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AS - N929 Pharmacology II > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

FAST Cardiac AP

A

Cardiomyocyte (cardiac cells) action potential

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2
Q

FAST Cardiac AP

Phase 0

A

Rapid depolarization

Na+ channel opens → Na+ inward flow

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3
Q

FAST Cardiac AP

Phase 1

A

Begin repolarization

Na+ channel closes

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4
Q

FAST Cardiac AP

Phase 2

A

Plateau
Slow Ca2+ channels open → Ca2+ flows inward
Ø net ion movement

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5
Q

FAST Cardiac AP

Phase 3

A

Repolarization
Ca2+ channel close
K+ channel open → slow outward K+ efflux

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6
Q

FAST Cardiac AP

Phase 4

A

Pacemaker potential
Return to resting membrane potential
Diastole -90mV

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7
Q

SLOW Cardiac AP

A

Pacemaker action potential

SA/AV node

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8
Q

SLOW Cardiac AP

Phase 4

A

No resting membrane potential
Gradual depolarization
Slow inward Na+ & Ca2+ currents
Funny channels

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9
Q

SLOW Cardiac AP

Phase 0

A

Slower depolarization
Ca2+ mediated
Upstroke
Threshold -40mV

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10
Q

SLOW Cardiac AP

Phase 3

A

VGCa2+ channels close rapidly
↓Na+ permeability
↑K+ permeability → repolarization

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11
Q

Cardiac Pacemaker

A

SA node

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12
Q

NSR

A

Normal sinus rhythm

60-100bpm (70-80)

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13
Q

AV Node Conduction Rate

A

40-60bpm

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14
Q

Purkinje Fibers Intrinsic Rate

A

15-40bpm

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15
Q

Arrhythmia

A

Disturbance in the heart electrical activity

Atrial, junctional, or ventricular

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16
Q

When to intervene & treat arrhythmias?

A

Arrhythmias → cardiac dysfunction

↑demand ↓CO → hemodynamic compromise

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17
Q

Arrhythmia Types

Altered Automaticity

A

Latent pacemaker cells take over the SA node role → ectopic beats

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18
Q

Arrhythmia Types

Delayed After-Depolarization

A

Normal cardiac cell AP triggers abnormal depolarizations

Repetitive discharge or arrhythmias

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19
Q

Arrhythmia Types

Re-Entry

A

Refractory tissues reactivated repeatedly & rapidly d/t unidirectional block → causes abnormal continuous circuit

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20
Q

Arrhythmia Types

Conduction Block

A

Impulse fail to propagate in non-conducting tissues d/t ischemia, scarring, fibrosis (damaged tissue)

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21
Q

Non-Pharmacological Arrhythmia Treatments

A 
Acute:
- Vagal maneuvers
- Cardioversion
Prophylactic:
- Radiofrequency catheter ablation
- Implantable defibrillator
Pacing - external, temporary, or permanent
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22
Q

Class I Antiarrhythmics

A

Phase 0 Na+ channel blockers → decreases AP propagation (depolarization rate) & slows conduction velocity
Sub-classes IA/B/C

Used to treat SVT, Afib, & Wolfe-Parkinson White

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23
Q

Class IA

A

Disopyramide (Norpace), Procainamide (ACLS), & Quinidine

Slow conduction velocity & pacemaker rate
Intermediate Na+ channel blocker (dissociation) ↓depolarization rate
Direct depressant effect on SA/AV node
↑AP duration

Used to treat atrial & ventricular arrhythmias

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24
Q

Class IA Prototype

A

Quinidine

No longer manufactured

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25
Q

Disopyramide (Norpace)

A

Class IA
Suppresses atrial & ventricular tachyarrhythmias
PO route
Significant myocardial depression & potential to precipitate CHF & HoTN

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26
Q

Procainamide

A

Class IA
1° used to treat ventricular tachyarrhythmias (less effective w/ atrial)
ACLS

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27
Q

Procainamide PK

A

15% protein binding

Elimination 1/2 time 2hrs

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28
Q

Procainamide Dose

A

Load 100mg IV Q5min until rate controlled
Max 15mg/kg
Followed by 2-6mg/min infusion

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29
Q

Procainamide SE

A

Myocardial depression → HoTN
Syndrome that resembles lupus erythematous
Monitor blood levels*

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30
Q

Therapeutic Procainamide Levels

A

4-8mcg/mL

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31
Q

What drugs replaced IA drugs? Why?

