Brainscape's Knowledge GenomeTM

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


See full index

Pharm I ( Melicia) > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

What are the 2 mechanisms of tachyarrhythmias?

A

Abnormality in impulse generation aka “automatic tachycardias”

abnormality in impulse conduction aka “reentrant” tachycardias

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

How do most antiarrhythmic drugs work?

A

by modulating the activity of ion channels in the plasma membranes

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

Generally, AADs alter cardiac rhythm by altering…

A
  • maximum diastolic potential of PPM cells
  • the rate of phase 4 depolarization
  • the threshold potential
  • the action potential duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Class I antiarrhythmics

A

Na+ channel blocks

Prototype: Procainamide, Lidocaine, Flecainide

Depress Na+ conduction in ischemic tissue greater than normal tissue

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

Class II antiarrhythmics

A

Beta adrenergic receptor antagonists

Prototype: Propranolol

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

Class III antiarrhythmics

A

K+ channel blockers

Prototype: Amiodarone

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

Class IV antiarrhythmics

A

Ca+ channel blockers

Prototype: Verapamil

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

Misc AADs include

A

Adenosine, Mg, K

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

Class IA prototype? MOA?

A

Procainamide

Inhibits Na+ channel, inhibits K+ current

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

Effects of Procainamide

A

Slows conduction velocity and PPM rate

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

Clinical applications for procainamide?

A

can be used to tx most atrial and ventricular arrhythmias

2nd choice for most sustained V arrhythmias associated with acute MI

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

Procainamide toxicities?

A

torsades de pointes in pts with renal failure

hypotension, long-term therapy produces reversible lupus related sxs

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

Disopyramide is also a class 1A Na+ channel blocker, how does it differ from Procainamide? What about Quinidine?

A

longer duration of action, toxicity includes antimuscarinic effects and HF

toxicity includes cinchonism (tinnitus, HA, GI disturbances) and thrombocytopenia

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

Class IB prototype? MOA?

A

Lidocaine

highly selective Na+ channel blocker

minimal effect in normal tissue

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

Clinical application for Lidocaine?

A

ventricular arrhythmias post MI

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

Lidocaine toxicities?

A

reduce dose in pts with HF or liver disease

neurological sxs: CNS sedation or excitation

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

Mexiletine is also a Class IB AAD, how does it differ from Lidocaine?

A

oral med

longer duration of action

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

Class IC prototype? MOA?

A

Flecainide

Na+ channel blocker

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

Effects of Flecainide?

A

dissociated from channel with slow kinetics, no change in action potential duration

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

Clinical application of Flecainide?

A

supraventricular arrhythmias in pts with normal heart, do not use in ischemic conditions (post MI)

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

Flecainide toxicities?

A

pro arrhythmic

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

Class II antiarrhythmics are useful in the treatment of…

A

supraventricular and ventricular arrhythmias precipitated by sympathetic stimulation

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

Class II prototype? MOA?

A

Propranolol

Beta-Adrenoceptor blocker

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

Effects of Propranolol?

A

direct membrane effects (Na channel block) and prolongation of action potential duration, slows SA node automaticity and AV nodal conduction velocity

25
Q

Clinical application of Propranolol?

A

Atrial arrhythmias

prevention of recurrent infarction/sudden cardiac death

26
Q

Propranolol toxicities?

A

asthma, AV block, acute HF

27
Q

Esmolol is also a class II BB, how does it differ from Propranolol?

A

Selective Beta 1 blockage, IV only, lasts 10 min. Used in perioperative and thyrotoxicosis arrhythmias

28
Q

Class III prototype? MOA?

A

Amiodarone

blocks K, Na and Ca channels, Beta adrenoceptors

29
Q

Effects of Amiodarone?

A

prolongs action potenital duration and QT interval, slows HR and AV node conduction

30
Q

Clinical applications of Amiodarone?

A

serious ventricular arrhythmias and supraventricular arrhythmias most commonly prescribed AAD

31
Q

Amiodarone PK

A

oral, IV

variable absorption and tissue accumulation

hepatic metabolism

32
Q

Amiodarone toxicities?

A

bradycardia and heart block in disease heart, peripheral vasodilation, pulmonary fibrosis, hepatic toxicity, tremor/ataxia, blue-gray skin

hyper or hypothyroidism

33
Q

Amiodarone drug interactions

A

lots, based on CYP metabolism

34
Q

What should you monitor in a pt taking Amiodarone

A

CXR (pulmonary fibrosis)

TFTs, ophtho exam, LFTs, ECG

35
Q

Dofetilide is a Class…drug, MOA?

A

III

K+ channel blocker

36
Q

Clinical application of Dofetilide?

A

Maintenance or restoration of SR in AFib

37
Q

Dofetilide toxicities?

A

torsades de pointes (initiate in hospital)

38
Q

Effects of Class IV AAD

A

CCB decrease the excitability of SA nodal cells and prolong AV nodal conduction, primarily by slowing the action potential upstroke in nodal tissue

39
Q

Name 2 Class IV AADs

A

Verapamil, Diltiazem

40
Q

Verapamil/Diltiazem MOA?

A

calcium channel blocker, slows conduction in AC node and pacemaker activity, PR interval prolongation

41
Q

Clinical applications of Verapamil?

A

AV nodal arrhythmias especially in prophylaxis

42
Q

Clinical applications of Diltiazem

A

rate control in Afib

43
Q

Toxicities of Verapamil and Diltiazem?

A

cardiac depression, constipation, hypotension

44
Q

Mg MOA?

A

interacts with Na/KATPase and Ca channel blockers

45
Q

Clinical applications of Mg?

A

torsades de pointes, digitalis induced arrhythmias

46
Q

Mg toxicities?

A

muscle weakness in OD

47
Q

K MOA?

A

increase K permeability, K currents

48
Q

effects of K?

A

slows ectopic pacemakers, slows conduction velocity

49
Q

Clinical applications of K?

A

digitalis induced arrhythmias, arrhythmias associated with hypokalemia

50
Q

K toxicities?

A

reentrant arrhythmias, fibrillation or arrest in OD

51
Q

Adenosine MOA?

A

activates inward rectifier K current, blocks Ca

52
Q

Effects of adenosine

A

very brief, usually complete AV blockade

53
Q

Clinical applications of Adenosine?

A

paroxysmal supraventricular tachycardias

54
Q

Adenosine PK

A

IV only, duration 10-15 sec

55
Q

Adenosine toxicities?

A

flushing, chest tightness, dizziness

56
Q

In Afib therapy is aimed at…

A

Controlling Ventricular rate
-Digoxin, non-DHP, CCBs, BB

Preventing thromboembolic complications
-Warfarin, ASA

restoring and maintaining SR
-AADs, direct current cardioversion

57
Q

Should you ever leave a pt in afib?

A

yes, rate control alone is often sufficient in pts who can tolerate it

58
Q

Sotalol is a Class….AAD, clinical applications?

A

Class III

ventricular arrhythmias, and Afib

Pharm I ( Melicia) (18 decks)

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