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Module 10 > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

where do supraventricular arrhythmias originate

A

in atria

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2
Q

where do ventricular arrhythmias originate

A

ventricles

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3
Q

what are two abnormalities that lead to arrhythmias

A
  1. abnormal impuses from ectopic foci

multiple spontaneous rhythms generated

  1. abnormal propagation: generation of re-entrant rhythm –> the damaged area conducts in one direction only –> permits continuous circilation of impulse to occur
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4
Q

what are the phases of cardiac action potential

A
  1. rapid depolarization
  2. partial repolarization
  3. plateau
  4. repolarization
  5. pacemaker depolarization
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5
Q

what are anti-arrhythmic drugs (AARD’s) used to treat

A
  1. tachyarrhythmias (vaughan williams classification –> class 1, 2, 3, 4 and digoxin)
  2. bradyarrhythmias (muscarinic antagonists, B-agonists, methylxanthines)
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6
Q

what is the mechanism of action of class 1 anti-arrhythmic drugs

A
  1. block sodium channels
  2. reduce the rate of depolarization during phase 0
  3. reduce slope of phase 0

use-dependent channel block

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7
Q

how are class 1 AARD’s subdivided

A

class 1a- intermediate dissociation

-prolong APD & RP

class 1b- fast dissociation

-slightly decrease APD & RP

class 1c- slow dissociation

-no effect on APD or RP

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8
Q

what is the major indication of class 1a AARD’s

A

hemodynamically significant or life threatening ventricular arrhythmias

to convert atrial fibrillation to sinus rhythm (quinidine in horses)

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9
Q

what are the side effects of class 1a AARD’s

A
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10
Q

what are the major indications of class 1b AARD’s

A

hemodynamically significant or life threatening ventricular arrhythmias

lidocaine effetive in recent onset arrhythmia in dogs

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11
Q

what are the side effects of 1b AARD’s

A
  1. tremor, shivering
  2. muscle fasciculations
  3. seizures

lidocaine also local anaesthetic

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12
Q

what are examples of class 2 AARDs

A

B-blockers

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13
Q

what are the types of B-blockers

A
  1. B1 and B2 receptors: Propanolol, Sotalol
  2. B1 receptors: Atenolol
  3. B1, B2, a1 receptors: Carvedilol
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14
Q

what are the effects of B-blockers

A
  1. reduce sympathetic drive: slow AV node conduction, negative inotropes
  2. reduce oxygen consumption: improve oxygenation
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15
Q

what are the indications of B-blockers

A
  1. arrhythmias (both SVA & VA)
  2. hypertrophic cardiomyopathy
  3. heart failure
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16
Q

what are the side effects of B-blockers

A
  1. worsening CHF
  2. negative inotropy
  3. lethargy, depression
  4. bradycardia
  5. bronchspasm
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17
Q

what are examples of class 3 AARDs

A

amiodarone, sotalol, bretylium

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18
Q

what are the effects of class 3 AARDs

A

block outward K channels

increase APD and RP

amiodarone –> Na channel blockade, a and B blocker, Ca channel blocker

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19
Q

what are the pharmacokinetics of class 3 AARDs

A

long t1/2

lipophilic

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20
Q

what are the side effects of AARDs

A
  1. elavated liver enzymes
  2. GI disturbances
  3. pulmonary fibrosis
  4. thyroid effects
21
Q

what are examples of class 4 AARDs

A

verapamil, diltiazem

22
Q

what are the mechanism of action of class 4 AARDs

A

calcium channel blockers

block L-type calcium channels –>

profound effect on nodal tissue (reduce AP height, prolong AP)

cardiomyocytes –> shorten AP (negative inotropes, positive lusitropes)

23
Q

what are the indications of class 4 AARDs

A

supraventricular arrhthymias

hypertrophic cardiomyopathy

24
Q

what is an example of cardiac glycosides

A

digoxin

25
Q

what are cardiac glycosides from

A

foxgloves and related plants

26
Q

what are the 3 components of cardiac glycosides

A

sugar, steroid, lactones

27
Q

what are the pharmacodynamics of cardaic glycosides

A
  1. antiarrhythmic effects
  2. baroreceptor/neuroendocrine effects
  3. positive inotropic effects
  4. diuretic effects
28
Q

how do cardiac glycosides lead to antiarrythmic effects

A
  1. increases parasympathetic activity –> decreases sinus rate
  2. inhibit AV node conduction –> prolong RP

overall: slow ventricular response to atrial flutter/fibrillation (supraventricular arrhythmias don’t pass down)

