Composition, form of production and packaging
Tablets from white to white with a creamy shade of color, round, with a fault line on one side, bevel from the edges to the fault line and with a facet on both sides, with the engraving of the heart symbol above the fault line and the figure "200" under the fault line.
amiodarone hydrochloride 200 mg
Excipients: lactose monohydrate, corn starch, magnesium stearate, povidone K90F, silicon dioxide colloidal anhydrous.
10 pieces. - blisters (3) - packs of cardboard.
INSTRUCTION FOR THE SPECIALIST.
Description of the drug approved by the manufacturer for the printed edition of 2015.
Antiarrhythmic drug. Amiodarone belongs to class III (a class of inhibitors of repolarization) and has a unique mechanism of antiarrhythmic action, in addition to the properties of class III antiarrhythmics (potassium channel blockade), it has the effects of class I antiarrhythmics (blockade of sodium channels), class IV antiarrhythmics (calcium channel blockade), and uncompetitive beta-adrenergic blocking action.
In addition to antiarrhythmic action, the drug has antianginal, coronary dilatation, alpha and beta-adrenergic blocking effects.
- an increase in the duration of the 3-phase potential action of cardiomyocytes, mainly due to blocking the ion current in potassium channels (the effect of class III antiarrhythmics according to Williams classification);
- a decrease in the automatism of the sinus node, leading to a decrease in heart rate;
- non-competitive blockade of? - and? -adrenoceptors;
- slowing of sinoatrial, atrial and AV-conduction, more pronounced with tachycardia;
- no changes in ventricular conduction;
- an increase in refractory periods and a decrease in the excitability of the myocardium of the atria and ventricles, as well as an increase in the refractory period of the AV node;
- slowing down and increasing the duration of the refractory period in additional beams of AV-conduction.
- absence of negative inotropic action when taken orally;
- decrease in oxygen consumption by myocardium due to a moderate decrease in OPSS and heart rate;
- increase in coronary blood flow due to direct effect on the smooth muscles of the coronary arteries;
- maintaining cardiac output by reducing the pressure in the aorta and reducing the OPSS;
- the effect on the exchange of thyroid hormones: inhibition of the conversion of T3 to T4 (blockade of thyroxine-5-deiodinase) and blocking the seizure of these hormones by cardiocytes and hepatocytes, leading to a weakening of the stimulating effect of thyroid hormones on the myocardium.
After the beginning of taking the drug inside, therapeutic effects develop on average a week (from several days to 2 weeks). After stopping its reception, amiodarone is determined in the blood plasma for 9 months. It should be taken into account the possibility of maintaining the pharmacodynamic action of amiodarone within 10-30 days after its withdrawal.
Bioavailability after oral administration varies from 30% to 80% in patients (mean value about 50%). After a single intake of amiodarone, Cmax in the blood plasma is reached after 3-7 hours. However, the therapeutic effect usually develops a week after the start of the drug (from several days to 2 weeks).
Binding to plasma proteins is 95% (62% - with albumin, 33.5% - with beta-lipoproteins). Amiodarone has a large V d . Amiodarone is characterized by a slow intake into tissues and high affinity for them. During the first days of treatment, the drug accumulates in almost all tissues, especially in adipose tissue and in addition to it in the liver, lungs, spleen and cornea.
Amiodarone is metabolized in the liver with the help of isozymes CYP3A4 and CYP2C8. Its main metabolite, desethylamiodarone, is pharmacologically active and can enhance the antiarrhythmic effect of the basic compound. Amiodarone and its active metabolite, dezetylamiodarone, in vitro have the ability to inhibit the isoenzymes CYP1A1, CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP3A4, CYP2A6, CYP2B6 and CYP2C8. Amiodarone and desethylamiodarone also demonstrated the ability to inhibit certain transporters, such as P-glycoprotein (P-gp) and an organic cation carrier (PKK2). In vivo, the interaction of amiodarone with the substrates of the isoenzymes CYP3A4, CYP2C9, CYP2D6 and P-gp was observed.
