Quinidine Sulfate — Veterinary Vademecum Drug Reference

Dosage & Administration Guidelines

Species	Route	Dose	Frequency	Duration & Clinical Notes
Dog	PO	6-20 mg/kg	q6-8h	Duration: As needed for arrhythmia control Notes: Start at lower end and titrate based on ECG monitoring and plasma levels (therapeutic range 2-5 mcg/mL).
Cat	PO	5-10 mg/kg	q6-8h	Duration: As needed Notes: Use cautiously; cats are sensitive to adverse effects.
Horse	PO (via nasogastric tube)	2.2 mg/kg every 2 hours until conversion or toxicity, then q6h for maintenance	Loading: q2h; Maintenance: q6h	Duration: Usually 1-3 days for conversion Notes: Monitor ECG and plasma levels; discontinue if QRS duration increases >25% or if hypotension occurs.
Cattle	PO	5-10 mg/kg	q6-8h	Duration: As needed Notes: Extra-label use; not FDA-approved for food animals.
Small Ruminants	PO	5-10 mg/kg	q6-8h	Duration: As needed Notes: Extra-label use; not FDA-approved.
Rabbit	PO	5-10 mg/kg	q6-8h	Duration: As needed Notes: Limited data; use with caution.

Clinical Indications & Species Uses

General Indications

Class 1A antiarrhythmic for atrial and ventricular arrhythmias

Dog (Canine)

Treatment of atrial fibrillation
Suppression of ventricular arrhythmias (e.g., premature ventricular contractions, ventricular tachycardia)
Management of supraventricular tachycardias

Cat (Feline)

Treatment of atrial fibrillation (rare)
Suppression of ventricular arrhythmias

Horse (Equine)

Treatment of atrial fibrillation
Management of ventricular arrhythmias (less common)

Pharmacology & Mechanism of Action

Drug Class: Class 1A Antiarrhythmic | Pharmacological Group: Sodium Channel Blocker

Mechanism of Action: Quinidine sulfate is a class 1A antiarrhythmic agent that blocks fast sodium channels in cardiac myocytes, slowing the rapid depolarization phase (phase 0) of the action potential. It also prolongs the effective refractory period and action potential duration by inhibiting potassium channels. Additionally, it has vagolytic (anticholinergic) effects and alpha-adrenergic blocking properties, which can lead to reflex tachycardia and hypotension. In atrial fibrillation, it can convert the rhythm to sinus by prolonging atrial refractoriness and slowing conduction.

Pharmacodynamics: Quinidine depresses myocardial automaticity, slows conduction velocity, and prolongs refractoriness. It increases the threshold for ventricular fibrillation and suppresses premature ventricular contractions. Its vagolytic effect can increase sinus rate, especially at low doses, while at higher doses it may depress sinus node function. It also has a negative inotropic effect, which may be clinically significant in patients with compromised cardiac function. In horses, it is used to treat atrial fibrillation by prolonging atrial refractory period and slowing conduction, allowing reversion to normal sinus rhythm.

⚡ Pharmacokinetics Summary

Absorption: Quinidine is well absorbed after oral administration, with peak plasma concentrations occurring within 1-3 hours in most species. Bioavailability may be reduced by food, but the extent is variable. In horses, oral absorption is rapid but may be erratic; peak levels occur in 1-2 hours.

Distribution: Quinidine is widely distributed throughout the body, with high concentrations in the heart, liver, kidneys, and skeletal muscle. It crosses the placenta and is distributed into milk. Protein binding is approximately 80-90% in dogs and cats, but lower in horses (about 60-70%).

Metabolism: Quinidine is extensively metabolized in the liver via cytochrome P450 enzymes (primarily CYP3A4) to active and inactive metabolites, including 3-hydroxyquinidine and quinidine-N-oxide. The extent of metabolism varies by species; in dogs, hepatic metabolism is significant, while in horses, a larger fraction is excreted unchanged.

Excretion: Renal excretion is the primary route of elimination, with both glomerular filtration and active tubular secretion. Approximately 20-50% of the drug is excreted unchanged in urine, depending on species and urine pH. Alkaline urine increases reabsorption, prolonging half-life. Biliary excretion also occurs, with enterohepatic recirculation.

Half-Life: Dogs: 5-7 hours; Cats: 2-4 hours; Horses: 6-8 hours; Cattle: 4-6 hours (estimated).

Bioavailability: Oral bioavailability is approximately 70-90% in dogs and cats, but may be lower and more variable in horses (around 50-70%).

Protein Binding: Dogs: 80-90%; Cats: 85-90%; Horses: 60-70%; Humans: 80-90%.

