Dopamine-Ferein, 0.5% 5 ml 10 pcs

Dopamine is a cardiotonic, hypertensive, vasodilator and diuretic.

It excites beta-adrenoreceptors (in small and medium doses) and alpha-adrenoreceptors (in large doses). Improvement of systemic hemodynamics leads to a diuretic effect. It has a specific stimulatory effect on postsynaptic dopamine receptors in vascular smooth muscle and the kidneys.

In low doses (0.5-3 µg/kg/min), it acts primarily on dopamine receptors, causing dilation of renal, mesenteric, coronary and cerebral vessels. Dilation of renal vessels leads to increased renal blood flow, increased rate of glomerular filtration, increased diuresis and sodium excretion; dilation of mesenteric vessels also occurs (this distinguishes dopamine action on renal and mesenteric vessels from action of other catecholamines).

In low and medium doses (2-10 µg/kg/min) it stimulates postsynaptic beta1-adrenoreceptors, which causes positive inotropic effect and increased minute blood volume.

Systolic blood pressure and pulse pressure may increase; diastolic blood pressure is unchanged or slightly increased. Total peripheral vascular resistance (TPR) is usually unchanged. Coronary blood flow and myocardial oxygen consumption tend to increase. At high doses (10 µg/kg/min or more), alpha1-adrenoreceptor stimulation predominates, causing increased ROS, heart rate, and renal vasoconstriction (the latter may reduce previously increased renal blood flow and diuresis). Both systolic and diastolic blood pressure increase as a consequence of increased minute blood volume and OPPS.

The onset of therapeutic effect is within 5 min against the background of intravenous administration and lasts for 10 min.

Pharmacokinetics

It is administered intravenously only. About 25% of the dose is taken up by neurosecretory vesicles, where hydroxylation occurs and norepinephrine is formed. It is widely distributed in the body and partially passes through the blood-brain barrier. The apparent volume of distribution (neonates) is 1.8 L/kg. Binding with blood plasma proteins is 50%.

The drug is rapidly metabolized in the liver, kidneys and blood plasma by monoaminoxidase and catechol-O-methyltransferase to inactive metabolites. Half-life of the preparation (T1/2) – adults: from blood plasma – 2 min, from body – 9 min; newborns – 6.9 min (within 5-11 min).

Extracted by the kidneys; 80% of the dose – as metabolites within 24 hours, in small amounts – unchanged.

Indications

Shock of various genesis, including cardiogenic, postoperative, infectious-toxic, anaphylactic, hypovolemic (only after the restoration of the blood circulation), acute cardiovascular failure, low ejection syndrome in cardiac surgery patients, severe arterial hypotension.

Poisonings (to enhance diuresis and to accelerate excretion of the xenobiotic).

Active ingredient

Composition

Active ingredient:

Dopamine hydrochloride;

Associates:

Sodium disulfite;

Hydrochloric acid 0.1M to pH 3.5-5.0,

water d/i

How to take, the dosage

It is administered intravenously by drip. The dose is set individually, depending on the severity of shock, the value of blood pressure and the patient’s response to treatment.

In order to enhance diuresis and obtain inotropic effect (increase myocardial contractile activity), it is administered at a rate of 100-250 mcg/min (1.5-3.5 mcg/kg/min) – low dose area. In intensive surgical therapy – 300-700 mcg/min (4-10 mcg/kg/min) – area of medium doses; in septic shock – 750-1500 mcg/min (10.5-21 mcg/kg/min) – area of maximum doses. In order to influence BP, it is recommended to increase the dose to 500 mcg/min or more, or with a constant dose of dopamine, norepinephrine (noradrenaline) is additionally prescribed in a dose of 5 mcg/min if the patient’s body weight is about 70 kg.

If cardiac rhythm abnormalities occur, regardless of the doses used, further dose increases are contraindicated.

In children, the dose is administered at 4-6 (maximum 10) mcg/kg/min. In contrast to adults, in children the dose should be increased gradually, that is, starting with the lowest dose.

