Bupivacaine Hydrochloride (Marcaine, Sensorcaine)

Max dose - 2 mg/kg WITHOUT epinephrine, 2.5 mg/kg WITH epinephrine Drug interactions - prolonged affects are produced by vasoconstrictors (eg. epinephrine), narcotics, and alpha-agonists (eg. clonidine). Bicarbonate is generally not added directly to bupivacaine.  If the pH is raised above 6.8, bupivacaine will precipitate. However, metabolic alkalization will increase the rate of onset and potency of local anesthetics, so give bicarbonate separately if this is the objective. Epidural chloroprocaine will antagonize the affects of epidural bupivacaine. Toxicity - Prior to toxicity, the patient may exhibit tongue or circumoral (around the mouth) numbness, metallic taste, tinnitus, tremors, restlessness, and anxiety. Toxicity symptoms include cardiopulmonary collapse and seizures. Toxicity risk may be decreased by adding epinephrine. Cardiotoxicity - bupivacaine is associated with more cardiotoxicity as compared to other amide local anesthetics. Order of neuronal loss - autonomic, pain, temperature, touch, proprioception, skeletal muscle tone (motor). OB - the parturient has reduced dose requirements to produce therapeutic affects. At high PLASMA levels, bupivacaine induces uterine vasoconstriction and thereby reduces uterine blood flow. This can occur after paracervical blocks (not after epidural/spinal anesthetics). Epinephrine adjuvant - improves quality and duration of bupivacaine.

Obstetric paracervical blocks - As mentioned, this can lead to uterine vasoconstriction and reduced blood flow to the fetus. Intravenous Regional Anesthesia (IVRA) - toxicity after tourniquet release. High concentrations - any concentration above 0.5% is contraindicated for anything other than spinal anesthesia. These concentrations are associated with toxicity and cardiac arrest. Use with caution - in patients with congestive heart failure, shock, heart blocks, or hypovolemia.

Bupivacaine inhibits ionic fluxes and thereby stabilizes neuronal membranes. This prevents the initiation of neuronal conduction impulses. Bupivacaine induces cardiac sodium blockade which is associated with cardiac depression of myocardial contractility and conduction. This combined with the slow offset of bupivacaine makes it more likely than other amides to produce cardiac toxicity.

Hepatic and Pulmonary

Toxicity: 20% Lipid emulsion (intralipid). 1-2 ml/kg bolus followed by a 0.25 ml/kg/min infusion for 30-60 minutes. Bolus doses can be repeated every 3-5 minutes to a max of 4 ml/kg. If sodium channel blockade is suspected as the source of cardiac toxicity, sodium bicarbonate can be administered (1-2 mEq/kg). Seizures or seizure prophylaxis can be treated with Versed (0.2 mg/kg IM, or 0.02-0.1 mg/kg IV). Bupivacaine-induced vasoconstriction: Calcium channel blockers (eg. verapamil and nifedipine) can reduce bupivacaine-induced vasoconstriction.