Cardiac vs Pulmonary Dyspnea - New tool to assess COPD/CHF

[GAmedic1506]

I know it sounds to simple to be true -- I will site you the threads you need (I am working, and do not have these stored on this computer), but its really common sense if you think about what happens to the body in CHF versus COPD or asthma (think alpha/beta) for your first clue. And I meant it works as fast as D50 in reversing the condition, not that it was a carbohydrate (and note that I said Dobutamine, not Dopamine -- many get confused by that). You will also note that I said Dobutamine for those who are drowning, not every CHF patient. Nitro is still the first drug followed by Morphine -- Dobutamine is used for those who do not respond, or who are already circling the drain. Dobutamine does not cause tachycardia -- that is dopamine (although many believe the two drugs work on the same receptor sites, they are totally opposite).

And techno, please cut back on the caffeine or increase the prozac -- you get worked up way too easy. I know it sounds to good to be true, and too simplistic, but it is, and it is the deciding trigger we have used for the past 3 years, and we have yet to be wrong. In fact, our Doctors are amazed at our accuracy in the absence of a chest x-ray.

[TechMedic05]

I know it sounds to simple to be true -- I will site you the threads you need (I am working, and do not have these stored on this computer), but its really common sense if you think about what happens to the body in CHF versus COPD or asthma (think alpha/beta) for your first clue. And I meant it works as fast as D50 in reversing the condition, not that it was a carbohydrate (and note that I said Dobutamine, not Dopamine -- many get confused by that).

The first half, I'm trying to follow, but sorry - I'm not completely getting what you're hinting at.

And I assumed you had meant onset - but it was not stated as such. And I think everyone knows you meant dobutamine, as myself and AZCEP both used dobutamine in our responses, as well.

Thanks for getting back to me - take your time on the information requested.

[GAmedic1506]

You are a smart guy techno, give it 10 minutes I know you will get it.

[TechMedic05]

I know it sounds to simple to be true -- I will site you the threads you need (I am working, and do not have these stored on this computer), but its really common sense if you think about what happens to the body in CHF versus COPD or asthma (think alpha/beta) for your first clue. And I meant it works as fast as D50 in reversing the condition, not that it was a carbohydrate (and note that I said Dobutamine, not Dopamine -- many get confused by that). You will also note that I said Dobutamine for those who are drowning, not every CHF patient. Nitro is still the first drug followed by Morphine -- Dobutamine is used for those who do not respond, or who are already circling the drain. Dobutamine does not cause tachycardia -- that is dopamine (although many believe the two drugs work on the same receptor sites, they are totally opposite).

And techno, please cut back on the caffeine or increase the prozac -- you get worked up way too easy. I know it sounds to good to be true, and too simplistic, but it is, and it is the deciding trigger we have used for the past 3 years, and we have yet to be wrong. In fact, our Doctors are amazed at our accuracy in the absence of a chest x-ray.

Okay, thank you GA for making this post, then editing it afterward, and still not actually answering our questions.

I had attempted to make the point that blood pressure alone is not a reliable determinant for assessing dyspnic patients.

Thankfully, AZCEP jumped in, as well with:

"The biggest issue is determining what the problem is. Is it truly pulmonary edema? Is it pneumonia, that is moving enough air to sound like coarse pulmonary edema? Is it in fact cardiac asthma?

Too many possibilities to say that the blood pressure will make the determination. If it could, don't you think someone would have used that method already? Blood pressure will guide treatment, but it does little to tell you what you are dealing with."

And he's right-on. It may help guide, but it's not reliable to make a definite diagnosis alone, like you were suggesting with:

"You dont need any fancy machines, just look at the blood pressure."

Regarding Dobutamine - This posting by Ace844 is a good reference, which includes the following statement:" Dobutamine is a catecholamine that acts directly on the beta-1 receptor, causing both a chronotropic and an inotropic response from the heart. Dopamine is also a catecholamine that increases both the chronotropic and inotropic responses of the heart. In addition to its beta-1 actions, dopamine also works on both alpha and dopaminergic receptors."

Maybe I'm a dumbie, or drinking too much caffeine and not eating enough of my SSRI's of choice for the day, but that sounds awfully similar to me. Dobutamine appears to be a bit more selective in it's actions, not exactly "totally opposite". I, myself, am not completely familiar with Dobutamine, so I may be incorrect. If so, please correct me. Please. I hate being wrong all the time.

And second to last: "and it is the deciding trigger we have used for the past 3 years, and we have yet to be wrong. In fact, our Doctors are amazed at our accuracy in the absence of a chest x-ray"

I know I'm still new and all, but I wish I was always right.

And: Worked up, eh? A little, but when someone comes on, throws around a few numbers based on 'personal observations' and their own systems' outcomes - I want more information. Something a little more legitimate for reference would be appreciated. Not too many can jump aboard, ruffle a lot of feathers in other threads, then throw around statistics without any backing other than 'I said so' and be taken seriously, and then have the audacity to state "And yes I could give you many long paragraphs explaining why, but this thread is already too long." to say C'mon, GA. You're smart, too. Should've seen this coming.

"You are a smart guy techno, give it 10 minutes I know you will get it."

The reason why I stated I didn't completely get it is because you haven't thoroughly and adequately stated an appropriate answer, that you tried to cover with laziness. I honestly don't thoroughly believe you know exactly what you're talking about. You know a lot, sir, but some things just aren't adding up to me yet.

And the name's TechMedic05. There's actually no "n's" or "o's" in it.

[AZCEP]

GA,

You will have to give us better responses than that.

There is no way that the only assessment your medics are using is the blood pressure to determine the presence of CHF. The list of differential's is just too long. I mentioned a couple in a previous post, but you and I both know that was merely the tip of the proverbial iceberg.

Blood pressure + JVD-->good possibility

Blood pressure + JVD + lung sounds--> even better

Blood pressure + JVD + lung sounds + Pt. history-->better still

Blood pressure + JVD + lung sounds + Pt. history + Fulminant-->slam dunk

Each step along the way the picture becomes more and more clear, but you can not determine the problem with an individual vital sign. Not even the utility of capnography can eliminate all of the possibilities. A BNP test from a lab, narrows things down, but you have to use it with all of the other clinical information.

I will admit, that if your crews are on the fence between CHF and cardiogenic shock, then yes, the distinction is made from the blood pressure. Otherwise, your argument is full of holes.

