Toxicology 2 – Sympathomimetics, Cardiac Medications & CNS Depressants

A set of question-and-answer flashcards covering recognition and management of sympathomimetic, calcium channel blocker, beta-blocker, digoxin, salicylate, acetaminophen, opioid, and benzodiazepine toxicities.

Which substances are common sympathomimetics that can cause stimulant toxicity?

Cocaine, amphetamines (Adderall, Vyvanse, methamphetamine, MDMA), novel synthetic cathinones (“bath salts”), and caffeine.

What are typical clinical features of sympathomimetic (stimulant) toxicity?

Agitation, sweating, nausea/vomiting, tachycardia, mydriasis, hypertension, arrhythmias, psychosis, seizures, chest pain, hyperthermia, and rhabdomyolysis.

What is the first-line drug class for managing agitation or seizures in stimulant toxicity?

Benzodiazepines.

Name the main classes of cardiac medications that may produce severe toxicities discussed in this lecture.

Calcium channel blockers (CCBs), beta-blockers, clonidine, digoxin, and salicylates.

Describe the primary hemodynamic effects of calcium channel blocker overdose.

Peripheral vasodilation plus decreased myocardial contractility, automaticity, and conduction velocity; also suppressed insulin release.

What key clinical signs suggest calcium channel blocker toxicity?

Bradycardia, hypotension, seizures, coma, metabolic acidosis, pulmonary edema, nausea/vomiting, and hyperglycemia.

List three adjunctive drug therapies (after supportive care) used in calcium channel blocker toxicity.

Intravenous calcium, vasopressors (norepinephrine and/or epinephrine), and high-dose insulin therapy.

Which beta-blocker is considered most toxic in overdose and why?

Propranolol, because it is lipophilic and has additional sodium-channel blocking properties.

What are common presentations of beta-blocker overdose?

Bradycardia, hypotension, and—especially with propranolol—seizures and cardiac conduction block.

What is the pharmacologic antidote for beta-blocker toxicity and its mechanism?

Glucagon; it increases intracellular cAMP in cardiac cells independent of β-adrenergic receptors.

When BB or CCB toxicity is refractory, what initial bolus of high-dose insulin is recommended?

1 unit/kg IV bolus followed by an infusion of 0.5–1 unit/kg/hour, titrated to hemodynamic response.

Which electrolyte abnormality must be corrected before starting high-dose insulin therapy?

Hypokalemia.

Which triad of symptoms is characteristic of digoxin toxicity?

Vomiting, hyperkalemia, and arrhythmias.

What is the specific antidote for severe digoxin poisoning?

Digoxin Immune Fab (DigiFab).

Approximately how much digoxin is bound by one 40-mg vial of DigiFab?

About 0.5 mg of digoxin.

If the amount of digoxin ingested is unknown, what initial DigiFab dose is recommended?

Give 10 vials initially; administer another 10 vials if needed based on clinical response.

An acute salicylate dose greater than what amount (mg/kg) is likely to cause toxicity?

200 mg/kg.

Which paired acid–base disturbances typify salicylate poisoning?

Early respiratory alkalosis with hyperventilation, followed by metabolic acidosis with an increased anion gap.

What therapy is used to alkalinize urine and enhance salicylate elimination?

Intravenous sodium bicarbonate infusion.

What is currently the leading cause of acute liver failure in the United States?

Acetaminophen (paracetamol) poisoning.

Within what time frame after acetaminophen ingestion is acetylcysteine most effective?

Within 10 hours of ingestion.

Give two mechanisms by which acetylcysteine protects the liver in acetaminophen overdose.

Replenishes hepatic glutathione stores and directly conjugates reactive metabolites (also provides sulfate).

In the oral 72-hour acetylcysteine regimen, what is the loading dose?

140 mg/kg orally.

How much total drug (mg/kg) is delivered in the standard 21-hour IV “three-bag” acetylcysteine regimen?

300 mg/kg (150 mg/kg + 50 mg/kg + 100 mg/kg).

According to the Rumack-Matthew nomogram, treatment is recommended when the serum acetaminophen level is above which reference?

The Rumack-Matthew treatment line (solid line).

List all four criteria that must be met to discontinue acetylcysteine therapy.

Serum acetaminophen <10 µg/mL, INR <2, liver enzymes normal or decreased ≥25–50% from peak, and the patient is clinically well.

What is the recommended maximum daily dose of acetaminophen for adults?

4 grams per day.

What classic constellation of findings signals opioid overdose?

Respiratory depression, lethargy → coma, pinpoint pupils, flaccid extremities, mild hypotension and bradycardia, and GI hypomotility.

Which medication rapidly reverses opioid-induced respiratory depression?

Naloxone, a competitive opioid antagonist.

Which opioid can cause QT-interval prolongation in overdose?

Methadone.

What unique adverse effect may occur after rapid IV fentanyl administration?

Acute muscular (chest-wall) rigidity.

What are typical manifestations of benzodiazepine overdose?

Drowsiness, confusion, and hypotension.

Which antagonist reverses benzodiazepine effects and what is the initial dose?

Flumazenil; 0.2 mg IV over 2 minutes.

Why must flumazenil be used cautiously in chronic benzodiazepine users or mixed overdoses?

It can precipitate seizures or arrhythmias.

What adjunctive measure may enhance elimination of lipophilic beta-blockers such as propranolol?

Intravenous lipid emulsion therapy.