Antidotes for Common Poisons: A Poison-to-Antidote Master Table for NEET PG
Reflex · 12 Nov 2026 · 12 min read
Last updated: 12 Nov 2026

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Antidotes are easiest to learn as pairs: one poison, one antidote, one mechanism and one trap. This post puts the common pairs into grouped tables so you can revise them in one sitting, then explains the few regimens that need more than a table cell.
Doses below are typical adult regimens from standard references, and sources differ slightly on some of them. Where they do, the post says so instead of picking one silently.
Key Takeaways
Organophosphate poisoning: atropine first (titrate to clear bronchorrhoea and bronchospasm), then pralidoxime.
Paracetamol: N-acetylcysteine, best started within 8 hours, loading then 4-hour and 16-hour infusions.
Opioids: naloxone. Benzodiazepines: flumazenil, which is contraindicated in seizure disorder and mixed overdose.
Methanol and ethylene glycol: fomepizole (or ethanol) to block alcohol dehydrogenase, with haemodialysis as definitive treatment.
Cyanide: hydroxocobalamin preferred. Iron: deferoxamine. Thallium: Prussian blue. Digoxin: digoxin-specific Fab.
Metals: dimercaprol, CaNa2 EDTA, succimer or penicillamine depending on the metal. In severe lead poisoning, dimercaprol goes before EDTA.
Indian snakebite: polyvalent anti-snake venom, plus a neostigmine trial for neurotoxic bites.
Once you have read the pairs below, test yourself with toxicology practice questions.
How to Use This Master Table of Antidotes
Read each table row as four questions: what blocks, binds or replaces the toxin, what is the typical dose, and what makes this antidote dangerous. The "caution" column is where most of the reasoning lives, so do not skip it.
Antidotes work in a few ways. Some compete at the receptor (naloxone, flumazenil), some block a toxic metabolite pathway (fomepizole, N-acetylcysteine), some bind the poison directly (chelators, Prussian blue, antibodies), and some restore a depleted substrate (pyridoxine, vitamin K). A useful revision habit is to group antidotes by mechanism rather than memorise a flat list.
An antidote never replaces supportive care. Airway, breathing, circulation and decontamination come first in most poisonings.
Antidotes for Pesticide and Cholinergic Poisoning
Organophosphate and carbamate poisoning is the classic antidote topic because it needs two drugs with different jobs. Atropine treats the muscarinic effects, and pralidoxime reactivates acetylcholinesterase that the organophosphate has inhibited (Merck Manual: Organophosphate and Carbamate Poisoning).
| Poison | Antidote | Mechanism | Typical adult regimen | Key caution |
|---|---|---|---|---|
| Organophosphate | Atropine, then pralidoxime | Atropine blocks muscarinic receptors; pralidoxime reactivates inhibited acetylcholinesterase | Atropine 2 to 3 mg IV, doubled every 3 to 5 minutes until effect. Pralidoxime 1 to 2 g IV over 15 to 30 minutes, then 8 mg/kg/h | Titrate atropine to clear bronchospasm and bronchorrhoea, not to pupil size or heart rate |
| Carbamate | Atropine; pralidoxime only when the agent is unknown | As above | As above | Effects usually clear within about 48 hours |
| Anticholinergic toxicity | Physostigmine | Inhibits acetylcholinesterase, raising acetylcholine | 1 to 2 mg IV over 5 minutes | Use is controversial; involve a toxicologist |
Atropine and pralidoxime in organophosphate poisoning
A 1 mg test dose that eases muscarinic signs supports the diagnosis, and the dose is then doubled every 3 to 5 minutes, sometimes reaching very large cumulative totals. Pralidoxime follows atropine, not the other way round. Benzodiazepines treat the seizures.
Do not treat pralidoxime as a sure thing. Rapid IV infusion can cause respiratory or cardiac arrest, it does not help once the enzyme has aged, and it penetrates the blood-brain barrier poorly. Systematic reviews of oxime therapy have shown no benefit or even possible harm (Chacko and Peter, Indian J Crit Care Med 2019). Dose schedules also vary: another reference gives 2 g over 20 minutes then 0.5 g/h.
A simple memory aid (our own, not a standard mnemonic): atropine dries the patient, pralidoxime frees the enzyme. If a stem asks what to titrate atropine against, the answer is secretions and bronchospasm, not the pupil.
