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Pharmacology II - CP > Antiarrhythmic Agents > Flashcards

Antiarrhythmic Agents Flashcards

1
Q

P wave

A

atria contraction

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2
Q

QRS wave

A

ventricular contraction

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3
Q

T wave

A

ventricular repolarization

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4
Q

PR interval

A

starts beginning of atrial depolarization to beginning of ventricular depolarization

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5
Q

ST segment

A

all cells depolarized

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6
Q

Phase 0 in Fast AP

A

rapid depolarization (fast Na+ channels open, influx of Na+)

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7
Q

Phase 1 in Fast AP

A

begin repolarization (K+ channels open, Na+ channels close)

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8
Q

Phase 2 in Fast AP

A

plateau phase (slow Ca++ channels open)

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9
Q

Phase 3 in Fast AP

A

repolarization (Ca++ channels close, K+ efflux)

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10
Q

Phase 4 in Fast AP

A

pacemaker potential, return to RMP

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11
Q

Refractory period

A

cannot generate another action potential, Na+ channels not in ready confirmation

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12
Q

Definition of arrhythmia

A

disturbance in the electrical activity of the heart

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13
Q

How are arrhythmias classified?

A

site of origin (atrial, junctional, vascular), complexes on ECG (narrow, broad), heart rhythm (regular, irregular), heart rate (increased, decreased)

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14
Q

Altered automaticity

A

latent pacemaker cells take over the SA node’s role, escape beats
ex. sinus bradycardia, tachycardia

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15
Q

Delayed after depolarization

A

normal action potential of cardiac cell triggers a train of abnormal depolarizations, leads to triggered arrhythmia

ex. Ca++ levels, R on T phenomena

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16
Q

Re-entry

A

refractory tissue reactivated repeatedly and rapidly d/t unidirectional block = abnormal continuous circuit

ex. WPW

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17
Q

Conduction block

A

impulse fail to propagate in non-conducting tissue

ex. heart blocks from tissue damage, fibrosis

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18
Q

Factors underlying cardiac arrhythmias

A

arterial hypoxemia, electrolyte imbalance, acid base abnormalities, myocardial ischemia, altered SNS activity, bradycardia, certain drugs, enlargement of a failing ventricle

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19
Q

Acute non-pharmacological treatment

A

vagal maneuvers, cardioversion, carotid massage

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20
Q

Prophylaxis non-pharmacological treatment

A

radiofrequency catheter ablation, implantable defibrillator

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21
Q

What non-pharmacological treatment can be external, temporary, or permanent?

A

pacing

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22
Q

Antiarrhythmic agents are used to..

A

prevent, suppress, or treat a disturbance in cardiac rhythm

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23
Q

Class I antiarrhythmic

A

sodium channel blockers - work at phase 0

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24
Q

Class II antiarrhythmic

A

beta adrenergic blockers - work at phase 4

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25
Q

Class III antiarrhythmic

A

potassium channel blockers - works at phase 2/3

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26
Q

Class IV antiarrhythmic

A

calcium channel blockers - works at phase 2

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27
Q

Class IA effect and drug examples

A

moderate depression and prolonged repolarization

ex. quinidine, procainamide, disopyramide

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28
Q

Class IB effect and drug examples

A

weak depression and shortened repolarization

ex. lidocaine, mexiletine, phenytoin, tocainide

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29
Q

Class IC effect and drug examples

A

strong depression with little effect on repolarization

ex. flecainide, propafenone, moricizine

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30
Q

Class II examples

A

esmolol, propranolol, metoprolol, timolol, pindolol, atenolol, acebutolol, nadolol, carvedilol

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31
Q

Class III examples

A

amiodarone, bretylium, sotalol, ibutilide, dofetilide

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32
Q

Class IV examples

A

verapamil, diltiazem

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33
Q

What rhythms are class I agents used to treat?

A

SVT, afib, WPW

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34
Q

How are Class IA agents eliminated?

A

hepatic metabolism

35
Q

Disopyramide - Class IA Agent

A

suppresses atrial and ventricular tachyarrhythmias
taken orally
significant myocardial depressant effects so can cause CHF and hypotension

36
Q

Why are Class IA agents not used commonly?

A

They cause toxicity that can lead to heart failure

37
Q

Procainamide - Class IA Agent

Use, Dose, Side Effects

A

Use: treatment of ventricular tachyarrhythmias
Dose: loading 100mg IV q 5 mins until rate controlled (max 15 mg/kg), 2-6 mg/min infusion
Elimination half time: 2 hours
Therapeutic level: 4 - 8 mcg/mL
S/E: myocardial depression, hypotension, syndrome resembling lupus erythematous

38
Q

Flecainide - Class IC Agent

A

treats ventricular PVCs, ventricular tachycardia, atrial tachyarrhythmias, WPW

oral agent
pro-arrhythmic side effects

39
Q

Propafenone - Class IC Agent

A

treats ventricular and atrial tachyarrhythmias

oral agent
pro-arrhythmic side effects (Torsades)

40
Q

Lidocaine - Class IB Agent

Pharmacokinetics

A

treats ventricular arrhythmias: ventricular tachycardia, fibrillation, PVCs (NOT SVT)
50% protein bound
hepatic metabolism - active metabolite

41
Q

What impairs Lidocaine’s metabolism?

