American Heart Association Guideline Update on Poisoning-Related Cardiac Arrest

The American Heart Association (AHA) released the 2023 focused update about resuscitation of patients with cardiac arrest, respiratory arrest, or life-threatening toxicity due to poisoning. The update was published in Circulation.

In the United States (US), more than 100,000 individuals died of poisoning and drug overdose in the 12 months preceding April 2021. This rate represented a 28.5% increase from the year before.

After poisoning, patients presenting with cardiac arrest may require specialized treatment. For example, following poisoning with β-adrenergic receptor antagonists or calcium channel antagonists, these patients will not respond to atropine, standard vasopressors, or cardiac pacing.

The guideline authors emphasized, “Treatment of cardiac arrest and life-threatening toxicity due to poisoning often requires specialized treatments that most clinicians do not use frequently such as antidotes and venoarterial extracorporeal membrane oxygenation, in addition to effective basic and advanced life support. Timely consultation with a medical toxicologist, clinical toxicologist, or regional poison center facilitates rapid and effective therapy.”

Opioids

Opioids are responsible for most poisoning events. In the US, and other countries, the opioid epidemic continues to worsen. Of the more than 100,000 deaths in the 12 months preceding April 2021, 75,673 involved opioids, a near 35% increase from the year prior.

The mainstay of patient care in the setting of opioid-associated toxicity is early identification and emergency response activation. An opioid overdose deteriorates to cardiopulmonary arrest making ventilation the highest priority. Administration of naloxone can restore respiration and airway reflexes in patients impaired by an opioid overdose. Alternatives to administering naloxone include observation, if the patient is breathing normally, or ventilatory support.

Administration of naloxone in cases with cardiac arrest has not been shown to improve patient outcomes. As such, the guideline authors emphasized that respiratory support should be the primary focus of treatment. Of note, responders to naloxone may develop recurrent central nervous system (CNS) or respiratory depression and need a longer observational period before discharge. In addition, some patients may require repeat doses of naloxone, as its duration of action can be shorter than the respiratory depressive effect of the opioids.

β-blockers

β-blockers are associated with one of the highest poisoning mortalities. Patients with β-blocker poisoning present with bradycardia and reduced cardiac contractility.

Common treatments for β-blocker poisoning include atropine, glucagon, calcium, vasopressors, high-dose insulin, and intravenous lipid emulsion. The guideline authors do not recommend for the use of nonadrenergic vasopressors (vasopressin, angiotensin II, amrinone, milrinone, methylene blue, and hydroxocobalamin).

Calcium channel blockers

Calcium channel blockers are also a leading cause of poisoning mortality, in part because these drugs are often prescribed in sustained-release forms and have long half-lives. Poisoning from both dihydropyridine and nondihydropyridine classes of calcium channel blockers present as severe shock from bradycardia, vasodilation, or loss of inotropy.

Treatment options for poisoning from calcium channel blockers include atropine, calcium, vasopressors, high-dose insulin therapy, nitric oxide inhibitors, and intravenous lipid emulsion therapy. As with β-blockers, the use of nonadrenergic vasopressors is not recommended.

Other poisonings

In addition to the most common (opioids) and most life-threatening (β- and calcium channel blockers) poisoning events, the guideline authors had specific recommendations about 9 additional poisonings.

• Benzodiazepines
  • Poisonings involving benzodiazepines often occur in combination with opioids and/or alcohol. Patients present with CNS depression with loss of protective airway reflexes. Benzodiazepine poisoning can be treated with flumazenil; however, this treatment can cause seizures or benzodiazepine withdrawal.
• Cocaine
  • Cocaine toxicity events are marked by tachycardia, hypertension, hyperthermia, diaphoresis, elevated psychomotor activity, and seizures. Benzodiazepines are recommended for initial management of blood pressure and psychomotor activity. For severe cases, calcium channel blockers, α1-adrenergic receptor antagonists, and nitrates may treat symptoms of hypertension and chest pain.
• Cyanide
  • This toxicity often affects laboratory or industrial workers or individuals exposed to structure fires. After exposure, poisoned individuals can develop rapid cardiovascular collapse, metabolic acidosis, depressed mental status, seizure, and death. These patients should be treated with hydroxocobalamin or alternatively, sodium nitrite plus sodium thiosulfate.
• Digoxin
  • Patients with digoxin and related cardiac glycoside poisoning can present with gastrointestinal symptoms, hyperkalemia, cardiac conduction abnormalities, and confusion. The recommended treatment is digoxin-specific immune antibody fragments (digoxin-Fab).
• Local anesthetics
  • Local anesthetic systemic toxicity (LAST) results in CNS toxicity with symptoms of seizure, agitation, syncope, dysarthria, perioral numbness, confusion, obtundation, and dizziness, and in some cases, with cardiovascular toxicity. The recommended treatment for LAST is intravenous lipid emulsion. If seizures occur, benzodiazepines are recommended.
• Methemoglobinemia
  • Patients with methemoglobinemia poisoning present as catatonic or with shortness of breath and fatigue. In severe cases, methemoglobinemia toxicity can lead to cardiovascular collapse and death. The best treatment for methemoglobinemia poisoning is methylene blue.
• Organophosphates and carbamates
  • These agents cause excess parasympathetic and nicotinic functioning and affect the CNS. Early treatment is important to prevent deterioration to respiratory and cardiac arrest. Treatment includes dermal decontamination, atropine, benzodiazepines, and oximes.
• Sodium channel blockers
  • Toxicity from sodium channel blockers causes QRS prolongation, hypotension, seizure, ventricular dysrhythmia, and cardiovascular collapse. Depending on the specific drug, additional effects on cardiac receptors or ion channels may occur. For the treatment of life-threatening cardiotoxicity, the recommended treatment is sodium bicarbonate.
• Sympathomimetics
  • This type of poisoning results in adrenergic nervous system activation. It is often difficult to determine the culprit substance, and clinicians must often rely on treating presenting symptoms. Some examples of symptom management include sedation for severe agitation, rapid external cooling for hyperthermia, vasodilators for coronary vasospasm, and mechanical circulatory support for cardiogenic shock. The authors noted that prolonged physical restraint without sedation can be potentially harmful.