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Succinylcholine and the Risk of Hyperkalemia

Succinylcholine and the Risk of Hyperkalemia

Background

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 [1]. 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.

Evidence

Based on multiple studies that included patients with normal renal function, succinylcholine leads to a serum potassium increase of  ~0.5 mEq/L [2-4]. This is likely clinically insignificant in most patients. In fact, an ED-based study found a variable response with serum potassium increasing in 46 cases, decreasing in 46 cases, and not changing in 8 cases [3]. It seems that even patients on chronic dialysis are not at increased risk of developing clinically-significant hyperkalemia from succinylcholine [5].

So, when should succinylcholine potentially be avoided specifically due to hyperkalemia concerns [6]?

  • Hyperkalemia with ECG changes present prior to succinylcholine administration
  • Denervating, crush, or burn injuries after 72 hours
  • Rhabdomyolysis
  • Prolonged total body immobilization
  • Denervating diseases (e.g., multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS))
  • Inherited myopathies (e.g., Duchenne muscular dystrophy (DMD))

In patients for whom succinylcholine is determined to be not an option, non-depolarizing muscular blocking agents (NMBAs), such as rocuronium, are still safe and do not lead to hyperkalemia.

Bottom Line

  • Succinylcholine-induced hyperkalemia is more likely to occur in patients with predisposing conditions
  • Development of hyperkalemia following succinylcholine is variable and not always predictable
  • If succinylcholine is not an option due to potential risk of hyperkalemia, NBMAs (i.e., rocuronium) are still safe and effective

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. Hovgaard HL, Juhl-Olsen P. Suxamethonium-induced hyperkalemia: a short review of causes and recommendations for clinical applications. Critical Care Research and Practice. 2021;2021:e6613118. doi: 10.1155/2021/6613118.
  2. Magee DA, Gallagher EG. “Self-taming” of suxamethonium and serum potassium concentration. Br J Anaesth. 1984;56(9):977-980. doi: 10.1093/bja/56.9.977. PMID: 6466531.
  3. Zink BJ, Snyder HS, Raccio-Robak N. Lack of a hyperkalemic response in emergency department patients receiving succinylcholine. Acad Emerg Med. 1995;2(11):974-978. doi: 10.1111/j.1553-2712.1995.tb03124.x. PMID: 8536123.
  4. Raman SK, San WM. Fasciculations, myalgia and biochemical changes following succinylcholine with atracurium and lidocaine pretreatment. Can J Anaesth. 1997;44(5 Pt 1):498-502. doi: 10.1007/BF03011938. PMID: 9161744.
  5. Thapa S, Brull SJ. Succinylcholine-induced hyperkalemia in patients with renal failure: an old question revisited. Anesth Analg. 2000;91(1):237-241. doi: 10.1097/00000539-200007000-00044 PMID: 10866919.
  6. Martyn JAJ, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology. 2006;104(1):158-169. doi: 10.1097/00000542-200601000-00022. PMID: 16394702.
By |2021-07-23T11:02:43-07:00Jul 31, 2021|EM Pharmacy Pearls, Tox & Medications|
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High-Dose Nitroglycerin for Sympathetic Crashing Acute Pulmonary Edema

Background

Nitroglycerin (NTG) is an important intervention to consider for patients with Sympathetic Crashing Acute Pulmonary Edema (SCAPE) as it significantly reduces preload, and even modestly reduces afterload with high doses. For acute pulmonary edema in the ED, NTG is often administered as an IV infusion and/or sublingual tablet. Starting the infusion at ≥ 100 mcg/min produces rapid effects in many patients and can be titrated higher as tolerated, with doses reaching 400 mcg/min or greater. Combined with noninvasive positive pressure ventilation (NIPPV) and in some cases IV enalaprilat, patients often turn around quickly, from the precipice of intubation to comfortably lying in bed [1, 2]. But what does the literature say about starting with a high-dose NTG IV bolus followed by an infusion?

Evidence

A 2021 prospective, pilot study of 25 SCAPE patients proposed a clear and systematic protocol (below) for treating these critically ill patients with a combination of high-dose NTG bolus (600 – 1000 mcg over 2 mins) followed by an infusion (100 mcg/min) and NIPPV [3].There were no cases of hypotension after the bolus and 24 of the 25 patients were able to avoid intubation. Additionally, an earlier PharmERToxGuy post summarizes some of the previous studies evaluating the use of a high-dose NTG IV bolus for acute pulmonary edema.

