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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
What phase of action potential dose quinidine effect
Vmax of phase 0, slows maximal rate of rise of cellular action potential
26
What does quinidine do to K+ channels
Blocks, prolongs depolarization
27
What receptors does quinidine bind/block and what is the effect
1. Muscarinic- increase HR and AV conduction (atropine-like) 2. Alpha receptors- hypotension and reflex tachycardia
28
What are the two mechanisms in which quinine increases HR
1. Muscarinic receptor blockade 2. Alpha receptor blockade via reflex tachycardia from hypotension
29
How does quinidine work
Binds to open and activated Na+ channels, prolonging AP duration and ERP
30
How is quinidine administered
Oral administration
31
Why is the bioavailability of quinidine variable
First pass effect
32
T or F: quinidine passes into milk and placenta
True
33
What is the t 1/2 of quinidine in dogs and horses
Dogs- 6 hours Horses- 8 hours
34
T or F: quinidine is used in cats
False
35
What is quinidine indicated for
1. Supraventricular arrhythmia’s 2. ventricular arrhythmia’s 3. Re-entry arrhythmias- ex: a-fib
36
When is quinidine contraindicated
Patients with myasthenia gravis, patients with AV block, patients with digoxin toxicity
37
What are some adverse effects of quinidine
Diarrhea, hypotension, widened QRS and QT complex, AV block, ventricular tachycardia
38
What are some adverse effects of quinidine in horses
Colic, ataxia, swelling of nasal mucosa, urticaria, laminitis
39
What does procainamide do
Binds to open and activated Na+ channels, prolongs AP and ERP
40
Quinidine or procainamide: less prominent Muscarinic and alpha receptor blockade
Procainamide
41
Procainamide is better at treating ___ than quinidine
Ventricular arrhythmias
42
Which has fewer drug interactions: quinidine or procainamide
Procainamide
43
Which is more effective at treating arrhythmias in horses: procainamide or quinidine
Quinidine
44
What does lidocaine do to treat arrhythmias
Blocks inactivated Na+ sodium channels, decreases APD and ERP due to block of slow na+ “window” currents
45
What arrhythmia is lidocaine only indicated for
Ventricular arrhythmias
46
How does lidocaine impact QRS or QT complex
It doesn’t
47
Lidocaine has little to no effect on myocardial ___
Contractility
48
T or F: lidocaine blocks vagal activity
False, but quinidine and procainamide do
49
How is lidocaine administered and what kind of dose is usually needed
IV, typically given a loading dose since t1/2=3hrs and takes 5 1/2 lives to reach steady state
50
Why can’t lidocaine be administered orally
First pass metabolism
51
Lidocaine is not effective at treating what arrhythmia and why
Supraventricular, only treats arrhythmia’s of ventricular origin
52
What is the loading dose for lidocaine
1-2mg/kg given every 3-5 minutes
53
To maintain an anti-arrhythmic effect of lidocaine what does the maintenance rate need to be
40-80ug/kg/min
54
What are lidocaine toxicity signs
Usually CNS related- drowsiness, agitated, muscle twitching, convulsions Hypotension can develop of bolus given too fast
55
How does propanolol bind
Beta receptor antagonist
56
What is propanolol indicated for
1. Supraventricular tachycardia 2. A-fib/a-flutter 3. Hypertrophic cardiomyopathy in ferrets 4. Hypertension 5. Thyrotoxicosis
57
What is more effective at treating ventricular tachycardia in horses: propanolol or lidocaine
Lidocaine
58
What does atenolol bind
B1 selective block agent
59
What does atenolol treat
1. Supraventricular tachyarrhythmia’s 2. Systemic hypertension 3. Hypertrophic cardiomyopathy in ferrets
60
How does esmolol bind
B1 specific blocker
61
What is esmolol used for
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
What does sotalol bind
Nonspecific beta receptor antagonist
63
How does sotalol and amiodarone tx arrhythmias
Inhibits K+ channels, prolongs AP and ERP
64
What arrhythmia does sotalol traditionally treat
Arrhythmogenic cardiomyopathy
65
A patient comes in with asthma and a ventricular arrhythmia, what drug should you NOT give them and why
Sotalol because Beta nonspecific antagonist- bind b2 causing bronchoconstriction
66
How does dilitiazem affect AV nodal conduction and HR
Slows AV node conduction and decreases HR by blocking Ca2+ channels
67
Does diltiazem cause vasodilation or vasoconstriction
Vasodilation
68
T or F: diltiazem produces reflex tachycardia
False, inhibits AV node (not like quinidine which blocks alpha receptor causing hypotension and reflex tachycardia)
69
When is diltiazem indicated
1. A-fib 2. Supraventricular tachycardia 3. Hypertrophic cardiomyopathy in cats and ferrets 4. Hypertension
70
What are some adverse effects of diltiazem
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
a patient with a supraventricular tachyarrythmias, what should you use: quinidine or diltiazem and why
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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