Lidocaine 2% Epinephrine Normon Actions

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Actions of Lidocaine 2% Epinephrine Normon in details

The action of the drug on the human body is called Pharmacodynamics in Medical terminology. To produce its effect and to change the pathological process that is happening the body and to reduce the symptom or cure the disease, the medicine has to function in a specific way. The changes it does to the body at cellular level gives the desired result of treating a disease. Drugs act by stimulating or inhibiting a receptor or an enzyme or a protein most of the times. Medications are produced in such a way that the ingredients target the specific site and bring about chemical changes in the body that can stop or reverse the chemical reaction which is causing the disease.

Pharmacology: Lignocaine, like other local anaesthetics, causes a reversible blockade of impulse propagation along nerve fibres by preventing the inward movement of sodium ions through the nerve membrane. Local anaesthetics of the amide-type are thought to act within the sodium channels of the nerve membrane.

Local anaesthetic drugs may have similar effects on excitable membranes in the brain and myocardium. If excessive amounts of drug reach the systemic circulation rapidly, symptoms and signs of toxicity will appear, emanating mainly from the central nervous system (CNS) and cardiovascular system.

Central nervous system toxicity usually precedes the cardiovascular effects as it occurs at lower plasma concentrations. Direct effects of local anaesthetics on the heart include slow conduction, negative inotropism and eventually cardiac arrest.

Indirect cardiovascular effects eg, hypotension and bradycardia, may occur after epidural or spinal administration depending on the extent of the concomitant sympathetic block.

Adrenaline acts on both α- and β-adrenergic receptors of tissue innervated by sympathetic nerves, except for the sweat glands and arteries of the face. It is the most important α-receptor activator. Adrenaline stimulates the heart to increase output; raises the systolic blood pressure; lowers diastolic blood pressure; relaxes bronchial spasm and mobilises liver glycogen, resulting in hyperglycaemia and possibly glycosuria.

Pharmacokinetics: Lignocaine has a rapid onset and a medium duration of action. The onset of action is 1-5 min following infiltration and 5-15 min following other types of administration.

The rate of absorption depends upon the dose, the route of administration and the vascularity of the injection site. Intercostal blocks give the highest peak plasma concentrations (approximately 1.5 mcg/mL for every 100 mg injected), while abdominal SC injections give the lowest (approximately 0.5 mcg/mL/100 mg injected). Epidural and major nerve block produce peak plasma levels intermediate between these.

The addition of adrenaline considerably slows the absorption of lignocaine, although the rate also depends on the site of injection. Peak plasma concentrations are reduced by 50% following SC injection, by 30% following epidural injection and by 20% following intercostal block if adrenaline 5 mcg/mL is added.

Absorption of lignocaine from the epidural space occurs in 2 phases; the 1st phase is in the order of 9 min and the 2nd is approximately 82 min. The slow absorption is the rate-limiting step in the elimination of lignocaine, which also explains the apparent elimination half-life following epidural injection is longer than after IV administration.

The plasma binding of lignocaine is dependent on drug concentration and the fraction bound decreases with increasing concentration. At concentrations of 1-4 mcg of free base/mL, 60-80% of lignocaine is protein bound. Binding is also dependent on the plasma concentration of the α1-acid glycoprotein.

Lignocaine crosses the blood-brain and placental barriers by passive diffusion. Since the degree of plasma protein-binding in the foetus is less than in the mother, although free lignocaine concentrations will be the same, the total plasma concentration will be greater in the mother.

Lignocaine has a total plasma clearance of 0.95 L/min, a volume of distribution at steady state of 91 L, an elimination half-life of 1.6 hrs and an estimated hepatic extraction ratio of 0.65. Approximately 90% of a parenteral dose of lignocaine is rapidly metabolised in the liver by de-ethylation to form monoethylglycinexylidide (MEGX) and glycinexylidide (GX) followed by cleavage of the amide bond to form xylidine and 4-hydroxyxylidine which are excreted in the urine. Less than 10% of a dose is excreted unchanged in the urine.

The principal metabolites, MEGX and GX, also possess pharmacological activity. The rate of metabolism of lignocaine appears to be limited by liver blood flow which may be reduced in patients after acute myocardial infarction and/or congestive heart failure. The rate of lignocaine metabolism may also be reduced in patients with liver or hepatic tissue necrosis, possibly because of altered perfusion.

The duration of action depends upon the concentration used, the dose given, the nerves to be blocked and the status of the patient. The 2% solution will produce an effect for 1½-2 hrs when given epidurally, and up to 5 hrs when given as a peripheral nerve block. When used in a 1% concentration, there is less effect on motor nerve fibres and the duration of effect is shorter.

Lidocaine 2% Epinephrine Normon pharmacology

Pharmacokinetics of a drug can be defined as what body does to the drug after it is taken. The therapeutic result of the medicine depends upon the Pharmacokinetics of the drug. It deals with the time taken for the drug to be absorbed, metabolized, the process and chemical reactions involved in metabolism and about the excretion of the drug. All these factors are essential to deciding on the efficacy of the drug. Based on these pharmacokinetic principles, the ingredients, the Pharmaceutical company decides dose and route of administration. The concentration of the drug at the site of action which is proportional to therapeutic result inside the body depends on various pharmacokinetic reactions that occur in the body.

Lidocaine 2% Epinephrine Normon acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Lidocaine 2% Epinephrine Normon has also been shown to bind or antagonize the function of N-methyl-D-aspartate (NMDA) receptors as well as nicotinic acetylcholine receptors and the serotonin receptor-ion channel complex.


  1. DailyMed. "LIDOCAINE; TETRACAINE: DailyMed provides trustworthy information about marketed drugs in the United States. DailyMed is the official provider of FDA label information (package inserts).". (accessed September 17, 2018).
  2. DailyMed. "EPINEPHRINE: DailyMed provides trustworthy information about marketed drugs in the United States. DailyMed is the official provider of FDA label information (package inserts).". (accessed September 17, 2018).
  3. NCIt. "Epinephrine Hydrochloride: NCI Thesaurus (NCIt) provides reference terminology for many systems. It covers vocabulary for clinical care, translational and basic research, and public information and administrative activities.". (accessed September 17, 2018).


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Information checked by Dr. Sachin Kumar, MD Pharmacology

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