[Ridryder 911]

I guess GAMedic never heard of pulmonary hypertension as well. Although, that may be an indicator of CHF, not all CHF patients has hypertension when in failure, in fact most patients in sever distress presents hypotension (shift from right side to left side) and decreases the work load for about 10 minutes.

Remember the true etiology of CHF is caused by poor pump failure such as in an AMI, poor ejection fraction, which the patient may not have hypertension. Dependent on just those findings is asking to eliminate other clinical symptoms as well.

R/r 911

[TechMedic05]

I guess GAMedic never heard of pulmonary hypertension as well. Although, that may be an indicator of CHF, not all CHF patients has hypertension when in failure, in fact most patients in sever distress presents hypotension (shift from right side to left side) and decreases the work load for about 10 minutes.

Remember the true etiology of CHF is caused by poor pump failure such as in an AMI, poor ejection fraction, which the patient may not have hypertension. Dependent on just those findings is asking to eliminate other clinical symptoms as well.

R/r 911

Excellent points, Rid!

And definitely, those pulmonary hypertension patients are rahter difficult to manage.

Above all, understanding that not all CHF is hypertensive, not all pulmonary is non-hypertensive, especially with multiple disease processes taking their toll.

[Ace844]

"GA,"

"TECHmedic," great post, very sucinct and well said. "GAmedic," I posted this study here because although I was initially skeptical of this machine, now having seen it work a few times in 'real time' I have started to come around. There are numerous posts here on CHF, cardiac phys, etc... feel free to do a search and read some of them.

Clinicians must continually integrate vast amounts of medical information with their skills in clinical decision making. They must be thorough yet efficient in gathering data and use strategies that promote maximal diagnostic proficiency while limiting time and performing maximal benefical intervention. These unique skills are neither adequately taught nor measured in medical schools, professional medical programms, and residencies. Emergency physicians, and other clinicians (READ PARAMEDICS AND EMS PROVIDERS) have become some of the most facile and rapid decision-makers in medicine. This is likely due to the nature of their specialty. Emergency physicians, and other clinicians (READ PARAMEDICS AND EMS PROVIDERS) are bombarded by diagnostic and management decisions throughout a clinical shift. Many pertain directly to diagnosing and managing a patient’s problem. Others relate to managing the scene, other agencies and providers, the clinical environment, and tranpsort destinations and decisions and interventions. As well as the risk-benefit ratios of all of the aforementioned as they apply to the patient. By better understanding the decision-making process of emergency provider, improved decision-making strategies can be developed and taught.

Both an adequate knowledge base of medical information and a repertoire of decision-making skills are necessary to diagnose and manage medical problems. Expert emergency care providers have learned to recognize disease and injury patterns and have developed sets of heuristics (rules of thumb) to make rapid decisions. When patient presentations do not fit an existing pattern or heuristic, EMS providers move between several levels of clinical decision making depending on their clinical experience, the clinical situation, and time constraints. Most errors in mental functioning affecting patient care can be traced to defects in one or more of these levels of clinical decision making.

Mental effort saved through improved decision making provides a “cognitive reserve” for emergency physicians, and other clinicians (READ PARAMEDICS AND EMS PROVIDERS) to control their hectic environment with decreased occupational stress and potential burnout. With greater reserve, emergency care providers are better able to consider patients’ values and expand their knowledge base.

In closing; please as 'AZCEP, TECHmedic, Ridryder," have written please take all of the time and space you need to explain your rationale and previous posts here. WE await your futher posts and explanations, and please peruse this post as well: Panel clarifies warnings for CHF medication.

Out Here,

ACE844

P.S. Here's some more information; first a MNEMONICthen more info. about DOBUTAMINE:

Non-Cardiogenic Pulmonary Edema, Causes of

PONS

P hosgene, paraquat, phenothiazines

O pioids/organophosphates

N itrous dioxide

S alicylates

Dobutamine

Dobutamine is a very useful inotropic agent for moderately decompensated HF.[127] As available clinically, dobutamine is a racemic mixture that stimulates both beta1 - and beta2 -adrenergic receptor subtypes (binding at an approximately 3:1 ratio)[124] and either binds to but does not activate alpha-adrenergic receptors ([+] enantiomer) or stimulates alpha1 and alpha2 receptor subtypes ([-] enantiomer). As discussed earlier, dobutamine also has a relatively high affinity for uptake1 . The affinity constants for racemic dobutamine binding to beta1 , beta2 , and alpha1B receptors are given in Table 23-5 , where it can seen that dobutamine is relatively nonselective for binding to beta1 versus beta2 receptors and binds to alpha1 receptors and uptake1 at a slightly higher affinity. When compared with isoproterenol, in human cardiac preparations, dobutamine is a partial beta-agonist with an intrinsic activity of approximately 0.5.[125] The binding to alpha receptors by each isomer of dobutamine results in a mixture of antagonist and agonist action that, when coupled with some peripheral vascular beta2 -agonism, usually produces a net mild degree of vasodilation at lower (≤5 µg/kg/min) doses. At these doses, dobutamine reduces aortic impedance and systemic vascular resistance, thus reducing afterload and improving ventricular-vascular coupling by reducing aortic impedance.[126] [127] In contrast, dopamine (see later) may either have no effect or increase ventricular afterload by increasing systemic vascular resistance and by causing a more rapid return of reflected aortic pressure waves, depending on the infusion rate. Therefore, dobutamine is preferable to dopamine for most patients with advanced decompensated HF who have not responded adequately to intravenous diuretics.

The neuronal reuptake inhibition of dobutamine means that in subjects with preserved neuronal uptake mechanisms, dobutamine may increase synaptic cleft area norepinephrine concentrations in the heart in addition to its intrinsic receptor-mediated actions. Dobutamine does not stimulate dopaminergic receptors and, unlike dopamine, does not selectively alter renal blood flow.[128] The importance of the vascular effects of dobutamine has been demonstrated by experiments in animals with artificial hearts.[129] [130] Even in the presence of a mechanical heart, dobutamine increased cardiac output by 10 to 15 percent and decreased systemic vascular resistance. Interestingly, dobutamine also decreases venous capacitance and increases right atrial pressure, possibly as a result of alpha1 -adrenergic agonism of the (-) enantiomer.[130] These experiments also demonstrated that the (+) enantiomer is responsible for the racemic drug's favorable effects on aortic input impedance, wave reflectance, and systemic vascular resistance.[129] The LV afterload-reducing effects are also responsible for the reduction in functional mitral regurgitation often observed concomitantly with dobutamine infusions in patients with large dilated ventricles and high LV end-diastolic pressure.[131] Dobutamine also causes a mild decline in pulmonary vascular resistance that is present regardless of chronic background vasodilator therapy.

