Local anesthetics decrease blood pressure and heart rate through alterations in electrical excitability of the heart, dilation of blood vessels, and inhibition of sinoatrial node firing. All local anesthetics have the potential to induce cardiac dysrhythmias. The negative inotropic action of local anesthetics is dose dependent, depresses myocardial contractility, and decreases cardiac output. Typical effects include widening of the QRS complex and lengthening of the PR interval [12].

The earliest signs of systemic toxicity are usually caused by blockade of inhibitory central nervous system pathways for unopposed excitatory nerve activity. Subjective symptoms include dizziness, confusion, tinnitus, difficulty focusing, shivering, tremors, and possible seizures. Symptoms of central nervous system depression, such as sedation, lack of responsiveness, and potential respiratory depression, follow soon after. These signs are rapidly reversed with discontinuation of the drug. Tissues with the highest aerobic demand and least tolerance for hypoxia, such as the heart, the lungs, and the central nervous system, are most vulnerable to the toxic effects of local anesthetics [5–7].

Initially, low serum levels of local anesthetic slightly increase cardiac output, blood pressure, and heart rate from increased sympathetic activity and vasoconstriction. As the blood levels rise, peripheral vasodilation of vascular smooth muscle and lower peripheral vascular resistance leads to hypotension and lower cardiac output [13]. Local anesthetic-induced arrhythmias can manifest as conduction delays, from prolonged PR interval to complete heart block, sinus arrest, and asystole. Conduction defects with IV lidocaine infusions are more prone to occur with preexisting bundle branch blocks [14, 15] (Table 7.2).