Barbiturate Toxicity Medication

Updated: Jan 14, 2017
  • Author: Keith A Lafferty, MD; Chief Editor: Asim Tarabar, MD  more...
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Medication

Medication Summary

GI decontamination with activated charcoal and urinary alkalinization may be beneficial in patient management. Also, pharmacologic support may be required in hypotensive patients with the use of pressor agents.

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GI decontaminants

Class Summary

These agents are used to minimize the amount of toxin absorbed from the GI tract into systemic circulation. Depending upon the amount of drug ingested and time from ingestion to treatment, gastric lavage may be used. Activated charcoal is beneficial in adsorbing the ingested agent and is considered safer than emetics.

Activated charcoal (Liqui-Char)

Prevents absorption by adsorbing drug in the intestine. Multidose charcoal may interrupt enterohepatic recirculation and enhance elimination by enterocapillary exsorption. Theoretically, by constantly bathing the GI tract with charcoal, the intestinal lumen serves as a dialysis membrane for reverse-absorption of drug from intestinal villous capillary blood back into the intestine.

Supplied as an aqueous mixture or in combination with a cathartic (usually sorbitol 70%).

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Alkalinizing agent

Class Summary

Sodium bicarbonate is the primary agent used clinically to enhance elimination. The goal of use is to alkalinize the urine to promote renal excretion and decrease elimination half-life of the barbiturate.

Sodium bicarbonate (Neut)

Goal is to maintain a urinary pH >7.5 and urine output >2 mL/kg/h. Monitor arterial or venous pH; a blood pH >7.55 may increase patient morbidity. This therapy is specific to long-acting barbiturates given their lower pKa, with ion trapping being the intended mechanism.

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Adrenergic Agonist Agents

Class Summary

These agents improve the hemodynamic status by increasing myocardial contractility and heart rate. This results in an increase in cardiac output. They also increase peripheral resistance by inducing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased blood pressure.

Norepinephrine (Levophed)

Stimulates beta1-adrenergic and alpha-adrenergic receptors, which, in turn, increases cardiac muscle contractility, heart rate, and vasoconstriction. As a result, systemic blood pressure and coronary blood flow increase.

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