moa arrhythmias Flashcards

(64 cards)

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
``` Beta blockers class 2 moa ```
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
26
``` Beta blockers class 2 se ```
SE: cold extremities, bradycardia
27
Beta blockers work on ____: AV and SA node and slow SA node firing, AV node conduction, and dec HR
nodal cells
28
Amiodarone moa
MOA: Complex drugs with effects on K+ (III), Na+ (acts like 1A), Ca (IV) channels, and beta adrenergic blocking properties (II)
29
amiodarone acts like a Na class ____
1a
30
Amiodarone se
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
Structurally similar to thyroxine/ T4 and contains iodine
Amiodarone
32
Pts must have PFT, thyroid test, and liver function test
Amiodarone
33
Amiodarone bbw
BBW: only use for life threatening arrhythmias; can cause pulmonary toxicity, hepatotoxicity, proarrhythmic effects
34
amiodarone pregnancy
D
35
PO half life PO onset: Can be in system up to ___ days after D/C of therapy
35-110 days 2 days-3 wks, peak response takes 1 wk to 5 mo 50
36
Dronedarone moa
MOA: Complex drugs with effects on K+ (III), Na+ (acts like 1A), CA (IV) channels, and beta adrenergic blocking properties (II)
37
“Less toxic amiodarone” but not as effective as amiodarone at maintaining sinus rhythm
Dronedarone
38
Dronedarone se
SE: long QT so don't use if your QT is over 500 ms
39
Not structurally related to thyroxine or iodine (amiodarone is)
Dronedarone
40
Dronedarone pregnancy
Pregnancy: X (weird bc amiodarone is D)
41
Dronedarone kinetics
Less toxic than amiodarone Shorter half life: 13-19 hrs Not as effective as amiodarone at maintaining sinus rhythm
42
Dronedarone bbw
BBW: inc risk of death, stroke, HF,
43
Dofetilide se
SE: long QT, torsades
44
Dofetilide bbw
BBW: must be in hospital for at least 3 days during initiation
45
Ibutilide se
SE: long QT, torsades
46
Ibutilide bbw
BBW: can cause fatal arrhythmias, monitor ECG, pts with AF over 2-3 days must be on anticoag
47
se sotalol
SE: proarrhythmic/abnormal ECG, MCC drug induced torsades, bradycardia
48
Sotalol | contra
Contra: asthma, long QT syndrome
49
Caution: give Betapace if pt has ventricular arrhythmia and Betapace AF if pt has atria arrhythmia
Sotalol
50
Sotalol | bbw
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
``` K+ channel blockers: class 3 moa ```
MOA: block K+ channels responsible for phase 3 repolarization causing slow repolarization and inc ERP
52
MC effect of all class 3 antiarrhythmics:
long qt
53
Very useful in suppressing tachyarrhythmias
K+ channel blockers: class 3
54
``` Ca2+ channel blockers: class 4 moa ```
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
``` Ca2+ channel blockers: class 4 se ```
SE: bradycardia and constipation
56
+ inotrope and - chronotrope: inc force of heart beat but dec HR
Digoxin
57
Digoxin moa
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
what does digoxin do to erp
inc
59
Digoxin se
SE: cardiac arrhythmias, visual disturbances (yellow or blurred vision… think Van Gogh), anorexia
60
when is digoxin mroe effective
hypokalemia
61
Half life of digoxin Normal renal function: __ hrs Renal failure: ___ hrs → adjust dose if pt has renal failure bc of its tissue binding availability
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
Distribution phase of digoxin: ____ hrs
Distribution phase: 6-12 hrs
63
Can take up to ___ days to reach steady state with digoxin
7
64
Adenosine moa
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