Cology, Antiarrhythmics, Drugs 1

Front 1

what decreases excitability

Back 1

Na channel blockers

Front 2

what prolongs action potential

Back 2

blocking K channels

Front 3

what prolongs AV refractories

Back 3

beta receptor blockade

Front 4

what decreases slow-response cells excitability

Back 4

Ca channel blockers

Front 5

what will prolong conduction

Back 5

beta receptor blockade

Front 6

what will increase energy required for fibrillation

Back 6

beta receptor blockade

Front 7

which class of Na blockers has the shortest recovery

Back 7

class 1B

Front 8

what class has the longest recovery

Back 8

class 1C

Front 9

what class the open is more than activated

Back 9

1A

1C

Front 10

in which class is receovery less than 1 sec

Back 10

inactivated more than open

Front 11

which classes have a higher affinity for the open channel

Back 11

1A

1C

Front 12

two Na gates

Back 12

M: activation

H: inactivation

Front 13

at rest the --- gate is open

Back 13

H. . . inactivation

Front 14

when does the M gate open

Back 14

depolarization

Na influx (out to in)

voltage increases

Front 15

when does the H gate close

Back 15

when voltage increase

Front 16

the absolute refractory period is the time for the -- gate to close and the -- gate to open

Back 16

M

H

Front 17

when the H gate closes what happens

Back 17

no more Na thru

Front 18

class 1A slows phase ----

Back 18

0

so longer to get to top, so the contraction is slowed down

less steep rise

Front 19

na ch blockers slows ----

Back 19

conduction

Front 20

na channel blockers --- action potential

Back 20

prolongs

Front 21

the channel affinity of the na channel blockers is ---- > ----

Back 21

open > inactivated

Front 22

how long is the dissociation of the 1A na channel blockers

Back 22

1-10 sec. . . slow

Front 23

is refractory increased or decreased in 1A na channel blockers

Back 23

increased

Front 24

a direct action fo quinidine is that it increases/slows conduction

Back 24

slows

Front 25

quinidine prolongs/decreases refractory period

Back 25

prolongs

Front 26

quinidine slows the rate of rise of phase ---

Back 26

0

Front 27

quinidine ----- threshold for excitability

Back 27

increases

more difficult to start 2nd action potential

Front 28

quinidine has increase/decrease automaticity

Back 28

decrease

Front 29

indirect actions of quinidine include

Back 29

anticholinergic

alpha blocker at higher doses

Front 30

what will anticholinergic effects of quinidine do

Back 30

increase conduction

Front 31

when will quinidine have alpha blocker effects

Back 31

at higher doses

this will affect bp

Front 32

quinidine maintains rhythm w/ ----- ---- or ----

Back 32

atrial flutter or fibrillation

keeps rapid rate from getting to the ventricles

(slows conduction, prolongs refractory, slows rise of Phase 0)

Front 33

quindine controls --- ---

Back 33

V tach

Front 34

t/f

a poplular use of quinidine is the conversion of a flutter and fib

Back 34

f

limited use

now cardioversion used

Front 35

since clots possible w/ a fib and flutter what do you give prior to conversion

Back 35

anticoagulants

dig: slow vent rates

Front 36

t/f

pt can revert after quinidine

Back 36

t

so, keep an eye on the pt

Front 37

quinidine has interactions w/ cyp ----- inhibitor

Back 37

2D6

Front 38

what meds will you be careful w/ when administering w/ quinidine

Back 38

morphine

codeine

Front 39

30-50% of pt's taking quinidine will have

Back 39

n/v/d

Front 40

t/f

quinidine users can have atrial arrhythmias only

Back 40

f

both atrial and ventricular

Front 41

quindine users can have ---tension

Back 41

hypo

Front 42

this can be fatal in quinidine users

Back 42

thrombocytopenia

Front 43

w/ ----- you can have tinnitus, dizziness, blurred vision

Back 43

cinchonism (quinidine toxicity)

Front 44

what do you call it when you're taking quindine, your arrhythmia is controlled and then you suddenly develop v tach, then death

Back 44

quinidine sudden death

Front 45

how do you prevent cinchonism

Back 45

decrease dose

or

d/c

Front 46

2-8% of quinidine users will develop

Back 46

torsades de pointes

Front 47

what's lengthened w/ torsades

Back 47

QT interval

so some beats are missed, you have abnorm contraction, and heart doesn't pump well

