By U. Nasib. Northwest Nazarene University.
Most ventricular arrhythmias were seenwithin 1hourofthedrug infusion 150mg bupron sr visa bipolar depression treatment resistant,butsome were seennearly 3 hours after the infusion generic 150 mg bupron sr with visa depression definition and symptoms. Itis thought that the arrhythmogenic potential of ibutilide is increasedwhenit is used with other drugs that prolong the duration of the actionpotential order 150mg bupron sr depression definition science. Ibutilide should also be avoided in patients receiving phenothiazines, tricyclic antidepressants, tetra- cyclic antidepressants, or antihistamineagents that block the H1 re- ceptor. Clinical utility of ibutilide The overall clinical utility of ibutilide probably ought to be con- sideredmarginal, mainly because of the disadvantages of the drug. The incidence of torsades de pointes with ibutilide is also troubling,and the relatively prolonged monitoring required after its use (regardless of whether it is effec- tive) can be quite inconvenient. Its major side effect, typical for drugs with these elec- trophysiologic properties, is torsades de pointes. While it iselim- inated by both the kidneys and the liver, the renal route of elimina- tionis particularly important clinically. The dosage of the drug needs to be carefully adjustedinpatients with reducedcreatinine clear- ances. The drug is available only to hospitals and physicians that have beencertiﬁed to administer itand is dispensed only by a limited number of pharmacies. Certiﬁcationisachieved by completing an educational programprovided by Pﬁzer, the manufacturer. If the creatinine clearance is greater than 60 mL/min, 500 µg of dofetilide is given twiceaday. If the creati- nine clearance is between40and 60 mL/min, 250 µg twiceaday is given. Indications Dofetilide is indicated for conversion to normal sinus rhythm,and especially for the maintenanceofsinus rhythm, in patients with atrial ﬁbrillation or atrial ﬂutter. Because of the drug’s narrow ther- apeutic to toxic ratio, and the extraordinary precautions that must be takeninusing it, dofetilide is generally reserved for patients whose arrhythmias are highly symptomatic. Dofetilide is moderately effective in converting atrial ﬁbrillation and atrial ﬂutter to sinus rhythm. W ith doses of 500 µg, conver- sionwithin 24–36 hours has been reported to occur in 30–70% of patients. Dofetilideappears to be more useful in maintaining sinus rhythm after successful conversion. Ifdosages of 500 µg twice per day can be maintained, 60–65% of patients treatedwith dofetilide have been reported to remain in sinus rhythm for up to 12months after con- version from atrial ﬁbrillation. Only very limitedinformationis available on the efﬁcacyof dofetilide for ventricular arrhythmias. Torsades de pointes was seeninas few as 1% butasmanyas>3% of patients givendofetilide in clinical trials. Reducing the oddsofexperiencing this arrhythmia requires carefultitration of the drug,and reduc- ing death from torsades de pointes requires prolongedin-hospital monitoring. The need to take such precautions has led to an ex- traordinarily restrictive approval status for dofetilide in the United States. Dofetilide has minimal hemodynamic effects and can be usedin patients with heart failure. Dofetilide has been reported to cause occasional noncardiac symp- toms, including headache, gastrointestinal disturbances, sleepdisor- ders, and ﬂulike symptoms. Dofetilide is completely contraindicatedwith drugs that can reduce its elimina- tion and thus increase its plasma concentration. These drugs include verapamil, cimetidine, trimethoprim, prochlorperazine, and mege- strol. It should be usedwith cautionwith triamterene, met- formin,and amiloride, which are drugs that compete with dofetilide for priority in the renal transport system. For many other calcium-blocking agents, suchasnifedipine, vasodilatory ef- fects predominate; for these agents, reﬂex responses to vasodilation appear to counteractand cancel any cardiac electrophysiologic ef- fects. Clinical pharmacology of verapamil and diltiazem When verapamil is given orally, more than 90% is absorbed,but ﬁrst-pass hepatic metabolism reduces bioavailability to 20–35%. Verapamil can be given as anintravenous bolus for the emergent termination of reentrant supraventricular arrhythmias. Diltiazem,like verapamil, is well absorbed but is also subjectto ﬁrst-pass metabolism,yielding abioavailability of about 40%. The drug is metabolizedinthe liver, and the elimination half-life isapproximately 3. Diltiazemis also available for intravenous infusion and isoccasionally usedinthis form to control heart rate during atrial ﬁbrillation or atrial ﬂutter. Dosage The usual dosage of verapamil is 240–360 mg/day in divideddoses given every 8 hours. Both drugs are also available in long-acting forms that can be given onceortwiceaday. Five to 10 mg is administered over a period of 2 minutes; an additional 10 mg can be given after 10 minutes. Infusion rates can be titrated to as muchas15mg/h, depending on the response of the heart rate. Continuing diltiazeminfusions for longer