MYOCARD-DX

MYOCARD-DX- dopamine hydrochloride and dextrose monohydrate injection
B. Braun Medical Inc.

DESCRIPTION

Dopamine Hydrochloride in 5% Dextrose Injection USP is prepared from Dopamine Hydrochloride and Hydrous Dextrose USP in Water for Injection USP. These solutions are for intravenous use only.

These solutions are sterile, nonpyrogenic, isotonic, and contain no bacteriostatic or antimicrobial agents or added buffers. They are intended for single use only. When smaller doses are required, the unused portion should be discarded.

Each 100 mL contains dopamine hydrochloride 80 mg or 160 mg and dextrose, hydrous, 5 g in water for injection, with sodium metabisulfite added 50 mg as a stabilizer; osmolar concentration, respectively 270 and 275 mOsmol/liter, pH 3.3 (2.5 — 4.5). pH may be adjusted with Hydrochloric Acid NF or Sodium Hydroxide NF, as required.

Dopamine administered intravenously is a myocardial inotropic agent which also may increase mesenteric and renal blood flow plus urinary output.

Dopamine hydrochloride is designated chemically, as 3,4-dihydroxyphenethylamine hydrochloride, a white crystalline powder freely soluble in water. Dopamine (also referred to as 3-hydroxytyramine) is a naturally occurring biochemical catecholamine precursor of norepinephrine.

The formulas of the active ingredients are:

IngredientsMolecular FormulaMolecular Weight
Hydrous Dextrose USPDextrose Molecule198.17
Dopamine Hydrochloride
Dopamine Formula
(click image for full-size original)
189.64

Dextrose MoleculeDopamine Formula

CLINICAL PHARMACOLOGY

Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system, especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves.

Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve ending.

Dopamine’s onset of action occurs within five minutes of intravenous administration, and with dopamine’s plasma half-life of about two minutes, the duration of action is less than ten minutes. If monoamine oxidase (MAO) inhibitors are present, however, the duration may increase to one hour. The drug is widely distributed in the body but does not cross the blood-brain barrier to a significant extent. Dopamine is metabolized in the liver, kidney, and plasma by MAO and catechol-O-methyltransferase to the inactive compounds homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid. About 25% of the dose is taken up into specialized neurosecretory vesicles (the adrenergic nerve terminals), where it is hydroxylated to form norepinephrine. It has been reported that about 80% of the drug is excreted in the urine within 24 hours, primarily as HVA and its sulfate and glucuronide conjugates and as 3,4-dihydroxyphenylacetic acid. A very small portion is excreted unchanged.

The predominant effects of dopamine are dose-related, although actual response of an individual patient will largely depend on the clinical status of the patient at the time the drug is administered. At low rates of infusion (0.5-2 mcg/kg/min) dopamine causes vasodilation that is presumed to be due to a specific agonist action on dopamine receptors (distinct from alpha- and beta-adrenoceptors) In the renal, mesenteric, coronary, and intracerebral vascular beds. At these dopamine receptors, haloperidol is an antagonist. The vasodilation in these vascular beds is accompanied by increased glomerular filtration rate, renal blood flow, sodium excretion, and urine flow. Hypotension sometimes occurs. An increase in urinary output produced by dopamine is usually not associated with a decrease in osmolarity of the urine.

At intermediate rates of infusion (2-10 mcg/kg/min) dopamine acts to stimulate the beta1 -adrenoceptors, resulting In improved myocardial contractility, increased SA rate and enhanced impulse conduction in the heart. There is little, if any, stimulation of the beta2 -adrenoceptors (peripheral vasodilation). Dopamine causes less increase in myocardial oxygen consumption than isoproterenol, and its use is not usually associated with a tachyarrhythmia. Clinical studies indicate that it usually increases systolic and pulse pressure with either no effect or a slight increase in diastolic pressure. Blood flow to the peripheral vascular beds may decrease while mesenteric flow increased due to increased cardiac output. At low and intermediate doses, total peripheral resistance (which would be raised by alpha activity) is usually unchanged.

