Amiodarone instructions

The main effect of amiodarone is to treat arrhythmias and promote blood circulation. It can also resist heart rhythm and reduce atrial functional diseases. It is of great help to the health of the body. All drugs should be used carefully before use to understand the relevant reactions of the drugs. This will help the condition and avoid harm to the human body caused by excessive intake.

Pharmacokinetics

Oral absorption is slow. The bioavailability is approximately 50%. The apparent distribution volume is large and it is mainly distributed in adipose tissue and fat-rich organs. Next are the heart, kidneys, lungs, liver and lymph nodes. The lowest are in the brain, thyroid gland and muscles. In plasma, 62.1% is bound to albumin and 33.5% may be bound to β-lipoprotein. It is mainly eliminated by metabolism in the liver. The half-life is 14 to 28 days, 4.6 hours for a single oral dose of 800 mg (uptake into tissues), and 13 to 30 days for long-term use. Blood drug concentration can still be measured six months after stopping the drug. Peak blood concentration is reached 4 to 6 hours after oral administration. The steady-state blood concentration can be reached in about 1 month, and the steady-state blood concentration is 0.92~3.75μg/ml. The effect begins in 4-5 days, reaches its maximum effect in 5-7 days, and can last for 8-10 days after drug discontinuation, occasionally up to 45 days. The effect starts 5 minutes after intravenous injection and can last for 20 minutes to 4 hours after drug withdrawal. The effective blood concentration is 1~2.5μg/ml, and the toxic blood concentration is above 1.8~3.7μg/ml. This product cannot be removed by hemodialysis.

Amiodarone is transported slowly in tissues with high affinity. Its bioavailability varies from person to person, ranging from 30% to 80% (average about 50%). Peak concentration is reached 3 to 7 hours after a single oral dose. The loading dose usually takes effect after a week (a few days to two weeks). The half-life of amiodarone is long and has significant individual differences (20~1Q0 days). During the first few days of treatment, most of the drug accumulates in tissues, especially adipose tissue, and begins to be cleared after a few days, reaching a steady-state concentration after one to several months, depending on the individual.

Due to the above characteristics, a loading dose should be given so that the tissue can be quickly saturated to exert a therapeutic effect.

Some of the iodine is removed from the molecule and excreted in the urine. Taking 200 mg of amiodarone per day can excrete the equivalent of 6 mg of iodine, so most of the remaining iodine is excreted through the liver and then excreted in the feces. Renal excretion is minimal, allowing patients with renal insufficiency to use conventional doses of amiodarone. Drug clearance may take several months after discontinuation of medication, and it should be noted that residual effects of the drug may last from 10 days to 1 month.

a. Prolong the phase III duration of cardiac fiber action potential to reduce potassium influx (Vaughar Williams classification is Class III), and this effect is independent of heart rate.

b. Reduced sinus node automaticity, which can lead to bradycardia that is unresponsive to atropine.

c. Non-competitive α- and β-adrenergic inhibition.

d. Slow down the conduction in the sinoatrial, intraatrial and nodal areas (more obvious when the heart rate is fast).

e.Does not change the intraventricular conduction.

f. Prolong the refractory period and reduce the excitability of the atria, nodes and ventricles.

g. Slow down the conduction of the atrioventricular accessory pathway and prolong its refractory period.

Anti-anginal effect

a. Reduce peripheral resistance, slow down heart rate and thus reduce oxygen uptake.

b. Non-competitive α- and β-adrenergic antagonism.

c. Directly acts on myocardial arterial smooth muscle to increase coronary artery output.

d. Reduce aortic pressure and peripheral resistance and maintain cardiac output.

3. Others have no obvious negative inotropic effect.

It is suitable for atrial premature beats, ventricular premature beats, transient atrial tachycardia, and recurrent supraventricular tachycardia. It is less effective than quinidine for persistent atrial fibrillation or flutter. The effect of maintaining sinus rhythm after cardioversion of atrial fibrillation is unsatisfactory. Intravenous injection is suitable for paroxysmal supraventricular tachycardia, especially for those with preexcitation syndrome. It is also used for patients with ventricular tachycardia who have not responded to lidocaine. This product is a broad-spectrum antiarrhythmic drug. It has significant therapeutic effects, but due to its many side effects, it is currently listed as a second-line antiarrhythmic drug.

For severe arrhythmias that are ineffective or unsuitable for other treatments:

1. Atrial arrhythmias (conversion of atrial flutter, atrial fibrillation and maintenance of sinus rhythm after conversion);

2. Nodal arrhythmia;

3. Ventricular arrhythmias (treatment of life-threatening premature ventricular contractions and ventricular tachycardia and prevention of ventricular tachycardia or ventricular fibrillation);

4. Arrhythmias associated with WPW syndrome

Based on its pharmacological characteristics, amiodarone is suitable for the above-mentioned arrhythmias, especially those combined with organic heart disease (coronary artery insufficiency and heart failure).