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N929 - Anesthesia Pharmacology > CV Drugs I - Antiarrhythmics > Flashcards

CV Drugs I - Antiarrhythmics Flashcards

1
Q

Class I Agents

A

Sodium Channel Blockers

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2
Q

Sodium Channel Blockers MOA

A
  • phase 0 of fast AP
  • block sodium channels which depresses phase 0 in depolarization of the cardiac AP
  • resultant decrease in AP propagation, decrease in depolarization rate, and slowing of conduction velocity
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3
Q

Sodium Channel Blockers clinical uses

A

-treat SVT, AF, WPW

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4
Q

Class IA agents

A
  • Quinidine (prototype)
  • Procainamide
  • Disopyramide
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5
Q

Class IA agents MOA

A
  • slow conduction velocity and pacemaker rate

- intermediate Na+ channel blocker (intermediate dissociation)

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6
Q

Class IA agents PK/PD

A

-hepatic metabolism

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7
Q

Class IA agents clinical use

A

-atrial and ventricular arrhythmias

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8
Q

Class IA agents effects

A
  • direct depressant effects on SA and AV node
  • decreased depolarization rate (phase 0)
  • prolonged repolarization
  • increased AP duration
  • not commonly used due to toxicity may precipitate HF*
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9
Q

Disopyramide dose/route

A

oral agent

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10
Q

Disopyramide clinical use

A

-suppression of atrial and ventricular tachyarrhythmias

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11
Q

Disopyramide effects

A

-significant myocardial depressant effects and can precipitate CHF and hypotension

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12
Q

Procainamide PK/PD

A
  • 15% protein bound

- elimination ½ is 2 hours

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13
Q

Procainamide dosing/routes

A

-Loading: 100 mg IV Q5min until rate controlled (max 15 mg/kg); then infusion 2-6 mg/min

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14
Q

Procainamide clinical use

A

-treatment of ventricular tachyarrhythmias (less effective with atrial)

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15
Q

Procainamide effects

A
  • myocardial depression –> hypotension

- syndrome that resembles lupus erythematous

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16
Q

Procainamide therapeutic level

A

-therapeutic blood level 4-8 mcg/mL

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17
Q

Class IC Agents

A
  • Flecainide (prototype)

- Propafenone

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18
Q

Class IC Agents MOA

A
  • slow Na+ channel blocker (slow dissociation), so does not vary much during cardiac cycle
  • potent decrease of depolarization rate phase 0, decreased conduction rate with increased AP
  • markedly inhibit conduction through the His-Purkinje system
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19
Q

Class IC Agents effects

A

-may have proarrhythmic side effects due to action in different cells

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20
Q

Flecainide route

A

oral

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21
Q

Flecainide clinical use

A
  • main use = paroxysmal afib
  • treatment of suppressing ventricular PVCs and ventricular tachycardia
  • atrial tachyarrhythmia treatment
  • WPW treatment
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22
Q

Flecainide effects/considerations

A
  • proarrhythmic effects

- no longer recommended for use of treatment of tachyarrhythmias post MI –> high incidence of Vfib and death

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23
Q

Propafenone route

A

oral

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24
Q

Propafenone clinical use

A

-suppression of ventricular and atrial tachyarrhythmias

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25
Q

Propafenone effects/considerations

A

-proarrhythmic effects

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26
Q

Class IB Agents

A
  • Lidocaine (prototype)
  • Mexiletine
  • Phenytoin
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27
Q

Class IB agents MOA

A
  • fast Na+ channel blocker (fast dissociation)
  • alters AP by inhibiting sodium ion influx via rapidly binding to and blocking sodium channels
  • produces little effect on maximum velocity depolarization rate, but shortens AP duration and shortens refractory period
  • decreases automaticity
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28
Q

Lidocaine PK/PD

A
  • 50% protein bound
  • hepatic metabolism
  • active metabolite, slows elimination half-time
  • metabolism may be impaired by drugs like cimetidine or propranolol or physiologic alter conditions like CHF, MI, liver dysfunction, GA
  • can be induced by drugs like barbiturates, phenytoin, or rifampin
  • 10% renal elimination
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29
Q

lidocaine dose/route

A

IV bolus: 1-1.5 mg/kg
IV infusion: 1-4 mg/min
MAX = 3 mg/kg

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30
Q

lidocaine clinical use

A
  • ventricular arrhythmias

- suppression of reentry rhythms – vtach, fibrillation, PVCs

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31
Q

lidocaine effects/considerations

A
  • no longer recommended for preventing v-fib after acute MI –> increased mortality d/t fatal brady arrhythmias
  • Adverse effects –> hypotension, bradycardia, seizures, CNS depression, 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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32
Q

Mexiletine dose/route

A

-oral agent

PO dose: 150-200 mg Q8H

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33
Q

Mexiletine clinical use

A

-chronic suppression of ventricular tachyarrhythmias

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34
Q

Mexiletine effects/considerations

A

-need cardiac clearance

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35
Q

Phenytoin PK/PD

A
  • metabolized in liver
  • excreted in urine
  • elimination ½ time 24 hours
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36
Q

Phenytoin dose/route

A

IV bolus: 1.5 mg/kg every 5 min up to 10-15 mg/kg

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37
Q

Phenytoin clinical use

A
  • suppression of ventricular arrhythmias associated with digitalis toxicity
  • also used for other ventricular tachycardias or torsades de pointes
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38
Q

Phenytoin effects/considerations

A
  • effects resemble lidocaine
  • can precipitate in D5W, mix in NS
  • can cause pain or thrombosis when given in peripheral IV
  • therapeutic blood level 10-18 mcg/mL
  • adverse effects  CNS disturbances, partially inhibits insulin secretion, bone marrow depression, nausea, hypotension with rapid admin, Stevens Johnson syndrome
  • toxicity = CNS disturbance, ataxia, slurred speech
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39
Q

Class II Beta Adrenergic Antagonists (Beta Blockers)

A
  • Propranolol (prototype)
  • Metoprolol
  • Esmolol
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40
Q

Beta blockers MOA

A
  • phase 4 of slow AP
  • depresses spontaneous phase 4 depolarization resulting in SA node discharge decrease
  • prevents catecholamine binding to beta receptors at SA node (slow HR, decrease MVO2)
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41
Q

Beta blockers clinical use

A
  • treat SVT, atrial and ventricular arrhythmias
  • suppress and treat ventricular dysrhythmias during MI and reperfusion
  • to treat tachyarrhythmias secondary do digoxin toxicity and SVT (atrial fib or flutter)
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42
Q

Beta blockers effects/considerations

A
  • drug-induced slowing of HR with resulting decrease in MVO2 – desirable for patients with CAD
  • slow speed of conduction of cardiac impulses through atrial tissues and AV node resulting in prolongation of PR interval on ECG
  • increased duration of AP in atria
  • decreased automaticity
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43
Q

Propranolol MOA

A

non-selective beta adrenergic antagonist

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44
Q

Propranolol PK/PD

A
  • onset: 2-5 min
  • peak: 10-15 min
  • DOA: 3-4 hours
  • elimination ½: 2-4 hours
45
Q

Propranolol clinical use

A

-used to prevent recurrence of tachyarrhythmias, both supraventricular and ventricular precipitated by sympathetic stimulation

46
Q

Propranolol effects/considerations

A

cardiac effects –> decreased HR, contractility, CO (increased filling, decreased MVO2); increased PVR, coronary vascular resistance, however decreased oxygen demand

47
Q

Metoprolol MOA

A

selective beta1 adrenergic antagonist

48
Q

Metoprolol PK/PD

A
  • onset: 2.5 min
  • half-life 3-4 hours
  • metabolized by liver
49
Q

Metoprolol dose/route

A

IV bolus: 5 mg over 5 min; max 15 mg over 20 min

50
Q

Metoprolol clinical use

A

can be used in mild CHF

51
Q

Esmolol MOA

A

selective beta1 adrenergic antagonist

52
Q

Esmolol PK/PD

A
  • DOA: <10 min

- hydrolyzed by plasma esterases

53
Q

Esmolol dose/route

A

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

54
Q

Esmolol effects/considerations

A
  • great choice for OR because short DOA

- effects HR without decreasing BP significantly in small doses

55
Q

Class III: Potassium Channel Blockers

A
  • Amiodarone (prototype)
  • Dronedarone
  • Ibutilide
  • Dofetilide
  • Sotalol
56
Q

Potassium Channel Blockers MOA

A
  • phase 3 of fast AP
  • block potassium channels resulting in prolongation of cardiac depolarization, increasing AP duration, and lengthening repolarization
  • decrease proportion of the cardiac cycle during which myocardial cells are excitable and thus susceptible to triggering event
57
Q

Potassium Channel Blockers clinical use

A
  • treat supraventricular and ventricular arrythmias
  • preventative therapy in patients who have survived sudden cardiac death who are not candidates for ICD
  • control rhythm in Afib
58
Q

Potassium Channel Blockers effects/considerations

A
  • can prolong QT interval and develop torsades

- prophylaxis in cardiac surgery patients r/t high incidence of Afib

59
Q

Amiodarone MOA

A

potassium/sodium/calcium channel blocker, alpha and beta adrenergic antagonist

60
Q

Amiodarone PK/PD

A
  • prolonged elimination ½ –> 29 days
  • hepatic metabolism, active metabolite
  • biliary/intestinal excretion
  • 96% protein bound
  • large Vd
61
Q

Amiodarone dose/route

A

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

62
Q

Amiodarone clinical uses

A
  • prophylaxis or acute treatment of atrial and ventricular arrhythmias (refractory SVR, refractory VT/VF, AF)
  • 1st line for VT/VF when resistant to electrical defibrillation
63
Q

Amiodarone considerations

A
  • therapeutic plasma level 1.0-3.5 mcg/mL
  • lengthens refractory period so susceptible to torsades (monitor Mg)
  • can give PO preop to decrease incidence of Vfib post CT surgery
  • many adverse effects, especially if given in high doses or over a long period of time
64
Q

Amiodarone adverse effects

A

-adverse effects – pulmonary toxicity (fibrosis develops), pulmonary edema, ARDS, photosensitive rashes, grey/blue discoloration of skin, thyroid abnormalities, corneal deposits, CNS/GI disturbances, pro-arrhythmic (torsades), heart block, hypotension, sleep disturbances, abnormal LFT, inhibits CYP450

65
Q

Sotalol class

A
  • II and III

- beta adrenergic antagonist (non-selective) and potassium channel blocker

66
Q

Sotalol PK/PD

A

excreted in urine

67
Q

Sotalol clinical use

A

treat severe sustained VT and VF

68
Q

Sotalol effects/considerations

A
  • side effects –> prolonged QT, bradycardia, myocardial depression, fatigue, dyspnea, AV block
  • caution with asthma (because of beta2 blockade)
69
Q

Dofetilide & Ibutilide clinical use

A

conversion of AF or aflutter to NSR

70
Q

Dofetilide & Ibutilide effects/considerations

A

proarrhythmic side effect (prolong QT)

71
Q

Class IV Calcium Channel Blockers

A
  • Verapamil (prototype)
  • Diltiazem
  • Nifedipine
72
Q

Calcium Channel Blockers MOA

A
  • phase 2 of fast AP
  • bind to the alpha1 subunit on the L type voltage-gated calcium ion channel maintaining an inactive or closed state
  • selectively interfere with inward calcium ion movement across myocardial and vascular smooth muscle cells
  • decreases conduction through AV node and shortens phase 2 of AP in ventricular myocytes
  • decreased contractility
73
Q

Calcium Channel Blockers clinical use

A

Vascular –> angina, systemic HTN, pulmonary HTN, cerebral arterial spasm, Raynaud’s disease, migraine
Non-vascular –> bronchial asthma, esophageal spasm, dysmenorrhea, premature labor
-treatment of SVT and ventricular rate control in Afib and Aflutter
-prevent recurrence SVT

74
Q

Calcium Channel Blockers effects

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)
75
Q

Calcium Channel Blockers drug interactions

A
  • myocardial depression and vasodilation with inhalational agents
  • can potentiate NMBD
  • verapamil and beta-blockers
  • verapamil increases risk of local anesthetic toxicity
  • verapamil and dantrolene can cause hyperkalemia d/t slowing of inward movement of K+ ions can result in cardiac collapse
  • interact with Ca2+ mediated platelet fxn
  • increase plasma dig concentration by decreasing clearance
  • H2 antagonists alter hepatic enzyme activity and increase plasma level of CCB
76
Q

Calcium Channel Blockers adverse effects

A

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

77
Q

Calcium channel blocker toxicity treatment

A

can be reversed with IV admin of calcium or dopamine

78
Q

Verapamil MOA

A
  • phenyl-alkyl-amines (AV node)

- intracellular pore blocking of channel at binding site

79
Q

Verapamil PK/PD

A
  • 87-98% protein bound
  • presence of lidocaine, diazepam, and propranolol increase activity
  • extensive 1st pass hepatic metabolism
  • peak: oral 30-45 min, IV 15 min
  • elimination ½: 6-12 hrs
  • hepatic metabolism, active metabolite (norverapamil)
  • excreted in urine/bile
80
Q

Verapamil dose/route

A

IV bolus: 2.5-10 mg over 1-2 min (max is 20mg)

IV infusion: 5 mcg/kg/min

81
Q

Verapamil clinical uses

A
  • SVT
  • vasospastic angina
  • HTN
  • hypertrophic cardiomyopathy
  • maternal and fetal tachyarrhythmias
  • premature onset of labor
82
Q

