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CP Test 1 > B4-017 CBCL: Dysrhythmias > Flashcards

B4-017 CBCL: Dysrhythmias Flashcards

1
Q
A

normal sinus rhythm

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2
Q

normal conduction velocity: PR interval

A

.2s

5 small boxes

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3
Q

normal conduction velocity: QRS

A

.12s

3 small boxes

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4
Q

normal conduction velocity: QT interval

A

.44s

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5
Q
  • time between start of SA node and AV firing
  • occurs due to “pause” effect of AV node
A

PR interval

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6
Q

time to depolarize all of the ventricular myocardium

A

QRS

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7
Q

time to repolarize all of ventricular myocardium

A

QT interval

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8
Q
A

first degree AV block

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9
Q
A

2nd degree AV block
Mobitz I

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10
Q
A

2nd degree AV block
Mobitz 2

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11
Q
  • progressive lengthening of PR until a beat is dropped
  • variable RR with a pattern
  • regularly irregular
  • usually asymptomatic
A

2nd degree AV block
Mobitz I

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12
Q
  • dropped beats that are not preceded by a change in PR interval
  • indicates structural issue: ischemia, fibrosis, sclerosis
  • requires pacemakers
A

2nd degree AV block
Mobitz II

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13
Q
  • P waves and QRS complexes are rhythmically dissociated
  • atria and ventricles beat independently of each other
  • atrial rate> ventricular rate
  • usually requires pacemaker
A

complete/ 3rd degree heart block

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14
Q
A

complete/3rd degree heart block

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15
Q
A

junctional rhythm

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16
Q
A

sinus bradycardia

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17
Q
A

asystole

check lead placement

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18
Q
A

sinus tachycardia

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19
Q
A

atrial flutter

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20
Q
A

atrial fibrillation

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21
Q
A

supraventricular tachycardia

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22
Q
A

monomorphic ventricular tachycardia

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23
Q
A

polymorphic ventricular tachycardia

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24
Q
A

ventricular fibrillation

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25
Q
A

torsades de pointes

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26
Q

irregularly irregular with no distinct p wave

A

atrial fibrillation

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27
Q

rapid succession of identical, consecutive artial depolarization waves causing a “sawtooth” appearance

A

atrial flutter

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28
Q
  • regular rhythm and rate
  • > 100 bpm
  • QRS > 120ms
  • commonly due to cardiomyopathy/ishchemia after infarction
  • high risk of sudden cardiac death
A

ventricular tachycardia

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29
Q

treatment of torsades de pointes

A

magnesium

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30
Q
  • polymorphic v tach
  • shifting sinusoidal waveforms
  • may progress to v fib
  • long QT interval predisposes risk
A

torsades de pointes

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31
Q

what causes drug induced long QT?

A

anti-Arrythmics
anti-Biotics
anti-Chychotics
anti-Depressants
anti-Emetics
anti-Fungals
Navir (protease inhibitors)
Opiods

ABCEDEF + NO

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32
Q
  • disorganized rhythm with no identifiable waves
  • fatal without immediate defibrillation
A

ventricular fibrillation

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33
Q
  • prolonged PR interval
  • benign and asymptomatic
A

first degree heart block

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34
Q

classes of drugs used for rate control

A
  • B-blocker
  • Ca+ channel blockers
  • digoxin
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35
Q

classes of drugs used for rhythm control

A
  • Na+ channel blockers
  • K+ channel blockers
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36
Q

class 1 of antiarrhythmic drugs are

A

Na+ channel blockers

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37
Q

class 2 antiarrhythmic drugs are

A

B blockers

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38
Q

class 3 antiarrhythmic drugs are

A

K+ channel blockers

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39
Q

class 4 antiarrhythmic drugs are

A

Ca+ channel blockers

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40
Q

Drugs in class IA

A
  • Procainaminde
  • Quinidine
  • Disopyramide

The queen proclaims Diso’s pyramid

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41
Q

Drugs in class 1B

A
  • Lidocaine
  • Mexiletine
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42
Q

drugs in class 1C

A
  • Flecainide
  • Propafenone
  • Moricizine
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43
Q

drugs in class 2

A
  • propranolol
  • metoprolol
  • esmolol
44
Q

drugs in class 3

A
  • amiodarone
  • dronedarone
  • sotalol
  • ibutilide
  • dofetilide
45
Q

drugs in class 4

A
  • verapamil
  • diltiazem
46
Q

other antiarrhythmic drugs

A
  • adenosine
  • digoxin
  • magnesium
47
Q

what class of drugs decrease the slope for phase 4 depolarization in SA node

A

Class 1

48
Q

what class of drugs decrease the heart rate but elevating the threshold for excitation

A

class 1

49
Q
  • moderate Na+ channel block
  • dissociate with intermediate kinetics
  • prolong APD
A

class 1A

50
Q
  • mild Na+ channel block
  • fast dissociation
  • shorten APD
A

class 1B

51
Q
  • strong Na+ channel block
  • slow dissociation
  • minimal effect on APD
A

class 1C

52
Q

has ganglion blocking activity which reduces peripheral vascular resistance and can cause hypotension

especially IV

A

procainamide

53
Q

long term therapy can cause a reversible lupus type syndrome
* rash
* arthralgia
* arthritis
* pericarditis

A

procainamide

54
Q

does procainamide elevate digoxin levels?

