LIDOCAINE HYDROCHLORIDE 0.2% IN DEXTROSE 5% IN PLASTIC CONTAINER

Clinical safety rating: safe

Beta-blockers may increase the risk of lidocaine toxicity Can cause CNS toxicity (seizures) and cardiovascular collapse.

How it works

Lidocaine is a sodium channel blocker that stabilizes the neuronal membrane by inhibiting the ionic fluxes required for initiation and conduction of impulses, resulting in local anesthetic and antiarrhythmic effects.

What the body does with it

Metabolism	Primarily hepatic metabolism via CYP1A2 to monoethylglycinexylidide (MEGX) and glycinexylidide (GX), both active metabolites.
Excretion	Renal excretion of unchanged drug and metabolites accounts for >95% of elimination, with ~10% as unchanged lidocaine and ~90% as metabolites (primarily 4-hydroxy-2,6-xylidine, with minor contribution from monoethylglycinexylidide and glycinexylidide). Biliary/fecal excretion is minimal (<1%).
Half-life	Terminal elimination half-life is approximately 1.5–2 hours (mean 1.8 h) in adults with normal hepatic function; may be prolonged in patients with hepatic impairment (e.g., cirrhosis) or heart failure (up to 10 h), and in neonates (3–6 h).
Protein binding	70–80% bound to alpha-1-acid glycoprotein (AAG) and, to a lesser extent, albumin. Binding is variable; decreases in conditions with low AAG (e.g., neonates) and increases in inflammatory states (elevated AAG).
Volume of Distribution	Volume of distribution is approximately 1.0–1.5 L/kg in adults (range 0.7–2.0 L/kg). Higher Vd in patients with heart failure (~2.5 L/kg) due to decreased tissue perfusion; lower Vd in elderly (0.5–1.0 L/kg). Indicates extensive tissue distribution (e.g., brain, heart, liver).
Bioavailability	Intravenous: 100%. Subcutaneous infiltration: essentially 100% (locally administered). Not administered orally due to extensive first-pass hepatic metabolism (<10% bioavailability).
Onset of Action	Intravenous (IV) administration: onset of antiarrhythmic effect is rapid (within 45–90 seconds). Subcutaneous infiltration: local anesthesia onset within 2–5 minutes.
Duration of Action	IV: antiarrhythmic effect lasts 10–20 minutes after a single bolus, necessitating continuous infusion. Subcutaneous infiltration: local anesthesia lasts 30–60 minutes, prolonged with epinephrine (up to 2 hours).

Classification & Brands

Dosing & administration

Intravenous infusion: 1-4 mg/min (0.2% solution = 2 mg/mL) for antiarrhythmic therapy; loading dose 1-1.5 mg/kg IV bolus, then infusion. Maximum infusion rate 4 mg/min.

Dosage form	INJECTABLE
Renal impairment	GFR > 10 mL/min: no adjustment. GFR ≤ 10 mL/min: reduce infusion by 50% or monitor for toxicity; prolonged half-life may require dose reduction.
Liver impairment	Child-Pugh A: no adjustment. Child-Pugh B: reduce dose by 25-50%. Child-Pugh C: reduce dose by 50-75% or consider alternative; increased risk of toxicity due to reduced metabolism.
Pediatric use	IV bolus: 1 mg/kg loading, then infusion 20-50 mcg/kg/min (0.03-0.05 mg/kg/min). Infusion rate may be titrated to effect; maximum infusion rate 50 mcg/kg/min.
Geriatric use	Elderly patients (≥65 years): reduce infusion rate by 50% and monitor for CNS and cardiac toxicity; lower hepatic clearance and reduced volume of distribution necessitate caution.

Use during pregnancy

1st trimester	Consult provider
2nd trimester	Consult provider
3rd trimester	Consult provider

Clinical note

Beta-blockers may increase the risk of lidocaine toxicity Can cause CNS toxicity (seizures) and cardiovascular collapse.

FDA category	Animal
Breastfeeding	Lidocaine is excreted into breast milk. M/P ratio approximately 0.4. Oral bioavailability in infant is low (<5%) due to first-pass metabolism; unlikely to cause adverse effects at maternal therapeutic doses. Use with caution in premature or ill infants.
Teratogenic Risk	Lidocaine crosses the placenta. First trimester: No well-controlled studies, but animal data show no teratogenicity at clinically relevant doses. Second/third trimester: Fetal bradycardia and CNS depression may occur with high maternal doses; use lowest effective dose. No structural malformations associated.

Warnings & precautions

■ FDA Black Box Warning

No FDA black box warning for lidocaine in dextrose solution.

