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Pharmacology 680 > Antidysrhythmics > Flashcards

Antidysrhythmics Flashcards

1
Q

Condition where spontaneous depolarizations occur due to abnormal impulse generation in sinus or ectopic foci

A

Automaticity cardiac dysrhythmias

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2
Q

explain the patho of re-entry cardiac dysrhythmias

A

impulses propagate more than one pathway.

i.e WPW

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3
Q

what type of cardiac dysrhythmias are Seen more with volatile anesthetics because of suppression of SA node and conduction pathway

A

re-entry dysrhythmias

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4
Q

8 factors that promote dysrhythmias

A 
electrolyte imbalance
hypoxemia
acid base imbalance
ischemia
bradycardia 
increased mechanical stretch
SNS 
drugs
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5
Q

what type of acid base balance is more prone to dysrthymias?

A

alkalosis

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6
Q

antidysrhythmic drugs mechanisms of action [basic]

A

Most work directly or indirectly by blocking various ion channels
[remember: there are different parts of action potential that we manipulate]

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7
Q

Blocking Na+ affects what part of action potential?

A

velocity of AP upstroke

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8
Q

Blocking K+ affects what part of action potential?

A

refractory

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9
Q

Blocking Ca+ affects what part of action potential

A

slope of phase 4 in nodal tissue

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10
Q

Newly developed brady or tachydysrhythmias resulting from chronic antidysrhythmic therapy

A

Prodysrhythmias

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11
Q

what is Torsades de Pointes

A

Polymorphic ventricular tachycardia

Ventricular Fibrillation

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12
Q

what causes Incessant Ventricular Tachycardia

A

Antidysrhythmic drugs that slow conduction can allow re-entrant impulses (Ia & Ib)

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13
Q

Wide Complex Ventricular Rhythm is usually seen with?

A

with class Ic drugs due to slow conduction.

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14
Q

phase 0 of action potential represents

[initial upstroke]

A

rapid depolarization from opening of Na channels and closing of K channels

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15
Q

phase 1 of action potential represents

[slight downstroke before plateau]

A

initial repolarization resulting from opening of K channels and closure of Na channels

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16
Q

phase 2 of action potential represents

[plateau]

A

plateau phase resulting from sustained Ca current

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17
Q

phase 3 of action potential represents

[downstroke]

A

repolarization from closure of Ca channels and opening of K channels

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18
Q

phase 4 represents

[resting, baseline]

A

resting potential - K channel open, Ca/Na channels closed

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19
Q

how do conduction myocytes (ventricular) differ from pacemaker cells?

A

“fast” action potentials that are dependent on Na for phase 0 (depolarization)
lower resting membrane potential

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20
Q

how do pacemaker (nodal) cells differ from conduction myocytes?

A

“slow” action potentials that rely on Ca for phase 0 (depolarization), leaky Na
less negative resting membrane potential

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21
Q

what does changing the rate of phase 4 depolarization do to the heart rate?

A

pns (ACh) stimulation elongates phase 4 which results in slower HR while sns (norepi) shortens phase 4 with causes an increase in the HR

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22
Q

Drug Classification I

A

membrane stabilizers

inhibit fast Na channels

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23
Q

Drug Classification II

A

beta adrenergic antagonists

decrease rate of depolarization

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24
Q

Drug Classification III

A

refractory prolongers

inhibit K

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25
Q

Drug Classification IV

A

calcium channel blockers

slow Ca channels

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26
Q

Decrease depolarizations & conduction velocity

**Blocking Na+ moves the threshold potential farther away from the resting potential

A

class I

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27
Q

describe Beta Adrenergic Antagonist and its effect on electrolytes

A

Decrease magnitude of Ca+ influx current

Decreases K+ current (Na+/K+ pump)

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28
Q

Useful in ischemic related dysrhythmias, reduces mortality

A

Beta Adrenergic Antagonist because it slows everything down

[slower phase 4, slower automaticity, slower AV node conduction]

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29
Q

these Interact with Beta Blockers

A

Refractory Prolongers, Class III r/t reduced automaticity and prolonged action potential duration (slows)

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30
Q

Useful in rate control for rapid ventricular response situations with A fib and A flutter, PSVT
Useful in ventricular tachycardia

A

Class IV, Cardiac Ca+ channel blockers

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31
Q

Have not been shown to reduce mortality after MI

A

Class IV, ca channel blockers

32
Q

Class Ia & Ib do what to mortality and ventricular dysrythmias?

A

↑ mortality and vent dysrhythmias

33
Q

Amiodarone & β Blockers do what to mortality post MI

34
Q

which can complicate CHF?

A

Class Ia & Ic

35
Q

what does Lidocaine do post MI?

