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PHARMACOLOGY I > antiarrhythmic agents > Flashcards

antiarrhythmic agents Flashcards

1
Q

what drugs are class I agents

A
  • quinidine (1A)
  • procainamide (1A)
  • lidocaine (1B)
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2
Q

what drugs are class II agents

A
  • propranolol
  • atenolol
  • esmolol

beta blockers

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3
Q

what drug is a class III agent

A

sotalol

K channel inhibitors, extend ERP

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4
Q

what drug is a class IV agent

A

diltiazem
inhibits SA node

calcium channel blocker, decreases HR and contractility

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5
Q

what are determining factors of the rate of pacemaker cells

A
  • duration of AP (longer AP = slower BP)
  • duration of diastolic interval
  • max diastolic potential (takes longer to reach threshold –> bradycardia)
  • slope of phase 4 depolarization
  • threshold potential
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6
Q

what is the goal of therapy for arrhythmias

A
  • reduce ectopic pacemaker activity
  • modify conduction or refractoriness to disable reentry
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7
Q

the SA node _____ APs
the AV node _____ APs

A

generates
conducts

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8
Q

what type of sodium channels are blocked by class 1A

A

open or activated sodium channels

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9
Q

what class 1 antiarrhythmic agent lengthens the duration of the action potential, increasing ERP, what agent shortens it

A

1A - lengthens
1B - shortens, decreasing time of ERP

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10
Q

what antiarrythmic agent can block both activated and inactivated sodium channel but has no effect on the duration of APs

A

1C

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11
Q

what class of antiarrhytmics reduces adrenergic activity on the heart by suppressing sympathetic effects

A

Class II, beta blockers

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12
Q

what class of antiarrhytmics are potassium channel blockers

A

Class III

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13
Q

what class of antiarrhytmics are calcium channel blockers

A

class IV

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14
Q

what is happening during phase 0 in cardiac cell AP

A

Ca channels slowly start to open, Na enters cell

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15
Q

what is happening during phase 1 in cardiac cell AP

A

K+ efflux

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16
Q

what is happening during phase 3 in cardiac cell AP

A

rapid repolarization as Ca channels gradually inactivate and K+ starts exciting cell

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17
Q

what is happening during phase 2 in cardiac cell AP

A

plateu of prolonged depolarization as K exits and Ca enters

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18
Q

what is the MOA of Quinidine

A
  • binds to open & activated Na channels
  • blocks K+ channels (prolongs depolarization)
  • muscarinic receptor blockade (increases HR and AV conduction)
  • blocks alpha receptors (hypotension)
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19
Q

BA of Quinidine

A

variable due to first pass effect

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20
Q

metabolism of Quinidine

A

80% liver
20 kidney

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21
Q

what is the half life of Quinidine

A

6 hrs in dogs, 8 hrs in horses

usually not used in cats

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22
Q

what is Quinidine useful in treating

A
  • supraventricular & ventricular arrythmias
  • re-entrant arrythmias (like atrial fibrillation)
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23
Q

contraindications of Quinidine

A

patients w/
* myasthenia gravis
* AV block
* digitalis toxicity or on digoxin

24
Q

adverse effects of Quinidine in dogs

A

anorexia, V+, negative inotropism (decreased contractility)

25
Q

adverse effects of Quinidine in horses

A

coloc, ataxia, swelling of nasal mucosa, urticaria, laminitis (rare)

26
Q

adverse effects of Quinidine (non-breed specific)

A

D+, hypotension, widened QRS complex, prolonged QT interval, AV block, ventricular tachycardia

27
Q

what are the differences b/w Quinidine and Procainamide

A

Procainamide….
* less prominant of a muscarinic and alpha receptor blocker
* more effective in treating ventricular arrhythmias
* has fewer drug interactions than quinidine
* is not as effective in horses

28
Q

what drug is used in the txt of arrhythmias of ventricular origin

A

Lidocaine

no vetmed product, all ELDU

29
Q

how does Lidocaine work

A
  • Binds to inactivated Na+ channels fast binding dissociates fast
  • Decreases action potential duration & shortens ERP due to blocking slow Na ‘window’ currents
30
Q

how is lidocaine administered

A

IV ONLY

31
Q

where is lidocaine metabolized

A

90-95% in liver

32
Q

lidocaine toxicity

A
  • Primarily CNS signs in dogs → muscle twitching, convulsions
  • Hypotension → if IV bolus given too rapidly
  • Cats → more susceptible to toxicity
33
Q

lidocaine effects

A
  • No significant effects on QRS, QT intervals
  • Decreases duration of APD and ERP
  • Causes less hypotension than procainamide
  • No depressant action on myocardial contractility
  • No vagal blocking
  • Not effective for supraventricular arrhythmias
34
Q

B1 selective blocking agent indicated for the treatment of supraventricular tachyarrhythmias, systemic hypertension and hypertrophic cardiomyopathy

A

Atenolol

35
Q

is propranolol or aetenolol longer acting

A

atenolol

36
Q

B1 specific blocking agent used in acute management of supraventricular tachycardia
and decreases HR in severe ventricular tachycardia in dogs/cats

A

Esmolol

37
Q

what is propranolol used in the treatment of

A
  • hypertrophic cardiomyopathy in ferrets
  • hypertension
  • thyrotoxicosis
  • ventricular tachycardia in horses

all extra label

38
Q

class III drug that is also a non-selective beta andrenergic blocker

A

sotalol

39
Q

what is sotalol traditionally used for

A

arrhythmogenic cardiomyopathy in boxers

40
Q

what type of arrhythmias are class IV drugs (Ca channel blockers) effective in treating

A

supraventricular tachyarrhythmias

41
Q

what drug produced vasodilation but not reflex tachycardia

A

Diltiazem

42
Q

what conditions is Diltiazem used to treat

A
  • atrial fibrilation (can be used in combination w/ quinidine in horses)
  • supraventricular tachycardia
  • hypertrophic cardiomyopathy in cats and ferrets
  • hypertension
43
Q

adverse effects of Diltiazem

A
  • bradycardia in dogs
  • V+ in cats
  • GI or CNS disturbances
  • increases liver enzymes
  • negative inotropic effect
44
Q

the blocking of _____ receptors by Quinidine results in an increased HR and AV node conduction

A

muscarinic

45
Q

because Quinidine blocks ___ receptors, it has the potential to cause reflex tachycardia

A

Alpha, which causes hypotension

46
Q

most common route of administration for Quinidine

A

oral, safe & rapid onset
- bioavailability is variable due to the first pass effect

47
Q

what animals is quinidine used in

A

dogs and horses

48
Q

what drug causes vasodilation w/out reflex tachycardia

A

Diltiazem

49
Q

what drug causes bradycardia in dogs & V+ in cats

A

Diltiazem

50
Q

what drug is only useful in treating arrhythmias of ventricular origin

A

lidocaine

51
Q

what drug has CNS toxicity in dogs

A

lidocaine

52
Q

what drug is used to see if long lasting beta blockers could be an effective treatment

A

Esmolol
ultrashort acting

53
Q

what drug can treat hypertrophic cardiomyopathy in both dogs and cats

A

Diltiazem

54
Q

what sodium channel blocker does NOT cause a decrease in contractility; therefore causing less hypotension than procainamide

A

Lidocaine

55
Q

what kind of arrhythmias are class IV Ca+ channel blockers effective at treating

A
  • they interupt atrial arrhythmias that rely on AV node re-entry
  • also useful in supraventricular tachycardia

PHARMACOLOGY I (21 decks)

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