HWN Suggests

Succinylcholine and the Risk of Hyperkalemia

Succinylcholine is frequently used in the ED to facilitate intubation, but it may be avoided in some cases due to the risk of hyperkalemia. The underlying physiology of this effect appears to be directly related to its therapeutic mechanism of action. When succinylcholine binds to and activates acetylcholine receptors, it leads to an influx of sodium and calcium and and an efflux of potassium into the extracellular space. Additionally, when these acetylcholine receptors are immature or denervated, it seems that these channels may stay open significantly longer, allowing for an increased amount of potassium to exit the cell, leading to an increased risk of hyperkalemia.

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Articles of Interest

An Analysis of Paralysis: Neuromuscular blocking agents in the Emergency Department

In this post, we will discuss the use of neuromuscular blocking agents (NMBAs) for intubation in the Emergency Department; we will focus on considerations in predicted difficult airways (RSI vs. awake intubation), Rocuronium vs. Succinylcholine, and the indications for Sugammadex.

Both Rocuronium and Succinylcholine Are Appropriate for Emergency Intubations

The two main paralytics used for U.S. emergency department (ED) intubations are rocuronium and succinylcholine. Succinylcholine has a faster onset, but rocuronium has fewer contraindications. While previous evidence showed that succinylcholine results in better intubating conditions in the controlled environment of the operating room, it is unclear if this difference translates to the ED. This analysis of the National Emergency Airway Registry compared first-pass success rates and adverse effects in all patients older than 14 who received either paralytic as part of rapid sequence intubation in 22 EDs during 2016.

Dilemma In Rapid Sequence Intubation: Succinylcholine Vs. Rocuronium

Introduced in 1952, SCh depolarizes the neuromuscular membrane and is structurally consisted of two acetylcholine molecules. It acts as a false transmitter of acetylcholine by avidly binding to postsynaptic cholinergic receptors, resulting in persistent depolarization and paralysis. This action is associated with muscle fasciculation which can lead to increased intracranial and intragastric pressures. The molecule is rapidly hydrolyzed by serine pseudocholinesterase. SCh is rapidly active within 60 seconds of administration by IV bolus. The clinical duration of action is 3 to 10 minutes and normal neuromuscular function returns within 15 minutes.

Does Succinylcholine Increase Mortality in Severe TBI Patients?

Succonylcholine may increase mortality in severe TBI patients undergoing RSI in the ED compared to rocuronium.

PharmD Pearls: Succinylcholine And Potassium

SCh binds to nicotinic receptors at motor end plates generating an action potential and causes prolonged depolarization and muscle paralysis. As a result of depolarization, K+ is released from cells causing an increase in serum potassium. Typically, the increase in K+ occurs within 3-5 minutes after administration of SCh and lasts less than 15 minutes.

Succinylcholine Dantrolene Controversy

Sounds like succinylcholine is a great drug and in many ways it is. However there are a variety of mild to severe side effects associated with succinylcholine. For example, some people experience annoying muscle pain lasting several days, heart rhythm changes that may be transient or in certain circumstances life threatening. As many of you who are interested in MH know already, succinylcholine is also a trigger of MH in the susceptible patient. Succinylcholine, because it produces paralysis, is rarely given by itself.

Sux vs Roc AND Roc Doesn’t Rock Unless A Pharmacist is in the House

In this episode, I’ll first review how Sux and Roc stack up in terms of onset, duration, efficacy, and safety. Then, I’ll explain the reason why Roc only rocks when you, Pharmacy Nation, are around.

ToxCard: Dangers of Succinylcholine

Succinylcholine is an analog of acetylcholine (ACh). In healthy patients, it binds ACh receptors at the neuromuscular junction (NMJ) causing depolarization of the cell membrane which results in muscular fasciculations.1 The fasciculations are secondary to the sustained endplate depolarization causing the Na+ channels to remain in the inactive state for a prolonged period. When the cell membrane is depolarized, sodium flows inward, and potassium flows out of the cell.