In addition, there is a growing abuse of tianeptine (street name “ZaZa”), which is an atypical tricyclic antidepressant. It also has opioid receptor agonism.⁸ Thus, patients will present with hypotension and respiratory depression with QRS widening. Treatment should include a combination of sodium bicarbonate and naloxone.⁸

Alpha-2 agonists such as xylazine and clonidine also have the potential for abuse. The primary mechanism for hypotension from these agents is direct vasodilation from the adrenergic alpha receptor blockade. Initial management of hypotension should include resuscitation with crystalloid fluid but these individuals may require vasopressor support to improve adrenergic activity at the alpha receptors.⁹ Vasopressor of choice should include norepinephrine or epinephrine. Finally, although xylazine is lipophilic, evidence of success in treating overdose with intralipid has not yet been shown.⁸

Hypotension from toxin ingestion could also be from hypovolemia from loss of fluids through vomiting or diarrhea. For instance, amanita mushroom toxicity specifically can cause large amounts of watery diarrhea, which can lead to hypovolemic shock.¹ Cholinergic toxicity can also lead to insensible fluid loss. Acetaminophen toxicity can also have a similar effect during stage two of disease. A combination of prolonged emesis and hepatic injury can lead to hypovolemia.¹⁰ Specific antidotes for each toxicity should also be given in addition to the management of hypotension. For example, Digibind should be given for digoxin toxicity.

Inhaled Toxins

Inhaled toxins such as cyanide, carbon monoxide, and arsenic can also cause hypotension. They present the unique challenge in decontamination. If there is concern for gastrointestinal ingestion, as in the case of cyanide and arsenic, activated charcoal should be utilized.⁵ Otherwise the individual should be physically washed and decontaminated in case there are remnants of the poison on clothes and skin.

Like the other toxins, treatment for hypotension includes supportive management and specific treatment with antidotes, if possible. In the case of cyanide, there is a halt in aerobic metabolism.¹¹ This can lead to build up of lactic acid and eventually cause tissue necrosis, and end-organ damage, including cardiogenic shock.

Treatment includes hydroxocobalamin or sodium thiosulfate with amyl nitrate (Cyanokit ®), which can help restore aerobic respiration. Hydroxocobalamin can also remove nitric oxide and improve vasoconstriction.⁵ Excessive carbon monoxide exposure can lead to cardiac ischemia from poor aerobic respiration. Management should include high oxygen therapy to improve oxygen saturation and consequently aerobic respiration.¹² If necessary, hyperbaric oxygen can be utilized. Finally, arsenic poisoning can lead to severe gastroenteritis that causes vomiting and diarrhea. This can precipitate hypovolemic shock. Consequently, as no specific antidote is available, aggressive fluid resuscitation is the mainstay of treatment.¹³