It is important to note that some institutions may not allow IV push NTG or may limit the use of NTG boluses. Providers may then opt to implement dosing strategies such as bolusing from an IV infusion pump or initiating the infusion at a high rate for a short period (e.g., NTG 300 mcg/min for 2-3 minutes) before reducing the rate to a more traditional infusion rate (e.g., 100 mcg/min).

Bottom Line

  • A few small ED studies support the use of an initial IV NTG bolus followed by an infusion compared to the infusion alone [1, 2]
  • There is a low risk of hypotension following a single IV NTG bolus
  • Consider using the following protocol to identify which doses may be best for specific patients based on initial systolic blood pressure

Click for full-sized version [3]

 

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. Wang K, Samai K. Role of high-dose intravenous nitrates in hypertensive acute heart failure. Am J Emerg Med. 2020;38(1):132-137. doi: 10.1016/j.ajem.2019.06.046. PMID: 31327485.
  2. Wilson SS, Kwiatkowski GM, Millis SR, Purakal JD, Mahajan AP, Levy PD. Use of nitroglycerin by bolus prevents intensive care unit admission in patients with acute hypertensive heart failure. Am J Emerg Med. 2017;35(1):126-131. doi: 10.1016/j.ajem.2016.10.038. PMID: 27825693.
  3. Mathew R, Kumar A, Sahu A, Wali S, Aggarwal P. High-dose nitroglycerin bolus for sympathetic crashing acute pulmonary edema: a prospective observational pilot study. The Journal of Emergency Medicine. Published online June 2021:S0736467921004674. doi: 10.1016/j.jemermed.2021.05.011.
By |2021-07-06T07:20:14-07:00Jul 10, 2021|EM Pharmacy Pearls, Pulmonary, Tox & Medications, Uncategorized|
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By |2021-07-06T16:58:37-07:00Jul 7, 2021|Expert Peer Reviewed (Clinical), Orthopedic, SplintER, Trauma|
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Beta-Blockers for Inhalant-Induced Ventricular Dysrhythmias

Background

There are a few unique scenarios when beta-blockers may be indicated for patients in cardiac arrest. Use of esmolol for refractory ventricular fibrillation was summarized in a 2016 PharmERToxGuy post with an accompanying infographic. Another potential use for beta-blockers is in the rare case of a patient with inhalant-induced ventricular dysrhythmias. The term ‘sudden sniffing death’ refers to acute cardiotoxicity associated with inhaling hydrocarbons. Check out this ACMT Toxicology Visual Pearl for more information about the background and diagnosis of inhalant abuse.

It is thought that inhalants causes myocardial sensitization via changes in various cardiac channels (e.g., sodium channels, potassium channels, calcium channels, or gap junctions) leading to prolonged repolarization and conduction [1, 2]. Additionally, chronic inhalant use can lead to structural heart damage. When the above alterations are combined with a sudden increase in catecholamines (e.g., exercise, caught sniffing), a dysrhythmia can develop which is often fatal [2-4].

Evidence

There are no case reports to support the use beta-blockers to treat inhalant-induced dysrhythmias. However, the case reports below include patients that ingested various hydrocarbons who developed ventricular dysrhythmias and improved following the initiation of beta-blockers. As the adverse cardiac effects should be similar between inhaled and ingested hydrocarbons, we can potentially extrapolate this data to patients with inhalant-induced dysrhythmias.

Demographics Agent(s) Ingested  Cardiac Effects Interventions Resolution of dysrhythmia following BB?
39 yo M [5] Trichloroethylene pVT/VF arrest Defibrillation, Propranolol bolus and infusion

Y
70 yo F [6] Trichloroethylene Bigeminy, Junctional rhythm Esmolol bolus and infusion

Y
23 yo F [7] Chloral hydrate VF arrest Esmolol bolus and infusion

Y
27 yo M [8] Chloral hydrate, Loxapine, Fluoxetine Stable VT Propranolol bolus and infusion

Y
3 yo M [9] Chloral hydrate Sinus tachycardia, Bigeminy, Trigeminy, NSVT Esmolol bolus and infusion

