Symptoms: ventricular paroxysmal tachycardia, ventricular extrasystole (often polytopic or bigeminia), nodal tachycardia, SA block, atrial flutter and flutter, AV block, decreased appetite, vomiting, diarrhea, abdominal pain, intestinal necrosis, perception of visual images in yellow — green color, flashing "flies" in front of the eyes, decreased visual acuity, perception of objects in a reduced or enlarged form, neuritis, sciatica, manic-depressive syndrome, paresthesia.
Treatment: withdrawal of cardiac glycosides, administration of antidotes (unitiol, EDTA), symptomatic therapy. As antiarrhythmic drugs-class I drugs (lidocaine, phenytoin). With hypokalemia-intravenous administration of potassium chloride (6-8 g/day at the rate of 1-1. 5 g per 0.5 liters of 5% dextrose solution and 6-8 units of insulin, administered drip, for 3 hours). In severe bradycardia, AV block — m-holinoblokatory. Beta-adrenostimulants are dangerous to administer because of the possible increase in the proarrhythmogenic effect of cardiac glycosides. With a complete transverse blockade with Morgagni-Adams-Stokes attacks, temporary pacing is performed.
hypersensitivity,
glycoside intoxication.
With caution: bradycardia, AV block and sinus node weakness syndrome (SSS) without an artificial pacemaker, paroxysmal ventricular tachycardia, hypertrophic obstructive cardiomyopathy (HOCMP), isolated mitral stenosis, acute myocardial infarction, unstable angina, WPW syndrome, chronic heart failure with impaired diastolic function (restrictive cardiomyopathy (CMP), amyloidosis of the heart, constrictive pericarditis, cardiac tamponade), extrasystole, cardiac asthma in patients with mitral stenosis (in the absence of tachysystolic form of atrial fibrillation), severe dilatation of the heart cavities, pulmonary heart. Electrolyte disorders (post-dialysis condition, diarrhea, taking diuretics or other drugs that cause electrolyte disorders, insufficient nutrition, prolonged vomiting): hypokalemia, hypomagnesemia, hypercalcemia, hypocalcemia. Hypothyroidism, alkalosis, myocarditis, obesity, old age, arteriovenous shunt, hypoxia
Beta-blockers, verapamil increase the severity of the decrease in AV conduction.
Quinidine, dopegit, clofelin, veroshpiron, cordarone, verapamil increase the concentration in the blood due to a competitive decrease in the secretion of the proximal tubules of the kidneys.
Corticosteroids, diuretics increase the risk of hypokalemia, hypomagnesemia, thiazides and Ca salts2 (especially when administered in / in) - hypercalcemia, cordarone, mercazolil, diacarb-hypothyroidism.
Ca Salts2 , catecholamines and diuretics increase the risk of glycoside intoxication.
Transparent colorless liquid with a bitter taste and the smell of chlorobutanol hydrate (preservative).
Cardiac glycosides 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 disorders, headache, dizziness.
The probability of intoxication increases with hypokalemia, hypomagnesemia, hypercalcemia, hypernatremia, hypothyroidism, severe dilatation of the heart cavities, myocarditis, obesity, and the elderly. With severe mitral stenosis and normal or bradycardia, heart failure develops due to a decrease in the diastolic filling of the left ventricle.
Korglikon, 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 exacerbate left ventricular failure.
In patients with mitral stenosis, cardiac glycosides are prescribed with the addition of right ventricular failure or in the presence of atrial tachyarrhythmia.
Corglycone in WPW syndrome, reducing AV conduction, promotes the conduction of impulses through additional pathways-bypassing the AV node, provoking the development of paroxysmal tachycardia.
As one of the methods of monitoring the level of digitalization in the appointment of cardiac glycosides, control of their plasma concentration is used.
atrial tachyarrhythmia,
atrial flutter (to reduce heart rate or convert atrial flutter to fibrillation with a controlled frequency of pulses through the AV node),
paroxysmal supraventricular tachycardia,
chronic heart failure,
acute left ventricular failure,
chronic pulmonary heart disease.
Cardiac glycoside, blocks the Na transport system /K -ATPase, resulting in the Na content in the cardiomyocyte increases, which leads to the opening of Ca2 - channels and incoming Ca2 into the cardiomyocytes. Excess Na results in faster Ca allocation2 from the sarcoplasmic reticulum, i.e. Ca concentration2 increases, which leads to the inhibition of the troponin complex, which has a depressing effect on the interaction of actin and myosin.
Increases the strength and speed of myocardial contraction (positive inotropic effect), by a mechanism different from the Frank-Starling mechanism, regardless of the degree of pre-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 (UOC and IOC). The final systolic and diastolic volume of the heart (CSR and BWW) decreases, which, along with an increase in myocardial tone, leads to a reduction in its size and t.about. to reduce the oxygen demand of the myocardium. The negative dromotropic effect is manifested in an increase in the refractoriness of the AV node. In atrial tachyarrhythmia, cardiac glycosides slow down the heart rate, lengthen the diastole, and improve intracardiac and systemic hemodynamics
The negative chronotropic effect (heart rate reduction) develops as a result of direct and indirect effects on the regulation of the heart rate. It has a direct vasoconstrictor effect (if 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 it causes an indirect vasodilating effect, reduces venous pressure, increases diuresis: reduces edema, shortness of breath.
The positive bathmotropic effect is manifested in subtoxic and toxic doses. With an intravenous injection, the action begins after 10 minutes and reaches a maximum after 2 hours.
In a dark place.
Keep out of reach of children.
Shelf life of the drug Korglikon® solution for injection 0.06%solution for intravenous administration of 0.06% — 3 years.
solution for intravenous administration of 0.6 mg / ml — 2 years.
Do not use after the expiration date indicated on the package.
Korglikon
Korglikon® solution for injection 0.06%
| Solution for intravenous administration | 1 ml |
| korglikon | 0.6 mg |
in ampoules of 1 ml (complete with an ampoule knife), in a contour cell package of 10 pcs.
Korglikon
Korglikon® solution for injection 0.06%
V/v slowly (for 4-5 minutes), 0.5–1 ml of 0.06% solution, 2 times a day (children 2-5 years — 0.2–0.5 ml, 6-12 years — 0.5–0.75 ml), before use, diluted in 10 or 20 ml of 40% dextrose solution or 0.9% sodium chloride solution. The highest single dose for intravenous administration is 1 ml, the daily dose is 2 ml.
C01AX Cardiac Glycosides other
