Antiarrhythmic drugs Flashcards

1
Q

Impulse propagation depends on –

A

conduction velocity and gNa+

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2
Q

conduction velocity depends on -

A

intracellular resistance and gNa+

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3
Q

gNa+ depends on

A

transmembrane [Na+] gradient and state of Na+ channel readiness

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4
Q

shortest interval at which a premature stimulus results in a propagated response

A

effective refractory period

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5
Q

sodium channel blockade

A

quinidine, lidocaine, encainide

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6
Q

beta-adrenergic blockade

A

propranolol

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7
Q

moderate phase-0 depression and slow conduction (usually long repolarization)

A

quinidine

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8
Q

minimal phase-0 depression and slow conduction (usually shorten repolarization)

A

lidocaine

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9
Q

marked phase-0 depression and slow conduction (little effect on repolarization)

A

encainide

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10
Q

prolong repolarization

A

amiodarone (and quinidine)

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11
Q

Ca2+ channel blockade

A

verapamil, diltiazem

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12
Q

adenosine, digitalis glycosides are – drugs

A

miscellaneous

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13
Q

Class IA antiarrhytmic drugs

A

quinidine

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14
Q

What does quinidine block (class IA)?

A

use-dependent block of Na+ channels

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15
Q

Class IA (quinidine) drugs have a similar action on the heart as –

A

peripheral nerves

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16
Q

Difference between the action of peripheral nerves and Class IA (quinidine) on the heart

A

Class IA (quinidine) affect the heart at lower concentrations

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17
Q

What treatments are Class IA (quinidine) used for?

A

prophylaxis
treatment of supraventricular arrhythmia
treatment of ventricle arrhythmia

18
Q

How can you decrease automaticity?

A

NT or drugs that increase K+ permeability or decrease Na+/Ca2+ permeability

19
Q

What causes the pacemaker potential?

A

net influx of positive charge

20
Q

How does a large membrane hyperpolarization affect the pacemaker potential?

A

longer to reach threshold (heart skips a beat)

21
Q

how can you change the pacemaker potential’s slope?

A

release Ach decreases slope

release NE increases slope

22
Q

what does a decreased slope of a pacemaker potential result in?

A

decreased HR

23
Q

How is the intensity of inward Na+ current reflected?

A

in the maximal rate of rise (Vmax) of AP phase-0 (depol)

24
Q

Effect of larger phase 0

A

more intense Na+ current –> increase conduction velocity

25
Q

relationship between the membrane potential of a myocardial cell at the time of stimulation and the maximal rate of rise of the AP

A

membrane responsiveness

26
Q

Na+ channel blockade reduces conduction velocity and mostly affects –

A

AV node

27
Q

What has a big effect on ERP

A

K channel blockers (more so than Na channel blockers)

28
Q

Use-dependent blockade of Na+ channels

A

drugs act on open Na channels to produce block

29
Q

Use dependent blockade of Na+ channels = the faster the AP discharge (during tx) –

A

the more Na channels blocked

30
Q

mexiletine and tocainide used for – vent arrhythmias (similar to lidocaine)

A

oral treatment

31
Q

side-effect of mexilentine and tocainide

A

GI and CNS effects

32
Q

side-effect of mexilentine and tocainide

A

GI an dCNS effects

33
Q

why can all antiarrhythmias cause arrhythmias?

A

they act on ion channels responsible for AP generation

34
Q

most reliable stimulus to increase HR and blood pressure

A

pain and stress

35
Q

non-selective beta blocker (propanolol) + EPI –>

A

increase in bp and reflex bradycardia

36
Q

most antiarrhythmic drugs produce –

A

hypotension

37
Q

don’t give another muscarinic block which will exasperate (with quinidine and disopyramide) –

A

salivary inhibition

38
Q

oral anticoagulants (warfarin) are used to prevent –

A

thrombosis

39
Q

– is an antiarrhymatic that has a high degree of plasma binding and can increase the risk of hemorrhaging after a dental procedure

A

phenytoin and quinidine

40
Q

new anticoagulant with fewer drug interactions

A

dabigatran

41
Q

most antiarrhymic drugs can cause –

A

hypotension