Strofantin-K - instructions for use, dose, side effects, contraindications

Clinical and pharmacological group: & nbsp

Cardiac glycosides and non-glycosidic cardiotonic agents

Included in the formulation

Strofantin® K

solution w / m in / in

GALICHFARM, PAO Ukraine

АТХ:

C.01.A Cardiac glycosides

Pharmacodynamics:

Strofantin K is a short-acting cardiac glycoside blocking the transport Na + / K + -ATPase, as a result, the content of sodium ions in cardiomyocytes increases, which leads to the opening of calcium channels and the entry of calcium ions into cardiomyocytes. Increases the strength and rate of contraction of the myocardium, which occurs by a mechanism different from the Frank-Starling mechanism, and does not depend on the degree of preliminary stretching of the myocardium; The systole becomes shorter and energy-efficient. As a result of increased myocardial contractility, the shock and minute volume of blood increases.

Reduces the end-systolic volume and the end-diastolic volume of the heart, which, along with an increase in the tone of the myocardium, leads to a reduction in its size, and so on. to a decrease in myocardial oxygen demand.

The negative dromotropic effect is manifested in the increased refractoriness of the atrioventricular node, which allows the drug to be used in paroxysms of supraventricular tachycardia and tachyarrhythmias. At ciliary tachyarrhythmia slows heart rate, lengthen diastole, improving intracardiac and systemic hemodynamics.Decrease in heart rate occurs as a result of direct and indirect effects on the regulation of the heart rhythm. Has a direct vasoconstrictive effect (in the event that the positive inotropic effect of cardiac glycosides is not realized - in patients with normal contractility or with excessive stretching of the heart); in patients with chronic heart failure causes mediated vasodilating effect, reduces venous pressure, increases diuresis: reduces edema, dyspnea. Positive batmotropic effect is manifested in sub-toxic and toxic doses. Has an insignificant degree of negative chronotropic action. With intravenous administration (IV), the effect begins 10 minutes and reaches a maximum after 15-30 minutes.

Pharmacokinetics:

There is practically no cumulative effect.

The distribution is relatively uniform; a little more concentrated in the tissues of the adrenal glands, pancreas, liver, kidneys. In the myocardium, 1% of the drug is found. Connection with blood plasma proteins - 5%.

It is not subjected to biotransformation, it is excreted by the kidneys unchanged.For 24 hours 85-90% of the drug is excreted; the concentration in the blood plasma decreases by 50% after 8 hours; completely excreted from the body after 1-3 days.

Indications:

- in the complex therapy of acute and chronic heart failure of the second functional class (in the presence of clinical manifestations), III-IV functional class according to the NYHA classification;

- tahisystolic form of flicker and atrial flutter of paroxysmal and chronic course (especially in combination with chronic heart failure).

ICD-10

IX.I30-I52.I48 Atrial fibrillation and flutter

IX.I30-I52.I50.0 Congestive heart failure

IX.I30-I52.I50.1 Left ventricular failure

Contraindications:

Hypersensitivity, glycosidic intoxication.

Carefully:

Bradycardia, AV blockade and sinus node weakness syndrome without pacemaker, paroxysmal ventricular tachycardia, hypertrophic obstructive cardiomyopathy, isolated mitral stenosis, acute myocardial infarction, unstable angina, WPW syndrome, chronic heart failure with diastolic dysfunction (restrictive cardiomyopathy, amyloidosis of the heart,constipative pericarditis, cardiac tamponade), extrasystole, cardiac asthma in patients with mitral stenosis (in the absence of tachysystolic form of atrial fibrillation), marked dilatation of the heart cavities, "pulmonary" heart. Electrolyte disorders (condition after dialysis, diarrhea, diuretics or other means that cause electrolyte disturbances, malnutrition, prolonged vomiting, etc.): hypokalemia, hypomagnesemia, hypercalcemia, hypocalcemia. Hypothyroidism, alkalosis, myocarditis, obesity, old age, arteriovenous shunt, hypoxia, chronic renal failure.

Pregnancy and lactation:

Application during pregnancy and during breastfeeding is contraindicated.

The category of FDA recommendations is not defined.

Dosing and Administration:

Strofantin K is used intravenously, intramuscularly, only in urgent situations when it is impossible to apply cardiac glycosides inside. For intravenous administration, a 0.025% solution of the drug is used. It is bred in 10-20 ml of a 5% solution of dextrose (glucose) or 0.9% sodium chloride solution. The introduction is slow, for 5 to 6 minutes (because a rapid injection can cause shock).Solution strofantina K can be administered and drip (in 100 ml of a 5% solution of dextrose (glucose) or 0.9% sodium chloride solution), because with this form of administration less toxic effect develops.

Higher doses of strophanthin K for adults are intravenous: single - 2 ml (2 ampoules), daily - 4 ml (4 ampoules).

If intravenous injection is not possible, the drug is administered intramuscularly. To reduce the sharp painfulness with intramuscular injection, 5 ml of a 2% solution of procaine are preliminarily injected, and then through the same needle - the required dose of strophanthin K diluted in 1 ml of a 2% solution of procaine. When administered intramuscularly, the doses increase 1.5 times.

