Bupivacaine

288.43

288.43

253-911-2

DTXSID2022703

N01B|N01BB01|N - Nervous system

32.3 Ų

3.41 (LogP)|log Kow = 3.41|3.6

1.032±0.06 g/cm3

107-108 °C

423.4±45.0 °C(Predicted)

Soluble in water, ethanol, chloroform (slightly ), and acetone (slightly ).

Store in tight container as defined in the USP-NF. This material should be handled and stored per label instructions to ensure product integrity. /Bupivacaine hydrochloride/|Bupivacaine hydrochloride solutions should be stored between 15-30 °C and freezing should be avoided; solutions containing epinephrine should be protected from light.

1.31X10-7 mm Hg at 25 °C (est)

14.85±0.70

Henry's Law constant = 1.79X10-10 atm-cu m/mol at 25 °C (est)

8.1|pKa = 8.09; also reported as 8.17

173.1 Ų [M+H]+ [CCS Type: TW, Method: Major Mix IMS/Tof Calibration Kit (Waters)]

Partition coefficient: (oleyl alcohol/water) 1565; (n-heptane/pH 7.4 buffer) 27.5|Hydroxyl radical reaction rate constant = 1.33X10-10 cu cm/molec-sec at 25 °C (est)

6.1

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, including bupivacane hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Bupivacane hydrochloride/

|Danger|H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]|P260, P262, P264, P270, P271, P280, P284, P301+P310, P302+P350, P304+P340, P310, P320, P321, P322, P330, P361, P363, P403+P233, P405, and P501|The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.|P260, P262, P264, P270, P271, P280, P284, P301+P310, P302+P350, P302+P352, P304+P340, P305+P351+P338, P310, P320, P321, P322, P330, P332+P313, P361, P362, P363, P403+P233, P405, and P501

Safety glasses with sideshields are recommended. Face shields or goggles may be required if splash potential exists or if corrosive materials are present. Approved eye protection (eg, bearing the ANSI Z87 or CSA stamp) is preferred. /Bupivacaine hydrochloride/|Where respirators are deemed necessary to reduce or control occupational exposures, use NIOSH-approved respiratory protection and have an effective respirator program in place. /Bupivacaine hydrochloride/|For handling of laboratory scale quantities, a cloth lab coat is recommended. Where significant quantities are handled, work clothing may be necessary to prevent take-home contamination. /Bupivacaine hydrochloride/

This material is assumed to be combustible. /Bupivacaine hydrochloride/

As with all fires, evacuate personnel to a safe area. Firefighters should use self-contained breathing equipment and protective clothing. /Bupivacaine hydrochloride/|Water spray, dry chemical, carbon dioxide, or foam as appropriate for surrounding fire and materials. /Bupivacaine hydrochloride/

Wear approved respiratory protection, chemically compatible gloves, and protective clothing. Wipe up spillage or collect spillage in appropriately labeled container for disposal. Wash spill site. /Bupivacaine hydrochloride/

Airborne exposure should be controlled primarily by engineering controls such as general dilution ventilation, local exhaust ventilation, or process enclosure. Local exhaust ventilation is generally preferred to general exhaust because it can control the contaminant at its source, preventing dispersion into the work area. An industrial hygiene survey involving air monitoring may be used to determine the effectiveness of engineering controls. Effectiveness of engineering controls intended for use with highly potent materials should be assessed by use of nontoxic surrogate materials Local exhaust ventilation such as a laboratory fume hood or other vented enclosure is recommended, particularly for grinding, crushing weighing, or other dust-generating procedures. /Bupivacaine hydrochloride/|As a general rule, when handling USP Reference Standards, avoid all contact and inhalation of dust, mists, and/or vapors associated with the material. Clean equipment and work surfaces with suitable detergent or solvent after use. After removing gloves, wash hands and other exposed skin thoroughly. /Bupivacaine hydrochloride/|For handling solutions, ensure that the glove material is protective against the solvent being used. Use handling practices that minimize direct hand contact. Employees who are sensitive to natural rubber (latex) should use nitrile or other synthetic nonlatex gloves. Use of powdered latex gloves should be avoided due to the risk of latex allergy. /Bupivacaine hydrochloride/|Maintain eyewash facilities in the work area. /Bupivacaine hydrochloride/|For more Preventive Measures (Complete) data for Bupivacaine (6 total), please visit the HSDB record page.

