Cardiac arrest from succinylcholine-induced hyperkalemia

Huggins, Rebecca M; Kennedy, W. Klugh; Melroy, Michael J; Tollerton, David G

doi:10.1093/ajhp/60.7.694

Cited by 22 publications

(7 citation statements)

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“…In association with surgical procedures, succinylcholine is widely used for the blockade of motor end plate function, and it has been repeatedly shown to induce hyperkalaemia, in some cases sufficient to cause cardiac arrest (for review see Huggins et al 2003). A subset of patients administered succinylcholine show an upregulation of skeletal muscle nACh receptors (Fung et al 1991), which is thought to be the source of the hyperkalaemia.…”

Section: Perspectivesmentioning

confidence: 99%

Na⁺–K⁺ pump stimulation restores carbacholine‐induced loss of excitability and contractility in rat skeletal muscle

Macdonald

Nielsen

Clausen

2005

The Journal of Physiology

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Intense exercise results in increases in intracellular Na + and extracellular K + concentrations, leading to depolarization and a loss of muscle excitability and contractility. Here, we use carbacholine to chronically activate the nicotinic acetylcholine (nACh) receptors to mimic the changes in membrane permeability, chemical Na + and K + gradients and membrane potential observed during intense exercise. Intact rat soleus muscles were mounted on force transducers and stimulated electrically to evoke short tetani at regular intervals. Carbacholine produced a 2.6-fold increase in Na + influx that was tetrodotoxin (TTX) insensitive, but abolished by tubocurarine, resulting in a significant 36% increase in intracellular Na + , and 8% decrease in intracellular K + content. The mid region, near the motor end plate, had much larger alterations than the more distal regions of the muscle, and showed a larger membrane depolarization from −73 ± 1 to −60 ± 1 mV compared with −64 ± 1 mV. Carbacholine (10 −4 M) significantly reduced tetanic force to 31 ± 3% of controls, which underwent significant recovery upon application of Na + -K + pump stimulators: salbutamol (10 −5 M), adrenaline (10 −5 M) and calcitonin gene-related peptide (CGRP; 10 −7 M). The force recovery with salbutamol was accompanied by a recovery of intracellular Na + and K + contents, and a small but significant 4-5 mV recovery of membrane potential. Similar results were obtained using succinylcholine (10 −4 M), indicating that Na + -K + pump stimulation may prevent or restore succinylcholine-induced hyperkalaemia. The stimulation of the Na + -K + pump allows muscle to partially recover contractility by regaining excitability through electrogenically driven repolarization of the muscle membrane.

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Section: Perspectivesmentioning

confidence: 99%

Na⁺–K⁺ pump stimulation restores carbacholine‐induced loss of excitability and contractility in rat skeletal muscle

Macdonald

Nielsen

Clausen

2005

The Journal of Physiology

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“…Reports of acute hyperkalemia precipitating cardiac arrest typically involve intravenous potassium loading, massive cell turnover, or shift of potassium in the setting of surgical anesthesia or critical illness. [10][11][12][13][14] In these cases, the measured potassium concentration was usually normal shortly before cardiopulmonary arrest; and only with rapid increases in serum potassium did the findings of tachy-and bradyarrhythmias associated with hyperkalemia become apparent. These extreme situations constitute a small minority of clinical hyperkalemia in humans which is often incidental, asymptomatic, and of unknown duration.…”

Section: Introductionmentioning

confidence: 99%

How Dangerous Is Hyperkalemia?

Montford

Linas

2017

JASN

162

131

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Hyperkalemia is a potentially life-threatening electrolyte disorder appreciated with greater frequency in patients with renal disease, heart failure, and with use of certain medications such as renin angiotensin aldosterone inhibitors. The traditional views that hyperkalemia can be reliably diagnosed by electrocardiogram and that particular levels of hyperkalemia confer cardiotoxic risk have been challenged by several reports of patients with atypic presentations. Epidemiologic data demonstrate strong associations of morbidity and mortality in patients with hyperkalemia but these associations appear disconnected in certain patient populations and in differing clinical presentations. Physiologic adaptation, structural cardiac disease, medication use, and degree of concurrent illness might predispose certain patients presenting with hyperkalemia to a lower or higher threshold for toxicity. These factors are often overlooked; yet data suggest that the clinical context in which hyperkalemia develops is at least as important as the degree of hyperkalemia is in determining patient outcome. This review summarizes the clinical data linking hyperkalemia with poor outcomes and discusses how the efficacy of certain treatments might depend on the clinical presentation.

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“…By binding to the two alpha subunits on the nicotinic receptor, a conformational change ensues and the channel opens, thereby permitting the influx of calcium and sodium, and the efflux of potassium (3,11,12). Because succinylcholine is not degraded by acetylcholinesterase, it remains bound to the receptor longer than acetylcholine itself would, resulting in a sustained depolarization (13). Once succinylcholine dissociates from the receptor and diffuses away from the neuromuscular junction, it is degraded by plasma cholinesterases, thus accounting for its relative short duration of action (11).…”

Section: Discussionmentioning

confidence: 99%

“…Succinylcholine-induced hyperkalemia has been described with a variety of conditions, including upper motor nerve injuries (e.g., spinal cord injury), lower motor nerve injuries (e.g., Guillain-Barré syndrome), prolonged chemical denervation, disuse atrophy, direct muscle trauma or inflammation, muscular dystrophies, burns, and sepsis (4)(5)(6)(7)(10)(11)(12)(13)15). Upregulation of the nicotinic-acetylcholine receptor on skeletal muscle seems to be the primary cause of the hyperkalemia (15).…”

Section: Discussionmentioning

confidence: 99%

Succinylcholine-induced Hyperkalemia in a Patient with Multiple Sclerosis

Levine

Brown

2012

The Journal of Emergency Medicine

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Cardiac arrest from succinylcholine-induced hyperkalemia

Cited by 22 publications

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Na⁺–K⁺ pump stimulation restores carbacholine‐induced loss of excitability and contractility in rat skeletal muscle

Na⁺–K⁺ pump stimulation restores carbacholine‐induced loss of excitability and contractility in rat skeletal muscle

How Dangerous Is Hyperkalemia?

Succinylcholine-induced Hyperkalemia in a Patient with Multiple Sclerosis

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Cardiac arrest from succinylcholine-induced hyperkalemia

Cited by 22 publications

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Na+–K+ pump stimulation restores carbacholine‐induced loss of excitability and contractility in rat skeletal muscle

Na+–K+ pump stimulation restores carbacholine‐induced loss of excitability and contractility in rat skeletal muscle

How Dangerous Is Hyperkalemia?

Succinylcholine-induced Hyperkalemia in a Patient with Multiple Sclerosis

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Na⁺–K⁺ pump stimulation restores carbacholine‐induced loss of excitability and contractility in rat skeletal muscle

Na⁺–K⁺ pump stimulation restores carbacholine‐induced loss of excitability and contractility in rat skeletal muscle