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10 free Paramedic practice questions: Toxicology and Overdose Management

These are real questions from the same bank the app draws from. Each one is written to the NREMT Paramedic content specifications and kept inside the Paramedic scope of practice. Pick an answer and you get the full rationale, including why the other three options are wrong.

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Question 1 of 10

A 51-year-old patient exposed to a spilled organophosphate insecticide has been decontaminated and is being ventilated with a BVM. Copious secretions are being suctioned from the airway, and wheezing is heard throughout. The vital signs are BP 96/60, P 48, and SpO₂ 90%, with respirations assisted at 12. Atropine is ordered. To what endpoint should the paramedic titrate the atropine?

Show the answer and rationale

Correct answer · Drying of the secretions

This patient has organophosphate poisoning, and you titrate atropine until the secretions dry. Copious secretions are being suctioned, and there is wheezing throughout. Organophosphates overstimulate the muscarinic receptors, and that overstimulation fills the airway with secretions. The secretions are what kill this patient. Atropine blocks those muscarinic receptors. When the drool and the bronchial secretions slow and the patient stops sounding wet, the atropine is working. Pupil size, heart rate, and blood pressure all change for their own reasons in this poisoning. None of those three reliably tells you the patient has had enough atropine. Expect to need far more atropine than the dose you use for bradycardia. Keep titrating until the secretions dry.

Why the others are wrong

A heart rate above 60: Atropine is the bradycardia drug, so heart rate sounds like the natural target. The heart rate usually comes up long before the airway dries. A crew that stops at a rate of 60 leaves a patient who is still filling with secretions.

Dilation of the pupils: Pinpoint pupils are one of the signs that point to this poisoning, so they sound like the sign that should clear first. Pupils respond unpredictably in organophosphate poisoning and can stay small long after the airway has dried. Dosing to the pupils can push you past the endpoint or leave you short of it, with no way to tell which.

A systolic pressure above 100: The pressure is low, and raising a low pressure sounds like the point of any drug you push. The low pressure here comes from the poisoning itself. The pressure comes up as the atropine blocks the cholinergic effects. Atropine is not a pressor you titrate to a number.

Question 2 of 10

A 39-year-old patient contaminated by a nerve agent has been decontaminated and given repeated doses of atropine. The salivation has stopped, the lungs are now clear, and the airway is dry. Over the next several minutes the patient develops visible twitching of the chest and face, a weakening grip, and cannot hold the head up off the cot. The vital signs are BP 118/74, P 96, R 24, and SpO₂ 94% on high flow oxygen. Which medication is indicated next?

Show the answer and rationale

Correct answer · A DuoDote autoinjector

This patient needs a DuoDote autoinjector. A nerve agent causes too much acetylcholine at two kinds of receptors, muscarinic and nicotinic. Atropine only blocks the muscarinic receptors. That's why the salivation stopped, the lungs cleared, and the airway is dry. The new findings are nicotinic. The twitching, the weak grip, and a head that cannot be held up all come from too much acetylcholine at the nicotinic receptors. The breathing muscles weaken the same way. Atropine does nothing for nicotinic findings. DuoDote carries an enzyme reactivator along with atropine. The enzyme reactivator restores the enzyme that breaks down acetylcholine, instead of blocking a receptor. The reactivator is the part of DuoDote that works on the nicotinic findings.

Why the others are wrong

Additional atropine boluses: Atropine is the drug for muscarinic findings like drooling and wheezing. Those findings have already cleared in this patient. Atropine has no effect on nicotinic receptors, no matter how much you give. This patient still needs the enzyme reactivator, and more atropine alone does not bring it.

Intravenous sodium bicarbonate: Sodium bicarbonate is used when a poisoning blocks sodium channels and causes a wide complex rhythm. Nothing in this question points to sodium channel blockade. Bicarbonate does nothing for a nerve agent that blocks the enzyme that clears acetylcholine.

Intravenous diphenhydramine: Diphenhydramine treats a dystonic reaction, which also causes abnormal muscle movement. A dystonic reaction comes from dopamine blockade. These twitches come from too much acetylcholine at the nicotinic receptors.

Question 3 of 10

A 46-year-old patient with a seizure disorder took an unknown number of clonazepam tablets about an hour ago. The patient is drowsy but rouses to voice, speech is slurred, and respirations are unlabored. The vital signs are BP 112/68, P 84, R 12, and SpO₂ 96% on room air. A family member asks whether there is a drug that reverses this. What is the most appropriate management?

