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2020 CPR II Cardio Exam 1 > Drugs for Cardiac Arrhythmia (Konorev) > Flashcards

Drugs for Cardiac Arrhythmia (Konorev) Flashcards

1
Q

What are the 3 class 1A antiarrhythmic drugs?

A
  • Quinidine
  • Procainamide
  • Disopyramide
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2
Q

What are the 2 class 1B antiarrhythmic drugs?

A
  • Lidocaine
  • Mexiletine
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3
Q

What are the 2 class 1C antiarrhythmic drugs?

A
  • Flecainide
  • Propafenone
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4
Q

What are the two class 2 antiarrhythmic drugs (beta-blockers)?

A
  • Esmolol
  • Propranolol
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5
Q

What are the four class 3 antiarrhythmic drugs?

A
  • Amiodarone
  • Sotalol
  • Dofetilide
  • Ibutilide
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6
Q

What are the two class 4 antiarrhythmic drugs?

A
  • Verapamil
  • Diltiazem
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7
Q

What is the one miscellaneous agents used as an antiarrhythmic drug?

A

Adenosine

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8
Q

What are the 3 cell types in the heart that exhibit fast AP?

A
  • Ventricular contractile cardiomyocytes
  • Atrial cardiomyocytes
  • Purkinje fibers
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9
Q

What are the 2 cell types in the heart that exhibit slow (pacemaker) AP’s?

A
  • SA node cells
  • AV node cells
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10
Q

Briefly describe the 5 phases of fast AP in cardiac muscle?

A
  • Phase 0: depolarization; inward Na+ flux
  • Phase 1: partial repolarization K+ efflux, while fast Na+ channels close
  • Phase 2: plateau, K+ exiting, offset by Ca<strong>2</strong>+ entering thru slow channels
  • Phase 3: Ca<strong>2</strong>+ channels close and K+ begins to exit rapidly = repolarization
  • Phase 4: stable RMP gradually restored by Na+/K+ ATPase and Na+/Ca2+ exchanger
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11
Q

Describe the ion currents involved in phase 4 of the slow (pacemarker) AP?

A
  • Poorly selective ionic influx (Na+, K+) known as pacemaker current (Funny current, If) - activated by hyperpolarization
  • Slow Ca2+ influx [via T-type (transient) channels]
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12
Q

What is responsible for the rapid upstroke of phase 0 and repolarization of phase 3 of the pacemaker AP?

A
  • Phase 0: influx of Ca2+ thru slow L-type (long-acting) Ca2+ channels
  • Phase 3: inactivation of Ca2+ channels w/ ↑ K+ efflux
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13
Q

How does a resting potential that is less negative affect the time needed for an AP to reach threshold and affect on firing rate?

A
  • Less time is needed to reach threshold
  • Firing rate ↑
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14
Q

What are the 3 states that the Na+ channel found on cardiac myocytes exists in and describe each?

A
  • Resting: the channel is closed but ready to generate AP
  • Activated state: depolarization to threshold opens m-gates greatly ↑ Na+ permeability
  • Inactivated state: h-gates are closed, inward Na+ flux is inhibited, the channl is not available for reactivation –> refractory period
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15
Q

Which channels are blocked by Class 1A antiarrhythmics?

A
  • Block Na+ channels
  • Block K+ channels
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16
Q

Class 1A antiarrhythmics block sodium channels in a state dependent manner, preferentially when in what state?

Cells with what characteristics will be preferentially targeted?

A
  • Preferentially bind to open (activated) Na+ channels
  • Ectopic pacemaker cells w/ faster rhythms will be preferentially targeted
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17
Q

What is the effect of Class 1A antiarrhythmics on the the different phases of the AP, QRS and QT intervals?

A
  • Decrease slope of phase 0 (blockade of Na+ channels)
  • Prolong AP duration (blockade of K+ channels)
  • Prolong QRS and QT intervals of the ECG
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18
Q

What is the clinical use of the class 1A antiarrhythmic, procainamide?

A
  • Tx sustained ventricular tachycardias, may be used in arrhythmias associated w/ MI
  • Paroxysmal supraventricular tachycardia (PSVT)
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19
Q

The class 1A antiarrhythmic, procainamide also has blocking effects where?

A
  • Antimuscarinic
  • Ganglion blocking
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20
Q

What are 3 cardiac AE’s associated with the class 1A antiarrhythmics, Procainamide and Quinidine?

A
  • QT interval prolongation
  • Induction of torsade de pointes arrhythmias and syncope
  • Excessive inhibition of conduction
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21
Q

What are some rare extra-cardiac and common AE’s associated with the class 1A antiarrhythmic, Procainamide?

A
  • Drug-induced lupus syndrome w/ arthritis, pleuritis, pulmonary dz, hepatitis
  • Agranulocytosis
  • Common = N/V, diarrhea, rash, fever, or hypotension
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22
Q

What is the clinical use for the class 1A antiarrhythmic, Quinidine?

A
  • Restoring rhythm in Afib/flutter pt’s w/ normal (but arrhythmic) hearts
  • Sustained ventricular arrhythmia
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23
Q

The class 1A antiarrhythmic, Quinidine, also has what other blocking effects?

A
  • Anticholinergic effects
  • Beta-blocking effects
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24
Q

What is the triad of Cinchonism and what class 1A antiarrhythmic may cause this as an AE?

A
  • HA, dizziness, and tinnitus
  • Quinidine
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25
Q

What are some of the extra-cardiac AE’s associated with the class 1A antiarrhythmic, Quinidine?

A
  • GI effects –> diarrhea + N/V
  • Cinchonism
  • Thrombocytopenia

- Hepatitis and fever

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26
Q

What is the main clinical implication for the class 1A antiarrhythmic, Disopyramide?

A

Prevent recurrence of ventricular tachycardia or ventricular fibrillation

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27
Q

Other than antiarrhythmic activity, what other type of effect does Disopyramide have and what are the AE’s associated with this effect?

A
  • Potent antimuscarinic effect
  • Dry mouth + blurred vision + constipation + urinary retention + exacerbation of glaucoma
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28
Q

What are the cardiac AE’s of the class 1A antiarrhythmic, Quinidine?

A
  • QT interval prolongation –> induction of torsade de pointes arrhythmia
  • Negative inotrope effect - may precipitate HF
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29
Q

Which ion channel(s) are blocked by the class 1B antiarrhythmic?

A

Na+ channels only

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30
Q

Class 1B antiarrhythmic exhibit state-dependent blocking of Na+ channels in which state?

Preferentially bind cells in what state of membrane potential?

A
  • Inactivated Na+ channels
  • Depolarized cells
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31
Q

What is the kinetics of dissociation from the Na+ channel like for the class 1A, 1B, and 1C antiarrhythmics and how does this correlate with their strength of blockade?

A
  • Class 1A = dissociate w/ intermediate kinetics = medium blockade
  • Class 1B = dissociate w/ fast kinetics = weak blockade
  • Class 1C = dissociate w/ slow kinetics = strong blockade
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32
Q

What is the effect of class 1B antiarrhythmics on AP and QT duration?

A
  • May shorten AP
  • Since do not block K+ channels, do not prolong AP or QT duration on ECG
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33
Q

Why is the class 1B antiarrhythmic, Lidocaine useful in damaged tissue based on its MOA?

A
  • Blocks inactivated Na+ channels (use-dependence)
  • Selectively blocks conduction in depolarized tissue, making damaged tissue “electrically silent.”
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34
Q

Why does the class 1B antiarrhythmic, Lidocaine have no effect on cardiac conductivity in normal tissue?

A

Rapid kinetics results in recovery from block between AP, exerts greater effects in depolarized (i.e., ischemic) and/or rapidly driven tissues

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35
Q

What are the 2 clinical indications for the use of the class 1B antiarrhythmic, Lidocaine?

