Source:http://www4.wiwiss.fu-berlin.de/dailymed/resource/drugs/481
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DOPamine Hydrochloride (Injection, Solution, Concentrate)
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WARNING: This is a potent drug;
it must be diluted before administration to the patient. Dopamine
Hydrochloride Injection, USP is administered (only after dilution) by intravenous
infusion. Suggested
Dilution���For the 40 mg/mL preparation, transfer by aseptic
technique the contents containing either 5 mL, 200 mg or 10 mL, 400 mg of
Dopamine Hydrochloride to either a 250 mL or 500 mL bottle of one of the sterile
I.V. solutions listed below. For the 80 mg/mL preparation, transfer by aseptic
technique the contents containing 10 mL, 800 mg of Dopamine Hydrochloride
to a 250 mL, 500 mL or 1000 mL bottle of one of the following sterile I.V.
solutions: 0.9% Sodium Chloride Injection, USP 5%
Dextrose Injection, USP 5% Dextrose and 0.9% Sodium
Chloride Injection, USP 5% Dextrose and 0.45% Sodium
Chloride Injection, USP 5% Dextrose and Lactated Ringer's
Injection Sodium Lactate Injection, USP 1/6 Molar Lactated
Ringer's Injection, USP The resultant dilutions
are summarized in the following chart: Dopamine Hydrochloride Injection, USP has been found to
be stable for a minimum of 24 hours after dilution in the foregoing I.V.
solutions. However, as with all I.V. admixtures, dilution should be made just
prior to administration. Do NOT add Dopamine Hydrochloride
to Sodium Bicarbonate Injection, USP or other alkaline I.V. solutions, since
the drug is inactivated in alkaline solution. Rate of Administration���Dopamine
Hydrochloride Injection, USP after dilution, is administered intravenously
by infusion via a suitable I.V. catheter or needle. When administering Dopamine
Hydrochloride (or any potent medication) by continuous intravenous infusion,
it is advisable to use a precision volume control I.V. set. Each patient must
be individually titrated to the desired hemodynamic or renal response to dopamine. In
titrating to the desired increase in systolic blood pressure, the optimum
dosage rate for renal response may be exceeded, thus necessitating a reduction
in rate after the hemodynamic condition is stabilized. Administration
at rates greater than 50 mcg/kg/min have safely been used in advanced circulatory
decompensation states. If unnecessary fluid expansion is of concern, adjustment
of drug concentration may be preferred over increasing the flow rate of a
less concentrated dilution. Suggested
Regimen:
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Dopamine, a sympathomimetic amine vasopressor, is the naturally
occurring immediate precursor of norepinephrine. Dopamine hydrochloride is
a white to off-white crystalline powder, which may have a slight odor of hydrochloric
acid. It is freely soluble in water and soluble in alcohol. Dopamine HCl is
sensitive to alkalies, iron salts, and oxidizing agents. Chemically itis
designated as 4-(2-aminoethyl) pyrocatechol hydrochloride, and its molecular
formula is CHNO���HCl. The
structural formula is: and the molecular weight is 189.64. Dopamine
hydrochloride injection is a clear, practically colorless, sterile, pyrogen-free,
aqueous solution of dopamine HCl for intravenous infusion after dilution.
Each milliliter of the 40 mg/mL preparation contains 40 mg of dopamine hydrochloride
(equivalent to 32.31 mg of dopamine base). Each milliliter of the 80 mg/mL
preparation contains 80 mg of dopamine hydrochloride (equivalent to 64.62
mg of dopamine base). Each milliliter of both preparations contains the following:
Sodium metabisulfite 9 mg added as an antioxidant; citric acid, anhydrous
10 mg; and sodium citrate, dihydrate 5 mg added as a buffer. May contain additional
citric acid and/or sodium citrate for pH adjustment. pH is 3.3 (2.5 to 5.0). Dopamine
must be diluted in an appropriate sterile parenteral solution before intravenous
administration. (See DOSAGE AND ADMINISTRATION)
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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 endings. 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. However, if monoamine oxidase (MAO) inhibitors
are present, 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 it should be noted
that 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 osmolality of the
urine. At intermediate rates of infusion (2���10 mcg/kg/min) dopamine acts to stimulate the beta-adrenoceptors,
resulting in improved myocardial contractility, increased SA rate and enhanced
impulse conduction in the heart. There is little, if any, stimulation of the
beta-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 increases due to increased cardiac
output. Total peripheral resistance (alpha effects) at low and intermediate
doses 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 naturesis.
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Dopamine HCl should not be used in patients with pheochromocytoma. Dopamine
HCl should not be administered to patients with uncorrected tachyarrhythmias
or ventricular fibrillation.
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*For use with LifeShield blunt
cannula. Avoid contact with alkalies (including
sodium bicarbonate), oxidizing agents or iron salts. Do
not use the injection if it is darker than slightly yellow or discolored in
any other way. Store at 20 to 25��C (68 to 77��F).
[See USP Controlled Room Temperature.] Revised: October,
2004 HOSPIRA, INC., LAKE FOREST,
IL 60045 USA
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IMPORTANT Antidote for Peripheral Ischemia: To prevent sloughing and necrosis in ischemic areas, the
area should be infiltrated as soon as possible with 10 to 15 mL of saline
solution containing from 5 to 10 mg of phentolamine mesylate, an adrenergic
blocking agent. A syringe with a fine hypodermic needle should be used, and
the solution liberally infiltrated throughout the ischemic area. Sympathetic
blockade with phentolamine causes immediate and conspicuous local hyperemic
changes if the area is infiltrated within 12 hours. Therefore, phentolamine
should be given as soon as possible after the extravasation is noted.
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General: 1. Monitoring���Careful monitoring of the following indices is necessary during dopamine HCl
infusion, as with any adrenergic agent: blood pressure, urine flow, and, when
possible, cardiac output and pulmonary wedge pressure. 2. Hypovolemia���Prior to treatment
with dopamine HCl, hypovolemia should be fully corrected, if possible, with
either whole blood or plasma as indicated. Monitoring of central venous pressure
or left ventricular filling pressure may be helpful in detecting and treating
hypovolemia. 3. Hypoxia,
Hypercapnia, Acidosis���These conditions, which may also
reduce the effectiveness and/or increase the incidence of adverse effects
of dopamine, must be identified and corrected prior to, or concurrently with,
administration of dopamine HCl. 4.
Decreased Pulse Pressure���If a disproportionate increase
in diastolic blood pressure and a marked decrease in pulse pressure are observed
in patients receiving dopamine HCl, the rate of infusion should be decreased
and the patient observed carefully for further evidence of predominant vasoconstrictor
activity, unless such effect is desired. 5.
Ventricular Arrhythmias���If an increased number of ectopic
beats are observed, the dose should be reduced if possible. 6. Hypotension���At lower infusion
rates, if hypotension occurs, the infusion rate should be rapidly increased
until adequate blood pressure is obtained. If hypotension persists, dopamine
HCl should be discontinued and a more potent vasoconstrictor agent such as
norepinephrine should be administered. 7.
Extravasation���Dopamine HCl should be infused into a large
vein whenever possible to prevent the possibility of extravasation into tissue
adjacent to the infusion site. Extravasation may cause necrosis and sloughing
of surrounding tissue. Large veins of the antecubital fossa are preferred
to veins in the dorsum of the hand or ankle. Less suitable infusion sites
should be used only if the patient's condition requires immediate attention.
The physician should switch to more suitable sites as rapidly as possible.
The infusion site should be continuously monitored for free flow. 8. Occlusive Vascular Disease���Patients with a history of occlusive vascular disease (for example, atherosclerosis,
arterial embolism, Raynaud's disease, cold injury, diabetic endarteritis,
and Buerger's disease) should be closely monitored for any changes
in color or temperature of the skin in the extremities. If a change in skin
color or temperature occurs and is thought to be the result of compromised
circulation in the extremities, the benefits of continued dopamine HCl infusion
should be weighed against the risk of possible necrosis. This condition may
be reversed by either decreasing the rate or discontinuing the infusion. IMPORTANT Antidote for Peripheral Ischemia: To prevent sloughing and necrosis in ischemic areas, the
area should be infiltrated as soon as possible with 10 to 15 mL of saline
solution containing from 5 to 10 mg of phentolamine mesylate, an adrenergic
blocking agent. A syringe with a fine hypodermic needle should be used, and
the solution liberally infiltrated throughout the ischemic area. Sympathetic
blockade with phentolamine causes immediate and conspicuous local hyperemic
changes if the area is infiltrated within 12 hours. Therefore, phentolamine
should be given as soon as possible after the extravasation is noted. 9. Weaning���When discontinuing the infusion, it may be necessary to gradually decrease
the dose of dopamine HCl while expanding blood volume with I.V. fluids, since
sudden cessation may result in marked hypotension.<br/>Drug Interactions:<br/>Pregnancy:: Teratogenic Effects:Pregnancy Category C Animal studies have revealed
no evidence of teratogenic effects due to dopamine. However, in one study,
administration of dopamine HCl to pregnant rats resulted in a decreased survival
rate of the newborn and a potential for cataract formation in the survivors.
