Brainscape's Knowledge GenomeTM

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


See full index

Cardio > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

class I

A

sodium channel blockers

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

class II

A

beta blockers

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

class III

A

potassium channel blockers

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

class IV

A

calcium channel blockers

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

class IA agents

A

quinidine, procainamide, disopyramide

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

class IB agents

A

lidocaine, mexiletine, phenytoin

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

class IC agents

A

flecainide, propafenone

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

class II agents

A

metoprolol, esmolol

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

class III agents

A

amiodarone, dronedarone, sotalol, dofetilide, ibutilide

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

class IV agents

A

verapamil, diltiazem

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

class I agents affect phase _ of the action potential

A

0

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

class IA cause Na channels to have a _______ recovery time

A

intermediate (intermediate potency)

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

class IA agents also inhibit _ channels

A

K+ (increasing action potential duration by prolonging repolarization)

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

class IB cause Na channels to have _____ recovery time

A

fast (low potency)

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

class IB ______ the action potential duration

A

decrease; shorten repolarization (opposite to IA agents)

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

class IC agents cause Na channels to have a ____ recovery time

A

slow (high potency)

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

effect of class IC agents on length of action potential duration

A

no effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

effects of quinidine on action potential

A

shifts phase 0 and phase 3 to the right, QT prolonged (torsades)

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

quinidine side effects that are mediated by blockade of autonomic nervous system receptors

A

anticholinergic effect (muscarinic receptors), increased HR, fast ventricular rate, hypotension (alpha receptor blockade)

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

therapeutic use of quinidine

A

limited, may be used for ventricular arrhythmias refractory to other therapies

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

other adverse effects of quinidine that lead to discontinuation

A

GI: diarrhea/n/v, cardiotoxicity, torsades, hypotension, cinchonism, increases plasma digitalis concentration and may precipitate digitalis toxicity

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

procainamide pearls

A

similar to quinidine but less anticholinergic effects, unique toxic effect: lupus erythematosus-like syndrome

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

disopyramide pearls

A

very anticholinergic, mostly used for a type of heart failure called hypertrophic cardiomyopathy

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

how is lidocaine administered

A

IV only (rapid first pass liver metabolism–> unsuitable for oral administration)

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

therapeutic use of lidocaine

A

ventricular arrhythmias only

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

adverse effects of lidocaine

A

it is lipophilic so crosses BBB so CNS effects– drowsiness, slurred speech, tremors, seizures

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

lidocaine effects on fast fibers

A

blocks Na channels–> channels unresponsive to stimulation for longer time–> channels in damaged tissue are in inactivated state longer–> decreases responsiveness/slows conduction in damaged tissue

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

what is mexiletine essentially

A

PO version of lidocaine

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

mexiletine therapeutic use

A

ventricular arrhythmias

30
Q

mexiletine side effects

A

significant GI effects

31
Q

flecainide mech

A

blocks sodium and some potassium channels

32
Q

flecainide therapeutic use

A

atrial arrhythmias like AF/AFl

33
Q

propafenone mech

A

blocks sodium and some potassium channels, some beta-blocking properties (structurally similar to propranolol)

34
Q

propafenone therapeutic use

A

atrial arrhythmias like AF/AFl

35
Q

what did the cardiac arrhythmia suppression trial demonstrate about flecainide and propafenone

A

they may actually exacerbate arrhythmia and worsen outcome in patients with structurally abnormal hearts (post-MI)

36
Q

how do beta blockers have antiarrhythmic action

A

they block effects of endogenous norepinephrine on beta-one receptors

37
Q

what are the actions of norepinephrine that lead to arrhythmia

A

increase the automaticity of normal and abnormal pacemaker cells, increase conduction velocity in the AV node

38
Q

what do you see on the ECG after beta-blocker administration

A

prolongation of PR interval

39
Q

beta blockers ____ the effective refractory period of AV node

A

increase

40
Q

how are beta blockers able to prevent fatal arrhythmias after MI

A

the presence of norepinephrine may lead to augmented automaticity of cardiac muscle cells, allowing them to generate abnormal rhythms, but beta blockers block the effects of norepi

