Antiarrhythmic Agents Flashcards
What is the greatest ADE of antiarrhythmic agents?
Arrhythmias
What is the refractory period in the cardiac cells?
The time between phase 0 and sufficient recovery of na channels in phase 3 to permit a new propagated response to external stimulus
What is the name of the late rectifier K current?
Human either Ago Go
All arrhythmias result from _____
Disturbances in impulse formation, disturbances in impulse conduction, or both
What causes depolarization of funny channels?
Opening of Ca slowly because they lack Na channels
What is the phase 4 depolarization slope susceptible to?
Parasympathetic outflow and drugs like BBs that slow the rate
What are EADS or DADS?
Early afterdepolarizations
Delayed afterdepolarizations
What type of disturbances are EADS or DADS?
Disturbances in electrical impulse formation
What are examples of disturbances in electrical impulse cunduction?
Heart blocks-usually in AV node or BBB
Reentry Arrhythmias- One impulse reenters and excites areas of the heart more than once
What is the usual treatment for reentry arrhythmias?
Drugs that slow conduction by blocking Na or Ca because they lengthen the refractory period
What three things need to be corrected before relying on drugs to correct arrhythmias?
Ensure ischemia is not present, correct electrolyte imbalances, change drugs that are possibly causing arrhythmias
What drugs can cause torsades?
Quinidine, sotalol, macrolides
What are the mentioned patient specific contraindications to antiarrhythmics?
HF and Dronedarone
Amiodarone can cause ILD and pulmonary fibrosis
What is the Singh/Vaughan-Williams classification for antiarrhythmic agents?
Class 1A-1C- Na channel blockers
Class 2- Blocking sympathetic autonomic effects-BBs
Class 3- Prolongation of AP duration and the effective refractory period
Class 4- Ca channel blockade
Lidocaine
Esmolol
Amiodarone
Diltiazem
Where on the ion channels do most antiarrhythmic drugs bind exactly?
Below the activation gate
What channel state do channel blocking agents have a low affinity to?
Resting
So why are hyperactive cardiac channels more susceptible to channel blockers?
Channels that are more frequently in the activated state, or inactivated state, are more likely to become blocked due to the channel blockers high affinity to them.
Why is antiarrhythmic agents such a gamble?
Because they can still cause inactivation of normal cardiac cells, but are just more likely to affect the abnormally firing cells. The “Do the math” concept
What are the class 1a na chanel blocking drugs?
Quinidines, procainamide, Disopyramide
What is quinidines MOA?
Blocks Na channels and prolongs potential duration (Through blocking K channels)
What is quinidines ADE?
Toxicity that causes prolonged QT and torsades
What are the class 1B blockers?
Lidocaine, mexiletine
What is an important pharmacokinetic point to understand about lidocaine?
It has extensive first pass metabolism, so poor oral bioavailability
What are the class 1C blockers?
Flecainide, propafenone
What makes class 1B and 1C different?
Class 1B dissociates rapidly from the channel, where 1C dissociates slowly
What is the main difference between class 1A and class 1B blockers?
1A blocks Na AND K, 1B is only a Na blocker
What is the MOA of class 2 drugs (beta blockers)?
They block B1, causing a decrease in Ca, reduced HR slows AV node conduction, and inhibits formation of afterdepolarization
What are the class 2 beta blockers to know?
Propanolol, sotalol, Acebutolol, and esmolol
APES
What makes esmolol unique?
It has significant K blockade in addition to beta, so high risk for torsades
What is class 3 blockers MOA?
Blocks K channels
What are the class 3 blockers?
Amiodarone, sotalol?, dronedarone, dofetilide, ibutilide
What are the class 4 blockers?
CCB
What is adenosines MOA?
Activates K current to shorten AP duration and cause hyperpolarization
What is digoxins MOA?
Increases parasympathetic outflow and influence on the heart, decreases sympathetic outflow
Slows AV nodal conduction