The removal of amiodarone begins in a few days, and the achievement of equilibrium between the intake and excretion of the drug (the achievement of C ss ) occurs after one to several months, depending on the individual characteristics of the patient. The main way to remove amiodarone is the intestine. Amiodarone and its metabolites are not excreted by hemodialysis. Amiodarone has a long T 1/2 with a large individual variability (therefore, when choosing a dose, for example, increasing or decreasing it, it should be remembered that at least 1 month is needed to stabilize the new plasma concentration of amiodarone).
Excretion during ingestion proceeds in 2 phases: initial T 1/2 (first phase) - 4-21 h, T 1/2 in the 2 nd phase - 25-110 days. After continued oral administration, the mean T 1/2 is 40 days. After the withdrawal of the drug, the complete removal of amiodarone from the body can continue for several months.
Each dose of amiodarone (200 mg) contains 75 mg of iodine. Part of the iodine is released from the drug and found in urine in the form of iodide (6 mg for 24 hours with a daily dose of amiodarone 200 mg). Most of the iodine that remains in the drug is excreted through the intestine after passing through the liver, but with prolonged administration of amiodarone, the concentration of iodine in the blood can reach 60-80% of the concentrations of amiodarone in the blood.
Features of the pharmacokinetics of the drug explains the use of loading doses, which is aimed at the rapid accumulation of amiodarone in tissues, in which its therapeutic effect is manifested.
Pharmacokinetics in special clinical cases
Due to the insignificant removal of the drug by the kidneys in patients with renal insufficiency, dose adjustment of amiodarone is not required.
- life-threatening ventricular arrhythmias, including ventricular tachycardia and ventricular fibrillation (treatment should be initiated in a hospital with careful cardiac monitoring).
- supraventricular paroxysmal tachycardia:
- documented attacks of recurrent persistent supraventricular paroxysmal tachycardia in patients with organic heart diseases;
- documented attacks of recurrent persistent supraventricular paroxysmal tachycardia in patients without organic heart disease, when antiarrhythmic drugs of other classes are not effective or there are contraindications to their use;
- documented attacks of recurrent persistent supraventricular paroxysmal tachycardia in patients with Wolff-Parkinson-White syndrome.
- atrial fibrillation (atrial fibrillation) and atrial flutter.
Preventing sudden arrhythmic death in high-risk patients
- patients after a recent myocardial infarction, having more than 10 ventricular extrasystoles per hour, clinical manifestations of chronic heart failure, and a reduced fraction of left ventricular ejection (less than 40%).
Cordarone В® can be used in the treatment of rhythm disturbances in patients with IHD and / or impaired left ventricular function.
The drug should be taken only as directed by a doctor.
Cordarone В® tablets are taken orally before meals and are washed down with a sufficient amount of water.
Load ("saturating") dose: various saturation schemes can be applied.
Inpatient: the initial dose divided into several receptions ranges from 600-800 mg (to a maximum of 1200 mg) / day until a total dose of 10 g (usually within 5-8 days).
Outpatient: the initial dose divided into several doses ranges from 600 to 800 mg per day until a total dose of 10 g is reached (usually within 10-14 days).
Supportive dose: can vary in different patients from 100 to 400 mg / day. A minimum effective dose should be applied in accordance with the individual therapeutic effect.
Because Cordarone В® has a very large T 1/2 , it can be taken every other day or take breaks in its reception 2 days a week.
The average therapeutic single dose is 200 mg.
The average therapeutic daily dose is 400 mg.
The maximum single dose is 400 mg.
The maximum daily dose is 1200 mg.
The incidence of adverse events was determined according to the WHO classification: very often (? 10%); often (? 1%, <10); infrequently (? 0.1%, <1%); rarely (? 0.01%, <0.1%); very rarely, including individual messages (<0.01%); the frequency is unknown (according to the available data, the frequency can not be determined).