41
Q

therapeutic use of beta blockers for arrhythmias

A

supraventricular arrhythmias: AF, AFl, paroxysmal atrial tachycardia

42
Q

what causes “sudden death” after MI

A

ventricular arrhythmia, ventricular tachycardia, ventricular fibrillation

43
Q

esmolol pearls

A

short acting beta blocker given IV, can be used in a clinical situation to suppress arrhythmias related to excess norepi

44
Q

class III mech

A

block K+ channels, prolong refractory period (repolarization)

45
Q

amiodarone has mechanistic properties of which classes

A

ALL: blocks inactivated Na channels, blocks Ca channels, blocks K channels, blocks beta receptors

46
Q

amiodarone therapeutic uses

A

oral therapy for severe ventricular arrhythmias (recurrent V tach or fib), also used for a fib and a flutter

47
Q

PK profile of amiodarone

A

variable absorption and hepatic metabolism (CYPA3A4) to active metabolite, very long half-life of approx. 50 days, highly lipophilic with extensive volume of distribution

48
Q

toxicity with amiodarone

A

PK profile explains multi-organ adverse effects: pulmonary fibrosis or pneumonitis, microdeposits in the cornea, thyroid toxicity (iodine-related, hypo or hyperthyroidism), skin blue-grey discoloration (smurf syndrome), photosensitivity, many others

49
Q

dronedarone therapeutic uses

A

paroxysmal or persistent AFib or AFL

50
Q

dronedarone is a derivative of _____

A

amiodarone; but it is free of iodine and less lipophilic than amio (less ADE but less effective)

51
Q

sotalol mech

A

prolongs action potential by blocking K channels, non-selective beta blocker with class III effect

52
Q

sotalol therapeutic uses

A

AFib/AFL, sometimes for ventricular arrhythmias

53
Q

dofetilide therapeutic uses

A

AFib/AFL

54
Q

what does dofetilide require

A

inpatient initiation with monitoring of QTc interval, creatinine clearance (renal dose adjustment), and screening for drug-drug interactions

55
Q

dofetilide pearls

A

PO only, pure class III K channel blocker

56
Q

Ibutilide pearls

A

pure class III K channel blocker, only available IV, higher risk of causing torsades

57
Q

ibutilide therapeutic uses

A

cardioversion of AFib/AFL

58
Q

calcium channel blockers mech for arrhythmias

A

decrease Ca current by blocking a fraction of the Ca channels participating in upstroke of AP–> slows conduction of AV node (slow response fibers). block activated and inactivated channels

59
Q

electrophysiologic effects of calcium channel blockers

A

decrease AV node conduction velocity, increase AV node refractory period

60
Q

effect of CCBs on ECG

A

prolongation of PR interval

61
Q

therapeutic uses of CCBs

A

slows ventricular RATE to supraventricular arrhythmias: treatment of reentrant supraventricular tachycardia when reentry circuit involves AV node, reduces ventricular response in AFib and AFL

62
Q

do not use CCBs in patients with ____

A

AV conduction problems, or severe ventricular dysfunction

63
Q

other antiarrhythmic agents

A

adenosine, digoxin, magnesium

64
Q

adenosine is a naturally occurring ____

A

nucleoside

65
Q

adenosine acts on ____

A

specific adenosine receptors (A1)

66
Q

why is adenosine’s use limited to the clinical setting

A

ultrashort half-life: given by rapid IV bolus administration, rapidly metabolized with a half-life of seconds

67
Q

the adenosine A1 receptor is a ______ receptor

A

G-protein coupled receptor

68
Q

adenosine therapeutic uses

A

acute termination of supraventricular tachycardia (SVT)

69
Q

what is digoxin used for

A

controlling ventricular response to AFib (common in heart failure)

70
Q

what is the mechanism of digoxin

A

increases vagal tone, slows conduction through AV node, decreases ventricular rate

71
Q

what is magnesium used for

A

Torsades first line, used to manage a variety of arrhythmias that occur in the setting of hypomagnesemia

72
Q

mech of magnesium

A

slows the rate of SA node impulse formation, prolongs conduction time. magnesium is necessary for movement of Ca, Na, and K and membrane stabilization

Cardio (26 decks)

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