Neuromuscular blockers

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Neuromuscular blockers

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A 59-year-old man was brought to the emergency department in winter after being found down in an alley. The patient was given naloxone prior to arrival with minimal change in arousal. Initial temperature is 35.0°C (95.0°F), pulse is 45/min, respirations are 9/min, blood pressure is 115/82 mmHg, and oxygen saturation is 88% on 6L nasal cannula. The patient is unresponsive to verbal or painful stimuli. Track marks are noted in the upper and lower extremities. There are pinpoint pupils bilaterally. The emergency medicine physician decides to intubate the patient using rocuronium and etomidate. During the procedure, the physician is unable to visualize the vocal cords due to copious secretions and an anterior airway. A decision is made to terminate the procedure. Repeat temperature is 33.0°C (91.4°F), pulse is 20/min, respirations are 7/min, blood pressure is 55/22 mmHg, and oxygen saturation is 56% on 6L nasal cannula. Administration of which of the following medications is the next best step in management?  

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Neuromuscular blockers are a class of medications that prevent acetylcholine from acting at the neuromuscular junction, which prevents the triggering of skeletal muscle contractions.

Okay, first things first. In order for a skeletal muscle to contract, your brain sends a signal, in the form of an action potential in an upper motor neuron.

The upper motor neuron then activates a lower motor neuron in the spinal cord.

From here, the action potential is sent through an axon down to its ending branches, called axon terminals, to muscle fibers which they innervate.

The place where an axon terminal meets the muscle fiber is the neuromuscular junction.

The neuromuscular junction has three main parts: a presynaptic membrane, which is the membrane of an axon terminal; a postsynaptic membrane, which is the membrane of a skeletal muscle fiber and is also called a motor end-plate; and a synaptic cleft, which is the gap between the presynaptic and postsynaptic membranes.

When an action potential reaches the axon terminal, synaptic vesicles that contain neurotransmitters, called acetylcholine, fuse with the cell membrane of the axon terminal, releasing the acetylcholine into the synaptic cleft.

The acetylcholine then diffuses over to the motor end plate on the muscle fiber and binds to ligand-gated ion channels, also called nicotinic receptors.

When that happens, these ligand-gated ion channels open up, letting lots of sodium ions rush into the skeletal muscle fiber, and a few potassium ions leak out of the cell as well. But overall there’s an increase in positive charge on the inside of the muscle fiber causing it to depolarize.

This causes the voltage-gated sodium ion channels on the membrane to open up, and there’s a huge influx of sodium ions into the muscle fiber.

This leads to a generation of an action potential, which rapidly spreads along the entire membrane, causing the whole muscle fiber to contract.

When the signal sent from the lower motor neuron stops, this causes synaptic vesicles full of acetylcholine to stop fusing with the membrane, while molecules of acetylcholine that are left behind within the synaptic cleft, are chopped up by an enzyme called acetylcholinesterase. And muscle contraction stops.

Summary

Neuromuscular blockers are medications used to relax the muscles during surgical procedures and mechanical ventilation. They work by inhibiting the actions of acetylcholine on nicotinic receptors at the neuromuscular junction. Inhibition of these receptors disrupts the transmission of nerve impulses to the muscles, thus causing them to become relaxed and unable to move.

Neuromuscular blockers are divided into non-depolarizing blockers, like atracurium, vecuronium, and rocuronium; and depolarizing agents like succinylcholine. Non-depolarizing blockers work by competing with acetylcholine for receptors. They are used in mechanical ventilation and to aid in surgery. On the other hand, depolarizing agents cause prolonged stimulation and subsequent desensitization of the receptors. They can facilitate tracheal intubation or short surgical procedures.

Sources

  1. "Katzung & Trevor's Pharmacology Examination and Board Review,12th Edition" McGraw-Hill Education / Medical (2018)
  2. "Rang and Dale's Pharmacology" Elsevier (2019)
  3. "Goodman and Gilman's The Pharmacological Basis of Therapeutics, 13th Edition" McGraw-Hill Education / Medical (2017)
  4. "Neuromuscular block" Br J Pharmacol (2006)
  5. "Activation and inhibition of human muscular and neuronal nicotinic acetylcholine receptors by succinylcholine" Anesthesiology (2006)
  6. "Atracurium: hypotension, tachycardia and bronchospasm" Anesthesiology (1985)
  7. "Laudanosine, an atracurium and cisatracurium metabolite" Eur J Anaesthesiol (2002)