Test 3: 34+35 antiarrhythmics Flashcards

1
Q

why use antiarrhythmic drugs

A

decrease symptoms: fainting
improve myocardial function

does not stop risk of sudden death

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2
Q

3 ways to treat arrhythmias

A

suppress/control with drugs

abolish arrhythmia: defibrillator, pacemaker

treat underlying disease: CHF, myocarditis, anemia

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3
Q

how do myocardial cells activate

A

influx of Na into the cell

goes from resting -90 to positive

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4
Q

how do SA and AV node activate

A

influx of Ca into the cell cause resting -40 mV to reach threshold

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5
Q

what part of the heart is activated by Calcium channels

A

SA node
AV node

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6
Q

what part of the heart is activited by Na channels

A

atrial myocardium
purkinje fibers
ventricular myocardium

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7
Q

how do pacemaker cells work

A

slow Na influx (funny channel)
Ca in ( T and L type)

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8
Q

how do myocardial cells work

A

fast Na in

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9
Q

how to block arrhythmia from pacemaker cell

A

block calcium channel

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10
Q

how to block arrhythmia from myocardial cell

A

block sodium channel
block potassium channel

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11
Q

class 1 anti Arrhythmics are

A

Na channel blockers

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12
Q

class II AA are

A

beta blockers
atenolol

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13
Q

class III AA are

A

K channel blockers

sotalol, amiodarone

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14
Q

class IV AA are

A

Ca channel blockers

Phenylalkylamines (Verapamil)
Benzothiazepines (Diltiazem)
Dihydropyridines (Amlodipine, Nifedipine)

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15
Q

which class 1 AA are these

A

IA: quinidine
IB: lidocaine

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16
Q

how do Na channel blockers effect the heart

A

work on myocardium to slow conduction of impulse

supress abnormal automaticity in non-nodal tissue and abolish reentry circuits

Do NOT affect SA and AV node (do not change HR)

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17
Q

lidocaine works on what channel (state)

A

inactivated Na channel
(use and state dependent)

class I AA (IB)

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18
Q

how does hyperkalemia effect class I drugs

A

high potassium causes the Na channel to get stuck in inactivated state

at this state lidocaine binds very well, would need to decrease dose of class I AA if high K

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19
Q

quinidine

A

class IA Na channel blocker

used to convert Afib in horses

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20
Q

side effects of quinidine

A

GI disturbances
* Hypotension
* Seizures
* Pro-arrhythmia: also blocks K channels
* Prolongs repolarization: long QT interval on ECG
* predispose to EADs and can cause ventricular tachycardia
* vagolytic
* negative inotrope

class IA Na channel blocker used to treat AFib in horses

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21
Q

procainamide

A

class IA Na channel blocker used in small animal

used to slow conduction velocity and abolish reentry circuits in myocardium

negative inotrope

not 1st choice AA, used when other drug like lidocaine does NOT work

short 1/2 life, oral dosing impractical need to give 3-4 times a day

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22
Q

how to give procainamide IV

A

used if other AA don’t work

give IV slowly over 10 mins, if works then CRI- can cause hypotension and reduced contractility (negative inotrope)

2nd line type 1A Na channel blocker used in dogs

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23
Q

how do class IB AA work

A

Na channel blocker: lidocaine binds to inactive state of Na channel

slows conduction velocity
abolish reentry circuits
supress abnormal automaticity in sick tissues

24
Q

what IV drug is used to treat ventricular tachycardia

A

lidocaine
class IB Na channel blocker

25
Q

mexiletine

A

Class IB Na channel blocker

similar to lidocaine, but not effective alone used in combo with other drugs (sotalol or beta blockers)

used to treat VT

side effects: GI, anorexia, vomiting

26
Q

class II AA work by

A

beta blockers

decrease sympathetic tone (NE) on the heart

cause decreased automaticity of the SA node by ↓ funny Na into the cell = ↓HR (chronotropy)

slows AV node conduction by inhibiting inward Ca (dromotropy)

reduce inotropy/contractility

27
Q

propranolol

A

class II AA: beta blocker

1st gen: non selective for B1 and B2 causes bronchoconstriction

↓ HR (↓Na into cell through funny channel)
↓ contractility
decrease sympathetic tone to heart
decrease Ca into cell= slow AV node conduction

28
Q

— are 2nd gen class II AA

A

beta blockers selective for B1

atenolol and esmolol

cause decreased SYM to SA node= ↓HR, slows AV node, ↓contractility

29
Q

when to use class II AA

A

sinus tachycardia
atrial tachycardia

ventricular arrhythmia (when used in combo with class 1 or class 3 drugs)

cats with hyperthyroidism with sinus trachycardia or VT

cats with HCM

dogs with congenital heart disease (SAS, PS- outflow obstruction)

beta blockers: 2nd gen: atenolol, esmolol
↓SYM to pacemaker cells in the heart: ↓HR, ↓contractility, slow AV node conduction

30
Q

atenolol side effects
what should you not combine with

A

selective B1 blocker: class II AA

bradycardia, AV block, fainting
DO NOT combine with Ca channel blocker, or animals with CHF

decreases SYM to SA node of heart: slows HR, ↓ contractility, slows AV node conduction

31
Q

esmolol

A

ultra short acting selective B1 blocker

very expensive- IV drug with very short half life

used to decrease HR

32
Q

propranolol

A

non selective B blocker that is not used often

PO q8 in cats

can cause bronchoconstriction (B2 receptor block)

