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N929 Pharmacology II > Anti-arrhythmic agents II > Flashcards

Anti-arrhythmic agents II Flashcards

1
Q

Class 1 agents work by

A

blocking sodium channels which depresses phase 0; decreases in action potential propagation (decrease in depolarization rate) and slowing of conduction velocity

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2
Q

Class 1 agents are used to treat

A

SVT, AF, and WPW

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3
Q

Class 1A agents have direct depressant effects on

A

the SA & AV node

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4
Q

Class 1A agents work by

A

slowing conduction velocity and pacemaker rate
intermediate Na+ channel blocker
decreases depolarization rate
prolongs repolarization

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5
Q

Class 1A agents are used for

A

atrial and ventricular arrhythmias

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6
Q

Class 1A agents are eliminated by

A

hepatic metabolism

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7
Q

Class 1A agents can cause

A

a reversible lupus like syndrome

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8
Q

The class 1A drugs include:

A

Quinidine-prototype
procainamide
disopyramide

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9
Q

Class 1A agents are not commonly used because

A

they can cause toxicity that may precipitate heart failure

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10
Q

Disopyramide is an

A

oral agent, used to suppress atrial and ventricular tachyarrhythmias, and has significant myocardial depressant effects and can precipitate CHF and hypotension

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11
Q

Procainamide is used

A 
in the treatment of ventricular tachyarrhythmias (less effective with atrial)
class 1A drug
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12
Q

Side effects of procainamide include

A

myocardial depression leading to hypotension & syndrome that resembles lupus erythematous

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13
Q

The dosage of procainamide is

A

loading 100 mg IV every 5 minutes until rate controlled (max 15 mg/kg); then infusion 2-6 mg/min.

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14
Q

Class 1C agents include:

A

flecainide- Class 1C prototype

propafenone (oral)

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15
Q

Class 1C agents work by

A

slowing Na+ channel blocker (slow dissociation)
potent decrease of depolarization rate phase 0 and decreased conduction rate with increased AP
markedly inhibits conduction through the His-Purkinje system

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16
Q

Propafenone is used for (& how supplied)

A

suppression of ventricular and atrial tachyarrhythmias
has pro-arrhythmic side effects
oral agent

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17
Q

Flecainide is effective in the treatment of

A

suppressing ventricular PVCs and ventricular tachycardia, also atrial tachyarrhythmias; Wolff-Parkinson-White syndrome

  • oral agent
  • has pro-arrhythmic side effects
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18
Q

Class 1B agents include:

A

lidocaine-prototype
Mexiletine (oral)
Phenytoin

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19
Q

Class 1B agents work by

A

fast dissociation on fast Na+ channel blocker
alters the AP by inhibiting sodium influx via rapidly binding to and blocking sodium channels (fast)
shortens AP duration and shortens refractory period
decreases automaticity

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20
Q

Lidocaine is used in the treatment of

A

ventricular arrhythmias- no longer recommended for preventing ventricular fibrillation after acute MI
particularly effective in suppression reentry rhythms: ventricular tachycardia, fibrillation, PVCs

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21
Q

Dosage of lidocaine includes:

A

1-1.5 mg/kg IV; infusion 1-4 mg/min (mas dose 3 mg/kg)

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22
Q

Lidocaine is metabolized in

A

the liver and is 50% protein bound

has active metabolite which prolongs elimination half-time

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23
Q

Lidocaine is eliminated

A

10% renally

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24
Q

Lidocaine metabolism may be impaired by

A

drugs such as cimetidine and propranolol or physiological altering conditions such as CHF, acute MI, liver dysfunction

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25
Q

Lidocaine metabolism might be induced by

A

drugs like barbiturates, phenytoin, or rifampin

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26
Q

Adverse effects of lidocaine include

A

hypotension, bradycardia, seizures, CNS depression, drowsiness, dizziness, lightheadedness, tinnitus, confusion, apnea, myocardial depression, sinus arrest, heart block, ventilatory depression, cardiac arrest, and can augment preexisting neuromuscular blockade

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27
Q

Mexiletine is used for

A

1B drug used for chronic suppression of ventricular cardiac tachyarrhythmias

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28
Q

Phenytoin is used for

A 
class 1B agent and is used in suppression of ventricular arrhythmias associated with digitalis toxicity
can also be used for ventricular tachycardias or torsade de pointes
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29
Q

Phenytoin dose:

A

1.5 mg/kg IV every 5 min up to 10-15 mg/kg
can cause pain or thrombosis when given peripheral IV
can cause severe hypotension if given rapidly

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30
Q

Therapeutic blood levels of phenytoin include:

A

10-18 mcg/mL

toxicity causes CNS disturbances

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31
Q

Phenytoin metabolism and excretion

A

liver; excreted urine

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32
Q

Elimination half time of phenytoin is

A

24 hours

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33
Q

Adverse effects of phenytoin include

A

CNS disturbances, partially inhibits insulin secretion, bone marrow depression, nausea, associated with Steven Johnson’s syndrome

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34
Q

Class II drugs include

A

beta-adrenergic antagonists and they work by depressing spontaneous phase 4 depolarization resulting in SA node discharge

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35
Q

Class II drugs work by

A

slow speed of conduction of cardiac impulses through atrial tissues; decreased automaticity; drug-induced slowing of heart rate with decreases in myocardial oxygen requirements is desirable in patients with CAD

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36
Q

Class II agents include

A

propanolol- prototype

esmolol

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37
Q

Class II agents are used to treat

A

SVT, atrial and ventricular arrhythmias
used to suppress and treat ventricular dysrhythmias during MI and reperfusion
treat tachyarrhythmias secondary to digoxin toxicity and SVT (afib or aflutter)

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38
Q

Class II agents help with tachyarrhythmias because

A

they prevent catecholamine binding to beta receptors
slow heart rate
decrease myocardial oxygen requirements

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39
Q

Propranolol is a

A

beta-adrenergic antagonist (non-selective)

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40
Q

Propranolol is used to prevent

A

reoccurrence of tachyarrhythmias both supraventricular and ventricular precipitated by sympathetic stimulation

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41
Q

Cardiac effects of propranolol include

A

decreased HR, contractility, CO; increased PVR, coronary vascular resistance, and lowered oxygen demand

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42
Q

The onset, peak, and elimination half time of propranolol include

A

Onset: 2-5 minutes
Peak: 10-15 minutes, duration 3-4 hours
elimination half-time: 2-4 hours

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43
Q

Metoprolol is a

A

beta-adrenergic antagonist (selective B1)

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44
Q

The dose of metoprolol is

A

5 mg IV over 5 minutes; max dose 15 mg over 20 min.

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45
Q

The onset and half life of metoprolol is

A

onset: 2.5 min.

half-life: 3-4 hours

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46
Q

Metoprolol is metabolized

A

by the liver & can be used in mild CHF

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47
Q

Esmolol is a

A

beta-adrenergic antagonist (selective Beta 1)

effects HR without decreasing BP significantly

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48
Q

The dose of esmolol is

A

0.5 mg/kg IV bolus over 1 minute then 50-300 mcg/kg/min

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49
Q

The duration of esmolol is

A

<10 minutes

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50
Q

Esmolol is metabolized by

A

plasma esterases

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51
Q

Class III drugs work by

A

blocking potassium ion channels
work at phase III of cardiac cycle and extend repolarization, prolong depolarization, and increase action potential duration

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52
Q

Class III agents are used to treat

A

supraventricular and ventricular arrhythmias, and control rhythm in afib
prophylaxis in cardiac surgery patients related to high incidence of afib
preventative therapy in patients who have survived sudden cardiac death who are not candidates for ICD

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53
Q

Class III agents can cause

A

prolonged QT interval and torsades development

54
Q

Class III agents include

A 
amiodarone- class III prototype (can have thyroid dysfunction b/c contain iodine)
dronedarone
Ibutilide
Dofetilide (oral)
Sotalol
55
Q

Amiodarone is a

A

class III antiarrhythmic drug with class I, II, and IV antiarrhythmic properties

56
Q

Amiodarone works by

A

blocking potassium, sodium, and calcium, alpha and beta adrenergic antagonist

57
Q

Amiodarone is used for

A

prophylaxis or acute treatment in the treatment of atrial and ventricular arrhythmias (refractory SVT, refractory VT/VF, AF)
1st line drug VT/VF when resistant to electrical defibrillation

58
Q

Amiodarone dose is

A

bolus 150-300 mg IV over 2-5 minutes, up to 5 mg/kg then 1 mg/hr x 6 hours, then 0.5 mg/hr x 18 hours

59
Q

Amiodarone half-life is

A

29 days

60
Q

Amiodarone is metabolized

A

in the liver and has active metabolite (hence long half-life)
biliary/intestinal excretion

61
Q

Therapeutic plasma levels of amiodarone are

A

1.0-3.5 micrograms/mL

62
Q

Amiodarone protein binding is

A

96% and has large volume of distribution

63
Q

Patients receiving amiodarone need to be

A

monitored for potassium increases because they are susceptible to torsades

64
Q

Adverse effects of amiodarone include:

A

pulmonary toxicity, pulmonary edema, ARDs, photosensitive rashes, grey/blue discoloration of skin, thyroid abnormalities, corneal deposits, CNS/GI disturbance, pro=arrhythmic effects (torsades de pointes), heart block, hypotension, sleep disturbances, abnormal LFT (20%), inhibits hepatic CYP450 so might see prolonged effects of muscle relaxants, coumadin, or digoxin

