28- Anti-Arrhythmics Flashcards
1
Q
amiodarone (Cordarone)
A
K+ Channel Blocker
- class III antiarrhythmic
- prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
- oral or IV
- used for: atrial and ventricular arrhythmias
- S/fx: bradycardia d/t B-blocking effects
- less arrhythmogenic in patients with HF or post-MI (probably d/t pleotropic effects on other channels)
- very lipid soluble so rapidly taken up into high fat tissues and take a long time before out of system
2
Q
dofetilide (Tikosyn)
A
K+ Channel Blocker
- oral class III antiarrhythmic started in hospital
- prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
- used for: atrial arrhythmias (relatively safe in HF)
- S/fx: marked QT prolongation– torsades de pointes
3
Q
ibutilide (Corvert)
A
K+ Channel Blocker
- IV class III antiarrhythmic, in hospital
- prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
- used for: acute conversion of A-fib/flutter
- S/fx: marked QT prolongation– torsades de pointes
4
Q
sotalol (Betapace)
A
K+ Channel Blocker
- class III antiarrhythmic
- prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
- oral, started in hospital d/t potential adverse effects
- used for: atrial and ventricular arrhythmias
- S/fx: bradycardia d/t B-blocking effects of L-isomer, marked QT prolongation– torsades de pointes
5
Q
dronedarone (Multaq)
A
K+ Channel Blocker
- oral class III antiarrhythmic
- prolong AP by blocking K channels and prolonging repolarization (lengthens effective refractory time)
- used for: atrial and ventricular arrhythmias
- lacks many of major s/fx of amiodarone but not as efficacious
6
Q
diltiazem (Cardizem LA)
A
Ca++ Channel Blocker
- oral or IV class IV antiarrhythmic
- used for: re-entry SVT’s involving AV node, slows AV node conduction
- S/fx: bradycardia, hypotension, negative inotrope
7
Q
verapamil (Covera-HS)
A
Ca++ Channel Blocker
- oral or IV class IV antiarrhythmic
- more cardio-selective then dilt
- used for: re-entry SVT’s involving AV node, slows AV node conduction
- S/fx: bradycardia, hypotension, negative inotrope
8
Q
delayed afterdepolarization (DAD)
A
- occur after cell has completely repolarized
- usually result from abnormal intracellular Ca handling that can occur from ischemia after MI or with digoxin use
- both occur from Ca overload leading to spontaneous cyclic activation of Ca pumps and exchangers
- DADs are more common in fast HR
9
Q
early afterdepolarization (EAD)
A
- occur before cell has completely repolarized
- depolarization-dependent triggered activity
- prolonged AP duration can cause EADs due to reactivation of VGCa channels before cell has fully repolarized which then triggers another AP through reactivation of VGCa channels
- EADs can lead to run of spontaneous extrasystolic beats
- can lead to torsades de pointes and are more common with slow heart rates, because AP duration correlates with HR
10
Q
effective (absolute) refractory period
A
- time from beginning of an action potential until cell is able to conduct another AP
- stimulating cell during this period will not fire AP because few to no VGNa channels have reactivated
11
Q
long QT syndrome
A
- mutations in hERG or certain drugs make K+ channels less effective in opening which can prolong repolarization and prolong QT interval
- this syndrome is predisposed to EADs, arrhythmias, and sudden cardiac death
- FDA now requires that all drugs be tested for effects on hERG
12
Q
reentry
A
- abnormal impulse conduction that occurs due to:
1. geometry for conduction loop
2. unidirectional conduction block
3. slow conduction (the effective refractory period must be less than propagation time around the loop) - if conduction too fast, will catch up to refractory period and transmission will cease
13
Q
relative refractory period
A
- time from end of effective refractory period until cell regains normal excitability
- stimulating cell during this phase will produce weaker then normal APs until all VGNa channels have recovered
- geometry can be anatomical or functional
14
Q
state-dependent block
