Initial low blood levels of local anesthetic typically increase most cardiac parameters, such as blood pressure, heart rate, and cardiac output. This is thought to be due to increased sympathetic tone and direct vasoconstriction. However, as the local anesthetic serum level rises, vasodilatation begins to predominate and leads to hypotension. Additionally, reduced cardiac output and dysrhythmias further worsen hypotension. This instability paves the way for cardiac arrest if not addressed immediately.

Prevention of local anesthetic toxicity is crucial due to the serious consequences of an overdose. Before any anesthetic employing local anesthetics is begun, safety equipment designed to treat emergencies, including airway equipment and resuscitative drugs, must be available. Additionally, carefully selecting the dose and concentration of local anesthetic is very important. The optimal dose is the lowest one that achieves the desired effect. Much effort has been made to develop an ideal test for detecting intravascular injection, and currently epinephrine is the most commonly used. Increases in heart rate by more than 10 bpm or systolic blood pressure by more than 15 mmHg or a decrease of 25% in the lead II T-wave amplitude are thought to be sensitive markers for intravascular injection [5]. Many problems do arise with epinephrine as a test dose, most notably in patients who are on beta-blockade therapy or those with low cardiac output states, which can delay circulation of the epinephrine. One more way of preventing intravascular injections is to use incremental dosing with frequent aspirations. Aspirating every 3–5 mL between injections and monitoring for toxicity can be instrumental in detecting intravascular injection in its earliest stages [1] (Table 27.2).

Once local anesthetic toxicity has been recognized, immediately stopping administration is of utmost importance. It is also crucial to maintain the airway and provide supplemental oxygen to the patient while assessing neurologic and cardiovascular parameters. Treatment of central nervous system toxicity is typically begun with a benzodiazepine (midazolam 0.05–0.1 mg/kg IV) to address any seizure activity. Lipid emulsion (i.e., Intralipid) is also useful in situations where cardiac toxicity is present. The current dosing guidelines recommend starting Intralipid 20% with a bolus of 1.5 mL/kg over 1 min followed by an infusion at 0.25 mL/kg/min. The bolus dose can be repeated, and the infusion rate doubled should hemodynamic instability persist [6]. Propofol is not an adequate substitute for lipid emulsion but can be used in low doses to treat seizure activity.

Dysrhythmias are managed using advanced cardiac life support modules, but providers must recognize a prolonged effort which may be required to provide enough circulation until the local anesthetic is either redistributed or metabolized. Epinephrine may aggravate some of the arrhythmias; therefore, many sources suggest vasopressin as an alternative agent [7]. The most current guidelines also recommend the use of amiodarone for local anesthetic overdose [8]. The use of lidocaine to treat dysrhythmias is controversial, with studies showing conflicting results. In instances where torsades de pointes develops, overdrive pacing may be required.