Show the answer and rationale

Correct answer · Supportive monitoring during transport

This patient has a benzodiazepine overdose from clonazepam, and the right care is supportive monitoring. The danger in a benzodiazepine overdose is the airway and the breathing. Right now both are holding. The patient rouses to voice, the respirations are unlabored at 12, and the SpO₂ is 96%. Flumazenil reverses benzodiazepines, and it is contraindicated in this patient. Flumazenil should not be given to anyone with a seizure disorder or with long-term benzodiazepine use. Reversing the drug suddenly in those patients can cause withdrawal seizures. In this patient, withdrawal seizures would bring back the seizures the clonazepam was preventing. Keep watching the airway and the rate and depth of breathing, and transport.

Why the others are wrong

Flumazenil titrated to alertness: Flumazenil is the reversal drug for benzodiazepines, so it can look like the definitive treatment. This patient's seizure disorder is the exact reason not to give flumazenil. Giving flumazenil here can cause seizures that were not happening before.

Naloxone by the intranasal route: Naloxone reverses an opioid overdose by working at the opioid receptors. Clonazepam is a benzodiazepine, so naloxone has no effect on it.

Activated charcoal by mouth: Activated charcoal is a common treatment for a recent ingestion. This patient is drowsy with slurred speech and is not reliably protecting the airway. Charcoal by mouth in this patient risks aspiration.

Question 4 of 10

A 37-year-old patient is carried out of a basement apartment fire. There is soot around the mouth and nose, the patient is confused and combative, and the skin is flushed. The vital signs are BP 84/50, P 128, R 32, and SpO₂ 99% on high flow oxygen. Carbon monoxide exposure is already assumed and oxygen is running. Which additional treatment does this presentation most strongly support?

Show the answer and rationale

Correct answer · A cyanide antidote kit per protocol

This patient has cyanide poisoning on top of the carbon monoxide. Burning household materials in a closed space release cyanide along with carbon monoxide. Cyanide stops the cells from using the oxygen the blood is still delivering. That's why the saturation can read 99% while the patient gets worse. The soot around the mouth and nose, the confusion, and the pressure of 84/50 after a closed space fire all point to cyanide. A good pulse oximeter reading does not rule cyanide out. Keep the oxygen running and give a cyanide antidote kit per protocol.

Why the others are wrong

Intravenous sodium bicarbonate: Cyanide causes a severe lactic acidosis, and sodium bicarbonate is the buffer on the truck. Buffering the blood does not let the cells use oxygen again, and that is the real injury here. Sodium bicarbonate is not the antidote for cyanide.

Nebulized ipratropium bromide: Soot and a fire scene raise concern for an inhalation injury that needs a bronchodilator. No wheezing is described here. A bronchodilator does nothing for a poison that works inside the cells.

Naloxone for the altered mental status: Naloxone is given for an opioid overdose. Nothing in this history points to an opioid. This patient is combative and breathing at 32, the opposite of the slow, quiet breathing an opioid causes.

Question 5 of 10

Which statement about activated charcoal in current EMS field practice is correct?

Show the answer and rationale

Correct answer · Its role has narrowed significantly and it is not a routine, universal field intervention

The role of activated charcoal in the field has narrowed. Charcoal works by binding toxin to its surface while the toxin is still in the gut, before it gets absorbed into the blood. Many common ingestions do not bind to charcoal at all, like alcohols, metals, and hydrocarbons. Charcoal also only helps within a short window after the ingestion. That's why charcoal is now given by protocol or by medical control in select cases. Those patients have a patent airway and took the poison recently enough for charcoal to help. Charcoal is not a default step on every ingestion call.

Why the others are wrong

It is administered routinely to every conscious patient with a suspected ingestion: Giving charcoal to every awake ingestion patient was the older teaching. Current field protocols have moved away from routine charcoal for every ingestion.

It is equally effective regardless of how much time has passed since ingestion: Charcoal binds toxin in the gut only within a limited window after the ingestion, often about the first hour. Once much of the drug has been absorbed, charcoal does little. The effect of charcoal is not the same no matter how much time has passed.

It eliminates the need for airway monitoring in poisoned patients: Charcoal can cut down further absorption of the toxin, but charcoal does nothing to protect the airway. A poisoned patient with a decreased level of consciousness still needs constant airway monitoring. Giving charcoal actually adds a risk of aspiration.

Question 6 of 10

A conscious 22-year-old patient reports swallowing an unknown quantity of pills 20 minutes ago and asks the paramedic to induce vomiting to remove the pills from their system. What is the correct action?

Show the answer and rationale

Correct answer · Do not induce vomiting; support the ABCs and transport

Do not induce vomiting in this patient. The patient swallowed an unknown number of pills 20 minutes ago, and nobody knows what the pills were. Vomiting does not reliably empty the stomach. If the patient's level of consciousness drops on the way, the patient can aspirate the vomit into the airway. If the pills were a caustic or a hydrocarbon, vomiting can injure the esophagus. With an unknown substance, you cannot rule any of that out. Protect the airway, support breathing and circulation, and transport quickly. The hospital can identify the substance and decontaminate the patient safely.

Why the others are wrong

Induce vomiting immediately: Inducing vomiting comes from older teaching, when vomiting was a first step for poisoning in the field. Current EMS practice does not support inducing vomiting in the field at all. With an unknown pill, you cannot rule out a caustic, and the patient can aspirate the vomit.

Administer activated charcoal followed by induced vomiting: Activated charcoal is a real decontamination tool for many swallowed poisons. Inducing vomiting after the charcoal brings the charcoal back up before the charcoal can bind anything. The vomiting still puts the patient at risk of aspiration.

Allow the patient to induce their own vomiting since they are conscious: This patient is conscious and is asking to vomit. Being awake now does not protect the airway if the reflexes change during vomiting. The risk of aspiration and caustic injury is the same no matter who starts the vomiting.

Question 7 of 10

A 26-year-old patient is found pacing and shouting in a parking lot after using methamphetamine. The patient pulls away from the paramedic and shouts, "They are coming for me!" The skin is hot and diaphoretic, and the pupils are dilated. The vital signs are BP 178/104, P 148, R 26, SpO₂ 97% on room air, and T 104°F. What medication should the paramedic administer?

Show the answer and rationale

Correct answer · Administer midazolam intramuscularly

This patient has sympathomimetic toxicity from methamphetamine. The skin is hot and diaphoretic, and the pupils are dilated. The pulse is 148, the BP is 178/104, and the patient is paranoid and agitated. The sweating is what confirms a stimulant. An anticholinergic overdose can look a lot like this, but the skin is dry and flushed instead. Methamphetamine causes a surge of catecholamines, the body's adrenaline. The surge drives the fast heart rate, the high blood pressure, the muscle activity, and the seizure risk. The muscle activity is also raising the temperature, which is 104°F. Midazolam is a benzodiazepine. Midazolam works on GABA receptors in the brain and blunts the catecholamine surge. The heart rate, blood pressure, muscle activity, temperature, and seizure risk all come down together. Give midazolam intramuscularly, because this patient is pulling away and has no IV. Start active cooling along with the sedation.

Why the others are wrong

Administer haloperidol intramuscularly: Haloperidol is used for agitation from a psychiatric cause, and it would calm this patient down. This patient already has a temperature of 104°F and a stimulant that raises the seizure risk. Haloperidol makes it harder for the body to get rid of heat. Haloperidol also lowers the seizure threshold, and it does nothing to blunt the catecholamine surge.

Administer naloxone intramuscularly: Naloxone reverses an opioid overdose. Opioids give you pinpoint pupils, slow shallow breathing, and a patient who is hard to wake up. This patient has dilated pupils, respirations of 26, and agitation. There is no opioid effect here for naloxone to reverse.

Administer flumazenil intravenously: Flumazenil reverses benzodiazepine sedation, the opposite of what this patient needs. Nothing here points to a benzodiazepine overdose. Taking away GABA activity in a stimulant overdose that is already at risk for seizures can cause a seizure.

Question 8 of 10

A 31-year-old patient is found unresponsive with respirations of 4 and pinpoint pupils. A family member states the patient takes methadone daily for chronic pain. Positive pressure ventilations are provided with a BVM, and naloxone is administered intranasally. Ten minutes later the patient opens the eyes to voice and is breathing at 14 with adequate tidal volume. The vital signs are BP 118/70, P 88, R 14, and SpO₂ 97% on room air. What is the most appropriate next action?

Show the answer and rationale

Correct answer · Monitor for recurrent respiratory depression during transport

This patient had an opioid overdose from methadone, and the naloxone has worked. The goal of naloxone is adequate breathing, not a fully awake patient. The patient is now breathing 14 times a minute with adequate tidal volume. The SpO₂ is 97% on room air, and the eyes open to voice. Methadone matters here because it lasts much longer than naloxone. As the naloxone wears off, the methadone still on the receptors can sedate the patient again and drop the breathing rate. Monitor for recurrent respiratory depression during transport. Keep the BVM within reach and be ready to give more naloxone.

Why the others are wrong

Administer flumazenil intravenously: Flumazenil reverses benzodiazepines. Its role is narrow, mostly a patient oversedated by a benzodiazepine given during medical care. This patient had respirations of 4 and pinpoint pupils and takes methadone every day. Methadone is an opioid, and the opioid reversal drug has already worked. Flumazenil acts on the wrong receptor, and it can cause seizures in a patient who takes benzodiazepines regularly.

Administer repeat naloxone until the patient is fully awake: Giving more naloxone until the patient is fully awake overshoots the goal. Breathing is already adequate, so more naloxone adds no benefit. More naloxone can cause acute withdrawal, with agitation and vomiting into an airway the patient may not be protecting yet.