From the cardiovascular system: often - bradycardia, usually mild, the severity of which depends on the dose of the drug; infrequent conduction disorder (sinoatrial block, AV block of various degrees), arrhythmogenic action (there are reports of the occurrence of new arrhythmias or aggravation of existing arrhythmias, in some cases - with subsequent cardiac arrest); on the basis of available data, it is impossible to determine whether the occurrence of these rhythm disturbances is due to the action of Cordarone В® , the severity of the cardiovascular pathology, or is a consequence of ineffective treatment. These effects are observed mainly in cases of the use of Cordarone В® together with drugs prolonging the period of cardiac ventricular repolarization (QT interval c ) or in disorders of the electrolyte content in the blood.
Very rarely - pronounced bradycardia or, in exceptional cases, stopping the sinus node, which were noted in some patients (patients with sinus node dysfunction and elderly patients), vasculitis; the frequency is unknown - the progression of chronic heart failure (with prolonged use), ventricular tachycardia of the "pirouette" type.
From the side of the digestive system: very often - nausea, vomiting, dysgeusia (dullness or loss of taste sensations), usually arising with the application of a loading dose and passing after its reduction.
On the part of the liver and bile ducts: very often - an isolated increase in the activity of transaminases in the blood serum, usually mild (exceeding the normal values вЂ‹вЂ‹by 1.5-3 times, decreases with decreasing dose or spontaneously); often - acute liver damage with increased transaminase activity and / or jaundice, including the development of liver failure, sometimes fatal; very rarely - chronic liver disease (pseudo-alcoholic hepatitis, cirrhosis), sometimes fatal. Even with a moderate increase in transaminase activity in the blood after treatment lasting more than 6 months, chronic liver damage should be suspected.
On the part of the respiratory system: often - pulmonary toxicity, sometimes fatal (alveolar / interstitial pneumonitis or fibrosis, pleurisy, bronchiolitis obliterans with pneumonia). Although these changes may lead to the development of pulmonary fibrosis, they are generally reversible in the early withdrawal of amiodarone and with or without the use of GCS. Clinical manifestations usually disappear within 3-4 weeks. Restoration of the radiographic picture and function of the lungs takes place more slowly (several months). The appearance of severe dyspnea or dry cough in the patient taking amiodarone, both accompanied and not accompanied by deterioration of the general condition (increased fatigue, weight loss, increased body temperature) requires chest X-ray and, if necessary, drug withdrawal.
Very rarely bronchospasm (in patients with severe respiratory failure, especially in patients with bronchial asthma), acute respiratory distress syndrome (sometimes fatal and sometimes immediately after surgery, it is assumed that it is possible to interact with a high concentration of oxygen).
The frequency is unknown - pulmonary hemorrhage.
From the side of the organ of vision: very often - microdeposition in the epithelium of the cornea, consisting of complex lipids, including lipofuscin, they are usually confined to the pupil area and do not require discontinuation of treatment and disappear after drug withdrawal, sometimes they can cause visual disturbances in the form of a color halo or fuzziness contours in bright light; very rarely - optic neuritis / visual neuropathy (the connection with amiodarone has not been established to date, however, since optic neuritis can lead to blindness, with blurred vision or reduced visual acuity, when taking Cordarone В®, it is recommended to perform a full ophthalmological examination, including fundoscopy, and in case of detection of optic neuritis, stop taking the drug).
On the part of the endocrine system: often - hypothyroidism (weight gain, chilliness, apathy, decreased activity, drowsiness, excessive, in comparison with the expected action of amiodarone, bradycardia). The diagnosis is confirmed by the detection of an elevated serum TSH level (using a supersensitive TSH assay);normalization of thyroid function is usually observed within 1-3 months after discontinuation of treatment; in life-threatening situations, amiodarone treatment can be continued with simultaneous additional administration of L-thyroxin under the control of serum TSH levels.
