Lidocaine (Xylocaine)

Anesthesia Implications

Therapeutic Effects: Local anesthetic, Neutrophil inhibitor

Anesthesia Implications

Used IV to reduce the pain associated with injections such as propofol or etomidate

Lidocaine is a CNS depressant, which decreases sympathetic, hemodynamic,  and intraocular pressure responses to laryngoscopy.

Reduces volatile anesthetic MAC by up to 40%

Lidocaine is used to help prevent and treat bronchospasm and laryngospasm, more especially during intubation and emergence.  HOWEVER, if the induction dose of lidocaine is too low, intratracheal or aerosolized lidocaine can actually induce a laryngo/bronchospasm.

Depresses hypoxic drive

Relaxes bronchial smooth muscle when administered IV

Potentiates Neuromuscular blockade

Cardiac: VENTRICULAR antiarrhythmic.  Depresses left ventricular contractility, which makes lidocaine especially useful for ventricular arrhythmias.  Left ventricular dysfunction can result with lidocaine overdose.  Does NOT effect SA/AV nodes firing rates or PR/QRS/QT intervals.  Decreases cardiac muscle refractory periods

Neuro: Reduces CMRO2, CBF, CBV, and ICP.  On the other hand, all of these can be increased as a result of lidocaine toxicity.  Lidocaine is thought to have some neuroprotective affects – infusions are sometimes utilized to prevent emergence delirium and opioid requirements.

Intermediate potency/toxicity when compared with other local anesthetics

Unintentional intravascular injections resulting in toxicity typically present as seizures.  Symptoms that may precede seizures include circumoral numbness, tinnitus, or a metallic taste.

Lidocaine has the highest neurotoxicity incidence when used for intrathecal anesthesia (lidocaine > tetracaine > bupivacaine > ropivicaine)

Spinal anesthesia with lidocaine can result in transient neurotoxicity.  Reported symptoms can include lower extremity and buttock dysesthesia, burning, and aching.  The risk factors are: outpatient spinal anesthesia, male gender, lithotomy position, and high concentrations (5%).  These symptoms usually resolve within 1-4 weeks

Clonidine, when added to lidocaine, will markedly prolong the anesthetic and analgesic properties

Mixtures of lidocaine with other local anesthetics should be anticipated to have additive effects

Reduces thrombosis and platelet aggregation.  Enhances Fibrinolysis.

Circumoral numbness, ringing in the ears, metallic taste, or apprehension can be early indications of intravenous injection.  Tell the patient to report these symptoms when injecting lidocaine.

Lidocaine, when injected directly into a muscle (such as trigger-point injections), can degenerate and necrose the muscle tissue.

Amiodarone is the preferred treatment of local anesthetic induced ventricular tachyarrhythmias.

5% lidocaine has been used for continuous spinal administration, but has a high incidence of neurotoxicity – specifically, cauda equina syndrome.

Patients with acute or chronic renal problems and/or advanced age should have a deceased dose. Typical doses can result in an accumulation of the drug and/or toxic metabolites.

Lidocaine has been demonstrated to improve outcomes following pulmonary acid aspiration (1.5 mg/kg following aspiration).  This protective effect is due to lidocaine’s inhibitory affect on neutrophils.

Lidocaine is used to treat symptomatic pre-ventricular contractions (PVC’s).  The dosing is 1.0 – 1.5 mg/kg as a bolus dose.  Infusion would be indicated if the PVC’s continue after the bolus.  Dosing is 1-4 mg/minute.

Lidocaine, by comparison to bupivacaine, is less protein-bound.  For this reason lidocaine will cross the placenta in greater quantities and is one of the primary culprits to cause fetal acidosis.

IV push dose

Adult induction/emergence: 1.5 mg/kg
Post-aspiration: 1.5 mg/kg
Treatment for symptomatic PVC’s: 1.0-1.5 mg/kg
Pediatric loading dose: 1.0 mg/kg

All of the toxic doses below are based on Ideal Body Weight

MAX adult dose of lidocaine WITHOUT epinephrine is 4.5 mg/kg, not to exceed 300 mg total.
MAX adult dose of lidocaine WITH epinephrine is 7 mg/kg, not to exceed 400 mg total.
MAX adult dose of lidocaine during tumescent anesthesia is 35-55 mg/kg

IV infusion dose

Adult : IV bolus 1.0-1.5 mg/kg + infusion of 1.5 – 3.0 mg/kg/hr has analgesic, antihyperalgesic, and antiinflammatory benefits

Pediatric: 20-50 mcg/kg/min

Epidural bolus dose:  

Classic “test” dose includes: 3 ml of 1.5% lidocaine with 1:200,000 epinephrine. Given BETWEEN contractions.

*The density motor blockade is directly related to the % given.  Anticipate dense motor blockade with 2% and above.

Differential Epidural Blockade
Sympatholysis: 0.5% lidocaine
Somatic: 1.0% lidocaine
All Fibers: 2.0% lidocaine

Spinal bolus dose: Cesarean section spinal: hyperbaric lidocaine: 50-60 mg (bupivacaine is a better option if the procedure is anticipated to last > 45min
Cesarean section epidural: 2%, 15-25 mL in 5 mL increments to avoid systemic toxicity

*spinal usage has fallen out of favor primarily because of its transient neurological symptoms and cauda equina syndrome (CES).
**Failed spinal blocks using lidocaine should not be repeated using lidocaine.

Regional bolus dose: Addition of sodium bicarbonate (1 mEq/10 mL of local anesthetic) accelerates the onset of neural blockade.

*Epinephrine should NEVER be added to solutions when performing digital or penile blocks

Classification: Local anesthetic (amide)

Time to Onset: IV: 1-2 minutes; Spinal: 3-5 minutes

Duration: Half-life: 1-2 hours. Epinephrine extends the duration 50%

Metabolism: Hepatic P-450. Relies on hepatic blood flow (flow-limited).

Elimination: Clearance is reduced by B-blockers and Histamine (H2) blockers

Additional Notes:
EMLA cream consists of a 1:1 ratio of 5% lidocaine and 5% prilocaine.

Used occasionally by surgeons to infiltrate the area around the carotid sinus to prevent pronounced or sustained reflex bradycardia or heart block during carotid artery surgery. Prophylactic infiltration can actually cause bradycardia

100-200 mg of lidocaine along with 1-2 g of magnesium is a common dose to give patients prior to removal of aortic cross-clamping. This is believed to reduce the likelihood of ventricular fibrillation.

Concentrations % include: 0.5, 1.0, 1.5, 2.0, 4.0, 5.0

References
Nagelhout. Nurse anesthesia. 5th edition. 2014. p. 137
Butterworth. Morgan & Mikhail’s Clinical Anesthesiology. 2013. p. 211, 230, 270-275, 281, 287, 349, 373, 386, 462, 482, 533, 584, 764, 856, 882, 958, 963, 1080
Barash. Clinical anesthesia. 7th edition. 2013. p. 161, 868