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Cardio Renal II Final > Pharmacology Anti-Arrhythmic 2 > Flashcards

Pharmacology Anti-Arrhythmic 2 Flashcards

1
Q

what are the cardiac effects of quinidine?

A

same as procainamide

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

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2
Q

what is the dosage form of quinidine?

A

oral - tablet
Iv - injecton

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3
Q

what are the pharmacokinetics of quinidine

A

absorbed in the GI tract
eliminated by hepatic metabolism - CYP3A4

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4
Q

what are the adverse effects of quinidine

A

qt interval prolongation
induction of torsades de pointes arrhythmia
excessive sodium channel blocked with slowed conduction throughout the heart

GI - NVD

CINCHONISM - HA dizzy tinnitus

immune - thrombocytopenia, hepatitis, angioneurotic edema, fever

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5
Q

does quinidine have DDI effects?

A

substrate of CYP3A4 - strong inhibitors and inducers

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6
Q

are there any contraindications for quinidine?

A

drugs causing QT prolongation and electrolyte imbalance

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7
Q

which drug from class IA has immediate release and controlled release capsules ?

A

disopyramide

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8
Q

how is disopyramide metabolized?

A

CYP3A4

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9
Q

T or F disopyramide needs dose adjustment in patients with renal impairment

A

T - decrease dose in renally impaired patietns

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10
Q

what is a major CI of disopyramide

A

may cause or worsen CHF - or produce severe hypotension as a consequence o its negative inotropic properties

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11
Q

disopyramide is given with

A

drugs slowing ventricular arrhythmia

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12
Q

what is a major adverse effect of disopyramide

A

atropine like activity - urinary retention, dry mouth, blurred vision, constipation and worsening of preexisting glaucoma

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13
Q

what is the mechanism of action of lidocaine

A

blocks activated and inactivated sodium chanells with rapid kinetics

exerts an antiarrhythmic effect by increasing the electric stimulation threshold of the ventricle during diastole

highly effective in arrhythmias associated with acute MI

greater effects on cells with long action potentials such as purkinje and ventricular cells compared with atrial cells

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14
Q

lidocaine is available as what dosage form

A

IV

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15
Q

how is lidocaine metabolized

A

extensive first pass metabolism
90% drug metabolized in liver - CYP1A2, 3A4 dealkylation

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16
Q

what is the half life of lidocaine

A

1-2 hours - loading and maintenance dose

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17
Q

lidocaine has high binding to _______

A

alpha acid glycoprotein

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18
Q

due to lidocaine high binding to alpha acid glycoprotein it is important to

A

measure plasma concentration for dose adjs - need higher dose

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19
Q

lidocaine dose should be decreased in patients who

A

have CHF
liver disease
take drugs that decrease liver perfusion - propanolol, cimetidine

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20
Q

therapeutic use of lidocaine

A

acute management of VA occurring during cardiac manipulations such as cardiac surgery
life threatening arrhythmias which are ventricular in origin occurring during acute MI

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21
Q

what are the CI of lidocaine

A

hypersensitivity to amide type anesthetics - lidocaine
stokes adams syndrome
wolf parkinson white syndrome
severe degrees of sinoatrial, atriovetricular or intraventricular block

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22
Q

which drug is the least cardiotoxic of the currently used Na+ channel blockers

A

lidocaine

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23
Q

what are the toxicities of lidocaine

A

may cause hypotension - partly by depressing myocardial contractility

CNS adverse effects - paresthesia, tremor, nausea of central orgin, lightheadedness, hearing disturbances, slurred speech, and convulsions

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24
Q

plasma levels of lidocaine need to be monitored and kept ______- to avoid side effects

A

9 ug/ml

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25
Q

what is the appropriate dosage form of mexiletine

A

oral, capsules

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26
Q

what are the similarities between mexiletine and lidocaine

A

structural similarities - local anesthetic properties

cardiac effects and properties

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27
Q

how is mexiletine metabolized?

