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pharmacology > moa arrhythmias > Flashcards

moa arrhythmias Flashcards

1
Q

Na+ Channel Blockers 1A/1B/1C

moa

A

Binds and block Na+ channels so rapid depolarization can’t occur. This dec slope of phase 0 and dec amplitude of the action potential
Dec conduction velocity in nodal tissue
Alter effective refractory period

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2
Q

which Na channel blocker dec slope of phase 0 the best? middle? worst?

A

cab

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3
Q

which Na+ Channel Blockers 1A/1B/1C inc erp?

A

1a

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4
Q

which Na+ Channel Blockers 1A/1B/1C dec erp?

A

1B

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5
Q

which Na+ Channel Blockers 1A/1B/1C has no effect on erp

A

1c

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6
Q

what are effects of erp related to

A

K channels involved in phase 3 repolarization

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7
Q

Inc ERP too much can cause

A

torsades

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8
Q

Na channel blockers inc survival in _____

A

non life threatening arrhythmias

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9
Q

which class 1a is a - inotrope

A

Disopyramide

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10
Q

Disopyramide se

A

SE: VERY anticholinergic so much that many pts cant tolerate drug (dec sludge)

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11
Q

Procainamide se

A

SE: INC antinuclear antibodies (ANA), + ANA can cause drug induced SLE, prolonged QT

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12
Q

Short half life: 2.5-4.5 hrs

A

Procainamide

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13
Q

50% metabolized by liver mostly d/t the active metabolite NAPA

A

Procainamide

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14
Q

_____ behaves like type II antiarrhythmic with renal excretion

A

NAPA

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15
Q

Quinidine se

A

SE: VERY irritating to the GI tract, cinchonism: quinidine is a stereoisomer of quinine & these cause blurred vision, tinnitus, hearing loss, diaphoresis, confusion, psychosis

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16
Q

lidocaine contra

A

Contra: stokes adam syndrome (suddenly collapse into unconscious bc you have a disorder in the heart rhythm where there is a slow or absent pulse) or WPW (accessory pathway between the atria and ventricles)

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17
Q

Mexiletine se

A

SE: extremely GI irritating with food (not starred)

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18
Q

flecainide and propafenone are ___ inotropes

A

-

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19
Q

Flecainide se

A

SE: VERY proarrhythmic

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20
Q

BBW: proarrhythmic effects- only use with life threatening ventricular arrhythmias bc of this

A

Flecainide

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21
Q

Propafenone se

A

SE: metallic taste (not bolded)

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22
Q

Propafenone contra

A

Contra: asthma and bronchospasms bc it has nonselective beta blocker activity too

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23
Q

Used for rapid control of arrhythmias
Works within 2-10 min of administration, and works for 10-30 min
Half life 9 min

A

Esmolol

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24
Q

Esmolol contra

A

asthma and copd

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25
Q 
Beta blockers class 2
 moa
A

MOA: inhibit sympathetic influences on cardiac electrical activity so sinus rate is dec, cardiac conduction velocity is dec, aberrant pacemaker activity is inhibited; beta blockers also inc action potential duration and ERP

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26
Q 
Beta blockers class 2
se
A

SE: cold extremities, bradycardia

27
Q

Beta blockers work on ____: AV and SA node and slow SA node firing, AV node conduction, and dec HR

A

nodal cells

28
Q

Amiodarone moa

A

MOA: Complex drugs with effects on K+ (III), Na+ (acts like 1A), Ca (IV) channels, and beta adrenergic blocking properties (II)

29
Q

amiodarone acts like a Na class ____

30
Q

Amiodarone se

A

SE: most effective antiarrhythmic for ventricular arrhythmias but is also most toxic, inc AST/ALT, pulm fibrosis, blue/grey skin, corneal deposits, hypo and hyperthyroidism, long QT

31
Q

Structurally similar to thyroxine/ T4 and contains iodine

A

Amiodarone

32
Q

Pts must have PFT, thyroid test, and liver function test

A

Amiodarone

33
Q

Amiodarone bbw

A

BBW: only use for life threatening arrhythmias; can cause pulmonary toxicity, hepatotoxicity, proarrhythmic effects

