Exam 7: Anti-arrhythmics Flashcards
Name 2 Class 1A Antiarrhythmics
Quinidine
Procainamide
Name one Class 1B Antiarrhythmic
Lidocaine
Name one Class 1C Antiarrhythmic
Flecainide
Name 3 Class II Antiarrhythmics
Propranolol
Acebutolol
Esmolol
Name 2 Class III Antiarrhythmics
Amiodarone
Dofetilide
Name 2 Class IV Antiarrhythmics
Verapamil
Diltiazem
Name an Antiarrhythmic used in treating SVT
Adenosine
What channels do Class I Antiarrhythmics generally affect?
Sodium
Quinidine and a Procainamide metabolite also block K channels
Main Mechanism of Class I Antiarrhythmics
Blockage of Na channels, especially during 0 phase (Depolarization) and phase 4 (pacemaker phase), lengthens action potentials, slowing conduction velocity and decreases their rate of spontaneous firing.
Main Mechanism of Class IA Antiarrhythmics
Na channel inhibition during 0 phase slows conduction velocity
Intermediate speed of interaction with 0 phase Na channels
K channel inhibition during phase 3 (repolarization) increases the length of refractory periods.
Main mechanism of Class 1B Antiarrhythmics
Less of a conduction slowing effect in phase 0 via Na channel inhibition
Rapidly interact with phase 0 Na channels
They inhibit Late Acting Na Channels, which decreases AP duration and refractory period (opposite of Class 1A)
Main Mechanism of Class 1C Antiarrhythmics
Marked inhibition of Na channels in phase 0 results in dramatic slowing of conduction velocity
Little to no affect on ERP (effective refractory period)
What is an affect that all Class I Antiarrhythmics share to varying degrees?
Increase the threshold of excitability
Quinidine Mechanism and Uses
Class IA Antiarrhythmic
Inhibits Na channels (slowing conduction rate) and K channels (Increasing length of ERP)
Recently increased use for V Fib in Brugada Syndrome and A Fib in Short QT syndrome
Quinidine Adverse Effects (3)
Can cause arrhythmias (Especially Torsades)
GI problems
Cinchonism (OD)- Kind of like Atropine poisoning (Increased HR, decreased BP,
Procainamide
Class IA Antiarrhythmic
Similar to Quinidine, but actions are caused by an acetylated metabolite produced in the liver (NAPA), which happens at different rates in different people.
Can cause Lupus syndrome
Also GI, CNS problems
Less likely to cause Torsades or Atropine-like problems than Quinidine
Lidocaine
Class IB Antiarrhythmic
Shortens ERP, phase 3 via inhibition of Late acting Na channels
Mainly treats ventricular arrhythmias caused by ischemia
Can cause CNS depression
Can cause arrhythmias, mainly in the presence of hyperkalemia
Flecainide Effects, Uses
Class IC Antiarrhythmic
Mostly slows conduction by markedly inhibiting Phase 0 Na channels
Little to no effect on ERP/AP duration
Used for severe arrhythmias resistant to other drugs
Flecainamide Adverse Effects (3)
Negative inotropic (exacerbates CHF)
Very pro-arrhythmic, especially with hyperkalemia
High mortality
Class II Antiarrhythmics Mechanism
Beta Blockers
Decrease inward Ca channel current, slowing conduction and depressing automaticity.
Useful in treating arrhythmias caused by too much sympathetic input
Treat supra ventricular arrhythmias
Propranolol
Good record of reducing incidence of sudden adrenergically‐driven arrhythmic death after myocardial infarction.
Theoretically could combat arrhythmias with membrane stabilization, but this would require way too high a dose to be safe.
Acebutolol
Beta 1 antagonist
Reduces risk of bronchospasm
Partial agonist property may decrease risk of too much suppression of cardiac function
Esmolol
Very short acting blocker used IV in acute arrhythmias occurring during surgery or emergency situations.
Beta Blocker Drug Interaction
Dont use them with Ca Channel Blockers, because that risks too much suppression of cardiac function
Class III Antiarrhythmics Mechanism
Mainly inhibit K channels during the AP, prolonging repolarization.
Prolongs ERP and AP duration without affecting other phases.
Amiodarone
Class III Antiarrhythmic
Prolongs ERP, AP by inhibiting K channels in Phase 3
Has complex secondary effects.
Used in severe tachyarrhythmias
Amiodarone Adverse Effects (3)
Lots of bad things that may persist long after the drug is stopped.
Interstitial pulm fibrosis
thyroid problems
Skin discoloration due to iodine build up.
Dofetilide
Pure Class III anti arrhythmic
Inhibits only K channels, prolonging AP, and ERP
Treats supra ventricular arrhythmias, especially A Fib
Can cause Torsades
Verapamil and Diltiazem
Class IV Antiarrhythmics
Calcium channel blockers
Work well at AV node, can stop AV node arrhythmias from reaching the ventricles
Dont combine with Beta blockers
Dont give when a fib is accompanied by WPW, or it may get worse.
Adenosine
Decreases conduction velocity and decreases abnormal impulse formation in the AV node
Decreases Ca influx and ACh sensitive phase 4 K current
Prolongs AV node refractory period
Drug of choice for paroxysmal supraventricular tachycardia (PSVT)
Short duration of action!
Can cause Flushing, SOB, and chest pain.
Procainamide Adverse Effects (4)
Lupus
CNS Problems
GI Problems
Arrhythmias (Less likely than with Quinidine)
Lidocaine Adverse Effects (2)
CNS Depression
Arrhythmias, especially in the presence of hyperkalemia
Class II Antiarrhythmic Uses
Arrhythmias caused my too much sympathetic input
Supra ventricular arrhythmias
Verapamil/Diltiazem Contraindications
Wolf Parkinson White (will make it worse) Beta blockers (will decrease cardiac function too much)