A

hepatically by CYP2D6 - 10% unchanged

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28
Q

what is the mechanism of action of mexiletine

A

blocks the fast sodium channel in cardiac tissues, especially the purkinje network without involvement of the autonomic system

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29
Q

mexiletine treats

A

life threatening ventricular arrhythmias such as sustained vtach

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30
Q

T or F mexiletine needs dose adjustment in patients with hepatic impairment

A

T - acidic pH increases clearance

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31
Q

what are the adverse effects of mexiletine

A

neurologic - tremor, blurred vision, lethargy

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32
Q

what is the mechanism of action of flecainide

A

potent blocker of sodium and potassium channels with slow unblocking kinetics

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33
Q

T or F flecainide prolongs APD

A

F
Flecainide does not prolong APD

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34
Q

flecainide treats what condition

A

supraventricular arrhythmias with normal heart

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35
Q

what is the dosage form of flecainide

A

oral - tablet

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36
Q

what are the effects of flecainide

A

decreases ventricular conduction

effective in suppressing premature ventricular contractions and vtach

no antimuscarinic effects

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37
Q

what is the pharmacokinetic profile flecainide

A

well absorbed
half life - 20 hours
hepatic metabolis m- CYP2D6
eliminated by kidneys

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38
Q

class 1C drugs cannot be given to

A

previous MI or Vtach - leads to higher mortality

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39
Q

flecainide is used for therapeutic treatment of

A

life threatening vtach, PSVT, pAF

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40
Q

which class IC drug is Proarrhythmogenic

A

flecainide

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41
Q

PSVT stands for

A

paroxysmal supraventricular tachyvardia

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42
Q

propafenone is indicated for patients who

A

have documented life threatening ventricular arrhythmias

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43
Q

what is the mechanism of action propafenone

A

prolongs teh time to recurrence of symptomatic atrial fibrillation in patients with episodic AF who do not have structural heart disease

of PSVT associated with disabling symptoms in pts who do not have structural heart disease

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44
Q

propafenone is similar to propranolol due to

A

both have weak beta blocking action

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45
Q

propafenone is similar in effects to quinidine except

A

action potential prolongation

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46
Q

propafenone has ______ channel kinetics similar to flecainide

A

sodium / Na+

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47
Q

what is the dosage form of propafenone

A

tablet - oral

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48
Q

how is propafenone metabolized

A

hepatic metabolism

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49
Q

what are the CI of propafenone

A

heart failure
cardiogenic shock
hypotension
disorders of impulse generation and conduction
COPD
bradycardia
electrolyte imbalance
brugada syndrome

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50
Q

propafenone should be avoided in pts using

A

a CYP2D6 inhibitor and CYP 3A4 inhibitor

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51
Q

propafenone increase plasma concentrations of

A

digoxin, warfarin and proponalol

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52
Q

what are the AE of propafenone

A

provoke HF
conduction issues
sudden death - exacerbate arrhythmias
agranulocytosis
exacerbation of myasthenia gravis

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53
Q

class III drugs are K+ channel blockers also known as

A

multichannel blockers

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54
Q

class 3 drugs increase

A

APD and ERP

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55
Q

what are the five Class 3 drugs

A

amiodarone
dronedarone
dofetilide
sotalol
ibutilide

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56
Q

patients who fall into the category of underlying structure heart disease are patients who

A

have HF, LVEF less than 35, CAD, valvular heart disease, LVH

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57
Q

what are the key characteristics of class 3 drugs

A

they block potassium channels in phase 3, or enhance inward current

prolong effective refractory period ERP

increases action potential duration APD

reverse use dependence - high APD slows rates - causing torsade de pointes

low effects when high rates

ALL CAUSE QT PROLONGATION

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58
Q

T or F amiodarone is widely used, useful against most arrhythmias

A

T

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59
Q

key components of amiodarone structure is

A

T4/ thyroxine , two iodine on ring

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60
Q

what are the foru types of arrhythmias that can be treated with amiodarone

A

recurrent ventricular fibrillation
recurrent hemodynamically unstable ventricular tachycardia
afib
ventricular tachy as adj therapy to decrease the freq of uncomfortable cardioverter defibrillator discharges

