Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CVS II Pharmacology > Antiarrhythmic drugs > Flashcards

Antiarrhythmic drugs Flashcards

(71 cards)

Start Studying
1
Q

list the 5 categories of the vaughn Williams classification of antiarrhythmic drugs

A
  1. Na+ channel blockers
  2. Beta blockers
  3. K+ channel blockers
  4. Calcium channel blockers
  5. Miscellaneous Drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 3 miscellaneous drugs in the vaughn Williams classification of antiarrhythmics

A

Adenosine, Digoxin, magnesium sulfate

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

what is phase 0 of the non-pacemaker action potential curve

A

activated Na+ channels open, Na+ ions inward

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

what is phase 1 of the non-pacemaker action potential curve

A

Na+ channels are inactivated, K+ outward

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

what is phase 2 of the non-pacemaker action potential curve

A

Plateau phase; Ca++ ions inward are balanced by K+ ions outward

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

what is phase 3 of non-pacemaker action potential curve

A

repolarization due to K+ ions outward and inactivation of Ca++ channels

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

what is phase 4 of non-pacemaker action potential curve

A

RMP by Na+/K+ ATPase pump

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

what is phase 0 of the pacemaker action potential curve

A

activation of L-type Ca++ channels

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

what is phase 3 of the pacemaker action potential curve

A

K+ ions outward

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

what is phase 4 of the pacemaker action potential curve

A

pacemaker current made of inward Na+/Ca++ ions and Outward K+

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

what is responsible for the depolarization of the action potential of pacemaker cells

A

Ca++

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

what maintains the RMP of non-pacemaker cells

A

K+

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

define effective refractory period (ERP)

A

impossible to produce a response regardless of the stimulus

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

define relative refractory period

A

period during which a strong impulse may elicit a response

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

define refractoriness

A

ERP/APD (as ERP decreases, you run a greater risk of the formation of premature impulses)

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

what are the 3 states the sodium channel toggles between

A

resting, active, and refractory (inactivated)

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

what class do quinidine, procainamide, and disopyramide belong to

A

Class 1a (Na+ channel blockers)

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

list the class 1a Na+ channel blockers

A

quinidine, procainamide and disopyramide

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

what is the MOA of class 1a Na+ channel blockers

A

decrease Vmax and prolong APD
(decrease rate of depolarization)

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

what is the clinical significance of prolonging the action potential duration (extend the refractory period)

A

it reduces the likelihood of arrhythmias

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

which of the class 1a drugs is most anticholinergic

A

disopyramide

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

what are the adverse effects of quinidine

A

tinnitus, GI upset, diplopia, increase QT interval (torsades de pointes); displaces digoxin from tissue binding sites

