Cardiovascular Drugs: Antidysrhythmics Flashcards
What is happening during the P wave
atrial depolarization
What is happening during the PR interval
impulse pauses at AV node
What is happening during the QRS complex?
ventricles depolarize
What is happening during ST interval?
ventricles pause before repolarization
What is happening during T wave?
ventricles repolarize
Where in the EKG do the atria repolarize?
Hidden within the QRS complex
What ions are involved with electrophysiology of myocyte?
Na+, K+, Cl-, Ca++
Which ion rushes into the myocyte to elicit contraction?
Na+
Which ion leaves the myocyte to allow for repolarization?
K+
Which ion prolongs repolarization in the myocyte?
Ca++
Which ion initiates depolarization of the SA node?
Na+ (funny current)
Which ion rushes in and elicits depolarization of SA node?
Ca++
Efflux of which ion results in SA node repolarization?
K+
List supraventricular arrhythmias
atrial fibrillation
atrial flutter
atrial tachycardia (like SVT)
List ventricular arrhythmias
ventricular fibrillation (vfib)
ventricular tachycardia (vtach)
PVCs
torsades
Two bradycardic arrhythmias
heart block
sick sinus syndrome
What ion do Class I antidysrhythmics inhibit?
Na+
What do class II antidysrhythmics inhibit?
B1 receptors
What ion do class III antidysrhythmics inhibit?
K+
What ion do class IV antidysrhythmics inhibit?
Ca++
List some class I antidysrhythmics
quinidine
procainamide
lidocaine
flecainide
propafenone
How do the class subtypes of class I antidysrhythmics differ?
IA = increase AP, ERP, QT interval
IB = decrease AP, ERP
IC = increase ERP in AV node only
Uses & AEs - Class IA
- uses = atrial & ventricular arrhythmias (SVTs & VTs)
- AE = anticholinergic
Uses & AEs: Class IB
- uses = post MI & other ventricular arrhythmias (affects ischemic tissues)
- AEs: toxicity at high doses
Uses & AEs: Class IC
- uses: SVTs & afib
- AE: can induce life threatening VT
Potency of Na channel blockade (Class I)
1C > IA > 1B
Increase in ERP: Class I
1A > 1C > 1B
- 1B decreases
which subtype of beta blockers are used as class II antidysrhythmics?
cardioselective usually 9atenolol, metoprolol, esmolol)
results of beta 1 antagonism
decreased HR
decreased contractility
decreased conduction through AV node
Uses for Class II
SVTs & VTs & post MI (improved O2 supply demand & decreased cardiac remodeling)
adverse effects of beta antagonism
bradycardia
hypotension
name a class III antidysrhythmic
amiodarone
What is amiodarone used for
ventricular tachycardias (vfib, vtach)
- off label for afib/flutter
Amiodarone MOA
- block K+ exit
- delayed repolarization, increased AP duration, increases ERP
- prolongs QT
how long is amiodarone’s half life?
25-60 days
adverse effects of amiodarone
pulmonary fibrosis
hypothyroidism
corneal microdeposits
skin discoloration
hepatotoxicity
*pro-dysrhythmic: torsades, bradycardia, AV block
What is a dihydropyridine
ca++ channel blocker that only impacts the vasculature (results in arteriole vasodilation)
What is a nondihydropyridine
ca++ channel blocker that works on the arteries (arterial vasodilation) AND on the heart (decreased contractility, HR, AV node conduction)
Which type of Ca++ blocker is used in treatment of dysrhythmias
nondihydropyridines
List some dihydropyridines
amlodipine
nifedipine
nicardipine
list some nondihydropyridines
diltiazem
verapamil
Class IV MOA
- blocks Ca influx
- decreases HR, decreased contractility, decreased conduction through AV node
Uses & AEs for class IV
- uses = SVTs
- AEs: bradycardia, AV block, hypotension
Which two classes of antidysrhythmics are contraindicated together?
Class II & Class IV
(beta blockers and Ca++ channel blockers)
What does adenosine do?
hyperpolarize cardiac membranes = no AP can occur
(kinda stops the heart for a sec!)
- K channel opening, hyperpolrization, inhibition of pacemaker cells & decreased HR
half life of adenosine
10 seconds
How to administer adenosine
rapid IV push followed immediately by rapid saline flush
adverse effects of adenosine
flushing
transient hypotension
transient flat line
transient chest pain
mechanism of action of digoxin
Na+/K+ ATPase inhibition = increased Na+ and therefore increased Ca++
= increased contractility
- longer phase 4 & 0 AP –> bradycardia
drug class of digoxin
cardiac glycoside
does digoxin cause tachycardia or bradycardia?
bradycardia potentially
adverse effect of digoxin
arrhythmias
AV block
toxicity
contraindications of digoxin
heart block
hypokalemia (can lead to drug toxicity)
WPW
advanced CKD
What class of medication is atropine
anticholinergic
(or muscarinic antagonist)
Cardiac effects of atropine
increased HR
uses for atropine as an antidysrhythmic
symptomatic bradycardia (1mg Q3-5mins)
adverse effects of atropine
decreased GI/GU
dry mouth
mydriasis
