Class I Antiarrhythmic Drugs Overview

What effect do Class I antiarrhythmic drugs have on myocardial membranes?

What happens to the blockade of Na+ channels when Class I drugs are used in alkaline blood pH?

What can prolonged procainamide therapy cause?

Which statement is true regarding the effective refractory period when Class I drugs are applied?

What side effect is associated with disopyramide?

What is the effect of Class I drugs on pacemaker cells?

Which condition exacerbates the rate and frequency of lupus syndrome during procainamide therapy?

What physiological change occurs when Class I drugs are administered in an acidic blood pH?

What type of symptoms may be observed with the use of disopyramide?

What happens to the conduction velocity when Class I antiarrhythmic drugs act on the myocardial membranes?

Class I Antiarrhythmic Drugs

All are weak bases
Bind and block sodium channels in their ionized form
Acidic blood pH enhances the blockade of Na+ channels
Alkaline blood pH decreases the blockade of Na+ channels
Class IA Antiarrhythmic Drugs act on nerve and myocardial membranes to slow conduction by blocking fast Na+ channels
Class IA Antiarrhythmic Drugs increase the threshold of excitability, increase the effective refractory period, decrease conduction velocity, and decrease spontaneous diastolic depolarization in pacemaker cells
Prolonged procainamide therapy can cause drug-induced Lupus
The effects of procainamide are reversed when the drug is removed
The rate and frequency of lupus syndrome increase with slow acetylators
Anticholinergic symptoms are seen with disopyramide

Class I Antiarrhythmic Drugs

Class I antiarrhythmic drugs are weak bases
They bind and block sodium channels in their ionized form
Acidic blood pH enhances the blockade of sodium channels
Alkaline blood pH decreases the blockade of sodium channels
This can be used as an antidote in case of overdose
Class IA antiarrhythmic drugs act on nerve and myocardial membranes to slow conduction by blocking fast sodium channels
They increase the threshold of excitability, increase the effective refractory period, decrease conduction velocity, and decrease spontaneous diastolic depolarization in pacemaker cells
Prolonged procainamide therapy can cause drug-induced lupus, which is reversible when the drug is removed
The rate and frequency of lupus syndrome are increased in slow acetylators
Anticholinergic symptoms are seen with disopyramide

This quiz covers the characteristics and mechanisms of Class I Antiarrhythmic Drugs, including their effects on sodium channels and their influence on cardiac conduction. Key concepts include the effects of blood pH on drug action and specific drug-related side effects such as drug-induced lupus and anticholinergic symptoms.