Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular > Elam Anti-arrhythmic agents > Flashcards

Elam Anti-arrhythmic agents Flashcards

1
Q

Diltiazem and Verapamil belong to the class of…

A

Non-Dihydropyridine Calcium Channel Blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Diltiazem and verapamil inhibit

A

L-Type–>voltage gated calcium channels

  • raises the threshold for cell of the SA and Av nodes
  • ->slows phase 0 depolarization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diltiazem and verapamil cause increases in (lengthens)…

A

R-R interval (slow the HR)

P-R interval–> slow conduction through the AV node–>this also slows heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Flecanide and other Sodium channel blockers work via

A

inhibition of voltage gated sodium channels

  • -> slow phase 0 depolarization
  • ->slow conduction speed through the atria, His-Purkinji system, and ventricles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

EKG changes brought about by sodium channel blockers

A

Widened QRS

Lengthened R-R Interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Potassium channel blocker work via..

A

slow repolarization of Atrial and ventricular myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Potassium channels blockers will show what EKG changes…

A

prolonged QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Adenosine is used to treat which cardiac condition

A

Supraventricular tachyarryhtmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Adenosine works to

A

slow conduction through the sinus node and to slow conduction through the AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

EKG changes brought about by bolus of adenosine

A
  • ->slows heart rate (lengthened R-R)

- ->increase in PR interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Beta blockers work via

A

simulate the effects of activating the sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Beta agonists are used to treat

A

bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Beta agonists cause which EKG change

A

> increase HR–(shortened R-R)
Shorten P-R interval
narrow the QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

name two beta agonists

A

isoproterenol

epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

beta agonists work via

A

> increase diastolic polarization of sinus node
increase rate of AV conduction
increase the rate of re-polarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

re-entrant imupulses can become what..

A

self-sustained ectopic pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pharmacologic treatment of re-entrant circuits are trying to…

A

alter the elctrophysiologic properties of the tissue by:

  • ->increasing the refractory period
  • ->or slowing conduction through the tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

drugs used to treat re-entrant circuitry clinically

A

–>Potassium channel blockers (AMIODARONE)
SOTATLOL, IBUTALIDE DOFETALIDE–>increase refractory period
*impulses re-entering are less likley to trigger the fast channels and the re-entrant impulse will die out
–>NA channel blockers–> LIDOCAINE AND FLECAINIDE
–> drugs that inhibit sodium and potassium channels (PROCAINAMIDE, QUINIDINE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MOST COMMON CAUSE OF DEATH IN PT.’S WITH MI OR TERMINAL HEART FAILURE

A

ARRHYTHMIAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

a normal AP is dependent on

A

sodium, potassium AND calcium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

2 major mechanisms for arrhythmias

A
  • ->re-entry

- -> automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ventricular arrhytmia often induced by anti-arrhythmic drugs

A

torsades de pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

which phase is the most important determinant for conduction velocity for most of the heart

A

phase 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

phase zero )upstroke determines what

A

conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

phase zero in non SA-AV cells in controlled by…

A

I-Na channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

therefore which ion regulates conduction velocity

A

I-Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

for SA and AV node which ion determines conduction velocity

A

Ca–>this is still set by the rate of Phase 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

phase 2 in most of the heart is determines by which ion

A

> calcium–> LTYPE–>
and one or more Potassium currents

*responsible for plateau phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Afib or Vfib is fatal

A

V fib if not corrected within minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

define Afib and Vfib

A

arrhythmias involving rapid reentry and chaotic movement of impulses through the tissues of the atria of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

define SVT

A

a reentrant arrhythmia that travels through the AV node, it may also be conducted through atrial tissue as part of reentrant circuit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Ventricular tachycardia

A

often associated with MI, abnormal automaticity or abnormal conduction–>impairs CO and may turn into Vfib–>requires PROMPT MANAGEMENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

time that must pass after and upstroke before a new AP will be conducted in that cell or tissue

A

Effective refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

which ion channel allows for rapid repolarization of non-pacemaker cells

A

inward rectifying Potassium channel (Ik)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

the Refractory period of sodium-dependent cardiac cells is a function of

A

how rapidly sodum channels recover (repolarize) from inactivation
*depends on repolarization time and extracellular potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

in the AV node–>rate of recovery is dependent upon

A

recovery from inactivation of calcium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

group 1 drugs belong to which class

A

sodium channel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

1A

A

procainamide (MAJOR)
quinidine
amiodarone (some class 3 activity)

39
Q

1B

A

LIDOCAINE

40
Q

1C

A

FLECAINIDE

41
Q

effect on AP for procainamide

A

prolonged AP

42
Q

effect on AP duration for lidocaine

A

shorten AP

43
Q

effect of AP for Flecainide

A

no change on AP

44
Q

All group 1 drugs work to

A

slow conduction in ischemic and depolarized cells and slow or abolish abnormal pacemakers (whenever they are dependent on Na channels)

45
Q

most selective of the Na channel blockers (group 1) for ISCHEMIC TISSUE

A

IB–>lidocaine
*LITTLE EFFECT ON OTHERS
1A AND 1C BLOCKERS–>REDUCE SODIUM IN EVEN NORMAL CELS

46
Q

NA CHANNEL BLOCKERS are all_____ which means_____.

