Pretreatment with a nondepolarizing muscle relaxant is least effective in attenuating which side effect of succinylcholine?

Pretreatment with a nondepolarizing muscle relaxant is least effective in attenuating which side effect of succinylcholine?

• A. Increased intragastric pressure
• B. Increased ICP
• C. Hyperkalemia
• D. Myalgias

Answer: (C)

The main idea here is how pretreatment with a nondepolarizing muscle relaxant changes the adverse effects of succinylcholine by reducing fasciculations. By competitively blocking nicotinic receptors, the pretreatment dampens the initial muscle contractions that succinylcholine would cause. Those contractions drive several side effects: they increase intragastric pressure from abdominal wall and diaphragmatic activity, raise intracranial pressure due to cerebral venous congestion, and contribute to post-twitch muscle pain (myalgias). Reducing the frequency and intensity of these fasciculations therefore helps lessen those effects. Hyperkalemia, however, arises from potassium efflux after succinylcholine depolarizes the motor endplates. This potassium release is driven by widespread receptor activation, including upregulated extrajunctional receptors in certain situations, and it can occur even when some receptors are blocked by a pretreatment dose. Because the potassium shift depends on depolarization at endplates that may still occur despite the block, pretreatment does not reliably prevent hyperkalemia. That makes hyperkalemia the side effect least attenuated by pretreatment.

The main idea here is how pretreatment with a nondepolarizing muscle relaxant changes the adverse effects of succinylcholine by reducing fasciculations. By competitively blocking nicotinic receptors, the pretreatment dampens the initial muscle contractions that succinylcholine would cause. Those contractions drive several side effects: they increase intragastric pressure from abdominal wall and diaphragmatic activity, raise intracranial pressure due to cerebral venous congestion, and contribute to post-twitch muscle pain (myalgias). Reducing the frequency and intensity of these fasciculations therefore helps lessen those effects.

Hyperkalemia, however, arises from potassium efflux after succinylcholine depolarizes the motor endplates. This potassium release is driven by widespread receptor activation, including upregulated extrajunctional receptors in certain situations, and it can occur even when some receptors are blocked by a pretreatment dose. Because the potassium shift depends on depolarization at endplates that may still occur despite the block, pretreatment does not reliably prevent hyperkalemia. That makes hyperkalemia the side effect least attenuated by pretreatment.