Corglikard, 10 pcs., 1 ml, 0.6 mg/ml, solution for intravenous administration
Adrenergic agonists.
The combined use of ephedrine hydrochloride, epinephrine hydrochloride or norepinephrine hydrotartrate, as well as selective beta-adrenergic agonists with cardiac glycosides may contribute to the occurrence of cardiac arrhythmia.
Aminazine and other phenothiazine derivatives
.
The effect of cardiac glycosides decreases.
Anticholinesterase drugs.
With simultaneous use of anticholinesterase drugs with cardiac glycosides, bradycardia increases. If necessary, it can be eliminated or weakened by the introduction of atropine sulfate.
Glucocorticosteroids.
If hypokalemia occurs as a result of prolonged treatment with glucocorticosteroids, the undesirable effects of cardiac glycosides may increase.
Diuretics.
When diuretics (which cause hypokalemia and hypomagnesemia, but increase the concentration of calcium ions in the blood) are combined with cardiac glycosides, the effect of the latter is enhanced. When using them simultaneously, you must adhere to the optimal dosage. You can periodically prescribe potassium-sparing diuretics (spironolactone, triamterene), which eliminate hypokalemia. However, hyponatremia may develop.
Potassium preparations.
Under the influence of potassium supplements/undesirable effects of cardiac/glycosides are reduced.
Calcium preparations.
When treating with cardiac glycosides, parenteral use of calcium preparations is dangerous, since the cardiotoxic effects (cardiac arrhythmias, etc.) are enhanced.
Ethylenediaminetetraacetic acid
,
disodium salt
.
There is a decrease in the effectiveness and toxicity of cardiac glycosides.
Drugs, corticotropin.
The effect of cardiac glycosides under the influence of corticotropin may be enhanced.
Xanthine derivatives.
Caffeine or theophylline drugs sometimes contribute to cardiac arrhythmias.
Sodium adenosine triphosphate.
Sodium adenosine triphosphate should not be prescribed simultaneously with cardiac glycosides.
Ergocalciferol.
With hypervitaminosis caused by ergocalciferol, the effect of cardiac glycosides may be enhanced due to the development of hypercalcemia.
Narcotic analgesics.
The combination of fentanyl and cardiac glycosides may cause hypotension.
Naproxen.
In healthy people, the combined use of cardiac glycosides with naproxen does not affect the results of psychological testing.
Paracetamol.
The clinical significance of this interaction has not been sufficiently studied, but there is evidence of a decrease in the excretion of cardiac glycosides by the kidneys under the influence of paracetamol.
Korglykard (Korglikon) solution IV 0.6 mg cor 1 ml x10
Trade name: Corglycard International name: Lily of the valley herb glycoside (Convallariae glycoside)
Release form: solution for intravenous administration 0.6 mg/ml (ampoules) 1 ml
Ingredients: lily of the valley leaf glycoside 0.6 mg - 1 ml
Pharmacological group: cardiotonic drug-cardiac glycoside
Pharmacological group according to ATK: C01AX (Other cardiac glycosides)
Pharmacological action: antiarrhythmic, diuretic, cardiotonic, cardiac glycoside,
Indications: Atrial fibrillation, atrial flutter (to reduce heart rate or convert atrial flutter into fibrillation with a controlled frequency of impulses through the AV node), paroxysmal supraventricular tachycardia, CHF, acute LV failure, chronic “pulmonary” heart disease.
Dosage regimen: IV slowly (over 4-5 minutes), 0.5-1 ml of 0.06% solution, 2 times a day (children 2-5 years old - 0.2-0.5 ml, 6-12 years old - 0.5-0.75 ml ), before use, dilute in 10 or 20 ml of 40% dextrose solution or 0.9% NaCl solution. The highest single dose for intravenous administration is 1 ml, daily dose is 2 ml.
Contraindications: Hypersensitivity, glycoside intoxication.