Hyperthyroidism, sometimes fatal, also occurs often during and after treatment (cases of hyperthyroidism that developed several months after amiodarone withdrawal were described). Hyperthyroidism proceeds more secretively with a small number of symptoms: a slight unexplained weight loss, a decrease in antiarrhythmic and / or antianginal efficacy; mental disorders in elderly patients or even the phenomenon of thyrotoxicosis. The diagnosis is confirmed by the detection of a reduced level of serum TSH (using a supersensitive TSH assay). If hyperthyroidism is detected, amiodarone should be withdrawn. Normalization of thyroid function usually occurs within a few months after drug withdrawal. In this case, the clinical symptoms are normalized earlier (3-4 weeks) than normalization of the level of thyroid hormones.Severe cases can lead to death, so in such cases, urgent medical intervention is required. Treatment in each case is selected individually. If the patient's condition worsens both because of thyrotoxicosis itself and because of the dangerous imbalance between myocardial oxygen demand and delivery, it is recommended that treatment be started immediately: the use of antithyroid drugs (which may not always be effective in this case), treatment with GCS ( 1 mg / kg), which lasts long enough (3 months), beta-blockers.
Very rarely - syndrome of ADH secretion.
From the skin and subcutaneous tissues: very often - photosensitivity; often (in the case of prolonged use of the drug in high daily doses) - grayish or bluish skin pigmentation (after the cessation of treatment, this pigmentation slowly disappears); very rarely - erythema (during radiotherapy), skin rash (usually mildly specific), alopecia, exfoliative dermatitis, alopecia; frequency unknown - hives.
From the nervous system: often - tremor or other extrapyramidal symptoms, sleep disorders, nightmares; infrequently - sensorimotor peripheral neuropathies and / or myopathy (usually reversible within a few months after drug withdrawal, but sometimes not completely); very rarely - cerebellar ataxia, benign intracranial hypertension (pseudotumor of the brain), headache.
From the genitals and the breast: very rarely - epididymitis, impotence.
From the hemopoietic system: very rarely - thrombocytopenia, hemolytic anemia, aplastic anemia.
Allergic reactions: the frequency is unknown - angioedema (Quincke's edema).
Laboratory and instrumental data: it is very rare to increase the concentration of serum creatinine.
General disorders: the frequency is unknown - the formation of granulomas, including bone marrow granuloma.
- SSSU (sinus bradycardia, sinoatrial blockade), except for cases of their correction by an artificial pacemaker (danger of "stopping" the sinus node);
- AV blockade II and III degree in the absence of an artificial pacemaker (pacemaker);
- interstitial lung disease;
- dysfunction of the thyroid gland (hypothyroidism, hyperthyroidism);
- congenital or acquired lengthening of the QT interval;
- combination with drugs that can prolong the QT interval and cause the development of paroxysmal tachycardias, including ventricular torsade de pointes: antiarrhythmic drugs of class IA (quinidine, hydroquinidine, disopyramide, procainamide); antiarrhythmic drugs of class III (dofetilide, ibutilid, brethilia tosilate);sotalol; other (non-antiarrhythmic) drugs, such as beprideal; vincamine; phenothiazines some neuroleptics (chlorpromazine, tsiamemazin, levomepromazine, thioridazine, trifluoperazine, fluphenazine), benzamides (amisulpride, sultopride, sulpiride, tiapride, veraliprid), butyrophenones (droperidol, haloperidol), sertindole, pimozide; cisapride; tricyclic antidepressants; macrolide antibiotics group (particularly erythromycin at / in the introduction, spiramycin); azoles; antimalarials (quinine, chloroquine, mefloquine, halofantrine); Pentamidine when administered parenterally; difemanila methyl sulfate; mizolastine; astemizole, terfenadine, fluoroquinolones;
- age under 18 years (efficiency and safety not established);
- lactation period;
- lactose intolerance (lactase deficiency) syndrome glucose-galactose malabsorption (formulation contains lactose);
- hypersensitivity to iodine, amiodarone or adjuvant formulation.