than24hours is not rec- ommended because longer infusionperiods have not been studied. Accordingly, the major electrophysiologic effects of calcium-channel blockers are limited to these two struc- tures. As a general rule, calcium blockers have minimal or no electro- physiologic effecton the atrial or ventricular myocardium. However, the slowcalcium channel has beeninvoked as a necessary com- ponent in the development of both early afterdepolarizationsand delayed afterdepolarizations. Accordingly, calcium-channel blockers can occasionally ameliorate afterdepolarizationsand the arrhyth- mias they cause. Further, it isapparent that the calcium channels might be re- sponsible, on occasion, for localized areas of slowconductioninthe ventricles. Thus, in relatively rare circumstances, calcium-channel blockers can be used to treat ventricular arrhythmias (see below, and Chapter 12) Like Class I antiarrhythmic drugs, calcium blockers exhibit use dependence—theirbinding and blocking of the calcium channels increases at more rapid heart rates. Clinical use of calcium-blocking agents Supraventricular tachyarrhythmias Verapamiland diltiazemcan be very useful in the management of manysupraventricular tachyarrhythmias either by affecting the 104 Chapter 6 mechanism of the arrhythmia itself and thus terminating or pre- venting it, or in slowing the ventricular response to the arrhythmia. Atrial tachyarrhythmias All these arrhythmias are localized to the atrial myocardium,socal- cium blockers have very little direct effecton them. Ingeneral, it is easier to control ventricular response during atrial ﬁbrillation thanit is during atrial ﬂutter or atrial tachycar- dia. On the other hand, controlling the ventricular response during chronic atrial ﬁbrillationis often quite achievable, thoughacombination of drugs may be required (calcium blockers plus beta blockers and/or digoxin). In the acute setting, intravenous infusionsofdiltiazem have proven to be very effective in controlling the ventricular rate during atrial tachycardias. Multifocal atrial tachycardia Multifocal atrial tachycardia isalmost exclusively seenduring acute illness, most oftenduring acute respiratory decompensation.
There’s a popular movement to favor bioidentical hormones over synthetic hormones order bupron sr 150 mg overnight delivery depression definition money. Bioidentical hormones are exact replicas of the hormones your body makes during your fertile years best bupron sr 150mg performance anxiety, including estradiol and progesterone order 150mg bupron sr depression symptoms help guide, which are the two hormones commonly referred to as “bioidenticals. Some alternative providers insist that bioidenticals solve every problem a menopausal woman has and are vastly superior to synthetic and animal-derived counterparts. When I counsel a woman about taking hormone therapy, I recommend bioidentical estrogen and progesterone, including transdermal estradiol and oral progesterone, but with an important caveat: I assume that the risks of bioidentical hormone therapy are the same as synthetic until proven otherwise. Overall, compounded bioidentical hormones often lack the regulatory oversight and rigorous testing that I believe women 57 deserve. Estrogen in Balance As I said at the beginning of this chapter, estrogen is the hormone that most defines you as a woman. When you’ve got your estrogen levels in balance, life feels joyous and right again. Signs of Estrogen Balance • You have regular periods (estrogen and progesterone work together on this one). Listen up: the combination of excessively high androgens is the most common hormone problem of women in their fertile years, and perhaps even before puberty. After menopause, high androgens are associated with serious health problems, such as heart disease, stroke, mood problems, and cancer. Androgens are a group of sex hormones that strongly affect your liveliness, libido, mood, and self-confidence. Virilization: Normal in Males, Abnormal in Females In males, androgens stimulate the embryo to increase the length and diameter of the penis and to develop the prostate and scrotum. The sex differentiation process that unfolds inside the uterus— and differentiates the boy from the girl fetus—is virilization, defined as the development of male physical characteristics such as the penis, and later, after puberty, muscle bulk, body hair on the chest and face, and a deep voice. In females, lack of androgens causes the embryo’s ambiguous genitalia to commit to a female pattern, as a default setting. In a young girl, mildly high androgens might range from nuisance symptoms, such as acne, to more severe and serious symptoms requiring an endocrinologist’s evaluation, such as early signs of puberty (pubic hair growth before age eight), or equally worrisome, signs of female virilization. In adolescent and adult females, virilization—as evidenced in enlargement of the clitoris, increased muscle strength, deepening of the voice, and/or menstrual irregularity due to lack of ovulation—indicates a problem. Most worrisome is that it may be a result of tumors of the ovaries, adrenals, or