Lidocaine Unit Converter
Lidocaine Unit Converter
Convert lidocaine — lignocaine in British usage — between µg/mL, mg/L and µmol/L, with the antiarrhythmic infusion range and the two facts that matter about it: toxicity is neurological before it is cardiac, and levels rise disproportionately in heart failure and liver disease.
Lidocaine converter
Mass ⇄ molarPlasma lidocaine 3 µg/mL during an antiarrhythmic infusion
The conversion
µg/mL = µmol/L ÷ 4.2673
because 4.2673 = 1 mg/L ÷ 234.34 g/mol, the molecular weight of lidocaine
- µg/mL = mg/L
- the same concentration written two ways. Lidocaine concentrations are almost always reported in µg/mL or mg/L; µmol/L appears on some European reports
- MW 234.34
- lidocaine, C₁₄H₂₂N₂O — <b>lignocaine</b> in British and Commonwealth usage, and the same molecule. The drug is given as the hydrochloride, whose salt weight is higher, but the assay measures the base
- MEGX and GX
- monoethylglycinexylidide and glycinexylidide, the active metabolites. Both accumulate during prolonged infusions and in renal impairment, and both contribute to neurological toxicity, so a total lidocaine concentration can understate the pharmacologically active load in a patient who has been infused for days
- α₁-acid glycoprotein
- lidocaine binds to it, and it is an acute-phase protein that rises after myocardial infarction. The measured TOTAL concentration therefore rises over the days after an infarct while the free, active concentration may not — one reason a total level can mislead in exactly the population being treated
Worked example
Plasma lidocaine 3 µg/mL during an antiarrhythmic infusion
3 µg/mL = 3.0 mg/L — the same concentration
3 × 4.2673 = 12.8 µmol/L
12.8 µmol/L sits inside the 1.5–5 µg/mL range, which is 6.4–21.3 µmol/L
It is not, however, a concentration to feel comfortable about: minor adverse effects appear in some patients above about 3 µg/mL, so this is the point at which to start asking about perioral tingling, tinnitus and drowsiness rather than the point at which to stop
Going back: 12.8 ÷ 4.2673 = 3.0 µg/mL
And in a patient with cardiac failure or cirrhosis the same infusion rate produces a higher concentration than this and takes longer to fall, because lidocaine clearance depends on hepatic blood flow
Concentration and effect
| Plasma concentration | µmol/L | What is typically seen |
|---|---|---|
| 1.5 – 5 µg/mL | 6.4 – 21.3 | The accepted antiarrhythmic range. Minor adverse effects begin in some patients above about 3 µg/mL |
| Above about 5 µg/mL | above 21.3 | Neurological symptoms become common: perioral and lingual paraesthesia, metallic taste, light-headedness, tinnitus, visual disturbance, drowsiness, agitation, muscle twitching, slurred speech |
| Higher still | — | Seizures, then respiratory depression and coma |
| Higher again | — | Cardiac effects — conduction slowing, widened QRS, hypotension, bradyarrhythmia and ultimately asystole |
Why heart failure and liver disease change everything
| Situation | Effect on lidocaine | Consequence |
|---|---|---|
| Cardiac failure or shock | Reduced hepatic blood flow reduces clearance; the volume of distribution is also smaller | A standard infusion rate produces a substantially higher concentration, and a standard loading dose a higher peak. Rates must be reduced |
| Hepatic impairment, cirrhosis | Reduced clearance, both from reduced blood flow and reduced enzyme capacity | Concentrations rise and fall slowly; accumulation over a prolonged infusion is the usual pattern |
| Prolonged infusion (over 24 hours) | The apparent half-life lengthens and the active metabolites MEGX and GX accumulate | Toxicity can appear on day two at an infusion rate that was safe on day one |
| Renal impairment | Little effect on lidocaine itself; the metabolites accumulate | Neurological toxicity out of proportion to the parent drug concentration |
| Days after myocardial infarction | α₁-acid glycoprotein rises, increasing protein binding | The measured total concentration rises while the free, active fraction may not — a total level can look toxic when it is not, or mask a change |
| Beta blockers, amiodarone, cimetidine | Reduced hepatic blood flow or inhibited metabolism | Higher concentrations on an unchanged rate |
When a lidocaine level is and is not the right test
| Setting | Is a level useful? |
|---|---|
