A patient is receiving a continuous IV infusion of lidocaine for the treatment of a dysrhythmia. Which of the following are consistent with lidocaine toxicity?

Introduction: Lidocaine is a Class 1B antiarrhythmic that works by blocking sodium channels in the myocardial conduction system, but it also crosses the blood-brain barrier. When serum levels exceed the therapeutic range, the medication causes significant neurotoxicity, progressing from mild sensory changes to severe central nervous system excitation. A. Lidocaine toxicity typically manifests as cardiovascular depression rather than stimulation. While early phases might show mild changes, severe toxicity is characterized by bradycardia, hypotension, and potential cardiac arrest due to the profound blockade of sodium channels across the cardiac conduction system and vascular smooth muscle. B. Respiratory symptoms like tachypnea and crackles are typically indicative of acute heart failure or pulmonary edema. While lidocaine can cause respiratory depression in late-stage toxicity, it does not typically present with the signs of fluid volume overload or pulmonary congestion associated with left-sided heart failure. C. The central nervous system is highly sensitive to lidocaine levels. Toxicity, often termed SAMS (Slurred speech, Altered central nervous system, Muscle twitching, Seizures), frequently presents as initial confusion and tremors. If the infusion is not stopped, this can rapidly progress to tonic-clonic convulsions and respiratory arrest. D. Blurred vision and seeing halos around objects are classic manifestations of digoxin toxicity, resulting from the inhibition of the sodium-potassium ATPase pump in the retina. While lidocaine can cause some visual disturbances, halos are specifically diagnostic for digitalis-induced xanthopsia rather than lidocaine-induced central nervous system toxicity.