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Pharmacological action of the drug Lanoxin
Cardiac glycoside, blocks the transport of Na + / K + -ATPase, as a result of which the Na + content in the cardiomyocyte increases, which leads to the opening of Ca2 + -channels and the entry of Ca2 + into cardiomyocytes. An excess of Na + also accelerates the release of Ca2 + from the sarcoplasmic reticulum.
An increase in Ca2 + concentration leads to inhibition of the troponin complex, which has a depressing effect on the interaction of actin and myosin. An increase in the force and rate of myocardial contraction occurs by a mechanism different from the Frank-Starling mechanism (does not depend on the degree of myocardial pre-stretching). The systole becomes shorter and more energy-efficient. As a result of an increase in myocardial contractility, the SVC and IOC increase.
Reduces the CSR and EDV of the heart, 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 is manifested in an increase in the refractoriness of the AV node, which makes it possible to use supraventricular tachycardias and tachyarrhythmias for paroxysms.
With atrial fibrillation, it slows down the heart rate, lengthens diastole, improves intracardiac and systemic hemodynamics. A decrease in heart rate occurs as a result of a direct and indirect effect on the regulation of the heart rate. The positive batmotropic effect is manifested when subtoxic and toxic doses are administered. The direct action is to reduce the automatism of the sinus node. Of greater importance in the formation of negative chronotropic action is a change in the reflex regulation of the heart rhythm: in patients with atrial fibrillation, blockade of the weakest impulses occurs; increased tone of n.vagus as a result of a reflex from the receptors of the aortic arch and carotid sinus with an increase in IOC; a decrease in pressure at the mouth of the vena cava and the right atrium (as a result of an increase in the contractility of the LV myocardium, its more complete emptying, a decrease in pressure in the pulmonary artery and hemodynamic unloading of the right heart), elimination of the Bainbridge reflex and reflex activation of the sympathoadrenal system (in response to an increase in IOC) ...
It has a direct vasoconstrictor effect, which is most clearly manifested in the event that a positive inotropic effect is not realized. At the same time, the indirect vasodilating effect (in response to an increase in the IOC and a decrease in excessive sympathetic stimulation of the vascular tone), as a rule, prevails over the direct vasoconstrictor effect, as a result of which the systemic vascular resistance decreases.
Indications for use Lanoxin
As part of the complex therapy of CHF II-IV f.c. (in the presence of clinical manifestations); tachysystolic form of atrial fibrillation and atrial flutter of paroxysmal and chronic course (especially in combination with CHF).
Interaction of the drug Lanoxin
Decreased bioavailability: activated charcoal, antacids, astringent drugs, kaolin, sulfasalazine, cholestyramine (binding in the lumen of the gastrointestinal tract); metoclopramide, proserin (increased gastrointestinal motility).
Increased bioavailability: broad-spectrum antibiotics that suppress the intestinal microflora (reduce destruction in the gastrointestinal tract).
Beta-blockers and verapamil increase the severity of the negative chronotropic effect, reduce the strength of the inotropic effect.
Quinidine, methyldopa, spironolactone, amiodarone, verapamil increase the concentration in the blood due to a competitive decrease in secretion by the proximal renal tubules.
GCS (development of hypokalemia) and thiazide diuretics (development of hypokalemia and hypercalcemia), Ca2 + salts (especially when administered intravenously) reduce the tolerance of cardiac glycosides.
Butadione, ibuprofen, reserpine, rifampicin, metoclopramide, potassium-sparing diuretics prevent the development of hypokalemia and reduce the risk of relative overdose.
Microsomal oxidation inducers (barbiturates, phenylbutazone, phenytoin, rifampicin, antiepileptic, oral contraceptives) can stimulate the metabolism of digitoxin (if they are canceled, digitalis intoxication is possible).
Co-administration with sympathomimetics increases the risk of arrhythmias.
Anticholinesterase drugs increase the likelihood of developing bradycardia.
How to apply: dosage and course of treatment
Inside, intravenously (drip, jet).
In the course of treatment, 2 periods are distinguished: the period of initial digitalization (saturation) and the period of maintenance therapy.
During the period of initial digitalization, the body is gradually saturated with cardiac glycoside until the optimal therapeutic effect is achieved. The individual saturating dose (IND) is the total dose (taking into account bioavailability and daily elimination), leading to an adequate level of digitalization of a particular patient. The appearance of signs of saturation with glycosides (primarily clinical) means that the patient has received IND.
The therapeutic effect of glycosides persists if the body contains at least 80% of the INI. Exceeding it by 50% usually leads to the development of intoxication. The average value of IND in patients without concomitant pathology of organs responsible for elimination and metabolism is the average saturating dose (SND). This is a dose of cardiac glycoside at which there is a full therapeutic effect in most patients without the appearance of toxic symptoms.
