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anti-arrhythmic agents Flashcards

1
Q

arrythmias are classified by

A

site of origin of abnormality
complex on ECG
rhythm
rate

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2
Q

what are the 4 mechanisms of arrhythmia production?

A

altered automaticity
delayed after-depolarization
re-entry
conduction block

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3
Q

altered automaticity

A

latent pacemaker cells tack over the SA node’s role

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4
Q

delayed after depolarization

A

normal action potential of cardiac cell triggers a train of abnormal depolarizations

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5
Q

re-entry

A

refractory tissue reactivated repeatedly and rapidly due to unidirectional block which causes abnormal continuous circuit of APs

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6
Q

conduction block

A

impulse fail to propagate in non-conducting tissue

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7
Q

when do cardiac arrhythmias require treatment

A

when they cannot be corrected by removing the precipitating cause

when hemodynamic stability is compromised

when it predisposes to more serious cardiac arrhythmias or co-morbities

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8
Q

name some non-pharmacologic treatments of arrhythmias

A

acute - vagal maneuvers, cardioversion

prophylaxis - radio-frequency catheter ablation, implantable defibrillator

pacing - external, temporary, permanent

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9
Q

class I agents - moa

A

block sodium channels

this depresses phase 0 of the fast action potential
= depresses depolarization (decreased rate and slowing conduction velocity)

aka “membrane stabilizing agents”

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10
Q

what are class I agents used to treat?

A

SVT, a fib, WPW

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11
Q

class IA agents moa

A

intermediate Na channel blocker

slows conduction velocity and pacemaker rate

  • decreased depol (phase 0)
  • prolonged repol (must block K channels to some degree)
  • increased AP duration

direct depressant effects on SA and AV node

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12
Q

what do you use class IA agents for

A

atrial and ventricular arrhythmias

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13
Q

name the class IA agents

A

quinimide (prototype) - no longer available
procainamide
disopyramide (Norpace)

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14
Q

why aren’t class IA drugs commonly used?

A

they cause toxicity and may precipitate heart failure

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15
Q

what is disopyramide

A

PO agent that suppresses atrial and ventricular tachyarrhythmias

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16
Q

what are the negative side effects of disopyramide

A

myocardial depressant effects and can precipitate CHF and hypotension

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17
Q

when do you use procainamide

A

used in the treatment of vent tachycardias (less effective with atrial)

was once part of ACLS algorithm

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18
Q

dose of procainamide

A

loading: 100 mg IV q5min until rate controlled (MAX = 15 mg/kg)

then

infusion: 2-6 mg/min

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19
Q

side effects of procainamide

A

myocardial depression leading to hypotension

syndrome that resembles lupus

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20
Q

therapeutic levels of procainamide

A

= 4-8 mcg/ml

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21
Q

how protein bound is procainamide

A

15%

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22
Q

what is the half life of procainamide

A

2h

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23
Q

what are the class IC agents

A

flecainide (prototype)

propafenone (PO)

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24
Q

class IC moa

A

slow Na+ channel blocker (slow dissociation) so does not vary much with cardiac cycle

causes potent decrease of depolarization rate (phase 0) and decreased conduction rate with increased AP

markedly inhibits conduction through His-Purkinje system

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25
Q

Flecainamide uses and side effects

A

effective in treatment of suppressing PVS and ventricular tach, also atrial tach, WPW (reentry syndrome)

PO

has pro-arrhythmic side effects **can cause sudden death with v-fib

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26
Q

propafenone uses and side effects

A

suppression of ventricular and atrial tachyarrhythmias

PO

has pro-arrhythmic side effects - can cause torsades and sudden death with vfib

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27
Q

what are the class IB agents

A

lidocaine (prototype)
mexiletine (PO)
phenytoin

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28
Q

class IB moa

A

fast Na channel blocker = fast dissociation
alters AP by inhibiting Na ion influx via rapidly binding to and blocking sodium channels

produces little effect on max velocity depol rate, but shortens AP duration adn shortens refractory period

decreases automaticity

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29
Q

lidocaine use and SE

A

used in treatment of ventricular arrhythmias
particularly effective with suppression reentry rhythm: V tach, v fib, PVCs

don’t use to treat v fib after acute MI because it increases mortality d/t bradyarrhythmias

