Ropivacaine produces less motor blockade than bupivacaine at equivalent analgesic concentrations. The pharmacological basis for this differential blockade is:

• A Ropivacaine's higher pKa causes greater ionisation at tissue pH, providing less penetration into myelinated motor fibres
• B Ropivacaine undergoes faster plasma ester hydrolysis before reaching motor endplates
• C Ropivacaine causes selective vasoconstriction in motor nerve territories, reducing local bioavailability
• D Ropivacaine is an S(-) enantiomer with inherently lower affinity for sodium channels in larger myelinated (Aβ) fibres ✓

Explanation

Ropivacaine is a pure S(-) enantiomer, whereas bupivacaine is a racemate. The S(-) enantiomer has lower intrinsic potency at sodium channels in large myelinated Aβ motor fibres but retains adequate potency at the smaller, less myelinated C and Aδ sensory fibres. This differential affinity produces sensory block disproportionate to motor block ('differential block'), making ropivacaine ideal for labour analgesia and ambulatory epidurals. Both agents have similar pKa values (~8.1 for ropivacaine, ~8.1 for bupivacaine), so ionisation differences are minimal.

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

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