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Introduction
Illustrated mechanism of action
Examples of Medication Brand Names (with Images)
Indication
Side Effects
Precautions & Contraindications
Monographs
Reference
HISTORY
HISTORY
Historical Background of Class 1A Antiarrhythmic Drugs:
The story of Class 1A antiarrhythmic drugs dates back to the early 20th century, when researchers began exploring natural and synthetic compounds for managing irregular heartbeats.
Quinidine
First discovered from cinchona bark
Used since the early 1900s to treat arrhythmias
One of the earliest known antiarrhythmic agents.
Procainamide
Developed in the 1950s as a safer, longer-acting derivative of procaine
Widely used for ventricular arrhythmias, especially in emergency settings.
Disopyramide
Introduced in the 1970s for oral long-term use
Notable for its anticholinergic effects.
Vaughan Williams Classification
Created in the 1970s, officially classified Class 1A as
Sodium channel blockers with moderate effects on conduction and prolonged repolarization.
Introduction
Class 1A antiarrhythmic drugs are a subgroup of sodium channel blockers used to manage various types of cardiac arrhythmias. These drugs work primarily by inhibiting fast sodium channels during the depolarization phase of the cardiac action potential, leading to a slower conduction velocity. In addition, they also prolong the repolarization phase by blocking some potassium channels, which results in an increased action potential duration and refractory period.
Class 1A antiarrhythmic drugs are a subgroup of sodium channel blockers used to manage various types of cardiac arrhythmias. These drugs work primarily by inhibiting fast sodium channels during the depolarization phase of the cardiac action potential, leading to a slower conduction velocity. In addition, they also prolong the repolarization phase by blocking some potassium channels, which results in an increased action potential duration and refractory period.
This dual effect helps stabilize the cardiac rhythm in patients suffering from both atrial and ventricular arrhythmias. Although effective, these drugs come with specific side effects and require careful monitoring, especially due to their potential to prolong the QT interval, increasing the risk of torsades de pointes.
This dual effect helps stabilize the cardiac rhythm in patients suffering from both atrial and ventricular arrhythmias. Although effective, these drugs come with specific side effects and require careful monitoring, especially due to their potential to prolong the QT interval, increasing the risk of torsades de pointes.
Illustrated mechanism of action
Class IA antiarrhythmic drug function by blocking fast sodium channels in cardiac cells. This action slows the rate of depolarization during phase 0 of the cardiac action potential, leading to decreased conduction velocity. Additionally, these drugs inhibit potassium channels, which prolongs repolarization (phase 3) and extends both the action potential duration and the effective refractory period. These combined effects help suppress abnormal electrical activity in the heart, making Class IA agents effective in treating various arrhythmias, including atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia.
Blocks Na⁺ channels → slows Phase 0 depolarization → ↓ conduction velocity.
Blocks some K⁺ channels → prolongs Phase 3 repolarization → ↑ action potential duration & refractory period.
ECG effect: ↑ QRS duration & ↑ QT interval.
Net result: Stabilizes heart rhythm by preventing early or fast re-excitation of heart cells.
Examples of Medication Brand Names
Procainamide Hydrochloride injection
Ethmozine
Quinidine Sulfate
Quinidine Gluconate
Norpace
Indication
1. Atrial Fibrillation (AF):
Used to control rhythm and reduce abnormal electrical activity.
2. Atrial Flutter:
Helps slow down and stabilize the rapid atrial impulses.
3. Paroxysmal Supraventricular Tachycardia (PSVT):
Treats episodes of sudden fast heart rates originating above the ventricles.
4. Ventricular Tachycardia (VT):
Effective in managing and preventing life-threatening ventricular arrhythmias.
5. Prevention of Recurrent Ventricular Arrhythmias (especially post-MI):
Sometimes used after myocardial infarction to prevent future arrhythmias (e.g., procainamide).
Side Effects
⚠️ Major Side Effects
1. Proarrhythmia
• QT interval prolongation, which can lead to torsades de pointes, a potentially fatal ventricular arrhythmia.
2. Cardiac Toxicity
• Conduction disturbances such as widened QRS complexes and heart block.
• Negative inotropic effects, particularly with disopyramide, which can exacerbate heart failure.
3. Drug-Specific Reactions
• Quinidine:
• Can cause cinchonism, characterized by tinnitus, headache, dizziness, nausea, and visual disturbances.
• Procainamide:
• Associated with a lupus-like syndrome, presenting with fever, rash, and joint pain.
• Disopyramide:
• Exhibits anticholinergic effects such as dry mouth, blurred vision, urinary retention, and constipation.
4. Hematologic Effects
• Thrombocytopenia (low platelet count).
• Agranulocytosis (severe reduction in white blood cells), particularly with procainamide.
5. Hypersensitivity Reactions
• Rashes, fever, and drug-induced lupus erythematosus.
🧠 Neurological and Gastrointestinal Effects
• Dizziness, headache, and mental confusion.
• Nausea, vomiting, and diarrhea.
Precautions & Contraindications
Precautions:
1. Cardiovascular conditions:
Hypotension: These drugs can cause hypotension, especially after intravenous administration.
Heart failure: They should be used cautiously in patients with heart failure as they may exacerbate the condition due to negative inotropic effects.
Bundle branch block: Caution in patients with conduction abnormalities, as they can worsen these conditions.
2. Electrolyte imbalances:
Electrolyte imbalances, particularly hypokalemia and hypomagnesemia, should be corrected before use, as these imbalances can increase the risk of arrhythmias.
3. Liver and renal impairment:
These drugs are metabolized in the liver and excreted in the kidneys, so caution is needed in patients with liver or kidney dysfunction.
4. QT prolongation:
Class 1A drugs can prolong the QT interval, increasing the risk of torsades de pointes (a life-threatening arrhythmia). Monitoring of the QT interval is recommended.
5. Drug interactions:
These medications may interact with other drugs, particularly those that affect the liver enzymes (e.g., CYP450 inhibitors/inducers) or drugs that alter the QT interval.
Contraindications:
1. Severe heart block: These drugs can worsen AV block, especially in patients with second- or third-degree heart block without a pacemaker.
2. Torsades de pointes: They are contraindicated in patients with a history of torsades de pointes or congenital long QT syndrome.
3. Severe hepatic or renal impairment: In severe cases, their clearance is impaired, and they may accumulate to toxic levels.
4. Hypersensitivity: Patients with known hypersensitivity or allergies to any of the class 1A drugs should avoid them.
Monographs
4_5785004713564969031.pdfDocument from Bassant Ahmed.pdfDocument from Bassant Ahmed.pdfDocument from Bassant Ahmed.pdfReference
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