A

increases bradydysrhythmias & mortality after and MI

36
Q

Prevent Supraventricular dysrhythmias, PVCs

Maintain sinus rhythm in Afib, Aflutter

37
Q

Mechanism of Action: quinidine

A

Decreases phase 4 slope, prolongs conduction

Blocks Na+ K+, alpha block, vagal inhibition

38
Q

SE of what drug? Prolongs QRS, QT, PR, hypotension, may increase NMB

39
Q

quinidine has a Depressant effect on myocardial contractility

A

but may offset this by an increase in HR

40
Q

indicated for Ventricular and atrial tachydysrhythmias

Premature ventricular contractions

A

Procainamide (Procan)

41
Q

Mechanism of Action: procainamide

A

Blocks Na+, K+ channels

Decreases automaticity, increases refractoriness

42
Q

Slowed conduction times
Prolongs QRS, QT,
Hypotension due to myocardial depression
Lupus-like symptoms

A

side effects procainamide

43
Q

indicated for Atrial & Ventricular Tachydysrhythmias

Maintain sinus rhythm in Afib, Aflutter

A

Disopyramide(Norpace)

44
Q

Mechanism of Action: disopyramide

A

Na+ channel block, anticholinergic actions

Slowed conduction

45
Q

adverse effects of what drug?
Myocardial depressant
Depresses contractility, aggravate CHF
Prolonged QT

A

Disopyramide(Norpace)

46
Q

indicated for:
Ventricular dysrhythmias
Little effect on supraventricular dysrhythmias
Re-entry cardiac dysrhythmias (PVCs, Vtach)

47
Q

Non-dysrhythmic use lidocaine?

A

ERAS - multimodal pain control

48
Q

Mechanism of Action: lidocaine

A

delays phase 4

49
Q

side effects lidocaine

A

May increase mortality after MI
Myocardial depressant
Neurologic, Seizures
Prolonged PR, QRS

50
Q

why use lidocaine?

A

More rapid than quinidine or procainamide

Easily titrated

51
Q

list Class I drugs

A

lidocaine
disopyramide (norpace)
procainamide (procan)
quinidine

52
Q

Beta Adrenergic Antagonists are effective in dysrhythmias

A

r/t increases in SNS

53
Q

Mechanism of Action: Beta Adrenergic Antagonists

A

Decrease spontaneous phase 4 depolarization

Decreased conduction through AV node

54
Q

Adverse effects Beta Adrenergic Antagonists

A

Prolonged PR, depressed myocardium

Bradycardia, hypotension, Bronchospasm

55
Q

Beta Adrenergic Antagonists are contraindicated for what patients?

A

CHF, RAD, AV block patients.

56
Q

Amiodarone (Cordorone) is what class?

57
Q

indications of what drug: Resistant V-tach, V-fib, A-fib, WPW
Acute termination of V-tach, V-fib (1st line treatment)

A

Amiodarone (Cordorone)

58
Q

Mechanism of Action amio?

A

Blocks Na+, reduces currents of K+, Ca+

Prolongs AP, refractory and conduction

59
Q

Alpha and beta antagonist of amio causes

A

vasodilation

60
Q

amio helps with chest pain how?

A

Dilates coronary arteries (antianginal)

61
Q

Adverse effects: amio

A 
Hypotension r/t vasodilation, LV depression
Pulmonary toxicity (lipophilic, slow elimination)
Altered thyroid function (resembles thyroid hormone)
62
Q

more side effects amio

A

Marked QT prolongation, bradycardia, AV block
Resistant to catecholamines,
Reduce oxygen concentrations

63
Q

Derivative of amiodarone

Prevents return to afib/flutter

A

Dronedarone (Multaq)

64
Q

dronedarone is Only for patients

A

currently in sinus rhythm which have been converted from afib/flutter

65
Q

side effect of dronedarone?

A

increase of heart failure

66
Q

these are indicated for Paroxysmal SVT, re-entrant tachy
Ventricular rate control in A-fib, A-flutter
Not effective in reducing ventricular ectopy

A

Verapamil and Diltiazem

67
Q

Mechanism of Action: verapemil, dilt

A

Block Ca+ in cardiac cells
Decreases spontaneous phase 4 depolarization
Vasodilation or coronary and peripheral arteries
Depress AV node, negative chronotropic SA node

68
Q

adverse effects verap, dilt

A

AV block, aggravates reduced LV fxn
Hypotension
Myocardial depression
NMB may be exaggerated

69
Q

Treat atrial tachydysrhythmias. Slow AV node conduction which slows ventricular response in A-fib. * Enhance assessory pathway conduction

70
Q

how does digitalis increase contractility?

A

Cardiac glycosides ultimately increase Ca+ which increases cardiac contractility. Can cause any cardiac dysrhythmia.

71
Q

slows sinus rate and conduction through AV node, Not effective in A-fib, A-flutter, V-tach

A

adenosine (asystole <5 seconds)

72
Q

useful in ventricular but not atrial dysrhythmias, digitalis toxicity induced ventricular dysrhythmias, Can depress sinus node

73
Q

Useful in preventing Torsades de Pointes, Digitalis-induced dysrhythmias and ventricular ectopy.

74
Q

other use for magnesium

A

eras - Anesthetic- and analgesic-sparing effect by enhancing the analgesic actions of opioids

75
Q

moves threshold potential further away from resting potential. Useful in hyperkalemia where resting potential is closer to threshold potential.

76
Q

Muscarinic antagonist prevents Ach from producing negative chronotropic, inotropic and dromotropic (conduction velocity) effects.

77
Q

produces negative lusitropic (myocardial relaxation) effects and potent coronary vasoconstriction

Pharmacology 680 (19 decks)

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