ich 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 hydrochloride, usp 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 hydrochloride, usp has resulted in an increase in urine flow, which in some cases reached normal levels. dopamine hydrochloride, usp 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 hydrochloride, usp 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 hydrochloride, usp as soon as a definite trend toward decreased systolic and diastolic pressure becomes evident.

e summarized in the following chart: dopamine hydrochloride injection 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 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: 1. when appropriate, increase blood volume with whole blood or plasma until central venous pressure is 10 to 15 cm h2o or pulmonary wedge pressure is 14 to 18 mm hg. 2. begin infusion of diluted solution at doses of 2 – 5 mcg/kg/min of dopamine hydrochloride in patients who are likely to respond to modest increments of heart force and renal perfusion. in more seriously ill patients, begin infusion of diluted solution at doses of 5 mcg/kg/min of dopamine hydrochloride and increase gradually using 5 to 10 mcg/kg/min increments up to a rate of 20 to 50 mcg/kg/min as needed. if doses in excess of 50 mcg/kg/min are required, it is advisable to check urine output frequently. should urinary flow begin to decrease in the absence of hypotension, reduction of dopamine dosage should be considered. multiclinic trials have shown that more than 50 percent of patients have been satisfactorily maintained on doses less than 20 mcg/kg/min. in patients who do not respond to these doses with adequate arterial pressures or urine flow, additional increments of dopamine may be given in an effort to produce an appropriate arterial pressure and central perfusion. 3. treatment of all patients requires constant evaluation of therapy in terms of blood volume, augmentation of cardiac contractility, and distribution of peripheral perfusion. dosage of dopamine should be adjusted according to the patient’s response, with particular attention to diminution of established urine flow rate, increasing tachycardia or development of new dysrhythmias as indices for decreasing or temporarily suspending the dosage. 4. as with all potent intravenously administered drugs, care should be taken to control the rate of administration to avoid inadvertent administration of a bolus of the drug. parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. dosage

buted 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 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 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.