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61
Q

what are the cardiac effects of amiodarone

A

prolongs APD
* blocks Ikr K+ channels - delayed rectifier
no reverse use dependence
blocks inavativated Na+ channels *
weak adrenergic inhibition and Ca++ bock
slows heart rate and AV node conduction
causes significant QT prolongation - low TdP incidence

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62
Q

what are the extra cardiac effects of amiodarone

A

peripheral vasodilation - IV

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63
Q

what dosage form is amiodarone available as

A

oral and iv

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64
Q

what is the bioavailability of the oral dosage form of amiodarone

A

tablet - 50

65
Q

what is the onset of action of amiodarone

66
Q

T or F Amiodarone is not effected by food

A

F, increased absorbtion with food

67
Q

T or F amiodarone is lipophillic

68
Q

where does amiodarone accumulate

A

in the adipose and thyroid tisseu

69
Q

how is amiodarone metabolized

A

hepatically, in liver,
CYP3A4, CYP2C8

70
Q

what is a major metabolite of amiodarone

A

desethylamiodarone
bioactive

71
Q

how is amiodarone excreted?

A

biliary excretion

72
Q

what is the half life of amiodarone

A

rapid component - 3-10 day , half the drug
slow component - several weeks

73
Q

how can one achieve rapid effects of amiodarone

A

via IV administration

74
Q

amiodarone has many DDI concerns, which drugs inhibit CYP3A4 and increase toxicity of amiodarone

A

protease inhibitors
loratidine
cimetidine
antidepressant - trazodone
grapefruit juice

75
Q

amiodarone has many DDI concerns, it can cause toxicity of which drugs due to enzyme and transporter inhibiton

A

cyclosporine
atorvastatin, simvastatin
digoxin
quinidine, procainamide, disopyramide
verapamil, propranolol
warfarin
clopidogrel

76
Q

amiodarone has many DDIs, including CYP3A4 inducers which decrease amiodarones efficacy

A

rifampin
st john wort

77
Q

what are miscellaneous substrates that amiodarone effects

A

increases fenatanyl , lidocaine

dextromethorpan increases
cholestyramine reduces amiodarone levels

78
Q

amiodarone and which drugs cause QT prolongation and lead to the higher risk of TdP

A

fluoroquinolones
macrolide abx
azoles

79
Q

what are the toxicities of amiodarone

A

pulmonary toxicity
bradycardia and heart block
worsened arrhythmia
thyrotoxicosis - blocks T4 to T3, large iodine in the body
liver injury
skin gray blue deposits
loss of vision - corneal microdeposits

80
Q

amiodarone may result in hypothyroidism which is known as

A

wolff chaikoff effect

81
Q

what is a structural analog of amiodarone

A

dronedarone

82
Q

how is dronedarone different from amiodarone

A

the iodine is removed, methanesulfonyl group on bezofuran

83
Q

what does the structural modification of amiodarone to dronedarone cause

A

there is no effect on the thyroxine metabolism but there is a decrease in half life

84
Q

what are key similarities between amiodarone and dronedarone?

A

cardiac effects
drug drug interactions
liver toxicity
absorption increases with food

85
Q

what are the key differences between amiodarone and dronedarone

A

no thyroid effects
no pulmonary toxicity

86
Q

what is the half life of dronedarone

87
Q

T or F dronedarone is both a substrate and inhibitor of CYP3A4

88
Q

T or F dronedarone is renally eliminated

89
Q

what is the black box warning for dronedarone

A

DO NOT USE IN HEART FAILURE PATIENTS

90
Q

what is a side effect of dronedarone?