A

Cimetidine, Propranolol, CHF, acute MI, liver dysfunction, GA

42
Q

What induces Lidocaine’s metabolism?

A

Barbiturates, Phenytoin, Rifampin

43
Q

Lidocaine

Dose, Side Effects

A

Not pro-arrhythmic!
Dose: 1-1.5 mg/kg IV, 1-4 mg/min infusion (max 3 mg/kg)

A/E: hypotension, bradycardia, seizures, CNS depression, drowsiness, dizziness, lightheadedness, tinnitus, confusion, apnea, myocardial depression, sinus arrest, heart block, cardiac arrest, augment NMB

44
Q

Mexiletine - Class IB Agent

A 
Oral agent
has an amine side group so it avoids the 1st pass effect
150-200 mg q8h
can be used for neuropathic pain
needs cardiac clearance before surgery
45
Q

Phenytoin - Class IB Agent

A

treat ventricular arrhythmias associated with digitalis toxicity, torsades de pointes
MIX IN NS not D5W!
Dose: 1.5 mg/kg IV q5min up to 10-15 mg/kg

Metabolized in the liver, excreted in urine
Elimination 1/2 time: 24 hours

46
Q

Phenytoin

Therapeutic level, toxicity, A/E

A

Therapeutic level 10-18 mcg/mL
can cause pain or thrombosis, bone marrow depression, nausea, Steven’s Johnson Syndrome, partially inhibits insulin secretion
severe hypotension if given rapidly
toxicity: CNS disturbances, vertigo, ataxia, slurred speech

47
Q

What arrhythmias are Class II agents used?

A

SVT, atrial and ventricular arrhythmias, ventricular dysrhythmias during MI and reperfusion, SVT, afib, aflutter, secondary to digoxin toxicity

48
Q

Propranolol - Class II Agent`

A 
Nonselective beta blocker
Onset: 2-5mins
Peak: 10-15mins
Elimination 1/2 time: 2-4hours
Cardiac effects: decreased HR, contractility, CO, increased PVR, coronary vascular resistance, lowered oxygen demand
49
Q

What is Propranolol used for?

A

prevent reoccurrence of tachyarrhythmias precipitated by sympathetic stimulation

50
Q

Metoprolol - Class II Agent

A 
selective Beta 1 
Dose: 5mg IV over 5 minutes, max 15 mg over 20 mins.
Onset: 2.5 min
Half life 3-4 hours
metabolized by liver
51
Q

Esmolol - Class II Agent

A 
selective Beta 1
Dose: 0.5 mg/kg IV bolus over 1 min, 50-300 mcg/kg/min
Duration: <10 minutes
Effects HR w/o decreasing BP
metabolized by plasma esterases
52
Q

Class III Agents are used to treat which arrhythmias?

A

supraventricular and ventricular arrhythmias, prophylaxis in cardiac surgery patients who are at risk of afib, those who are not eligible for ICD, afib

53
Q

Amiodarone - Class III Agent

A

also has Class I, II, and IV properties

used for prophylaxis or acute treatment for atrial and ventricular arrhythmias (refractory SVT, VTach, VFib, AF)

54
Q

Which agent is the 1st line drug for refractory vtach/vfib to defibrillation?

A

Amiodarone

55
Q

Amiodarone

Pharmacokinetics

A 
Dose: bolus 150-300 mg IV over 2-5minutes up to 5mg/kg, 1mg/hr x 6 hours then 0.5 mg/hr x 18 hours
elimination half life 29 DAYS!
hepatic metabolism, active metabolite
extensive protein bound
large Vd
56
Q

Amiodarone Adverse Effects

A

pulmonary toxicity, pulmonary edema, ARDS, photosensitive rashes, discoloration, thyroid abnormalities, corneal deposits, CNS/GI disturbance, proarrhythmic effects, heart block, hypotension, sleep disturbances, abnormal LFT, inhibits hepatic P450

57
Q

Sotalol - Class II and III Agent

A

nonselective beta blocker and K+ channel blocker
treat severe sustained vtach/vfib, prevent reoccurrence of tachyarrhythmias (afib and flutter)
S/E: prolonged QT interval, bradycardia, myocardial depression, fatigue, dyspnea, AV block
excreted in urine

58
Q

Which agent(s) should be avoided in patients with asthma?

A
  • sotalol d/t beta blocker effect on beta 2 receptors causing bronchoconstriction
  • adenosine can cause bronchospasm, dyspnea
59
Q

Dofetilide and Ibutilide - Class III Agents

A

used for conversion of afib or flutter to NSR

proarrhythmic - prolongs QT interval

60
Q

Where are calcium ion channels?

