Pcol Test 4 Arrhythmias Drugs

Front 1

what are the properties of class 3 drugs

Back 1

K channel blockers

Front 2

what does K channel blocking do

Back 2

prolongs EFR/repolarization and increases APD

Front 3

how do K channel blockers treat arr

Back 3

they prolong ERP thereby slowing atrial rate in flut/fib

Front 4

how do K channels blockers treat re-entry

Back 4

by prolonging the ERP

Front 5

what does prolonging AP, delaying repolarization, widening QT have the potential to cause

Back 5

torsades de pointes

Front 6

what K channel is prominent contribultor to repolarization in both ventricular and atrial muscle

Back 6

IKr

Front 7

what is the problem w/ K channel blockers targeting IKr

Back 7

not only will they increase ERP and APD in the atrial muscle but also in the ventricle which could lead to prolonged QT that can cause torsades

Front 8

what is the pro-arr action of class 3 drugs

Back 8

prolongation of QT (this is a property of K channel blockers)

Front 9

how can diuretics cause an arrhythmia

Back 9

diuretics have a tendency to cause electrolyte disturbances which can lead to arrhythmias

diuretics electrolyte disturbances: hypokalemia, hypomagnesemia these are common contributors to Torsades

Front 10

why are knowing electrolyte values important when dealing with arrythmias

Back 10

sometimes arryhthmia can be corrected by restoring electrolyte balance

Front 11

what are the properties of Amiodarone and what class is it

Back 11

class 3
K channel blocker
Na, Ca channel blocking properties

Front 12

what class 3 agent is effective against Atrial fib/flutter and why

Back 12

amiodarone

since it has Na and Ca channel blocking properties it can treat the rate and rhythm

Front 13

how do you carry out rhythm control

Back 13

prolonging repolarization/erp it will slow the atrial rhythm down

Front 14

what is the most effective way to combat afib/flutter

Back 14

prolonging repolarization

Front 15

does amiodarone cause torsades

Back 15

no

Front 16

what are the undesired effects of amiodarone

Back 16

hypo-hyperthyroidism (b/c it contains iodine)
pulmonary fibrosis
huge accumulation in fatty tissue (due to it being highly lipophilic and having a long HL)

Front 17

what is the structural analog of amiodarone

Back 17

dronedarone

Front 18

what are the properties of dronedarone

Back 18

lacks iodine
less accumulation in fatty tissue (less lipophilic/shorter HL)
no pulmonary fibrosis
no torsades de pointes

Front 19

what type of agent is sotalol

Back 19

class 3

Front 20

what are the properties of sotalol

Back 20

weak beta blocker properties
at high doses cause torsades de pointes

Front 21

what does a pure K blocker do to incidence of torsades

Back 21

increases likelyhood

Front 22

what class 3 agent is IV only

Back 22

ibulitide

Front 23

what are the 2nd generation class 3 drugs

Back 23

ibulitide
dofetilide

Front 24

what is ibulitide indicated for

Back 24

rapid conversion of aflut/fib to normal sinus rhythm

Front 25

what are the properties of ibulitide

Back 25

pure k channel blocker
at high doses causes torsades

Front 26

what class 3 drug is oral use only

Back 26

dofetilide

Front 27

what is dofetilide indicated for

Back 27

maintenance and conversion of aflut/fib

Front 28

what are the K channels found in atrium but not ventricles

Back 28

Ikur
IkACh

Front 29

what was the first selective atrial K channel blocker and what channels does it block

Back 29

vernakalant

blocks IKur

blocks INa also

Front 30

what are the properties of vernakalant

Back 30

terminates/prevents recurrence of afib/flut <48hrs >7days

Front 31

how does atrial flut/fib cause cardiac remodeling the longer the afib/flut persists

Back 31

as the atrial flut/fib persists IKr declines
IKur is upregulated

Front 32

all the drugs before vernakalant blocked what K channel

Back 32

IKr

Front 33

what are the properties of lidocaine/mexilitene

Back 33

depress conduction velocity @ normal HR and will eliminate re-entry

Front 34

what is the most important diff between lidocaine and mexilitene

Back 34

lidocaine has 1st pass and can only be given via IV in hospital

mexilitene is a lidocaine analog and is not subject to 1st pass so it can be given orally

lidocaine doesn't have vasodilator or cardiodepressant action. has a short duration of action.