29
Q

how do cardiac glycosides effect baroreceptors

A

baroreceptors functions are decreased in heart failure

glycosides increase function –> decrease sympathetic activity, and decrease [catecholamine]

not a primary indication of digoxin

30
Q

how do cardiac glycosides have a positive inotropic effect

A
  1. inhibits Na/K ATPase

–> increases [Na+] in the cardiomyocyte –> slows extrusion of Ca via the Na/Ca exchange transporter –> increases [Ca] stored in SR –> increase Ca released by each AP

mild positive inotrope

31
Q

explain what this data is showning

A

control: when cell is stimulated Ca increases and increases contraction

after cardiac glycoside is added: the transient Ca is larger and therefore the contraction is larger

32
Q

how do cardiac glycosides cause diuretic effects

A

Na/K ATPase on basolateral aspect of renal tubular epithelial cells –> promote tubular reabsorption of sodium

inhibition –> diuretic effect

33
Q

what are the pharmacokinetics of digoxin (6)

A
  1. oral admin 60-75% bioavailability
  2. 25% plasma protein bound
  3. large Vd (skeletal muscle reservoir)
  4. t1/2 dog 24-30 hours (cats 36 hours)
  5. approx 7 days to steady state
  6. renal excretion
34
Q

what are the adverse effects of cardiac glycosides (3)

A
  1. disturbances of rhythm: block AV conduction, increased ectopic pacemaker activity
  2. effects of glycosides increased if plasma [K+] decreases
  3. narrow therapeutic index: excessive borborygmi, depression, anorexia, vomiting, diarrhea, cardaic arrhythmia
35
Q

what are predispositions to cardiac glycoside toxicity (9)

A
  1. thin, cachexic
  2. obese
  3. ascites
  4. hypoproteinemia
  5. hypothyroidism
  6. impaired renal function
  7. electrolyte disturbance
  8. other drugs
  9. dobermans
36
Q

how is cardiac glycoside toxicity prevented (5)

A
  1. start on low dose
  2. dose by body surface area
  3. avoid loading dose
  4. reduce dose if predisposed
  5. check serum level after 7 days
37
Q

how is cardiac glycoside toxicity dealt with

A
  1. stop for 3-5 days
  2. start again at lower dose
  3. check electrolytes, acid base balance
  4. treat arrhythmias
  5. overdose –> activated charcoal/cholestyramine resin, digibind (if in circulation antibody used to encapsulate drug)
38
Q

what is the mechanism of action of muscarinic antagonists

A

antagonism of muscarinic acetylcholine receptors

39
Q

when are muscarinic antagonists indicated

A

bradyarrhythmias associated with high vagal tone

40
Q

what are the side effects of muscarinic antagonists (4)

A
  1. constipation
  2. sinus tachycardia
  3. urinary retention
  4. dry mucous membranes
41
Q

what are examples of muscarinic antagonists

A

atropine

propanthaline

42
Q
A
43
Q

what are examples of B-agonists

A

isoprenaline (B1)

terbutaline (B2)

44
Q

what are the mechanism of action of B-agonists

A

stimulation of B-adrenergic receptors

45
Q

what are the indications of B-agonists

A

sinus arrest, AV block

bronchodilator

46
Q

what are the side effects of B-agonists

A
  1. isprenaline: ventricular arrhthymia
  2. terbutaline: tremor, tachycardia, hypotension
47
Q

what are examples of methylxanthines

A

theophylline, aminophylline, etamiphylline

48
Q

what is the mechanism of action of methylxanthines

A

mild PDE inhibition

enhanced sympathetic drive –> mild positive inotropic and chronotropic effects

49
Q

what are the indications of methylxanthines

A

widely used in HF in past

now bronchodilation

Module 10 (27 decks)

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