Side effects:

From the digestive tract: a decrease in appetite, nausea, vomiting, diarrhea.

From the cardiovascular system: bradycardia, extrasystole, atrioventricular block, ventricular paroxysmal tachycardia, ventricular fibrillation.

From the side of the central nervous system: headache, dizziness, sleep disorders, fatigue, impaired color perception, depression, drowsiness, psychosis, confusion.

Other: allergic reactions, urticaria, petechiae, thrombocytopenia, thrombocytopenic purpura, nosebleeds, gynecomastia. With intramuscular route of administration, soreness at the site of administration.

Overdose:

Symptoms:

From the cardiovascular system: arrhythmias, including bradycardia, atrioventricular block, ventricular paroxysmal tachycardia, ventricular fibrillation, ventricular extrasystole (bigemia, polytopic), nodular tachycardia, sinoatrial blockade, flicker and atrial flutter.

From the digestive tract: anorexia, nausea, vomiting, diarrhea.

From the side of the central nervous system and sensory organs: headache, fatigue, dizziness, rarely - dyeing of surrounding objects in green and yellow colors, the sensation of flickering flies before the eyes, reduced visual acuity, scotoma, macro and micropsia; very rarely, confusion, syncopal states.

Treatment: withdrawal of the drug or reduction of subsequent doses and increasing the time intervals between drug administration, administration of antidotes (sodium dimercaptopropanesulfonate), symptomatic therapy (antiarrhythmic drugs - lidocaine, phenytoin, amiodarone; preparations of potassium; m-holinoblokatory - atropine sulfate). As antiarrhythmic drugs - preparations of I class (lidocaine, phenytoin). With hypokalemia - IV injection of potassium chloride (6-8 g / day at the rate of 1-1.5 g per 0.5 L of a 5% solution of dextrose (glucose) and 6-8 units of insulin, injected drip, for 3 hours).With severe bradycardia, atrioventricular blockade - m-holinoblokatory. Beta-adrenomimetics is dangerous because of the possible increase in the arrhythmogenic effect of cardiac glycosides. With a full transverse blockade with attacks of Morgagni-Adams-Stokes temporary pacing is shown.

Interaction:

When strophanthin K is used together with barbiturates (phenobarbital and others), the cardiotonic effect of glycoside decreases. Simultaneous use of strophanthin K with sympathomimetics, methylxanthines, reserpine and tricyclic antidepressants increases the risk of arrhythmias. The concentration of strophanthin K in the blood plasma increases with simultaneous use of quinidine, methyldopa, amiodarone, captopril, calcium antagonists, erythromycin and tetracycline. Against the background of magnesium sulfate, the possibility of slowing the conduction and occurrence of atrioventricular blockade of the heart increases. Diuretics (mostly thiazide and inhibitors of carbonic anhydrase), corticotropin (adrenocorticotropic hormone) preparation, glucocorticosteroids, insulin, calcium preparations, laxatives, carbenoxolone, amphotericin B, benzylpenicillin, salicylates increase the risk of developing glycosidic intoxication. Beta-adrenoblockers, antiarrhythmics, verapamil can not only increase the severity of decreasing atrioventricular conduction (negative dromotropic action), but also potentiate the negative chronotropic effect of strophanthin K (decreasing heart rate). Inductors of microsomal liver enzymes (phenytoin, rifampicin, phenobarbital, phenylbutazone), and neomycin and cytostatic agents reduce the concentration of strophanthin K in the blood plasma. Glycoside intoxication can be caused by the development of hypokalemia, the inhibitor of carbonic anhydrase, mineralocorticoids, so when used simultaneously with cardiac glycosides, it is required to regularly determine the potassium content in the blood plasma. Drugs of potassium salts can not be used if under the influence of cardiac glycosides there are conduction disorders on the electrocardiogram, however, potassium salts are often prescribed together with digitalis preparations to prevent cardiac rhythm disturbances.

Anticholinesterase drugs increase bradycardia with simultaneous use with cardiac glycosides;edetic acid reduces the efficacy and toxicity of cardiac glycosides; should not be used in conjunction with cardiac glycosides trifosadenine; hypervitaminosis, caused by vitamin D, increases the action of cardiac glycosides due to the development of hypercalcemia; there is evidence of a decrease in kidney secretion of cardiac glycosides under the influence of paracetamol. Glucocorticosteroids and diuretics increase the risk of hypokalemia and hypomagnesemia, angiotensin converting enzyme inhibitors and angiotensin II receptor blockers - reduce.

Special instructions:

ECG monitoring.

- Distinguishing characteristics.

Cardiac glycoside of low lipophilicity, is unstable, inefficient at ingestion, slightly cumulates.

With rapid on / in the introduction of possible bradyarrhythmia, ventricular tachycardia, AV blockade and cardiac arrest. At the peak of the effect, extrasystoles may appear, sometimes in the form of bigeminy. To prevent this effect, the dose can be divided into 2-3 IV injections or one of the doses administered in / m. If the patient has previously been assigned other cardiac glycosides, it is necessary to make an interruption (5-24 days - depending on their cumulative properties) before / in the introduction of strophanthin-K.

Instructions

Strophantine-K (Strophanthinum K)