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Hypotension may be due to poisoning by many different drugs, including antihypertensives, beta-blockers, calcium channel blockers, disulfiram (ethanol interaction), iron, trazodone, quetiapine, and other antipsychotic agents and antidepressants. Poisons causing hypotension include cyanide, carbon monoxide, hydrogen sulfide, aluminum or zinc phosphide, arsenic, and certain mushrooms.

Hypotension in the poisoned or drug-overdosed patient may be caused by venous or arteriolar vasodilation, hypovolemia, depressed cardiac contractility, or a combination of these effects.


Most hypotensive poisoned patients respond to empiric treatment with repeated 200 mL intravenous boluses of 0.9% saline or other isotonic crystalloid up to a total of 1–2 L; much larger amounts may be needed if the victim is profoundly volume depleted (eg, as with massive diarrhea due to Amanita phalloides mushroom poisoning). Monitoring the central venous pressure (CVP) can help determine whether further fluid therapy is needed. Consider bedside cardiac ultrasound or pulmonary artery catheterization (or both) to assess CVP. If fluid therapy is not successful after adequate volume replacement, give dopamine or norepinephrine by intravenous infusion.

Hypotension caused by certain toxins may respond to specific treatment. For hypotension caused by overdoses of tricyclic antidepressants or other sodium channel blockers, administer sodium bicarbonate, 50–100 mEq by intravenous bolus injection. Norepinephrine 4–8 mcg/min by intravenous infusion is more effective than dopamine in some patients with overdoses of tricyclic antidepressants or of drugs with predominantly vasodilating effects. For beta-blocker overdose, glucagon (5–10 mg intravenously) may be of value. For calcium channel blocker overdose, administer calcium chloride, 1–2 g intravenously (repeated doses may be necessary; doses of 5–10 g and more have been given in some cases). High-dose insulin (0.5–1 unit/kg/h intravenously) euglycemic therapy may also be used (see the sections Beta-Adrenergic Blockers and Calcium Channel Blockers, below). Intralipid 20% lipid emulsion has been reported to improve hemodynamics in some cases of intoxication by highly lipid-soluble drugs such as bupivacaine, bupropion, clomipramine, and verapamil. Intravenous methylene blue and extracorporeal membrane oxygenation (ECMO) have been employed in a few refractory cases; ECMO may offer temporary hemodynamic stabilization while the offending drug is eliminated.

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Heise  CW  et al. Two cases of refractory cardiogenic shock secondary to bupropion successfully treated with veno-arterial extracorporeal membrane oxygenation. J Med Toxicol. 2016 Sep;12(3):301–4.
[PubMed: 26856351]
Kryshtal  DO  et al. In vitro studies indicate intravenous lipid emulsion acts as lipid sink in verapamil poisoning. J Med Toxicol. 2016 Jun;12(2):165–71.
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Laes  JR  et al. Improvement in hemodynamics after methylene blue administration in drug-induced vasodilatory shock: a case report. J Med Toxicol. 2015 Dec;11(4):460–3.
[PubMed: 26310944]
Woodward  C  et al. High dose insulin therapy, an evidence-based approach to beta blocker/calcium channel blocker toxicity. ...

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