A

it increases tubular secretion of creatinine which leads to 10-20% increase in creatinine

91
Q

what is the mechanism of action of sotalol

A

beta adrenergic receptor blocking Class 2 and action potential prolonging Class 3 actions

92
Q

what are the therapeutic uses of sotalol

A

life threatening ventricular arrhythmias and the maintenance of sinus rhythm in patients with afib

pediatric arrhythmias

decreases threshold for cardiac defib

WPW syndrome

93
Q

in what dosage forms is sotalol available

94
Q

what is the distribution of sotalol

A

well absorbed with a 100% bioavailability

95
Q

T or F sotalol binds to 50% of plasma proteins

A

F, no binding to plasma proteins

96
Q

how is sotalol metabolized

A

NO METABOLISM

97
Q

how is sotalol excreted

A

unchanged during eliminiation in urine

98
Q

what is the half life of sotalol

99
Q

what are the toxicities of sotalol

A

dose related incidence of torsafes de pointes

can cause serious ventricular arrhythmia
caution in using with drugs that prolong QT interval
caution in patients with HF
BRONCHOSPASM
anaphylaxis
caution in patients with heart block

100
Q

what is the mechanism of action of dofetilide

A

class 3 purely
dose dependent blockade of the delayed rectifier potassium current
blockade of IKr increases hypokalemia

101
Q

T or F Dofetilide shows moderate reverse use dependence

102
Q

what is the bioavailability of dofetilide

103
Q

what is the metabolism of dofetilide

A

20% metabolized, metabolites are inactive

104
Q

how is dofetilide eliminated

A

in the urine

105
Q

what drug increases the peak plasma concentration of dofetilide

106
Q

does dofetilide need to be adjusted for renally impaired patients

107
Q

drugs like cimetidine which inhibit the renal cation secretion mechanism cause what effect when taken with dofetilide

A

prolong the half life of dofetilide

108
Q

what are the therapeutic uses of dofetilide

A

effective in restoring the normal sinus rhythm in patients with afib

second to amiodarone in arrhythmia with HF

109
Q

what are the toxicities of dofetilide

A

ventricular arrhythmia
QT prolongation
Tdp
TdP risk higher with k depleting diuretics
caution with drugs that prolong QT and antiarrhythmic agents

110
Q

Dofetilide is CI in

A

Qt prolongation
bradycardia
hypokalemia

111
Q

Ibutilide is a therapeutic agent for patients with

A

atrial flutter
afib

112
Q

what is the mechanism of action of ibutilide

A

class 4 - blocks Ikr and activation of slow inward sodium current

113
Q

what is the dosage form of ibutilide

114
Q

how is ibutilide metabolized

A

rapidly by the liverh

115
Q

how is ibutilide excreted

A

excreted by KIDNEYs

116
Q

what is the half life ibutilide

117
Q

what are the adverse effects of ibutilide

A

qt prolongation
tdp

moitor ECG for 4 hours after IV administration till QT returns to normal

118
Q

what are the calcium channel blockers for antiarrhythmia

A

verapamil
diltiazem

119
Q

T or F DHP like nifedipine also share antiarrhythmic efficacy

A

F, they do not and may precipitate arrhythmias

120
Q

what is the mechanism of action of class IV drugs

A

block both activated and inactivates L type calcium channels

decreases SA node and AV node rate

121
Q

______ can decrease both early and delayed after depolarization

122
Q

what are the misc agents that have anti-arrhythmic properties

A

adenosine
ranolazine
ivabradine
magnesium

123
Q

_____ is a naturally occuring nucleoside

124
Q

what is the mechanism of action of adenosine

A

activates GPCR in the heart, Gi coupled which leads to the activation of inward rectifier K current leading
inhibition of calcium curent