Possible eye, skin, ... and/or respiratory tract irritation. /Bupivacaine hydrochloride/

The mean seizure dosage of bupivacaine in rhesus monkeys was found to be 4.4 mg/kg with mean arterial plasma concentration of 4.5 mcg/mL. The intravenous and subcutaneous LD 50 in mice is 6 to 8 mg/kg and 38 to 54 mg/kg respectively. Recent clinical data from patients experiencing local anesthetic induced convulsions demonstrated rapid development of hypoxia, hypercarbia, and acidosis with bupivacaine within a minute of the onset of convulsions. These observations suggest that oxygen consumption and carbon dioxide production are greatly increased during local anesthetic convulsions and emphasize the importance of immediate and effective ventilation with oxygen which may avoid cardiac arrest.

In clinical trials with the amide local anesthetics, serum aminotransferase and alkaline phosphatase elevations were rarely reported and were generally no more common than with placebo or comparator injections. Despite widespread use for many decades, the local amide anesthetics, when given as single or limited injections or infusions, have not been convincingly linked to instances of clinically apparent liver injury, and liver toxicity is not mentioned in product labels. Nevertheless, there have been several case series of jaundice arising a few days to as long as a month after use of bupivacaine given over several days as a constant infusion or as repeated injections into a localized area of pain. Some reports mentioned concurrent administration of an antibiotic such as cefazolin during the perioperative period, which might have accounted for the liver injury. However, in other reports, only bupivacaine was given. The liver injury was mixed or cholestatic and mild-to-moderate in severity, resolving within 1 to 2 months of onset without residual evidence of liver injury. In many instances, there was an accompanying low grade fever, rash or eosinophilia, suggesting a hypersensitivity reaction.

Solutions of Bupivacaine Hydrochloride containing a vasoconstrictor, such as epinephrine, should be used with extreme caution in patients receiving monoamine oxidase inhibitors (MAOI) or antidepressants of the triptyline or imipramine types, because severe prolonged hypertension may result.|Bupivacaine Hydrochloride with epinephrine 1:200,000 or other vasopressors should not be used concomitantly with ergot-type oxytocic drugs, because a severe persistent hypertension may occur.

LD50 Mouse sc 38-54 mg/kg|LD50 Mouse iv 6-8 mg/kg

Pending accumulation of further data on the use of the drug in pediatric patients, bupivacaine hydrochloride solutions should not be used in children younger than 12 years of age and the solution for spinal anesthesia should not be used in children younger than 18 years of age.|Because amide-local anesthetics such as Bupivacaine Hydrochloride are metabolized by the liver, these drugs, especially repeat doses, should be used cautiously in patients with hepatic disease. Patients with severe hepatic disease, because of their inability to metabolize local anesthetics normally, are at a greater risk of developing toxic plasma concentrations. Local anesthetics should also be used with caution in patients with impaired cardiovascular function because they may be less able to compensate for functional changes associated with the prolongation of AV conduction produced by these drugs.|Local anesthetics should also be used with caution in patients with hypotension or heartblock.|Newborns and infants seem to be at greater risk of bupivacaine cardiotoxicity than adults do.|This case suggests that carnitine deficiency may increase susceptibility to bupivacaine cardiotoxicity.

95%

For the production of local or regional anesthesia or analgesia for surgery, for oral surgery procedures, for diagnostic and therapeutic procedures, and for obstetrical procedures.|FDA Label|Postsurgical analgesia|Zynrelef is indicated for treatment of somatic postoperative pain from small- to medium-sized surgical wounds in adults (see section 5.1).|Treatment of acute postoperative pain|Exparel is indicated as a brachial plexus block or femoral nerve block for treatment of post-operative pain in adults, and as a field block for treatment of somatic post-operative pain from small- to medium-sized surgical wounds in adults.,

The amide local anesthetics including lidocaine, bupivacaine and ropivacaine are commonly used for pain control during minor surgery or invasive procedures such as biopsies, small excisions or dental work. These local anesthetics have not been linked to serum enzyme elevations, but when given as constant infusions or repeated injections have been occasionally mentioned as possible causes of clinically apparent liver injury.