There are no adequate and well-controlled studies in pregnant women and it
is not known if dopamine crosses the placental barrier. Because animal reproduction
studies are not always predictive of human response, this drug should be used
during pregnancy only if, in the judgment of the physician, the potential
benefit justifies the potential risk to the fetus.<br/>Labor and Delivery: In obstetrics, if vasopressor drugs are used to correct hypotension
or are added to a local anesthetic solution, some oxytocic drugs may cause
severe persistent hypertension and may even cause rupture of a cerebral blood
vessel to occur during the postpartum period.<br/>Nursing Mothers: It is not known whether this drug is excreted in human milk.
Because many drugs are excreted in human milk, caution should be exercised
when dopamine HCl is administered to a nursing woman.<br/>Pediatric Use: Safety and effectiveness in children have not been established.
Dopamine HCl has been used in a limited number of pediatric patients, but
such use has been inadequate to fully define proper dosage and limitations
for use.
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In the case of accidental overdosage, as evidenced by excessive
elevation of blood pressure, reduce rate of administration or temporarily
discontinue dopamine HCl until patient's condition stabilizes. Since
dopamine's duration of action is quite short, no additional remedial
measures are usually necessary. If these measures fail to stabilize the patient's
condition, use of the short-acting alpha-adrenergic blocking agent phentolamine
should be considered.
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Dopamine Hydrochloride
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DOPamine Hydrochloride (Injection, Solution, Concentrate)
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The following adverse reactions have been observed, but there
are not enough data to support an estimate of their frequency. Cardiovascular System: ventricular
arrhythmia (at very high doses) ectopic beats tachycardia anginal
pain palpitation cardiac conduction
abnormalities widened QRS complex bradycardia hypotension hypertension vasoconstriction Respiratory System: dyspnea Gastrointestinal System: nausea vomiting Metabolic/Nutritional System: azotemia Central Nervous System: headache anxiety Dermatological System: piloerection Other: Gangrene of the extremities
has occurred when high doses were administered for prolonged periods or in
patients with occlusive vascular disease receiving low doses of dopamine HCl.
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Contains sodium metabisulfite, a sulfite that may cause allergic-type
reactions including anaphylactic symptoms and life-threatening or less severe
asthmatic episodes in certain susceptible people. The overall prevalence of
sulfite sensitivity in the general population is unknown and probably low.
Sulfite sensitivity is seen more frequently in asthmatic than in nonasthmatic
people. Do NOT add dopamine HCl to any alkaline diluent
solution since the drug is inactivated in alkaline solution. Patients
who have been receiving MAO inhibitors prior to the administration of dopamine
HCl will require substantially reduced dosage. See Drug
Interactions below.
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Dopamine HCl is indicated for the correction of hemodynamic
imbalances present in the shock syndrome due to myocardial infarction, trauma,
endotoxic septicemia, open-heart surgery, renal failure, and chronic cardiac
decompensation as in congestive failure. Patients most
likely to respond adequately to dopamine HCl 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 blood volume correction and dopamine HCl, the better the prognosis.
Where appropriate, blood volume restoration with a suitable plasma expander
or whole blood should be accomplished prior to administration of dopamine
HCl. Poor Perfusion
of Vital Organs���Urine flow appears to be one of the better
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 reversal of 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 HCl is administered before urine flow has diminished to levels of
approximately 0.3 mL/minute, prognosis is more favorable. Nevertheless, in
a number of oliguric or anuric patients, administration of dopamine HCl has
resulted in an increase in urine flow, which in some cases reached normal
levels. Dopamine HCl 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. 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 movements 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 HCl 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 HCl as soon as a definite
trend toward decreased systolic and diastolic pressure becomes evident.
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DOPamine Hydrochloride
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