At higher doses, the (-) isomer of dobutamine begins to exert alpha1 -adrenergic agonist action, thereby preventing progressive vasodilation and usually leading to minimal changes in preload and afterload. The advantage of this alpha-adrenergic effect of dobutamine is that because preload and afterload do not change dramatically, dobutamine can be administered without pulmonary artery catheter monitoring of LV filling pressure. Another advantage of the relative lack of vasodilation coupled to the partial agonist action is that dobutamine does not produce much increase in the heart rate at doses of 10 µg/kg/min or less. Because of its partial agonist activity, desensitization to prolonged infusions of dobutamine is not pronounced.[132] Dobutamine infusions are initiated at 2 to 3 µg/kg/min and are titrated upward according to the patient's hemodynamic response (usually not higher than 20 µg/kg/min).[127] [128]

The limitations of dobutamine are that it (1) is a relatively weak beta-agonist,[125] (2) only modestly lowers elevated pulmonary artery pressure, (3) eventually produces desensitization phenomena when used chronically,[132] [133] and (4) cannot be effectively used in the presence of high levels of beta-adrenergic receptor blockade.[119] [120] The first three of these limitations can be overcome by combining dobutamine with a phosphodiesterase inhibitor (see below), which results in additive effects on myocardial performance,[134] substantial reductions in pulmonary wedge and pulmonary artery pressure,[134] and a protective effect on desensitization[133] related to being able to lower the dobutamine dose. The fourth limitation is best dealt with by avoiding dobutamine and using a PDEI alone in patients receiving carvedilol or high doses of beta1 -blocking agents; in the presence of carvedilol, dobutamine produces little or no increase in stroke volume and increases systemic vascular resistance.[119] [120] On the other hand, favorable hemodynamic responses to the PDEIs, enoximone or milrinone, are enhanced by either carvedilol[119] [120] or metoprolol.

(Dobutamine: Drug information

Copyright 1978-2006 Lexi-Comp @ Inc. All rights reserved.)

PHARMACOLOGIC CATEGORY

Adrenergic Agonist Agent

DOSING: ADULTS — Cardiac decompensation: I.V. infusion: 2.5-20 mcg/kg/minute; maximum: 40 mcg/kg/minute, titrate to desired response; see table.

I.V. Infusion Guidelines

To deliver 2.5 mcg/kg/minute:

Using 500 mcg/mL solution1; infuse at 0.005 mL/kg/minute.

Using 1000 mcg/mL solution2; infuse at 0.0025 mL/kg/minute.

To deliver 5 mcg/kg/minute:

Using 500 mcg/mL solution1; infuse at 0.01 mL/kg/minute.

Using 1000 mcg/mL solution2; infuse at 0.005 mL/kg/minute.

To deliver 7.5 mcg/kg/minute:

Using 500 mcg/mL solution1; infuse at 0.015 mL/kg/minute.

Using 1000 mcg/mL solution2; infuse at 0.0075 mL/kg/minute.

To deliver 10 mcg/kg/minute:

Using 500 mcg/mL solution1; infuse at 0.02 mL/kg/minute.

Using 1000 mcg/mL solution2; infuse at 0.01 mL/kg/minute.

To deliver 12.5 mcg/kg/minute:

Using 500 mcg/mL solution1; infuse at 0.025 mL/kg/minute.

Using 1000 mcg/mL solution2; infuse at 0.0125 mL/kg/minute.

To deliver 15 mcg/kg/minute:

Using 500 mcg/mL solution1; infuse at 0.03 mL/kg/minute.

Using 1000 mcg/mL solution2; infuse at 0.015 mL/kg/minute.

1500 mg/L or 250 mg per 500 mL of diluent.

21000 mg/L or 250 mg per 250 mL of diluent.

DOSING: PEDIATRIC — Cardiac decompensation: Refer to adult dosing.

(For additional information see "Dobutamine: Pediatric drug information")

DOSING: ELDERLY — Refer to adult dosing.

DOSAGE FORMS

Infusion, as hydrochloride [premixed in dextrose]: 1 mg/mL (250 mL, 500 mL); 2 mg/mL (250 mL); 4 mg/mL (250 mL)

Injection, solution, as hydrochloride: 12.5 mg/mL (20 mL, 40 mL, 100 mL) [contains sodium bisulfite]

DOSAGE FORMS: CONCISE

Infusion [premixed in dextrose]: 1 mg/mL (250 mL, 500 mL); 2 mg/mL (250 mL); 4 mg/mL (250 mL)

Injection, solution: 12.5 mg/mL (20 mL, 40 mL, 100 mL)

GENERIC EQUIVALENT AVAILABLE — Yes

ADMINISTRATION — Use infusion device to control rate of flow; administer into large vein. Do not administer through same I.V. line as heparin, hydrocortisone sodium succinate, cefazolin, or penicillin.

(show formula)

COMPATIBILITY — Stable in D5LR, D51/2NS, D5NS, D5W, D10W, LR, 1/2NS, NS, mannitol 20%; not stable in sodium bicarbonate 5%; variable stability (consult detailed reference) in peritoneal dialysis solutions

Y-site administration: Compatible: Amifostine, amiodarone, atracurium, aztreonam, bretylium, calcium chloride, calcium gluconate, ciprofloxacin, cisatracurium, cladribine, clarithromycin, diazepam, diltiazem, docetaxel, dopamine, dopamine with lidocaine, dopamine with nitroglycerin, dopamine with sodium nitroprusside, doxorubicin liposome, enalaprilat, epinephrine, etoposide, famotidine, fentanyl, fluconazole, gatifloxacin, gemcitabine, granisetron, haloperidol, hydromorphone, inamrinone, insulin (regular), labetalol, levofloxacin, lidocaine, lidocaine with nitroglycerin, lidocaine with sodium nitroprusside, linezolid, lorazepam, magnesium sulfate, meperidine, milrinone, morphine, nicardipine, nitroglycerin, nitroglycerin with sodium nitroprusside, norepinephrine, pancuronium, potassium chloride, propofol, ranitidine, remifentanil, sodium nitroprusside, streptokinase, tacrolimus, theophylline, thiotepa, tolazoline, vecuronium, verapamil, zidovudine. Incompatible: Acyclovir, alatrofloxacin, alteplase, aminophylline, amphotericin B cholesteryl sulfate complex, cefepime, foscarnet, indomethacin, phytonadione, piperacillin/tazobactam, thiopental, warfarin. Variable (consult detailed reference): Furosemide, heparin, midazolam