At higher rates of infusion (10-20 mcg/kg/min) there is some effect on alpha-adrenoceptors, with consequent vasoconstrictor effects and a rise in blood pressure. The vasoconstrictor effects are first seen in the skeletal muscle vascular beds, but with increasing doses they are also evident in the renal and mesenteric vessels. At very high rates of infusion (above 20 mcg/kg/min), stimulation of alpha-adrenoceptors predominates and vasoconstriction may compromise the circulation of the limbs and override the dopaminergic effects of dopamine, reversing renal dilation and natriuresis.

Dextrose provides a source of calories. Dextrose is readily metabolized, may decrease losses of body protein and nitrogen promotes glycogen deposition and decreases or prevents ketosis if sufficient doses are provided.

INDICATIONS AND USAGE

Dopamine Hydrochloride in 5% Dextrose Injection USP is indicated for the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarctions, trauma, endotoxic septicemia, open heart surgery, renal failure, and chronic cardiac decompensation as in congestive heart failure.

Where appropriate, restoration of blood volume with a suitable plasma expander or whole blood should be instituted or completed prior to administration of dopamine.

Patients most likely to respond adequately to administration of dopamine are those in whom physiological parameters such as urine flow, myocardial function, and blood pressure, have not undergone profound deterioration. Multiclinic trials indicate that the shorter the time interval between onset of signs and symptoms and initiation of therapy with volume correction and dopamine, the better the prognosis.

Poor Perfusion of Vital Organs — Urine flow appears to be one of the diagnostic signs by which adequacy of vital organ perfusion can be monitored. Nevertheless, the physician should also observe the patient for signs of reversal of confusion or comatose condition. Loss of pallor increase in toe temperature, and/or adequacy of nail bed capillary filling may also be used as indices of adequate dosage. Clinical studies have shown that when dopamine is administered before urine flow had diminished to levels approximately 0.3 mL/minute, prognosis is more favorable.

Nevertheless, in a number of oliguric or anuric patients, administration of dopamine has resulted in an increase in urine flow which in some cases reached normal levels. Dopamine may also increase urine flow in patients whose output is within normal limits and thus may be of value in reducing the degree of pre-existing fluid accumulation. It should be noted that at doses above those optimal for the individual patient, urine flow may decrease, necessitating reduction of dosage. Concurrent administration of dopamine and diuretic agents may produce an additive or potentiating effect.

Low Cardiac Output — Increased cardiac output is related to dopamine’s direct inotropic effect on the myocardium. Increased cardiac output at low or moderate doses appears to be related to a favorable prognosis. Increase in cardiac output has been associated with either static or decreased systemic vascular resistance (SVR). Static or decreased SVR associated with low or moderate increments in cardiac output is believed to be a reflection of differential effects on specific vascular beds with increased resistance in peripheral beds (e.g., femoral) and concomitant decreases in mesenteric and renal vascular beds. Redistribution of blood flow parallels these changes so that an increase in cardiac output is accompanied by an increase in mesenteric and renal blood flow. In many instances the renal fraction of the total cardiac output has been found to increase. Increase in cardiac output produced by dopamine is not associated with substantial decreases in systemic vascular resistance as may occur with isoproterenol.

Hypotension — Hypotension due to inadequate cardiac output can be managed by administration of low to moderate doses of dopamine, which have little effect on SVR. At high therapeutic doses, dopamine’s alpha adrenergic activity becomes more prominent and thus may correct hypotension due to diminished SVR. As in the case of other circulatory decompensation states, prognosis is better in patients whose blood pressure and urine flow have not undergone profound deterioration. Therefore, it is suggested that the physician administer dopamine as soon as a definite trend toward decreased systolic and diastolic pressure becomes evident.

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