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Cardiac Dysrhythmias
Caused by changes in the ionic currents through ion channels of the myocardial cell membrane:
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What changes cause cardiac dystrhythmias
–Sodium-influx into cell
–Potassium-extruded from cell
- –Calcium-influx into cell
- Magnesium, Phosphorous
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Any drug used to treat an arrhythmia (dysrhythmia) can also cause
an arrhythmia = proarrhythmia
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How many Classes of Dysrhythmic agents
5
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Class 1 dysrhythmic agents
Sodium Channel Blockers
Block cardiac sodium channels
slow impulse conduction in the atria, ventricles , and His-Purkinjie System
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Class II Dysrhythmic agents
Beta adrenergic blocking agents
block adrenergic receptors, producing antisympathetic properties
- SA node: Reduce automaticity, slow conduction
- velocity, and reduce contractility
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Class III Dysrhythmic agents
Potassium Channel Blockers
- –lengthen the action potential duration and
- effective refractory period
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Class IV Dysrhythmic agents
Calcium Channel Blockers
- –Same effects as beta blockers – reduction of
- automaticity in the SA node, delay of conduction through AV node, and reduction
- of myocardial contractility
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Other dysrhythmic drugs
–Adenosine and Digoxin
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Class IA dysrhythmic agent
Quinidine (Quinidex extendtabs)
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Quinidine (Quinidex extendtabs) Other drugs in class
- Procainamide (Pronestyl, Procanbid),
- dispyramide (Norpace),
- tocainide (Tococard),
- propafenone (Rythmol)
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Quinidine (Quinidex extendtabs) Therapeutic Uses
Used to treat supraventricular and ventricular arrhythmias
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Quinidine (Quinidex extendtabs) Physiologic Actions
Slows impulse conduction by blocking sodium channels
Decreases myocardial excitability, conduction velocity, and contractility
Prevents reentry phenomenon
Strongly anticholinergic effects (atropine-like) increases ventricular rate
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Quinidine (Quinidex extendtabs) Side Effects
Serious adverse effect: Cardiotoxicity, arterial embolism, hypotension with IV use
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