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30
Q

dose of lidocaine

A

IVP: 1-1.5 mg/kg
gtt: 1-4 mg/min (max dose 3 mg/kg)

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31
Q

how protein bound is lidocaine

A

50%

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32
Q

how is lidocaine metabolized

A

hepatic metabolism - cyp450
- active metabolite prolongs elimination half time

extensive first pass metabolism when taken PO

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33
Q

what can alter metabolism of lidocaine

A

impaired by

  • drugs such as cimetidine and propanolol
  • CHF, acute MI, liver dysfunction
  • General anesthesia

can be induced by barbs, phenytoin, or rifampin

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34
Q

describe lidocaine elimination

A

10% eliminated renally

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35
Q

adverse effects of lidocaine

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 pre-existing neuromuscular blockade

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36
Q

what is mexiletine used for

A

chronic suppression of ventricular tachyarrhythmias - PO agent

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37
Q

dose of mexiletine

A

150-200 mg Q8H

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38
Q

why can mexilitine be taken orally and lidocaine cannot

A

amine side group allows for PO admin because it avoids first pass metabolism

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39
Q

phenytoin uses

A

effects resemble lidocaine
used in suppression of ventricular arrhythmias associated with digitalis toxicity

can also be used for other ventricular tachycardias or torsades

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40
Q

how is phenytoin given

A

IV in NS

will precipitate in D5W

can be painful in peripheral IV

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41
Q

dose of phenytoin

A

1.5 mg/kg every 5 minutes up to 10-15 mg/kg

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42
Q

therapeutic blood levels of phenytoin

A

10-18 mcg/ml

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43
Q

how is phenytoin metabolized

A

by the liver

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44
Q

how is phenytoin excreted

A

in the urine

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45
Q

what is the elimination half time of phenytoin

A

24 hours

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46
Q

what are the adverse effects of phenytoin

A

CNS disturbances, partially inhibits insulin secretion, bone marrow depression, nausea, ataxia, slurred speech, severe hypotension with rapid admin

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47
Q

class II moa

A

beta-adrenergic agonists

depress spontaneous phase 4 depolarization resulting in SA node discharge decrease = slowing of heart rate and decreased mvo2

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48
Q

class II moa

A

beta-adrenergic agonists

depress spontaneous phase 4 depolarization resulting in SA node discharge decrease = slowing of heart rate and decreased mvo2

slows speed of conduction of cardiac impulses through atrial tissues and AV node resulting in prolongation of PR interval, increased duration of AP, decrease automaticity

prevents catecholamine binding to beta receptors

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49
Q

what are class II agents used for

A

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

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50
Q

What are the class II agents

A

propanolol (prototype)
esmolol
metoprolol

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51
Q

what is the selectivity of propanolol

A

non-selective

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52
Q

what is the use of propanolol

A

to prevent reoccurence of tachyarrhythmia, both supraventricular and ventricular precipitated by SYMPATHETIC STIMULATION

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53
Q

what is the onset of propanolol

A

2-5 minutes

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54
Q

when would you expect peak effects of propanolol

A

10-15 minutes after given

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55
Q

what is the duration of propanolol

A

3-4 hours

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56
Q

what is the elimination half time of propanolol

A

2-4 hours

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57
Q

what are the cardiac effects of propanolol

A

decreased HR, contractility, and CO

increased PVR (bronchoconstriction d/t beta2 block), coronary vascular resistance

Decreased MVO2 (demand)

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58
Q

what is the selectivity of metoprolol

A

beta 1 selective

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59
Q

dose of metoprolol

A

5mg over 5 min

max dose 15 mg over 20 min

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60
Q

onset of metop

A

2.5 min

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61
Q

duration/half-life of metop

A

3-4 hours

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62
Q

how is metop metabolized

A

liver

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63
Q

when do you use metop

A

mild CHF

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64
Q

what is the selectivity of esmolol

A

selective for beta 1

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65
Q

what is the dose of esmolol

A

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

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66
Q

what is the duration of esmolol

A

<10 mins = quick acting, short acting

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67
Q

how is esmolol metabolized

A

hydrolyzed by plasma esterases

68
Q

in small doses, how does esmolol effect HR and BP

A

effects HR (decrease) without significantly decreasing BP

69
Q

class III agents moa

A

block potassium channels which

  • prolongs cardiac depolarization (cells don’t start to repol because VGKs dont open)
  • increased AP duration (because K can’t efflux to bring cells back to baseline)
  • lengthening repolarization (same as above)

PROPORTION OF CARDIAC CYCLE WHERE CELLS ARE EXCITABLE IS DECREASED = aka longer time in refractory aka cell isn’t susceptible to AP trigger

70
Q

class III agent uses

A

treat supraventricular and ventricular arrhythmias

preventative in patients who have survived sudden cardiac death who are not candidates for ICD

control rhythm in Afib
- this is given prophylactically in cardiac surgery patients because there is a high incidence of afib

71
Q

what is a negative ekg change caused by class III agents

A

prolongation of QT interval can lead to torsades

72
Q

what are the class III agents

A 
amiodarone (prototype)
dronedarone
ibutilide
dofetilide (PO)
sotalol
73
Q

amiodarone moa

A 
characterized as class III but also has I, II, and IV properties
 - aka it blocks K, Na, and Ca channels and its a beta agonist

however, it works primarily in phase II and III as a k channel blocker

74
Q

uses of amiodarone

A

prophylaxis or acute treatment for atrial and ventricular arrhythmias (refractory SVT, refractory VT/VF, AF)

1st line drug for VT/VF when resistant to electrical defibrillation

“one of the most effective drugs at preventing arrhythmias in patients with HF”

75
Q

dose of amiodarone

A

bolus 150-300 mg IV over 2-5 minutes, up to 5 mg/kg

then

1 mg/hr for 6 hours

then

0.5 mg/hr for 18 hours

76
Q

what is the elimination half life

A

29 days - prolonged

77
Q

how is amiodarone metabolized

A

hepatic with active metabolite

78
Q

how is amiodarone excreted

A

biliary/intestinal excretion

79
Q

what is the therapeutic plasma level for amio

A

1.0-3.5 mcg/ml

80
Q

is amio protein bound?

A

yes 96%, extensively

81
Q

describe the volume of distribution of amiodarone

A

large

82
Q

amiodarone adverse effects

A 
PULM TOXICITY (lung fibrosis d/t free O2 radicals in drugs)
pulm edema
ARDS
abnormal LFT
photosensitive rash
grey/blue skin discoloration
thyroid abnormalities
corneal deposits
TORSADES (arrhythmic effects)
HEART BLOCK 
HYPOTENSION
sleep disturbances
CYP450 INHIBITOR!!!!!!
83
Q

sotalol moa

A 
primarily class III drug with some class II action 
aka K channel blocker with some nonselective beta agonism included
84
Q

uses of sotalol

A

used to treat severe sustained v tach and v fib, to prevent reoccurrence of tachyarrhythmias (especially afib and aflutter)

85
Q

side effects of sotalol

A 
prolonged qt interval 
bradycardia
myocardial depression
fatigue
dyspnea
av block
86
Q

what is a patient population you should use caution with when giving sotalol (think respiratory)

A

asthma because non selective beta antagonism action

87
Q

how is sotalol excreted

A

urine

88
Q

dofetilide and ibutilide uses and main SE

A

class III

used for conversion of afib or aflutter to NSR
used for maintenance of SR after afib or conversion of afib to sinus

SE: pro-arrhythmic d/t prolongation of QT interval

89
Q

name the class IV calcium channel blockers

A

verapamil
diltiazem
nifedipine

90
Q

where are calcium ion channels?

A 
skeletal muscle cell membrane
VSMC
cardiac muscle
mesenteric muscle
neurons
glandular cells
coagulation
91
Q

calcium channel blockers moa

A

block L-type channels selectively to interfere with inward calcium ion movement across myocardial and vascular smooth muscle cells

92
Q

structure and area of action of verapamil

and moa at channel

A

phenyl-alkyl-amine at AV node

intracellular pore blocking of channel at binding site

93
Q

structure and area of action of diltiazem

and moa

A

benzothiazepine at AV node

mechanism unclear

94
Q

structure and area of action of nifedopine

and moa

A

1, 4-dihydropyridine at arterial beds

extracellular allosteric modulation of channel at binding site

95
Q

structure and importance of L-type calcium channel

A

5 subunits
alpha 1 is the central part of channel and provides main path for Ca2+ to enter
this is a slow channel

important in determining vascular tone and cardiac contractility

96
Q

vascular uses of calcium channel blockers

A 
angina
systemic hypertension
pulmonary hypertension
cerebral arterial spasm
raynauds
migraine

ca channel blockers dilate coronary arteries and decrease contractility of VSMC

97
Q

non-vascular uses of calcium channel blockers

A

bronchial asthma
esophageal spasm
dysmenorrhea
premature labor (prevention)

98
Q

effects of ca channel blockers

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 and BP
- arterial > venous
decreased mvo2 (demand)

99
Q

uses for calcium channel blockers

A

treatment of SVT, ventricular rate control in afib and aflutter
prevention of reoccurrence of SVT

NOT used in ventricular arrhythmias

100
Q

verapamil structure highlights

A

phenylakylamine
synthetic derivative of papaverine
levoisomer is specific for the slow calcium channel

101
Q

moa verapamil

A

depresses the AV node
negative chronotropic effects on SA node aka decreased HR
negative inotropic effects on myocardial muscle aka decreased contractility
moderate vasodilation on coronary as well as systemic arteries

102
Q

clinical uses for verapamil

A 
SVT
vasospastic angina pectoris
HTN
hypertrophic cardiomyopathy
maternal and fetal tachydysrhythmias
premature onset of labor
103
Q

protein binding of verapamil

A

highly protein bound - presence of other agents that are protein bound such as lidocaine, diazepam, propanolol increase its activity

104
Q

absorption of verapamil

A

orally almost completely absorbed with extensive hepatic metabolism and almost none of the drug appears unchanged in the urine

105
Q

oral and IV peak of verapamil

A 
PO = 30-45 minutes
IV = 15 minutes
106
Q

elimination half time of verapamil

A

6-12 hours

6-8 on later slide?

107
Q

dose of verapamil

A

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

continuous gtt 5 mcg/kg/min

108
Q

what med is iv verapamil contraindicated with

A

beta blockers because it can cause a heart block

109
Q

how is verapamil metabolized

A

hepatic with active metabolite norverapamil

110
Q

how is verapamil excreted

A

in the urine and bile

111
Q

side effects of verapamil

A

myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs effects of NMBDs

112
Q

site of action of diltiazem

A

AV node is prinicple site of action

113
Q

what is the first line treatment for SVTs

A

diltiazem

114
Q

what is the relative potency of diltiazem in comparison to the other class IV calcium channel blockers

A

intermediate between verapamil and nifedipine

115
Q

what is the extent of CV depressant effects of diltiazem

A

minimal

116
Q

clinical uses of diltiazem

A 
SVT***
vasospastic angina pectoris
HTN
hypertrophic cardiomyopathy
maternal and fetal cardiac dysrhythmias
117
Q

dose of diltiazem

A

0.25-0.35 mg/kg over 2 minutes, can repeat in 15 minutes

infusion = 10 mg/h

118
Q

oral onset and peak of diltiazem

A

15 minutes peaks in 30

119
Q

protein binding of diltiazem

A

70-80%

120
Q

excretion of diltiazem

A

bile and urine

121
Q

what patients would need a decrease in dose of verapamil

A

liver disease

122
Q

clinical uses of nifedipine

A

angina pectoris

123
Q

primary site of action of nifedipine

A

peripheral arterioles

124
Q

clinical effect on SA/AV node?

A

little to no effect

125
Q

what is a HR concern for nifedipine

A

reflex tachycardia

126
Q

what patients are at risk for myocardial depression with nefedipine?