65
Q

Sotalol side effects

A

prolonged QT interval, bradycardia, myocardial depression, fatigue, dyspnea, AV block

66
Q

Sotalol should be used in caution with

A

asthmatics

67
Q

Sotalol is excreted in

A

the urine

68
Q

Sotalol is used to treat

A

severe sustained ventricular tachycardia and ventricular fibrillation; to prevent reoccurrence of tachyarrhythmias especially aflutter and AF

69
Q

Sotalol is a

A 
Class II & class III antiarrhythmic drug 
beta-adrenergic antagonist (non-selective) and potassium channel blocker
70
Q

Dofetilide and Ibutilide are

A

Class III antiarrhythmics and are used for conversion of afib or aflutter to NSR
used for maintenance of NSR after afib or conversion of afib to sinus
proarrhythmic

71
Q

Class IV calcium channel blockers include

A

verapamil
diltiazem
nifedepine

72
Q

Calcium channel blockers work by

A

binding to the receptor on voltage-gated calcium ions maintaining the channels in an inactive or closed state

73
Q

Calcium ion channels are present in

A

cell membranes of skeletal muscle, vascular smooth muscle, cardiac muscle, mesenteric muscle, neurons, and glandular cells

74
Q

Calcium channel blockers are classified based on

A

structure
phenyl-alkyl-amines-AV node (Verapamil)
benzothiazepines-AV node (diltiazem
1,4- dihydrophyridines-arterial beds (Nifedipine)

75
Q

Calcium channel blockers work by

A

selectively interfering with inward calcium ion movement across myocardial and vascular smooth muscle cells

76
Q

Calcium channel blocker uses include

A

Vascular- angina, systemic hypertension, pulmonary hypertension, cerebral arterial spasm, Raynaud’s disease, migraine
Non-vascular- bronchial asthma, esophageal spasm, dysmenorrhea, premature labor

77
Q

Calcium channel blockers block

A

slow calcium channels and their primary site is the AV node during phase 2 (shortens phase 2)
contractility of the heart decreases

78
Q

Calcium channel blockers have several subtypes

A

and the L type channel is important in determining vascular tone and cardiac contractility
Decreased Ca+ keeps intracellular Ca+ low

79
Q

The effects of calcium channel blockers include

A

decreased contractility, decreased HR, decreased activity of SA node, decreased rate of conduction of impulses via AV node, vascular smooth muscle relaxation: decreased SVR & BP (arterial>venous)

80
Q

Calcium channel blockers are used to treat

A

SVT, ventricular rate control in afib & aflutter, used to prevent reoccurrence of SVT
not used in ventricular arrhythmias

81
Q

Calcium channel blockers include

A 
verapamil- class IV prototype
diltiazem
82
Q

Clinical uses of verapamil include

A

SVT, vasospastic angina pectoris, HTN, hypertrophic cardiomyopathy, maternal and fetal tachydysrhythmias, premature onset of labor

83
Q

Verapamil is a

A 
class IV antiarrhythmic
synthetic derivative of papaverine 
its levoisomer is specific for the slow calcium channel
84
Q

The primary site of verapamil is the

A

AV node
it depresses the AV node, negative chronotropic effect on SA node, negative inotropic effect on myocardial muscle, moderate vasodilation on coronary as well as systemic arteries

85
Q

Verapamil peak and half-life

A

oral: 30-45 minutes/IV 15 minutes

half life is 6-12 hours

86
Q

Verapamil is highly

A

protein bound & the presence of other agents such as lidocaine, diazepam, propranolol increase its activity

87
Q

Verapamil is (metabolism)

A

almost completely absorbed with extensive first pass metabolism and almost none of the drug appears unchanged in the urine

88
Q

Verapamil dose is

A

2.5-10 mg IV over 1-3 minutes (max dose 20 minutes)

continuous infusion 5 mcg/kg/minute

89
Q

Verapamil should not be given with

A

beta blockers as it leads to heart blocks

90
Q

Verapamil half life is

A

6-8 hours

91
Q

Verapamil is metabolized and excreted

A

metabolized in the liver with active metabolite

excreted in the urine and bile

92
Q

Verapamil side effects are

A

myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs effects of neuromuscular blockers

93
Q

Diltiazem is a

A

calcium channel blocker and benzothiazepine derivative

94
Q

Clinical uses of diltiazem include

A

similar to verapamil, SVT, vasospastic angina pectoris, HTN, hypertrophic cardiomyopathy, maternal and fetal tachydysrhythmias

95
Q

Diltiazem administration:

A

PO or IV
Dose is 0.25-0.35 mg/kg over 2 minutes can repeat in 15 minutes
IV infusion 10 mg/hr

96
Q

The principle site of action of diltiazem includes

A

the AV node

97
Q

The 1st line of treatment for SVT is

A

diltiazem

98
Q

Diltiazem has (potency)

A

intermediate potency between verapamil and nifedipine

also has minimal CV depressant effects

99
Q

The onset of action, peak, and elimination half- life of diltiazem is

A

oral onset: 15 minutes
peaks: 30 minutes
elimination half-life of 4-6 hours

100
Q

Diltiazem is excreted

A

in the bile and urine

also highly protein bound 70-80%

101
Q

General side effects of calcium channel blockers include:

A

cancer, cardiac problems, bleeding, constipation

102
Q

Nifedipine is a

A

dihydrophyridine derivative

calcium channel blocker

103
Q

Clinical uses of nifedipine include

A

angina pectoris

104
Q

The primary site of action of calcium channel blockers is

A

peripheral arterioles

has coronary and peripheral vasodilator properties > verapamil

105
Q

Nifedipine can cause

A

reflex tachycardia due to decreased SVR & BP
can produce myocardial depression in patients with LV dysfunction or on beta blockers
has little to no effect on SA or AV node

106
Q

Nifedipine can be administered

A

IV, oral, or sublingual

107
Q

Nifedipine is metabolized

A

in the liver and excreted in the urine

90% protein bound

108
Q

Drug interactions with calcium channel blockers include:

A

verapamil- increases risk of local anesthetic toxicity
beta blockers- can put someone into heart block
can potentiate neuromuscular blockers
can cause myocardial depression and vasodilation with inhalational agents
verapamil and dantrolene can cause hyperkalemia and can result in cardiac collapse

109
Q

Toxicity of calcium channel blockers may be reversed

A

with IV administration of calcium or dopamine

110
Q

Calcium channel blockers can interact with

A

calcium mediated platelet function
digoxin: CCBs can increase the plasma concentration of digoxin
H2 antagonists: ranitidine and cimetidine alter hepatic enzyme activity and thus could increase plasma levels of CCB

111
Q

Side effects of calcium channel blockers include

A

vertigo, HA, flushing, hypotension, paresthesias, muscle weakness, can induce renal dysfunction, coronary vasospasm with abrupt discontinuation

112
Q

_____ has the greatest coronary artery dilation among the calcium channel blockers

A

nicardipine

113
Q

Adenosine works by

A

binding to A1 purine nucleotide receptors (activates adenosine receptors to open K+ channels and increase K+ currents)
slows AV nodal conduction

114
Q

Adenosine is used for

A

termination of SVT/ diagnosis of VT

and to stop arrhythmia from occurring

115
Q

The dose of adenosine is

A

6 mg IV rapid bolus

repeated if necessary after 3 minutes, 6-12 mg IV

116
Q

The half-life of adenosine is

A

<10 seconds

117
Q

Adenosine is eliminated by

A

plasma and vascular endothelial cell enzymes in RBCs

118
Q

The side effects of adenosine include:

A

excessive AV or SA nodal inhibition, facial flushing, HA, dyspnea, chest discomfort, nausea, bronchospasm
contraindicated in asthma, heart block

119
Q

Digoxin is a

A

cardiac glycoside

positive inotrope- used to treat CHF

120
Q

Digoxin works by

A

increasing vagal activity and thus decreasing activity of SA node and prolongs conduction of impulses thru the AV node
decreases HR, preload, and afterload
slows AV conduction by increasing AV node refractory period

121
Q

Digoxin is used for the management of

A

atrial fibrillation or flutter (controls ventricular rate), especially with impaired heart function

122
Q

Digoxin dose is

A

0.5-1 mg in divided doses over 12-24 hours

123
Q

The onset of action of digoxin is

A

30-60 minutes

124
Q

The half time of digoxin is

A

36 hours

125
Q

Digoxin dosing needs to be reduced in

A

elderly & renal impairment

126
Q

Digoxin is excreted

A

by the kidneys

127
Q

Digoxin has a narrow

A

therapeutic index
0.5-1.2 ng/mL
need to check levels

128
Q

Magnesium works by

A

working at sodium, potassium, and calcium channels

129
Q

Magnesium can be used for

A

torsades de pointes

130
Q

Magnesium dose is

A

1 gm IV over 20 minutes and can be repeated

131
Q

The adverse effects of digoxin include

A

arrhythmias, heart block, anorexia, nausea, diarrhea, confusion, agitation
potentiated by hypokalemia and hypomagnesaemia

132
Q

The toxicity treatment for digoxin includes

A

phenytoin for ventricular arrhythmias, pacing, and atropine

N929 Pharmacology II (16 decks)

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