Compatibility in syringe: Compatible: Heparin, ranitidine. Incompatible: Doxapram

Compatibility when admixed: Compatible: Amiodarone, atracurium, atropine, dopamine, enalaprilat, epinephrine, flumazenil, hydralazine, isoproterenol, lidocaine, meperidine, meropenem, metaraminol, morphine, nitroglycerin, norepinephrine, phentolamine, phenylephrine, procainamide, propranolol, ranitidine. Incompatible: Acyclovir, alteplase, aminophylline, bumetanide, calcium gluconate, diazepam, digoxin, floxacillin, furosemide, insulin (regular), magnesium sulfate, phenytoin, potassium phosphates, sodium bicarbonate. Variable (consult detailed reference): Bretylium, calcium chloride, heparin, nitroglycerin with sodium nitroprusside, potassium chloride, verapamil

USE — Short-term management of patients with cardiac decompensation

USE - UNLABELED / INVESTIGATIONAL — Positive inotropic agent for use in myocardial dysfunction of sepsis

ADVERSE REACTIONS SIGNIFICANT — Incidence of adverse events is not always reported.

Cardiovascular: Increased heart rate, increased blood pressure, increased ventricular ectopic activity, hypotension, premature ventricular beats (5%, dose related), anginal pain (1% to 3%), nonspecific chest pain (1% to 3%), palpitation (1% to 3%)

Central nervous system: Fever (1% to 3%), headache (1% to 3%), paresthesia

Endocrine & metabolic: Slight decrease in serum potassium

Gastrointestinal: Nausea (1% to 3%)

Hematologic: Thrombocytopenia (isolated cases)

Local: Phlebitis, local inflammatory changes and pain from infiltration, cutaneous necrosis (isolated cases)

Neuromuscular & skeletal: Mild leg cramps

Respiratory: Dyspnea (1% to 3%)

CONTRAINDICATIONS — Hypersensitivity to dobutamine or sulfites (some contain sodium metabisulfate), or any component of the formulation; idiopathic hypertrophic subaortic stenosis (IHSS)

WARNINGS / PRECAUTIONS — May increase heart rate. Patients with atrial fibrillation may experience an increase in ventricular response. An increase in blood pressure is more common, but occasionally a patient may become hypotensive. May exacerbate ventricular ectopy. If needed, correct hypovolemia first to optimize hemodynamics. Ineffective in the presence of mechanical obstruction such as severe aortic stenosis. Use caution post-MI (can increase myocardial oxygen demand). Use cautiously in the elderly starting at lower end of the dosage range.

DRUG INTERACTIONS

Beta-blockers (nonselective ones) may increase hypertensive effect; avoid concurrent use.

(For additional information: Launch Lexi-Interact™ Drug Interactions Program )

Cocaine may cause malignant arrhythmias; avoid concurrent use.

Guanethidine can increase the pressor response; be aware of the patient's drug regimen.

MAO inhibitors potentiate hypertension and hypertensive crisis; avoid concurrent use.

Methyldopa can increase the pressor response; be aware of patient's drug regimen.

Reserpine increases the pressor response; be aware of patient's drug regimen.

TCAs increase the pressor response; be aware of patient's drug regimen.

PREGNANCY RISK FACTOR — B (show table)

LACTATION — Excretion in breast milk unknown

MONITORING PARAMETERS — Blood pressure, ECG, heart rate, CVP, RAP, MAP, urine output; if pulmonary artery catheter is in place, monitor CI, PCWP, and SVR; also monitor serum potassium

TOXICOLOGY / OVERDOSE COMPREHENSIVE — Symptoms include fatigue, nervousness, tachycardia, hypertension, and arrhythmias. Reduce rate of administration or discontinue infusion until condition stabilizes.

CANADIAN BRAND NAMES — Dobutrex®

INTERNATIONAL BRAND NAMES — Butamine® (IL); Cardiject® (ID, TH); Cloridrato de Dobutamina® (BR); DBL Dobutamine® (TH); Dobucor® (ES); Dobuject® (CZ, FI, ID, IL, MX, PL, SG, TH); Dobutamin Fresenius® (DE); Dobutamin Giulni® (SI); Dobutamin Hexal® (DE, HU, PL, RU); Dobutamin Liquid Fresenius® (CH); Dobutamin Nycomed® (AT); Dobutamin Ratiopharm® (DE); Dobutamin Solvay® (AT, DE, HU); Dobutamin-Guilini® (AT, RO, RU); Dobutamina Abbott® (ES); Dobutamina Bioindustria Lim® (IT); Dobutamina Clorhidrato® (CL); Dobutamina DBL® (IT); Dobutamina Duncan® (AR); Dobutamina Fabra® (AR); Dobutamina Gray® (AR); Dobutamina Inibsa® (ES); Dobutamina Richet® (AR); Dobutamina Rovi® (ES); Dobutamina® (CL); Dobutamine Abbott® (TH); Dobutamine Antigen® (TH); Dobutamine Faulding® (BE); Dobutamine Hcl Abbott® (ID); Dobutamine Hydrochloride® (AU, NZ, TR); Dobutamine Solvay® (TH); Dobutamine® (ID, PL, TR); Dobutamin® (BG, CZ, NO); Dobutam® (IL); Dobutrex® (AU, BE, BR, CA, CH, CL, CZ, DK, ES, FI, FR, GB, HK, HR, HU, ID, IE, IN, IT, MX, NL, NO, NZ, PL, RO, RU, SE, TH, TR, YU, ZA); Duvig® (AR); E.M.C.® (AR); Inotop® (AT, SI); Inotrop® (ID); Miozac® (IT); Oxiken® (MX); Posiject® (GB, IE, ZA)

MECHANISM OF ACTION — Stimulates beta1-adrenergic receptors, causing increased contractility and heart rate, with little effect on beta2- or alpha-receptors

PHARMACODYNAMICS / KINETICS

Onset of action: I.V.: 1-10 minutes

Peak effect: 10-20 minutes

Metabolism: In tissues and hepatically to inactive metabolites

Half-life elimination: 2 minutes

Excretion: Urine (as metabolites)

Use of UpToDate is subject to the Subscription and License Agreement.

