Test 3: 34+35 antiarrhythmics Flashcards
why use antiarrhythmic drugs
decrease symptoms: fainting
improve myocardial function
does not stop risk of sudden death
3 ways to treat arrhythmias
suppress/control with drugs
abolish arrhythmia: defibrillator, pacemaker
treat underlying disease: CHF, myocarditis, anemia
how do myocardial cells activate
influx of Na into the cell
goes from resting -90 to positive
how do SA and AV node activate
influx of Ca into the cell cause resting -40 mV to reach threshold
what part of the heart is activated by Calcium channels
SA node
AV node
what part of the heart is activited by Na channels
atrial myocardium
purkinje fibers
ventricular myocardium
how do pacemaker cells work
slow Na influx (funny channel)
Ca in ( T and L type)
how do myocardial cells work
fast Na in
how to block arrhythmia from pacemaker cell
block calcium channel
how to block arrhythmia from myocardial cell
block sodium channel
block potassium channel
class 1 anti Arrhythmics are
Na channel blockers
class II AA are
beta blockers
atenolol
class III AA are
K channel blockers
sotalol, amiodarone
class IV AA are
Ca channel blockers
Phenylalkylamines (Verapamil)
Benzothiazepines (Diltiazem)
Dihydropyridines (Amlodipine, Nifedipine)
which class 1 AA are these
IA: quinidine
IB: lidocaine
how do Na channel blockers effect the heart
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)
lidocaine works on what channel (state)
inactivated Na channel
(use and state dependent)
class I AA (IB)
how does hyperkalemia effect class I drugs
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
quinidine
class IA Na channel blocker
used to convert Afib in horses
side effects of quinidine
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
procainamide
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
how to give procainamide IV
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
how do class IB AA work
Na channel blocker: lidocaine binds to inactive state of Na channel
slows conduction velocity
abolish reentry circuits
supress abnormal automaticity in sick tissues
what IV drug is used to treat ventricular tachycardia
lidocaine
class IB Na channel blocker
mexiletine
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
class II AA work by
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
propranolol
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
— are 2nd gen class II AA
beta blockers selective for B1
atenolol and esmolol
cause decreased SYM to SA node= ↓HR, slows AV node, ↓contractility
when to use class II AA
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
atenolol side effects
what should you not combine with
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
esmolol
ultra short acting selective B1 blocker
very expensive- IV drug with very short half life
used to decrease HR
propranolol
non selective B blocker that is not used often
PO q8 in cats
can cause bronchoconstriction (B2 receptor block)
how do class III AA work
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)
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)
why should you not combine class III AA drugs with quinidine
class III: K channel blocker: sotalol
can cause prolonged QT → long Action Potential Duration →Torsade de Pointe
class IA: Na channel blocker: Quinidine (horse)
sotalol
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
— is the first line PO drug choice for treatment of life-threatening ventricular tachycardia
sotalol
class III AA: K channel blocker, also a class II (non selective B blocker)
which class III AA can be used to cardiovert Afib
amiodarone
K channel blocker
sotaolol is a class III AA: but is not effective against Afib
amiodarone
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
side effects of amiodarone
- 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
nexterone
IV amiodarone
class III : K channel blocker used to treat VT
how to treat? Boxer with history of collapse
VPCs
treat with sotalol (class III K channel blocker)
class IV AA are used to treat
supraventricular arrhythmias (Afib)
Ca channel blockers that slow AV node conduction velocity
class IV AA are divided into what three catagories
- 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)
amlodipine
class IV: Ca channel blocker
Dihydropyridines- used to treat HTN unlike other Class IV that are used to treat Afib (diltiazem)
dilacorXR
extended release diltiazem- can give BID
class IV: Ca channel blocker → slows AV node conduction → treats Afib
Benzothiazepines group of Class IV AA
side effects of diltiazem
- 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)
what drug can cause this
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
Moderate reduction in phase 0 slope, lengthen APD, increases ERP
IA Na channel blocker
quinidine, Procainamide
Small reduction in phase 0, shortens APD, decreases ERP, increases post-repolarization refractoriness
IB Na channel blocker
Lidocaine, Mexiletine
Slows rate of spontaneous depolarization and conduction velocity in SA and AVN
Class II beta blockers: atenolol, esmolol, propranolol (sotalol class III)
class IV Ca channel blockers: diltiazem, verapamil
Markedly prolongs repolarization (phase 3), lengthen ERP and APD
class III K channel blocker: amiodarone, sotalol
when to use digoxin
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
side effect of digoxin
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.
what class of drugs used to treat VT
class I: Na channel blocker: quinidine, lidocaine
class III: K channel blocker: amiodarone, sotaolol
what class of AA to treat SVT
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
how to treat bradycardia
can try anticholinergic drug: atropine
can try sypathomimetic drug Terbutaline (β2 agonist)
best treatment pacemaker