Antiarryhthmics Flashcards

(56 cards)

1
Q

action Class 1A Na channel blockers

(quinidine, procainamide, dispyramide)

A

moderate 0 deepression

slowed conduction (+2)

shorten repol

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1
Q

phase 2 =

A

plateau phase

blanced inward Ca and outward K

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1
Q

action of Sotalol

A

block IKr channel

B block

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2
Q

Ic na channel blockers

A

flecainide

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3
Q

action class IV drugs

verapamil, diltiazem

A

Ca channel blockers

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3
Q

side effects Lidocaine

A

dizziness

seizures

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4
Q

side effects Beta blockers

A

negative ionotropic

heart block,

bradycardia

bronchospasm

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5
Q

catecholamine impact on depolarization

A

enhance depl in slow response cells (no impact in fast response cells)

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6
Q

specific side effects, diltiazem (less so in other Ca blockers )

A

interact with digitalis to slow AV conduction > heart block (and verapamil)

compete for digitalis renal excretion (and verapamil)

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7
Q

indications sotalol

A

VF VT

supravent tachycardia

a fib

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8
Q

impact, flecainide

threshold

vmax

A

increase threshold

decrease Vmax

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8
Q

main physiological effect of fleccainide

A

strongest change in depol (slight in duration)

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8
Q

side effects amiodarone

A

triggered arrhythmias (torases de pointes rare)

altered thyroid fxn (inhibts T4>T3) > hypothyroidism

pulmonary fibrosis (reversible)

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9
Q

impact, Na channel blockers (Class I)

membrane responsiveness

threshold

Vmax

Refractory

A

reduce mem responsiveness

increase threshold

decrease Vmax

increase refractory

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10
Q

indirect effects QUinidine, class Ia na blockers

A

block K channels early after depol (EAD)

Vagolytic effect - enahnce communication across AV > Vtach

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11
Q

phase 3 =

A

rapid repolarization

(L type close while K still open)

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12
Q

indications flecainide

A

approved in life-threatenign when supraventricular and ventricular arrhythmias are resistant to other drugs

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13
Q

action of class II drugs

Propanolol, esmolol

A

beta adrenergic blockers

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13
Q

class III K channel blockers

A

amiodarone

sotalol

dofetilide

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14
Q

class IV Ca channel blockers

A

verapamil

diltiazem

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15
Q

since beta blockers do not _____, they are safe for pt with Long Qt

A

prolong repolarizaation

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16
Q

indications Adenosine

A

supraventricular tachycardia (slows AV conduction and heart rate)

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18
Q

1-4-dihydropyridines are not used as antiarrhythmics because,

they are used, however, to relieve

A

primarily target vascular cells (vs cardiac)

used to relieve angia pectoris to relieve chest spasms

19
Q

Class IV Ca blockers (Diltiazem and Verapamil) act primary on ___ cells
which are dependent on ___ for AP depol

A

act primarily on slow response cells (AV and SA nodes) which are dependent on Ca influx for AP

20
action 1C Na blockers flecainide
Marked 0 depression slow conduction (4+) little impact on repol
21
triggered automaticity after repolarization excerbated by
fast rates high intracellular Ca
23
class IA Na Channel blockers
quinidine procainamide disopyramide
24
action 1b Na blockers | (lidocaine)
minimal phase 0 depression slow conduction (0- 1+) shorten repol
26
indications lidocain
Vtach Digitalis - induced arrhthmias Safe for pts with long QT syndrome
27
indications Ca blockers
**Atrial tachycardia** paroxysmal supraventricular tachycardia
28
mechanism DIoxin
enhances vagal parasympathetic activity \> slow conduction at AV node
29
mechanism Adenosine
**rapidly** activates K channels to slow phase 4 depol at AV node blocks cAMP enhance Ca channel activity at AV node
30
nifedipine specific side effects (weaker in other Ca blockers)
peripheral edema
31
side effects felcainide
pro-arrhtyhmic (CAST trial)
32
all actions of amiodarone (class III)
**K blocker ** Modest Na, Ca blocker modest B adenoreceptor blocker
33
ach impact on depolarization
significantly depresses depol in slow response cells (no effect inf ast)
34
indications, Beta blockers
arrhythmias VF vT with high catecholamine (SA and AV node highly innervated)
35
action calsss III drugs amiodarone, sotalol, dofetilide
K channel blockers
36
triggered automaticity, intterupted repolarization exacerbated by
long QT syndrome
38
phase 1
inactivation of fast Na chennels (or closure of L-type Ca)
39
Torsade de Pointes in pt on sotalol
U wave likely due to long repol of purkinje fibers post ectopic pause + long QT
40
phase 4 =
resting membrane potential | (mostly K)
41
4 ways antiarrhythmic drugs reduced spontaneous discharge
1 decrease phase 4 slope (slow rate) 2. increase max diastolic potential (more negative, further from threshold) 3. Increase threshold 4. increase AP duration \> increase refractory period
42
phase 0
rapid depol of AP phase (Na in fast cells, Ca L-type in slow cells)
43
impact, lidocaine threshold AP refractory rate
increase threshold decrease AP duration decrease refractory
44
Class II beta adrenergic blockers
propanolol, esmolol
45
class IB Na channel blockers
Lidocaine
46
verapamil side effects (less so in other Ca blockers )
constipation interaction with digitalis to slow conduction velocity in AV \> hear block (and verapamil) increase plasma digitalis levels by competing for renal excertion (and verapamil)
48
short, long acting B blockers
propanolol - long, oral esmolol - short, IV
49
indications Digoxin
Afib and supravent tachycardia | (to control ventricular response rate)
50
major side effects Ca blockers
Negative chronotropic effect - decreases automaticity of SA (brady) Negative ionotropic (decrease Ca influx) hypotension (decrease Ca into smooth muscle)
51
indication amiodarone (class III)
VF VT prevention of reccurent paroxysmal a fib or flutter
52
most common target of Class III (amiodarone, sotalol)
IKr channel (increases Refractory peirod) (possible arrhytmias)
53
indications quinidine
atrial flutter A fib prevent VF VT
54
action of beta blockers in presence of catecholamines
slow rate of diastolic (phase 4) depolarization)
55
major side effects QUinidine
Severe GI Vagolytic inhibits p450s Proarrhythmic, reduced renal clearance of digitalis metabolized by liver (renal failre pt OK)