REFERENCES

1. Bax, JJ, Poldermans, D, Elhendy, A, et al. Improvement of Left Ventricular Ejection Fraction, Heart Failure Symptoms and Prognosis After Revascularization in Patients With Chronic Coronary Artery Disease and Viable Myocardium Detected by Dobutamine Stress Echocardiography. J Am Coll Cardiol 1999; 34:163.

2. Leier, CV, Webel, J, Bush, CA. The Cardiovascular Effects of the Continuous Infusion of Dobutamine in Patients With Severe Cardiac Failure. Circulation 1977; 56:468.

3. Patel, MB, Kaplan, IV, Patni, RN, et al. Sustained Improvement in Flow-Mediated Vasodilation After Short-Term Administration of Dobutamine in Patients With Severe Congestive Heart Failure. Circulation 1999; 99:60.

4. Paulman, PM, Cantral, K, Meade, JG, et al. Dobutamine Overdose. JAMA 1990; 264:2386.

5. Practice Parameters for Hemodynamic Support of Sepsis in Adult Patients in Sepsis. Task Force of the American College of Critical Care Medicine, Society of Critical Care Medicine. Crit Care Med 1999; 27(3):639-60. Available at: http://www.sccm.org/pdf/Hemodynamic%20Support.pdf. Accessed August 13, 2003.

6. Rich, MN, Woods, WL, Davila-Roman, VG, et al. A Randomized Comparison of Intravenous Amrinone Versus Dobutamine in Older Patients With Decompensated Congestive Heart Failure. J Am Geriatr Soc 1995; 43:271.

7. Rivers, E, Nguyen, B, Havstad, S, et al. Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock. N Engl J Med 2001; 345:1368

Dobutamine — Dobutamine (Dobutrex®) is not a vasopressor but rather is an inotrope that causes vasodilation. Dobutamine's predominant beta-1 adrenergic receptor effect increases inotropy and chronotropy and reduces left ventricular filling pressure. In patients with heart failure this results in a reduction in cardiac sympathetic activity [26]. However, minimal alpha- and beta-2 adrenergic receptor effects result in overall vasodilation, complemented by reflex vasodilation to the increased CO. The net effect is increased CO, with decreased SVR with or without a small reduction in blood pressure.

Dobutamine is most frequently used in severe, medically refractory heart failure and cardiogenic shock and should not be routinely used in sepsis because of the risk of hypotension. Dobutamine does not selectively vasodilate the renal vascular bed, as does dopamine at low doses. (See "Inotropic agents in heart failure due to systolic dysfunction").

Dobutamine Hydrochloride (001099)

CATEGORIES:

Ingredients: Dobutamine Hydrochloride

Indications: Decompensation, cardiac

Pregnancy Category B

FDA Approved 1978-07-01

DRUG CLASS: Adrenergic agonists; Inotropes

Brand Names: Butamine (Israel); Cardiject (India); Cardiomin (Philippines); Dobuject (China, Czech-republic, Denmark, Finland, Indonesia, Israel, Korea, Mexico, Russia, Singapore, Sweden, Thailand); Dobumine (Korea); Dobutamina (Ecuador); Dobutamin Giulini (Germany); Dobutamin Hexal (Germany); Dobutamin-Ratiopharm (Germany); Dobutrex (US); Inotrex (Greece, Portugal); Inotrop (Indonesia); Oxiken (Mexico)

(International brand names outside U.S. in italics)

HCFA JCODES: J1250

Cost of Therapy: $33.29 (Cardiac Decompensation-short term; 12.5 mg/ml; 100 ml; Generic Injection (Abbott Hosp.); 1450 mg/day; 2 day supply); $50.75 (Cardiac Decompensation-short term; 12.5 mg/ml; 20 ml; Generic Injection (Bedford); 1450 mg/day; 2 day supply)

DESCRIPTION:

Dobutamine in 5% dextrose injection is a sterile, nonpyrogenic, prediluted solution of dobutamine hydrochloride and dextrose in water for injection. It is administered by intravenous infusion.

Each 100 ml contains dobutamine HCl equivalent to 50, 100, 200, or 400 mg of dobutamine; dextrose, hydrous 5 g in water for injection, with sodium metabisulfite 25 mg and edetate disodium, dihydrate 10 mg added as stabilizers; osmolar concentration, respectively, 260, 263, 270, or 284 mOsmol/L (calc.). The pH is 3.0 (2.5-5.5). May contain hydrochloric acid and/or sodium hydroxide for pH adjustment. Dobutamine in 5% dextrose injection is oxygen sensitive.

Dobutamine HCl is chemically designated (±)-4-[2-[[3-(p-hydroxyphenyl)-1-methylpropyl]amino]ethyl]-pyrocatechol HCl. It is a synthetic catecholamine.

Dextrose, USP is chemically designated D-glucose monohydrate (C16H12O6·H2O), a hexose sugar freely soluble in water.

Water for injection is chemically designated H2O.

The flexible plastic container is fabricated from a specially formulated nonplasticized, thermoplastic co-polyester (CR3). Water can permeate from inside the container into the overwrap but not in amounts sufficient to affect the solution significantly. Solutions inside the plastic container also can leach out certain of its chemical components in very small amounts before the expiration period has attained. However, the safety of the plastic has been confirmed by tests in animals according to USP biological standards for plastic containers.

CLINICAL PHARMACOLOGY:

Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the β-receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. It does not cause the release of endogenous norepinephrine, as does dopamine. In animal studies, dobutamine produces less increase in heart rate and less decrease in peripheral vascular resistance for a given inotropic effect than does isoproterenol.

In patients with depressed cardiac function, both dobutamine and isoproterenol increase the cardiac output to a similar degree. In the case of dobutamine, this increase is usually not accompanied by marked increases in heart rate (although tachycardia is occasionally observed), and the cardiac stroke volume is usually increased. In contrast, isoproterenol increases the cardiac index primarily by increasing the heart rate while stroke volume changes little or declines.

Facilitation of atrioventricular conduction has been observed in human electrophysiologic studies and in patients with atrial fibrillation.

Systemic vascular resistance is usually decreased with administration of dobutamine. Occasionally, minimum vasoconstriction has been observed.