With caution should be used with decompensated or chronic severe (III-IV functional class NYNA classification), heart failure, liver failure, asthma, severe respiratory failure in elderly patients (high risk of severe bradycardia), with AV-blockade of I degree .
PREGNANCY AND LACTATION
Currently available clinical data is insufficient to determine the possibility or impossibility of the occurrence of malformations in the embryo in the application of amiodarone in the I trimester of pregnancy.
Since the fetal thyroid gland begins to bind iodine with only 14 weeks of pregnancy (amenorrhea), it is not expected to impact on it of amiodarone in the case of his earlier application. Excess iodine when using the drug after this period may cause symptoms of hypothyroidism laboratory newborn or even to form it clinically significant goiter.
In view of the impact of the drug on the fetal thyroid, amiodarone is contraindicated during pregnancy, except in special cases when the expected benefits outweigh the risks (with life-threatening ventricular arrhythmias).
Amiodarone is released in breast milk in significant amounts, so it is contraindicated during lactation (in this period, the drug should be discontinued or stop breastfeeding).
APPLICATION FOR FUNCTIONS OF THE LIVER
Slight excretion of the drug in urine allows you to assign the drug in renal failure in high doses. Amiodarone and its metabolites do not undergo dialysis.
APPLICATION FOR VIOLATIONS OF THE FUNCTION OF KIDNEYS
Use with caution in liver failure.
APPLICATION FOR CHILDREN
Contraindications: childhood and adolescence to 18 years (effectiveness and safety have been established).
APPLICATION IN ELDERLY PATIENTS
With caution should be used in elderly patients (high risk of severe bradycardia).
Because side effects of amiodarone are dose-dependent, it is necessary to treat patients minimally effective dose to minimize the possibility of their occurrence.
Patients should be warned that they are at the time of treatment to avoid exposure to direct sunlight or take protective measures (for example, the use of sunscreen, wearing appropriate clothing).
Before taking amiodarone is recommended to perform a study ECG and determining the content of potassium in the blood. Hypokalemia should be adjusted prior to use of amiodarone. During treatment, the ECG must be checked regularly (every 3 months) and transaminase activity and other indicators of liver function.
Additionally due to the fact that amiodarone can cause hypothyroidism or hyperthyroidism, especially in patients with thyroid diseases in history, before taking amiodarone should conduct the clinical and laboratory (TSH concentration in the serum, determined by ultrasensitive assay for TSH) screening for identify functional disorders and thyroid disease. During amiodarone therapy and for several months following termination of the patient should be evaluated regularly in order to identify clinical or laboratory signs of thyroid function changes. For suspected thyroid dysfunction necessary to determination of TSH concentration in the serum (using ultrasensitive assay for TSH).
In patients receiving long-term treatment for arrhythmia, cases have been reported to increase the frequency of ventricular defibrillation and / or increasing the threshold triggering a pacemaker or implanted defibrillator, which may reduce the effectiveness of these devices. Therefore, before starting or during treatment with amiodarone should regularly check the correctness of their functioning.
Regardless of whether or not during treatment with amiodarone pulmonary symptoms is recommended every 6 months X-ray examination of the lungs and pulmonary function tests.
The appearance of dyspnea or dry cough, both isolated and accompanied by a deterioration of the general condition (fatigue, weight loss, fever) may indicate pulmonary toxicity, such as interstitial pneumonitis, suspected that the development requires a radiographic lung studies and conducting pulmonary function samples.
Because prolongation of repolarization of the ventricles of the heart, the pharmacological effect of the drug Kordaron В® causes certain changes in ECG intervals QT prolongation, QT c (korregirovat) may cause waves U. permissible increase QT interval withnot more than 450 ms or no more than 25% of the initial value. These changes are not a manifestation of the toxic effect of the drug, however, require monitoring and dose adjustment for evaluation of possible actions proaritmogennoe Kordaron preparation В® .
With the development of AV-blockade II and III degree sinoatrial block or two-beam intraventricular blockade treatment should be discontinued. When an AV-I blockade degree should enhance observation.
Although the noted occurrence of arrhythmia or exacerbation of existing arrhythmias, sometimes fatal, proaritmogennoe effect of amiodarone is weakly expressed (less pronounced than most antiarrhythmic drugs), and usually manifests itself in the context of the factors which increase the duration of the interval QT, such as interaction with other drugs and / or in violation of electrolytes in blood. Although amiodarone ability to increase the duration of the interval QT, it has shown low activity in respect of provoking ventricular tachycardia type "pirouette".
If blurred vision or decreased visual acuity is an urgent need to conduct an eye examination, including fundus examination. With the development of neuropathy or optic neuritis caused by amiodarone, a drug should be abolished because of the risk of blindness.
Since Kordaron В®contains iodine, it may interfere with the reception of the absorption of radioactive iodine and distort the results of radioisotope studies of the thyroid gland, but the drug does not affect the accuracy of the determination of the content of T3, T4 and TSH levels in the blood plasma. Amiodarone inhibits the peripheral conversion of thyroxine (T4) into triiodothyronine (T3) and can cause isolated biochemical changes (increase in free T4 concentration in serum at slightly reduced or even normal concentration of free T3 in serum) in clinically euthyroid patients that does not cause to cancel amiodarone.
Development hypothyroidism can be suspected following the appearance of clinical signs, usually weakly expressed: weight gain, intolerance to cold, reduced activity, excessive bradycardia.
Before surgery should inform the anesthetist that the patient is taking Cordarone В® .
Prolonged treatment with Kordaron В® can enhance hemodynamic risk inherent local or general anesthesia. In particular it relates to its bradycardic and hypotensive effects, reduction in cardiac output and conduction disturbances.
Moreover, in patients taking Kordaron В® , in rare cases directly after surgery noted acute respiratory distress syndrome. When mechanical ventilation such patients require careful monitoring.
Recommended careful monitoring of liver function tests (determination of the activity of transaminases) before ingestion Kordaron В® and regularly during drug treatment. Before the drug Kordaron В® possible acute liver disorders (including hepatocellular insufficiency or hepatic failure, sometimes fatal) and chronic liver disease. Therefore, treatment must be discontinued amiodarone with increasing transaminase activity, 3 times the ULN.
Clinical and laboratory signs of chronic liver failure in receiving amiodarone administration can be minimally expressed (hepatomegaly, increased transaminases, 5 times the ULN) and reversible upon discontinuation of the drug, however, reported cases of death in lesions of the liver.
Impact on the ability to drive vehicles and manage mechanisms
Based on safety data, there is no evidence that amiodarone impairs the ability to drive vehicles or to engage in other potentially hazardous activities. However, as a precaution, patients with severe paroxysmal rhythm disturbance during treatment with Cordarone В® is desirable to refrain from driving and classes of potentially hazardous activities that require high concentration and psychomotor speed reactions.
Symptoms: The ingestion of very high doses described several cases of sinus bradycardia, heart failure, attacks of ventricular tachycardia, paroxysmal ventricular tachycardia type "pirouette" and liver damage. May slow AV-conduction, increasing the already existing heart failure.
Treatment: gastric lavage, administration of activated carbon, if the drug has recently accepted, in other cases, symptomatic therapy: bradycardia - beta adrenostimulyatorov or installation pacemaker with ventricular tachycardia type "pirouette" - in / or administration of the magnesium salt pacing.
Neither amiodarone nor its metabolites are not removed by hemodialysis. There is no specific antidote.
