Exam #02 - Anti-arrhythmic Drugs Flashcards
Quinidine
Class IA Na+ and K+ channel blocker
SOA: contractile cells & pacemaker cells
Primary Therapeutic Use:
effective for almost any type of arrhythmia
Effects on pacemaker cell AP: decrease spontaneous depolarization decrease pacemaker rate decrease excitability of conducting system increase AP duration increase refractory period
Effects on contractile cell AP: decrease AP rate of rise decrease AP amplitude increase AP duration increase refractory period
AE
Significant digoxin interaction - displaces digoxin from plasma proteins and increases plasma levels
Anti-cholinergic effect - blocks ACh release from vagus nerve, decreases parasympathetic tone - leads to increase in HR in some patients
Cinchonism syndrome - blurred vision, tinnitus, psychosis, hallucinations
Procainamide
Class IA Na+ and K+ channel blocker
SOA: contractile cells & pacemaker cells
Primary Therapeutic Use:
effective for almost any type of arrhythmia
Effects on pacemaker cell AP: decrease spontaneous depolarization decrease pacemaker rate decrease excitability of conducting system increase AP duration increase refractory period
Effects on contractile cell AP: decrease AP rate of rise decrease AP amplitude increase AP duration increase refractory period
AE
No digoxin interaction
No anti-cholinergic effect
Lupus-like syndrome (reversible) - stop taking drug if experiencing these symptoms and they’ll go away
Disopyramide
Class IA Na+ and K+ channel blocker
SOA: contractile cells & pacemaker cells
Primary Therapeutic Use:
effective for almost any type of arrhythmia
Effects on pacemaker cell AP: decrease spontaneous depolarization decrease pacemaker rate decrease excitability of conducting system increase AP duration increase refractory period
Effects on contractile cell AP: decrease AP rate of rise decrease AP amplitude increase AP duration increase refractory period
AE
No digoxin interaction
Significant anti-cholinergic effect- blocks ACh release from vagus nerve, decreases parasympathetic tone - leads to increase in HR in some patients (much more significant than quinidine)
Lidocaine
&
Mexiletine
Class IB Voltage-gated Na+ channel blocker
SOA: contractile cells
MOA: Class IB anti-arrythmia drugs have greater affinity for open Na+ channels and since ischemic tissue is more often depolarized with its Na+ channels open, the drugs selectively bind to damaged tissue
Primary Therapeutic Use:
ventricular arrhythmias associated with MI
Effects on pacemaker cell AP:
none - does NOT block Na+ leak channels
Effects on contractile cell AP:
decrease AP rate of rise
decrease AP amplitude
may shorten AP duration slightly
Flecainide
&
Propafenone
Class IC Na+ channel blocker
SOA: all excitable tissue
Primary Therapeutic Use:
used only in life-threatening arrhythmias in the hospital
Effects on pacemaker cell AP:
decrease spontaneous depolarization
decrease pacemaker rate
decrease excitability of conducting system
Effects on contractile cell AP:
decrease AP rate of rise
decrease AP amplitude
AE
binds to ALL Na+ channel conformations so it targets damaged and healthy tissue
Propanolol
Class II Beta-adrenoreceptor blocker
SOA: everywhere beta-1 receptors are located (SA and AV node, and contractile cells in both atria and ventricles)
Primary Therapeutic Use:
useful in preventing sudden arrythmic deaths following an MI
useful in treating supraventricular tachycardia
Major effects occur at pacemaker cells:
decrease pacemaker activity (automaticity)
decrease spontaneous depolarization
decrease HR
Minor effects occur at contractile cells:
decrease contractility leads to reduced O2 demand and reduces risk of myocardia ischemia (this effect is more important in treating angina)
Metoprolol
Class II Beta-adrenoreceptor blocker
SOA: everywhere beta-1 receptors are located (SA and AV node, and contractile cells in both atria and ventricles)
Primary Therapeutic Use:
useful in preventing sudden arrythmic deaths following an MI
useful in treating supraventricular tachycardia
Major effects occur at pacemaker cells:
decrease pacemaker activity (automaticity)
decrease spontaneous depolarization
decrease HR
Minor effects occur at contractile cells:
decrease contractility leads to reduced O2 demand and reduces risk of myocardia ischemia (this effect is more important in treating angina)
Esmolol
Class II Beta-adrenoreceptor blocker
SOA: everywhere beta-1 receptors are located (SA and AV node, and contractile cells in both atria and ventricles)
Primary Therapeutic Use:
useful in preventing sudden arrythmic deaths following an MI
useful in treating supraventricular tachycardia
Major effects occur at pacemaker cells:
decrease pacemaker activity (automaticity)
decrease spontaneous depolarization
decrease HR
Minor effects occur at contractile cells:
decrease contractility leads to reduced O2 demand and reduces risk of myocardia ischemia (this effect is more important in treating angina)
Amiodarone
Class III K+ channel blocker
SOA: everywhere voltage-gated K+ channels are located (SA/AV node, contractile cells (atria and ventricles)
Primary Therapeutic Use:
prevent re-entry arrythmias
Major effects: has therapeutic activity from all arrythmic classes but for K+ channel blocker: increases depolarization phase duration increases AP duration increases refractory period
AE:
most common: GI - N, V, constipation
less common: CNS effects - dizzy, HA
rare: pulmonary toxicity (lethal), alteration of thyroid metabolism - results in blue/green discoloration in skin/eyes
Increased likelihood of QT prolongation b/c of prolonged refractory period and therefore predisposed to torsades de pointe. Out of all class III’s, least likely to cause torsades (ventricular tachycardia)
Sotalol
Class III K+ channel blocker
SOA: everywhere voltage-gated K+ channels are located (SA/AV node, contractile cells (atria and ventricles)
Primary Therapeutic Use:
useful in treating pediatric arrythmias
Major effects: increases depolarization phase duration increases AP duration increases refractory period also has class II beta-1 agonist action
AE:
Lowest SE profile
Increased likelihood of QT prolongation b/c of prolonged refractory period and therefore predisposed to torsades de pointe (ventricular tachycardia)
Dofetilide
Class III K+ channel blocker
SOA: everywhere voltage-gated K+ channels are located (SA/AV node, contractile cells (atria and ventricles)
Primary Therapeutic Use:
prevent re-entry arrythmias
Major effects:
increases depolarization phase duration
increases AP duration
increases refractory period
AE:
Increased likelihood of QT prolongation b/c of prolonged refractory period and therefore predisposed to torsades de pointe (ventricular tachycardia)
Ibutilide
Class III K+ channel blocker
SOA: everywhere voltage-gated K+ channels are located (SA/AV node, contractile cells (atria and ventricles)
Primary Therapeutic Use:
prevent re-entry arrythmias
Major effects:
increases depolarization phase duration
increases AP duration
increases refractory period
AE:
Increased likelihood of QT prolongation b/c of prolonged refractory period and therefore predisposed to torsades de pointe (ventricular tachycardia)
Verapamil
Class IV Ca+2 channel blocker
SOA: pacemaker cells and contractile cells
Primary Therapeutic Use:
arrhythmia
Effects on pacemaker cell AP:
decrease AP amplitude
decrease AP rate of rise
decrease conduction
Effects on contractile cell AP:
decrease AP duration
decrease refractory period
Diltiazem
Class IV Ca+2 channel blocker
SOA: pacemaker cells and contractile cells
Primary Therapeutic Use:
arrhythmia
Effects on pacemaker cell AP:
decrease AP amplitude
decrease AP rate of rise
decrease conduction
Effects on contractile cell AP:
decrease AP duration
decrease refractory period
