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Module 10 > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

(49 cards)

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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

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

what are examples of class 4 AARDs

Study These Flashcards
A

verapamil, diltiazem

22
Q

what are the mechanism of action of class 4 AARDs

Study These Flashcards
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

Study These Flashcards
A

supraventricular arrhthymias

hypertrophic cardiomyopathy

24
Q

what is an example of cardiac glycosides

25
what are cardiac glycosides from
foxgloves and related plants
26
what are the 3 components of cardiac glycosides
sugar, steroid, lactones
27
what are the pharmacodynamics of cardaic glycosides
1. antiarrhythmic effects 2. baroreceptor/neuroendocrine effects 3. positive inotropic effects 4. diuretic effects
28
how do cardiac glycosides lead to antiarrythmic effects
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
how do cardiac glycosides effect baroreceptors
baroreceptors functions are decreased in heart failure glycosides increase function --\> decrease sympathetic activity, and decrease [catecholamine] not a primary indication of digoxin
30
how do cardiac glycosides have a positive inotropic effect
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
explain what this data is showning
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
how do cardiac glycosides cause diuretic effects
Na/K ATPase on basolateral aspect of renal tubular epithelial cells --\> promote tubular reabsorption of sodium inhibition --\> diuretic effect
33
what are the pharmacokinetics of digoxin (6)
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
what are the adverse effects of cardiac glycosides (3)
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
what are predispositions to cardiac glycoside toxicity (9)
1. thin, cachexic 2. obese 3. ascites 4. hypoproteinemia 5. hypothyroidism 6. impaired renal function 7. electrolyte disturbance 8. other drugs 9. dobermans
36
how is cardiac glycoside toxicity prevented (5)
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
how is cardiac glycoside toxicity dealt with
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
what is the mechanism of action of muscarinic antagonists
antagonism of muscarinic acetylcholine receptors
39
when are muscarinic antagonists indicated
bradyarrhythmias associated with high vagal tone
40
what are the side effects of muscarinic antagonists (4)
1. constipation 2. sinus tachycardia 3. urinary retention 4. dry mucous membranes
41
what are examples of muscarinic antagonists
atropine propanthaline
42
43
what are examples of B-agonists
isoprenaline (B1) terbutaline (B2)
44
what are the mechanism of action of B-agonists
stimulation of B-adrenergic receptors
45
what are the indications of B-agonists
sinus arrest, AV block bronchodilator
46
what are the side effects of B-agonists
1. isprenaline: ventricular arrhthymia 2. terbutaline: tremor, tachycardia, hypotension
47
what are examples of methylxanthines
theophylline, aminophylline, etamiphylline
48
what is the mechanism of action of methylxanthines
mild PDE inhibition enhanced sympathetic drive --\> mild positive inotropic and chronotropic effects
49
what are the indications of methylxanthines
widely used in HF in past now bronchodilation

Module 10 (27 decks)

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