A
  • In mono- and polymorphic ventricular tachycardias
  • Very efficient in arrhythmias assoc. w/ acute MI
36
Q

What is the pharmacokinetics of the class 1B antiarrhythmic, Lidocaine like and needs to be given via which route?

A

Extensive first-pass metabolism; must give IV

37
Q

What is the least toxic of all class 1 antiarrhythmics?

A

Lidocaine (class 1B)

38
Q

What are some of the CV and neurological AE’s associated with the class 1B antiarrhythmic, Lidocaine?

A
  • CV = may cause hypotension in pt’s w/ HF by inhibiting contractility
  • Neuro = paresthesias, tremor, slurred speech, and convulsions
39
Q

Which class 1B antiarrhythmic is a lidocaine analog modified to reduce first-pass metabolism and permit chronic oral therapy?

A

Mexiletine

40
Q

The electrophysiological and antiarrhythmic effects of the class 1B antiarrhythmic, Mexiletine are similar to what?

A

Lidocaine (since is a modified analog)

41
Q

What are the 2 clinical uses for the class 1B antiarrhythmic, Mexiletine?

A
  • Ventricular arrhythmias
  • Relieve chronic pain, especially pain due to diabetic neuropathy and nerve injury
42
Q

What are 4 AE’s associated with the class 1B antiarrhythmic, Mexiletine?

A
  • Tremor
  • Blurred vision
  • Nausea
  • Lethargy
43
Q

Which ion channel(s) are blocked by class 1C antiarrhythmics?

A
  • Block Na+ channels
  • Block certain K+ channels
44
Q

What is the strength of the Na+ channel block associated with class 1C antiarrhythmics and preferentially block channels in which state?

A
  • Strong/long-lasting block due to slow dissociation from channel
  • Preferentially bind Na+ channel in open (activated) state
45
Q

Which interval is prolonged by the class 1C antiarrhythmics due to blockage of certain K+ channels?

A
  • Prolong QRS interval
  • NO effect on AP or QT duration
46
Q

What is the clinical use of the class 1C antiarrhythmic, Flecainide?

Patients with which cardiac status specifically?

A
  • In pts with normal hearts
  • Tx of supraventricular arrhythmias including atrial fibrillation, paroxysmal SVT (AV nodal reentrant tachy, AV reentrate tachy)
  • Life-threatening ventricular arrhythmias, such as sustained V-Tach
47
Q

The class 1C antiarrhythmic, Flecainide may be very effective in suppressing premature ventricular contractions, but pt’s with what cardiac status are at risk for AE’s and what are these effects?

A
  • May cause severe exacerbation of ventricular arrhythmias if given to:
  • Pts w/ preexisting ventricular tachyarrhythmias, a previous MI, or those w/ ventricular ectopic rhythms
48
Q

Which class 1C antiarrhythmic also possesses weak β-blocking activity?

A

Propafenone (kind of sounds like propranolol)

49
Q

What are the 2 clinical uses of the class 1C antiarrhythmic, Propafenone?

Specifically pt’s with what cardiac status?

A
  • Pt’s WITHOUT structural disease
  • Prevent paroxysmal atrial fibrillation and SVT
  • Used in sustained ventricular arrhythmias
50
Q

The class 1C antiarrhythmic, Propafenone, should not be combined with inhibitors of what 2 enzymes as the risk of proarrhythmia may be increased?

A

CYP2D6 and CYP3A4 inhibitors

51
Q

What are 3 AE’s associated with the class 1C antiarrhythmic, Propafenone?

A
  • Exacerbation of ventricular arrhytmias
  • Metallic taste
  • Constipation
52
Q

What is the effect of the sympathetic NS on the If, T-type and L-type Ca2+ channels involved in pacemaker action potentials?

A
  • ↑ slope of phase 4 due to effects on If and T-type Ca2+ channels
  • Effect on L-type Ca2+ channels = lowers the threshold
53
Q

What is the effect of the class 2 antiarrhythmic (beta-blockers) at the SA and AV node?

Effect on which 2 intervals?