Anesthetics, Local

Bupivacaine hydrochloride is used for infiltration anesthesia and for peripheral, sympathetic nerve, and epidural (including caudal) block anesthesia. A 0.75% solution of the drug in 8.25% dextrose is used for spinal anesthesia. Bupivacaine is not used for obstetric paracervical block or topical anesthesia. /Use Included in US product label/|Bupivacaine Hydrochloride is indicated for the production of local or regional anesthesia or analgesia for surgery, dental and oral surgery procedures, diagnostic and therapeutic procedures, and for obstetrical procedures. Only the 0.25% and 0.5% concentrations are indicated for obstetrical anesthesia. /Use Included in US product label/

The 0.75% solution of bupivacaine hydrochloride is no longer recommended for obstetric anesthesia, since use of this concentration for epidural anesthesia in obstetric patients has been associated with cardiac arrest with difficult resuscitation or death. Cardiac arrest has occurred after seizures resulting from systemic toxicity, apparently following inadvertent intravascular injection.|Local anesthetics should only be employed by clinicians who are well versed in diagnosis and management of dose-related toxicity and other acute emergencies which might arise from the block to be employed, and then only after insuring the immediate availability of oxygen, other resuscitative drugs, cardiopulmonary resuscitative equipment, and the personnel resources needed for proper management of toxic reactions and related emergencies. delay in proper management of dose-related toxicity, under ventilation from any cause, and/or altered sensitivity may lead to the development of acidosis, cardiac arrest and, possibly, death. /Local anesthetics/|Pending accumulation of further data on the use of the drug in pediatric patients, bupivacaine hydrochloride solutions should not be used in children younger than 12 years of age and the solution for spinal anesthesia should not be used in children younger than 18 years of age.|Some commercially available formulations of bupivacaine hydrochloride contain sodium metabisulfite, a sulfite that may cause allergic-type reactions, including anaphylaxis and life-threatening or less severe asthmatic episodes, in certain susceptible individuals. The overall prevalence of sulfite sensitivity in the general population is unknown but probably low; such sensitivity appears to occur more frequently in asthmatic than in nonasthmatic individuals.|For more Drug Warnings (Complete) data for Bupivacaine (18 total), please visit the HSDB record page.

Bupivacaine is a widely used local anesthetic agent. Bupivacaine is often administered by spinal injection prior to total hip arthroplasty. It is also commonly injected into surgical wound sites to reduce pain for up to 20 hours after surgery. In comparison to other local anesthetics it has a long duration of action. It is also the most toxic to the heart when administered in large doses. This problem has led to the use of other long-acting local anaesthetics:ropivacaine and levobupivacaine. Levobupivacaine is a derivative, specifically an enantiomer, of bupivacaine. Systemic absorption of local anesthetics produces effects on the cardiovascular and central nervous systems. At blood concentrations achieved with therapeutic doses, changes in cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance are minimal. However, toxic blood concentrations depress cardiac conduction and excitability, which may lead to atrioventricular block, ventricular arrhythmias and to cardiac arrest, sometimes resulting in fatalities. In addition, myocardial contractility is depressed and peripheral vasodilation occurs, leading to decreased cardiac output and arterial blood pressure. Following systemic absorption, local anesthetics can produce central nervous system stimulation, depression or both.

Drugs that block nerve conduction when applied locally to nerve tissue in appropriate concentrations. They act on any part of the nervous system and on every type of nerve fiber. In contact with a nerve trunk, these anesthetics can cause both sensory and motor paralysis in the innervated area. Their action is completely reversible. (From Gilman AG, et. al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed) Nearly all local anesthetics act by reducing the tendency of voltage-dependent sodium channels to activate. (See all compounds classified as Anesthetics, Local.)