Side effects: Digitalis intoxication - decreased appetite, nausea, vomiting, diarrhea, arrhythmias, AV block, drowsiness, confusion, delirious psychosis, decreased visual acuity, thrombocytopenia, allergic reactions, thrombocytopenic purpura, nosebleeds, petechiae, gynecomastia, sleep disturbances, headache, dizziness. Intoxication: ventricular paroxysmal tachycardia, ventricular extrasystole (often polytopic or bigeminy), nodal tachycardia, SA block, atrial fibrillation and flutter, AV block, decreased appetite, vomiting, diarrhea, abdominal pain, intestinal necrosis, yellow-green coloring of visible objects color, flashing “fly spots” before the eyes, decreased visual acuity, perception of objects in a reduced or enlarged form, neuritis, radiculitis, manic-depressive syndrome, paresthesia. Overdose. Treatment: withdrawal of cardiac glycosides, administration of antidotes (unithiol, EDTA), symptomatic therapy. Class I drugs (lidocaine, phenytoin) are used as antiarrhythmic drugs. For hypokalemia - intravenous administration of KCl (6-8 g/day at the rate of 1-1.5 g per 0.5 l of 5% dextrose solution and 6-8 units of insulin, administered by drip over 3 hours). For severe bradycardia and AV block, use m-cholinergic blockers. It is dangerous to administer beta-agonists due to the possible enhancement of the arrhythmogenic effect of cardiac glycosides. In case of complete transverse block with Morgagni-Adams-Stokes attacks - temporary cardiac pacing.
Pharmacodynamics: Cardiac glycoside blocks the transport Na+/K+-ATPase, as a result, the Na+ content in the cardiomyocyte increases, which leads to the opening of Ca2+ channels and the entry of Ca2+ into the cardiomyocytes. Excess Na+ leads to an acceleration of the release of Ca2+ from the sarcoplasmic reticulum, i.e. the Ca2+ concentration increases, which leads to inhibition of the troponin complex, which has an inhibitory effect on the interaction between actin and myosin. Increases the force and speed of myocardial contraction (positive inotropic effect), which occurs by a mechanism different from the Frank-Starling mechanism, and does not depend on the degree of preliminary stretching of the myocardium, systole becomes shorter and energy-efficient. As a result of increased myocardial contractility, SV and IOC increase. The ESR and EDV of the heart decrease, which, along with an increase in myocardial tone, leads to a reduction in its size, etc. to reduce myocardial oxygen demand. The negative dromotropic effect manifests itself in increased refractoriness of the AV node. With atrial fibrillation, cardiac glycosides slow heart rate, lengthen diastole, improving intracardiac and systemic hemodynamics. The negative chronotropic effect (decrease in heart rate) occurs as a result of direct and indirect effects on the regulation of heart rate. It has a direct vasoconstrictor 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 CHF it causes an indirect vasodilating effect, reduces venous pressure, increases diuresis: reduces swelling, shortness of breath . Positive bathmotropic effect is manifested in subtoxic and toxic doses. When administered intravenously, the effect begins within 10 minutes and reaches a maximum after 2 hours.
Special instructions: The likelihood of intoxication increases with hypokalemia, hypomagnesemia, hypercalcemia, hypernatremia, hypothyroidism, severe dilatation of the heart cavities, cor pulmonale, myocarditis, obesity, and old age. With severe mitral stenosis and normo- or bradycardia, HF develops due to a decrease in LV diastolic filling. Strophanthin, increasing the contractility of the right ventricular myocardium, causes a further increase in pressure in the pulmonary artery system, which can provoke pulmonary edema or aggravate LV failure. For patients with mitral stenosis, cardiac glycosides are prescribed when right ventricular failure occurs or in the presence of atrial fibrillation. Korglykon in WPW syndrome, reducing AV conductivity, promotes the conduction of impulses through accessory pathways - bypassing the AV node, provoking the development of paroxysmal tachycardia. As one of the methods for monitoring the level of digitalization when prescribing cardiac glycosides, monitoring their plasma concentration is used. Carefully. Bradycardia, AV block and CVS without a pacemaker, paroxysmal ventricular tachycardia, HOCM, isolated mitral stenosis, acute myocardial infarction, unstable angina, WPW syndrome, CHF with impaired diastolic function (restrictive cardiomyopathy, cardiac amyloidosis, constrictive pericarditis, cardiac tamponade), extrasystole , cardiac asthma in patients with mitral stenosis (in the absence of the tachysystolic form of atrial fibrillation), severe dilatation of the heart cavities, “pulmonary” heart. Electrolyte disturbances (condition after dialysis, diarrhea, taking diuretics or other drugs that cause electrolyte disturbances, malnutrition, prolonged vomiting, etc.): hypokalemia, hypomagnesemia, hypercalcemia, hypocalcemia. Hypothyroidism, alkalosis, myocarditis, obesity, old age, arteriovenous shunt, hypoxia, chronic renal failure.