Verapamil effects/considerations

A
  • primary site of action is AV node  depresses AV node, negative chronotropic effect on SA node, negative inotropic effect on myocardial muscle, moderate vasodilation on coronary as well as systemic arteries
  • do not use in combination with beta-blocker (can induce heart block)
  • side effects –> myocardial depression, hypotension, constipation, bradycardia, nausea, prolongs effects of NMBDs
83
Q

Diltiazem MOA

A
  • benzothiazepines (AV node)
  • unclear mechanism
  • principal site of action is AV node
84
Q

Diltiazem PK/PD

A
  • onset: oral 15 min, peak 30 min
  • 70-80% protein bound/excreted in bile and urine
  • elimination ½: 4-6 hrs
  • liver disease may require decreased dose
85
Q

Diltiazem dose/route

A

-PO or IV
IV bolus: 0.25-0.35 mg/kg over 2 min (can repeat in 15min)
IV infusion: 10 mg/hr

86
Q

Diltiazem clinical use

A
  • SVT (1st line treatment)
  • vasospastic angina
  • HTN
  • hypertrophic cardiomyopathy
  • maternal and fetal tachyarrhythmias
87
Q

Diltiazem effects/considerations

A
  • intermediate potency between verapamil and nifedipine
  • minimal CV depressant effects
  • side effects –> constipation, hypotension, bradycardia
88
Q

Nifedipine MOA

A
  • 1,4-dihydropyridines (arterial beds)
  • extracellular allosteric modulation of channel at binding site
  • primary site of action = peripheral arterioles
89
Q

Nifedipine PK/PD

A
  • oral onset 20 min
  • oral peak 60-90 min
  • 90% protein bound
  • hepatic metabolism
  • excreted in urine
  • elimination ½: 3-7 hrs
90
Q

Nifedipine dose/route

A

IV, oral, or sublingual

91
Q

Nifedipine clinical use

A

angina pectoris

92
Q

Nifedipine effects/considerations

A
  • coronary and peripheral vasodilator properties (decreases SVR and BP)
  • little to no effect on SA or AV node
  • reflex tachycardia
  • can produce myocardial depression in patients with LV dysfunction or beta blockers
  • side effects –> cancer, cardiac problems, bleeding, constipation, heart block
93
Q

Adenosine MOA

A

binds to A1 purine nucleotide receptors – activates adenosine receptors to open K+ channels and increase K+ currents

94
Q

Adenosine PK/PD

A
  • t ½ < 10 seconds

- eliminated by plasma and vascular endothelial cell enzymes

95
Q

Adenosine dose/route

A

IV RAPID bolus: 6 mg; repeat after 3 min 6-12 mg IV

96
Q

Adenosine clinical use

A

acute treatment, termination of SVT

97
Q

Adenosine effects/considerations

A
  • slows AV nodal conduction
  • side effects –> excessive AV or SA nodal inhibition, facial flushing, HA, dyspnea, chest discomfort, nausea, bronchospasm, impending doom
  • contraindicated –> asthma, heart block
98
Q

Digoxin MOA

A

increases vagal activity, decreasing activity of SA node, prolongs conduction of impulses through AV node

99
Q

Digoxin PK/PD

A
  • onset: 30-60 min
  • t ½: 36 hrs
  • weak protein binding
  • 90% excreted by kidneys
  • reduce dose in elderly or renal impairment
100
Q

Digoxin dose/route

A

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

101
Q

Digoxin clinical use

A
  • CHF

- management of afib or aflutter, especially with impaired heart function

102
Q

Digoxin effects/considerations

A
  • decreases HR, preload, and afterload
  • slows AV conduction by increasing AV node refractory period
  • positive inotrope
  • narrow therapeutic index (0.5-1.2 mcg/mL)
  • adverse effects  arrhythmias, heart block, anorexia, nausea, diarrhea, confusion, agitation
103
Q

digoxin toxicity treatment

A

phenytoin (vent arrhythmias), pacing, atropine

104
Q

Magnesium

A
  • works at sodium, potassium, and calcium channels
  • treatment –> torsades de pointes
  • IV bolus: 1 g over 20 min; can be repeated
105
Q

Atropine

A

-muscarinic receptor antagonist

106
Q

atropine PK/PD

A
  • metabolized in liver
  • onset <1 min
  • DOA: 30-60 min
107
Q

atropine dose

A

IV bolus: 0.4-1 mg; repeat as necessary

108
Q

atropine clinical use

A

unstable bradyarrhythmias

109
Q

atropine considerations

A

caution dosing <0.4 mg –> can have paradoxical response

N929 - Anesthesia Pharmacology (12 decks)

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