Bradycardia in a patient shortly after reversal with pyridostigmine is most likely due to:

Bradycardia in a patient shortly after reversal with pyridostigmine is most likely due to:

• A. Recurarization
• B. Oxymorphone
• C. Pyridostigmine
• D. Propranolol

Answer: (C)

Bradycardia shortly after reversing a neuromuscular block is most likely due to the reversal agent increasing acetylcholine at muscarinic receptors in the heart. Pyridostigmine inhibits acetylcholinesterase, boosting acetylcholine levels. At the heart, this heightened acetylcholine stimulates M2 receptors via the vagus nerve, slowing the SA node and slowing AV conduction, which produces bradycardia. This is a predictable muscarinic side effect of acetylcholinesterase inhibitors used for reversal, especially if anticholinergic countermeasures like atropine or glycopyrrolate aren’t given. Recurarization would present with renewed muscle weakness from return of NMBA effect rather than isolated bradycardia. An opioid such as oxymorphone can cause bradycardia but not as a direct consequence of NMBA reversal timing. Propranolol would cause bradycardia through beta-blockade, not through reversal-related muscarinic effects.

Bradycardia shortly after reversing a neuromuscular block is most likely due to the reversal agent increasing acetylcholine at muscarinic receptors in the heart. Pyridostigmine inhibits acetylcholinesterase, boosting acetylcholine levels. At the heart, this heightened acetylcholine stimulates M2 receptors via the vagus nerve, slowing the SA node and slowing AV conduction, which produces bradycardia. This is a predictable muscarinic side effect of acetylcholinesterase inhibitors used for reversal, especially if anticholinergic countermeasures like atropine or glycopyrrolate aren’t given.

Recurarization would present with renewed muscle weakness from return of NMBA effect rather than isolated bradycardia. An opioid such as oxymorphone can cause bradycardia but not as a direct consequence of NMBA reversal timing. Propranolol would cause bradycardia through beta-blockade, not through reversal-related muscarinic effects.