Lidocaine serves multiple therapeutic roles in anesthesia, including its use as a local anesthetic and a neutrophil inhibitor. It is commonly used intravenously to alleviate the pain associated with injections of agents like propofol or etomidate. Lidocaine acts as a CNS depressant, reducing sympathetic and hemodynamic responses as well as intraocular pressure during laryngoscopy. It also diminishes the minimum alveolar concentration (MAC) of volatile anesthetics by up to 40% and is effective in preventing and treating bronchospasm and laryngospasm, particularly during intubation and emergence, although an insufficient induction dose might paradoxically trigger spasms.
Lidocaine also depresses the hypoxic drive and relaxes bronchial smooth muscles when administered intravenously, enhancing the effects of neuromuscular blockade. It serves as a class IB ventricular antiarrhythmic, blocking sodium channels in ischemic ventricular tissue with minimal effect on contractility at therapeutic doses, useful specifically for ventricular arrhythmias while not affecting the sinoatrial or atrioventricular nodes' firing rates or the PR/QRS/QT intervals. Lidocaine reduces cerebral metabolic rate for oxygen (CMRO2), cerebral blood flow (CBF), cerebral blood volume (CBV), and intracranial pressure (ICP); however, increases in these parameters can occur as a result of toxicity. Intravenous lidocaine has also been used to prevent emergence delirium and reduce opioid requirements due to its neuroprotective effects.
Despite its intermediate potency and toxicity among local anesthetics, lidocaine carries the highest risk of neurotoxicity when used for intrathecal anesthesia. Symptoms of toxicity generally manifest first as circumoral numbness, tinnitus, or a metallic taste, potentially escalating to seizures. It also reduces thrombosis and platelet aggregation while enhancing fibrinolysis.
In obstetric applications, lower doses of lidocaine are necessary as high plasma levels can induce uterine vasoconstriction, reducing uterine blood flow and potentially causing fetal bradycardia or death. Lidocaine is not recommended for obstetric paracervical blocks due to these risks. Clonidine can significantly extend the anesthetic and analgesic effects of lidocaine, and the drug should be used judiciously in patients with renal issues or advanced age to avoid accumulation and toxicity.
For infiltration and regional anesthesia, the maximum lidocaine dosages are prescribed based on the presence of epinephrine and the specific application. For adult patients without epinephrine, the maximum dose of lidocaine is set at 4.5 mg/kg, with a total limit not exceeding 300 mg. When lidocaine is used with epinephrine, the maximum allowable dose increases to 7 mg/kg, but should not exceed a total of 500 mg. In the case of tumescent anesthesia, which often requires larger volumes of anesthetic, the maximum dose of lidocaine can range from 35-55 mg/kg, significantly higher than in other contexts. These guidelines are crucial to adhere to, in order to prevent toxicity and ensure patient safety during procedures requiring lidocaine.
Metabolism occurs predominantly in the liver via the P450 enzyme system, and its clearance can be influenced by beta-blockers and histamine (H2) blockers. In regional anesthesia, the addition of sodium bicarbonate can accelerate the onset of neural blockade, although epinephrine should never be added when performing digital or penile blocks due to the risk of severe vasoconstriction.
Overall, lidocaine is a versatile agent in the anesthetic toolkit, used across various settings from intravenous administration to epidural and spinal anesthesia, albeit with caution due to its potential for severe side effects and systemic toxicity.
