Digoxin Reneval, tablets 0.25 mg 56 pcs
€2.24 €1.87
Pharmacodynamics
Digoxin is a cardiac glycoside. It has a positive inotropic effect due to the direct inhibitory effect of sodium-potassium ATPase of cardiomyocyte membranes, which leads to an increase in intracellular sodium ions content and, consequently, a decrease in potassium ions.
Increased content of sodium ions causes activation of sodium-calcium metabolism, increased content of calcium ions, resulting in increased myocardial contractility. As a result of increased myocardial contractility, the stroke volume of blood increases. The final systolic and final diastolic volumes of the heart decrease, which, along with an increase in myocardial tone, leads to a reduction in myocardial size and thus reduces myocardial oxygen demand.
It has a negative chronotropic effect, reduces excessive sympathetic activity by increasing the sensitivity of cardiopulmonary baroreceptors. By increasing the activity of the vagus nerve, it has an antiarrhythmic effect due to the decrease in the rate of impulse conduction through the atrioventricular node and prolongation of the effective refractory period. This effect occurs as a result of mediated action on the atrioventricular node.
Negative dromotropic effect is manifested by increased refractoriness of the atrioventricular node, which determines the use in paroxysms of supraventricular tachycardia and tachyarrhythmias.
In atrial fibrillation it helps slow down the rate of ventricular contractions, prolongs diastole, improves intracardiac and systemic hemodynamics. The positive butotropic effect is manifested at subtoxic and toxic doses.
It has a direct vasoconstrictor effect, which is most clearly manifested in the absence of peripheral edema stasis. At the same time, the indirect vasodilatory effect (in response to an increase in the minute blood volume and reduction of excessive sympathetic stimulation of vascular tone) usually prevails over the direct vasoconstrictor effect, resulting in a decrease in total peripheral vascular resistance.
Pharmacokinetics
Absorption of digoxin from the gastrointestinal tract is variable, is 70-80% of the dose and depends on the motility of the gastrointestinal tract, drug form, concomitant ingestion, interaction with other drugs. Bioavailability is 60-80 %.
Under normal gastric acidity a small amount of digoxin is destroyed, under hyperacidic conditions more of it may be destroyed. For complete absorption sufficient intestinal exposure is required: with decreased motility of the gastrointestinal tract bioavailability is maximum, with increased peristalsis – minimum.
The ability of digoxin to accumulate in tissues (cumulate) explains the lack of correlation at the beginning of treatment between the severity of pharmacodynamic effect and its concentration in blood plasma. Binding with blood plasma proteins is 25%.
Apparent volume of distribution is 5 l/kg. It is metabolized in liver. It is excreted mainly by kidneys (60-80% unchanged), half-life is about 40 hours (determined by the kidney function). The intensity of renal excretion is determined by the value of glomerular filtration.
In mild chronic renal insufficiency decrease in renal excretion of digoxin is compensated by hepatic metabolism to inactive compounds. In hepatic insufficiency, compensation is due to increased renal excretion of digoxin.
Indications
Arrhythmia, Heart Failure As part of the complex therapy of chronic heart failure II (in the presence of clinical manifestations) and III-IV functional class according to the classification NYHA; tachysystolic form of atrial fibrillation and flutter paroxysmal and chronic course (especially in combination with chronic heart failure).
Active ingredient
Digoxin
Composition
Each tablet contains:
active ingredient:
digoxin – 0.25 mg
excipients:
potato starch – 6.25 mg
sucrose (sugar) – 15 mg
calcium stearate – 0.5 mg
dextrose monohydrate – 20 mg
lactose monohydrate (milk sugar) – 7.5 mg
talc – 0.5 mg
How to take, the dosage
Oral.
As for all cardiac glycosides, the dose should be chosen with caution, individually for each patient. If a patient has taken cardiac glycosides before the appointment of digoxin, in this case the dose of the drug should be reduced.
Adults and children over 10 years old – the dose of digoxin depends on the required speed of achieving therapeutic effect:
- Moderately fast digoxin (24-36 hours) used in emergency cases: daily dose of 0.75-1.25 mg divided into 2 doses, with ECG monitoring before each subsequent dose. After reaching saturation, switch to maintenance treatment;
- slow digitalization (5-7 days): a daily dose of 0.125-0.5 mg administered once daily for 5-7 days (until saturation is achieved), after which switch to maintenance treatment.