Interaction: Beta-blockers, verapamil increase the severity of the decrease in AV conductivity. Quinidine, dopegyt, clonidine, veroshpiron, cordarone, verapamil increase the concentration in the blood due to a competitive decrease in secretion by the proximal tubules of the kidneys. GCS, diuretics increase the risk of developing hypokalemia, hypomagnesemia, thiazides and Ca2+ salts (especially with intravenous administration) - hypercalcemia, cordarone, Mercazolil, Diacarb - hypothyroidism. Ca2+ salts, catecholamines and diuretics increase the risk of developing glycoside intoxication.
Drug registration number: P No. 016062/01
Date of registration (re-registration) of the drug: 08/04/2006
Corglycard
Adrenergic agonists.
The combined use of ephedrine hydrochloride, epinephrine hydrochloride or norepinephrine hydrotartrate, as well as selective beta-agonists with cardiac glycosides may contribute to the occurrence of cardiac arrhythmia.
Aminazine and other phenothiazine derivatives.
The effect of cardiac glycosides decreases.
Anticholinesterase drugs.
With simultaneous use of anticholinesterase drugs with cardiac glycosides, bradycardia increases. If necessary, it can be eliminated or weakened by the introduction of atropine sulfate.
Glucocorticosteroids.
If hypokalemia occurs as a result of prolonged treatment with glucocorticosteroids, the undesirable effects of cardiac glycosides may increase.
Diuretics.
When diuretics (which cause hypokalemia and hypomagnesemia, but increase the concentration of calcium ions in the blood) are combined with cardiac glycosides, the effect of the latter is enhanced. When using them simultaneously, you must adhere to the optimal dosage. You can periodically prescribe potassium-sparing diuretics (spironolactone, triamterene), which eliminate hypokalemia. However, hyponatremia may develop.
Potassium preparations.
Under the influence of potassium preparations, the undesirable effects of cardiac glycosides are reduced.
Calcium preparations.
When treating with cardiac glycosides, parenteral use of calcium preparations is dangerous, since the cardiotoxic effects (cardiac arrhythmias, etc.) are enhanced.
Ethylenediaminetetraacetic acid
disodium salt.
There is a decrease in the effectiveness and toxicity of cardiac glycosides.
preparations
.
The effect of cardiac glycosides under the influence of corticotropin may be enhanced.
Xanthine derivatives.
Caffeine or theophylline drugs sometimes contribute to cardiac arrhythmias.
Sodium adenosine triphosphate.
Sodium adenosine triphosphate should not be prescribed simultaneously with cardiac glycosides.
Ergocalciferol.
With hypervitaminosis caused by ergocalciferol, the effect of cardiac glycosides may be enhanced due to the development of hypercalcemia.
Narcotic analgesics.
The combination of fentanyl and cardiac glycosides may cause hypotension.
Naproxen.
In healthy people, the combined use of cardiac glycosides with naproxen does not affect the results of psychological testing.
Paracetamol.
The clinical significance of this interaction has not been sufficiently studied, but there is evidence of a decrease in the excretion of cardiac glycosides by the kidneys under the influence of paracetamol.
