Precautions for the use of amiodarone, precautions for the clinical use of amiodarone include:

Answers]: a, b, c, d

This question examines the dos and don'ts of amiodarone. The precautions for amiodarone are: (1) Use with caution in the following situations:

sinus bradycardia, prolonged Q-T syndrome, noisy hypotension, hypoglycetic liver function, severe congestive heart failure, pulmonary insufficiency, and hypokalemia. (2) The elderly need to closely monitor the electrocardiogram and lung function when applying. (3) Blood pressure, electrocardiogram (especially pay attention to Q-T interval), liver function, thyroid function, lung function and eyes should be checked regularly during the medication.

Therefore, the answer is ABCD.

Answer]: The pharmacological effect of amiodarone is mainly to block sodium, calcium, and potassium channels, and only disturb non-competitive blocking and receptors; It significantly inhibits repolarization and prolongs APD and ERP of atrial muscle, ventricular muscle, and conduction system. It can reduce the automaticity of the sinus node and Xiyipu system, increase the threshold of ventricular fibrillation, and reduce the conductivity of Pukenye fiber and sinus node, so the correct answer is a.

Answer] :d amiodarone is a benzofuran derivative, which belongs to a class of broad-spectrum antiarrhythmic drugs that mainly prolong the action potential, and its main mechanism of action is to prolong the action potential time course and effective refractory period of the atrium, atrioventricular refractory node and ventricle by blocking potassium ion outflow, so that the difference between the refractory period of the Lie manuscript between cardiomyocytes is reduced, the action potential tends to be consistent, and the establishment of micro-reentry is prevented, which is conducive to eliminating the reentry activation and inhibiting atrioventricular fibrillation and slowing down the automaticity of the sinus node. Slows conduction, slows the heart rate, and terminates ventricular tachycardia. Therefore, choose D.

Test center: The role and use of amiodarone.

pharmachologic effect].

Mechanism of action of amiodarone: blockade of sodium, calcium, potassium channels, non-competitive blockade and receptor action.

It significantly inhibits repolarization and prolongs APD and ERP of atrial muscle, ventricular muscle, and conduction system.

It can reduce the automaticity of the sinus node and the His-Pur system, increase the threshold of ventricular fibrillation, and reduce the conductivity of Purkinje fibers and the sinus node.

It has a relaxing effect on smooth muscles such as coronary blood vessels, dilates coronary blood vessels, reduces peripheral vascular resistance, reduces myocardial work and oxygen consumption, and protects ischemic myocardium. There is little negative inotropic effect.

Antiarrhythmic effect.

A prolongation of the heart fiber action potential phase course to reduce potassium influx (Vaughar Williams classification class), an effect independent of heart rate.

b Decreases sinus node automaticity, as it can lead to bradycardia that does not respond to atropine.

c Non-competitive - and - adrenergic inhibitions.

d Slows conduction in the sinus, intra-atrium, and nodal areas (more pronounced when the heart rhythm is fast).

e does not alter intraventricular conduction.

f Prolongs the refractory period and decreases myocardial excitability in the atria, nodal area, and ventricles.

g Slows down the conduction of the atrioventricular bypass pathway and prolongs its refractory period.

Antianginal effect.

a Lowers peripheral resistance and slows heart rate to reduce oxygen uptake.

b Non-competitive - and - adrenergic antagonism.

c Acts directly on the smooth muscles of the myocardial arteries to increase coronary output.

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

3. Other no obvious negative inotropic effects.

Indications: Oral is suitable for atrial premature contractions and premature ventricular contractions; Recurrent paroxysmal supraventricular tachycardia, atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation can prevent reversal, and can also prevent the onset of pre-excitation syndrome with supraventricular arrhythmias and maintenance of atrial fibrillation or atrial flutter after electrical reversion. Secondly, it has an antianginal effect.

Intravenous injection is indicated for paroxysmal supraventricular tachycardia, especially in patients with preexcitation syndrome, and for ventricular tachycardia that does not respond to lidocaine**.

It is suitable for atrial premature contractions, ventricular premature contractions, transient atrial tachycardia, and retroactive supraventricular tachycardia, and has poor efficacy for persistent atrial fibrillation or flutter, which is not as good as quinidine. Not satisfied with the effect of maintaining sinus rhythm after cardioversion of atrial fibrillation. Intravenous injection is indicated for paroxysmal supraventricular tachycardia, especially in patients with preexcitation syndrome.

It is also used in patients with ventricular tachycardia who do not respond to lidocaine**. This product is a broad-spectrum antiarrhythmic drug. The efficacy is significant, but it is currently listed as a second-line antiarrhythmic drug because of the large number of anti-arrhythmic drugs.

For severe arrhythmias that are ineffective or inappropriate for others:

1 atrial arrhythmias (maintenance of atrial flutter, atrial fibrillation and post-conversion sinus rhythm);

2 Nodal arrhythmias;

3 Ventricular arrhythmias (** life-threatening premature ventricular systoles and ventricular tachycardia and prevention of ventricular tachyarrhythmia or ventricular fibrillation);

4 Arrhythmias with w-p-w syndrome.

According to its pharmacological characteristics, amiodarone is suitable for the above arrhythmias, especially those with structural heart disease (coronary insufficiency and heart failure).

Pharmacological characteristics of amiodarone:

1 Decreased automaticity (blockade of NA, CA influx, blockade ).

2. Slowing conduction (mainly atrioventricular node, Purs' fiber).

3 Prolongation of APD, ERP (related to blockade of K efflux and inactivation of NA channels).

4. Broad-spectrum antiarrhythmic drugs, long-term oral administration can prevent ventricular tachycardia, ventricular fibrillation**, and reduce the rate of sudden death in patients with structural heart disease.

5 Adverse reactions are gastrointestinal reactions (loss of appetite, nausea and vomiting, etc.), hyperthyroidism or hypothyroidism, causing hepatitis, the most serious is interstitial pneumonia, forming pulmonary fibrosis, intravenous injection can cause arrhythmia or aggravate cardiac insufficiency. Combined with class I, II, III drugs, it can enhance the effect, cause sinus bradycardia, and even asystole.