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10 free AEMT practice questions: Respiratory Emergencies and Nebulized Medications

These are real questions from the same bank the app draws from. Each one is written to the NREMT AEMT content specifications and kept inside the AEMT 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 33-year-old patient with asthma has difficulty breathing. The AEMT applies waveform capnography through a nasal sampling cannula. The waveform shows a slow rising upstroke with no flat plateau, and EtCO₂ reads 48 mmHg. What does the shape of this waveform indicate?

Show the answer and rationale

Correct answer · Obstructed airflow in the lower airways

A normal capnogram has a sharp upstroke and a flat plateau, because the alveoli empty together. When the lower airways are narrowed, different parts of the lung empty at different speeds, the plateau never flattens, and the tracing climbs the whole way across. That sloping shape is the shark fin, and it means bronchospasm. Read the shape as well as the number, because the fin can show up before the reading moves and it flattens back out as the airways open.

Why the others are wrong

A leak in the capnography sampling line: A sampling cannula sits loose in the nose, so suspecting the equipment when a tracing looks odd is a fair first thought. A leak in the sampling line makes the waveform small or ragged and drags the reading down, rather than tilting the upstroke. What is described is a steady slow climb, which is an airflow problem and not a sampling problem.

A fall in the patient's cardiac output: Capnography reports circulation as well as ventilation, so a perfusion problem belongs on the list of things an abnormal tracing could mean. Falling cardiac output lowers the height of the waveform, because less blood carries carbon dioxide to the lungs. That changes the size of the tracing, not the slope of the upstroke.

Ventilations being delivered too quickly: A patient in respiratory distress is usually breathing fast, and a rate problem is the first thing an abnormal capnogram suggests. Ventilating too fast blows carbon dioxide off and lowers the reading, and this patient is breathing on their own with a reading of 48 mmHg. Rate errors move the number, while narrowed airways change the shape.

Question 2 of 10

A 6-year-old patient with asthma has been struggling to breathe for an hour. On arrival the patient is limp, the breathing effort has faded, P 150, R 8, and SpO₂ 84% on room air. The AEMT begins positive pressure ventilations with a BVM. At what rate should the ventilations be delivered?

Show the answer and rationale

Correct answer · One breath every 2 to 3 seconds

A child who has a pulse but is not breathing adequately is ventilated at one breath every 2 to 3 seconds, which comes out to roughly 20 to 30 breaths a minute. Children burn through oxygen faster and hold less reserve than adults, which is why their assisted rate is quicker than the adult rate. Aim for gentle chest rise with each breath instead of squeezing the bag hard, since extra volume pushes air into the stomach and makes ventilation harder. Count out loud, because the easiest mistake with a sick child is drifting faster than you meant to.

Why the others are wrong

One breath every 6 seconds: the adult rate for a patient with a pulse, and using it on a child underventilates them. The higher oxygen demand of a child is exactly why the pediatric rate is faster.

One breath every 10 seconds: Slowing down is the drilled correction for the most common error at the bag, so the slowest rate on the list can look like the careful answer. One breath every 10 seconds is 6 breaths a minute, slower than the assisted rate for a patient of any age. A child ventilated that slowly keeps falling rather than recovering.

Two breaths after every 30 compressions: This is the compression to ventilation ratio for CPR, and this child has a pulse of 150. Ventilation rates and CPR ratios are separate numbers, and confusing them leads to compressions on a patient who is still perfusing.

Question 3 of 10

A 66-year-old patient with chronic obstructive pulmonary disease has been on oxygen for 10 minutes and has finished a nebulized bronchodilator treatment. The SpO₂ has come up to 90%, but the patient is now harder to rouse, with R 8 and shallow and very little chest movement. What should the AEMT do next?

Show the answer and rationale

Correct answer · Begin positive pressure ventilations with a BVM

The saturation looks acceptable, and that is the trap in this patient. A saturation number tells you about oxygen, while a falling level of consciousness with R 8 and shallow breathing tells you carbon dioxide is climbing and ventilation is failing. A chronic lung patient in respiratory failure gets assisted ventilation, delivered slowly with a long time to exhale so the trapped air can escape. Never take oxygen away from a patient as a treatment for sleepiness, because the fix for failing ventilation is ventilation.

