Bupivacaine is administered with specific dosage guidelines: the maximum dose without epinephrine is 2 mg/kg, and with epinephrine, it is 3 mg/kg. The inclusion of vasoconstrictors such as epinephrine, narcotics, and alpha-agonists like clonidine can prolong the effect of the drug. It's important not to directly add bicarbonate to bupivacaine, as increasing the pH above 6.8 causes precipitation. However, separately administered bicarbonate can enhance the onset and potency of local anesthetics. Notably, epidural chloroprocaine can negate the effects of epidural bupivacaine.
Toxicity symptoms may precede more severe reactions and include tongue or circumoral numbness, a metallic taste, tinnitus, tremors, restlessness, and anxiety, escalating to cardiopulmonary collapse and seizures. Bupivacaine is notably associated with higher cardiotoxicity compared to other amide local anesthetics. The sequence of nerve block typically progresses from autonomic to pain, temperature, touch, proprioception, and finally to motor nerves affecting skeletal muscle tone.
In obstetrics, reduced doses of bupivacaine are required, and care must be taken as high plasma levels can induce uterine vasoconstriction, reducing blood flow, especially concerning in obstetric paracervical blocks. Bupivacaine's utility is enhanced with epinephrine, which improves both the quality and duration of anesthesia.
However, there are specific contraindications to consider. Bupivacaine should not be used in obstetric paracervical blocks due to the risk of uterine vasoconstriction or in intravenous regional anesthesia (IVRA), where toxicity risks increase after tourniquet release. The 0.75% concentration is contraindicated for obstetric epidural anesthesia after reports of refractory cardiac arrest from accidental intravascular injection; labor analgesia uses dilute solutions. Caution is advised when using bupivacaine in patients with congestive heart failure, shock, heart blocks, or hypovolemia.
The drug's method of action involves inhibiting ionic fluxes which stabilize neuronal membranes and prevent the initiation of nerve conduction impulses, and it has a notable impact on cardiac sodium channels, contributing to its potential for inducing cardiac toxicity. Bupivacaine is metabolized primarily in the liver, with significant first-pass pulmonary uptake, with the time to onset varying by administration method, ranging from under one minute for spinal applications to 4-17 minutes for epidural, and its effects can last between 200-400 minutes, extended further with the addition of epinephrine.