| Prolonged antiarrhythmic infusion, particularly with cardiac failure or hepatic impairment | Sometimes — to confirm accumulation or to explain neurological symptoms, alongside the clinical picture |
| Suspected toxicity during an infusion, with equivocal symptoms | Occasionally, as supporting evidence. Management does not wait for it |
| Local anaesthetic systemic toxicity after infiltration, a block or tumescent anaesthesia | No. This is a clinical emergency treated on recognition with lipid emulsion and resuscitation; a level arrives far too late to be of use and must never be waited for |
| Routine monitoring of a short antiarrhythmic infusion in a stable patient | Rarely. Monitoring is by rhythm, blood pressure and symptoms |
| Topical, dental or dermatological use | No |
Lignocaine by another name, neurology before cardiology, and a clearance that depends on blood flow
Lidocaine — lignocaine in British and Commonwealth usage, and the same molecule either way — is reported in micrograms per millilitre, identically in milligrams per litre, or occasionally in micromoles per litre. Its molecular weight is 234.34, so one microgram per millilitre is 4.2673 micromoles per litre and a concentration of 3 µg/mL is 12.8 µmol/L. The generally accepted therapeutic range for lidocaine as an antiarrhythmic is 1.5 to 5 µg/mL, which is 6.4 to 21.3 µmol/L, and minor adverse effects begin to appear in some patients above about 3 µg/mL — so the middle of the range is not a place to relax.
Monitoring lidocaine is uncommon. Its role as a routine antiarrhythmic has shrunk considerably since prophylactic lidocaine after myocardial infarction was abandoned, and most lidocaine given today is given as a local anaesthetic, where dosing is by milligrams per kilogram and no plasma concentration is involved. Where a level is sent, it is almost always to make sense of a prolonged antiarrhythmic infusion — to explain neurological symptoms, or to confirm accumulation in a patient whose liver or heart makes it likely.
The clinically essential fact about lidocaine toxicity is its order. The central nervous system fails before the heart does. The sequence begins with perioral or lingual paraesthesia, a metallic taste, light-headedness and tinnitus; it moves on to visual disturbance, agitation, drowsiness, muscle twitching, slurred speech and confusion; then seizures, respiratory depression and coma; and only at higher concentrations still do the cardiac effects appear — conduction slowing, a widened QRS, hypotension, bradyarrhythmia and ultimately asystole. Anyone looking after a lidocaine infusion is therefore watching for tingling lips and ringing ears, because those are the early signals and they arrive while there is still time. Individual thresholds vary too widely for a number to be the trigger. Local anaesthetic systemic toxicity after infiltration, a nerve block or tumescent anaesthesia follows the same progression, and is a clinical emergency treated on recognition with lipid emulsion and resuscitation: a plasma level has no part in that decision and must never be waited for.
The second essential fact is pharmacokinetic. Lidocaine has a high hepatic extraction ratio, which means its clearance is limited by how much blood reaches the liver rather than by enzyme capacity — flow-dependent clearance. Cardiac failure and shock reduce hepatic blood flow, so the same infusion rate produces a substantially higher concentration, and the volume of distribution is smaller as well, so a standard loading dose produces a higher peak. Hepatic impairment reduces clearance for both reasons at once. The result is an unwelcome coincidence: the patients most likely to receive an antiarrhythmic lidocaine infusion — those with a failing or recently infarcted heart — are the patients in whom it accumulates fastest. Two further complications sit on top of that. The active metabolites monoethylglycinexylidide and glycinexylidide build up during infusions lasting more than a day and in renal impairment, contributing neurological toxicity that the parent concentration understates; and α₁-acid glycoprotein, which binds lidocaine, rises as an acute-phase protein after myocardial infarction, so the measured total concentration can climb while the free, active fraction does not. A lidocaine level is therefore a piece of evidence about an infusion, to be read with the patient’s symptoms, their liver and cardiac function and how long the infusion has been running. It does not set the rate.
