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Pharmacology > Lecture 20: Antiarrhythmic agents > Flashcards

Lecture 20: Antiarrhythmic agents Flashcards

1
Q

What happens during phase O of cardiac AP

A

Voltage gated Na+ channels open causing depolarization

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2
Q

What happens during Phase 1 of cardiac action potentials

A

Na+ channels remain open, correct overshoot

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3
Q

What happens during phase 2 cardiac action potentials

A

Ca2+ channels open and release more ca2+ from sarcoplasmic reticulum

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4
Q

What happens during phase 3 cardiac action potentials

A

K+ enters to hyperpolarize

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5
Q

What happens during phase 4 action potentials

A

Begin slow depolarization back up to threshold

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6
Q

What are the 2 causes of clinical arrhythmia’s

A
  1. Disturbances in impulse formation
  2. Disturbances in impulse conduction
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7
Q

What factors play a role in disturbances in impulse formation

A
  1. Duration of action potential
  2. Duration of diastolic interval
    - maximum diastolic potential
    - slope of phase 4 depolarization
    - threshold potential
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8
Q

Black is normal and purple is abnormal, what is the change a result of

A

Change in maximum diastolic potential causing a greater hyperpolarization resulting in longer time to reach threshold and fire a new action potential. Will decrease HR

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9
Q

Black is normal, purple is abnormal, what is the change a result of and what nerve is stimulated

A

Change in the slope of phase 4 depolarization, result of activation of the vagus nerve via ACh on M2 receptors- prolonging depolarization to threshold

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10
Q

Black is normal, purple is abnormal what is this change

A

Increase in threshold potential required to generate AP

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11
Q

Black is normal, purple is abnormal what is the cause of this change

A

Lengthen duration of AP

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12
Q

What are the 2 primary mechanisms that can a disturbance in impulse conduction

A
  1. Simple block (AV node or bundle branch)
  2. Recently mechanism- unidirectional block
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13
Q

Describe the normal electrical impulse conduction

A

Two impulses extinguish each other due to trying to activate cells in the effective refractory period, all electrical activity stops and ion channels reset

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14
Q

Describe what happens in a unidirectional block and reentry

A

Impulse traveling through the unidirectional block is extinguished in anterograde direction but it will re-enter in retrograde direction and cause re-entry arrhythmia circuit

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15
Q

What are the 2 aims of therapy for arrhythmias

A
  1. Reduce ectopic pacemaker activity (premature heartbeat)
  2. Modify conduction or refractories to disable reentry
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16
Q

What are the 4 mechanisms to coutneract arrhythmias

A
  1. Na+ channel blockade
  2. Blockade of SNS effects
  3. Prolong effective refractory period
  4. Ca2+ channel blockade
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17
Q

What do Class I channels do

A

Block Na+ channels

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18
Q

What do class I type A Antiarrhythmic drugs do and what are they

A

Preferentially block open or activated sodium channels, lengthening the direction of AP and ERP

Drugs:
1. Quinidine
2. Procainamide

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19
Q

What do class A type B Antiarrhythmic drugs do and what are they

A

Preferentially block inactivated sodium channels (prevent recycling) and shorten the duration of AP and ERP

Drugs:
1. Lidocaine

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20
Q

What do class I type C Antiarrhythmic drugs do and what are they

A

Block activated and inactivated Na+ channels and have no effect on duration of AP

Drugs:
1. Flecainide

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21
Q

What type of class I Antiarrhythmic drugs are most likely to cause arrhythmias

A

Type C

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22
Q

What do Class II Antiarrhythmic drugs do and what are they

A

Reduce adrenergic activity on the heart

Drugs: beta blockers

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23
Q

What do class III Antiarrhythmic drugs do and what are they

A

K+ channel inhibitors, increasing ERP

Drugs:
Sotalol, amiodarone

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24
Q

What do class IV Antiarrhythmic drugs do and what are they

A

Calcium channel blockers, decrease HR and contractility

Drugs: diltiazem

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25
Q

What phase of action potential dose quinidine effect

A

Vmax of phase 0, slows maximal rate of rise of cellular action potential

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26
Q

What does quinidine do to K+ channels

A

Blocks, prolongs depolarization

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27
Q

What receptors does quinidine bind/block and what is the effect

A
  1. Muscarinic- increase HR and AV conduction (atropine-like)
  2. Alpha receptors- hypotension and reflex tachycardia
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28
Q

What are the two mechanisms in which quinine increases HR

A
  1. Muscarinic receptor blockade
  2. Alpha receptor blockade via reflex tachycardia from hypotension
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29
Q

How does quinidine work

A

Binds to open and activated Na+ channels, prolonging AP duration and ERP

30
Q

How is quinidine administered

A

Oral administration

31
Q

Why is the bioavailability of quinidine variable

A

First pass effect

32
Q

T or F: quinidine passes into milk and placenta

33
Q

What is the t 1/2 of quinidine in dogs and horses

A

Dogs- 6 hours
Horses- 8 hours

34
Q

T or F: quinidine is used in cats

35
Q

What is quinidine indicated for

A
  1. Supraventricular arrhythmia’s
  2. ventricular arrhythmia’s
  3. Re-entry arrhythmias- ex: a-fib
36
Q

