Card Set Information
heart arrhythmia pharmacology
Class and use, MoA, Adverse Effects, Contraindications
Binds to inactivated Na+ channels (primary MoA)
: acute ventricular arrhythmias, digitalis toxicity, (prevention of ventricular arrhythmia - controversial)
decreases APD and ERP in normal cells
: CNS at therapeutic doses (sleepiness, dizziness, paresthesia); CVS effects and allergic reaction at high doses
: 2nd or 3rd degree heart block, A-fib, sick sinus syndrome*note: lidocaine is the least cardiotoxic anti-arrhythmic
Which is the only supraventricular arrhythmia that can be treated with Lidocaine?
What makes phenytoin different from all other class I anti-arrhythmic agents?
It is a weak acid, while all of the others are weak bases.
Binds to activated Na+ channels (primary MoA)
(also has anti-muscarinic and alpha-1 antagonist activity)
: Ventricular ectopic beats, A-fib and A-flutter after cardioversion, chronic control of SVT and VT
: rarely used as a first line treatment
Increases APD and ERP; decreases conduction velocity (slope of phase 0)
: Cinchonism, arrhythmia or asystole, torsade de pointes, sycope or sudden death
: torsade de pointes, wide QRS, long QT, heart block, digoxin induced arrythmia
What should be given to treat Quinidine toxicity?
What happens when digoxin and quinidine are given together?
Digoxin clearance and volume of distribution become greatly reduced,
which leads to an increased steady-state concentration. Essentially,
this can lead to digitalis toxicity.
How is procainamide different from quinidine?
1. Less anti-muscarinic activity
2. Less effect on Ca++ channels
3. Less alpha-1 antagonist activity
What is one major potential adverse effect of procainamide?
SLE-like (lupoid) syndrome.
gets metabolized by acetylation. In slow metabolizers, more
procainamide remains in the system. Procainamide also haptens to be a
good hapten. So, if it combines with a protein, it can trigger a
Blocks activated Na+ channels (primary MoA)
(blocks K+ channels)
: A-flutter, A-fib
: has a very limited use because it is proarrhythmogenic; second-choice drug
No effect on APD or ERP; large effect on phase 0
: arrhythmias, dizziness, sudden death
: Structural cardiac disease
: treatment of digitalis-induced arrhythmia
: also used as an anti-convulsant
Beta blockers (MoA)
: chronic control of A-fib
and A-flutter, supraventicular reentry arrhythmias, arrhythmias caused
by increased adrenergic activity (thyroid, adrenal tumor)
: Esmolol is used in ICU because of its short half-life
decrease cardiac contractility, decrease HR (and therefore cardiac output)
What effects will a beta blocker have on an EKG?
-on PR interval
-on QT interval
-on QRS duration
PR interval will be increased, QT interval and QRS duration will not be affected.
Blocks K+ channels and inactivated Na+ channels
: A-fib, A-flutter, SVT, V-fib prophylaxis
: most effective and most commonly prescribed anti-arrhythmic
increases refractoriness (phase 3); decreases automaticity (phase 4)
: Affects every organ system - hypothyroidism, corneal deposits, torsade de pointes
: Long QT syndrome, pregnancy, sick sinus, torsade, cardiogenic shock
What effects will amiodarone have on an EKG?
PR interval will slightly increase, QRS will increase, and QT interval will markedly increase
Class III, also has Class II activity
Blocks K+ channels
: Supraventricular and ventricular arrhythmias
increases refractoriness (phase 3)
: caused by beta blocker activity, can lead to torsade de pointes
Blocks K+ channels and activates inward Na+ channels
: A-flutter, A-fib
: AV block, BBB, V-tach, torsade
: Long QT syndrome, V-tach
Block Ca++ channels in pacemaker cells (phase 0)
: SVT, chronic A-flutter and A-fib
decreased conduction, increased refractoriness, decreased automaticity
: WPW, long QRS complex
What effects do Class IV agents have on the EKG?
Only PR interval is increased. QRS and QT are unaffected.
activates Ach-sensitive K+ channels => hyperpolarization
inhibits cAMP-induced influx of Ca++ (secondary MoA)
: acute PSVT
decreased automaticity, decreased conduction, increased refractoriness
Where in the heart does adenosine act?
SA node (decreases automaticity) and AV node (decreases conduction and increases refractoriness).
What are the clinical uses of IV Magnesium sulfate?
1. To prevent recurrent torsade de pointes.
2. To treat digitalis induces arrhythmia.
parasympathomimetic activity in the heart
: A-fib and A-flutter in patients with cardiac failure
Eliminates AV nodal reentrant tachycardia