Side Effect Profile

Common Effects	ventricular arrhythmias
Serious Effects

Absolute Contraindications

["Hypersensitivity to lidocaine or amide-type anesthetics","Adams-Stokes syndrome or severe sinoatrial block","Hypovolemia or severe hypotension","In patients with history of sensitivity to lidocaine"]

Clinical Precautions

Precautions

["Continuous monitoring of ECG and vital signs required during IV administration","Risk of CNS toxicity (seizures, respiratory depression) with high doses","Caution in patients with hepatic impairment or severe heart failure","May exacerbate pre-existing arrhythmias in some patients"]

Clinical Tips & Counseling

Drug interactions

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LIDOCAINE HYDROCHLORIDE 0.2% IN DEXTROSE 5% IN PLASTIC CONTAINER

Clinical safety rating: safe

Beta-blockers may increase the risk of lidocaine toxicity Can cause CNS toxicity (seizures) and cardiovascular collapse.

How it works

What the body does with it

Metabolism	Primarily hepatic metabolism via CYP1A2 to monoethylglycinexylidide (MEGX) and glycinexylidide (GX), both active metabolites.
Excretion	Renal excretion of unchanged drug and metabolites accounts for >95% of elimination, with ~10% as unchanged lidocaine and ~90% as metabolites (primarily 4-hydroxy-2,6-xylidine, with minor contribution from monoethylglycinexylidide and glycinexylidide). Biliary/fecal excretion is minimal (<1%).
Half-life	Terminal elimination half-life is approximately 1.5–2 hours (mean 1.8 h) in adults with normal hepatic function; may be prolonged in patients with hepatic impairment (e.g., cirrhosis) or heart failure (up to 10 h), and in neonates (3–6 h).
Protein binding	70–80% bound to alpha-1-acid glycoprotein (AAG) and, to a lesser extent, albumin. Binding is variable; decreases in conditions with low AAG (e.g., neonates) and increases in inflammatory states (elevated AAG).
Volume of Distribution	Volume of distribution is approximately 1.0–1.5 L/kg in adults (range 0.7–2.0 L/kg). Higher Vd in patients with heart failure (~2.5 L/kg) due to decreased tissue perfusion; lower Vd in elderly (0.5–1.0 L/kg). Indicates extensive tissue distribution (e.g., brain, heart, liver).
Bioavailability	Intravenous: 100%. Subcutaneous infiltration: essentially 100% (locally administered). Not administered orally due to extensive first-pass hepatic metabolism (<10% bioavailability).
Onset of Action	Intravenous (IV) administration: onset of antiarrhythmic effect is rapid (within 45–90 seconds). Subcutaneous infiltration: local anesthesia onset within 2–5 minutes.
Duration of Action	IV: antiarrhythmic effect lasts 10–20 minutes after a single bolus, necessitating continuous infusion. Subcutaneous infiltration: local anesthesia lasts 30–60 minutes, prolonged with epinephrine (up to 2 hours).

Classification & Brands

Dosing & administration

Intravenous infusion: 1-4 mg/min (0.2% solution = 2 mg/mL) for antiarrhythmic therapy; loading dose 1-1.5 mg/kg IV bolus, then infusion. Maximum infusion rate 4 mg/min.

Dosage form	INJECTABLE
Renal impairment	GFR > 10 mL/min: no adjustment. GFR ≤ 10 mL/min: reduce infusion by 50% or monitor for toxicity; prolonged half-life may require dose reduction.
Liver impairment	Child-Pugh A: no adjustment. Child-Pugh B: reduce dose by 25-50%. Child-Pugh C: reduce dose by 50-75% or consider alternative; increased risk of toxicity due to reduced metabolism.
Pediatric use	IV bolus: 1 mg/kg loading, then infusion 20-50 mcg/kg/min (0.03-0.05 mg/kg/min). Infusion rate may be titrated to effect; maximum infusion rate 50 mcg/kg/min.
Geriatric use	Elderly patients (≥65 years): reduce infusion rate by 50% and monitor for CNS and cardiac toxicity; lower hepatic clearance and reduced volume of distribution necessitate caution.

Use during pregnancy

1st trimester	Consult provider
2nd trimester	Consult provider
3rd trimester	Consult provider

Clinical note

Beta-blockers may increase the risk of lidocaine toxicity Can cause CNS toxicity (seizures) and cardiovascular collapse.

FDA category	Animal
Breastfeeding	Lidocaine is excreted into breast milk. M/P ratio approximately 0.4. Oral bioavailability in infant is low (<5%) due to first-pass metabolism; unlikely to cause adverse effects at maternal therapeutic doses. Use with caution in premature or ill infants.
Teratogenic Risk	Lidocaine crosses the placenta. First trimester: No well-controlled studies, but animal data show no teratogenicity at clinically relevant doses. Second/third trimester: Fetal bradycardia and CNS depression may occur with high maternal doses; use lowest effective dose. No structural malformations associated.

Warnings & precautions

■ FDA Black Box Warning

No FDA black box warning for lidocaine in dextrose solution.

Side Effect Profile

Common Effects	ventricular arrhythmias
Serious Effects