Most clinical experience with dobutamine is short-term-not more than several hours in duration. In the limited number of patients who were studied for 24, 48, and 72 hours, a persistent increase in cardiac output occurred in some, whereas output returned toward baseline values in others.

The onset of action of dobutamine in 5% dextrose injection is within 1 or 2 minutes; however, as much as 10 minutes may be required to obtain the peak effect of a particular infusion rate.

The plasma half-life of dobutamine in humans is 2 minutes. The principal routes of metabolism are methylation of the catechol and conjugation. In human urine, the major excretion products are the conjugates of dobutamine and 3-O-methyl dobutamine. The 3-O-methyl derivative of dobutamine is inactive.

Alteration of synaptic concentrations of catecholamines with either reserpine or tricyclic antidepressants does not alter the actions of dobutamine in animals, which indicates that the actions of dobutamine are not dependent on presynaptic mechanisms.

INDICATIONS AND USAGE:

Dobutamine in 5% dextrose injection is indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of adults with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures.

In patients who have atrial fibrillation with rapid ventricular response, a digitalis preparation should be used prior to institution of therapy with dobutamine.

CONTRAINDICATIONS:

Dobutamine in 5% dextrose injection is contraindicated in patients with idiopathic hypertrophic subaortic stenosis and in patients who have shown previous manifestations of hypersensitivity to dobutamine.

Dextrose solutions without electrolytes should not be administered simultaneously blood through the same infusion set because of the possibility that pseudoagglutination of red cells may occur.

WARNINGS:

1. Increase in Heart Rate or Blood Pressure: Dobutamine HCl may cause a marked increase in heart rate or blood pressure, especially systolic pressure. Approximately 10% of patients in clinical studies have had rate increases of 30 beats/minute or more, and about 7.5% have had a 50 mm Hg or greater increase in systolic pressure. Usually, reduction of dosage promptly reverses these effects. Because dobutamine facilitates atrioventricular conduction, patients with a trial fibrillation are at risk of developing rapid ventricular response. Patients with preexisting hypertension appear to face an increased risk of developing an exaggerated pressor response.

2. Ectopic Activity: Dobutamine may precipitate or exacerbate ventricular ectopic activity, but it rarely has caused ventricular tachycardia.

3. Hypersensitivity: Reactions suggestive of hypersensitivity associated with administration of dobutamine in 5% dextrose injection, including skin rash, fever, eosinophilia, and bronchospasm, have been reported occasionally. Addictive medications should not be delivered via this solution.

4. Dobutamine in 5% dextrose injection contains sodium bisulfite, 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.

PRECAUTIONS:

1. During the administration of dobutamine in 5% dextrose injection solution, as with any adrenergic agent, ECG and blood pressure should be continuously monitored. In addition, pulmonary wedge pressure and cardiac output should be monitored whenever possible to aid in the safe and effective infusion of dobutamine in 5% dextrose injection.

2. Hypovolemia should be corrected with suitable volume expanders before treatment with dobutamine in 5% dextrose injection is instituted.

3. Animal studies indicated that dobutamine may be ineffective if the patient has recently received a β-blocking drug. In such a case, peripheral vascular resistance may increase.

4. No improvement may be observed in the presence of marked mechanical obstruction, such as severe valvular aortic stenosis.

5. Dobutamine, like other β-agonists, can produced a mild reduction in serum potassium concentration, rarely to hypokalemic levels. Accordingly, consideration should be given to monitoring serum potassium.

6. Excess administration of potassium-free solutions may result in significant hypokalemia. The intravenous administration of these solutions can cause fluid and/or solute overloading resulting in dilution of serum electrolyte concentrations, overhydration, congested states or pulmonary edema.

7. Avoid bolus administration of the drug. (See DOSAGE AND ADMINISTRATION.) Clinical evaluation and periodic laboratory determinations are necessary to monitor changes in fluid balance, electrolyte concentrations and acid-base balance during prolonged parenteral therapy or whenever the condition of the patient warrants such elevation. Solutions containing dextrose should be used with caution in patients with known subclinical or overt diabetes mellitus.

8. Dobutamine in 5% dextrose injection may exhibit a pink color that, if present, will increase with time. This color change is due to slight oxidation of the drug, but there is no significant loss of potency during the time of administration. Do not administer unless solution is clear and container is undamaged. Discard unused portion.

Usage Following Acute Myocardial Infarction

Clinical experience with dobutamine following myocardial infarction has been insufficient to establish the safety of drug for this use. There is concern that any agent that increases contractile force and heart rate may increase the size of an infarction by intensifying ischemia, but it is not known whether dobutamine does so.

Carcinogenesis, Mutagenesis, and Impairment of Fertility

Studies to evaluate the carcinogenic or mutagenic potential of dobutamine or the potential of the drug to affect fertility adversely have not been performed.

Pregnancy Category B

Reproduction studies performed in rats and rabbits have revealed no evidence of harm to the fetus due to dobutamine. The drug, however, has not been administered to pregnant women and should be used only when the expected benefits clearly outweigh the potential risks to the fetus.

Pediatric Use

The safety and effectiveness of dobutamine in 5% dextrose injection for use in children have not been studied.

INTERACTIONS:

There was no evidence of drug interactions in clinical studies in which dobutamine HCl was administered concurrently with other drugs, including digitalis preparations, furosemide, spironolactone, lidocaine, glyceryl trinitrate, isosorbide dinitrate, morphine, atropine, heparin, protamine, potassium chloride, folic acid, and acetaminophen. Preliminary studies indicate that the concomitant use of dobutamine and nitroprusside results in a higher cardiac output and, usually, a lower pulmonary wedge pressure than when either drug is used alone.

ADVERSE REACTIONS:

Increased Heart Rate, Blood Pressure, and Ventricular Ectopic Activity

A 10-20 mm increase in systolic blood pressure and an increase in heart rate of 5-15 beats/minute have been noted in most patients (see WARNINGS regarding exaggerated chronotropic and pressor effects). Approximately 5% of patients have had increased premature ventricular beats during infusions. These effects are dose related.

Hypotension

Precipitous decreases in blood pressure have occasionally been described in association with dobutamine therapy. Decreasing the dose or discontinuing the infusion typically results in rapid return of blood pressure to baseline values. In rare cases, however, intervention may be required and reversibility may not be immediate.

Reactions at Sites of Intravenous Infusion

Phlebitis has occasionally been reported. Local inflammatory changes have been described following inadvertent infiltration.