Why the others are wrong

Remove the oxygen and watch the breathing: This choice rests on the belief that the oxygen suppressed the breathing, which is not real physiology. Pulling oxygen off a patient who was hypoxic ten minutes ago makes them hypoxic again and leaves the failing ventilation untouched.

Sit the patient up and reassess in 5 minutes: Sitting a patient up supports a patient who is still moving air and doing the work of breathing. A patient at R 8 who is hard to rouse has run out of the effort that position is meant to help, and 5 minutes is far too long to wait.

Repeat the nebulized bronchodilator treatment: A nebulized treatment only works if the patient can pull the mist deep into the lungs, and this patient is barely moving air. Medication cannot reach airways that air is not reaching.

Question 4 of 10

A 34-year-old patient with a history of asthma is sitting upright with audible expiratory wheezing in both lung fields after running out of a rescue inhaler. The patient is alert, speaking in short sentences, with BP 128/78, P 104, R 26, and SpO₂ 92% on room air. Which nebulized dose of albuterol should the AEMT prepare?

Show the answer and rationale

Correct answer · 2.5 mg mixed with saline and driven by oxygen flow

Lock 2.5 mg in as the number you reach for. That is the standard adult nebulizer dose, mixed with saline and driven by oxygen flow, and protocols that go higher for severe bronchospasm top out around 5 mg rather than four times the standard dose. If you remember one albuterol number for the exam, make it this one, because almost every respiratory scenario you see will start with it.

Why the others are wrong

1 mg mixed with saline and driven by oxygen: 1 mg is under the standard dose. Nebulized albuterol is not titrated down for an adult with active bronchospasm, and a smaller dose simply treats the patient less.

0.3 mg mixed with saline and driven by oxygen: 0.3 mg is the adult epinephrine auto-injector dose, not an albuterol dose. Mixing those two numbers up is common, so tie 0.3 mg to anaphylaxis and 2.5 mg to the nebulizer.

10 mg mixed with saline and driven by oxygen: 10 mg is double even the highest documented range. Protocols that allow more than the standard dose reach about 5 mg for severe bronchospasm, not 10 mg.

Question 5 of 10

A 66-year-old patient has had a fever and a productive cough for three days and now has difficulty breathing. Auscultation finds coarse, low-pitched sounds over the right lower lobe that change after the patient coughs, with clear sounds elsewhere. BP 118/72, P 104, R 24, T 101.8°F, SpO₂ 91% on room air. Which condition do these findings best support?

Show the answer and rationale

Correct answer · Pneumonia, because secretions sit in the larger airways

The sound tells you where the problem is, and where the problem is tells you what it is. Coarse, low-pitched sounds that clear or change with a cough are rhonchi, and rhonchi come from secretions and sputum sitting in the larger airways. Pair that with fever, a productive cough, and findings focused over one lobe, and you have pneumonia. Hold the pairing steady in your head: fluid down in the alveoli gives crackles, secretions up in the bigger tubes give rhonchi, and the two are never swapped.

Why the others are wrong

Acute pulmonary edema, because fluid has filled the alveoli: Pulmonary edema puts fluid in the alveoli, and the sound that makes is crackles at the bases spreading upward, heard on both sides rather than over one lobe.

An acute asthma attack, because the lower airways have narrowed: An asthma attack narrows the small airways and gives you wheezing across both lung fields with a long exhale, not focal coarse sounds that change after a cough.

A spontaneous pneumothorax, because air has entered the pleural space: A pneumothorax gives decreased or absent sounds over the affected side with sudden onset, not coarse sounds that clear with a cough after three days of fever.

Question 6 of 10

A 31-year-old patient with severe asthma has had two back to back nebulized albuterol treatments and continues to worsen, with faint wheezing, single-word speech, and SpO₂ falling from 91% to 87% on oxygen. There are no hives and no swelling, and BP 118/70. Which additional treatment has a recognized role here where protocol authorizes it?