A
  • SA node = ↓ HR (increase RR interval)
  • AV node = ↓ AV conductance (increase PR interval)
54
Q

What is the effect of the class 2 antiarrhythmic (beta-blockers) on the slop of phase 4 and the threshold of the pacemarker AP?

A
  • Decreased slope due to effects on If and T-type Ca2+ channels
  • Increased threshold due to effect on L-type Ca2+ channels

*Net effect = slow AP + ↓ HR + ↓ AV conductance

55
Q

What are the 4 clinical indications for the use of the class 2 antiarrhythmic, Propranolol for arrhythmias?

Decrease mortaility from arrhythmias in which pt’s?

A
  • Arrhythmias associated w/ STRESS (i.e., catecholamines)
  • Re-entrant arrhythmias that involve AV node –> AVNRT and AVRT
  • Afib and flutter
  • Arrhythmias associated w/ MI –> ↓ mortality in pt’s with acute MI
56
Q

Which class of antiarrhythmics is reserved for use in pt’s with a structually normal heart?

A

Class 1C = Flecainide and Propafenone

57
Q

Which class 2 antiarrhythmic is a short-acting (t1/2 5-10 min) SELECTIVE β1-blocker?

58
Q

Due to it’s short half-life how is Esmolol administered clinically as an antiarrhythmic?

A

Continous IV infusion when rapid adrenergic blockade is desired

59
Q

What are the 3 clinical uses for the class II antiarrhythmic, Esmolol?

A
  • Supraventricular arrhythmias
  • Arrhythmias association with thyrotoxicosis, myocardial ischemia/infarction
  • As an adjunct drug in general anesthesia to control arrhythmias in perioperative period
60
Q

List some of the AE’s associated with the class 2 antiarrhythmic, beta-blockers.

A
  • Bradycardia + Bronchoconstriction
  • Impaired liver glucose mobilization
  • Worsens blood lipid profile
  • Sedation + depression + fatigure
  • Rapid withdrawl –> rebound HTN
61
Q

What are 6 contraindications for the the class 2 antiarrhythmic, beta-blockers?

A
  • Asthma
  • Peripheral vascular disease
  • Raynaud’s
  • Type 1 DM on insulin
  • Bradyarrhythmias, AV conduction problems
  • Severe depression of cardiac function
62
Q

Which K+ channels in the heart are open in the resting state?

A

Inward rectifying K+ channels

63
Q

Class 3 antiarrhytmics block which ion channel and in which state?

A

Bind K+ channels in the resting state = reverse use dependence

64
Q

What is the effect of class 3 antiarrhytmics on the AP, QT interval and refractory period?

A
  • Prolong AP duration
  • Prolong QT interval
  • Prolong refractory period
65
Q

K+ channels in the heart are responsible regulating which parts of the membrane potential?

A
  • Regulation of resting potential via inward rectifying K+ channels which are open in resting state
  • Regulation of AP via voltage-gate K+ channels which repolarize and limit the frequence of AP’s (regulate duration of the refractory period)
66
Q

Which class 3 antiarrhytmic prolongs QT interval and APD uniformly over a wide range of heart rates and in all cardiac tissues?

A

Amiodarone

67
Q

What are the 2 clinical uses for the class 3 antiarrhytmic, Amiodarone?

A
  • Tx of ventricular arrhythmias
  • Atrial fibrillation
68
Q

What is unique about the pharmacokinetics of the class 3 antiarrhytmic, Amiodarone, including t1/2, elimination, and interactions?

A
  • Major metabolite has t1/2 = ~ 50 days
  • Effects maintainied for 1-3 months after discontinuation and metabolites may be found in tissues 1 year later (highly lipophilic)
  • Inhibits many CYP enzymes so can affect metabolism of other drugs
69
Q

Which class 3 antiarrhythmic has a lower incidence of torsade de pointes as an AE compard to others in the class?

A

Amiodarone

70
Q

What are 5 of the extra-cardiac AE’s associated with the class 3 antiarrhytmic, Amiodarone?