Miscellaneous Uncommon Effects

The following adverse effects have been reported in 1-3% of patients: nausea, headache, anginal pain, nonspecific chest pain, palpitations, and shortness of breath.

Administration of dobutamine, like other catecholamines, can produce a mild reduction in serum potassium concentrations, rarely to hypokalemic levels (see PRECAUTIONS.)

Longer-Term Safety

Infusions of up to 72 hours have revealed no adverse effects other than those seen with shorter infusions.

OVERDOSAGE:

Overdoses of dobutamine have been reported rarely. The following is provided to serve as a guide if such an overdose is encountered.

Signs and Symptoms

Toxicity from dobutamine HCl is usually due to excessive cardiac β-receptor stimulation. The duration of action of Dobutamine HCl is generally short (T½ = 2 minutes) because it is rapidly metabolized by catechol-O-methyltransferase. The symptoms of toxicity may include anorexia, nausea, vomiting, tremor, anxiety, palpitations, headache, shortness of breath, and anginal and nonspecific chest pain. The positive inotropic and chronotropic effects of Dobutamine on the myocardium may cause hypertension, tachyarrhythmias, myocardial ischemia, and ventricular fibrillation. Hypotension may result from vasodilation.

If the product is ingested, unpredictable absorption may occur from the mouth and the gastrointestinal tract.

Treatment

To obtain up-to-date information about the treatment of overdose, a good resource is your certified Regional Poison Control Center. In managing overdosage, consider the possibility of multiple drug overdosage, interaction among drugs, and unusual drug kinetics in your patient.

The initial actions to be taken in a dobutamine HCl overdose are discontinuing administration, establishing an airway, and ensuring oxygenation and ventilation. Resuscitative measures should be initiated promptly. Severe ventricular tachyarrhythmias may be successfully treated with propranolol or lidocaine. Hypertension usually responds to a reduction in dose or discontinuation of therapy.

Protect the patient's airway and support ventilation and perfusion. If needed, meticulously monitor and maintain, within acceptable limits, the patient's vital signs, blood gases, serum electrolytes, etc. Absorption of drugs from the gastrointestinal tract may be decreased by giving activated charcoal, which, in many cases, is more effective than emesis or lavage; consider charcoal instead of or in addition to gastric emptying. Repeated doses of charcoal over time may hasten elimination of some drugs that have been absorbed. Safeguard the patient's airway when employing gastric emptying or charcoal.

Forced diuresis, peritoneal dialysis, hemodialysis, or charcoal hemoperfusion have not been established as beneficial for an overdose of dobutamine HCl.

DOSAGE AND ADMINISTRATION:

Do NOT add sodium bicarbonate or other alkalinizing substance, since dobutamine is inactivated in alkaline solution. Dobutamine in 5% dextrose injection is administered only intravenously via a suitable catheter or needle infusion. The less concentrated 0.5 mg/ml solution may be preferred when fluid expansion is not a problem. The more concentrated 1 mg/ml, 2 mg/ml, or 4 mg/ml solutions may be preferred in patients with fluid retention or when a slower rate of infusion is desired.

Recommended Dosage

The rate of infusion needed to increase cardiac output usually ranged from 2.5-15 μg/kg/min. On rare occasions, infusion rates up to 40 μg/kg/min have been required to obtain the desired effect.

Rate of Administration

When administering dobutamine (or any potent medication) by continuous intravenous infusion, it is advisable to use a precision volume control IV set.

Each patient must be individually titrated to the desired hemodynamic response to dobutamine. The rate of administration and the duration of therapy should be adjusted according to the patient's response as determined by heart rate, presence of ectopic activity, blood pressure, urine flow, and, whenever possible, measurement of central venous or pulmonary wedge pressure and cardiac output.

As with all potent intravenously administered drugs, care should be taken to control the rate of infusion so as to avoid inadvertent administration of a bolus of the drug.

Parenteral drug products should be visually inspected for particulate matter and discoloration prior to administration, whenever solution and container permit (see PRECAUTIONS and TABLE 1 through TABLE 4B.

TABLE 1 Dobutamine Infusion Rate (ml/h) Chart Using 500 μg/ml Concentration Patient Body Weight (kg)

* 30 40 50 60 70 80 90 100 110 120

2.5 9 12 15 18 21 24 27 30 33 36

5 18 24 30 36 42 48 54 60 66 72

7.5 27 36 45 54 63 72 81 90 99 108

10 36 48 60 72 84 96 108 120 132 144

12.5 45 60 75 90 105 120 135 150 165 180

15 54 72 90 108 126 144 162 180 198 216

17.5 63 84 105 126 147 168 189 210 231 252

* Infusion rate (μg/kg/min).

TABLE 2 Dobutamine Infusion Rate (ml/h) Chart Using 1000 μg/ml Concentration Patient Body Weight (kg)

* 30 40 50 60 70 80 90 100 110 120

2.5 4.5 6 7.5 9 10.5 12 13.5 15 16.5 18

5 9 12 15 18 21 24 27 30 33 36

7.5 13.5 18 22.5 27 31.5 36 40.5 45 49.5 54

10 18 24 30 36 42 48 54 60 66 72

12.5 22.5 30 37.5 45 52.5 60 67.5 75 82.5 90

15 27 36 45 54 63 72 81 90 99 108

17.5 31.5 42 52.5 63 73.5 84 94.5 105 115.5 126

* Infusion rate (μg/kg/min).

