Chapter 23 Flashcards
antiarrhythmic drug
drug used to restore normal cardiac rhythm
arrhythmia
disorder of cardiac conduction and electrical impulse formation
cinchonism
quinidine toxicity, which is characterized by ringing in the ears (tinnitus), dizziness, and headache
ectopic focus
area of the heart from which abnormal impulses originate
premature atrial contraction (PAC)
premature contraction of the atria, usually caused by an ectopic focus
premature ventricular contraction (PVC)
premature contraction of the ventricles, usually caused by an ectopic focus
proarrhythmia
an arrhythmia caused by administration of an antiarrhythmic drug
supraventricular arrhythmia
arrhythmia that originates above the AV node in the atria
torsade de pointes
a type of proarrhythmia that causes ventricular tachycardia and fainting
ventricular fibrillation
the most serious arrhythmia; usually a terminal event where ventricular contractions are no longer able to effectively pump blood
What are Arrhythmias Caused by?
Electrolyte disturbances
Overstimulation of the heart
Where do arrhythmias originate?
Can originate anywhere in the heart
Types of Arrhythmias (3)
Tachycardias
Premature contractions
Flutters and fibrillations
Supraventricular arrhythmias
Originate in the atria and atrioventricular (AV) nodal areas
Include paroxysmal atrial tachycardia, atrial flutter, atrial fibrillation, and premature atrial contractions (PACs)
Ventricular arrhythmias
Originate below the AV node
Include premature ventricular contractions (PVC), ventricular tachycardia, and ventricular fibrillation
ECG monitoring
Arrhythmias cause abnormalities in the appearance of waves and ECG intervals.
Electrophysiology of the Heart
Generated by sodium (Na+), calcium (Ca2+), and potassium (K+) ions Phases of cardiac action potential Phase 0 - Generation of action potential Phase 1–3 - Repolarization of membrane Phase 4 - Resting level
Electrophysiologic Properties of the Heart
Conduction – Na+ rapidly moves to the inside of the cell, causing reversal of the membrane potential (depolarization)
Refractoriness – K+ moves to the outside of the cell, bringing the membrane potential back to its resting level (repolarization)
Automaticity – A latent property of ventricular muscle; in pacemaker cells, there is a slow inward movement of Na+ and Ca++ and an outward movement of K+, which “automatically” excites the membrane and begins another membrane depolarization
Therapeutic effects of Antiarrhythmic drugs
Influence the movement of ions
Act on a specific phase of the action potential
Can cause arrhythmia to become worse, or cause a proarrhythmia, a new arrhythmia
Class 1 Antiarrhythmic Drugs: Sodium Channel Blockers
Block Na ion influx during depolarization of nerves and excitable membranes
Prolong depolarization and conduction during phase 0
Class 1A drugs prolong efflux of K ion during repolarization
Class 1 A
Antiarrhythmic Drugs: Sodium Channel Blockers
Class 1A
Quinidine
Cardiac depressant, produces anticholinergic and alpha-blocking effects
Procainamide
Produces less anticholinergic and alpha-blocking actions than quinidine
Disopyramide
Produces decreased conduction and prolonged refractory period
Class 1B
Antiarrhythmic Drugs: Sodium Channel Blockers
Class 1B
Lidocaine
-Prevents ventricular arrhythmias, depresses automaticity
Mexiletine - Derivative of lidocaine
Class 1 C
Antiarrhythmic Drugs: Sodium Channel Blockers
Class 1C
Flecanide and propafenone
-Used to treat arrhythmias that are unresponsive to other antiarrhythmic drugs
Class 2 Antiarrhythmic Drugs: Beta-Blockers
Decrease heart rate, AV conduction, and automaticity of the SA and AV nodes and of atrial and ventricular muscle
- Propranolol - Possesses beta-blocking and depressant effects
- Esmolol - Affects beta-1 receptors in the heart
Class 3 Antiarrhythmic Drugs: Potassium Channel Blockers
Block potassium channels
Interfere with the efflux of K+ during repolarization Phases 1 through 3
Amiodarone
-Used for most supraventricular and ventricular arrhythmias
Sotalol
-Treats ventricular arrhythmias and atrial fibrillation
Dofetilide
-Helps in the treatment of atrial fibrillation
Ibutilide
-Indicated for the conversion of atrial flutter and atrial fibrillation to normal sinus rhythm
Special Considerations
ECGs of heart patients must be constantly monitored.
Infusion rate of antiarrhythmic drug should be adjusted to its proper rate of delivery.
Awareness of the adverse effects of antiarrhythmic drugs is important.
One must be alert for their appearance.
Preferred Therapy for Selected Arrhythmias
Sinus bradycardia
- Atropine
- Nonpharmacologic therapy - Cardiac pacemakers
Atrial flutter and atrial fibrillation
- Beta blockers, calcium channel blockers, and digoxin stabilize and protect the ventricles.
- Anticoagulants prevent atrial blood clots
- Electrical cardioversion helps terminate arrhythmia.
Preferred Therapy for Selected Arrhythmias
Paroxysmal supraventricular tachycardia
- Acute therapy - Adenosine
- Chronic therapy
- Drugs that slow AV conduction, beta-blockers, calcium channel blockers, and digoxin
Supraventricular tachycardia
- Propranolol or metoprolol
- Verapamil or diltiazem
Ventricular arrhythmias
- Acute therapy
- IV administration of amiodarone or lidocaine
- Chronic therapy
- Amiodarone