125
Q

what is the therapeutic use of adenosine

A

acute termination of reentrant supraventricular arrhythmias

126
Q

what are the cardiac effects of adenosine

A

activates ach sensitive K+ current in the atrium, snius and av nodes
this leads to shortened action potential duraton, hyperpolarization and slowing of automaticity

slow HR, slow AV conduction

DECREASES INTRACELLULAR EFFECTS OF CYCLIC AMP decreases ca++currents

127
Q

what is the dosage form of adenosine

A

IV bolus only

128
Q

what is the half life of adenosine

A

seconds, rapid uptake

129
Q

how is adenosine metabolized

A

deamination

130
Q

what are the adverse effects of adenosine

A

safer - rapid clear
transient asystole
chest fullness and dyspnea when therapeutic doses

afib bronchospasm is rare

131
Q

DDI of adenosine

A

potentiation with dipyridamole
caffeine and theophylline have antagonising effects

132
Q

what is the dose of magnesium typically used

A

1g as sulfate given IV for 20 minutes

133
Q

what is the mechanism of action of magnesium

A

unknown, influences na K atpase, na channels , some k channels and ca channels

134
Q

magnesium is used to treat patients with

A

digitalis induced arrhythmias if hypomg

torsades de pointes even if normal mg

135
Q

which antianginal and anti-arrhythmic agent is a piperazine derivative

A

ranolazine

136
Q

ranolazine is a ____ and blocks late __ current

A

metabolic modulator
Na+

137
Q

what is the moA of ranolazine

A

inhibits late inward sodium current in heart muscle

138
Q

what is the result of the moa of ranolazine

A

leads to reductions in elevated intracellular calcium levels which leads to reduced tension in the heart wall leading to o2 requirements reducing for the muscle

139
Q

the effects of ranolazine are

A

increased glucose oxidation
increasing cardiac atp prod
prolongs APD an QT interval
decreasing edematous end products
decreases FA oxidation

DECREASES MYOCARDIAL O2 REQUIREMENTS
DECREASE CELL CONTRACTURE AND RUPTURE BY BALANCING NA CA CHANNEL
DECREASE MYOCARDIAL CELL SWELLING

140
Q

what is the normal adult dosage form of ranolazine and dose

A

extended release tablets
500 mg orally twice daily

141
Q

how is ranolazine metabolized

142
Q

how is ranolazine excreted

A

urine, monitor renal function

143
Q

DDI of ranolazine

A

cyp3a4 inducers and inhibition

144
Q

what is the CI of ranolazine

A

liver cirrhosis
strong CYP3A4 inhibitors and inducers

145
Q

what are the ADR of ranolazine

A

constipation
nausea
dizzy
asthenia - weakness loss of energy
qt prolongation but no Tdp

146
Q

what is the mechanism of action of ivabradine

A

selective blocker of hyperpolarization - activated HCN ion channels - called class 0 action

147
Q

with ivabradine , __ node function is regulated

148
Q

what is the caridac effect of ivabradine

A

decreases heart rate and thus oxygen demand

149
Q

what drug is a parasympatholytic

150
Q

what is the therapeutic use of atropine

A

symptomatic bradycardia
bradycardia with malignant escape rhythms and asystole

151
Q

how is atropine administered

152
Q

what is a caution to be aware of giving pts atropine

A

there is a paradoxical decrease in HR in AV block patientswha

153
Q

what are the AE of atropine

A

dry mouth
blurred vison
urinary retention
higher doses lead to CNS effects

154
Q

what is a general problem with anti arrhythmic drugs

A

can cause cardiac arrest at high doses by inhibiting all pacemaker activity

155
Q

many anti arrhythmic drugs are _____ especially at high doses by slowing conduction (RE ENTRY)

A

pro arrhythmic

156
Q

T or F some of the side effects of anti arrhythmic drugs are IRREVERSIBLE

157
Q

what are the general adverse effects of anti arrhythmic drugs

A

torsades
cinchonism
lupus
cholinergic
seizures
ataxia
nystagmus
sudden death
pulmonary fibrosis

158
Q

what is a key thing to remember when determining use of anti arrhythmic drugs

A

must determine whether the benefit of treatment outweights the liabiliteis of drug administration

Cardio Renal II Final (8 decks)

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