A
- refers to how smart drugs, such as lido, only block channels when in activated or inactivated state
- these drugs come off channel when channel is in resting state
15
Q
supraventricular tachycardia
A
- usually narrow complex QRS because it uses the normal His/Purkinje system to conduct implulse
- can be atrial or nodal
16
Q
torsades de pointes
A
- common ventricular arrhythmia that occurs after EAD
- rotating ectopic folci causing ventricular depolarizations
17
Q
unidirectional block
A
- tissue that allows impulse transmission in one direction but not the other
- usually happens in ischemic tissue that results from MI
18
Q
use-dependent block
A
-refers to how smart drugs, such as lido, increases binding to channels that are activated more often as in tachycardia
19
Q
ventricular tachycardia
A
-usually wide complex because they originate in the ventricles and do not use His/Purkinje system to conduct impulse
20
Q
metoprolol
A
cardioselective beat-blocker
- Class II antiarrhythmic
- reduce AV conduction and slope of phase 4
- PO or IV
- Use: atrial arrhythmias,slow AV node conduction, prevent sudden cardiac death post-MI
- S/E: bradycardia, negative inotropy
21
Q
atenolol
A
cardioselective beat-blocker
- Class II antiarrhythmic
- reduce AV conduction and slope of phase 4
- PO or IV
- Use: atrial arrhythmias,slow AV node conduction, prevent sudden cardiac death post-MI
- S/E: bradycardia, negative inotropy
22
Q
esmolol
A
cardioselective beat-blocker
- Class II antiarrhythmic
- reduce AV conduction and slope of phase 4
- IV
- Use: atrial arrhythmias,slow AV node conduction
- S/E: bradycardia, negative inotropy
- metabolized by ester hydrolysis (very short t1/2)
23
Q
propranolol
A
Non-cardioselective beta-blocker (beta1 and beta2)
- Class II antiarrhythmic
- reduce AV conduction and slope of phase 4
- PO or IV
- Use: atrial arrhythmias,slow AV node conduction
- S/E: bradycardia, negative inotropy, bronchoconstriction/bronchospasm
24
Q
digoxin
A
Cardiac glycoside
- inhibits the Na/K ATPase leading to a decrease Na gradient and an inhibition in the NCX. This causes an increase in intracellular Ca leading to a stronger contraction and increases vagal tone on the heart (slows HR).
- Inhibits ICa
- Use: atrial arrhythmias (slows ventricullar response in AF/A flutter).
- S/E: Arrhythmogenic in doses that produce inotropy.
25
Q
adenosine
A
Misc anti-arrhythmic
- Acts on A-1 receptors and increases I-K while inhibiting I-Ca.
- Uses: SVT; aid in Dx of AF/A Flutter
- S/E: asystole (transient), AV node block
26
Q
procainamide
A
class 1A Na+ channel blocker
- block K+ channels
- prolong AP
- unbind with medium kinetics
- oral or IV
- use- ventricular or recurrent atrial arrhythmia
- side effects- lupus like effects, nausea
- metabolite NAPA- prolongs QT predisposing patient to EADs and arrhythmia
27
Q
quinidine
A
class 1A Na+ channel blocker
- block K+ channels
- prolong AP
- unbind with medium kinetics
- oral or IV
- use- ventricular or recurrent atrial arrhythmia
- side effects- diarrhea
28
Q
disopryamide
A
class 1A Na+ channel blocker
- block K+ channels
- unbind with medium kinetics
- oral
- use- ventricular or recurrent atrial arrhythmia
- side effects- negative inotrope (avoid in heart failure)
29
Q
lidocaine
A
class 1B Na+ channel blocker
- IV
- unbind with fast kinetics- shortens AP
- use- acute ventricular arrhythmia
- side effects- CNS toxicity
30
Q
mexiletine
A
class 1B Na+ channel blocker
- oral
- unbind with fast kinetics- shortens AP
- use- chronic ventricular arrhythmia
- side effects- CNS toxicity
31
Q
flecainide
A
class 1C Na+ channel blocker
- oral
- unbind with slow kinetics- no effect on AP
- use- recurrent atrial arrhythmia
- side effects- arrhythmogenic
- avoid in patients with underlying structural heart disease or post-MI
32
Q
propafenone
A
class 1C Na+ channel blocker
- oral
- unbind with slow kinetics- no effect on AP
- use- recurrent atrial arrhythmia
- side effects- arrhythmogenic
- avoid in patients with underlying structural heart disease of post MI