The speed of administration should be chosen individually to achieve an optimal patient response. Most patients are able to maintain a satisfactory condition with doses of dopamine less than 20 µg/kg/min.

Length of administration: the duration of infusions depends on individual patient characteristics. There is a positive experience of infusion duration up to 28 days. After the clinical situation has stabilized, the drug should be withdrawn gradually.

Rules for solution preparation: 0.9 % sodium chloride solution, 5 % dextrose solution (including their mixtures), 5 % dextrose solution in Ringer lactate solution, sodium lactate solution and Ringer lactate solution are used for dilution. In order to prepare a solution for intravenous infusion, 400-800 mg of dopamine should be added to 250 ml of solvent (dopamine concentration will be 1.6-3.2 mg/ml). The infusion solution should be prepared immediately before use (solution stability is maintained for 24 h, except for mixture with Ringer-lactate solution – maximum 6 h). The dopamine solution should be clear and colorless.

Interaction

Pharmaceutically incompatible with alkaline solutions (inactivate dopamine), oxidants, iron salts, thiamine (promotes destruction of vitamin B1).

The sympathomimetic effect is enhanced by adrenostimulants, monoamine oxidase inhibitors (including furazolidone, procarbazine, selegiline), guanethidine (increasing the duration and enhancement of cardio-stimulating and pressor effects); diuretic – diuretics; cardiotoxic effects – inhalation drugs for general anesthesia, hydrocarbon derivatives – such as cyclopropane, chloroform, enflurane, halothane, isoflurane, methoxyflurane (increased risk of severe atrial or ventricular arrhythmias), tricyclic antidepressants including maprotiline (risk of cardiac rhythm disturbances, severe hypertension or hyperpyrexia), cocaine, other sympathomimetics impair – butyrophenones and beta-adrenoblockers (propranololol).

Limits the hypotensive effect of guanadrel, guanethidine, mecamylamine, methyldopa, rauwolfia alkaloids (the latter prolong the effect of dopamine).

In concomitant use with levodopa – increased likelihood of arrhythmias; with thyroid hormones – possible increase in the effect of both dopamine and thyroid hormones.

Ergometrine, ergotamine, methylergometrine, and oxytocin increase the vasoconstrictor effect and the risk of ischemia and gangrene as well as severe arterial hypertension, up to intracranial hemorrhage.

Phenytoin may contribute to arterial hypotension and bradycardia (depending on the dose and speed of administration); ergot alkaloids to vasoconstriction and gangrene.

Compatible with cardiac glycosides (increased risk of cardiac arrhythmias, additive inotropic effect possible, ECG monitoring required).

Decreases the antianginal effect of nitrates, which in turn may decrease the pressor effect of sympathomimetics and increase the risk of arterial hypotension (simultaneous use is permitted depending on achieving the desired therapeutic effect.

Special Instructions

Contraindications

Hypersensitivity, hypertrophic obstructive cardiomyopathy, pheochromocytoma, ventricular fibrillation.

Side effects

Nervous system and sense organs: headache, anxiety, motor restlessness, hand tremor.

Cardiovascular system and blood (hematopoiesis, hemostasis): angina, tachycardia or bradycardia, palpitations, pain behind the chest, increased or decreased BP, conduction disorders, QRS complex expansion, vasospasm, increased left ventricular end-diastolic pressure; when used in high doses – ventricular or supraventricular arrhythmias.

Gastrointestinal disorders: nausea, vomiting.

Allergic reactions: in patients with bronchial asthma – bronchospasm, shock.

Others: dyspnea, azotemia, piloarreaction; rarely, polyuria (when administered in low doses); local reactions: necrosis of the skin, p/c cellulose if the drug gets under the skin.

Overdose

Symptoms: excessive rise in BP, peripheral arterial spasm, tachycardia, ventricular extrasystoles, angina pectoris, dyspnea, headache, psychomotor agitation.

Treatment: due to rapid elimination of dopamine from the body these phenomena are controlled by dose reduction or discontinuation of administration; if ineffective – short-acting alpha-adrenoblockers (for excessive increase in blood pressure) and beta-adrenoblockers (for heart rhythm disorders).