Systemic absorption of local anesthetics is dose- and concentration-dependendent on the total drug administered. Other factors that affect the rate of systemic absorption include the route of administration, blood flow at the administration site, and the presence or absence of epinephrine in the anesthetic solution.|Only 6% of bupivacaine is excreted unchanged in the urine.|After absorption into the blood, bupivacaine hydrochloride is more highly bound to plasma proteins than are any other local anesthetics; bupivacaine is reportedly 82-96% bound. Bupivacaine hydrochloride has the lowest degree of placental transmission of parenteral local anesthetics and may cause the least fetal depression.|Pregnant rats received an intravenous infusion of bupivacaine at a rate of 0.33 mg. kg-1. min-1 over a period of 15 min. The fetuses were delivered either at the end of infusion or at 2 or 4 hr after dosing. Maternal and fetal blood and tissue samples were obtained for the assays of bupivacaine and its metabolites using capillary gas chromatography-mass spectrometry. The elimination half-life of bupivacaine was 37.7 min. The major metabolite was 3'-hydroxybupivacaine. Bupivacaine and 3'-hydroxybupivacaine were present in all samples at the end of administration. The fetal to maternal concentration ratio of bupivacaine in plasma was 0.29, and in the placenta was 0.63. The amnion contained the highest bupivacaine concentration: threefold higher in the maternal and 11-fold higher than in the fetal plasma. At 4 hr after dosing, bupivacaine was no longer detectable in any maternal and fetal samples, whereas 3'-hydroxybupivacaine was still present in all tissues except the fetal plasma and heart. These data indicate that a considerable amount of bupivacaine is taken up by both sides of the placenta, as well as the amnion and myometrium. 3'-Hydroxybupivacaine was present in all tissues except the fetal plasma and heart samples, even after the parent compound became no longer detectable.|After injection of Bupivacaine Hydrochloride for caudal, epidural, or peripheral nerve block in man, peak levels of bupivacaine in the blood are reached in 30 to 45 minutes, followed by a decline to insignificant levels during the next three to six hours.|Pharmacokinetic studies on the plasma profile of Bupivacaine Hydrochloride after direct intravenous injection suggest a three-compartment open model. The first compartment is represented by the rapid intravascular distribution of the drug. The second compartment represents the equilibration of the drug throughout the highly perfused organs such as the brain, myocardium, lungs, kidneys, and liver. The third compartment represents an equilibration of the drug with poorly perfused tissues, such as muscle and fat. The elimination of drug from tissue distribution depends largely upon the ability of binding sites in the circulation to carry it to the liver where it is metabolized.|For more Absorption, Distribution and Excretion (Complete) data for Bupivacaine (6 total), please visit the HSDB record page.

Amide-type local anesthetics such as bupivacaine are metabolized primarily in the liver via conjugation with glucuronic acid. The major metabolite of bupivacaine is 2,6-pipecoloxylidine, which is mainly catalyzed via cytochrome P450 3A4.|Pregnant rats received an intravenous infusion of bupivacaine at a rate of 0.33 mg. kg-1. min-1 over a period of 15 min. The fetuses were delivered either at the end of infusion or at 2 or 4 hr after dosing. Maternal and fetal blood and tissue samples were obtained for the assays of bupivacaine and its metabolites using capillary gas chromatography-mass spectrometry. The elimination half-life of bupivacaine was 37.7 min. The major metabolite was 3'-hydroxybupivacaine. Bupivacaine and 3'-hydroxybupivacaine were present in all samples at the end of administration. The fetal to maternal concentration ratio of bupivacaine in plasma was 0.29, and in the placenta was 0.63. The amnion contained the highest bupivacaine concentration: threefold higher in the maternal and 11-fold higher than in the fetal plasma. At 4 hr after dosing, bupivacaine was no longer detectable in any maternal and fetal samples, whereas 3'-hydroxybupivacaine was still present in all tissues except the fetal plasma and heart. These data indicate that a considerable amount of bupivacaine is taken up by both sides of the placenta, as well as the amnion and myometrium. 3'-Hydroxybupivacaine was present in all tissues except the fetal plasma and heart samples, even after the parent compound became no longer detectable.|Bupivacaine hydrochloride is principally metabolized to pipecolylxylidine (PPX) by N-dealkylation, probably in the liver. Bupivacaine is excreted in urine as small amounts of PPX, unchanged drug (5%), and other metabolites as yet unidentified.