For the receptor pharmacology behind this, see our notes on cholinergic drugs and organophosphate poisoning.
Specific Antidotes for Common Drug Overdoses
Drug overdose pairs are short to learn but each carries a contraindication. Learn the antidote and the one situation where giving it is harmful.
| Poison | Antidote | Mechanism | Typical adult regimen | Key caution |
|---|---|---|---|---|
| Paracetamol | N-acetylcysteine | Supplies cysteine for glutathione, which neutralises the toxic metabolite NAPQI | IV 150 mg/kg loading, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours | Best started within 8 hours, but still given later |
| Opioids | Naloxone | Competitive antagonist at mu, delta and kappa receptors | 0.4 to 2 mg IV every 2 to 3 minutes | Short half-life, so repeat doses; can precipitate withdrawal |
| Benzodiazepines | Flumazenil | Competitive antagonist at the benzodiazepine site of GABA-A | 0.1 to 0.2 mg IV every minute, maximum 2 mg | Contraindicated in seizure disorder, mixed overdose, benzodiazepine tolerance and prolonged QRS |
| Isoniazid | Pyridoxine | Replenishes vitamin B6 and supports GABA production | Gram for gram with the amount ingested; if the amount is unknown, a large empirical IV dose (references differ on the figure) | Treats the seizures |
| Beta-blockers | Glucagon | Raises cAMP independent of beta receptors | 5 to 10 mg IV loading | Second-line; causes nausea and vomiting |
| Local anaesthetic toxicity | 20% IV lipid emulsion | "Lipid sink" | 1.5 mL/kg bolus, then 0.25 mL/kg/min for 30 to 60 minutes | Evidence is mostly animal and case reports |
N-acetylcysteine for paracetamol poisoning
N-acetylcysteine is the drug in this section with the most timing detail to learn. It works best when started within 8 hours of ingestion, and one review advises starting ideally between 4 and 8 hours and not later than 14 hours. Another reference still recommends treatment beyond 24 hours in a patient with significant toxicity (Merck Manual: Acetaminophen Poisoning).
The treatment nomogram line is 150 mcg/mL at 4 hours: a level at or below this line in a patient with no symptoms makes hepatotoxicity very unlikely. It applies only to a single acute ingestion with a known time. The loading infusion runs over 15 minutes in the Merck protocol and over 60 minutes in some other references, so learn the three-bag pattern (150, 50, 100 mg/kg) rather than a single loading time.
Naloxone and flumazenil: two competitive antagonists
Both reverse their target drug quickly, and both can cause harm by doing so. Naloxone can precipitate withdrawal, and if there is no response after 10 mg, reconsider the diagnosis. A lower starting dose of 0.04 mg is used when dependence is suspected (Chacko and Peter, 2019).
Flumazenil can provoke seizures when benzodiazepines are masking a tricyclic antidepressant overdose, and in dependent patients it can cause withdrawal (Merck Manual: Symptoms and Treatment of Specific Poisons). Resedation is possible as it wears off.
Antidotes for Toxic Alcohols and Cyanide
Methanol, ethylene glycol and cyanide share one theme: the parent compound is not the main danger, so the antidote either blocks conversion or mops up the poison. Early treatment matters in all three.
| Poison | Antidote | Mechanism | Typical adult regimen | Key caution |
|---|---|---|---|---|
| Methanol | Fomepizole (preferred) or ethanol | Inhibits alcohol dehydrogenase, blocking formation of toxic metabolites | Fomepizole 15 mg/kg IV, then 10 mg/kg every 12 hours. Ethanol 10% in 5% dextrose, 10 mL/kg over 1 hour, then 1 to 2 mL/kg/h, targeting 100 mg/dL | Give early; haemodialysis is definitive |
| Ethylene glycol | Fomepizole or ethanol | As above | 15 mg/kg IV, then 10 mg/kg every 12 hours | Haemodialysis is definitive |
| Cyanide | Hydroxocobalamin (preferred); sodium nitrite and sodium thiosulfate kit | Hydroxocobalamin binds cyanide to form cyanocobalamin; thiosulfate donates sulfur to form thiocyanate | Hydroxocobalamin typically 5 g IV | Give 100% oxygen as well |
| Methaemoglobinaemia | Methylene blue | Converted to leucomethylene blue, which reduces methaemoglobin | 1% solution, 1 to 2 mg/kg IV slowly | Inject slowly |
| Carbon monoxide | 100% oxygen | Oxygen is the treatment | Consider hyperbaric oxygen if COHb is above about 25% | Hyperbaric oxygen is a consideration, not a routine step |
Fomepizole schedules differ between references, with a longer schedule that steps the dose up after four doses and continues until ethanol falls below 20 mg/dL (Chacko and Peter, 2019). The principle is the same: block the enzyme early and keep blocking it until the toxin is cleared.