Show the answer and rationale

Correct answer · Epinephrine given by the intramuscular route

Epinephrine is not only an anaphylaxis drug. In severe asthma that is not responding to nebulized treatment, intramuscular epinephrine has a recognized role at the same dose you would use for anaphylaxis, where your protocol authorizes it. The absence of hives and swelling does not take it off the table, because the indication here is failure of the nebulized treatment rather than an allergic picture. Read the trend: faint wheezing, single-word speech, and a saturation moving the wrong way on oxygen all say this patient is not responding, so repeating the same treatment a third time is not the escalation this call needs.

Why the others are wrong

Nebulized epinephrine at the same dose as albuterol: Nebulized epinephrine has a role in croup, where it shrinks swollen tissue below the cords. It is not the recognized route for a severe asthma patient failing nebulized bronchodilators.

Intravenous magnesium given over twenty minutes: Magnesium given by the intravenous route for severe asthma sits above the AEMT level, so it is not a treatment you would be reaching for on this call.

A third nebulized albuterol treatment run continuously: Two treatments have already failed and the patient is worse. Running a third continuously is more of the therapy that is not working, and the lesson is explicit that a failing patient needs escalation instead.

Question 7 of 10

A 70-year-old patient with chronic obstructive pulmonary disease reports that breathing has been worse for two days, that the cough has increased, and that the sputum has changed color and thickness. Auscultation finds diminished sounds with wheezing plus coarse, low-pitched sounds. Which explanation accounts for the coarse, low-pitched sounds?

Show the answer and rationale

Correct answer · Large volumes of sputum sitting in the larger airways

Rhonchi are a large airway sound, and patients with this disease make a lot of sputum, so hearing them here is ordinary rather than alarming. An exacerbation usually shows up as three things together: breathing that has gotten worse, more coughing, and a change in the sputum, which is exactly the history given. Diminished sounds with wheezing is the chronic background, and the coarse low-pitched layer on top of it is the secretions. Keep the pairing straight in your head: crackles come from fluid down in the alveoli, and rhonchi come from secretions up in the bigger tubes.

Why the others are wrong

Fluid filling the alveoli behind a failing left ventricle: Fluid in the alveoli produces crackles, described as fine popping. It is a different sound produced at a different level of the lung.

Air trapped behind small airways that cannot empty fully: Air trapping is real in this disease and it is why exhalation drags out, but trapped air does not make a coarse low-pitched sound. It shows up as diminished sounds and wheezing.

Narrowing of the upper airway above the level of the vocal cords: Narrowing above the vocal cords produces stridor, which is heard on inspiration and is not a coarse sound rising from the chest.

Question 8 of 10

An AEMT is comparing an asthma exacerbation with a chronic obstructive pulmonary disease exacerbation. Both narrow the lower airways through smooth muscle tightening. Which feature is characteristic of the chronic obstructive pulmonary disease patient rather than the asthma patient?

Show the answer and rationale

Correct answer · Daily breathlessness between flares

Daily breathlessness between flares is the deciding finding. In COPD, structural damage, alveolar destruction in emphysema and airway wall thickening with mucus hypersecretion in chronic bronchitis, permanently narrows the airways, so smooth muscle relaxation from a bronchodilator can't restore normal caliber. Asthma's obstruction is bronchospasm and reversible inflammation, so that patient returns to baseline once treated. This baseline dyspnea tells you the exacerbation is layered on chronic disease rather than starting from clear lungs, so you're aiming to return the patient to their usual shortness of breath, not to a normal airway.

Why the others are wrong

Wheezing heard through both lung fields: shows up in both asthma and COPD attacks, since both involve bronchospasm narrowing the same small airways. It doesn't separate the two conditions, and the question asks for the feature unique to COPD.

