Question

A young male was given regional anaesthesia with 0.25% bupivacaine. The patient became unresponsive & pulse became unrecordable. Best Management would be

• A. CPCR with 20% Intralipid
• B. CPCR with sod. Bicarbonate
• C. CPCR with dobutamine
• D. CPCR with calcium

Hint:

Bupivacaine toxicity causing cardiac arrest has a specific antidote that works by sequestering the lipophilic drug away from cardiac tissue.

Answer 1

The Correct Option is A

Lipid sink theory for Local Anaesthetic Systemic Toxicity (LAST):

Bupivacaine is highly lipophilic (protein binding ~95%). In LAST, it accumulates in myocardial tissue, blocking $\text{Na}^+$ channels and impairing mitochondrial fatty acid oxidation, causing refractory cardiac arrest.

$\textbf{Intralipid 20%}$ (lipid emulsion therapy) reverses this by:

• Creating a lipid compartment in plasma that acts as a "lipid sink" -- bupivacaine partitions into the lipid phase, reducing free drug concentration at cardiac receptors.
• Restoring mitochondrial function by providing fatty acid substrate.

Dosing protocol:

• Bolus: $1.5 \text{ ml/kg}$ of Intralipid 20% IV over 1 minute
• Infusion: $0.25 \text{ ml/kg/min}$ for at least 10 minutes
• Repeat bolus once or twice if cardiovascular collapse persists

Other options are ineffective for this specific mechanism:

• Sodium bicarbonate: used for tricyclic antidepressant toxicity
• Dobutamine: inotropic support, not antidotal
• Calcium: used for calcium channel blocker toxicity

\[\boxed{\text{CPCR with 20\% Intralipid}}\]