Interaction
When concomitant use of digoxin and drugs that cause electrolyte imbalance, in particular, hypokalemia (mineral and glucocorticosteroids, insulin, beta-adrenomimetics, amphotericin B, carboangiradase inhibitors, corticotropin, diuretics, promoting excretion of fluid and potassium (bumetanide, ethacrynic acid, furosemide, indapamide, mannitol and thiazide derivatives), sodium phosphate), the risk of arrhythmias and other toxic effects of digoxin increases, so continuous monitoring of blood potassium is required.
Special Instructions
Throughout the duration of treatment with digoxin, the patient should be under medical supervision in order to avoid side effects resulting from overdose.
The dose of digoxin should be reduced in patients with chronic pulmonary heart disease, coronary artery disease, water-electrolyte balance disorders, renal or hepatic failure.
In elderly patients also require careful dose selection, especially if they have one or more of the above conditions. It should be borne in mind that in these patients even with impaired renal function creatinine clearance values may be within normal limits due to a decrease in muscle mass and decreased creatinine synthesis.
Since in renal failure pharmacokinetic processes are impaired, the dose selection should be conducted under monitoring the blood serum digoxin concentration.
If this is not feasible, the following recommendations can be used: the dose should be reduced by approximately the same percentage as the creatinine clearance is reduced. If creatinine clearance has not been determined, it can be approximately calculated from the serum creatinine concentration (CSC) using the Cockcroft-Gault formula. For men: (140 – age [in years]) – weight [in kg] / (72 – BAC [mg/dL]). For women, the result obtained should be multiplied by 0.85.
In severe renal failure, the serum digoxin concentration should be determined every 2 weeks, at least during the initial period of treatment.
In idiopathic subaortic stenosis (left ventricular exit tract obstruction by asymmetrically hypertrophic interventricular septum), administration of digoxin leads to an increase in the severity of obstruction.
In severe mitral stenosis and normo- or bradycardia, heart failure develops due to decreased diastolic filling of the left ventricle. Digoxin, by increasing myocardial contractility of the right ventricle, causes a further increase in pressure in the pulmonary artery system, which may provoke pulmonary edema or exacerbate left ventricular failure.
Patients with mitral stenosis are prescribed cardiac glycosides if right ventricular insufficiency is present, or if atrial fibrillation is present.
In patients with atrioventricular block degree II the prescription of cardiac glycosides may worsen it and lead to Morgania-Adams-Stokes attack.
The prescription of cardiac glycosides for 1st degree atrioventricular block requires caution, regular ECG monitoring, and in some cases – pharmacological prophylaxis with agents that improve atrioventricular conduction.
Digoxin in Wolff-Parkinson-White syndrome, by slowing atrioventricular conduction, promotes impulses through additional conduction pathways to bypass the atrioventricular node and thereby provokes the development of paroxysmal tachycardia.
The likelihood of glycoside intoxication increases in hypokalemia, hypomagnesemia, hypercalcemia, hypernatriemia, hypothyroidism, marked cardiac cavity dilatation, “pulmonary” heart, myocarditis and in elderly patients.
Plasma concentration monitoring of cardiac glycosides is used as one of the methods to control digitalization when prescribing cardiac glycosides.
Allergic reactions to digoxin and other cardiac glycosides are rare. If hypersensitivity occurs to any one cardiac glycoside, other members of this group can be used, since cross-sensitivity to cardiac glycosides is not characteristic.
The patient must accurately follow the following instructions:
– use the drug only as prescribed, do not change the dose yourself;
– each day use the drug only at the prescribed time;
– if the heart rate is below 60 bpm.
– if the heart rate is below 60 bpm, you should immediately consult the physician;
– if the next dose is missed it should be taken as soon as possible and then continue the course according to the prescribed scheme.
– It is prohibited to increase or double the dose;
– If the patient did not take the drug for more than 2 days it is necessary to inform the physician;
– Before discontinuing the drug it is necessary to inform the doctor;
– In case of vomiting, nausea, diarrhea, increased pulse rate it is necessary to immediately contact a physician;
– Before surgical operations or in case of emergency it is necessary to inform the physician about the use of the drug;
– It is not advisable to use other medicinal products without the permission of the physician.