A

no

55
Q

least useful class 1A drug due to short half life and adverse effects

A

procainamide

56
Q

drug of second or third choice for sustained ventricular arrhythmias associated with myocardial infarction

A

procainamide

57
Q

similar to procainamide, with modest antimuscarinic effect

A

quinidine

58
Q
  • blocks a-adrenergic receptors to cause vasodilation
  • marked hypotension and reflex tachycardia
A

quinidine

59
Q

adverse effects

  • increase plasma digoxin
  • thrombocytopenia
  • adverse GI effects
A

quinidine

60
Q

rarely used because of cardiac and extracardiac adverse effects and better bioavailbility of other drugs

A

quinidine

61
Q

similar effects to quindine and procainamide, but more antimuscarinic effects

A

disopyramide

62
Q

adverse effects:

  • urinary retention
  • dry mouth, blurred vision, constipation
  • worsening of glaucoma

atropine-like activity

A

disopyramide

63
Q
  • not used very often because of antimuscarinic effects
  • only approved in USA to treat ventricular arrhythmias
A

disopyramide

64
Q

must be given IV due to high first-pass hepatic metabolism

A

lidocaine

65
Q
  • treats unstable v tach
  • relatively uneffective for atrial flutter or fibrillation
A

lidocaine

66
Q

low incidence of toxicity and high degree of effectiveness

A

lidocaine

67
Q

lidocaine analog, but resistant to first-pass metabolism

A

mexiletine

68
Q
  • useful for ventricular arrythmias
  • can be used off label for diabetic neuropathy
A

mexiletine

69
Q

adverse effects

predominantly neurologic:
* tremor
* blurred vision
* lethargy
* nausea

A

mexiletine

70
Q

increase mortality from cardiac arrest or arrhythmic sudden death in patients with recent MI

A

Class 1C antiarrhythmics

71
Q
  • no QT prolongation
  • no antimuscarinic effects
  • used to treat supraventricular arrhythmias
  • effictive in suppressing PVCs
A

flecainide

72
Q
  • blocks Na+ channels, weak B blocker
  • has metallic taste
  • may exacerbate arrythmias and cause constipation
A

propafenone

73
Q
  • antiarrhythmic phenothatzine derivative
  • used for ventricular arrhythmias
  • withdrawn from US market
A

moricizine

74
Q
  • frequently used for rate control
  • treat supraventricular and ventricular arrythmias causes by SNS
  • prevent ventricular fibrillation

2

A

propranolol (nonselective)
atenolol (b1 selective)

75
Q
  • short acting drug
  • IV
  • used for acute tachycardias occurring during surgery
A

esmolol (b1 selective)

76
Q

harmful effect of Class 2: b-blockers

A

negative inotrope

77
Q
  • dimish SNS activation of the heart and vessels
  • dimish cardiac workload
  • clear mortality benefit in CHF
A

Class 2: b- blockers

78
Q
  • oral or IV
  • treats atrial fibrillation
A

amiodarone

79
Q
  • prolongs AP duration by blocking K+ channels
  • decreases rate of firing in pacemaker cells by blocking Na+ channels
  • blocks a- and b- adrenergic receptors and Ca+ channels
  • bradycardia
A

amiodarone

80
Q

causes peripheral vasodilation after IV administration

A

amiodarone

81
Q

can cause pulmonary fibrosis

A

amiodarone

82
Q

can cause gray-blue skin discoloration

A

amiodarone

83
Q

can cause corneal microdeposits and blindess

A

amiodarone

84
Q

can cause hypo or hyper thyroidism

A

amiodarone

85
Q
  • long half life
  • measurable even after a year
A

amiodarone

86
Q
  • metabolized by CYP3A4
  • can elevate digoxin or warfarin
A

amiodarone

87
Q

structural analog of amiodarone, no iodine

A

dronedarone

88
Q

can cause severe liver toxicity to the point of requiring transplant

A

dronedarone

89
Q

“black box” FDA warning regarding an increased risk of death, stroke, and heart failure in patients with decompensated heart failure or permanent a fin

A

dronedarone

90
Q
  • non selective b-blocker that prolongs ADP
  • treatment of life-threatening ventricular arrhythmias in pediatrics
A

sotalol

91
Q

dofetilide is administed

A

orally

92
Q

ibutilide is administered

A

IV

93
Q
  • block rapid component of delayed rectifier K+ current to slow cardiac repolarization
  • good to restore normal sinus rhythm in a fib or flutter

2

A

dofetilide or ibutilide

94
Q
  • orally active
  • block L type Ca+ channels
  • rate control for a fib

2

A

verapamil, diltiazem

95
Q

opens inward rectifier K+ channels –> hypopolarization

A

adenosine

96
Q
  • inhibits L type calcium channels
  • mainly effects AV node, not SA node
  • very short half life
  • treats paroxysmal supraventricular tachycardia
A

adenosine

97
Q

adverse effects

  • flushing
  • SOB
  • chest burning
  • headache
  • hypotension
  • nausea
  • paresthesia
A

adenosine

98
Q
  • potent and selective NaKATPase inhibitor
  • positive inotrope
A

digoxin

99
Q
  • stimulates vagus nerve to decrease heart rate without affecting blood pressure
  • used in a fib
A

digoxin

100
Q
  • very narrow therapeutic window
  • many drug-drug interactions
A

digoxin

101
Q

drugs that enhance digoxin toxicity

A
  • quinidine
  • amiodarone
  • captopril
  • verapamil
  • dilitiazem
  • cyclosporine
102
Q
  • GI: nausea, vomiting, diarrhea, abdominal discomfort
  • Cardiac: can lead to almost all arryhthmias
A

digoxin toxicity

103
Q

administed parenterally

A

magnesium

104
Q

used to prevent/treat torsades de pointes
and digoxin induced arrhythmias

A

magnesium

105
Q
  • effective mainly in the treatment of ventricular arrhythmias
  • stable v tach
A

magnesium

CP Test 1 (16 decks)

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