Acute toxic ingestions are a common reason for presentation to the emergency department (ED) and clinical scenarios range from benign accidental ingestions to large overdoses resulting in hemodynamic instability. A wide variety of toxins cause hemodynamic instability, from cardiotoxic medication to plant-based toxins, and even inhaled substances.¹ In the ED, the most important consideration in management of these toxicities involves decontamination, evaluating for airway protection, and managing any hemodynamic instability.¹

Medications such as beta blockers, calcium channel blockers, and digoxin can cause cardiogenic shock secondary to decreased inotropic and chronotropic effects. If the ingestion was within the first hour, activated charcoal should be considered for gastrointestinal decontamination and may prevent progression of toxidrome. The dose is 25 g- 100 g for adults and 0.5 g/kg-1 g/kg with maximum dose of 50 g in children.¹ Whole-bowel irrigation can be considered; however, it is not recommended in unstable patients or those at risk for aspiration.

Fluid resuscitation is the initial management of hypotension. However, it should be used with caution in patients with cardiogenic shock. One to two liters of crystalloid is a reasonable starting amount.^1,2 Reversal agents should be used for specific toxins such as digoxin immune fab for digoxin toxicity high-dose insulin for beta blocker toxicity, or calcium for calcium channel blocker toxicity.^2,3 Vasopressors, ideally norepinephrine or epinephrine, are the next step if fluid resuscitation and antidotes are not successful.^2,3

Atropine or temporary pacing can be used for treatment of bradycardia. Lipid emulsion can be used as an adjunct to therapy and can act to bind lipophilic substrates of toxins and expedite their excretion. In addition, it is proposed to improve fatty acid phosphorylation, adenosine triphosphate production, and decrease nitric oxide production, which reduces vasodilation.^4,5 Amlodipine and verapamil toxicity have been shown to be responsive to this treatment.⁶

Methylene blue is an additional adjunct that can inhibit formation of nitric oxide, thus increasing vascular tone and blood pressure.⁵ Finally, extracorporeal membrane oxygenation (ECMO) can be used temporarily if all other measures fail.¹ Some evidence suggests improved mortality in patients who received veno-arterial (VA) ECMO for refractory toxin-induced shock.⁷ During this time, consultation with a cardiologist, intensivist, and medical toxicologist is required.

Dysrhythmias from Toxin Ingestion

Dysrhythmias can also be associated with toxin ingestion leading to cardiogenic shock. For example, tricyclic antidepressant overdose can lead to sodium channel blockade, which can cause QRS widening. In addition to supportive measures, sodium bicarbonate should be given as an initial bolus of 50 milliequivalents (mEq) to 100 mEq (or one mEq/kg-two mEq/ kg ).⁷ A continuous sodium bicarbonate infusion can also be started at 150 mEq in 1 L D5W at 250 mL per hour over four hours after the initial bolus.⁷ Toxicity from selective serotonin reuptake inhibitors and antipsychotic medications can lead to corrected QT interval (QTc) prolongation, which can lead to torsades de pointes. Ideally, these patients should be treated with magnesium sulfate until QTc normalizes.¹