Breathing that returns to normal between flares: This is the true picture of asthma: bronchospasm and inflammation reverse fully, so breathing normalizes between attacks. COPD's damage, alveolar breakdown in emphysema and thickened, mucus-clogged airways in chronic bronchitis, doesn't resolve, so that patient never returns to normal, only to their own baseline dyspnea. This describes the other patient in the comparison, not the one asked about.

A prolonged expiratory phase during the attack: A prolonged expiratory phase happens with any narrowed lower airway, since air trapping slows exhalation in both asthma and COPD attacks. It's part of the asthma picture too, so it doesn't distinguish COPD from asthma.

Question 9 of 10

A 6-year-old patient weighing 20 kg is having an asthma exacerbation with wheezing throughout both lung fields, retractions, and SpO₂ 91% on room air. The patient is alert and speaking in short phrases. Which nebulized albuterol dose should the AEMT give?

Show the answer and rationale

Correct answer · 2.5 mg, which is the same dose used for an adult patient

This is one of the few places where the pediatric number is the easy one, because it is the same number you use for an adult. Nebulized albuterol is given at 2.5 mg for a wheezing child with suspected asthma, and it is not scaled down by weight. The reason is that a nebulizer delivers a mist the child breathes in, and a smaller child simply takes in less of it. Do not let the weight in the scenario pull you into a calculation, because that weight is there to test whether you know this dose is flat.

Why the others are wrong

0.5 mg, which is one fifth of the usual adult dose: Cutting the dose to a fifth undertreats a child in active bronchospasm. The nebulized dose is not scaled by body size the way an injected or intravenous drug is.

1.25 mg, calculated at half of the adult dose: Halving the adult dose looks like careful pediatric practice, but it is the wrong instinct for a nebulized bronchodilator, where the standard dose is the same as for an adult.

0.1 mg per kilogram, which comes to 2 mg here: A per-kilogram calculation is right for many pediatric drugs and wrong for this one. The presence of a weight in the scenario does not make the dose weight-based.

Question 10 of 10

A 74-year-old patient with cardiogenic pulmonary edema is placed on CPAP. Within several minutes, the SpO₂ rises and the patient's breathing becomes visibly less labored. What explains this improvement?

Show the answer and rationale

Correct answer · It reopens collapsed alveoli and pushes fluid back into the pulmonary circulation

The finding that decides this is the pattern itself: SpO₂ climbing and work of breathing dropping within minutes of starting CPAP, not minutes of giving a bronchodilator or a higher-flow oxygen device. CPAP holds a continuous positive pressure in the airway throughout inspiration and expiration, which recruits and re-expands alveoli that have collapsed or filled with edema fluid, raising functional residual capacity. That same positive pressure raises hydrostatic pressure on the alveolar side, driving interstitial and alveolar fluid back into the pulmonary capillaries and improving the alveolar-capillary interface for gas exchange. This is why CPAP is the priority noninvasive intervention in cardiogenic pulmonary edema before you consider bagging or intubating.

Why the others are wrong

It provides a much higher oxygen concentration than an NRB delivers: This looks appealing because CPAP is often paired in your head with "more oxygen delivery," and it's true that FiO2 can be titrated on a CPAP circuit, but an NRB at 15 liters per minute already approaches 100% delivered oxygen, so the rapid SpO₂ improvement here can't be explained by CPAP simply out-concentrating an NRB; the change comes from the pressure effect on the alveoli, not from a richer oxygen mixture.

It relaxes bronchial smooth muscle to reverse the airway constriction causing this: This describes the mechanism of a bronchodilator like albuterol reversing bronchoconstriction in asthma or COPD, where wheezing from smooth muscle tightening is the problem. Cardiogenic pulmonary edema fills alveoli with fluid, it doesn't constrict bronchial smooth muscle, so there's no airway constriction here for CPAP to reverse.

It actively suctions the accumulated fluid out of the alveoli through the mask: CPAP has no suction function built into the mask or circuit; it works entirely by generating and maintaining positive pressure. The fluid shift happens because pressure pushes it back into the pulmonary circulation, not because anything is pulling it out through the mask.

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