Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens during Phase 1 of cardiac action potentials

A

Na+ channels remain open, correct overshoot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What happens during phase 2 cardiac action potentials

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What happens during phase 3 cardiac action potentials

A

K+ enters to hyperpolarize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What happens during phase 4 action potentials

A

Begin slow depolarization back up to threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 2 causes of clinical arrhythmia’s

A
  1. Disturbances in impulse formation
  2. Disturbances in impulse conduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Black is normal, purple is abnormal what is this change

A

Increase in threshold potential required to generate AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

Lengthen duration of AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do Class I channels do

A

Block Na+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Type C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What do Class II Antiarrhythmic drugs do and what are they

A

Reduce adrenergic activity on the heart

Drugs: beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do class III Antiarrhythmic drugs do and what are they

A

K+ channel inhibitors, increasing ERP

Drugs:
Sotalol, amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What do class IV Antiarrhythmic drugs do and what are they

A

Calcium channel blockers, decrease HR and contractility

Drugs: diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What phase of action potential dose quinidine effect

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What does quinidine do to K+ channels

A

Blocks, prolongs depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

A

True

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

A

False

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

A

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

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions