Contraindications
Absolute contraindications for the use of lidocaine include:

Heart block, second or third degree (without pacemaker)
Severe sinoatrial block (without pacemaker)
Serious adverse drug reaction to lidocaine or amide local anesthetics
Hypersensitivity to corn and corn-related products (corn-derived dextrose is used in the mixed injections)
Concurrent treatment with quinidine, flecainide, disopyramide, procainamide (class I antiarrhythmic agents)
Prior use of amiodarone hydrochloride
Adams-Stokes syndrome
Wolff-Parkinson-White syndrome
Lidocaine viscous is not recommended by the FDA to treat teething pain in children and infants.Exercise caution in patients with any of these:

Hypotension not due to arrhythmia
Bradycardia
Accelerated idioventricular rhythm
Elderly
Ehlers–Danlos syndromes; efficiency of local anesthetics can be reduced
Pseudocholinesterase deficiency
Intra-articular infusion (this is not an approved indication and can cause chondrolysis)
Porphyria, especially acute intermittent porphyria; lidocaine has been classified as porphyrogenic because of the hepatic enzymes it induces, although clinical evidence suggests it is not. Bupivacaine is a safe alternative in this case. Impaired liver function – people with lowered hepatic function may have an adverse reaction with repeated administration of lidocaine because the drug is metabolized by the liver. Adverse reactions may include neurological symptoms (e.g. dizziness, nausea, muscle twitches, vomiting, or seizures). Overdosage
Overdoses of lidocaine may result from excessive administration by topical or parenteral routes, accidental oral ingestion of topical preparations by children (who are more susceptible to overdose), accidental intravenous (rather than subcutaneous, intrathecal, or paracervical) injection, or from prolonged use of subcutaneous infiltration anesthesia during cosmetic surgery. Such overdoses have often led to severe toxicity or death in both children and adults.
Lidocaine and its two major metabolites may be quantified in blood, plasma, or serum to confirm the diagnosis in potential poisoning victims or to assist forensic investigation in a case of fatal overdose. Lidocaine is often given intravenously as an antiarrhythmic agent in critical cardiac-care situations. Treatment with intravenous lipid emulsions (used for parenteral feeding) to reverse the effects of local anaesthetic toxicity is becoming more common. Postarthroscopic glenohumeral chondrolysis
Lidocaine in large amounts may be toxic to cartilage and intra-articular infusions can lead to postarthroscopic glenohumeral chondrolysis. Pharmacology
Mechanism of action
Lidocaine alters signal conduction in neurons by prolonging the inactivation of the fast voltage-gated Na+ channels in the neuronal cell membrane responsible for action potential propagation. With sufficient blockage, the voltage-gated sodium channels will not open and an action potential will not be generated. Careful titration allows for a high degree of selectivity in the blockage of sensory neurons, whereas higher concentrations also affect other types of neurons. The same principle applies for this drugs actions in the heart. Blocking sodium channels in the conduction system, as well as the muscle cells of the heart, raises the depolarization threshold, making the heart less likely to initiate or conduct early action potentials that may cause an arrhythmia. Pharmacokinetics
When used as an injectable it typically begins working within four minutes and lasts for half an hour to three hours. Lidocaine is about 95% metabolized (dealkylated) in the liver mainly by CYP3A4 to the pharmacologically active metabolites monoethylglycinexylidide (MEGX) and then subsequently to the inactive glycine xylidide.