2.7 hours in adults and 8.1 hours in neonates|Pregnant rats received an intravenous infusion of bupivacaine at a rate of 0.33 mg. kg-1. min-1 over a period of 15 min. The fetuses were delivered either at the end of infusion or at 2 or 4 hr after dosing. Maternal and fetal blood and tissue samples were obtained for the assays of bupivacaine and its metabolites using capillary gas chromatography-mass spectrometry. The elimination half-life of bupivacaine was 37.7 min.|The elimination half-life of bupivacaine hydrochloride is 1.5-5.5 hours in adults and 8.1 hours in neonates.

Local anesthetics such as bupivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. Bupivacaine prevents depolarization by bindng to the intracellular portion of sodium channels and blocking sodium ion influx into neurons. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: (1) pain, (2) temperature, (3) touch, (4) proprioception, and (5) skeletal muscle tone. The analgesic effects of Bupivicaine are thought to potentially be due to its binding to the prostaglandin E2 receptors, subtype EP1 (PGE2EP1), which inhibits the production of prostaglandins, thereby reducing fever, inflammation, and hyperalgesia.|Local anesthetics block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. In general, the progression of anesthesia is related to the diameter, myelination, and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: (1) pain, (2) temperature, (3) touch, (4) proprioception, and (5) skeletal muscle tone.

Emergency and supportive measures: Maintain an open airway and assist ventilation if necessary. Treat coma, hypotension, arrhythmias, and anaphylaxis if they occur. Extracorporeal circulatory assistance (eg, balloon pump or partial cardiopulmonary bypass) has been used for short-term support for patients with acute massive overdose with 20% lidocaine solution and inadvertent intravascular administration of bupivacaine. Monitor vital signs and ECG for at least 6 hours. /Anesthetics, local/|Decontamination: Parenteral exposure: Decontamination is not feasible. Ingestion: Administer activated charcoal orally if conditions are appropriate. Gastric lavage is not necessary after small to moderate ingestions if activated charcoal can be given promptly. /Anesthetics, local/|Accidental intravascular administration of bupivacaine during performance of a brachial block precipitated convulsions followed by asystole. The patient was rapidly resuscitated using cardiopulmonary resuscitation, supplemented by 150 mL of 20% lipid emulsion. Nonetheless, cardiac toxicity reappeared 40 min after completion of the lipid emulsion. In the absence of further lipid emulsion, amiodarone and inotropic support were used to treat cardiotoxicity. This case suggests that local anesthetic systemic toxicity may recur after initial lipid rescue. Since recurrence of toxicity may necessitate administration of additional doses of lipid emulsion, a sufficient quantity of lipid emulsion should be available when regional anesthesia is performed.|Management of Local Anesthetic Emergencies: The first consideration is prevention, best accomplished by careful and constant monitoring of cardiovascular and respiratory vital signs and the patient's state of consciousness after each local anesthetic injection. At the first sign of change, oxygen should be administered. The first step in the management of systemic toxic reactions, as well as underventilation or apnea due to unintentional subarachnoid injection of drug solution, consists of immediate attention to the establishment and maintenance of a patent airway and effective assisted or controlled ventilation with oxygen with a delivery system capable of permitting immediate positive airway pressure by mask. This may prevent convulsions if they have not already occurred. If necessary, use drugs to control the convulsions. A bolus IV injection of succinylcholine will paralyze the patient without depressing the central nervous or cardiovascular systems and facilitate ventilation. A bolus IV dose of diazepam or of thiopental will permit ventilation and counteract central nervous system stimulation, but these drugs also depress central nervous system, respiratory, and cardiac function, add to postictal depression and may result in apnea. Intravenous barbiturates, anticonvulsant agents, or muscle relaxants should only be administered by those familiar with their use. Immediately after the institution of these ventilatory measures, the adequacy of the circulation should be evaluated. Supportive treatment of circulatory depression may require administration of intravenous fluids, and when appropriate, a vasopressor dictated by the clinical situation (such as ephedrine or epinephrine to enhance myocardial contractile force). Endotracheal intubation, employing drugs and techniques familiar to the clinician, may be indicated after initial administration of oxygen by mask if difficulty is encountered in the maintenance of a patent airway, or if prolonged ventilatory support (assisted or controlled) is indicated. Recent clinical data from patients experiencing local anesthetic-induced convulsions demonstrated rapid development of hypoxia, hypercarbia, and acidosis with bupivacaine within a minute of the onset of convulsions. These observations suggest that oxygen consumption and carbon dioxide production are greatly increased during local anesthetic convulsions and emphasize the importance of immediate and effective ventilation with oxygen which may avoid cardiac arrest. If not treated immediately, convulsions with simultaneous hypoxia, hypercarbia, and acidosis plus myocardial depression from the direct effects of the local anesthetic may result in cardiac arrhythmias, bradycardia, asystole, ventricular fibrillation, or cardiac arrest. Respiratory abnormalities, including apnea, may occur. Underventilation or apnea due to unintentional subarachnoid injection of local anesthetic solution may produce these same signs and also lead to cardiac arrest if ventilatory support is not instituted. If cardiac arrest should occur, successful outcome may require prolonged resuscitative efforts. The supine position is dangerous in pregnant women at term because of aortocaval compression by the gravid uterus. Therefore during treatment of systemic toxicity, maternal hypotension or fetal bradycardia following regional block, the parturient should be maintained in the left lateral decubitus position if possible, or manual displacement of the uterus off the great vessels be accomplished.|For more Antidote and Emergency Treatment (Complete) data for Bupivacaine (7 total), please visit the HSDB record page.

