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
T or F VF is rapidly fatal, because the ventricles quiver and stop pumping blood
T
24
torsades de pointes is a type of
V tach
25
what does torsades de pointes mean
polymorphic ventricular tachycardia
26
what are the ion movements of the NA K ATPase pum
1 ATP pumps out 3 Na+= and 2 K+
27
What is the ion movement of the Na+ Ca++ exchanger
3 Na + in, 1 Ca++ out
28
electrical activity of the heart is maintained by
pumps ion channels autonomic nervous system
29
what is the mechanism of arrhythmias
distrubance of impulse formation
30
which class of anti arrhythmic drugs decrease phase 4 slope?
class 2
31
what class of antiarrthymic drugs increase threshold?
class 1 and class 4
32
what class of antiarrthymic drugs increase the maximum diastolic potential
adenosine and acetylcholine
33
what class of antiarrhythmic drugs increase action potential duration?
class 3
34
what are two ways to increase refractoriness?
in early after depolarization and delayed afterdepolarization
35
what are some examples of class III drugs?
amiodarone dofetilide sotalol
36
what are some examples of class II drugs
beta blockers like propranolol, atenolol, metoprolol
37
what are some examples of class IV drugs
non DHP calcium channel blockers like verapamil and diltiazem
38
what is the mechanism of action of class I drugs?
sodium channel blockade
39
which class of drugs reduces phase 0 slope and peak of AP
class I
40
which subclass of class I drugs are moderate
A
41
which subclass of Class I drugs are strong
C
42
which subclass of class I drugs are weak
B
43
which class of drugs has a moderate reduction in phase 0 slope with an increased APD
IA
44
which class of drugs reduced APD
IB
45
which class of drugs has no effect on APD
IC
46
what is the mechanism of action of Class II drugs
beta blockade, blocks sympathetic activity, reducing rate and conduction
47
what is the mechanism of action of Class III drugs
potassium channel blockade
48
what class of drugs has delay repolarization in phase 3 thereby increasing APD and ERP
class III
49
what is the mechanism of action of class IV drugs
calcium channel blockade
50
which class of drugs blocks L type calcium channels and is most effective at the SA and AV nodes, reducing rate and conduction
class IV
51
what are the Class IA drugs?
procainamide quinidine disopyramide
52
what are the Class IB drugs
lidocaine mexiletine
53
what are the class IC drugs
flecainide propafenone
54
which class I subclass dissociates with the channel with rapid kinetics?
IB
55
which class I subclass dissociates with the channel with intermediate kinetics?
Class IA
56
which class I subclass dissociates with the channel with slow kinetics?
class IC
57
procainamide is effective against
most atrial and ventricular arrhythmias WPW syndrome
58
what are the cardiac effects of procainamide?
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
what are the extracardiac effects of procainamide?
has ganglion blocking properties and causes hypotension
60
what are the dosage forms of procainamide?
oral iv - slow infusion im
61
how is procainamide metabolized?
hepatic NAPA - n acetyl procainamide
62
NAPA has class _ effects causing
3 torsades de pointes
63
how is procainamide excreted?
renally
64
T or F procainamide does not need dose adjustment for patients in renal or heart failure
F , needed because eliminated renally
65
who is contraindicated for procainamide
hypersensitivity CHF renal failure shock patients
66
are there DDI concerns with procainamide?
YES potentiate cardiac effects of beta blockers hypotensive effect of thiazides anticholinergic effects neuromuscular blocking effects
67
what are the toxicities of procainamide
cardiotoxicity immunity issues blood dyscrasia pulmonary toxicity
68
what are the cardiotoxicity effects of procainamide?
excessive action potential prolongation QT interval prolongation induction of torsades de pointes arrhythmia syncope
69
1/3 of patients who take procainamide experience immune toxicities, what is that?
lupus erythematosus, arthralgia and arthritis
70
what kind of toxicities, blood dyscrasias, does procainamide have?
agranulocytosis bone marrow depression neutropenia hypoplastic anemia thrombocytopenia