When is quinidine contraindicated

A

Patients with myasthenia gravis, patients with AV block, patients with digoxin toxicity

37
Q

What are some adverse effects of quinidine

A

Diarrhea, hypotension, widened QRS and QT complex, AV block, ventricular tachycardia

38
Q

What are some adverse effects of quinidine in horses

A

Colic, ataxia, swelling of nasal mucosa, urticaria, laminitis

39
Q

What does procainamide do

A

Binds to open and activated Na+ channels, prolongs AP and ERP

40
Q

Quinidine or procainamide: less prominent Muscarinic and alpha receptor blockade

A

Procainamide

41
Q

Procainamide is better at treating ___ than quinidine

A

Ventricular arrhythmias

42
Q

Which has fewer drug interactions: quinidine or procainamide

A

Procainamide

43
Q

Which is more effective at treating arrhythmias in horses: procainamide or quinidine

44
Q

What does lidocaine do to treat arrhythmias

A

Blocks inactivated Na+ sodium channels, decreases APD and ERP due to block of slow na+ “window” currents

45
Q

What arrhythmia is lidocaine only indicated for

A

Ventricular arrhythmias

46
Q

How does lidocaine impact QRS or QT complex

A

It doesn’t

47
Q

Lidocaine has little to no effect on myocardial ___

A

Contractility

48
Q

T or F: lidocaine blocks vagal activity

A

False, but quinidine and procainamide do

49
Q

How is lidocaine administered and what kind of dose is usually needed

A

IV, typically given a loading dose since t1/2=3hrs and takes 5 1/2 lives to reach steady state

50
Q

Why can’t lidocaine be administered orally

A

First pass metabolism

51
Q

Lidocaine is not effective at treating what arrhythmia and why

A

Supraventricular, only treats arrhythmia’s of ventricular origin

52
Q

What is the loading dose for lidocaine

A

1-2mg/kg given every 3-5 minutes

53
Q

To maintain an anti-arrhythmic effect of lidocaine what does the maintenance rate need to be

A

40-80ug/kg/min

54
Q

What are lidocaine toxicity signs

A

Usually CNS related- drowsiness, agitated, muscle twitching, convulsions

Hypotension can develop of bolus given too fast

55
Q

How does propanolol bind

A

Beta receptor antagonist

56
Q

What is propanolol indicated for

A
  1. Supraventricular tachycardia
  2. A-fib/a-flutter
  3. Hypertrophic cardiomyopathy in ferrets
  4. Hypertension
  5. Thyrotoxicosis
57
Q

What is more effective at treating ventricular tachycardia in horses: propanolol or lidocaine

58
Q

What does atenolol bind

A

B1 selective block agent

59
Q

What does atenolol treat

A
  1. Supraventricular tachyarrhythmia’s
  2. Systemic hypertension
  3. Hypertrophic cardiomyopathy in ferrets
60
Q

How does esmolol bind

A

B1 specific blocker

61
Q

What is esmolol used for

A
  1. Acute management of supraventricular tachycardia
  2. Decrease heart rate in severe ventricular tachycardia in dogs and cats
  3. Test drug to determine if long lasting B-blockers are effective to
62
Q

What does sotalol bind

A

Nonspecific beta receptor antagonist

63
Q

How does sotalol and amiodarone tx arrhythmias

A

Inhibits K+ channels, prolongs AP and ERP

64
Q

What arrhythmia does sotalol traditionally treat

A

Arrhythmogenic cardiomyopathy

65
Q

A patient comes in with asthma and a ventricular arrhythmia, what drug should you NOT give them and why

A

Sotalol because Beta nonspecific antagonist- bind b2 causing bronchoconstriction

66
Q

How does dilitiazem affect AV nodal conduction and HR

A

Slows AV node conduction and decreases HR by blocking Ca2+ channels

67
Q

Does diltiazem cause vasodilation or vasoconstriction

A

Vasodilation

68
Q

T or F: diltiazem produces reflex tachycardia

A

False, inhibits AV node

(not like quinidine which blocks alpha receptor causing hypotension and reflex tachycardia)

69
Q

When is diltiazem indicated

A
  1. A-fib
  2. Supraventricular tachycardia
  3. Hypertrophic cardiomyopathy in cats and ferrets
  4. Hypertension
70
Q

What are some adverse effects of diltiazem

A
  1. Bradycardia
  2. GI or CNS disturbances
  3. Increase bioavailability of Beta-blockers so should not be used together
  4. Negative inotropic effect and/or AV block
71
Q

a patient with a supraventricular tachyarrythmias, what should you use: quinidine or diltiazem and why

A

Diltiazem because quinidine tx supraventricular arrhythmias but can cause reflex tachycardia by blocking alpha receptor causing hypotension and reflex tachycardia

Pharmacology (14 decks)

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