A
  • Pulmonary fibrosis (can be fatal)
  • Hepatitis
  • Hyperthyroidism or hypothyroidism
  • Corneal micro-deposits
  • Bluish discoloration of the skin
71
Q

What are the 2 MOA’s of the class 3 antiarrythmic, Sotalol?

A
  • Non-selective β-AR antagonist (class 2)
  • Blocks inward-rectifier K+ channels (class 3) = prolongs ADP
72
Q

What are the 2 clinical uses of the class 3 antiarrhythmic, Sotalol?

A
  • Tx of life-threatening ventricular tachyarrhythmias
  • Maintenance of sinus rhythm in pt’s w/ atrial fibrillation
73
Q

What are the 2 major AE’s associated with the class 3 antiarrhytmic, Sotalol?

A
  • Depression of cardiac function (same as β-blockers)
  • Provokes torsade de pointes
74
Q

What is the specific MOA of the class 3 antiarrhythmic, Dofetilide?

Effect of drug is most pronounced at which HR’s?

A
  • Potent and “pure” IKr (inward K+ rectifier) blocker
  • More pronounced effect at lower HR’s
75
Q

Why does the class 3 antiarrhythmic, Dofetilide have a narrow therapeutic window?

A

Majority is excreted by kidneys; must adjust dose based on Cr clearance

76
Q

What are the major AE’s of the class 3 antiarrhythmic, Dofetilide?

A
  • Torsades de pointe

- QT interval prolongation and ↑ risk of ventricular arrhythmias

77
Q

What is the clinical use for the class 3 antiarrhytmic, Dofetilide?

A

Maintenance of normal sinus rhythm in pt’s with chronic atrial fibrillation/atrial flutter AFTER cardioconversion

78
Q

What is the specific MOA of the class 3 antiarrhytmic, Ibutilide?

A

Similar to dofetilide, slows cardiac repolarization as a IKr blocker

79
Q

How is the the class 3 antiarrhytmic, Ibutilide adminstered and it’s clinical use?

A

Via rapid IV infusion for immediate conversions of acute atrial fibrillation or flutter —> sinus rhythm

80
Q

What are the AE’s associated with the class 3 antiarrhytmic, Ibutilide?

Due to AE’s pt’s require what?

A
  • Torsades de pointes, requires immediate cardioconversion
  • Must monitor EKG continously unti QTc returns to baseline
  • Incrased risk of other arrhytmias
81
Q

Which specific channels and in which state do the class 4 antiarrhytmics (verapamil and diltiazem) block?

A

Both activated and inactivated L-type Ca2+ channels

82
Q

What is the effect of the class 4 antiarrhytmics on the slope of phase 0, threshold potential at the SA node, and refractory period?

A
  • Decrease the slope of phase 0
  • ↑ L-type Ca2+ threshold potential in SA node = slows depolarization –> bradycardia
  • Prolongs refractory period in AV node = prolongs APD and conduction time
83
Q

What are the 2 clinical uses for the class 4 antiarrhythmics?

A
  • Prevention of paroxysmal SVT
  • Rate control in atrial fibrillation and atrial flutter
84
Q

What are the cardiac and extracardiac AE’s of the class 4 antiarrhythmics?

A
  • CHF (negative inotropy)
  • AV block
  • SA node arrest
  • Bradyarrhythmias
  • Hypotension
  • Constipation
85
Q

What is the MOA of adenosine in the heart (ie., receptors and effect)?

A
  • Activates K+ current and inhibits Ca2+ and Funny current
  • Causes marked hyperpolarization and suppression of AP’s in SLOW cells
  • Inhibits AV conduction and increases nodal refractory period
86
Q

What is the clinical use of Adenosine for arrhythmias?

A

Conversion to sinus rhythm in paroxysmal SVT

87
Q

What are 5 AE’s associated with Adenosine?

A
  • SOB
  • Bronchoconstriction (both A1 and A2B adenosine receptors)
  • Chest burning/fullness
  • AV block
  • Hypotension

2020 CPR II Cardio Exam 1 (31 decks)

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