pituitary glands. Because they control the development of typically male characteristics, androgens are considered “masculinizing” hormones, but they also account for emotional well- being, assertiveness, and sense of agency—the capacity a person has to act powerfully in his social structure or an innate sense of belonging. Androgens are the biochemical underpinnings of dominance and desire, and even though males have more androgens than females do, having the right amount of androgens is just as essential to women’s health and well- being. The Science of High Androgens The best-known androgen is testosterone, the hormone that inspires motocross, wrestling, and bar fights. Although it is often thought of as the male hormone, women need to have some testosterone in their bodies as well. The difference between men and women lies in the quantity of testosterone: women produce approximately 250 micrograms (0. Of all the androgens circulating in your blood and tissues, testosterone is the superstar. It promotes muscles, bigger bones, and immune function, including the bone-marrow manufacture of red blood cells. Androgens normally decrease by 1 to 2 percent per year beginning in your twenties, so higher levels of androgens are less common after menopause. In men, testosterone is produced in the testes and adrenal glands; in women, it is produced in the ovaries and adrenal glands. In general, testosterone is released throughout the body, sending word to your erogenous zones that you are ready for sex. When testosterone is functioning properly, it revs up the hypothalamus, boosting erotic feelings and sensations. Growing research supports the role of testosterone in female desire, with evidence of low desire associated with low testosterone and increased desire with replacement. Women reach their peak testosterone levels in their midtwenties, after which comes a slow but steady decline, about 1 to 2 percent per year, of available testosterone. By menopause, testosterone levels are at half the peak level, mostly due to decline in adrenal production. Since ovaries produce testosterone, women whose ovaries have been excised are suddenly operating with 75 percent less testosterone. Most of these women feel the drop almost immediately, often with hot flashes and a substantial decline in libido, confidence, and verve. If all this talk about mood and libido sounds familiar, it should: testosterone has an overlapping role with our old friend estrogen. You see, testosterone can be converted to estrogen; fat cells contain an enzyme, called aromatase, that converts testosterone to estradiol. The more fat you have, the more likely it is that you’ll create an excess of both androgens and estrogens. We know that excess estrogen may make it extremely difficult to lose weight, which then reinforces the cycle of more fat, estrogen, and weight. We also know that too much testosterone is associated with mood problems such as depression and anxiety, weight gain, and what we call sexual issues (as in, “Back off, Cowboy! Women with too much testosterone have deeper voices, more pubic and facial hair, and more muscular builds than women with normal amounts of this hormone (Figure 4, page 207). Occasionally, high testosterone is so significant that it causes balding, a full beard, or growth of the clitoris. We also know that criminal violence and aggressive dominance in women are linked to higher testosterone. Measuring testosterone levels in the saliva on two occasions two years apart, the researchers found that the women with the highest testosterone levels were the most likely to gamble. Testosterone levels also predicted ultimate career choice: women with higher testosterone were more likely to have chosen riskier careers, such as investment banking and finance. These jobs tend to have fatter salaries, but also less security and a higher probability of turnover. Her libido had been abysmal for the past ten years, yet she loves her new husband and wanted to feel more passionate toward him. Her woes led her to a doctor, who prescribed 2 percent testosterone cream, which she applied to her vagina. Within a few weeks, Cheryl had large, painful pimples on her cheeks and jawline and had to wash her hair more often. The clitoris has a wide normal range and engorges with blood during sexual arousal; the nonaroused clitoris is normally 3 to 4 mm wide by 4 to 5 mm long. The testosterone in her blood was, not surprisingly, elevated: the normal range of free testosterone—I’ll explain what that is in a minute—is 0. After checking Cheryl’s liver enzymes and doing a cholesterol test, I was relieved to find normal levels.
