The recommended management of local anaesthetic systemic toxicity (LAST) presenting as cardiac arrest includes 20% lipid emulsion (Intralipid) bolus. The proposed mechanism by which lipid emulsion rescues cardiac toxicity from bupivacaine is:

• A Direct pharmacological reversal of sodium channel blockade by lipid binding to bupivacaine-channel complex
• B Creation of a lipid 'sink' in plasma that sequesters free bupivacaine away from cardiac tissue
• C Provision of fatty acid substrate to overcome bupivacaine-mediated mitochondrial inhibition in cardiomyocytes
• D Both lipid partitioning ('sink') and direct fatty acid resuscitation of mitochondrial function contribute ✓

Explanation

The mechanisms of lipid emulsion rescue in LAST are multifactorial. The 'lipid sink' hypothesis proposes that the intravenous lipid creates a large hydrophobic compartment in plasma that sequesters free bupivacaine (which is highly lipophilic), reducing the free fraction available to bind cardiac sodium channels. Additionally, bupivacaine impairs mitochondrial fatty acid oxidation in cardiomyocytes, and the exogenous lipid substrate (triglycerides and fatty acids from the emulsion) partially overcomes this metabolic blockade. Direct sodium channel reversal (option A) is not the mechanism. Both contributing mechanisms are acknowledged in current guidelines.

Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.