Analgesics, Sedative-Hypnotics, and Cardiovascular Drugs
Acetaminophen and salicylates
Acetaminophen overdose is diagnosed by the Rumack-Matthew nomogram applied to a level drawn at least four hours after a single acute ingestion. The treatment line begins at 150 µg/mL at 4 hours. N-acetylcysteine replenishes glutathione and is most effective early, but remains beneficial in late presentation. Salicylate poisoning produces a mixed respiratory alkalosis plus metabolic acidosis, tinnitus, hyperthermia, and hypoglycemia; treatment is sodium bicarbonate to alkalinize serum and urine, plus hemodialysis for severe toxicity, altered mentation, pulmonary edema, or renal failure.
Sedative-hypnotics
Opioids cause miosis, hypoventilation, and CNS depression; titrate naloxone to adequate respiration, not full arousal, and use an infusion because naloxone is shorter-acting than methadone. Benzodiazepines alone rarely kill adults but cause profound depression with co-ingestants. Flumazenil is the classic trap: it is contraindicated in benzodiazepine-tolerant patients and in suspected tricyclic co-ingestion because it precipitates seizures.
Cardiovascular drugs
- Sodium-channel blockers (tricyclics, flecainide, cocaine): wide QRS, hypotension, seizures - give sodium bicarbonate.
- Beta blockers: glucagon, high-dose insulin with dextrose, vasopressors, pacing.
- Calcium channel blockers: intravenous calcium, high-dose insulin euglycemia therapy, vasopressors; avoid calcium in verapamil toxicity? Not absolute, but high-dose insulin is the mainstay.
- Digoxin: hyperkalemia, bradyarrhythmias, and GI/visual symptoms; digoxin-specific Fab fragments.
- Sulfonylureas cause refractory hypoglycemia; octreotide suppresses insulin release.
Rule of thumb: for any poisoning with a widened QRS, think sodium-channel blockade and reach for bicarbonate before other antiarrhythmics.