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Lidocaine (Lignocaine Local anaesthetic) Pharmacology

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Lidocaine is an amide local anaesthetic agent and a class 1B antiarrhythmic drug. It is an amide, because it has an amine bond similar to that amino acids. This amide contains a nitrogen-hydrogen group tat is  bound to a carbon-oxygen, double bond.

The nitrogen-hydrogen (NH) group is a benzene that has two methyl groups on both of it’s ortho positions. The carbon-oxygen (CO) group is a carbon bound to a nitrogen molecule to which two ethane groups are attached.

Local anesthetics are drugs that are used to provide regional anesthesia to aid in  painless surgical procedures..


Ester local anesthetics have just one “i” in their names I.e procaine and cocaine while amide local anesthetics have more than one “i” in their names such as lidocaine and, bupivacaine.

Lignocaine is the most widely used local anaesthetic in the UK.


Lidocaine is the best drug used in the management of ventricular tachycardia associated with acute myocardial infarction (MI)

The agent is also used in open-heart surgery,

It is used in management of ventricular arrhythmias associated with digoxin toxicity.When given judiciously via an intravenous route, it is an effective antiarrhythmic agent

With or without adrenaline, lidocaine is injected into the eyelids for minor surgeries and for surgical procedures on the globe of the eye.

The drug doesn’t slow conduction therefore it has little effect on atrial function.

Lignocaine is used for infiltration block, peripheral nerve block, and for epidural

and spinal anesthesia.

In addition to injection, lidocaine can be administered topically as a gel or aerosol. It is used in all forms of local anaesthesia.

Lidocaine Mechanism of Action

Lidocaine is a class Ib agent that blocks sodium channels,therefore reducing the rate of increase of the cardiac action potential and increasing the effective refractory period.

Lidocaine works by selectively blocking open (inactivated) sodium channels and dissociates rapidly. This prevents the sodium ions from going through the voltage-gated channels stopping the nerve impulses or signals before their generation.

The function of the voltage-gated channels is to allow movement of sodium ions from outside the cell into the cell. This creates a flow of positive ions, making the voltage that stimulates the central nervous system. Then the sodium potassium pump actively throws out the sodium ions out of the cell.

Lidocaine is known to act exclusively on both activated and inactivated sodium channel and it is highly selective for damaged tissues.

As mentioned above, lidocaine is an amide. This amide component allows it to act like an amino acid therefore interacting with the active sites in the sodium channel domains.

This interaction prevents the transfer of sodium ions.

Lidocaine is known to interact with sodium ions in a 1:1 ration. This simply means that one molecule of lidocaine blocks one molecule of sodium

Local anesthetic agents have the ability to inhibit electrical excitation of nociceptive nerve fibers.

This agent weakly blocks sodium channels shortening action potential.

Pharmacodynamics and Pharmacokinetics

Lidocaine has a poor oral bioavailability due to presystemic or first-pass metabolism therefore it  is must be given intravenously. It is known to have a quick onset and medium duration of action.

The agent is metabolized in the liver and its clearance is limited by hepatic blood flow.

Its clearance from the body is reduced in patients with heart failure. This predisposes the patient to developing lidocaine toxicity unless the dose is reduced. Lidocaine has a very small difference between a therapeutic and toxic plasma concentrations.

The mean half-life of lidocaine is approximately two hours in healthy subjects.

Local anesthetics are readily cleaved making them unsuitable for oral administration.

Lidocaine is broken down primarily in the liver by a process known as oxidative N-dealkylation by liver amidases.

Absorption following topical application can be rapid such as from the larynx, bronchi or urethra.

The agent has a rapid onset and intermediate duration of action of about 1–2 hours.

The therapeutic drug range for lidocaine is 1.5 to 5.0 mcg/mL.

While generally safe , lidocaine can be toxic if administered inappropriately.


When given parenterally, an effective plasma concentration is rapidly achieved by administering a bolus loading dose intravenously followed by a constant rate infusion.

The dose must be adjusted in patients with congestive heart disease or hepatic disease.

For minor operation, 1% plain lidocaine is used and,

For dental operation, 2% lidocaine with epinephrine is employed.

Side effects

Adverse drug reactions of lidocaine mainly affect two systems. The central venous system and cardiovascular system.

These include the following:

In the central nervous systemine is associated with; drowsiness, twitching, paraesthesia, nausea and vomiting.

The patient may also develop focal seizures followed by generalized seizures.

In the cardiovascular system, there is an associated bradycardia, cardiac depression as an effect of negative inotropic effect and asystole.

Of the conventional anti-arrhythmic drus, lidocaine is less cardiotoxic.

Systemic allergy is uncommon.

Like other local anaesthetics, lidocaine is associated with concomitant cardiac inhibition known as cardiodepression. Though this effect is useful in the management of cardiac arrythmias.


Negative inotropic agents are known to reduce lidocaine clearance by reducing hepatic blood flow. This predisposes and individual to accumulation and toxicity.


Toxicity occurs when the levels are greater than 5mcg/mL. A high-yield mnemonic to use in mastering features of toxicity is SAMS

  • slurred speech
  • altered Central nervous system
  • muscle twitching
  • S-Seizures

Post References

  • Katzung basic and clinical pharmacy

  • Revised on: 2021-06-24 09:31:44