33
Q

how do class III AA work

A

K channel blockers

delay repolarization
lengthens refractory period and makes beats longer and more uniform

used for ventricular arrhythmias and SVT (some Afib)

sotalol (also acts as B blocker- negative inotrope)
amiodarone (Afib)

34
Q
A

torsade de pointe

long QT can lead to long Action Potential Duration that cause arrhythmias

this can happen if too high a dose of Class III AA: K channel blockers: sotalol, amiodarone

do not combine class III drugs with quinidine (class IA: Na blocker)

35
Q

why should you not combine class III AA drugs with quinidine

A

class III: K channel blocker: sotalol

can cause prolonged QT → long Action Potential Duration →Torsade de Pointe

class IA: Na channel blocker: Quinidine (horse)

36
Q

sotalol

A

class III antiarrhythmic (K blocker) effects combined with class II (non-selective β blocker)

Ø increases atrial, AV- nodal, accessory pathway and ventricular refractoriness and ventricular repolarization

quick onset, high bioavailability

37
Q

— is the first line PO drug choice for treatment of life-threatening ventricular tachycardia

A

sotalol

class III AA: K channel blocker, also a class II (non selective B blocker)

38
Q

which class III AA can be used to cardiovert Afib

A

amiodarone
K channel blocker

sotaolol is a class III AA: but is not effective against Afib

39
Q

amiodarone

A

class III AA
K channel blocker

also works as weak Na, Ca, β and ⍺ channel blocker

does not work as negative inotrope like sotalol →Good for dogs with myocardial failure: Boxer or Doberman with cardiomyopathy

used to treat VT and cardiovert AFib

works well but expensive and lots of side effects: use as last resort

40
Q

side effects of amiodarone

A
  • anorexia, vomiting, lethargy
  • elevation of liver enzymes (Doberman!)
  • Check liver enzymes every 2 months
  • Liver toxicity is reversible
  • Neutropenia reversible

class III K channel blocker

41
Q

nexterone

A

IV amiodarone
class III : K channel blocker used to treat VT

42
Q

how to treat? Boxer with history of collapse

A

VPCs

treat with sotalol (class III K channel blocker)

43
Q

class IV AA are used to treat

A

supraventricular arrhythmias (Afib)

Ca channel blockers that slow AV node conduction velocity

44
Q

class IV AA are divided into what three catagories

A
  • Phenylalkylamines (Verapamil)
  • Benzothiazepines (Diltiazem) → used to treat Afib
  • Dihydropyridines (Amlodipine, Nifedipine) →used to treat HTN

Ca channel blockers that slow AV node conduction velocity → treat supraventricular arrhythmias (Afib)

45
Q

amlodipine

A

class IV: Ca channel blocker

Dihydropyridines- used to treat HTN unlike other Class IV that are used to treat Afib (diltiazem)

46
Q

dilacorXR

A

extended release diltiazem- can give BID

class IV: Ca channel blocker → slows AV node conduction → treats Afib

Benzothiazepines group of Class IV AA

47
Q

side effects of diltiazem

A
  • 2nd or 3rd degree AV block/bradycardia if dosing at high end of range
  • cats: anorexia

class IV: Ca channel blocker used to treat Afib (slows AV node conduction)

48
Q

what drug can cause this

A

diltazem
class IV Ca channel blocker

slows conduction through AV node

second EKG still has rapid P (from atria contracting) but only a few signals get through to ventricules (QRS less frequent)

pt healthier with AV block and HR slower

49
Q

Moderate reduction in phase 0 slope, lengthen APD, increases ERP

A

IA Na channel blocker
quinidine, Procainamide

50
Q

Small reduction in phase 0, shortens APD, decreases ERP, increases post-repolarization refractoriness

A

IB Na channel blocker

Lidocaine, Mexiletine

51
Q

Slows rate of spontaneous depolarization and conduction velocity in SA and AVN

A

Class II beta blockers: atenolol, esmolol, propranolol (sotalol class III)

class IV Ca channel blockers: diltiazem, verapamil

52
Q

Markedly prolongs repolarization (phase 3), lengthen ERP and APD

A

class III K channel blocker: amiodarone, sotalol

53
Q

when to use digoxin

A

Afib

blocks Na/K pump

indirect antiarrhythmic effect: vagomimetic → slows AV node conduction
weak antiarrhythmic

used in combo with Class IV Ca channel blockers or Class II Beta Blockers to further slow AV conduction

54
Q

side effect of digoxin

A

can cause toxicity

measure serum levels after 5-7 days

side effects: GI, anorexia, arrhythmias, depression

stop med and then restart at lower dose

digoxin: used to treat Afib usually in combo with other med.

55
Q

what class of drugs used to treat VT

A

class I: Na channel blocker: quinidine, lidocaine

class III: K channel blocker: amiodarone, sotaolol

56
Q

what class of AA to treat SVT

A

class II: B blocker(atenolol) or class IV: Ca channel blocker (diltiazem)

class III: K channel blocker: amiodarone, sotalol

or

digoxin and class IV Ca channel blocker: Diltiazem

57
Q

how to treat bradycardia

A

can try anticholinergic drug: atropine

can try sypathomimetic drug Terbutaline (β2 agonist)

best treatment pacemaker