Recovery is available even to persons who may not at first be able to perceive this hope effective bupron sr 150 mg anxiety drugs, especially when the focus is on linking the health consequences to the disease of addiction order bupron sr 150mg without a prescription depression test learnmyself. As in other health conditions discount 150 mg bupron sr fast delivery bipolar depression medication and weight loss, self-management, with mutual support, is very important in recovery from addiction. Peer support such as that found in various “self-help” activities is beneficial in optimizing health status and functional outcomes in recovery. The neurobiology of reward has been well understood for decades, whereas the neurobiology of addiction is still being explored. Current neuroscience recognizes that the neurocircuitry of reward also involves a rich bi-directional circuitry connecting the nucleus accumbens and the basal forebrain. It is the reward circuitry where reward is registered, and where the most fundamental rewards such as food, August 15, 2011 Page 6 hydration, sex, and nurturing exert a strong and life-sustaining influence. Alcohol, nicotine, other drugs and pathological gambling behaviors exert their initial effects by acting on the same reward circuitry that appears in the brain to make food and sex, for example, profoundly reinforcing. Other effects, such as intoxication and emotional euphoria from rewards, derive from activation of the reward circuitry. While intoxication and withdrawal are well understood through the study of reward circuitry, understanding of addiction requires understanding of a broader network of neural connections involving forebrain as well as midbrain structures. Selection of certain rewards, preoccupation with certain rewards, response to triggers to pursue certain rewards, and motivational drives to use alcohol and other drugs and/or pathologically seek other rewards, involve multiple brain regions outside of reward neurocircuitry itself. These five features are not intended to be used as “diagnostic criteria” for determining if addiction is present or not. Although these characteristic features are widely present in most cases of addiction, regardless of the pharmacology of the substance use seen in addiction or the reward that is pathologically pursued, each feature may not be equally prominent in every case. The diagnosis of addiction requires a comprehensive biological, psychological, social and spiritual assessment by a trained and certified professional. In this document, the term "addictive behaviors" refers to behaviors that are commonly rewarding and are a feature in many cases of addiction. Exposure to these behaviors, just as occurs with exposure to rewarding drugs, is facilitative of the addiction process rather than causative of addiction. The state of brain anatomy and physiology is the underlying variable that is more directly causative of addiction. Thus, in this document, the term “addictive behaviors” does not refer to dysfunctional or socially disapproved behaviors, which can appear in many cases of addiction. Behaviors, such as dishonesty, violation of one’s values or the values of others, criminal acts etc. The anatomy (the brain circuitry involved) and the physiology (the neuro-transmitters involved) in these three modes of relapse (drug- or reward-triggered relapse vs. Reward-triggered relapse also is mediated by glutamatergic circuits projecting to the nucleus accumbens from the frontal cortex. Relapse triggered by exposure to conditioned cues from the environment involves glutamate circuits, originating in frontal cortex, insula, hippocampus and amygdala projecting to mesolimbic incentive salience circuitry. Relapse triggered by exposure to stressful experiences involves brain stress circuits beyond the hypothalamic-pituitary-adrenal axis that is well known as the core of August 15, 2011 Page 7 the endocrine stress system. Pathologically pursuing reward (mentioned in the Short Version of this definition) thus has multiple components. In addiction, pursuit of rewards persists, despite life problems that accumulate due to addictive behaviors, even when engagement in the behaviors ceases to be pleasurable. Similarly, in earlier stages of addiction, or even before the outward manifestations of addiction have become apparent, substance use or engagement in addictive behaviors can be an attempt to pursue relief from dysphoria; while in later stages of the disease, engagement in addictive behaviors can persist even though the behavior no longer provides relief. Permission to make digital or hard copies of this work for personal or classroom use is granted without fee provided that copies are not made or distributed for commercial, advertising or promotional purposes, and that copies bear this notice and the full citation on the first page. Re publication, systematic reproduction, posting in electronic form on servers, redistribution to lists, or other uses of this material, require prior specific written permission or license from the Society. Excerpting any statement for any purpose requires specific written permission from the Society. The cover photo shows a bioreactor at Roche’s Penzberg facility and conveys at least a rough of idea of the sophisticated technical know-how and years of experience required to manufacture biopharma- ceuticals. Modern biotechnology plays a crucial role both in the elucidation of the molecular causes of disease and in the development of new diagnostic methods and better target- ed drugs. These developments have led to the birth of a new economic