Available Formulations & Strengths

Oral Tablet 100 mg, 200 mg, 300 mg (PO)

Oral Capsule 200 mg, 300 mg (PO)

Injectable Solution 200 mg/mL (as gluconate) (IV/IM)

Contraindications & Clinical Warnings

Contraindications:

Known hypersensitivity to quinidine or cinchona derivatives
Complete AV block or severe intraventricular conduction defects
Digitalis-induced arrhythmias (unless specifically indicated)
Myasthenia gravis
Severe hepatic or renal impairment (use with caution)
Concurrent use with drugs that prolong QT interval (e.g., amiodarone, sotalol) due to additive effects

Warnings & Clinical Precautions:

Use with caution in animals with congestive heart failure, hypotension, or electrolyte imbalances (especially hypokalemia or hypomagnesemia).
Monitor ECG regularly for QRS widening, QT prolongation, or new arrhythmias.
Monitor plasma quinidine levels; therapeutic range is 2-5 mcg/mL; toxicity increases above 5 mcg/mL.
In horses, rapid IV administration can cause severe hypotension and collapse; use oral route preferentially.
May cause cinchonism (tinnitus, headache, visual disturbances) in humans; monitor for similar signs in animals.
Use with caution in animals with hepatic or renal disease; dose adjustment may be necessary.
Discontinue if severe gastrointestinal upset or allergic reactions occur.

Adverse Effects & Reactions

Common:

Gastrointestinal upset (vomiting, diarrhea, anorexia)
Hypotension
Tachycardia (due to vagolytic effect)
ECG changes (QRS widening, QT prolongation)

Serious / Severe:

Ventricular arrhythmias (torsades de pointes)
Complete heart block
Severe hypotension or shock
Hepatotoxicity
Thrombocytopenia or agranulocytosis (rare)

Rare:

Allergic reactions (rash, fever, anaphylaxis)
Cinchonism (tinnitus, visual disturbances)
Hemolytic anemia
Lupus-like syndrome

Key Drug Interactions

Interacting Drug / Class	Clinical Effect & Mechanism	Severity
Digoxin	Quinidine increases digoxin plasma levels by decreasing its clearance and volume of distribution, potentially leading to digoxin toxicity.	High
Beta-blockers (e.g., propranolol)	Additive negative inotropic and chronotropic effects; may cause severe bradycardia or hypotension.	High
Calcium channel blockers (e.g., verapamil, diltiazem)	Additive depression of cardiac contractility and conduction; increased risk of hypotension and AV block.	High
Amiodarone	Additive QT prolongation and risk of torsades de pointes.	High
Phenobarbital or phenytoin	Induce hepatic metabolism of quinidine, reducing its plasma levels and efficacy.	Moderate
Cimetidine	Inhibits hepatic metabolism of quinidine, increasing its plasma levels and risk of toxicity.	Moderate
Antacids (aluminum/magnesium)	May reduce absorption of quinidine; separate administration by 2 hours.	Mild

Overdose & Toxicity Management

Signs of Toxicity:

Severe hypotension
Widening of QRS complex
Ventricular arrhythmias (including torsades de pointes)
Complete heart block
Seizures
Respiratory depression
Coma

Emergency Treatment Protocol: Immediate supportive care: discontinue drug, provide IV fluids for hypotension, and correct electrolyte imbalances (especially potassium and magnesium). For severe arrhythmias, administer sodium bicarbonate to alkalinize plasma and counteract sodium channel blockade. Use lidocaine or phenytoin for ventricular arrhythmias if needed. In severe cases, consider temporary cardiac pacing. Activated charcoal may be used if ingestion is recent. Hemodialysis may be considered in severe cases, but is rarely used in veterinary medicine.

Food Animal Withdrawal Times

🥩 Meat: 14 days🥛 Milk: 3 days

Withdrawal times are not established for quinidine in food animals; these are estimates based on pharmacokinetic data. Consult regulatory authorities for specific guidance.

Storage, Handling & Regulatory Information

Storage Temperature: Store at controlled room temperature (20-25°C, 68-77°F).

Light Sensitivity: Light-sensitive — protect from direct exposure.

Handling & Special Conditions: Protect from light and moisture. Keep in tightly closed container.

Dispensing Status: Prescription Required (Rx Only)

Approval Status: Quinidine sulfate is FDA-approved for human use, but not specifically approved for veterinary use. However, it is commonly used in veterinary medicine under extra-label regulations.

Extra-Label (Off-Label) Use: In the US, extra-label use of quinidine in food animals is permitted under AMDUCA with a valid veterinarian-client-patient relationship, but requires a withdrawal time extension and may not be used in feed. In horses, it is not approved for use in horses intended for human consumption.

Clinical Pearls & Practice Notes

💡 Clinical Insights: Quinidine sulfate is a valuable antiarrhythmic agent in veterinary medicine, particularly for the treatment of atrial fibrillation in horses and ventricular arrhythmias in dogs. Due to its narrow therapeutic index and potential for serious adverse effects, therapy should be initiated under close veterinary supervision with ECG monitoring. Plasma levels should be monitored when possible, and dosage adjustments made based on clinical response and toxicity. In horses, oral administration via nasogastric tube is preferred to avoid the severe hypotension associated with rapid IV administration. For food animals, strict adherence to withdrawal times is essential to prevent drug residues in meat and milk. Always consider alternative therapies and individual patient factors when prescribing quinidine.

References & Literature

📚 Plumb's Veterinary Drug Handbook
📚 Papich Veterinary Pharmacology and Therapeutics
📚 Compendium of Veterinary Products (CVP)