Frequently asked questions
How do you convert lidocaine from µg/mL to µmol/L?
Multiply by 4.2673, which is one milligram per litre divided by lidocaine’s molecular weight of 234.34 g/mol. A concentration of 3 µg/mL is 12.8 µmol/L, and dividing by the same factor goes back. µg/mL and mg/L are the same number, so no conversion is needed between them.
Is lignocaine the same as lidocaine?
Yes — lignocaine is the British and Commonwealth name and lidocaine the international non-proprietary name for the same molecule, C₁₄H₂₂N₂O, molecular weight 234.34. Older UK reports, textbooks and local protocols may use either, and no conversion or adjustment is involved. The drug is given as lidocaine hydrochloride, but the assay measures the base, so the salt weight does not enter the arithmetic.
What is the therapeutic range for lidocaine?
1.5–5 µg/mL, equivalently 1.5–5 mg/L or 6.4–21.3 µmol/L, for lidocaine used as an antiarrhythmic by intravenous infusion — with minor adverse effects appearing in some patients above about 3 µg/mL. It does not apply to local anaesthetic use, where dosing is by milligrams per kilogram and toxicity is recognised clinically rather than measured.
What are the first signs of lidocaine toxicity?
Neurological, not cardiac. Perioral or lingual numbness and tingling, a metallic taste, light-headedness and tinnitus come first, followed by visual disturbance, agitation, drowsiness, muscle twitching, slurred speech and confusion, then seizures. Cardiac effects — conduction slowing, a widened QRS, hypotension, bradyarrhythmia and at extreme concentrations asystole — appear only at higher concentrations. That order is why a patient on an infusion who reports tingling lips or ringing ears is taken seriously immediately.
Why do lidocaine levels rise so much in heart failure and liver disease?
Because lidocaine has a high hepatic extraction ratio, so its clearance is limited by hepatic blood flow rather than by enzyme capacity. Cardiac failure and shock reduce that flow, and the volume of distribution is smaller too, so the same infusion rate yields a considerably higher concentration and the same loading dose a higher peak. Hepatic impairment reduces clearance by both mechanisms. Infusion rates have to be reduced in these patients, and a concentration that has risen falls more slowly than expected.
Should you wait for a lidocaine level in suspected local anaesthetic systemic toxicity?
No, never. Local anaesthetic systemic toxicity after infiltration, a nerve block or tumescent anaesthesia is a clinical emergency recognised from its progression — perioral tingling, tinnitus and confusion moving to seizures and cardiovascular collapse — and treated immediately with stopping the injection, airway and seizure management, lipid emulsion and full resuscitation. A plasma level takes far too long to return and contributes nothing to that decision.
Related calculators
References
- Bauer LA. Lidocaine. In: Applied Clinical Pharmacokinetics. 2nd ed. New York: McGraw-Hill; 2008: chapter 7. “The generally accepted therapeutic range for lidocaine is 1.5–5 µg/mL”; minor adverse effects above 3 µg/mL in some patients.
- Collinsworth KA, Kalman SM, Harrison DC. The clinical pharmacology of lidocaine as an antiarrhythmic drug. Circulation. 1974;50(6):1217–1230.
- Thomson PD, Melmon KL, Richardson JA, et al. Lidocaine pharmacokinetics in advanced heart failure, liver disease, and renal failure in humans. Ann Intern Med. 1973;78(4):499–508.
- Neal JM, Neal EJ, Weinberg GL. American Society of Regional Anesthesia and Pain Medicine local anesthetic systemic toxicity checklist: 2020 version. Reg Anesth Pain Med. 2021;46(1):81–82.
- Torp KD, Metheny E, Simon LV. Lidocaine toxicity. In: StatPearls. Treasure Island FL: StatPearls Publishing; 2024.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.