TABLE 3A Dobutamine Infusion Rate (ml/h) Chart Using 2000 μg/ml Concentration Patient Body Weight (kg)

Infusion rate (μg/kg/min) 30 40 50 60 70

2.5 2.25 3 3.75 4.5 5.25

5 4.5 6 7.5 9 10.5

7.5 6.75 9 11.25 13.5 15.75

10 9 12 15 18 21

12.5 11.25 15 18.75 22.5 26.25

15 13.5 18 22.5 27 31.5

17.5 15.75 21 26.25 31.5 36.75

TABLE 3B Dobutamine Infusion Rate (ml/h) Chart Using 2000 μg/ml Concentration Patient Body Weight (kg)

Infusion rate (μg/kg/min) 80 90 100 110 120

2.5 6 6.75 7.5 8.25 9

5 12 13.5 15 16.5 18

7.5 18 20.25 22.5 24.75 27

10 24 27 30 33 36

12.5 30 33.75 37.5 41.25 45

15 36 40.5 45 49.5 54

17.5 42 47.25 52.5 57.75 63

TABLE 4A Dobutamine Infusion Rate (ml/h) Chart Using 4000 μg/ml Concentration Patient Body Weight (kg)

Infusion rate (μg/kg/min) 30 40 50 60 70

2.5 1.125 1.5 1.875 2.25 2.625

5 2.25 3 3.75 4.5 5.25

7.5 3.375 4.5 5.625 6.75 7.875

10 4.5 6 7.5 9 10.5

12.5 5.625 7.5 9.375 11.25 13.125

15 6.75 9 11.25 13.5 15.75

17.5 7.875 10.5 13.125 15.75 18.375

TABLE 4B Dobutamine Infusion Rate (ml/h) Chart Using 4000 μg/ml Concentration Patient Body Weight (kg)

Infusion rate (μg/kg/min) 80 90 100 110 120

2.5 3 3.375 3.75 4.125 4.5

5 6 6.75 7.5 8.25 9

7.5 9 10.125 11.25 12.375 13.5

10 12 13.5 15 16.5 18

12.5 15 16.875 18.75 20.625 22.5

15 18 20.25 22.5 24.75 27

17.5 21 23.625 26.25 28.875 31.5

Instructions For Use

To Open: Tear outer wrap at notch and remove solution container. Some opacity of the plastic due to moisture absorption during the sterilization process may be observed. This is normal and does not affect the solution quality or safety. The opacity will diminish gradually.

Preparation for Administration (use aseptic technique)

1. Close flow control clamp of administration set.

2. Remove cover from outlet port at bottom of container.

3. Insert piercing pin of administration set into port with a twisting motion until the set is firmly seated. Note: See full directions on administration set carton.

4. Suspend container from hanger.

5. Squeeze and release drip chamber to establish proper fluid level in chamber.

6. Open flow control clamp and clear air from set. Close clamp.

7. Attach set to venipuncture device. If device is not indwelling, prime and make venipuncture.

8. Regulate rate of administration with flow control clamp.

WARNING: Do not use flexible container in series connections.

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HOW SUPPLIED:

Dobutamine in 5% Dextrose Injection is supplied in 250 and 500 ml LifeCare flexible containers.

Exposure of pharmaceutical products to heat should be minimized.

Avoid excessive heat. Protect from freezing. It is recommended that the product be stored at room temperature (25°C); however, brief exposure up to 40°C does not adversely affect the product.

--------------------------------------------------------------------------------

HOW SUPPLIED - RATED THERAPEUTICALLY EQUIVALENT:

Solution -- Intravenous -- 5%;50 mg/100 ml:

250.0 ml x 12.0 $731.70 GENERIC Abbott Pharmaceutical 00074234532

500.0 ml x 12.0 $535.50 GENERIC Abbott Pharmaceutical 00074234534

Solution -- Intravenous -- 12.5 mg/ml:

20.0 ml $9.89 GENERIC Abbott Pharmaceutical 00074234401

20.0 ml $9.89 GENERIC Abbott Pharmaceutical 00074344010

20.0 ml $21.00 GENERIC Bedford Laboratories 55390056020

20.0 ml x 10.0 $43.75 GENERIC Bedford Laboratories 55390056090

20.0 ml x 10.0 $50.00 GENERIC Abbott Pharmaceutical 00074202520

20.0 ml $51.88 GENERIC Lilly, Eli and Company 00702737501

20.0 ml x 10.0 $59.38 GENERIC Lilly, Eli and Company 00702737510

20.0 ml x 10.0 $92.60 GENERIC Abbott Pharmaceutical 00074234402

20.0 ml x 10.0 $120.00 Dobutrex Lilly, Eli and Company 00002717510

20.0 ml x 10.0 $120.00 Dobutrex Lilly, Eli and Company 00002737510

20.0 ml x 10.0 $122.13 GENERIC Abbott Pharmaceutical 00074344020

20.0 ml x 10.0 $169.20 GENERIC SICOR Pharmaceuticals Inc 00703181503

40.0 ml x 10.0 $79.80 GENERIC Abbott Pharmaceutical 00074202554

40.0 ml x 10.0 $234.00 GENERIC Sanofi-Synthelabo Inc 00024059401

100.0 ml $14.35 GENERIC Abbott Pharmaceutical 00074472901

Solution -- Intravenous -- 5%;100 mg/100 ml:

250.0 ml x 12.0 $244.92 GENERIC Abbott Pharmaceutical 00074234632

250.0 ml x 18.0 $334.13 GENERIC Baxter I.V. Systems Division 00338107302

500.0 ml x 12.0 $710.52 GENERIC Baxter I.V. Systems Division 00338107303

500.0 ml x 12.0 $732.74 GENERIC Abbott Pharmaceutical 00074234634

Solution -- Intravenous -- 5%;200 mg/100 ml:

250.0 ml x 12.0 $367.32 GENERIC Abbott Pharmaceutical 00074234732

250.0 ml x 18.0 $1549.26 GENERIC Baxter I.V. Systems Division 00338107502

Solution -- Intravenous -- 5%;400 mg/100 ml:

250.0 ml x 12.0 $489.72 GENERIC Abbott Pharmaceutical 00074372432

250.0 ml x 18.0 $2617.65 GENERIC Baxter I.V. Systems Division 00338107702

--------------------------------------------------------------------------------

HOW SUPPLIED - EQUIVALENTS NOT AVAILABLE:

Solution -- Intravenous -- 5%;50 mg/100 ml:

500.0 ml x 12.0 $596.64 GENERIC Baxter I.V. Systems Division 00338107103

Solution -- Intravenous -- 12.5 mg/ml:

20.0 ml x 10.0 $31.30 GENERIC American Regent Laboratories Inc 00517207510

Solution -- Intravenous -- 5%;100 mg/100 ml:

250.0 ml x 18.0 $601.88 GENERIC Lilly, Eli and Company 00002749601

Solution -- Intravenous -- 5%;200 mg/100 ml:

250.0 ml x 18.0 $216.00 GENERIC Lilly, Eli and Company 00002749801

Solution -- Intravenous -- 5%;400 mg/100 ml:

250.0 ml $126.88 GENERIC B. Braun/McGaw Inc 00264982359

250.0 ml x 18.0 $337.50 GENERIC Lilly, Eli and Company 00002750001

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