Obtain a refusal of transport from the patient: Many of these patients want to refuse once they feel better. A refusal needs a patient who is alert and oriented, and this patient only opens the eyes to voice. Methadone is the other problem. Naloxone wears off well before methadone does, and the patient can slip back into respiratory depression with nobody around. Transport keeps the patient watched while the methadone outlasts the naloxone.

Question 9 of 10

A 58-year-old patient is drowsy after an intentional ingestion of a prescribed medication about an hour ago. The pupils are 4 mm and reactive, and the respirations are unlabored with adequate tidal volume. The vital signs are BP 76/44, P 42, R 16, and SpO₂ 97% on room air. The blood glucose level is 268 mg/dL. Which class of medication was most likely ingested?

Show the answer and rationale

Correct answer · Calcium channel blocker

This is a calcium channel blocker overdose. A slow heart rate with low blood pressure after an overdose narrows the list to a few drug classes. The blood glucose is what separates them. The pancreas needs calcium to enter its cells through calcium channels before it can release insulin. When those channels are blocked, insulin release shuts down and the glucose climbs. This patient has a glucose of 268 with no reported diabetes, a pulse of 42, and a pressure of 76/44. That combination points to a calcium channel blocker. The pupils are 4 mm and reactive, and the respirations are unlabored at 16 with adequate tidal volume. Those findings rule out an opioid, the other common slow and sedated overdose. The field treatment is different too, because calcium channel blocker overdose responds to IV calcium. Calcium is given along with the glucagon, fluid, and vasopressors these poisonings share.

Why the others are wrong

Alpha-2 adrenergic agonist: An alpha-2 agonist like clonidine does cause a slow heart rate, low blood pressure, and sedation. In children, clonidine can look a lot like an opioid overdose. Clonidine does not raise the blood glucose, so the glucose of 268 goes unexplained.

Beta-adrenergic blocker: A beta blocker gives the same slow heart rate and low blood pressure through a similar effect on the same conduction system. The glucose goes the other way. Beta blockade blocks the release of stored glucose, so the level is usually normal or low, not 268. The two overdoses look alike at the bedside, and calcium is where their treatments differ.

Opioid pain medication: An opioid overdose gives you a drowsy patient with pinpoint pupils and slow, shallow breathing, and naloxone is the treatment. This patient's pupils are 4 mm and reactive. The respirations are unlabored at 16 with adequate tidal volume. Opioids also do not cause a pulse of 42 with a glucose of 268.

Question 10 of 10

A 46-year-old patient reports a headache, nausea, and lightheadedness that have worsened through the morning at home. Two other people in the house report headaches that started the same morning. A family member states the furnace was serviced the day before. The patient is alert and answers slowly. The skin is warm and dry. The vital signs are BP 138/84, P 104, R 20, and SpO₂ 99% on room air. After the fire department clears the scene and the patient is moved outside, what should the paramedic do next?

Show the answer and rationale

Correct answer · Apply high-flow oxygen by NRB

This patient has carbon monoxide poisoning. The headache, nausea, and lightheadedness got worse through the morning at home. Two other people in the house have headaches that started the same morning, and the furnace was serviced the day before. A standard pulse oximeter cannot tell carbon monoxide on the hemoglobin apart from oxygen on the hemoglobin. In carbon monoxide poisoning, the SpO₂ reads normal or high while the blood carries very little usable oxygen. That's why the 99% reading does not reassure you. Give high-flow oxygen by NRB no matter what the SpO₂ says. A high concentration of oxygen pushes carbon monoxide off the hemoglobin faster. Transport so the hospital can measure the carboxyhemoglobin, which is the carbon monoxide level in the blood.

Why the others are wrong

Withhold oxygen because the SpO₂ is normal: Withholding oxygen for a normal SpO₂ would only make sense if the pulse oximeter could see carbon monoxide. A standard pulse oximeter cannot. Trusting that number is how these patients end up going back into the exposure. Treat the carbon monoxide poisoning that the scene and the symptoms show you.

Give oxygen by nasal cannula at 2 liters each minute: Two liters by nasal cannula is fine for raising the saturation of a mildly hypoxic patient a little. The goal here is to give enough oxygen to shorten the time carbon monoxide stays on the hemoglobin. A low-flow nasal cannula barely changes that time, so most of the benefit is lost.

Obtain a 12-lead ECG before deciding on oxygen: A 12-lead ECG is a reasonable thing to get in carbon monoxide exposure. Less oxygen reaching the heart can cause ischemia, especially in an older patient with coronary disease. The 12-lead does not need to come before oxygen. Putting a test in front of a treatment that is clearly needed only delays the oxygen.

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