Pharmacology Anti-Arrhythmic 1 Flashcards

1
Q

DAD stands for

A

delayed afterdepolarization

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2
Q

EAD stands for

A

early after-depolarization

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3
Q

ERP stands for

A

effective refractory period

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4
Q

define arrhythmia

A

abnormal heart rhythm/rate affects cardiac output

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5
Q

_________ increases risk for stroke and heart failure

A

arrhythmia

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6
Q

What are the different causes of arrhythmia?

A

genetic - wolff parkinson white syndrome
drug induced - digitalis
anesthetized patients
heart dysfunction/ acute mi

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7
Q

What are some nonpharmacologic therapies?

A

pacemakers
cardioversion
catheter ablation
surgery

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8
Q

What is bradycardia?

A

slow heart beat

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9
Q

less than 60 bpm is

A

bradycardia

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9
Q

more than 100 bpm is

A

tachycardia

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10
Q

what is normal sinus rhythm?

A

between 60 to 100 bpm

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10
Q

tachycardia is

A

rapid heart beat

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11
Q

an abnormality in impulse initiation and/or impulse propagation

A

arrhythmia

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12
Q

what are the three types of atrial arrhythmias?

A

premature atrial contractions
paroxysmal atrial tachycardia
atrial fibrillation

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13
Q

a premature atrial contraction triggerering a flurry of atrial activity, with ventricles still able to keep pace and the heart rate jumping to 180 bpm is known as

A

paroxysmal atrial tachycardia

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14
Q

impulses moving over the arial surface at rates of perhaps 500 beats per minute with quivers instead of an organized contraction is known as

A

atrial fibrillation

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15
Q

what are the types of ventricular arrhythmia

A

premature ventricular contractions
ventricular tachycardia
ventricular fibrillation

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16
Q

what type of atrial arrhythmias occur in often healthy individuals

A

PACs

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17
Q

what is known as a surprise atrial contraction

A

PACs

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18
Q

what increases incidences of PACs

A

stress, caffeine, and various drugs

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19
Q

what type of ventricular arrhythmia occurs when a purkinje cell or ventricular myocardial cell depolarizes to threshold and triggers a premature contractions

A

PVCs

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20
Q

which cell is responsible for PVCs

A

ectopic pacemaker

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21
Q

what arrhythmia is defined as four or more PVCswithout intervening normal beats

A

ventricular tachycardia

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22
Q

what arrhythmia is responsible for cardiac arrest

A

ventricular fibrillation

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23
Q

T or F VF is rapidly fatal, because the ventricles quiver and stop pumping blood

A

T

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24
Q

torsades de pointes is a type of

A

V tach

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25
Q

what does torsades de pointes mean

A

polymorphic ventricular tachycardia

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26
Q

what are the ion movements of the NA K ATPase pum

A

1 ATP pumps out 3 Na+= and 2 K+

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27
Q

What is the ion movement of the Na+ Ca++ exchanger

A

3 Na + in, 1 Ca++ out

28
Q

electrical activity of the heart is maintained by

A

pumps
ion channels
autonomic nervous system

29
Q

what is the mechanism of arrhythmias

A

distrubance of impulse formation

30
Q

which class of anti arrhythmic drugs decrease phase 4 slope?

31
Q

what class of antiarrthymic drugs increase threshold?

A

class 1 and class 4

32
Q

what class of antiarrthymic drugs increase the maximum diastolic potential

A

adenosine and acetylcholine

33
Q

what class of antiarrhythmic drugs increase action potential duration?

34
Q

what are two ways to increase refractoriness?

A

in early after depolarization and delayed afterdepolarization

35
Q

what are some examples of class III drugs?

A

amiodarone
dofetilide
sotalol

36
Q

what are some examples of class II drugs

A

beta blockers like propranolol, atenolol, metoprolol

37
Q

what are some examples of class IV drugs

A

non DHP calcium channel blockers like verapamil and diltiazem

38
Q

what is the mechanism of action of class I drugs?

A

sodium channel blockade

39
Q

which class of drugs reduces phase 0 slope and peak of AP

40
Q

which subclass of class I drugs are moderate

41
Q

which subclass of Class I drugs are strong

42
Q

which subclass of class I drugs are weak

43
Q

which class of drugs has a moderate reduction in phase 0 slope with an increased APD

44
Q

which class of drugs reduced APD

45
Q

which class of drugs has no effect on APD

46
Q

what is the mechanism of action of Class II drugs

A

beta blockade, blocks sympathetic activity, reducing rate and conduction

47
Q

what is the mechanism of action of Class III drugs

A

potassium channel blockade

48
Q

what class of drugs has delay repolarization in phase 3 thereby increasing APD and ERP

49
Q

what is the mechanism of action of class IV drugs

A

calcium channel blockade

50
Q

which class of drugs blocks L type calcium channels and is most effective at the SA and AV nodes, reducing rate and conduction

51
Q

what are the Class IA drugs?

A

procainamide
quinidine
disopyramide

52
Q

what are the Class IB drugs

A

lidocaine
mexiletine

53
Q

what are the class IC drugs

A

flecainide
propafenone

54
Q

which class I subclass dissociates with the channel with rapid kinetics?

55
Q

which class I subclass dissociates with the channel with intermediate kinetics?

56
Q

which class I subclass dissociates with the channel with slow kinetics?

57
Q

procainamide is effective against

A

most atrial and ventricular arrhythmias
WPW syndrome

58
Q

what are the cardiac effects of procainamide?

A

slows the upstroke of the AP
slows conduction
prolongs the QRS duration of ECG
prolongs the APD - class 3
has direct depressant actions on SA and AV nodes
all 1a show reverse use dependence

59
Q

what are the extracardiac effects of procainamide?

A

has ganglion blocking properties and causes hypotension

60
Q

what are the dosage forms of procainamide?

A

oral
iv - slow infusion
im

61
Q

how is procainamide metabolized?

A

hepatic
NAPA - n acetyl procainamide

62
Q

NAPA has class _ effects causing

A

3
torsades de pointes

63
Q

how is procainamide excreted?

64
Q

T or F procainamide does not need dose adjustment for patients in renal or heart failure

A

F , needed because eliminated renally

65
Q

who is contraindicated for procainamide

A

hypersensitivity
CHF
renal failure
shock patients

66
Q

are there DDI concerns with procainamide?

A

YES
potentiate cardiac effects of beta blockers
hypotensive effect of thiazides
anticholinergic effects
neuromuscular blocking effects

67
Q

what are the toxicities of procainamide

A

cardiotoxicity
immunity issues
blood dyscrasia
pulmonary toxicity

68
Q

what are the cardiotoxicity effects of procainamide?

A

excessive action potential prolongation
QT interval prolongation
induction of torsades de pointes arrhythmia
syncope

69
Q

1/3 of patients who take procainamide experience immune toxicities, what is that?

A

lupus erythematosus, arthralgia and arthritis

70
Q

what kind of toxicities, blood dyscrasias, does procainamide have?

A

agranulocytosis
bone marrow depression
neutropenia
hypoplastic anemia
thrombocytopenia