A

Class IC

Toxicity potential to precipitate heart failure

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32
Q

Class IB

A

Lidocaine, Mexiletine, & Phenytoin

Fast Na+ channel blocker (dissociation)
Inhibits Na+ ion influx 
Minimal effect on max velocity depolarization rate
Shortens AP duration & refractory period
↓automaticity
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33
Q

Lidocaine

A

Class IB prototype

Used to treat ventricular arrhythmias; particularly effective to suppress re-entry rhythms (Vtach, fibrillation, PVCs)

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34
Q

Lidocaine PK

A

50% protein binding
Extensive 1st pass effect
Hepatic metabolism w/ active metabolite that prolong elimination 1/2 time
10% renal elimination

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35
Q

Lidocaine Dose

A

1-1.5mg/kg IV
Infusion 1-4mg/min
Max dose 3mg/kg

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36
Q

Lidocaine SE

A

Toxicity
HoTN, bradycardia, seizures, CNS depression, drowsiness, dizziness, lightheaded, tinnitus, confusion, apnea, myocardial depression, sinus arrest, heart block, ventilatory depression, cardiac arrest, potential to augment pre-existing neuromuscular blockade

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37
Q

Mexiletine

A

Class IB
PO agent
Chronic ventricular tachyarrhythmias suppression
- Consider cardiac clearance prior to surgery
150-200mg Q8H
Amine group avoids hepatic 1st pass metabolism

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38
Q

Phenytoin (Dilantin)

A

Class IB
Used to suppress ventricular arrhythmias associated w/ dig toxicity, other ventricular tachycardias, or torsades de pointes

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39
Q

Phenytoin PK

A 
IV mix in NS (precipitates in D5W)
Pain or thrombosis when admin in peripheral IV
Rapid infusion → HoTN
Hepatic metabolism; renal excretion
Elimination 1/2 time 24hrs
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40
Q

Phenytoin Dose

A

1.5mg/kg IV Q5min up to 10-15mg/kg

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41
Q

Phenytoin SE

A

CNS disturbances, partially inhibits insulin secretion, bone marrow suppression, nausea
Associated w/ Stevens-Johnson syndrome
Toxicity - CNS symptoms, vertigo, ataxia, slurred speech

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42
Q

Therapeutic Phenytoin Levels

A

10-18mcg/mL

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43
Q

Class IC

A

Flecainide & Propafenone

Slow Na+ channel blocker (dissociation)
Potent ↓depolarization rate (phase 0) & conduction rate ↑AP & shortens AP duration
Suppresses SA node w/ marked His-Purkinje conduction inhibition

Used to treat PVCs or Vtach & atrial Wolfe-Parkinson White

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44
Q

Class IC Prototype

A

Flecainide
PO agent

Used to suppress PVCs, ventricular tachycardia, atrial tachyarrhythmias, Wolf-Parkinson White syndrome
Pro-arrhythmic SEs

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45
Q

Propafenone

A

Class IC
PO agent

Suppresses ventricular & atrial tachyarrhythmias
Pro-arrhythmic SEs

46
Q

Class II Antiarrhythmics

A

β adrenergic blockers (phase 4) ↓SA node discharge → slows HR ↓myocardial oxygen requirements
Slower conduction via atrial tissues & AV node → prolonged PRI interval ↑AP duration ↓automaticity

Used to treat SVT, atrial (fib or flutter) & ventricular arrhythmias, suppress & treat ventricular dysrhythmias during MI & reperfusion, tachyarrhythmias 2° dig toxicity

Propranolol, Esmolol, Metoprolol, & -olols

47
Q

Class II Prototype

A

Propranolol
Non-selective β adrenergic antagonist
Used to prevent supra-/ventricular tachyarrhythmias reoccurrence precipitated by sympathetic stimulation
↑SA node conduction

48
Q

Propranolol PK

A

Onset 2-5min
Peak 10-15min
DOA 3-4hrs
Elimination 1/2 time 2-4hrs

49
Q

Propranolol SE

A 
↓HR, contractility, CO 
↑SVR & coronary vascular resistance
Improved filling
↓MVO2
Bronchoconstriction
50
Q

Metoprolol

A

Class II

Selective β1 antagonist

51
Q

Metoprolol Dose

A

5mg IV over 5min

Max dose 15mg over 15min

52
Q

Metoprolol PK

A

Onset 2.5min
DOA 3-4hrs
Hepatic metabolism

Okay in mild CHF

53
Q

Esmolol

A

Class II

Selective β1 antagonist

54
Q

Esmolol Dose

A

0.5mg/kg IV bolus over 1min

Infusion 50-300mcg/kg/min

55
Q

Esmolol DOA

A

< 10min

Hydrolysis via plasma esterases

56
Q

Esmolol SE

A

Effects HR w/o significantly ↓BP (in small doses)

57
Q

Class III Antiarrhythmics

A

K+ channel blockers (phase 2/3)
Prolongs cardiac depolarization ↑AP duration & lengthens repolarization

Used to treat supra- & ventricular arrhythmias, prophylaxis in cardiac surgery patients w/ Afib, control rhythm in Afib, preventative therapy in patients not candidates to receive internal cardiac defibrillator

Amiodarone, Sotalol. Dofetilide, & Ibutilide

58
Q

Class III Prototype

A

Amiodarone
Class I, II, & IV antiarrhythmic properties
K+/Na+/Ca2+ channel blocker
α & β adrenergic antagonist

Used in prophylaxis or treatment atrial & ventricular arrhythmias (refractory SVT/Vtach/Vfib or atrial fibrillation)

59
Q

Amiodarone PK

A 
Extensive protein binding 96%
Lipophilic w/ large Vd
Prolonged elimination 1/2 life 29 days
Hepatic metabolism w/ active metabolite
Biliary & intestinal excretion
60
Q

Amiodarone Dose

A

Bolus 150-300mg IV over 2-5min up to 5mg/kg

Followed by 1mg/hr infusion x6hrs then 0.5mg/hr x18hrs

61
Q

Amiodarone SE

A 
Pulmonary toxicity/edema
ARDS
Photosensitivity rashes
Grey/blue skin discoloration
Thyroid abnormalities
Corneal deposits
CNS/GI disturbances
Pro-arrhythmic effects (Torsades de pointes)
Heart block
HoTN
Sleep disturbances
Abnormal LFTs
Inhibits hepatic P450
62
Q

Therapeutic Amiodarone Level

A

1-3.5mcg/mL

63
Q

What’s the 1st line Vtach or Vfib treatment when resistant to electrical defibrillation?

A

Amiodarone

64
Q

Sotalol

A

Class II/III
Non-selective β adrenergic antagonist & K+ channel blocker
*Caution in patients w/ asthma

Used to treat severe sustained ventricular tachycardia & Vfib, prevent tachyarrhythmias reoccurrence, especially atrial fib & flutter

Renal excretion

65
Q

Sotalol SE

A 
Prolonged QT interval
Bradycardia
Myocardial depression
Fatigue
Dyspnea
AV block
66
Q

Dofetilide & Ibutilide

A

Class III

Used to convert atrial fib or flutter to NSR & maintenance NSR after conversion
Pro-arrhythmic prolongs QT interval

67
Q

Class IV Antiarrhythmics

A

Calcium channel blockers (phase 2) block slow Ca2+ channels

Used to treat vascular (angina, HTN, pulm HTN, cerebral artery spasm, Raynaud, migraine) & non-vascular conditions (asthma, esophageal spasm, dysmenorrhea, premature labor)

Verapamil, Diltiazem, & Nifidipine

68
Q

Ca2+ Ion Channels

Locations

A
  • Skeletal muscle cell membranes
  • Vascular smooth muscle
  • Cardiac muscle
  • Mesenteric muscle
  • Neurons
  • Glandular cells
69
Q

Ca2+ Channel Blockers

MOA

A

Bind to the receptor on VGCa2+ ions to maintain the channels in an inactive or closed state
Block slow Ca2+ channels → decreases conduction through the AV node and shortens phase 2 (ventricular myocytes AP plateau)
Interfere with inward Ca2+ ion movement across myocardial & vascular smooth muscle cells
- Primary site at AV node
↓heart contractility

70
Q

Ca2+ Channel Blockers

Subtypes

A

L, T, N, & P channels

71
Q

L-type Ca2+ channel determines ______

A

Vascular tone & cardiac contractility

↓Ca2+ keeps intracellular Ca2+ levels low

72
Q

Ca2+ Channel Blockers

CV Effects

A

↓contractility/inotropy
↓HR
↓SA node activity
↓conduction rate & impulses via AV node

→ vascular smooth muscle relaxation ↓SVR & BP (arterial > venous)

73
Q

Ca2+ channel blockers are used to treat:

A
  • SVT & ventricular rate control in A fib & A flutter
  • Used to prevent SVT reoccurrence

NOT used to treat ventricular arrhythmias

74
Q

Class IV Prototype

A

Verapamil

  • Synthetic papaverine derivative
  • Less vasodilation
75
Q

Verapamil 1° Action Site

A

AV node

  • 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
76
Q

Verapamil Clinical Usages

A

SVT, vasospastic angina pectoris, HTN, hypertrophic cardiomyopathy, maternal & fetal dysrhythmias, premature labor onset

77
Q

Verapamil PK

A

Highly protein bound
PO absorption w/ extensive hepatic 1st pass
Active metabolite - Norverapamil
Renal & bile excretion (urine almost unchanged)
Oral peak 30-45min
IV peak 15min
Elim 1/2 time 6-12 hours

78
Q

Verapamil SE

A

Myocardial depression, HoTN (treatment = 1G Ca2+ gluconate), bradycardia, constipation, nausea, potentiates NMB effects

LA activity or toxicity w/ regional

79
Q

Verapamil Dose

A

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

Continuous infusion 5mcg/kg/min

80
Q

Do NOT administer Verapamil IV w/ ______

A

β blocker

81
Q

Verapamil Drug Interactions

A

Verapamil & β-blockers → heart block
Verapamil ↑LA toxicity risk
Verapamil & Dantrolene → hypokalemia d/t slowing inward K+ ions movement → CV collapse

82
Q

Diltiazem

A

Class IV
Benzothiazepine derivative
Principle action site = AV node

Intermediate potency b/w Verapamil & Nifedipine
Minimal CV depressant effects

Used to treat SVTs & HTN

83
Q

Diltiazem Clinical Usages

A

SVT, vasospastic angina pectoris, HTN, hypertrophic cardiomyopathy, maternal & fetal tachydysrhythmias

84
Q

1st line SVT treatment

A

DILTIAZEM

85
Q

Diltiazem PK

A 
PO onset 15min
Peak in 30min
70-80% protein bound
Excreted via bile & urine (inactive metabolite)
Elim 1/2 time 4-6 hours

↑dose w/ hepatic disease
Mixed cardiac & vascular effects - myocardial depression, HoTN, bradycardia, & constipation

86
Q

Nifedipine

A

Class IV
Dihydropyridine derivative

Used to treat angina pectoris

1° action site = peripheral arterioles

87
Q

Nifedipine PK

A 
IV, PO, or sublingual 
PO effects in 20min
Peaks in 60-90min
90% protein bound
Hepatic metabolism
Renal excretion
Elim 1/2 time 3-7 hours
88
Q

Nifedipine SE

A

Coronary & peripheral vasodilation (properties > Verapamil)
Little to no effect on the SA or AV node
↓SVR & BP
Reflex tachycardia
→ myocardial depression in patients w/ LV dysfunction or on β-blockers

89
Q

Ca2+ Channel Blockers SE

A

Cancer w/ prolonged administration
Cardiac problems → hear block
Bleeding d/t platelet dysfunction
GI constipation

Vertigo, HE, flushing, HoTN, paresthesias, & muscle weakness
Induce renal dysfunction
Coronary vasospasm w/ abrupt discontinuation (slow wean to discontinue)

90
Q

Ca2+ Channel Blockers

Drug Interactions

A

Myocardial depression & vasodilation w/ inhalational agents
Potentiate NMBs
Interact w/ Ca2+ mediated platelet dysfunction
↑plasma Digoxin concentration via ↓plasma clearance
H2 antagonists (Ranitidine & Cimetidine) alter hepatic enzyme activity → potential to ↑Ca2+ channel blockers plasma levels

91
Q

Ca2+ Channel Blockers Toxicity

A

↑chronotropy

Reverse w/ IV Ca2+ or Dopamine administration

92
Q

What Ca2+ channel blocker has the greatest impact on coronary artery dilation?

A

Nicardipine

Table 18-2
Ca2+ channel blocker pharmacologic effects (Verapamil, Nifedipine, Nicardipine, & Diltiazem)

93
Q

Clevidipine

A

Class IV
Dihydropyridine

Blocks 1° L-type channels
POTENT vasodilator

Metabolism via plasma esterases → reflex tachycardia & rebound HTN when d/c

94
Q

Clevidipine Dose

A

Bolus 1mg
1-2mg/hr double every 90sec
MAX 20mg/hr (up to 32mg/hr short duration)

95
Q

Clevidipine Onset

A

< 30 seconds

96
Q

Clevidipine DOA

A

< 1 min

97
Q

Class V Antiarrhythmics

A

Other (unclassified drugs)
Different MOA - not on ion channels or unknown

Adenosine, Digoxin, Phenytoin (Dilantin), Atropine, & Magnesium

98
Q

Adenosine

A

Class V

Acute treatment ONLY
Used to treat SVT or diagnose V tach

99
Q

Adenosine MOA

A

Binds to A1 purine nucleotide receptors (activates adenosine receptors to open K+ channels & ↑K+ currents) shortens AP
Slows AV node conduction
↓excitability (hyperpolarization)

100
Q

Adenosine PK

A

Elim 1/2 time < 10 seconds

Metabolism via plasma & vascular endothelial cell enzymes

101
Q

Adenosine Dose

A

6mg IV rapid bolus 1st dose 60% effective
Repeat after 3min 6-12mg 2nd dose 90%
20mL rapid flush via large bore PIV or central line
Access closest to the heart

102
Q

Adenosine SE

A

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

Contraindicated in asthma or heart block (slows AV node conduction)

103
Q

Digoxin

A

Class V
Cardiac glycoside

Used to treat A fib or A flutter (controls ventricular rate) especially w/ impaired heart function

104
Q

Digoxin MOA

A

↑vagal activity ↓SA node activity & prolongs conduction impulses via AV node
↓HR, preload, & afterload
Slows AV conduction via ↑AV node refractory period

Positive inotropy used to treat CHF

105
Q

Digoxin PK

A 
Onset 30-60min
Elim 1/2 time 36 hours
Narrow therapeutic index
Weak protein binding
90% renal excretion

Reduce dose in elderly or renal impaired patients

106
Q

Digoxin Dose

A

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

107
Q

Therapeutic Digoxin Level

A

0.5-1.2ng/mL

108
Q

Digoxin SE

A

Arrhythmias, heart block, agitation, anorexia, nausea, diarrhea, confusion
- Potentiated by hypokalemia & hypomagnesemia

109
Q

Digoxin Toxicity Treatment

A

Phenytoin (ventricular arrhythmias)
Pacing
Atropine

Maintain normal electrolyte levels

110
Q

Magnesium

A

Class V
MOA at Na+, K+, & Ca2+ channels

Used to treat Torsades de pointes

111
Q

Magnesium Dose

A

1 gram IV over 20min

112
Q

Antiarrhythmic Agents

A

Used to prevent, suppress, or treat a disturbance in cardiac rhythm
- A fib, A flutter, SVT, V tach, V fib, brady arrhythmias, heart block

AS - N929 Pharmacology II (10 decks)

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