34
Q

amiodarone pregnancy

35
Q

PO half life
PO onset:
Can be in system up to ___ days after D/C of therapy

A

35-110 days
2 days-3 wks, peak response takes 1 wk to 5 mo
50

36
Q

Dronedarone moa

A

MOA: Complex drugs with effects on K+ (III), Na+ (acts like 1A), CA (IV) channels, and beta adrenergic blocking properties (II)

37
Q

“Less toxic amiodarone” but not as effective as amiodarone at maintaining sinus rhythm

A

Dronedarone

38
Q

Dronedarone se

A

SE: long QT so don’t use if your QT is over 500 ms

39
Q

Not structurally related to thyroxine or iodine (amiodarone is)

A

Dronedarone

40
Q

Dronedarone pregnancy

A

Pregnancy: X (weird bc amiodarone is D)

41
Q

Dronedarone kinetics

A

Less toxic than amiodarone
Shorter half life: 13-19 hrs
Not as effective as amiodarone at maintaining sinus rhythm

42
Q

Dronedarone bbw

A

BBW: inc risk of death, stroke, HF,

43
Q

Dofetilide se

A

SE: long QT, torsades

44
Q

Dofetilide bbw

A

BBW: must be in hospital for at least 3 days during initiation

45
Q

Ibutilide se

A

SE: long QT, torsades

46
Q

Ibutilide bbw

A

BBW: can cause fatal arrhythmias, monitor ECG, pts with AF over 2-3 days must be on anticoag

47
Q

se sotalol

A

SE: proarrhythmic/abnormal ECG, MCC drug induced torsades, bradycardia

48
Q

Sotalol

contra

A

Contra: asthma, long QT syndrome

49
Q

Caution: give Betapace if pt has ventricular arrhythmia and Betapace AF if pt has atria arrhythmia

50
Q

Sotalol

bbw

A

BBW: hospitalize pt at least 3 days, proarrhythmic effects so it can cause life threatening VT associated with long QT interval, do NOT substitute Sotalol for Sotalol AF

51
Q 
K+ channel blockers: class 3
moa
A

MOA: block K+ channels responsible for phase 3 repolarization causing slow repolarization and inc ERP

52
Q

MC effect of all class 3 antiarrhythmics:

53
Q

Very useful in suppressing tachyarrhythmias

A

K+ channel blockers: class 3

54
Q 
Ca2+ channel blockers: class 4
moa
A

MOA: dec conduction velocity and prolong repolarization at the AV node (this prolongs phase2/plateau phase). Overall: dec SA node firing, slows AV node conduction → slower HR

55
Q 
Ca2+ channel blockers: class 4
se
A

SE: bradycardia and constipation

56
Q

+ inotrope and - chronotrope: inc force of heart beat but dec HR

57
Q

Digoxin moa

A

MOA: blocks Na/K ATPase pump which reduces the number of signals traveling through the AV node. It also stimulates the PSNS via vagus n leading to SA and AV node effects → dec HR

58
Q

what does digoxin do to erp

59
Q

Digoxin se

A

SE: cardiac arrhythmias, visual disturbances (yellow or blurred vision… think Van Gogh), anorexia

60
Q

when is digoxin mroe effective

A

hypokalemia

61
Q

Half life of digoxin
Normal renal function: __ hrs
Renal failure: ___ hrs → adjust dose if pt has renal failure bc of its tissue binding availability

A

Half life:
Normal renal function: 36 hrs
Renal failure: 72 hrs → adjust dose if pt has renal failure bc of its tissue binding availability

62
Q

Distribution phase of digoxin: ____ hrs

A

Distribution phase: 6-12 hrs

63
Q

Can take up to ___ days to reach steady state with digoxin

64
Q

Adenosine moa

A

MOA: causes transient heart block in the AV node and interrupts reentry pathways. Used for rapid trmt of supraventricular arrhythmias… its a potent vasodilator, but VERY short acting

pharmacology (16 decks)

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