The cyanide kit sequence
The older kit works in a fixed order. Amyl nitrite is inhaled first, then 3% sodium nitrite 10 mL IV (given slowly), then 25% sodium thiosulfate 25 to 50 mL. Thiosulfate is slow and penetrates cells poorly, so it is usually considered when hypoxia persists despite maximum hydroxocobalamin.
Chelating Antidotes for Heavy Metal and Iron Poisoning
Chelators bind the metal and let the kidney or gut clear it. The choice depends on the metal, so learn the metal-to-chelator mapping first and doses second (Merck Manual: Chelation Therapy for Heavy Metal Poisoning).
| Poison | Antidote | Typical regimen | Key caution |
|---|---|---|---|
| Lead (severe poisoning) | Dimercaprol plus CaNa2 EDTA | Dimercaprol 3 to 4 mg/kg IM every 4 hours on day 1, then tapering; CaNa2 EDTA 25 to 35 mg/kg IM or slow IV every 12 hours for 5 to 7 days | Dimercaprol first, to avoid redistributing lead to the brain |
| Lead (occupational adult exposure, or children with blood lead above 45 mcg/dL) | Succimer | 10 mg/kg orally every 8 hours for 5 days, then every 12 hours for 14 days | Oral option |
| Arsenic and mercury | Dimercaprol and succimer for both; penicillamine is also listed for arsenic | Penicillamine 5 to 7.5 mg/kg orally four times daily, maximum 2 g/day | Dimercaprol is used for arsenic when oral therapy is not possible |
| Copper (Wilson disease) | Penicillamine; trientine | Trientine 750 to 1250 mg/day in 2 to 4 doses, age 13 and over | Trientine is approved for Wilson disease only |
| Thallium | Prussian blue | 60 mg/kg four times daily via nasogastric tube | Avoid penicillamine, which can redistribute thallium to the CNS |
| Iron | Deferoxamine | IV infusion starting at 15 mg/kg/h, titrated to blood pressure | Hypotension: give IV fluids |
Why dimercaprol goes before EDTA
In severe lead poisoning, dimercaprol should precede EDTA to avoid redistribution of lead to the brain (Chacko and Peter, 2019). Dimercaprol dosing differs between references, so the table gives the Merck schedule as a typical regimen.
Deferoxamine for iron overdose
Deferoxamine chelates free serum iron. IV therapy is reserved for severe poisoning, such as acidosis, shock, severe gastroenteritis or a serum iron above 500 mcg/dL (Merck Manual: Iron Poisoning).
The Prussian blue dose also differs: another review lists 20 g/day, so treat the figure above as one reference's regimen. Prussian blue works because it traps thallium in the gut, where about 99% is then excreted in faeces.
Antidotes for Anticoagulant, Digoxin and Other Reversals
These are reversal agents, so the useful skill is matching each agent to its drug. Match the drug to its reversal and note the one limitation.
| Drug or poison | Antidote | Mechanism | Key point |
|---|---|---|---|
| Warfarin | Vitamin K1, plus FFP or prothrombin complex concentrate for rapid reversal | Directly antagonises warfarin | IV vitamin K only if oral is not possible, because of anaphylactoid risk |
| Heparin | Protamine sulfate | Forms an inactive complex | Give slowly over 10 to 15 minutes; only partly neutralises LMWH |
| Digoxin | Digoxin-specific Fab | Antibody fragments bind digoxin | Each vial binds 0.5 mg; 10 vials for an unknown adult ingestion |
Five more pairs are best learned as straight poison-to-antidote matches (Merck Manual: Common Specific Antidotes).
| Poison or drug | Antidote |
|---|---|
| Tricyclic antidepressants | Sodium bicarbonate |
| Sulfonylureas | Octreotide |
| Methotrexate | Leucovorin or glucarpidase |
| Dabigatran | Idarucizumab |
| Ionising radiation | Potassium iodide |
Digoxin Fab is not for asymptomatic patients, and digoxin levels read falsely high for at least 3 weeks after Fab therapy. That is a useful reasoning point if a stem shows a high level after treatment.