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

which class 1a drug doesnt have alpha blocking activity

A

procainamide

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

what are the adverse side effects of procainamide

A

agranulocytosis and SLE like syndrome in slow acetylators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how do class 1b drugs differ from class 1a na+ channel blockers
they have no effect on Vmax and they have a preference for ischemic tissue bc they only work on inactivated Na+ channels, and they increase the threshold for V fib
26
what class of drugs do lidocaine, tocainide, and mexiletine belong to?
class 1b Na+ channel blockers
27
what is lidocaine indicated for?
vtac after MI
28
what is the most notable adverse effect of lidocaine
convulsions (be careful with dose)
29
what two class 1b na+ channel blockers are given orally
mexiletine and tocainide
30
what are the three class 1b Na+ channel blockers
lidocaine, tocainide, and mexiletine
31
what are the three class 1c Na+ channel blockers
flecainide, propafenone, and moricizine
32
what class of drugs do flecainide, propafenone, and moricizine belong to
class 1c Na+ channel blockers
33
what is the MOA of class 1c Na+ channel blockers
decrease Vmax significantly but no effect on APD
34
what is the main difference between class 1a, 1b and 1c Na+ channel blockers with regard to MOA
1a. decrease Vmax and APD 1b. no effect on Vmax and only effective at inactive Na+ channels 1c. no effect on APD
35
What are the clinical uses for flecainide, propafenone and moricizine (Na+ channel blockers)
life-threatening Vtac and Vfib
36
what are the adverse effects of the class 1c Na+ channel blockers
proarrhythmic effect risk of sudden death and cardiac arrest decrease in LV function after MI
37
what are the class 2 beta blockers used to treat arrhythmias
metoprolol, propranolol, acebutolol and Esmolol
38
what is the MOA of class 2 beta blockers
decrease SA and AV nodal conduction and decrease the slope of phase 4
39
what are the clinical uses of the class 2 beta blockers: metoprolol, propranolol, acebutolol, and esmolol
prophylaxis for ventricular arrhythmias post MI
40
what are the adverse effects of class 2 beta blockers
proarrhythmic: can cause AV block
41
what is esmolol indicated for
emergency rx of SVT
42
what beta blocker is used in an emergency rx of SVT
esmolol
43
what are the 5 class 3 K+ channel blocker drugs
amiodarone, dofetilide, ibutilide, sotalol, and dronaderone
44
what is the MOA of class 3 K+ channel blockers
increase APD, and ERP; prolong repolarization and lengthen phase 2
45
what class of antiarrhythmic drugs do amiodarone, dofetilide, ibutilide, sotalol, and dronaderone belng to?
class 3 K+ channel blockers
46
what is the significance of amiodarone
is mimics class 1, 2, 3, and 4 binds to Na+ Channel (inactivated) blocks K+ and Ca++ channels non-competitive inhibitor of beta receptors long 1/2 life: 25-60 days
47
what are the clinical uses of class 3 antiarrhythmic K+ channel blockers
atrial fibrillation and Vtach
48
what are the adverse effects of amiodarone, dofetilide, ibutilide, sotalol, and dronaderone (K+ channel blockers)
pulmonary fibrosis, hepatotoxicity, smurf skin, hypothyroidism, and hyperthyroidism and notably TdP.
49
what are the 2 class 3 K+ channel blocker antiarrhythmics that selectively block outward potassium channel called delayed rectifier potassium channel
Ibutilide and deofetilide
50
what is the significance of ibutilide and deofetilide selectively blocking delayed rectifier potassium channels
it prolongs the ventricular repolarization and increases the QT interval
51
what are the uses of ibutilide and dofetilide
used for pharmacological cardioversion of atrial fibrillation and flutter
52
what makes Sotalol unique as an antiarrhythmic drug?
it has properties of both Class 2 and class 3 drugs (beta blocker and a K+ channel blocker)
53
what are the 2 MOAs of sotalol
decrease heart rate and AV conduction and prolong APD and ERP
54
what is the clinical use of sotalol
A fib, and life-threatening ventricular arrhythmias
55
what are the adverse effects of Sotalol
TdP, headache, depression, and impotence use with caution in asthmatics
56
what are the class 4 CCB antiarrhythmic drugs
Diltiazem and verapamil
57
what class of antiarrhythmic drugs wo diltiazem and verapamil belong to
class 4: CCB
58
what is the MOA of the class 4 CCB drugs, Diltiazem and verapamil
decrease SA and AV conduction and slope of phase 4
59
what is the clinical use of diltiazem and verapamil
PSVT due to AV nodal re-entry
60
what are the adverse effects of diltiazem and verapamil
orthostatic hypotension, reduce cardiac output, lower extremity edema, constipation Verapamil displaces digoxin, increasing its toxicity Proarrhythmic AV block if used with beta blockers Caution: Atrial tachycardia due to WPW
61
what are the miscellaneous antiarrhythmic drugs
Adenosine, Digoxin, and magnesium sulfate
62
what is the MOA of adenosine
AV nodal blocker
63
what are the clinical uses of adenosine
drug of choice for PSVT
64
what is the prophylaxis drug of choice after administration of adenosine for SVT
class 2 (b blocker) or class 4 (ccb)
65
what drugs increase risk of torsade de pointes
amiodarone, quinidine, sotalol, thioridazine, and TCAs
66
what is the mechanism behind antiarrhythmics causing torsades de pointes
prolongation of QT intervals
67
what is the rescue therapy for torsades de pointes
mg sulfate and K+
68
what is the clinical use of digoxin
heart failure and to control ventricular rates in afib and afluter
69
what is the antagonist of adenosine
theophylline
70
what is the antidote for digitalis toxicity
digifab (digibind)
71
what drugs are proven to decrease mortality in hear failure
ACEI and MRA (i.e. spirinolactone)

CVS II Pharmacology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions