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N929 Pharmacology > Exam 2 Week 1- Anti-arrhythmic Agents > Flashcards

Exam 2 Week 1- Anti-arrhythmic Agents Flashcards

1
Q

Phase 0 (Cardiac Cell)

A

rapid depolarization (fast sodium channels open; fast inward flow of Na+)

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2
Q

Phase 1 (Cardiac Cell)

A

beginning of repolarization (sodium channels close)

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3
Q

Phase 2 (Cardiac Cell)

A

plateau (slow calcium channels open; slow inflow of Ca2+)

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4
Q

Phase 3 (Cardiac Cell)

A

repolarization (calcium channels close; potassium channels open; slow outward K current)

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5
Q

Phase 4 (Cardiac Cell)

A

pacemaker potential; returning to resting membrane potentials

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6
Q

Refractory period (Cardiac Cell)

A

phases 1-3

periods of repolarization

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7
Q

Phase 0 (SA/AV Node)

A

upstroke
critical firing threshold (-40mV)
slower and Ca2+ mediated

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8
Q

Phase 3 (SA/AV Node)

A

repolarization
inactivation of Ca2+ and Na+ channels
activation of K channels

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9
Q

Phase 4 (SA/AV Node)

A

gradual depolarization

slow inward Na and Ca2 currents

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10
Q

What node is the cardiac pacemaker?

A

Sino-atrial

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11
Q

Normal sinus rhythm is

A

60-100bpm

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12
Q

Which node conducts more slowly then the SA?

A

AV node

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13
Q

Which node conducts faster then the AV node?

A

Purkinje fibers

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14
Q

P wave indicates

A

Atrial depolarization

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15
Q

QRS complex represents

A

ventricular depolarization

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16
Q

T wave represents

A

ventricular repolarization

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17
Q

What is an arrhythmia

A

is the disturbance in the electrical activity of the heart

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18
Q

Classification of arrhythmia

A

site of origin of abnormality (atrial/junctional/ventricular)
complexes on ECG
Heart Rhythm (regular/irregular)
Heart rate is increased or decreased

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19
Q

Mechanisms of arrhythmia production

A

Altered automaticity
delayed after-depolarization
re-entry
conduction block

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20
Q

Altered automaticity

A

latent pacemarker cells take over the SA node’s role; escape beats

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21
Q

Delayed after-depolarization

A

normal action potential of cardiac cell triggers

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22
Q

Re-entry

A

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

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23
Q

Conduction Block

A

impulse fail to propagate in non-conducting tissue

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24
Q

Supraventricular Drugs

A

adenosine IV
digoxin
verapamil

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25
Q

Stress Induced Drugs

A

Class 2

beta blockers, propanolol, atenolol, sotalol

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26
Q

Sinus Bradycardia drugs

A

atropine IV

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27
Q

Ventricular and supra-ventricular drugs

A

Class 3- amiodarone, sotalol
Class 1A- procainamide and disopyramide
Class 1C- flecanide, propafenone

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28
Q

Ventricular Drugs

A

class 1B- lidocaine, mexlietine

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29
Q

Factors underlying cardiac arrhythmias

A 
arterial hypoxemia
electrolyte imbalance
acid-base abnormalities
myocardial ischemia
altered sympathetic nervous system activity
bradycardia
administration of certain drugs
enlargement of a failing ventricle
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30
Q

When do cardiac arrhythmias require treatment?

A

they cannot be corrected by the removing the precipitating cause
hemodynamic stability is compromised
the disturbance predisposed to more serious cardiac arrhythmias or co-morbidities

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31
Q

Non-pharmacological treatment

A

acute: vagal manuevers/cardioversion
Prophylaxis: radiofrequency catheter ablation/ implantable defibrillator
Pacing: External, temporary, permanent

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32
Q

What anti-arrhythmic agents utilized for?

A

used to prevent, suppress or treat a disturbance in cardiac rhythm

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33
Q

Class 1 Anti-arrhythmic Drug Class

A

Sodium Channel Blockers/Phase 0

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34
Q

Class 2 Anti-arrhythmic Drug Class

A

Beta adrenergic blocker/ Phase 4

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35
Q

Class 3: Anti-arrhythmic Drug Class

A

Potassium Channel Blockers

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36
Q

Class 4: Anti-arrhythmic Drug Class

A

Calcium Channel blockers

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37
Q

Class 5: Anti-arrhythmic Drug Class

A

Unclassified drugs

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38
Q

Electrophysiologic Effect of Class 1 Anti-Arrhythmic Drugs

A

depression of phase 0 depolarization (block of sodium channels)
Results in decreases in action potential propogation (decrease in depolarization rate) and slowing conduction velocity
membrane stabilizing agents
Binds to open or inactive gate best, not resting state

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39
Q

Electrophysiologic Effect of Class 1A Anti-Arrhythmic Drugs

A

Moderate depression and prolonged repolarization

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40
Q

Electrophysiologic Effect of Class 1B Anti-Arrhythmic Drugs

A

weak depression and shortened repolarization

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41
Q

Electrophysiologic Effect of Class 1C Anti-Arrhythmic Drugs

A

strong depression with little effect on repolarization

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42
Q

Electrophysiologic Effect of Class 2 Anti-Arrhythmic Drugs

A

Beta adrengeric blocking effects

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43
Q

Electrophysiologic Effect of Class 3 Anti-Arrhythmic Drugs

A

prolongs repolarization (blocks potassium channels)

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44
Q

Electrophysiologic Effect of Class 4 Anti-Arrhythmic Drugs

A

Calcium channel-blocking effects

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45
Q

Other Anti-arrhythmic Drugs

A

Adenosine, adenosine triphosphate, digoxin, and atropine

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46
Q

Class 1A Drugs

A

quindine, procainamide, disopyramide

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47
Q

Class 1B Drugs

A

lidocaine, mexiletine, phenytoin, tocainide

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48
Q

Class 1C drugs

A

flecainide, propafenone, moricizine

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49
Q

Class 2 drugs

A

esmolol, propanolol, metoproplol, timolol, pindolol, atenolol, acebutuolol, nadolol, carvedilol

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50
Q

Class 3 drugs

A

amiodarone, bretylium, sotalol, ibutilide, dafetilide

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51
Q

Class 4 Drugs

A

verampil, dilitiazem

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52
Q

Class 1 Agents treat

A

SVT, AF, WPW

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53
Q

Class 1A Agents

A

slow conduction velocity and pacemaker rate
intermediate sodium channel blocker (immediate dissociation)
direct depressant effects on SA and AV node (decrease automaticity)
Decreased depolarization rate (phase 0)
prolonged repolarization
Increased AP duration
Used for atrial and ventricular arrhythmias
Eliminated by hepatic metabolism
Implication in reversible lupus like syndrome
increases QT duration

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54
Q

Disopyramide

A

suppresses atrial and ventricular tachyarrhythmias
oral agent
has significant myocardial depressant effects and can precipitate congestive HF and hypotension

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55
Q

Procainamide

A

used in treatment of ventricular tachyarrhythmias (less effective with atrial)
15% protein bound
2 hour elimination time

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56
Q

Procainamide Dose

A

Loading 100mg IV Q5mins until rate controlled
max: 15mg/kg
Infusion 2-6mg/min

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57
Q

Procainamide Side Effects

A

myocardial depression leading to hypotension
syndrome that resembles lupus erythematous
Check blood levels 4-8mcg/ml

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58
Q

Class 1C Agents are good for

A

Block fast Na+ channels but slow dissociation

Good for PVC and Vtach but better for atrial arrhythmias like WPW

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59
Q

Flecainide

A

effective in the treatment of suppressing ventricular PVCs and ventricular tachycardia; also atrial tachyarrthymias; WPW
oral agent
has pro-arrhythmic side effects

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60
Q

Propafenone

A

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

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61
Q

Class 1C Agents MOA

A

Slow sodium channel blocker (slow dissociation) so does not vary much during the cardiac cycle
potent decrease of depolarization rate phase 0 and decreased conduction rate, with increased AP
marked inhibit conduction through the his purkinje system

62
Q

Class 1B Agents MOA

A

fast Na+ channel blocker (fast dissociation)
alters the action potential by inhibiting sodium ion influx via rapidly binding to an blocking sodium channels (fast)
produces little effect on maximum velocity depolarization rate, but shortens AP duration and shortens refractory period
decreases automaticity

63
Q

Lidocaine

A

used in the treatment of ventricular arrhythmias
(no longer recommended for preventing ventricular fibrillation after acute MI)
Particularly effective in suppression re-entry rhythms: ventricular tachycardia, fibrillation, PVCs

64
Q

Pharmokinetics of Lidocaine

A

Dose: 1-1.5 mg/kg IV
Infusion 1-4 mg/min (max dose 3mg/kg)
50% protein binding
Hepatic Metabolism (active metabolism, prolongs elimination)
Metabolism affected by CYP inhibitors and inducers
10% renal elimination
extensive first pass
NOT a pro-arrhythmic b/c dissociates too quickly

65
Q

Adverse Effects of Lidocaine

A

hypotension, bradycardia, seizures, CNS depression, drowsiness, dizziness, lightheadness, tinnitus, confusion, apnea, myocardial depression, sinus arrest, heart block, ventilatory depression, cardiac arrest and can augment pre-existing neuromuscular blockade

66
Q

Mexilentine

A

oral agent
chronic suppression of ventricular cardiac tachyarrhythmias
cardiac clearance required
150-200mg Q8H
amine side group that allows to be adminstered oral
Can also be seen in neuropathetic pain

67
Q

Phenytoin

A 
effects resemble lidocaine
class 1b agent
used in suppression of ventricuar arrhythmias associated withe digitalis toxicity
can also be used with other ventricular tachycardias or torsades de pointes
given IV (must be saline)
68
Q

dose of phenytoin

A

1.5mg/kg IV every 5 mins, up to 10-15 mg/kg

69
Q

Therapeutic Phenytoin Blood level

A

10-18 mcg/ml

70
Q

Pharmacokinetics of Phenytoin

A

metabolized in the liver
excreted in urine
elimination 1/2 time @ 24 hours

71
Q

Phenytoin adverse effects

A

CNS disturbances, partially inhibits insulin secretion, bone marrow depression, nausea
SJS

72
Q

Class 2 Agents MOA

A

drug induced slowing of the heart rate with resulting decreases in myocardial oxygen requirements is desirable in patients with CAD
slow speed of conduction of cardiac impulses through atrial tissues and AV node resulting in prolongation of the PR interval on EKG, increased duration of the action potential in atria
decreased automaticity
prevents catecholamine binding to beta receptors
slowing of heart rate
decrease myocardial oxygen requirements

73
Q

Class 2 agents are used to treat

A

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

74
Q

Propranolol

A

prototype
beta adrenergic antagonist
used to prevent reoccurance of tachyarrhythmias, both supraventricular and ventricular precipated by sympathetic stimulation

75
Q

Onset of propanolol

A

2-5 minutes

76
Q

Peak effect of Propanolol

A

10-15 minutes

77
Q

Duration of Propanolol

A

3-4 hours

78
Q

Elimination half time of propanolol

A

2-4 hours

79
Q

Cardiac Effects of Propanolol

A

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

80
Q

Metoprolol

A

Beta adrenergic Antagonist (selective B1)

81
Q

Dose of metoprolol

A

5 mg IV of 5 mins

max dose: 15 mg over 20 minutes

82
Q

Onset of metoprolol

A

2.5 minutes

83
Q

1/2 life of metoprolol

A

3-4 hours

84
Q

Metoprolol is metabolized in

A

liver

85
Q

Is metoprolol okay to used in CHF?

A

Only mild cases

86
Q

Esmolol

A

Beta adrenergic antagonist (selective B1)

Effects without decreasing BP significantly in small doses

87
Q

Dose of Esmolol

A

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

88
Q

Duration of Esmolol

A

less then 10 minutes

89
Q

Class 3 Agents MOA

A

K ion channels blocked causes prolongation of cardiac depolarization and increasing action potential duration, and lengthening repolarization
decreases proportion of the cardiac cycle during which myocardial cells are excitable and thus susceptible to a triggering event

90
Q

Class 3 agents treat

A

supraventricular and ventricular arrhythmias
can prolong QT interval and develop torsades
prophylaxis in cardiac surgery patients d/t high incidence of afib
preventative therapy in patients who have survived sudden cardiac death who are not candidates for ICD
control rhythm in afib

91
Q

amiodarone

A

potassium, sodium, calcium channel blocker and alpha and beta adrenergic antagonist
used for prophylaxis or acute treatment in the treatment of atrial and ventricular arrhythmias (refactory SVT, refractory VT/VF, AF)
1st line drug VT/VF when resistant to electrical defibrillation

92
Q

Dose of amiodarone

A

bolus 150-300 mg IV over 2-5 minutes, up to 5mg/kg then 1mg/hr x6 hours then 0.5mg/hr x 18 hrs

93
Q

Pharmacokinetics of Amiodarone

A 
prolonged elimination half-time (29 days)
hepatic metabolism, active metabolite
biliary/intestinal excretion
extensive protein binding 96%
large volume of distribution
94
Q

Therapeutic Plasma Level of Amiodarone

A

1-3.5ug/ml

95
Q

Adverse effects of Amiodarone

A 
pulmonary toxicity
pulmonary edema
ARDs
photosensitivity rashes
grey/blue discolouration of skin
thyroid abnormalities
corneal deposits
CNS/GI disturbances
pro-arrhythmic effects (torsades de pointes)
heart block
hypotension
sleep disturbances
abnormal LFT 20%
inhibits hepatic P450
96
Q

Sotalol

A

Class 2 and 3 antiarrhythmic
beta adrenergic antagonist (nonselective) and potassium channel blocker
used to treat severe sustained ventricular tachycardia and ventricular fibrillation; to prevent reoccurance of tachyarrhythmias, especially aflutter and afib
excreted in urine

97
Q

Side effects of sotalol

A

prolonged QT interval, bradycardia, myocardial depression, fatigue, dyspnea, AV block,
caution in asthmatics

98
Q

Dofetilide and Ibutilide

A

class 3 antirrhythmics
used for conversion of afib or aflutter to NSR
used for maintenance of sinus rhythm after Afib or conversion of Afib to sinus
pro-arrhythmic

99
Q

Calcium Channel Blockers are located in

A 
cell membranes of skeletal musle
vascular smooth muscle
cardiac muscle
mesenteric muscle
neurons
glandular cells
100
Q

Calcium Channel blockers bind to

A

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

101
Q

Calcium channel blockers

A

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

102
Q

Calcium channel blockers are classified by:

A

phenyl-alkyl amines- AV node (verapamil)
Benzothiazepines-AV (diltiazem)
1,4 dyhydropyrindines-arterial beds (nifedopine)

103
Q

Vascular Uses of CCBs

A 
angina
systemic hypertension
pulmonary hypertension
cerebral arterial spasm
raynaud's disease
migraine
104
Q

Nonvascular Uses of CCBs

A

bronchial asthma
esophageal spasm
dysmenorrhea
premature labor

105
Q

MOA of CCB

A

primary site AV node
blocks slow calcium channels, which decreases conduction through AV node and shortens phase 2 of the action potential in ventricular myocytes
contracility of the heart decreases

106
Q

L type calcium channel is important in

A

determining vascular tone and cardiac contractility

decreased Ca keeps intracellular Ca+ low

107
Q

CCB effects

A

decreased contractility
decrease HR
decreased activity of SA node
decreased rate of conduction of impulses via AV node
vascular smooth muscle relxation: decrease SVR and BP (arterial> venous)

108
Q

CCB is used to

A

used in the treatment of SVT and ventricular rate control in Afib and Aflutter
Used to prevent reoccurrence of SVT

109
Q

Verapamil

A

synthetic derivative of papaverine
Primary site of action is the AV node
Depresses the AV node
negative chronotropic effect on SA node

110
Q

Clinical Uses of CCB

A

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

111
Q

Pharmacokinetic Verapamil

A

highly protein bound (presence of other agents such as lidocaine, diazepam, propranolol increase its activity)
Hepatic first pass metabolism and almost none of the drug appears unchanged in the urine
active metabolite, norverampil
excreted in urine and bile

112
Q

Verapamil Peaks

A

Oral: 30-45 minutes
IV: 15 minutes

113
Q

Elimination 1/2 Time of Verapamil

A

6-8hours

114
Q

Dose of Verapamil

A

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

Continuous gtt: 5 ug/kg/min

115
Q

Do not mix verapamil with

A

a beta blocker

116
Q

Verapamil Side Effects

A

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

117
Q

Diltiazem is a

A

benzothiazepines derviative

118
Q

Site of Action of Diltiazem

A 
AV node
1st line treatment of SVT
HTN
intermediate potency between verapamil and nifedipine
minimal CV depressant effects
119
Q

Clinical Uses of Diltiazem

A

similar to verapamil
SVT
vasospastic angina pectoris, HTN, hypertrophic cardiomyopathy, maternal and fetal tachydysrhymthmias
premature onset of labor

120
Q

Dose of Diltiazem

A

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

IV infusion 10mg/h

121
Q

Forms of Diltiazem

A

PO or IV

122
Q

Pharmacokinetics of Diltiazem

A

oral onset 15 minute
peaks in 30 minutes
70-80% protein bound/ excreted in the bile and urine (inactive metabolite)
Elimination 1/2 time: 4-6 hours
Liver disease may require a decrease dose

123
Q

Side effects of Diltiazem

A

myocardial demand
decrease HTN
constipation
bradycardia

124
Q

Nifedipine is a

A

dihydropyridine derviative

125
Q

Clinical uses of Nifedipine

A

angina pectoris

126
Q

Primary site of action of Nifedipine

A

peripheral arterioles
coronary and peripheral vasodilator properties then verpamil
little to no effect on SA or AV node
decrease SVR, BP
reflex tachycardia
can produce myocardial depression in patients with LV dysfunction or on beta blockers

127
Q

Routes of Nifedipine

A

IV oral Sublingual

128
Q

Pharmacokinetics of Oral Nifedipine

A

effects in 20 minutes
peaks in 60-90 minutes
90% protein bound/ hepatic metabolism, excreted in urine
Elimination 1/2 life is 3-7 hours

129
Q

Side effects of Nifedipine

A

cancer
cardiac problems
bleeding (prolonged)
GI constipation

130
Q

CCB Drug interactions Cause

A

myocardial depression and vasodilation with inhalation agents
can potentiate NMB
interact with calcium mediated platelet function

131
Q

Verapamil and BB

A

potentiate HR block

132
Q

Verapamil increase the risk

A

of local anesthetic toxicity

133
Q

Verapamil and Dantrolene can cause

A

hyperkalemia due to slowing of inwawrd movement of K ions can result in cardiac collapse

134
Q

Digoxin and CCBs

A

increase the plasma concentration of digoxin by decreasing its plasma clearance

135
Q

H2 antagonist and CCBs

A

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

136
Q

Toxicity of CCB

A

may be reversed with IV administration of calcium or dopamine

137
Q

Side Effects of CCB

A 
vertigo
headache
flushing
hypotension
paresthesias
muscle weakness
can induce renal dysfunction
coronary vasospasm with abrupt discontinuation
138
Q

Other CCBs

A 
clevidipine
dihydropyridine
potent vasodilator
broken down by plasma esterases
4-6 mg/ hr IV. start at 1-2 mg/hr and titrate up to 32mg/hg
139
Q

Adenosine

A

binds to A1 purine nucleotide receptors (activated adenosine receptors to open K+ channels and increase K+ currents
slows AV nodal conduction
used for acute Rx only
used for termination of SVT /diagnosis of VT

140
Q

Dose of Adenosine

A

6mg IV bolus, rapid

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

141
Q

T1/2 of Adenosine

A

<10 seconds

142
Q

how is adenosine eliminated?

A

plasma and vascular endothelial cell enzymes

143
Q

Side effects of adenosine

A

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

144
Q

Digoxin

A

cardiac glycoside
increases vagal activity thus decreasing activity of SA node and prolongs conduction of impulses through the AV node
Decreases HR, preload and afterload
slows AV conduction by increasing AV node refractory period
positive inotrope- used to treat CHF

145
Q

Pharmacokinetics of Digoxin

A 
used for management of atrial fibrillation or flutter (controls ventricular rate), especialy withe impaired heart function
narrow therapeutic index 
levels: 0.5-1.2ng/ml
Week protein binding
90% excreted by kidneys
reduce dose in elderly/ renal impairment
146
Q

Dose of Digoxin

A

0.5-1mg divided into doses of 12-24 hours

147
Q

Onset of action of Digoxin

A

30-60 minutes

148
Q

T1/2 of digoxin

A

36 hours

149
Q

Adverse effects of Digoxin

A

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

150
Q

Digoxin Toxcity treatment

A

phenytoin for ventricular arrthymias
pacing
atropine

151
Q

Magnesium

A

works at sodium, potassium, calcium channels
can be used with torsaded de pointes
dose 1 gm IV over 20 minutes; can be repeated

152
Q

Atropine

A 
muscarinic receptor antagonist
unstable bradyarrhythmias
0.4-1mg and repeat as neccessary
metabolized by liver
onset less then 1 mint
DOA 30-60 minutes
caution dosing < 0.4 mg-> paradoxical response

N929 Pharmacology (16 decks)

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