Drugs that can cause bidirectional ventricular tachycardia type "pirouette" or prolong the QT interval
drugs that can cause ventricular tachycardia type "pirouette"
Combination drug therapy which can induce ventricular tachycardia type "pirouette" contraindicated because It increases the risk of potentially lethal ventricular tachycardia type "pirouette". These include:
- antiarrhythmics: Class IA (quinidine, gidrohinidin, disopyramide, procainamide), sotalol, bepridil;
- others (not antiarrhythmic) drugs, such as vincamine; some neuroleptics: phenothiazines (Chlorpromazine, tsiamemazin, levomepromazine, thioridazine, trifluoperazine, fluphenazine), benzamides (amisulpride, sultopride, sulprid, tiapride, veraliprid), butyrophenones (droperidol, haloperidol), sertindole, pimozide; tricyclic antidepressants; cisapride; macrolide antibiotics (erythromycin at / in the introduction, spiramycin); azoles; antimalarials (quinine, chloroquine, mefloquine, halofantrine, Lumefantrine); Pentamidine when administered parenterally; difemanila methyl sulfate; mizolastine; astemizole; terfenadine.
Drugs that can prolong the QT interval
Co-administration of amiodarone with drugs capable of increasing the duration of the interval QT, should be based on a careful assessment of each patient's ratio of expected benefits and potential risks (the possibility of increasing the risk of ventricular tachycardia type "pirouette"), with the use of such combinations is necessary to continuously monitor the patient's ECG (for identifying lengthening QT interval), potassium and magnesium contents in the blood.
In patients taking amiodarone, should avoid the use of fluoroquinolones, including moxifloxacin.
Drugs that slows the heart rate or causing automaticity or conduction disorders
Combination therapy with these drugs is not recommended.
Beta-blockers, calcium channel blockers slow, reduce heart rate (verapamil, diltiazem) may cause disturbances automatism (development of excessive bradycardia) and conductivity.
Drugs that can cause hypokalemia
- with laxatives, stimulating peristalsis, which can cause hypokalemia, which increases the risk of ventricular tachycardia type "pirouette". When combined with amiodarone should be used laxatives other groups.
Combinations requiring caution when applying
- diuretics causing hypokalemia (in monotherapy or in combination with other drugs);
- with systemic corticosteroids (glucocorticoids, mineralocorticoids) tetrakozaktidom;
- with amphotericin B (/ introduction).
It is necessary to prevent the development of hypoglycemia, and in case of occurrence of restoring to the normal level of potassium in the blood, to control the concentration of electrolytes in blood and ECG (for possible lengthening QT interval), and in case of ventricular tachycardia type "pirouette" should not apply antiarrhythmics (, possibly in / introduction magnesium salts ventricular pacing should be started).
Preparations for inhalation anesthesia
has been reported that the development of these severe complications in patients taking amiodarone, during their general anesthesia: bradycardia (refractory to atropine), lower blood pressure, conduction disturbances, reduced cardiac output.
There were very rare cases of serious complications from the respiratory system, sometimes fatal (acute adult respiratory distress syndrome, which developed immediately after surgery, and the occurrence of which is associated with high concentrations of oxygen).
Drugs that slows the heart rate (clonidine, guanfacine, cholinesterase inhibitors (donepezil, galantamine, rivastigmine, tacrine, ambenonium chloride, pyridostigmine, neostigmine bromide), pilocarpine
risk of excessive bradycardia (cumulative effects).
The effect of amiodarone on other drugs
Amiodarone and / or its metabolite dezetilamiodaron inhibit isozymes CYP1A1, CYP1A2, CYP3A4, CYP2C9, CYP2D6 and P-glycoprotein may increase the systemic exposure of drugs which are their substrates. Due to the long T 1/2 amiodarone this interaction can be observed even after a few months after stopping its administration.
Drugs that are substrates of P-gp
Amiodarone is an inhibitor of P-gp. That it will co-administration with drugs that are substrates of P-gp, will lead to increased systemic exposure of the latter.
Cardiac glycosides (digitalis preparations)
The potential for violations