Exam 3: Anti-Arrhythmic Agents Flashcards
Phase 0:
Rapid depolarization; fast inward Na+ flow; upstroke of action potential graph
Phase 1:
Partial repolarization; Na+ channels close; ‘peak’ of AP graph
Phase 2:
Plateau; slow Ca2+ channels open; flat ‘pause’ on AP graph
Phase 3:
Repolarization; Ca2+ channels close; K+ channels open; downstroke on AP graph
Phase 4:
Pacemaker potential; slow upward stroke between APs
Which phases are refractory?
1-3
Normal SA rate:
60-100
Normal AV rate:
40-60
SA node resting potential:
-55 mV
Purkinje fiber firing rate:
15-30
Receptors in the atria that affect the SA node:
β1 and M2
Two types of defects in electrical activity:
Defect in formation of impulse
Defect in conduction of impulse
Define altered automaticity:
Latent pacemaker cells take over the SA node’s role; escape beats
Define delayed after-depolarization:
Normal AP of cardiac cell triggers train of abnormal depolarizations
Define re-entry:
Refractory tissue reactivates repeatedly/rapidly due to unidirectional block, which causes a circuit effect
Define conduction block:
Impulses that fail to propagate in non-conducting tissue (like MI-injured heart)
Causes of delayed after-depolarization:
Electrolyte abnormalities
Drug toxicities
Most common way arrhythmias are formed:
Re-entry
Arrythmias require tx when:
Cause cannot be corrected
Hemodynamic function compromised
Arrhythmia can cause more serious arrhythmias or comorbidities
Acute non-pharmacological tx of arrhythmias:
Vagal maneuvers
Cardioversion
Prophylactic non-pharmacological tx of arrhythmias:
Radiofrequency catheter ablation
Implantable defibrillator
Class I antiarrhythmic drugs:
Na+ channel blockers
Class II antiarrhythmic drugs:
β-blockers
Class III antiarrhythmic drugs:
K+ channel blockers
Class IV antiarrhythmic drugs:
Ca+ channel blockers
Class V antiarrhythmic drugs:
Unclassified
Class Ia agents are:
Intermediate Na+ channel blockers
Effects of class Ia agents:
↓ depolarization rate
↓ conduction velocity
Prolonged repolarization
↑ AP duration
Class Ia prototype and examples:
Quinidine*
Procainamide
Disopyramide
Moricizine
Indications for disopyramide:
Suppress atrial/ventricular tachyarrhythmia
S/E of disopyramide:
Myocardial depression
Can precipitate CHF/HoTN
Class Ib agents are:
Fast Na+ channel blocker
MoA of class Ib agents:
Blocks Na+ channels; doesn’t affect the rate of depolarization, but shortens AP duration and refractory
Prototype and examples of class Ib agents:
Lidocaine*
Mexiletine
Tocainide
Phenytoin
Indications for lidocaine:
Acute tx/prevention of ventricular dysrhythmias esp. immediately after MI
Lidocaine used after MI because:
Raises the vfib threshold
Dosing for lidocaine:
1 - 1.5 mg/kg IV
Infusion: 1-4 mg/min
Max dose: 3 mg/kg
PK of lidocaine:
50% protein bound
Hepatic metabolism with an active metabolite
10% renal elimination
Drugs/conditions that impair metabolism of lidocaine:
Cimetidine
Propranolol
CHF, MI, liver dysfunction, GA
Drugs that induce metabolism of lidocaine:
Barbiturates
Phenytoin
Rifampin
Half-time of lidocaine:
1.4 - 8 hrs
Therapeutic concentration of lidocaine:
1-5 mcg/ml
Indication for mexiletine:
Oral/chronic suppression of ventricular tachyarrhythmias
Class Ic agents are:
Slow Na+ channel blockers
MoA of class Ic agents:
Potent decrease of depolarization rate, decrease of conduction rate, increased AP
Prototype and examples of class Ic agents:
Flecainide*
Propafenone
Indications for flecainide or propafenone:
Ventricular PVCs, v-tach
Atrial tachyarrhythmias
WPW (flecainide)