Snakebite: Anti-Snake Venom and the Neostigmine Trial
In India, the antidote for venomous snakebite is polyvalent anti-snake venom (ASV), and neurotoxic bites also get a neostigmine trial. The figures below come from one ICU series that cites the National Snakebite Management Protocol, so treat them as that series' regimen (Saini et al., IJCCM 2014).
| Item | Detail |
|---|---|
| Initial ASV | 8 to 10 vials IV over 1 hour |
| Maximum ASV | 30 vials for haemotoxic bites; 20 vials for neurotoxic bites |
| Atropine then neostigmine regimen | Atropine 0.6 mg (child 50 mcg/kg) first, then neostigmine 0.01 to 0.04 mg/kg every 1 to 3 hours, maximum 10 mg/24 hours IM or IV |
Neostigmine likely does not work in presynaptic envenoming (krait, Russell's viper) but can work in postsynaptic envenoming (cobra). Antivenom has not been shown to reverse established presynaptic paralysis (Toxins 2023 review). Anaphylaxis can follow any amount of ASV, and routine premedication remains controversial (Lancet Reg Health SE Asia 2025).
The atropine given before neostigmine blocks the muscarinic side effects of neostigmine. Remember that sequence as "atropine first, then neostigmine".
Common Mistakes When Revising Antidotes
Most mistakes in this topic come from mixing near-neighbours. These are the ones to guard against.
- Pupils as the atropine endpoint. The endpoint is clearing of bronchorrhoea and bronchospasm.
- Flumazenil in any benzodiazepine overdose. It is unsafe in seizure disorder, mixed overdose and tolerance.
- Giving EDTA before dimercaprol in severe lead poisoning.
- Penicillamine for thallium. Prussian blue is the antidote, and penicillamine can move thallium into the CNS.
- Calling pralidoxime curative. Its benefit in trials is mixed.
- Forgetting that neostigmine depends on the venom type (postsynaptic versus presynaptic).
A good revision method is to cover the antidote column and recall it from the poison, then cover the caution column and recall it from the antidote. Repeat until the pairs come without prompting.
You can then check your recall with pharmacology toxicology and antidotes practice.
Conclusion
Antidotes become manageable once you sort them by mechanism: receptor antagonists, enzyme blockers, chelators, binders and reversal agents. For each pair, hold on to the one caution that changes management, such as the atropine endpoint, the flumazenil contraindications, dimercaprol before EDTA and the presynaptic limits of neostigmine. Practise the pairs with toxicology questions after each pass through the tables.
Practise this on Reflex
Turn what you just read into recall with 14 years of tagged PYQs.
FAQ
Frequently asked questions
The questions aspirants ask most about this topic.
Atropine is given first and doubled every 3 to 5 minutes, titrated to clear bronchospasm and bronchorrhoea rather than pupil size or heart rate. Pralidoxime follows to reactivate inhibited acetylcholinesterase, although trials of oximes show mixed benefit.
N-acetylcysteine. It supplies cysteine for glutathione, which neutralises the toxic metabolite NAPQI. It works best when started within 8 hours of ingestion, and a typical IV regimen is 150 mg/kg loading, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours.
Flumazenil should not be used in seizure disorder, mixed overdose, benzodiazepine tolerance or prolonged QRS. It can provoke seizures when benzodiazepines are masking a tricyclic antidepressant overdose and can cause withdrawal in dependent patients.
Fomepizole is preferred, with ethanol as the alternative. Both inhibit alcohol dehydrogenase so that toxic metabolites do not form. Haemodialysis is the definitive treatment.
Giving EDTA first can redistribute lead into the brain. Dimercaprol is started first to avoid this, and CaNa2 EDTA follows.
No. It is likely to be ineffective in presynaptic envenoming such as krait or Russell's viper bites, and effective in postsynaptic envenoming such as cobra bites. It is given after atropine as a test and treatment for neurotoxic bites.
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