100814 antiarrthymic drugs

Question 1

what inhibitors depolarization of fast response cells in the myocardium?

Answer 1

class I antiarrhythmics

Question 2

inhibitors of depolariztion for slow response cells of myocardium?

Answer 2

calcium entry blockers (verapamil, diltiazem)

Question 3

diff btwn fast and slow response cells

Answer 3

diastolic depolarization-in slow response cells usually

fast response cells-their level of resting membrane potential determines maximum upstroke or conduction velocity of the action potential

effective refractory period (minimum interval btwn two propagating impulses): slow response cells have delayed recovery

Question 4

3 mechanisms of arrhythmias

Answer 4

increased automaticity

triggered automaticity (normal AP is interrupted or followed by an abnormal depoliariztion; afterdepolarizations)

reentry (abnormal impulse conduction)

Question 5

what is early afterdepolarization exacerbated by?

Answer 5

long QT syndrome-Torsades de Pointes results

Question 6

what is delayed afterdepolarization exacerbated by?

Answer 6

fast rates, high intracellular calcium, digitalis toxicity, catecholamines, ischemia

delayed afterdepolarizations occur AFTER repolarization

Question 7

two types of reentry

Answer 7

functionally defined reentry (tissue with ischemia, hypoxia)

anatomic reentry (reentry in AV node)

Question 8

four ways in which antiarrhyth drugs work

Answer 8

decrease phase 4 slope
increase threshold
increase maximum diastolic potential (making it more negative)
increase action potential duration

Question 9

class IA drugs action

Answer 9

sodium channel blocker

moderate phase 0 depression and slowed conduction; prolong repolarization

Question 10

examples of class IA drugs

Answer 10

quinidine
procainamide
disopyramide

Question 11

class IB drugs action

Answer 11

sodium channel blocker

minimal phase 0 depression and slow conduction; shorten reploarization

Question 12

ex of class IB drug

Answer 12

lidocaine

Question 13

class IC drugs action

Answer 13

sodium channel blocker

marked phase 0 depression and slow conduction
little effect on repolarization

Question 14

ex of class IC drug

Answer 14

flecainide

Question 15

class II drug action

Answer 15

beta adrenergic blocker

Question 16

ex of class II drugs

Answer 16

proproanolol, esmolol

Question 17

class III drug action

Answer 17

K+ channel blocker-prolong repolarization

Question 18

ex of class III drug

Answer 18

amiodarone
sotalol
dofetilide

Question 19

class IV drug action

Answer 19

calcium channel blocker

Question 20

ex of class IV drug

Answer 20

verapamil

diltiazem

Question 21

MOA of class I

Answer 21

reduce membrane responsiveness
increase threshold of AP firing
reduce Vmax (depress conduction velocity)
prolong effective refractive period

Question 22

what kind of cells do class I drugs act on

Answer 22

fast response cells

Question 23

uses of class IA drugs

Answer 23

atrial flutter or fibrillation

prevent ventricular tachycardia and fibrillation

Question 24

side effects of class IA drugs

Answer 24

block K channels so can get early afterdepolarizations

vagolytic effect (if used on atrial fibrillation, can decrease atrial firing but this may increase AV nodal firing due to giving AV node enough time to surpass refractory period)

severe GI

inhibits P450

proarrhythmic

reduces renal clearance of digitalis

metabolized by liver actually

SO MANY SIDE EFFECTS OVERALL

Question 25

class IB MOA

Answer 25

increase AP threshold block Na+ channels at high HR (greater than 120, so it's use dependent) and in depolarized cells (so could target disease ischemic cells)... binds preferably in Na+ inactivated channel state decrease AP duration and ERP

Question 26

use of class IB

Answer 26

ventricular tachycardia digitalis induced arrhythmias safe for patients with long QT syndrome

Question 27

class IC MOA

Answer 27

``` increase AP threshold decrease Vmax (conduction velocity) ``` dissociates from Na channel slowly

Question 28

side effects of class IC

Answer 28

pro arrhythmic

Question 29

use of class IC

Answer 29

life threatening situations when supraventricular and ventricular arrhythmias are resistant to other drugs

Question 30

class II drugs act on what phase of AP?

Answer 30

phase 4--prolongs it in the slow response cells

Question 31

uses of beta blockers

Answer 31

all atrial arrhythmias, ventricular tachycardia and fibrillation most useful antiarrhytmic drugs due to safety record and wide clinical applications

Question 32

side effects of beta blockers

Answer 32

negative inotropic effect heart block bradycardia bronchospasm

Question 33

MOA of class III

Answer 33

prolong AP repolarization

Question 34

uses of amiodarone

Answer 34

ventricular tachyarrhytmias and fibrillation | prevention of recurrent paroxysmal atrial fibrillation or flutter

Question 35

side effects of amiodarone

Answer 35

triggered arrhthmias, but rarely associated with Torsades de Pointes altered thyroid fxn pulmonary fibrosis

Question 36

most serious side effect of sotalol

Answer 36

triggered arrhytmias, with Torsades de Pointes

Question 37

uses of sotalol

Answer 37

ventricular tachyarrhtmias and fibrillation supraventricular tachycardias, atrial fibrillation

Question 38

class IV drugs act most on what type of cells

Answer 38

slow response cells

Question 39

MOA of calcium channel blockers

Answer 39

increase threhold for AP firing in nodal cells increase nodal cell refractory period depress conduction velocity in SA and AV nodes

Question 40

uses of calcium channel blockers

Answer 40

paroxysmal supraventricular tachycardia note: rarely used for ventricular tachycardia

Question 41

side effects of calcium ch blockers

Answer 41

negative chronotropic effect (decreases automaticity of SA node, bradycardia) negative inotropic effect (decreases calcium influx during plateau phase of ventricular AP) hypotension (decreases calcium influx into vascular sm muscle cells) constipation (verapamil) interacts with digitalis to slow conduction velocity in AV node, leading to heart block (verapamil and diltiazem) increase plasma digitalis levels for competing for renal excretion (verapamil and diltiazem)

Question 42

adenosine MOA

Answer 42

VERY RAPIDLY activates K channels to slow phase 4 depolarization AV node (half life of 10 seconds) blocks cAMP enhanced Calcium channel activity at AV node

Question 43

uses of adenosine

Answer 43

supraventricular tachycardia-slows AV conduction and heart rate

Question 44

digoxin MOA

Answer 44

enhances vagal parasympathetic activity to slow conduction at the AV node

Question 45

uses of digoxin

Answer 45

atrial fibrillation and supraventircular tachycardia to control ventricular response rate

Question 46

what should you be careful of with flecainide?

Answer 46

increases risk of death in pts with CAD

Question 47

adenosine may be better than diltiazem and metoprolol for AV nodal reentrant tachycardia b/c

Answer 47

adenosine targets directly the AV node although all three could be used

Question 48

what has been shown to be most effective for long QT syndrome?

Answer 48

propranolol