The ability to affect the reaction rate when driving motor transport or operating other mechanisms
Studies to assess the effect of digoxin on the ability to drive vehicles and operate mechanisms that require high concentration and speed of psychomotor reactions are insufficient, but caution should be exercised.
Contraindications
Hypersensitivity to drug components, glycoside intoxication, Wolf-Parkinson-White syndrome, grade II atrioventricular block, ventricular tachycardia and ventricular fibrillation, intermittent complete block, children under 3 years of age; patients with rare hereditary diseases: Lactose intolerance, fructose intolerance, lactase, sucrose/isomaltase deficiency or glucose-galactose malabsorption.
With caution
Comparing benefit/risk: Grade I atrioventricular block, sinus node weakness syndrome without a pacemaker, possibility of unstable conduction through the atrioventricular node, history of Morgans-Adams-Stokes attacks, hypertrophic obstructive subaortic stenosis, isolated mitral stenosis with a rare heart rate cardiac asthma in patients with mitral stenosis (in the absence of tachysystolic atrial fibrillation), acute myocardial infarction, unstable angina pectoris, arteriovenous shunt, hypoxia, heart failure with impaired diastolic function (restrictive cardiomyopathy, cardiac amyloidosis, constrictive pericarditis, cardiac tamponade), extrasystole, marked heart cavity dilatation, “pulmonary” heart; water-electrolyte disorders: hypokalemia, hypomagnesemia, hypercalcemia, hypernatriemia; hypothyroidism, alkalosis, myocarditis, old age, renal and/or liver failure, obesity.
Side effects
Cardiovascular system: paroxysmal ventricular tachycardia, ventricular extrasystole (bigemia, polytopic ventricular extrasystole), nodal tachycardia, sinus bradycardia, sinoauricular block, atrial fibrillation and flutter, atrioventricular block; on ECG – ST segment decrease with formation of biphasic wave.
Gastrointestinal tract: anorexia, nausea, vomiting, diarrhea, abdominal pain, intestinal necrosis.
Central nervous system: sleep disorders, headache, dizziness, neuritis, radiculitis, manic-depressive syndrome, paresthesias and fainting, disorientation and confusion (mainly in elderly patients with atherosclerosis), monochrome visual hallucinations.
Comparing benefit/risk: Grade I atrioventricular block, sinus node weakness syndrome without rhythm driver, possibility of unstable conduction through the atrioventricular node, history of Morgania-Adams-Stokes seizures, hypertrophic obstructive subaortic stenosis, isolated mitral stenosis with a rare heart rate, cardiac asthma in patients with mitral stenosis (in the absence of tachysystolic atrial fibrillation),
Overdose
Symptoms: decreased appetite, nausea, vomiting, diarrhea, abdominal pain, intestinal necrosis; Ventricular paroxysmal tachycardia, ventricular extrasystole (often polytopic or bigemia), nodal tachycardia, sinoauricular block, atrial fibrillation and flutter, atrioventricular block, drowsiness, confusion, delirium psychosis, decreased visual acuity, yellow-green coloring of visible objects, flicker of “flies” before eyes, perception of objects in reduced or enlarged form; neuritis, radiculitis, manic-depressive syndrome, paresthesias.
Treatment: Digoxin withdrawal, activated charcoal administration (to reduce absorption), antidotes (sodium dimercaptopropanesulfonate, sodium edetate (EDTA), symptomatic therapy. Continuous ECG monitoring should be performed.
Pregnancy use
Foxglove drugs penetrate through the placenta. Digoxin according to the safety of its use in pregnancy belongs to the category “C”. Studies in pregnant women are insufficient, the drug may be prescribed only when the estimated benefit to the mother exceeds the potential risk to the fetus.
Digoxin is excreted into the breast milk. Since there are no data on the effect of the drug on infants, it is recommended to stop breastfeeding if therapy is required during this period.
Weight | 0.020 kg |
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Shelf life | 2 years. |
Manufacturer | Update PFC AO, Russia |
Medication form | pills |
Brand | Update PFC AO |
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