sec- tor, the biotech industry, associated mostly with small start-up companies. For their part, the more established healthcare com- panies have also been employing these modern techniques, known collectively as biotechnology, successfully for many years. By studying the molecular foundations of diseases they have developed more specific ways of combating diseases than ever before. This new knowledge permits novel approaches to treatment, with new classes of drug – biopharmaceuticals – at- tacking previously unknown targets. Increasing attention is also being paid to differences between individual patients, with the result that in the case of many diseases the goal of knowing in advance whether and how a particular treatment will work in a given patient is now within reach. When a disease, rather than being diagnosed on the ba- sis of more or less vague signs and symptoms, can be detected on the basis of molecular information, the possibility of suc- cessful treatment depends largely on what diagnostic techniques are available. To the healthcare industry this represents a major development in that diagnosis and treatment are growing ever closer together, with clear benefits for companies that possess competence in both these areas. To patients, progress in medical biotechnology means one thing above all: more specific, safer and more successful treatment of their illnesses. For example,more than 40% of the sales of Roche’s ten best-sell- ing pharmaceutical products are currently accounted for by bio- pharmaceuticals, and this figure is rising. This booklet is intended to show what has already been achieved via close cooperation between basic biological research, applied science and biotechnologically based pharmaceutical and diag- nostic development. Just as in the past the development of beer, bread and cheese were major breakthroughs, another revolution is now about to overtake medicine: compounds produced using biotechnological methods are opening up entirely new possibilities in medical diagnostics and therapy, and in so doing are bringing about a major restructuring of markets. From knowledge to science: the history of biotechnology Babylonian biotechnologists were a highly regarded lot. Their products were in demand among kings and slaves and were ex- ported as far as Egypt. They are even mentioned in the Epic of Gilgamesh, the world’s oldest literary work – the Babylonian brewers, with their 20 different types of beer. Their knowledge was based on a biological technology that was already thousands of years old – fermentation Terms by yeast. Biopharmaceuticals drugs manufactured using biotech- Though it may sound nological methods. The only thing that is relatively new about the biotechnology industry is its name. Stone Age, Iron Age, The term ‘biotechnology’ was first used in a 1919 Age of Biochemistry publication by Karl Ereky, a Hungarian engineer and economist. He foresaw an age of biochemis- try that would be comparable to the Stone Age and the Iron Age in terms of its historical significance.
Monitoring Measure Frequency Rationale Creatinine and At least daily in folinic acid * Dose of disodium levofolinate is methotrexate levels rescue dependent on these parameters in ‘rescue’ buy 150 mg bupron sr amex molal depression constant definition. Additional information Common and Immediate:Pyrexialreactions generic bupron sr 150mg overnight delivery bipolar depression 45,anaphylaxisand urticariahave beenreportedrarely order bupron sr 150 mg line depression symptoms spanish. Significant * Levofolinate may #levels or effect of the following drugs: interactions possible #efficacy of folic acid antagonists, e. This assessment is based on the full range of preparation and administration options described in the monograph. Pre-treatment checks * Avoid in severe heart failure, second- and third-degree heart block and sinus node dysfunction (unless a pacemaker is fitted) and cardiogenic shock. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Disopyramide | 267 Technical information Incompatible with No information Compatible with Flush: NaCl 0. This is more likely in patients with cardiomyopathy or uncompensated congestive heart failure. Additional information Common and serious Anticholinergic effects such as dysuria, acute urinary retention (more undesirable effects likely in patients with prostatic enlargement), disorders of accommodation, diplopia, dry mouth. This assessment is based on the full range of preparation and administration options described in the monograph. Its use requires intensive haemodynamic monitoring and ideally should be confined to the critical care setting. Dobutamine | 269 * It may also be used in cardiac stress testing if the patient cannot undergo a period of exercise or if the exercise yields no useful information (dobutamine stress echocardiography). Pre-treatment checks * Do not use in mechanical obstruction of ventricular filling and/or outflow, hypovolaemia. Biochemical and other tests (not all are necessary in an emergency situation) Bodyweight Electrolytes: serum K Dose Inotropic effect: initiate at 2. Cardiac stress