Because amide-local anesthetics such as Bupivacaine Hydrochloride are metabolized by the liver, these drugs, especially repeat doses, should be used cautiously in patients with hepatic disease. Patients with severe hepatic disease, because of their inability to metabolize local anesthetics normally, are at a greater risk of developing toxic plasma concentrations. Local anesthetics should also be used with caution in patients with impaired cardiovascular function because they may be less able to compensate for functional changes associated with the prolongation of AV conduction produced by these drugs.|Injection of repeated doses of local anesthetics may cause significant increases in plasma levels with each repeated dose due to slow accumulation of the drug or its metabolites, or to slow metabolic degradation. Tolerance to elevated blood levels varies with the status of the patient. Debilitated, elderly patients and acutely ill patients should be given reduced doses commensurate with their age and physical status. Local anesthetics should also be used with caution in patients with hypotension or heartblock.|Some commercially available formulations of bupivacaine hydrochloride contain sodium metabisulfite, a sulfite that may cause allergic-type reactions, including anaphylaxis and life-threatening or less severe asthmatic episodes, in certain susceptible individuals. The overall prevalence of sulfite sensitivity in the general population is unknown but probably low; such sensitivity appears to occur more frequently in asthmatic than in nonasthmatic individuals.|Systemic absorption of local anesthetics produces effects on the cardiovascular and central nervous systems (CNS). At blood concentrations achieved with normal therapeutic doses, changes in cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance are minimal. However, toxic blood concentrations depress cardiac conduction and excitability, which may lead to atrioventricular block, ventricular arrhythmias, and cardiac arrest, sometimes resulting in fatalities. In addition, myocardial contractility is depressed and peripheral vasodilation occurs, leading to decreased cardiac output and arterial blood pressure. Recent clinical reports and animal research suggest that these cardiovascular changes are more likely to occur after unintended intravascular injection of bupivacaine. Therefore, incremental dosing is necessary.|For more Human Toxicity Excerpts (Complete) data for Bupivacaine (20 total), please visit the HSDB record page.

1-Butyl-N-(2,6-dimethylphenyl)-2-piperidinecarboxamide

Table: Bupivacaine Hydrochloride Preparations [Table#7475]|Table: Bupivacaine Hydrochloride in Dextrose Preparations [Table#7476]

2-Piperidinecarboxamide, 1-butyl-N-(2,6-dimethylphenyl)-: ACTIVE

Human Drugs -> EU pediatric investigation plans|Human drugs -> Zynrelef -> EMA Drug Category|Anesthetics -> Human pharmacotherapeutic group|Human drugs -> Exparel liposomal -> EMA Drug Category|Amides, Anesthetics, local -> Human pharmacotherapeutic group|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients|Pharmaceuticals