A

patients with LV dysfunction or those on beta blockers

127
Q

what are the routes of admin for nifedipine

A

IV, PO, sublingual

128
Q

oral onset and peak

A

onset 20 minutes

peak 60-90 minutes

129
Q

protein binding of nifedipine

A

90% protein bound

130
Q

metabolism of nifedipine

A

hepatic

131
Q

excretion of nifedipine

A

urine

132
Q

elimination half time of nifedipine

A

3-7 hours

133
Q

side effects of calcium channel blockers

A

cancer with long term use
cardiac problems
bleeding d/t interference with platelet function
constipation

vertigo, HA, flushing, hypotension, paresthesias, muscle wekaness

can induce renal dysfunction

134
Q

what is the drug interaction of calcium channel blockers with inhalational agents

A

myocardial depression

135
Q

what is the drug interaction of calcium channel blockers with NMBDs

A

can potentiate blocks

136
Q

what is the drug interaction of calcium channel blockers with beta blockers

A

risk for heart block - particularly with verapamil

137
Q

what is the drug interaction of calcium channel blockers with local anesthetics

A

verapamil increases risk of LA toxicity

138
Q

what is the drug interaction of calcium channel blockers with dantrolene

A

verapamil and dantrolene can cause hyperkalemia due to slowing of inward movement of K ions which can result in cardiac collapse

139
Q

what is the drug interaction of calcium channel blockers with digoxin

A

can increase the plasma concentration of digoxin by decreasing its plasma clearance

140
Q

what is the drug interaction of calcium channel blockers with H2 antagonists

A

ranitidine and cimetidine alter hepatic enzyme activity and thus could increase plasma levels of CCBs

141
Q

how do you reverse calcium channel blocker toxicity?

A

IV administration of calcium or dopamine

142
Q

why are patients on CCB a bleeding risk

A

they interfere with calcium mediated platelet function

143
Q

what can happen with abrupt d/c of CCBs

A

coronary vasospasm

144
Q

adenosine moa

A

binds to A1 purine nucleotide receptors

  • activates adenosine receptors to open K channels and increase K currents
  • slows AV nodal conduction
145
Q

what is adenosine used for

A

acute only to terminate SVT or for diagnosis of VT

146
Q

dose of adenosine

A

6mg iv rapid bolus

repeated if necessary after 3 minutes, 6-12 mg iv rapid bolus

147
Q

how affective is the first dose of adenosine vs the second dose

A

effective on first dose 60%

effective on second dose 90%

148
Q

half life of adenosine

A

<10 seconds

149
Q

elimination of adenosine

A

via plasma and endothelial cell enzymes

150
Q

side effects of adenosine

A

excessive AV or SA nodal inhibition, facial flushing, HA, dyspnea, chest discomfort, nausea, bronchospasm

151
Q

adenosine is contraindicated in which patients

A 
asthma (causes bronchospasm)
heart block (slows AV conduction)
152
Q

digoxin mechanism of action

A

comes from foxblood plant - cardiac glycoside

increases vagal activity, thus decreasing activity of SA node and prolongs conduction of impulses through AV node by increasing refractory period

decreases HR, preload, and afterload

153
Q

digoxin uses

A

for management of afib/flutter (controls ventricular rate) especially with impaired heart function

used to treat chf because it is a positive inotrope

154
Q

dose of digoxin

A

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

155
Q

onset of action of digoxin

A

30-60 minutes

156
Q

half life of digoxin

A

36 hours

157
Q

describe the therapeutic index of digoxin

A

narrow

0.5-1.2 ng/ml

158
Q

describe the protein binding of digoxin

A

weak

159
Q

how is digoxin excreted

A

90% by kidneys

160
Q

considerations for elderly or those with renal impairment?

A

reduce dose and frequently check levels

161
Q

adverse effects of digoxin

A

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

162
Q

how to treat digoxin toxicity

A

phenytoin for ventricular arrhythmias
pacing
atropine

163
Q

magnesium moa

A

works at sodium, potassium, and calcium channels

164
Q

when do you use magnesium

A

torsades

165
Q

dose of magnesium

A

1g IV over 20 minutes, can be repeated

Advanced Pharm (11 decks)

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