The maximum tolerated dose of cardiac glycoside (without intoxication phenomena) - the individual maximum tolerated dose may exceed the average saturating dose, coincide with it and be less than SND. IND ranges from 50 to 200% of the average full dose. A significant decrease in the individual maximum tolerated dose is found in patients with severe myocardial damage and advanced decompensation, with myocardial infarction, pulmonary heart. In these patients, signs of intoxication develop earlier than the clinical manifestations of the positive inotropic action of cardiac glycosides. Digoxin elimination rate - 20%; SND - 3 mg; SPD (average maintenance dose) - 0.6 mg. With moderately rapid digitalization, it is prescribed orally, at 0.25 mg 4 times a day or 0.5 mg 2 times a day. When administered intravenously, a daily dose of 0.75 mg of digoxin is required in 3 injections. Digitalization is achieved on average after 2-3 days. Then the patient is transferred to a maintenance dose, which is usually 0.25-0.5 mg / day when administered orally and 0.125-0.25 mg when administered intravenously.
With slow digitalization, treatment is immediately started with a maintenance dose (0.25-0.5 mg / day in 1 or 2 doses). Digitalization in this case occurs in a week in most patients. Patients with hypersensitivity to cardiac glycosides are prescribed lower doses and digitalization is performed at a slow pace.
When switching from one dosage form to another, it may be necessary to adjust the dosage regimen (different dosage forms have differences in bioavailability). A dose of 100 μg in the form of a solution for injection is bioequivalent to a dose of 125 μg in the form of tablets or an elixir.
In case of paroxysmal supraventricular arrhythmias, 1-4 ml of a 0.025% solution (0.25-1 mg) in 10-20 ml of 20% dextrose solution is injected intravenously. For intravenous drip, the same dose is diluted in 100-200 ml of 5% dextrose solution or 0.9% NaCl solution. The saturating dose for children is 0.05-0.08 mg / kg; this dose is administered over 3-5 days with moderately rapid digitalization or 6-7 days with slow digitalization. The maintenance dose for children is 0.01-0.025 mg / kg / day.
In case of impaired renal excretory function, it is necessary to reduce the dose of digoxin: with a CC of 50-80 ml / min, the SPD is 50% of the SPD for persons with normal renal function; with CC less than 10 ml / min - 25% of the usual dose.
The drug in question is contraindicated for use in cases where the patient has severe hypersensitivity (allergy) to the main or one of the auxiliary components.
It is also contraindicated if the patient has:
- glycosidic intoxication;
- WPW syndrome;
- AV block II degree;
- intermittent complete blockade.
Caution should be exercised when using if the patient has:
- severe bradycardia;
- AV blockade I degree;
- isolated mitral stenosis, hypertrophic subaortic stenosis;
- acute myocardial infarction;
- unstable angina pectoris;
- cardiac tamponade, extrasystole, ventricular tachycardia.
Use during pregnancy and lactation
Use during pregnancy is possible only under the supervision of a physician, only if the expected benefits to the health of the mother outweighs the risk of adverse effects in the fetus.
Do not process the mammary glands before feeding the baby.
When a large amount of the drug is swallowed, glycosidic intoxication may occur, which has symptoms such as:
- development of sinus bradycardia;
- ventricular premature beats;
- atrial tachycardia;
- ventricular fibrillation;
- slowing down of atrioventricular conduction and atrioventricular blockade.
Dyspeptic disorders are possible.
In case of an overdose, it is necessary to flush the stomach, take enterosorbents, treat the symptoms and stop taking the drug.
Digitalis intoxication: on the part of the CVS - ventricular paroxysmal tachycardia, ventricular premature beats (often polytopic or bigeminy), nodal tachycardia, sinus bradycardia, SA blockade, atrial fibrillation and flutter, AV block.
From the digestive system: decreased appetite, nausea, vomiting, diarrhea, abdominal pain, intestinal necrosis.
From the senses: coloring visible objects in a yellow-green color, flashing "flies" before the eyes, decreased visual acuity, perception of objects in a reduced or enlarged form.
From the nervous system: sleep disorders, headache, dizziness, neuritis, radiculitis, manic-depressive syndrome, paresthesia.
On the part of the hematopoietic system and the hemostatic system: thrombocytopenic purpura, epistaxis, petechiae.
Others: hypokalemia, gynecomastia, allergic reactions. Overdose. Treatment: abolition of cardiac glycosides, administration of antidotes (unitiol, EDTA, antibodies to digoxin), symptomatic therapy. Class I drugs (are used as antiarrhythmic drugs lidocaine, phenytoin). In case of 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 U of insulin; injected drip, within 3 hours). With severe bradycardia, AV blockade - m-anticholinergics. It is dangerous to administer beta-adrenostimulants due to the possible increase in the arrhythmogenic effect of cardiac glycosides. With complete transverse blockade with attacks of Morgagni-Adams-Stokes, temporary pacing is indicated.