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

Step 1: Identify the diagnosis. The patient received bupivacaine for regional anaesthesia and developed sudden unresponsiveness with unrecordable pulse. This is a classic presentation of Local Anaesthetic Systemic Toxicity (LAST), specifically bupivacaine-induced cardiotoxicity.

Step 2: Understand bupivacaine cardiotoxicity.

• Bupivacaine is a long-acting amide local anaesthetic that can cause severe cardiac toxicity if accidentally administered intravascularly or in excessive doses.
• It inhibits cardiac sodium channels (Na+ channels) and also impairs mitochondrial fatty acid metabolism in cardiac cells, leading to refractory cardiac arrest.
• Manifestations: ventricular arrhythmias, cardiac arrest, CNS toxicity (seizures, loss of consciousness).

Step 3: Management -- Lipid Emulsion Therapy.

• Immediate cardiopulmonary resuscitation (CPR) must be initiated.
• The specific antidote for bupivacaine toxicity is Intravenous Lipid Emulsion (Intralipid 20%).
• Mechanism: the lipid emulsion acts as a "lipid sink," sequestering the lipophilic bupivacaine molecules from cardiac tissues, reducing their toxic effect.
• Dose: Intralipid 20% -- bolus 1.5 ml/kg IV, followed by infusion.
• Other options (sodium bicarbonate, dobutamine, calcium) are not specific antidotes for bupivacaine toxicity.

Step 4: Conclusion. CPCR (CPR) combined with 20% Intralipid is the standard management for bupivacaine-induced cardiac arrest. Answer: CPCR with 20% Intralipid.