answer 15

post-MI and digoxin toxicity. this is the least cardiotoxic of conventionals.

Question 16

SE of lidocaine

Answer 16

CNS toxic -seizures.

Question 17

class IC

Answer 17

blocks fast sodium channels especially His-purkinje. these are proarrhythmogenic. there is no effect on APD, no ANS SE.

Question 18

class IC agents

Answer 18

flecainide

Question 19

flecainide

Answer 19

last ditch drug, limited due to it s proarrhythmogenicity. there is increased sudden death post-MI.

Question 20

class II antiarrhythmetics

Answer 20

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.

Question 21

what is the primary use for beta blockers

Answer 21

post-MI prophylaxis and SVT.

Question 22

class III antiarrhythmogenic.

Answer 22

blocks potassium channels. causing a drastic elongation in the time to repolarize. slows potassium current of phase III.

Question 23

class III agents

Answer 23

amiodarone and sotalol

Question 24

amiodarone

Answer 24

mimics class I, II, III, IV. increases the APD and ERP in all cardiac tissues. used in many arrhythmias.

Question 25

what is the biggest problem of amiodarone

Answer 25

half-life of 80 days. loves to bind to proteins increasing its Vd.

Question 26

SE of amiodarone

Answer 26

pulmonary fibrosis, blue skin, hepatic necrosis. phototoxic, corneal deposits, thyroid dysfunction.

Question 27

what are the uses of sotalol

Answer 27

V-tach.

Question 28

class IV antiarrhythmics

Answer 28

calcium channel blockers. blocks slow calcium channels L-type. decreases phase 0, IV. decreases SA and AV nodal activity.

Question 29

class IV agents.

Answer 29

verapamil and diltiazem.

Question 30

what are the uses of the class IV.

Answer 30

SVT.

Question 31

SE of the class IV

Answer 31

well tolerated. constipation, dizziness, flushing, hypotension, AV-block.

Question 32

what happens if BB or digoxin is taken with CCB

Answer 32

there is the potential for AV-block.

Question 33

what are the interactions for the CCB

Answer 33

displaces digoxin.

Question 34

adenosine

Answer 34

activates adenosine receptors causing Gi-coupled decreases i cAMP. this decreases SA and AV nodal arrhythmia.

Question 35

where else are adenosine receptors found

Answer 35

in the bronchial tree.

Question 36

what is adenosine used for?

Answer 36

DOC for paroxysmal SVT and AV nodal arrhythmia.

Question 37

what is the halflife of adenosine

Answer 37

<10 sec

Question 38

SE of adenosine

Answer 38

flushing, sedation, dyspnea. antagonized by methylxanthines.

Question 39

magnesium used for?

Answer 39

torsades. it is similar to calcium and impairs its function.

Question 40

what are the drugs that cause torsades

Answer 40

potassium channel blockers (1A, III)
antipsychotics
TCA