List of Common Antidotes Nurses Should Know

Drug toxicity and overdose are emergencies, and the right antidote given fast reverses the damage and saves the patient. An antidote neutralizes a poison's effect: it can bind the toxin, block its absorption, speed its elimination, or reverse its physiology. The word is Greek for "given against." For the floor and for the NCLEX, you need to know the common antidotes and how they work.

What is an Antidote?

An antidote neutralizes or counteracts the harmful effects of a poison or toxin. It can bind the toxin, prevent absorption, enhance elimination, or reverse the physiologic effect. Know the indications, administration, and mechanism for each.

How Antidotes Work

1. Neutralization. The antidote chemically reacts with the toxin to form a less harmful or inert compound. Antacids like calcium carbonate neutralize acidic substances.
2. Chelation. Chelating agents bind metal ions, such as heavy metals, into stable complexes that are excreted in the urine. EDTA for lead poisoning, dimercaprol (BAL) for heavy metal poisoning.
3. Enhanced elimination. The antidote increases excretion through urine, bile, or other routes. Activated charcoal adsorbs toxins in the GI tract and carries them out in the feces.
4. Receptor blockade. The antidote blocks the toxin at its receptor. Flumazenil blocks benzodiazepine receptors, reversing the sedation and respiratory depression of a benzodiazepine overdose.
5. Antagonism. The antidote opposes the toxin's action directly. Vitamin K antagonizes warfarin's anticoagulant effect by promoting the synthesis of clotting factors.
6. Metabolic conversion. The antidote shifts the toxin toward less toxic metabolites. Acetylcysteine drives acetaminophen toward nontoxic metabolites in an acetaminophen overdose.