A

cell membranes of skeletal muscle, vascular smooth muscle, cardiac muscle, mesenteric muscle, neurons, glandular cells

61
Q

How are calcium channel blockers classified?

A

Based on structure:
Phenyl-alkyl-amines AV node (Verapamil)
Benzothiazepines-AV node (Diltiazem)
1,4-dihydropyridines-arterial beds (Nifedipine)

62
Q

Vascular uses for calcium channel blockers

A

angina, systemic HTN, pulmonary HTN, cerebral arterial spasm, Raynaud’s disease, migraine

63
Q

Nonvascular uses for calcium channel blockers

A

bronchial asthma, esophageal spasm, dysmenorrhea, premature labor

64
Q

Which agents are complementary to nitrates and good at dilating the coronary arteries?

A

Class IV Agents - Calcium channel blockers

decrease contractility

65
Q

Which Calcium channel subtype is important in determining vascular tone and cardiac contractility?

A

L type channels

66
Q

Calcium channel blocker effects

A

decreased contractility, HR, SA node activity, rate of conduction of impulses via AV node, vascular smooth muscle relaxation (decreased SVR and BP), decreased O2 demand

67
Q

What arrhythmias are treated by Class IV agents?

A

SVT and ventricular rate control in afib/flutter, prevent reoccurrence of SVT

NOT used in ventricular arrhythmias

68
Q

Verapamil - Class IV Agent

A

depresses the AV node, negative chronotropy, inotropy, moderate vasodilation

used for SVT, vasospastic angina pectoris, HTN, HCM, premature onset of labor
highly protein bound
hepatic first pass metabolism, active metbolite
oral peak: 30-45 mins, 15 mins IV
elimination 1/2 time: 6-12 hours

69
Q

Verapamil

Dosing, Side Effects

A

Dose: 2.5-10 mg IV over 1-3min (max 20mg), 5 mcg/kg/min infusion

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

70
Q

What can we give to decrease the chance of hypotension with administration of Verapamil?

A

Calcium gluconate

71
Q

Which class of drugs should not be given with Verapamil?

A

Beta blockers = will cause heart block

72
Q

Which drug has local anesthetic activity?

A

Verapamil, increases the risk of local anesthetic toxicity

73
Q

Diltiazem - Class IV Agent

A

1st line for SVT, also used for HTN, vasospastic angina, HCM
minimal CV depressant effects
Dose: 0.25-0.35 mg/kg over 2 mins can repeat in 15 minutes, 10 mg/hour infusion
Onset: 15 minutes
Peak: 30 minutes
highly protein bound
elimination 1/2 time 4-6 hours

74
Q

Nifedipine - Class IV Agent

A 
used for angina pectoris
coronary and peripheral vasodilator properties
little to no effect on SA and AV node
Onset: 20 minutes
Peak: 60-90 minutes
highly protein bound
hepatic metabolism
elimination 1/2 time: 3-7 hours
75
Q

Calcium Channel Blockers Drug interactions

A
  • myocardial depression and vasodilation with inhalational agents
  • potentiate NMB
  • verapamil and beta blockers = heart block
  • verapamil increases risk of LA toxicity
  • verapamil and dantrolene = hyperkalemia d/t slowing of K+ movement = cardiac collapse
  • CCBs interact w/ calcium mediated platelet function
  • digoxin w/ CCB increases plasma concentration of digoxin
  • H2 antagonists increase plasma levels of CCB
76
Q

Toxicity of CCB can be reversed by

A

IV admin of calcium or dopamine

77
Q

Abrupt discontinuation of CCB can cause

A

coronary vasospasm

78
Q

Adenosine MOA

A

binds to A1 purine nucleotide receptors to open K+ channels and increase K+ currents, slows AV nodal conduction

used for SVT/diagnosis of VT

79
Q

Adenosine

Pharmacokinetics/Dosing

A

Dose: 6 mg rapid bolus, after 3 minutes 6-12 mg
onset: <10 seconds
eliminated by plasma and vascular enzymes in RBCs
S/E: excessive AV or SA node inhibition, flushing, HA, dyspnea, chest discomfort, nausea, bronchospasm

80
Q

Digoxin - cardiac glycoside

A

increases vagal activity, decreases SA node activity and prolongs conduction of impulses thru the AV node
positive inotrope by blocking the Na+/K+ ATP pump, increasing Ca++

81
Q

Digoxin Dosing and Pharmacokinetics

A

dose: 0.5-1 mg over 12-24 hours
onset: 30-60 mins
elimination 1/2: 36 hours
weak protein binding
excreted by kidneys
narrow therapeutic index: 0.5-1.2 ng/mL

82
Q

Digoxin Adverse Effects

A

arrhythmias, heart block, anorexia, nausea, diarrhea, confusion, agitation

83
Q

How to treat digoxin toxicity

A

phenytoin, pacing, atropine

84
Q

Magnesium

A

works at Na+, K+, Ca++ channels
used for torsades de pointes
dose: 1 gm over 20 minutes

Pharmacology II - CP (12 decks)

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