Dobutamine
Risk Factor: BM
Class: AUTONOMICS
/ Sympathomimetics (Adrenergics)
Contents of this page:
Fetal Risk Summary
Breast Feeding Summary
References
Questions and Answers
Fetal Risk Summary
Dobutamine, an inotropic agent, is structurally related to dopamine. Reproduction studies in rats (at doses up to the normal human dose10 g/kg/min for 24 hours for a total daily dose of 14.4 mg/kg [NHD]) and rabbits (at doses up to twice the NHD) did not reveal any evidence of fetal harm (1).
No reports describing the placental transfer of dobutamine or studying its effects during human pregnancy have been located (see also Dopamine). The relatively low molecular weight (about 301), however, probably indicates that transfer to the fetus occurs. Short-term use in one patient with a myocardial infarction at 18 weeks' gestation was not associated with any known adverse effects (2).
Breast Feeding Summary
No data are available.
References
- Product information. Dobutrex. Eli Lilly and Company, 2000.
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Stokes IM, Evans J, Stone M. Myocardial infarction and cardiac arrest in the second trimester followed by assisted vaginal delivery under epidural analgesia at 38 weeks gestation. Case report. Br J Obstet Gynaecol 1984;91:1978.
Questions and Answers
Has anyone had a family member die from a heart attack during a dobutamine stress test?, My father died in 2005 during a doubutamine stress test. It's an non-invasive test used to eval CAD (coronary artery disease) for people who can't exercise on a treadmill. There is only a 1% chance of the test actually causing a heart attack that results in death. I just want to know if someone else has had this experience?
I used to assist with the stress tests at a hospital that I worked and I have never seen that happen. That is very rare, but I'm sure it makes it no less bearable for you. I'm sorry for your loss.
what are the differences of levophed,dopamine and dobutamine in terms of their action?, can this three medication administer to the patient all at the same time?
Levophed (norepinephrine) acts predominantly on alpha-adrenergic receptors to produce constriction of resistance and capacitance vessels, thereby increasing systemic blood pressure and coronary artery blood flow. Norepinephrine also acts on beta1-receptors, although quantitatively less than either epinephrine or isoproterenol. In relatively lower doses, the cardiac-stimulant effect of norepinephrine is predominant; with larger doses, the vasoconstrictor effect predominates.
Similar to epinephrine, norepinephrine has direct agonist effects on effector cells that contain alpha- and beta-receptors. As with other catecholamines, the intracellular action of norepinephrine is mediated via cyclic adenosine monophosphate (cAMP), the production of which is augmented by beta stimulation and attenuated by alpha stimulation.
The primary pharmacodynamic effects of norepinephrine are cardiac stimulation, particularly at lower doses, and vasoconstriction, which tends to predominate with moderate to higher doses of the drug. Metabolic effects observed with epinephrine, such as glycogenolysis, inhibition of insulin release, and lipolysis, also occur with norepinephrine but are much less pronounced.
The hemodynamic consequences of norepinephrine's cardiovascular stimulation include increases in systolic, diastolic, and pulse pressures. Cardiac output is generally unaffected, although it can be decreased, and total peripheral resistance is also elevated. The elevation in resistance and pressure result in reflex vagal activity, which slows the heart rate and increases stroke volume. The elevation in vascular tone or resistance reduces blood flow to the major abdominal organs as well as to skeletal muscle. As with epinephrine, however, coronary blood flow is substantially increased secondary to the indirect effects of alpha stimulation. Therefore, unlike epinephrine, norepinephrine does not significantly increase myocardial oxygen consumption, except in patients with variant angina who are hyperresponsive to alpha stimulation.
Norepinephrine is ineffective orally, and subcutaneous absorption is poor. As a result, it is recommended that norepinephrine be administered only via the intravenous route. Following IV administration, the onset of activity is rapid, with a short duration of action of only 1—2 minutes following discontinuation of the infusion. The short half-life of norepinephrine is due to the fact that the drug is rapidly inactivated by catechol-O-methyltransferase and monoamine oxidase in the liver and other tissues. The pharmacologic activity of norepinephrine is rapidly terminated by uptake and metabolism in the synaptic cleft. Negligible amounts of norepinephrine are excreted unchanged in urine. Most of the drug is eliminated renally as sulfate- or glucuronide-conjugated metabolites. The drug crosses the placenta but not the blood-brain barrier.
Dopamine is a neurotransmitter that possesses intrinsic activity, as well as serving as the metabolic precursor of norepinephrine and epinephrine. Endogenous dopamine is synthesized from tyrosine. During gestation, the adrenal medulla is formed in parallel with the peripheral sympathetic nervous system; hence there are two CNS and peripheral sources of catecholamines in the body. Once synthesized, dopamine is converted to norepinephrine and norepinephrine is converted to epinephrine in peripheral sites. In the CNS, dopamine is secreted to stimulate central dopamine receptors directly, however, exogenous dopamine does not cross the blood-brain barrier.
Dopamine receptors are subdivided into D1 and D2, and exogenous dopamine stimulates both. DA1 receptors are postsynaptic receptors and mediate vasodilation in renal, mesenteric, coronary, and cerebral blood vessels. DA2 are presynaptic receptors located on postganglionic sympathetic nerves and, when stimulated, norepinephrine release from sympathetic nerve endings is inhibited.
The clinical effects of exogenous dopamine vary depending on the rate of infusion. At low doses (0.5—2 mcg/kg/min), dopamine principally acts on specific dopaminergic receptors in the renal, mesenteric, coronary, and intracerebral vasculature, resulting in vasodilation. The most clinically significant effect of this vasodilatory response is increased renal blood flow. This increase improves GFR which can be critical in patients with diminished renal perfusion. The corresponding increase in urinary output serves as an indirect marker of increased perfusion to other vital organs. At moderate therapeutic doses (2—10 mcg/kg/min), dopamine also stimulates beta1-adrenergic receptors, resulting in increased cardiac output while maintaining the dopaminergic-induced vasodilatory effects. Compared to isoproterenol, dopamine exerts selectively greater effects on contractility than on heart rate. At high dopamine doses (> 10 mcg/kg/min), alpha-adrenergic agonism predominates, and increased peripheral vascular resistance and renal vasoconstriction result. Interestingly, fenoldopam and bromocriptine, selective agonists at D1- and D2-receptors, respectively, both lower blood pressure in hypertensive patients.
Following administration of continuous IV dopamine infusion, the onset of action occurs within 5 minutes and persists for less than 10 minutes. The plasma half-life is about 2 minutes. Distribution occurs throughout the body; however, dopamine does not significantly cross the blood-brain barrier. Dopamine is metabolized in the liver, kidneys, and plasma to inactive compounds by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT). About 25% of dopamine is metabolized to norepinephrine within adrenergic nerve terminals. Excretion occurs in the urine, mainly as metabolites and conjugates.
Dobutamine is a direct-acting sympathomimetic. It is primarily an agonist at beta1-adrenergic receptors, with minor beta2 and alpha1 stimulatory effects. Clinical actions reflect both beta agonism by the (+) isomer and the alpha agonism by the less potent (-) isomer. Agonism at the beta1-adrenergic receptor predominates and increases myocardial contractility and stroke volume with modest chronotropic effects, resulting in increased cardiac output. The inotropic effects are dose-dependent. Dobutamine's secondary hemodynamic effects include decreases in systemic vascular resistance (afterload) and ventricular filling pressure (preload). Systolic blood pressure is generally elevated as a consequence of increased stroke volume, although diastolic blood pressure and mean arterial pressure are usually unchanged with normal doses in normotensive patients. Increased myocardial contractility results in increased coronary blood flow and myocardial oxygen consumption. Dobutamine has minimal effect on pulmonary vascular resistance. Unlike dopamine, dobutamine does not affect dopaminergic receptors, nor does it cause release of norepinephrine from sympathetic nerve endings. Urinary output can increase, however, secondary to increased cardiac output. Electrophysiologically, dobutamine can facilitate AV nodal conduction, particularly in patients with concomitant atrial fibrillation.
Onset of action occurs within 2 minutes, although peak pharmacodynamic activity can be delayed up to 10 minutes. The plasma half-life of dobutamine is about 2 minutes. The drug is metabolized in the liver enzymatically by catechol-O-methyltransferase and by glucuronidation to inactive metabolites. Excretion occurs mainly by the kidney as the metabolites and conjugates.
The answer to you second question, in the clinical setting you wouldn't normally administer all 3 drugs at the same time and they shouldn't be.
Why cant you have caffiene before a dobutamine nuclear stress test?,
Dobutamine increases your heart rate and heart contraction. Caffeine also increases your heart rate. So taking caffeine beforehand will make the results inaccurate since it is interfering and affecting the beating and work of the heart. Basically you will be unable to tell if your are making the heart work harder ("stressing the heart") due to the Dobutamine or the caffeine.
Does anyone know the formula for computing dopamine/dobutamine?, I'm taking my nclex exam at the end of the month and I just want to be prepared in case there's a question regarding dopamine.
A good rule of thumb is the number TWO.
TWO milligrams per kilogram for lidocaine bolus.
TWO milligrams per minute for infusion for lidocaine, procainamide, bretylium, labetolol,
TWO Micrograms per kilogram for isopreterenol, norepinephrine, amrinone, and epinephrine
TWO Micrograms per kilogram per minute for dopamine, dobutamine, sodium nitroprusside,
Start with TWO and titrate up or down based upon response.
A second rule of thumb.never EVER do these calculations in your head. If you write them down on paper, make sure the paper becomes part of the chart to show you did them right.
If you use a calculator make sure you understand the formulas and are not just plugging in numbers. ((I use a slide rule and can do it faster than with a calculator. Very impressive in court when they question your calculations. But then again, I am an old nurse with a strong background in math..))
What is "Dobutamine, Stress Echocardiography criteria"?, What criteria can be recognized as serious coronary artery disease? Thanks.
Dobutamine is the chemical they use for non-exercise stress tests. IOW, there are some people who simply can't run on a treadmill, so they have to make their heart work and act like it's on a treadmill... without the running part. What they do is they use dobutamine intravenously to raise the heart rate and BP.
my husband is to have a stress echocardiogram he will be having dobutamine injected?, he is really worried about it as he keeps losing his breath and he is wooried he will not be able to breath has any one had one and is it as bad as he thinks it will be
There is no real need for you to worry. The dobutamine infusion will only slowly increase his heart rate and blood pressure in a controlled way whilst he is being monitored. The rate of the infusion is increased every three minutes until target heart rate is achieved ( this is determined by the Doctor and will be based on your husbands age and physical condition).
His BP will be monitored and ECG tracing will be made routinely throughout the infusion. If your husband starts to feel pain or discomfort he can ask to stop the infusion at anytime.This will all be explained when you get there but your husband should immediately inform the technologist if he feels any chest pain, breathing difficulties, sweating, or heart palpitations during the test. The rare risks associated with this test are just that, rare.
Dobutamine Question for doctors and nurses!!?, A pt goes into heart failure and the MD orders Dobutamine a 3 mcg/kg/min. The pt weighs 240 pounds. What rate will the nurse set the IV pump to run at? ______ml/hr
Mom's takin a test and need to ace it so please help me out can you explain how you got the answer too but if not the answer is fine. but yeah
first u have to find out what is the strength of the drug (dobutamine) like how many mg/ml
anyway its 327mcg/min for a pt of 240 lbs hope thats helpful
How do you solve this equation?, You receive an order to prepare 250 mg of dobutamine in a 100-ml pump cassette with NS as the diluent. Dobutamine is available as a 12.5-mg/ml solution. How many milliliters of dobutamine do you need to prepare this prescription?
If you need 250 mg of dobutamine in 100 ml, that is 2.5mg/ml. (250mg/100ml = 2.5mg/ml)
the equation is
2.5 mg/ml * 100ml = 12.5 mg/ml * xml
x = 20 ml
100ml = total volume needed, and x = volume of the 12.5mg/ml solution needed
So that would be 20 ml of 12.5mg/ml solution + 80 ml of the NS.
Hope that helps
REASONS why dobutamine is medicine of choice in :?, CARDIOGENIC SHOCK
and CARDIAC FAILURE?
It has no renovasculature effect, urine output increases BP IMPROVES.
It reduces systemic resistance and improves cardiac performance, thereby decreasing both after load and ventricular filling pressures.
Greater improvement in cardiac out put as compared to dobutamine, for a given increase in myocardial consumption.
