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2023 AHA Focused Updates: Poisoning

Drew Kalnow, DO and Andy Little, DO

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The summary below is from an episode of ERcast: Clinical Perspectives

Poisoning resuscitations hinge on recognizing the toxin-specific physiology behind shock, dysrhythmia, and respiratory failure. The 2023 AHA focused update sharpens emergency management for opioid, benzodiazepine, beta-blocker, calcium channel blocker, cyanide, digoxin, local anesthetic, organophosphate, cocaine, methemoglobinemia, and sodium-channel blocker poisoning.

Airway and antidote priorities

  • Opioid arrest priorities: In suspected opioid overdose with cardiac arrest, high-quality CPR and ventilation come before naloxone; if there is a pulse with inadequate breathing, naloxone is reasonable.
  • Post naloxone observation: Recurrent opioid toxicity is common after an initial response, so patients need monitored observation until breathing, mental status, and vital signs have normalized.
  • Selective flumazenil use: Flumazenil belongs only in carefully selected pure benzodiazepine poisoning; seizure history and benzodiazepine or alcohol dependence are major reasons to avoid it.
  • Naloxone before flumazenil: When opioid and benzodiazepine co-ingestion is possible, naloxone is the first antidote for respiratory depression. We get into the practical sequencing in the episode.

Cardiotoxic overdose management

  • High dose insulin backbone: For beta-blocker and calcium channel blocker poisoning with hypotension, high-dose insulin is a first-line therapy alongside vasopressors rather than a late salvage move.
  • Glucagon's narrower role: Glucagon remains reasonable for beta-blocker poisoning with bradycardia or hypotension, but its benefit in calcium channel blocker toxicity is much less certain.
  • Lipid emulsion boundaries: IV lipid emulsion is not routinely recommended for beta-blocker or calcium channel blocker poisoning, but it remains indicated for local anesthetic systemic toxicity.
  • ECMO rescue threshold: VA-ECMO has a defined role in refractory cardiogenic shock from beta-blocker, calcium channel blocker, local anesthetic, and sodium-channel blocker poisoning. We cover where that escalation fits on the show.
  • Dialyzable exceptions: Hemodialysis may help in severe atenolol or sotalol poisoning, a useful reminder that not all beta-blocker overdoses behave the same way.

Sodium channel blockade syndromes

  • Bicarbonate first line: Sodium bicarbonate is the cornerstone therapy for life-threatening cardiotoxicity from tricyclic antidepressants and other sodium-channel blocker poisonings.
  • Cocaine wide complex treatment: In cocaine poisoning with wide-complex tachycardia, sodium bicarbonate is reasonable and lidocaine is also supported, reflecting sodium-channel toxicity rather than simple stimulant excess.
  • Local anesthetic dysrhythmias: Local anesthetic systemic toxicity with wide-complex tachycardia also responds to sodium bicarbonate, while seizures should be treated with benzodiazepines.
  • Lipid as rescue: For sodium-channel blocker poisoning, lipid emulsion is a rescue therapy after standard measures fail rather than an early routine antidote. We walk through that distinction in the chapter.

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References:

  1. Lavonas EJ, Akpunonu PD, Arens AM, et al. 2023 American Heart Association Focused Update on the Management of Patients With Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2023;148(16):e149-e184. PMID: 37721023

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