Y
44 yo M [10] Chloral hydrate Stable VT Propranolol bolus, Labetalol infusion

Y

BB=beta-blocker; pVT=polymorphic ventricular tachycardia; VT=ventricular tachycardia; VF=ventricular fibrillation; NSVT=non-sustained ventricular tachycardia

Bottom Line

  • Patients presenting to the ED with cardiopulmonary manifestations of inhalant use should have routine electrolytes and an ECG to assess cardiac status
  • A quiet environment is important to decrease stimulation and minimize catecholamine surges
  • For both stable and non-perfusing dysrhythmias, propranolol or esmolol are reasonable choices to counteract the catecholamine effects, in addition to standard care [5-10]
    • Consider avoiding epinephrine and other catecholamines unless necessary, as they may worsen the dysrhythmia

Want to learn more about EM Pharmacology?

Read other articles in the EM Pharm Pearls Series and find previous pearls on the PharmERToxguy site.

References

  1. Nelson LS. Toxicologic myocardial sensitization. J Toxicol Clin Toxicol. 2002;40(7):867–79. doi: 10.1081/clt-120016958. PMID: 12507056.
  2. Tormoehlen LM, Tekulve KJ, Nañagas KA. Hydrocarbon toxicity: A review. Clin Toxicol (Phila). 2014 Jun;52(5):479–89. doi: 10.3109/15563650.2014.923904. PMID: 24911841.
  3. Bass M. Sudden sniffing death. JAMA. 1970 Jun 22;212(12):2075–9. PMID: 5467774.
  4. Baydala L. Inhalant abuse. Paediatr Child Health. 2010 Sep;15(7):443–54. doi: 10.1093/pch/15.7.443. PMID: 21886449.
  5. Gindre G, Le Gall S, Condat P, Bazin JE. [Late ventricular fibrillation after trichloroethylene poisoning]. Ann Fr Anesth Reanim. 1997;16(2):202–3. doi: 10.1016/s0750-7658(97)87204-8. PMID: 9686084.
  6. Mortiz F, de La Chapelle A, Bauer F, Leroy JP, Goullé JP, Bonmarchand G. Esmolol in the treatment of severe arrhythmia after acute trichloroethylene poisoning. Intensive Care Med. 2000 Feb;26(2):256. doi: 10.1007/s001340050062. PMID: 10784325.
  7. Shakeer SK, Kalapati B, Al Abri SA, Al Busaidi M. Chloral hydrate overdose survived after cardiac arrest with excellent response to intravenous β-blocker. Oman Med J. 2019 May;34(3):244–8. doi: 10.5001/omj.2019.46. PMID: 31110633.
  8. Zahedi A, Grant MH, Wong DT. Successful treatment of chloral hydrate cardiac toxicity with propranolol. Am J Emerg Med. 1999 Sep;17(5):490–1. doi: 10.1016/s0735-6757(99)90256-5. PMID: 10496517.
  9. Nordt SP, Rangan C, Hardmaslani M, Clark RF, Wendler C, Valente M. Pediatric chloral hydrate poisonings and death following outpatient procedural sedation. J Med Toxicol. 2014 Jun;10(2):219–22. doi: 10.1007/s13181-013-0358-z. PMID: 24532346.
  10. Wong O, Lam T, Fung H. Two cases of chloral hydrate overdose. Hong Kong Journal of Emergency Medicine. 2009 Jul;16(3):161–7. doi: 10.1177/102490790901600307.
By |2021-06-23T11:18:43-07:00Jun 26, 2021|Cardiovascular, Critical Care/ Resus, EM Pharmacy Pearls, Tox & Medications|
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SplintER Series: To Immobilize or Not to Immobilize: That is the Question

A patient presents to the Emergency Department after sustaining a twisting knee injury while skiing. She felt a pop and was unable to bear weight afterward secondary to pain and a feeling of instability. Shortly after the injury, she noted increased swelling and pain. On examination, she has a moderate effusion and a positive Lachman test. An x-ray was obtained and is shown above (Image 1. Case courtesy of Mikael Häggström, M.D. – Author info – Reusing images, CC0, via Wikimedia Commons).

 

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By |2026-06-16T16:17:25-07:00Jun 25, 2021|Expert Peer Reviewed (Clinical), Orthopedic, SplintER|
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