Common Drug Antidotes

Indication	Antidote	Mode of Action
Acetaminophen (Tylenol) toxicity	N-acetylcysteine (Mucomyst)	Acetylcysteine replenishes glutathione stores, enhancing the non-toxic metabolism of acetaminophen, thereby preventing liver damage.
Various oral poisonings and overdoses except for cyanide, iron, lithium, caustics, and alcohol .	Activated charcoal	Activated charcoal adsorbs toxins in the gastrointestinal tract, reducing their systemic absorption.
Cholinergic crisis, Organophosphate or carbamate insecticide poisoning, certain mushroom poisonings	Atropine (Atropen)	Atropine blocks acetylcholine receptors, reversing cholinergic effects like salivation, bronchial secretions, and bradycardia .
Magnesium Sulfate overdose, hyperkalemia, calcium channel blocker overdose	Calcium gluconate	Calcium gluconate stabilizes cardiac membranes and counteracts the effects of hyperkalemia and calcium channel blockers.
Fluoride ingestion	Calcium chloride or calcium gluconate	Calcium chloride binds to fluoride ions, forming insoluble calcium fluoride, reducing fluoride toxicity, especially on the cardiovascular and nervous systems.
Iron poisoning	Deferoxamine (Desferal)	Deferoxamine binds free iron in the bloodstream, forming a complex that can be excreted in the urine .
Digoxin toxicity	Digoxin immune fab (DigiFab/Digibind)	Digoxin immune fab binds to digoxin molecules, forming a complex that is then excreted by the kidneys, thereby neutralizing its effects.
Heavy metal poisoning, such as lead, arsenic, mercury, copper, and thallium.	Dimercaprol (BAL)	Dimercaprol chelates heavy metals, forming stable complexes that can be excreted in the urine, thereby reducing their toxicity.
Extrapyramidal symptoms (EPS)	Diphenhydramine (Benadryl)	Diphenhydramine blocks histamine (H1) and muscarinic (M1) receptors, which reduces the excessive cholinergic activity in the central nervous system that contributes to EPS.
Heavy metal poisoning, such as lead, copper, and mercury	D- penicillamine (Cuprimine)	D-penicillamine works by forming stable complexes with the metal ions, which are then excreted from the body.
Lead poisoning	Edetate calcium disodium (Calcium EDTA), dimercaprol (BAL), Succimer Dimercaptosuccinate (DMSA)	EDTA: Chelates lead by binding to it, forming a water-soluble complex that is excreted in the urine .
Benzodiazepine overdose	Flumazenil (Romazicon)	Flumazenil competitively inhibits benzodiazepine binding at the GABA receptor, reversing sedation and respiratory depression .
Ethylene glycol (antifreeze), Methanol poisoning	Fomepizole (Antizol) Ethanol, Hemodialysis	Fomepizole inhibits alcohol dehydrogenase, preventing the metabolism of toxic alcohols into their harmful metabolites.
Beta-blockers overdose, calcium channel blockers overdose, hypoglycemia	Glucagon	Glucagon increases cyclic AMP in cardiac cells, improving heart contractility and counteracting the effects of beta-blockers.
Insulin reaction	Glucose (Dextrose 50%)	Glucose rapidly raises blood sugar levels, providing immediate energy to counteract insulin -induced hypoglycemia and alleviate symptoms like dizziness and weakness .
Cyanide poisoning	Hydroxocobalamin (1st line) Nitrites and thiosulfate (2nd line)	Hydroxocobalamin binds to cyanide to form cyanocobalamin, a non-toxic compound that is excreted by the body.
Methotrexate toxicity	Leucovorin Calcium (folinic acid)	Leucovorin calcium acts as a folate precursor, counteracting methotrexate toxicity by restoring normal cell function, especially in rapidly dividing tissues like the bone marrow and GI tract.
Cyclophosphamide toxicity	Mesna	Mesna works by binding to acrolein, a toxic metabolite of Cyclophosphamide, preventing damage to the bladder and reducing the risk of hemorrhagic cystitis .
Chemical producing severe methemoglobinemia. Ifosamide-induced encephalopathy.	Methylene blue	Methylene blue works by reducing methemoglobin back to hemoglobin, restoring the oxygen -carrying capacity of the blood.
Opioids (Narcotic) overdose	Naloxone (Narcan)	Naloxone competitively binds to opioid receptors, reversing the effects of opioids like respiratory depression and sedation.
Anticholinergics	Neostigmine	Anticholinesterase which causes accumulation of acetylcholine at cholinergic receptor sites.
Carbon Monoxide poisoning	100% Oxygen	Administering high-flow oxygen helps to rapidly displace carbon monoxide from hemoglobin, restoring oxygen delivery to tissues and reducing the risk of tissue hypoxia and organ damage.
Hypertensive crisis due to catecholamine excess (e.g., pheochromocytoma)	Phentolamine (Regitine)	Phentolamine blocks alpha-adrenergic receptors, causing vasodilation and reducing blood pressure .
Anticholinergic toxicity, Tricyclic antidepressants, anticholinergic, diphenhydramine dimehydrinate overdose	Physostigmine	A reversible anticholinesterase which effectively increases the concentration of acetylcholine at the sites of cholinergic transmission.
Warfarin (Coumadin) overdose	Phytomenadione (Vitamin K)	Vitamin K is essential for the synthesis of clotting factors II, VII, IX, and X, reversing the anticoagulant effects of warfarin .
Organophosphate poisoning	Pralidoxime (2-PAM, Protopam)	Pralidoxime reactivates acetylcholinesterase that has been inactivated by organophosphates, restoring normal neuromuscular function.
Heparin overdose	Protamine sulfate	Protamine sulfate binds to heparin, forming a stable complex that neutralizes its anticoagulant effect.
Isoniazid overdose, monomethyl hydrazine poisoning. Adjunctive therapy in ethylene glycol poisoning.	Pyridoxine (Vitamin B6)	Vitamin B6 serves as a cofactor for pyridoxal kinase, converting isoniazid (INH) into less toxic metabolites, thereby decreasing the risk of neurological side effects from INH overdose.
Cobra bite	Snake antivenom	Neutralizes venom by binding with circulating venom components and with locally deposited venom by accumulating at the bite site.
Tricyclic Antidepressant (TCA) overdose, salicylate poisoning, metabolic acidosis, hyperkalemia, chlorine gas inhalation	Sodium Bicarbonate	Sodium bicarbonate alkalinizes the blood and urine, enhancing the elimination of certain drugs and counteracting metabolic acidosis .
Alcohol-induced Wernicke-Korsakoff syndrome, acute thiamine deficiency	Thiamine (Vitamin B1)	Thiamine replenishes deficient levels, crucial for glucose metabolism, preventing and treating neurological damage in Wernicke-Korsakoff syndrome and acute thiamine deficiency.