Front 48

w/ quinidine you can have ---- reactions

Back 48

immunological

Front 49

procainamide has a long/short duration

Back 49

short

3-4 hrs

Front 50

to solve the short duration problem procainamide now come in a --- ----- ---

Back 50

slow release preparation

Front 51

which has more anticholinergic properties: quinidine or procainamide

Back 51

quinidine

Front 52

t/f

procainamide has alpha blocking activity

Back 52

f

no alpha blocking activity

Front 53

procaiamide has active/inactive acetylated metobolite

Back 53

active

Front 54

procainamide is an active ---- metabolite

Back 54

acetylated

NAPA

Front 55

what can the fast acetylators do w/ procanamide

Back 55

increase active metabolite

Front 56

t/f

since there's no alpha blocking activity procainamide does not cause hypotension

Back 56

f

can cause hypotension

Front 57

procainamide involved in the slowing of ---

Back 57

conduction

Front 58

due to NAPA what can occur w/ procainamide

Back 58

nausea

Front 59

25-25 % of pt taking procainamide will develop---- ------

why?

Back 59

lupus like syndrome

mostly in slow acetylators

Front 60

what arrhythmia can procainamide cause

Back 60

torsades de pointes

Front 61

0.2% of pt taking procainamide can develop

Back 61

bone marrow suppression

Front 62

which better tolerated quinidine IV or procainamide IV

Back 62

procainamide IV

Front 63

t/f

oral procainamide better tolerated long term

Back 63

f

poorly tolerated long term

Front 64

actions of Disopyramide effects are similar to ----

Back 64

quinidine

Front 65

which has more anticholinergic effects quinidine or disopyramide

Back 65

disopyramide

problem: increase in SE

Front 66

t/f

disopyramide has alpha blocking activity

Back 66

f

no alpha blocking activity

Front 67

t/f

disopyramide has positive inotripic effects

Back 67

f

negative

Front 68

clinical indications for disopyramide include ---- tach and ------

Back 68

ventricular

supraventricular (flutter and fib)

Front 69

due to more anticholinergic actions of disopyramide has ----- effects

Back 69

antimuscarinic effects

Front 70

disopyramide has ---- disturbances

Back 70

conduction

Front 71

disopyramide can lead to ------ due to decreased contractility

Back 71

CHF

Front 72

arrhythmia due to disopyramide

Back 72

torsades de pointes

Front 73

CI of disopyramide

Back 73

heart block

hypersensitivity

gluacoma

Front 74

why is heart block CI w/ disopyramide

Back 74

already slowed conduction

Front 75

class 1 B Na ch blockers have a shorten phase ---

Back 75

3

Front 76

class 1B has decreased ---- foci automaticity

Back 76

ectopic

Front 77

1B Na channel blockers have a higher affinity for inactivated/open

Back 77

inactivated

higher affinity in ischemic tissue, little effect in normal tissue

Front 78

t/f
class 1 B has a slow dissociation

Back 78

f

rapid

< 1 sec

Front 79

Class 1 B speeds/slows action potential

Back 79

speeds up/shortens

Front 80

if class 1B speeds up the action potential what will happe w/ the refractory period

Back 80

shorten

so decreased ectopic (no time to allow an ectopic to work)

hopefully, heart will follow the faster rate of the SA node, if that's not the ectopic site

Front 81

which class is there an increase likelihood of following the SA node and not ectopic

Back 81

Class 1B

Front 82

in which disease is there extra cardiac tissue that causes impulses to cross from atria to ventricles

how do you tx

Back 82

Wolff-Parkinson-White

Lidocaine and surgical ablation

Front 83

Clinical indications of lido

Back 83

wolff-parkinson's

v tach, premature beats

v fib

acute MI (increase mortality)

Front 84

route of lido

why

Back 84

IV

extensive 1st pass metabolism

Front 85

lidocaine binds to which Na channel

Back 85

open or inactivated

Front 86

recovery of lido: rapid or slow

Back 86

rapid

more affinity to inactive channels

Front 87

t/f

lidocaine has high effect on normal tissue

Back 87

f

less effect

Front 88

t/f

CI for lido include atrial arrhythmias

Back 88

f

no effective on against atrial arrhythmias

Front 89

name some CNS toxicities of lido

Back 89

drowsiness

confusion

restlessness

muscle twitches

seizures

nystagmus

Front 90

an early sign of toxicity of lido

Back 90

nystagmus

Front 91

other toxicity of lido

Back 91

hypersensitivity

increased AV conduction

Front 92

CI of lido

Back 92

seizures

age

Front 93

tocanide --- removed

Back 93

analog

Front 94

tocanide can cause:

pulmonary ----

--- ----- suppression

Back 94

pulmonary fibrosis

bone marrow suppression

Front 95

how is mexiletine metabolized

Back 95

hepatically

Front 96

mexiletine has --- bioavailability

Back 96

oral

Front 97

mexilitine has decreased -----, ---- in ventricles

Back 97

automaticity

conduction

Front 98

mexiletine is effective in congenital long --- syndrome

Back 98

QT

Front 99

toxicity of mexiletine:

Back 99

n/v

tremor

blod dyscrasis

CNS effects

hepatotoxicity

Front 100

affintiy of receptors w/ mexiletine

Back 100

close > open

Front 101

class 1C has a slow phase -

Back 101

0

Front 102

class 1C has slow ---

Back 102

conduction

Front 103

effect of Class 1C on refractory

Back 103

questionable

Front 104

t/f

class 1 C will effect the normal heart

Back 104

t

Front 105

channel affinity of class 1C

Back 105

open > inactivated

Front 106

t/f

class 1 c is fast

Back 106

f

dissociatin slow

> 10 sec

Front 107

flecanide blocks Na channels and -- channels in the ---

Back 107

K

ventricles

Front 108

flecainide prolongs ---, ---, and -- intervals

Back 108

PR

QRS

QT

Front 109

flecainide prevents ----

Back 109

PVC

Front 110

t1/2 of flecainide

Back 110

14 hrs

long t1/2

Front 111

route of flecainide

Back 111

oral

IV

Front 112

save flecainide for pt's w/o. . .

Back 112

significant structrual damage to heart

Front 113

CIinical indications of flecainide

Back 113

life threatening sustained vent arrhythmias

Supraventricular arrhythmias

Front 114

toxicity of flecanide include:

--- vision

--- tach

tremors

---- spasm

----cytopenia

increase/decrease mortality in MI patients

Back 114

blurred

V tach

bronchospasms

thrombocytopenia (like quinidine)

increased

seizures

Front 115

what has teh same mechanism as flecainide

Back 115

propafenone

Front 116

propafenone also has -- blocking activity

Back 116

Beta

this can be beneficial

Front 117

toxicity of propafenone include:

-- arrhythmia

--- vision

---cardia

Back 117

proarrhythmia

blurred vision

bradycardia

dizziness

Front 118

toxicity of propafenone include

--- spasm

-- adrenergic blockade

Back 118

brocho

Beta

Front 119

blood problems r/t propafenone

Back 119

agranulocytosis

anemia

thrombocytopenia (like Flecanide and Quinidine)

Front 120

propafenone can worsen ---

Back 120

CHF (like Disopyramide)

Front 121

class 2 bb slow/increase conduction

Back 121

slow

Front 122

t/f

class 2 bb increase automaticity

Back 122

f

decrease

Front 123

class 2 bb prolong/decrease AV conduction

Back 123

prolong

(like lidocaine)

Front 124

class 2 bb prolong -- conduction

Back 124

AV

Front 125

class 2 bb decrease phase -- depolarization

Back 125

4

Front 126

class 2 bb affect the -- node

Back 126

AV

Front 127

class 2 bb block -- channel in SA and AV node

Back 127

K

Front 128

w/ class 2 bb the rise in phase 4 is slowed so you don't reach the ----

Back 128

threshold as quickly

Front 129

propanonolol is selective/nonselective bb

Back 129

nonselective

Front 130

propanolol reduces phase --- activation

Back 130

4

Front 131

propanonolol slows --- conduction

Back 131

AV

Front 132

propanolol slow AV ---

Back 132

conduction

Front 133

propanolol has neg --- and --- effects

Back 133

inotrophic

choronic

Front 134

propranolol suppress --- ---- beats

Back 134

premature ventricular

Front 135

propranonolol is ---- stabilizing

Back 135

membrane

Front 136

CIinical indications of propanolol

Back 136

supraventricular arrhythimias

Vent. ectopic beats

MI: decrease O2 demand and prevent arrhythmias

Front 137

propranolol toxicity include:

heart ---- and ----

Back 137

heart failure

heart block

Front 138

propranolol tox include:

--- tension

----glycemia

---spasm

Back 138

hypotension

hyperglycemia

bronchospasm

Front 139

what med should you watch when give w/ propanolol

Back 139

dig

they both slow conduction, so can generate ectopic beats

Front 140

b1 selective blockers that can be used for arrhythmias

Back 140

metropolol

acebutalol

Front 141

which has less bronchospasms:

metroprolol or propranolol

Back 141

metroprolol/acebutalol

Front 142

metroprolol/acebutalol can induce:

Back 142

CHF

Front 143

se of metroprolol/acebutaolol

Back 143

CNS

sedation

fatigue

Front 144

only iv b1 selective

Back 144

esmolol

also short acting

used in ER and then switch to PO for long term tx.

Front 145

only iv b1 selective

Back 145

esmolol

also short acting

used in ER and then switch to PO for long term tx.