A 45-year-old quadriplegic man with suspected bacterial pneumonia is admitted to the hospital and started on intravenous antibiotics. Over the next 24 hours, he develops progressive respiratory failure requiring mechanical ventilation. Prior to intubation, a skeletal muscle relaxant is administered and the patient subsequently goes into cardiac arrest. His attached cardiac monitor shows ventricular fibrillation. While he is being resuscitated, his serum potassium level is drawn and later comes back as 9.5 mEq/L. Administration of which of the following agents is most likely responsible for this patient's condition?

Question

A 45-year-old quadriplegic man with suspected bacterial pneumonia is admitted to the hospital and started on intravenous antibiotics.  Over the next 24 hours, he develops progressive respiratory failure requiring mechanical ventilation.  Prior to intubation, a skeletal muscle relaxant is administered and the patient subsequently goes into cardiac arrest.  His attached cardiac monitor shows ventricular fibrillation.  While he is being resuscitated, his serum potassium level is drawn and later comes back as 9.5 mEq/L.  Administration of which of the following agents is most likely responsible for this patient's condition?

Quizplus · Accepted Answer

11ec160b_3c13_bb13_9249_5d315bc1d28e_MD0001_00 Succinylcholine is a depolarizing neuromuscular-blocking agent that, like acetylcholine, attaches to the nicotinic acetylcholine receptor (nAChR) and depolarizes the neuromuscular end plate. Unlike acetylcholine, succinylcholine is not degraded by acetylcholinesterase, resulting in continuous stimulation of the endplate (reflected by initial transient fasciculations). However, the sodium channels surrounding the end plate rapidly become inactivated and cannot reopen until the end plate is repolarized. Thus, succinylcholine-induced depolarization remains isolated to the end plate, resulting in development of a flaccid paralysis (phase 1 block). Eventually, with continued administration of succinylcholine, the continuous depolarization of the endplate gives way to gradual repolarization as the nAChR becomes desensitized to the effects of succinylcholine. This is termed phase II block and is similar to non-depolarizing blockade. Because the nAChR is a nonselective cation channel, its opening not only allows sodium influx but also potassium release. Exaggerated hyperkalemia and life-threatening arrhythmias can occur in patients with crush or burn injuries, denervating injuries or diseases (eg, quadriplegia and Guillain-Barré syndrome), and myopathies. These pathologic states cause up-regulation of muscle nAChRs and/or rhabdomyolysis, which can result in the release of large amounts of potassium when succinylcholine is administered. In these patients, non-depolarizing agents such as vecuronium or rocuronium are better choices (Choice E). (Choice A) The nondepolarizing neuromuscular-blocking agent atracurium releases histamine and can produce a fall in blood pressure, flushing, and bronchoconstriction. It is also metabolized to laudanosine, which can provoke seizures. (Choice B) Baclofen is a muscle relaxant that affects GABA_B receptors at the level of the spinal cord. (Choice C) Dantrolene is a muscle relaxant effective in malignant hyperthermia. It acts on ryanodine receptors on the sarcoplasmic reticulum and prevents release of calcium into the cytoplasm of muscle fibers. Educational objective: Succinylcholine can cause significant potassium release and life-threatening arrhythmias in patients at high risk for hyperkalemia, including those with burns, myopathies, crush injuries, and denervating injuries or disease. __________ References: Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. (http://www.ncbi.nlm.nih.gov/pubmed/16394702)

A 45-Year-Old Quadriplegic Man with Suspected Bacterial Pneumonia Is Admitted