testing: initially 5 micrograms/kg/minute for 3--8 minutes increasing by 5 micrograms/kg/minute every 3--8 minutes, up to a usual maximum of 20 micrograms/kg/minute (occasionally up to 40 micrograms/kg/minute may be required). Continuous intravenous infusion via a syringe pump The concentration used is dependent on the patient’s dosage and fluid requirements but the final concentration must be no greater than 5mg/mL. Withdraw 250mg (20mL) of the concentrate and make up to 50mL in a syringe pump with Gluc 5% or NaCl 0. Cap the syringe and mix well to give a solution containing 5mg/mL (5000 micrograms/mL). Inspect visually for particulate matter or discoloration prior to administration and discard if present. Calculation of infusion rate: Weight ðkgÞÂrequired rate ðmicrograms=minuteÞÂ60 Infusion rate ðmL=hourÞ¼ Concentration of prepared infusion ðmicrograms=mLÞ See Table D6 below for a dosage chart detailing pre-calculated infusion rates for each bodyweight using a 5mg/mL (5000 micrograms/mL) solution. Aciclovir, alteplase, aminophylline, amphotericin, bumetanide, calcium gluconate, ceftazidime, digoxin, doxapram, drotrecogin alfa, flucloxacillin, foscarnet, furosemide, heparin sodium, insulin (soluble), micafungin, midazolam, pantoprazole, phenytoin sodium, phytomenadione, piperacillin with tazobactam. Stability after From a microbiological point of view, should be used immediately; however, preparation prepared infusions may be stored at 2--8 C and infused (at room temperature) within 24 hours. Blood glucose At least 12-hourly * May see "insulin requirements in patients with diabetes mellitus. Response to therapy After 72 hours * Tolerance may develop after 72 hours of therapy. Other: headache, bronchoconstriction, eosinophilia, #platelet aggregation with prolonged therapy, nausea, urinary urgency. This assessment is based on the full range of preparation and administration options described in the monograph. T able D obutam in e rate ofin fusion usin g dobutam in e 2 m g m ade up to5 m L in a 5 - m L syrin ge pum p ( 5 m icrogram s/ m L I nfusi onrate ( m i crog ram s/ kg / i nute) 1 W ei g h t R ate ofi nfusi on( m h our) i nkg 4 4 5 5 6 6 7 7 8 8 9 9 1 1 1 1 1 Dopamine hydrochloride | 273 Dopam ine hydrochloride 40mg/mL and 160mg/mL solution in 5-mL ampoules 40mg/mL solution in 5-mL and 10-mL vials 400mg (1. Its use requires intensive haemodynamic monitoring and ideally should be confined to the critical care setting. Pre-treatment checks * Do not use in phaeochromocytoma, hyperthyroidism, uncorrected atrial or ventricular tachy- arrhythmias, ventricular fibrillation. Continuous intravenous infusion The concentration used is dependent on the patient’s dosage and fluid requirements. The solution should be clear and almost colourless (the concentrate may have a pale straw colour). Inspect visually for particulate matter or discoloration prior to administration and discard if present. Continuous intravenous infusion via a syringe pump For administration via a central line only. Withdraw 200mg of the concentrate and make up to 50mL in a syringe pump with NaCl 0. Cap the syringe and mix well to give a solution containing 4mg/mL (4000 micrograms/mL). The solution should be clear and almost colourless (the concentrate may have a pale straw- colour). Inspect visually for particulate matter or discoloration prior to administration and discard if present. Calculation of infusion rate: Weight ðkgÞÂrequired rate ðmicrograms=minuteÞÂ60 Infusion rate ðmL=hourÞ¼ Concentration of prepared infusion ðmicrograms=mLÞ See Tables D8, D9 and D10 below for dosage charts detailing pre-calculated infusion rates for each bodyweight using 1. Dopamine hydrochloride | 275 Technical information Incompatible with Sodium bicarbonate. Aciclovir, amphotericin, ampicillin, alteplase, benzylpenicillin (penicillin G), furosemide, gentamicin, insulin (soluble). Stability after From a microbiological point of view, should be used immediately; however, preparation prepared infusions may be stored at 2--8 C and infused (at room temperature) within 24 hours. Monitoring Measure Frequency Rationale Blood pressure Continuously * Response to therapy. Infusion site * Possible necrosis on extravasation; see Additional information below for management. Benefits of continued dopamine infusion should be weighed against the risk of possible necrosis. Renal function Periodically * Monitor particularly during high dose regimens (>20 and serum Na microgram/kg/minute) as decreased renal blood flow can and K occur. Additional information Common and serious Infusion-related: Local: Extravasation -- necrosis and sloughing of the undesirable effects surroundingtissue. Ischaemiacanbe reversedbyinfiltrationofthe affectedarea with phentolamine (see the Phentolamine monograph). This assessment is based on the full range of preparation and administration options described in the monograph. Dopamine hydrochloride | 277 Table D8 Dopamine rate of infusion using dopamine 400 mg in a 250-mL infusion bag, i. It stimulates beta -adrenoceptors and2 peripheral dopamine receptors; it inhibits neuronal uptake of noradrenaline.