both have SE that effect the CNS

Front 35

why is a short duration of action desirable for anti arr drug

Back 35

because they can also contribute to arr. for example since most depress conduction, if that lasts too long that can actually create an arr

Front 36

what class 1a drug has the least (muscarinic properties) atropine like effect

Back 36

procainamide

Front 37

what class 1a drug has the most atropine (muscarinic properties) like effect

Back 37

disopyramide

Front 38

what class 1a drug is a cardiodepressant and what is its effect on HF

Back 38

disopyramide

being a cardiodepressant has negative effect on force of contraction and can aggravate heart failure

Front 39

what drug may produce lupus like syndrome w/ chronic treatment

Back 39

procainamide

Front 40

what are the class 1c drugs

Back 40

flecainide
propafenone

Front 41

what are the properties of flecainide

Back 41

can have cardiodepressant action
may also increase ERP
high incidence of CNS side effects

Front 42

what are the properties propafenone

Back 42

weak BB
weak Ca channel blocking properties
widen both PR interval and QRS

Front 43

what calcium channel blockers are not part of Class 4 and why

Back 43

dihydropyridines (nifedipine, amlodipine, felodipine) this is due to them having little to no effect on the heart therefore they're not used as anti-arrhythmic drugs plus THEY HAVE A REFLEX EFFECT IN WHICH SNS ACTIVITY INCREASES

Front 44

what is DHP used to treat

Back 44

HTN via vasodilation

Front 45

what would happen if you treated someone w/ aflutter/fib w/ DHP

Back 45

DHP would cause a drop in BP
reflex tachycardia would result
SNS activity would go up resulting in increase ventricular rate
THIS IS WHAT YOU DON'T WANT

Front 46

what are the properties of class 4 arr drugs

Back 46

Ca channel blockers
decrease conduction velocity and increase ERP in AV node

Front 47

can class 4 drugs be used to treat atrial fib/flut

Back 47

yes b/c they decrease CV in AV node and increase ERP in AV node
both of which slow ventricular rate

Front 48

how does class 4 drugs effect re-entry in AV node

Back 48

via increasing ERP and decreasing conduction velocity

Front 49

what drugs can be used to treat super ventricular tachycardia

Back 49

class 4
class 2

Front 50

what are the class 4 drugs

Back 50

verapamil
dilitiazem

Front 51

what is a negative effect of CCB

Back 51

may decrease cardiac contractility

Front 52

what is the pro-arrhythmic effect of class 4 drugs

Back 52

wolff parkinson white syndrome which can be aggrevated by CCB

Front 53

what is WPW syndrome

Back 53

a condition where there is a fast conducting pathway (accessory pathway) in the AVN that leads to AVN re-entry

there is competition between the fast conducting pathway (accessory) and the slow conducting pathway and results in some parts of the AV node getting activated early

Front 54

what are the properties of verapamil

Back 54

more potent than diltiazem in terms of cardiodepressant therefore more like to decrease cardiac contractility

may cause significant vasodilation and hypotension

Front 55

what are the properties of diltiazem

Back 55

less cardiodepression than verapamil
more selective for heart therefore less vasodilator than verapamil

Front 56

what are the causes of supraventricular tachycardia and why is it paraoxymal

Back 56

re-entry
WPW syndrome

paroxysmal because the ANS is constantly fine tuning AV conduction

Front 57

what can be used to treat torsades de pointes

Back 57

magnesium even if Mg is normal
class 1B

Front 58

what can be used to treat digoxin induced arrhythmia

Back 58

magnesium if Mg is low
class 1B

Front 59

what are the properties of digoxin

Back 59

slows AV node conduction
due to effects on AVN can slow ventricular rate in Atrial fib/flutt

Front 60

how can digoxin convert a fib to a flutter

Back 60

by shortening the atrial ERP

Front 61

what can be useful to counteract the effects of class 1a drugs

Back 61

digoxin