Master Class I Antiarrhythmics (Na+ Channel Blockers) Overview with Picmonic for Medicine

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Class I Antiarrhythmics (Na+ Channel Blockers) Overview

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Class I Antiarrhythmics (Na+ Channel Blockers) Overview

(1) Wand Ant-Tie-Arrhythmia-Drummer (Salt Shaker Channel Blocked)

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Class I Antiarrhythmics treat tachyarrhythmias by blocking fast Na⁺ channels and there are several subcategories of drug based on their specific effect on cardiac action potentials. These drugs are used to restore normal pacemaker and conduction activity, and are selective for depolarized tissue, which is known as state dependant. Class I antiarrhythmic drug's blockade of Na⁺ channels reduces rate of phase 0 depolarization and prolongs effective refractory period. This Na⁺ blockade also increases the threshold for firing within abnormal pacemaker cells. These drugs are contraindicated in hyperkalemic states, as excess potassium increases resting membrane potential and can produce a sodium-channel blockade so pronounced that asystole may result in patients taking Class I antiarrhythmics.

7 KEY FACTS

These drugs are indicated for arrhythmias, which generally refer to abnormal heart rate or regularity. They can be caused by either irregular impulse conduction or impulse generation.

Class I antiarrhythmics also have local anesthetic properties.

Class I drugs act by blocking fast sodium channels. This slows or halts conduction, especially within depolarized cells.

Blockage of Na+ channels reduces rate of phase 0 depolarization and prolongs effective refractory period.

Because of the Na+ channel blockage, these drugs increase the threshold for firing within abnormal pacemaker cells.

The drugs in this class are state dependant, meaning they selectively depress tissue that is frequently depolarized, versus normally polarized tissue. This can include ischemic tissue.

These drugs are contraindicated in hyperkalemic states as they cause increased toxicity for all class I agents. This is because excess potassium increases resting membrane potential and can produce a sodium-channel blockade so pronounced that asystole may result.

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