Cardiac or central nervous system toxicity may result when standard lignocaine doses are administered to patients with circulatory failure. This may be due to the following reason :
Cardiac or central nervous system toxicity may result when standard lignocaine doses are administered to patients with circulatory failure. This may be due to the following reason :
💡 Explanation
## **Core Concept**
The question revolves around the pharmacokinetics and toxicodynamics of lignocaine (lidocaine), a local anesthetic and antiarrhythmic drug. Lignocaine is primarily metabolized by the liver and its metabolites are excreted by the kidneys. In patients with circulatory failure, there can be alterations in hepatic blood flow and renal function, potentially affecting lignocaine's pharmacokinetics.
## **Why the Correct Answer is Right**
The correct answer, , implies that decreased hepatic blood flow in patients with circulatory failure can lead to reduced first-pass metabolism of lignocaine. Lignocaine undergoes extensive first-pass metabolism in the liver. When hepatic blood flow is decreased, more lignocaine reaches systemic circulation in its active form, increasing its plasma concentration. High plasma concentrations of lignocaine can cause central nervous system (CNS) toxicity (e.g., dizziness, tremors, seizures) and cardiac toxicity (e.g., arrhythmias, decreased cardiac contractility).
## **Why Each Wrong Option is Incorrect**
- **Option A:** This option does not directly relate to the pharmacokinetic alterations seen in circulatory failure that would increase lignocaine toxicity.
- **Option B:** While decreased renal function can affect the clearance of lignocaine metabolites, the primary concern with lignocaine toxicity is its parent compound, which is metabolized by the liver.
- **Option C:** This option does not directly pertain to a mechanism by which circulatory failure would increase the risk of lignocaine toxicity.
## **Clinical Pearl / High-Yield Fact**
A key clinical point to remember is that lignocaine toxicity can be exacerbated in patients with liver dysfunction or decreased hepatic blood flow, as these conditions reduce the drug's clearance and increase its risk of CNS and cardiac toxicity. Dose adjustments are often necessary in such patients.