A

USE DEPENDENT/STATE DEPENDENT:

THEY ALL BIND MORE READILY IN THE OPEN OR INACTIVATED STATE–>than when fully repolarized (therfore are selective for abnormal tissue)

47
Q

USE DEPENDENT NA CHANNEL BLOCKERS WILL INHIBIT CHANNELS…

A

UNDERGOING RAPID DEPOLARIZATION
>TACHYCARDIA
> HYPOXIA

48
Q

Antiarrhythmic drug with group 1A and group 3 actions

A

amiodarone

49
Q

Na channel blockers are useful in both ____ and ___ arrhytmias.

A

Atrial and ventricular

50
Q

Blocking I-Na will bring about

A

–>slower conduction velocity in the atria, PF’s, and Ventricles

51
Q

high doses of Na channel blockers might

A

slow AV conduction

52
Q

drugs with 1B action

A

Lidocaine–>major
mexilitine
sometimes phenytoin

53
Q

1B drugs are selective for

A

ischemic OR DEPOLARIZED PF’s or ventricles

little to no effects on the atria

54
Q

1B drugs work via

A

reduce AP duration

prolong effective refractory period

55
Q

because !b agents have little to no effect on normal cardiac cells

A

little to no EKG changes

56
Q

Group 1C drugs

A

flecainide

57
Q

flecainide (1C) works via

A

slowing conduction velocity in atria and ventricles
increase QRS on EKG
>no effect on ventricular AP duration or Qt interval

58
Q

Indications for procainamide…

A

any type of arrhythmia and during the acute phase of MI

59
Q

quinidine reduces clearance of

A

digoxin

60
Q

all group 1 drugs prolong

A

ERP by slowing recovey of sodium channels from inactivation

61
Q

Group 1 drug useful in acute ischemic ventricular arrhythmias

A

lidocaine

62
Q

lidocaine nver given orally because

A

first pass degration

metabolites are cardiotoxic

63
Q

group 1 drug toxicities are aggrevated by

A

hyperkalemia

*counteract by sodium lactate

64
Q

all drugs that prolong AP duration can case

A

torsades de pointes

65
Q

Group 2 Antiarrhythmics=

A

beta blockers

66
Q

protypical drugs in group 2

A

Propranolol

Esmolol

67
Q

MOA for beta blockers

A

beta receptor blockade and reduction in cAMP–>reduces both SODIUM AND CALCIUM currents
–>supresses abnormal pacemakers

68
Q

Cardiac are particularly sensitive to beta blockers

A

AV node

69
Q

group 3 drugs with some group 2 activity

A

amiodarone (also 1a) and sotalol (2)

70
Q

Beta blocker with shortest half life

A

esmolol

71
Q

side effects of beta blockers

A

AV block, heart failure, decrease CO, and bronchospasm

72
Q

beta blockers with beta and alpha antagonistic properties

A

labetolol

carvedilol

73
Q

beta blocker with partial beta 2 agonist activity

A

labetolol

74
Q

do group 2 drugs affect phase 0

A

NO

75
Q

Name the group 3 drugs

A

Dofetilide
Ibutilide
Sotalol (group 2 and 3)
Amiodarone (1a, 2, and 3)

76
Q

hallmark of group 3 drugs

A

prolongation of the AP duration
by blockage of Potassium channel (cheifly I-Kr) responsible for phase 2
*very drawn out repolarization

77
Q

prolongation of AP–>

A

lengthened ERP

*reduces the ability of the heart to respond to rapid tachycardias

78
Q

Group 1A and Group 3 drugs all prolong

A

QT interval

–>inhibit rate of depolarization–>therefore prolong AP and increase ERP

79
Q

do group 3 drugs affect upstroke

A

no–>only rate or repolarization

80
Q

most eficacious of all antiarrhythmic drugs

A

amiodarone

81
Q

amiodarone blocks…

A

calcium, sodium, potassium, and beta receptors

82
Q

greatest effect of blockade by amiodarone is….

A

potassium receptors–>therefore it is a group 3 drug

83
Q

Group 4 antiarrhythmic agents

A

CCB’s

84
Q

name the protype CCB and the less effective on

A

verapamil (phenylalkylamine) and the diltiazem (benzothiazepine)

these drugs cannot be given with a Beta Blocker because that would cause heart block

85
Q

are DHP drugs useful in tx of arrhythmias

A

NO–.they are selective and only work in the vasculature

86
Q

CCB’s are most effective against

A

AV nodal arrhythmias–>these tissues are calcium dependent

87
Q

Verapamil and Diltiazem in AV nodal tissues cause

A

state and use dependent selective depression of Calcium conductivity–>this slow AV nodal condution velocity and causes prolonged PR interval and ERP

88
Q

which drug can conver AV nodal tachycardia back into normal sinus rhythm

A

CCB’s

89
Q

drug that works via increasing Ik1 conduction and hyperpolarizing AV nodal cells in high doses

A

adenosine bolus–> AV block in high doses

90
Q

Misc. DOC for AV nodal arrhythmia

A

adenosine–>15 second half life

91
Q

Misc. drug for supression of ectopic pacemakers inclduing those caused by digitalis toxicity

A

potassium ion

92
Q

hypokalemia leads to

A

arrhythmias (especically in pt.’s with digoxin tx.)

93
Q

hyperkalemia leads to

A

reentrant arrhythmias

Cardiovascular (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions