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Free NREMT practice questionsFree AEMT practice questions · Airway, Respiration & Ventilation

10 free AEMT practice questions: Ventilation and Oxygenation Support

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 supraglottic airway has been placed and confirmed in a 64-year-old patient in cardiac arrest. Compressions have been running at 30 to 2. How do compressions and ventilations run from this point?

Show the answer and rationale

Correct answer · Continuous compressions with one breath every 6 seconds

Placing an advanced airway changes the choreography. Before it, ventilation has to happen in the gaps, so you run 30 compressions to 2 breaths and the compressor stops for the breaths. Once a device is sealing the airway, the breaths no longer need a pause, so compressions run continuously at 100 to 120 per minute and the breaths go in around them, one every 6 seconds for an adult and one every 2 to 3 seconds for an infant or a child. The whole point is that interruptions in compressions cost perfusion, and now you have a way to avoid them. Keep counting the breaths, because it is easy to speed up once nobody is pausing for you.

Why the others are wrong

Continuous compressions with one breath every 3 seconds: One breath every 3 seconds is 20 per minute, and the urge to bag that fast during an arrest is strong. That is the pediatric rate, and in an adult it raises intrathoracic pressure and reduces the blood your compressions are returning to the heart.

Continuous compressions with one breath every 10 seconds: One breath every 10 seconds is 6 per minute, and it is where you land after being warned how much harm fast ventilation does during an arrest. Six breaths a minute does not clear the carbon dioxide your compressions are delivering to the lungs, and this patient has no breathing of their own to make up the difference.

Cycles of 30 compressions to 2 breaths, continued as before: Staying at 30 to 2 is safe in the sense that it is what the crew was already doing well. It also gives up the reason you placed the device, since every pause for breaths is a pause in the perfusion your compressions are generating.

Question 2 of 10

A 55-year-old patient is in respiratory arrest with a pulse and a partner is ventilating with a BVM, squeezing about every 2 seconds. The chest rises fully with each breath and there is no gastric distention. Over the next two minutes the blood pressure falls from 118/70 mmHg to 84/50 mmHg and the pulse climbs from 96 to 124. What best explains the falling blood pressure?

Show the answer and rationale

Correct answer · Higher pressure inside the chest is cutting venous return

Every positive pressure breath you deliver raises the pressure inside the chest, and that pressure has to fall back down between breaths for blood to refill the heart. Squeeze again before it falls and the pressure stacks, so the chest never returns to a level that lets venous blood in. Less blood coming back means less blood going out, and the pressure drops while the heart rate climbs to compensate. This is why ventilating too fast is the most common harmful error in prehospital airway management, and it hits hardest in the patients who can least afford it: the hypotensive patient and the patient in arrest, where the drop in preload works directly against your compressions. An adult in respiratory arrest with a pulse gets one breath every 6 seconds, which is 10 breaths per minute, and a timer or the rate display on your capnography is how you actually hold that.

Why the others are wrong

Each breath is delivering a lower oxygen concentration: Rate and delivered concentration do feel like they should be linked, and a bag without a reservoir really does deliver far less oxygen. The concentration coming out of the bag is set by the flow and the reservoir, not by how often you squeeze, and a change in concentration would not drop a blood pressure in two minutes.

The fast rate is raising the carbon dioxide and dropping the pressure: Watching a carbon dioxide number move with your ventilation rate is exactly the right habit, and carbon dioxide does affect vessel tone. The direction is backwards here: ventilating faster clears more carbon dioxide and drives the number down rather than up, so a level that is falling is not what dropped this pressure.

The shortened breaths are making the patient hypoxic: Fast shallow breathing does leave a patient hypoxic, and that pattern is worth recognizing in a spontaneously breathing patient. The chest is rising fully with each delivered breath, so volume is not the problem here, and hypoxia this early would show as a falling saturation rather than a falling pressure.

Question 3 of 10

A single AEMT is ventilating a 48-year-old patient who is apneic with a BVM. The chest barely moves with each squeeze, air leaks audibly with every breath, and the upper abdomen is becoming visibly distended. An oropharyngeal airway is already in place and the reservoir is inflated on 15 liters per minute. What should the AEMT do first?

Show the answer and rationale

Correct answer · Reposition the head and recheck the mask seal

When the chest does not rise, the air you are delivering is going somewhere, and the two places it goes are out around the mask and down into the stomach. Both of those are fixed at the top of the list rather than the bottom. Run the recheck in order: head position first, then the mask seal, then a look for something needing suction, then two providers on the mask, and only then a supraglottic airway if the patient meets the indications. Gastric distention compounds while you work, because a full stomach pushes the diaphragm up, which makes the chest harder to ventilate, which tempts you to squeeze harder, which puts more air in the stomach. One provider trying to seal, hold the jaw, and squeeze at the same time is the setup for exactly this, so getting a second set of hands on the mask is the next thing after the position and the seal.

Why the others are wrong

Squeeze the bag with more force on each breath: More force does move more air when the resistance is in the lungs, and the instinct when nothing is working is to do it harder. Force is what drives air into the stomach in the first place, and with a leaking seal and a partly closed airway the extra pressure takes the easier path every time.

Place a supraglottic airway device now: An advanced airway does solve a mask seal problem, and this patient may well end up with one. It sits at the end of the recheck list rather than the start, because head position and a seal are free, immediate, and fix this far more often than the device does.

Switch to a smaller mask and try the same breaths: Mask fit is a real cause of a leak, and matching the mask to the face is part of doing this well. A smaller mask on an adult face usually leaks more rather than less, and changing equipment before you have corrected the head position skips the step that fixes most of these.

Question 4 of 10

An AEMT is ventilating a 60-year-old patient who has a supraglottic airway in place after a drug overdose, and the patient has a strong pulse at 88 with a blood pressure of 122/74 mmHg. Over ten minutes the end-tidal carbon dioxide has drifted from 38 mmHg down to 23 mmHg. The waveform is still a clean rectangle that returns to the baseline, chest rise is good, and the partner on the bag is squeezing about every 3 seconds. What should the AEMT do?

Show the answer and rationale

Correct answer · Slow the rate to 10 breaths per minute

Read a capnogram in two parts and it stops being intimidating. The shape tells you about the airway and the lungs, and a clean rectangle that returns to the baseline says both are fine. The height tells you about ventilation and perfusion, and a number that falls while the shape holds means carbon dioxide is leaving faster than the body is making it. Ventilating too fast is the most common cause of that, and a squeeze every 3 seconds is 20 breaths a minute in an adult who should be getting 10. Slow to 10 breaths a minute, which is one every 6 seconds, and the number should climb back toward the normal range of 35 to 45 mmHg. Falling perfusion also drives the number down, which is why you check the rate first: when the rate is correct, the concern becomes how much blood is reaching the lungs.

Why the others are wrong

Give an isotonic crystalloid bolus for poor perfusion: A low carbon dioxide number really can mean less blood is reaching the lungs, and that is the second cause on the list worth knowing. This patient has a strong pulse at 88 and a blood pressure of 122/74, so perfusion is not what changed, and the rate in front of you explains the number without adding fluid.

Remove the device and ventilate with a BVM: Pulling a device when the capnogram changes is a habit that saves patients at the confirmation moment. The rule for removing a device belongs to a waveform that never establishes itself or one that disappears, and this tracing is a clean rectangle with good chest rise, which means the device is doing its job.

Increase the oxygen flow running to the bag: More oxygen feels like a safe move whenever a number on the monitor is heading the wrong way. Oxygen flow sets the concentration in the bag and has no effect on the carbon dioxide number, which is driven by how much air you move and how much blood reaches the lungs.

Question 5 of 10

An AEMT is treating a 68-year-old patient with a history of chronic obstructive pulmonary disease (COPD) who has difficulty breathing. The patient is on oxygen by NRB at 15 liters per minute, and the SpO₂ has risen from 82% to 86%. The patient's usual saturation is not known. A crew member states that the oxygen should be turned down to protect the patient's drive to breathe. Which action does the AEMT take?

Show the answer and rationale

Correct answer · Continue oxygen and titrate toward an SpO₂ of 88% to 92%

Hypoxia is the emergency in front of you. An SpO₂ of 86% means this patient is still short of oxygen, and oxygen is never withheld or reduced in a hypoxic patient, whatever the history says. A patient with COPD gets oxygen titrated toward that patient's own baseline saturation, and when the baseline is unknown, 88% to 92% is the working proxy target. Titrating means adjusting the flow to reach that window as the saturation climbs, which is a different action from pulling oxygen back because of what someone on the crew believes about the drive to breathe.

Why the others are wrong

Reduce the oxygen flow to protect the drive to breathe: This is the belief the crew member voiced, and it is the one you do not act on. Oxygen is never withheld or reduced in a hypoxic patient, and at 86% this patient is hypoxic, so cutting the flow treats a theory instead of the number in front of you.

Switch the patient to a nasal cannula at 2 liters per minute: A blanket rule that a patient with COPD gets low flow no matter what the saturation reads is common enough to carry into this question. Titration follows the saturation rather than the diagnosis, and dropping a hypoxic patient to 2 liters per minute is a reduction dressed up as a device change.

Continue oxygen until the SpO₂ reaches 100%: Running oxygen until the number reads 100% treats more as always better and ignores the target entirely. The window you are titrating toward is 88% to 92% when the baseline is unknown, and driving straight past it means you never titrated at all.

Question 6 of 10

A trauma patient in shock has significant hypoxia and is breathing adequately on their own. The AEMT applies an NRB at 15 L/min. Five minutes later the oxygen saturation remains at 85% with no change in the patient's breathing effort. What is the most appropriate next action?

Show the answer and rationale

Correct answer · Assist ventilations with a BVM, synchronized with the patient's breathing

The deciding finding is the oxygen saturation of 85% after five full minutes on a nonrebreather at 15 L/min, unchanged despite maximal passive FiO2. That tells you the problem isn't lack of inspired oxygen, it's inadequate alveolar ventilation and gas exchange; passive flow alone can't force enough oxygen across the alveolar membrane. Assisting with a BVM timed to the patient's own inspiratory effort increases tidal volume and alveolar recruitment, which raises oxygenation where more passive flow cannot. This shifts the priority from supplemental oxygen to active ventilatory support.

Why the others are wrong

Continue the NRB unchanged and reassess again in five minutes: Reassessing in five minutes is the right move when an intervention hasn't been given time to work, but this patient already had five full minutes at maximal NRB flow with the saturation still at 85%. Repeating the same unchanged step delays the ventilatory support the failed trial already tells you this patient needs.

Switch to a nasal cannula, which delivers a lower oxygen concentration: A nasal cannula is the right call for a patient needing a lower, titratable FiO2, such as a stable COPD patient. An oxygen saturation of 85% after maximal NRB flow calls for more ventilatory support, not a device that delivers less oxygen.

Withhold further intervention, since the patient is still breathing on their own: Adequate spontaneous respiratory effort justifies withholding ventilatory support only when oxygenation is also adequate. The saturation of 85% despite maximal passive oxygen shows the breathing effort present isn't achieving adequate gas exchange, so it answers the rate question, not the oxygenation question this scenario asks.

Question 7 of 10

An AEMT administers nebulized albuterol to a wheezing asthma patient. After the treatment, the wheezing is louder and more audible than before, and the patient reports easier breathing with an improved capnography waveform. How should the AEMT interpret this change?

Show the answer and rationale

Correct answer · The patient is moving more air than before, consistent with improvement

The deciding finding is that the wheeze got louder while the patient reports easier breathing and the capnography waveform improves. Wheezing is turbulent airflow moving through narrowed bronchioles; when airflow stops almost completely, as in a silent chest, there is not enough turbulence left to hear anything at all. Albuterol relaxes bronchial smooth muscle, so more air is now pushing through those airways than before, and that increased flow is what makes the sound louder. This tells the AEMT the treatment is working, so you continue the current plan and reassess rather than escalating or withholding further nebulized doses.

Why the others are wrong

The patient is deteriorating and bronchospasm is worsening: A worsening bronchospasm would drive airflow down, not up, so the wheeze would trend quieter or disappear entirely as the airway closes, the opposite of what the patient's report and capnography waveform show here.

The louder wheeze indicates the treatment failed and a repeat dose is contraindicated: A louder wheeze can mean failure when it shows up alongside worsening distress or a flattening capnography trend, but here the patient reports easier breathing and the waveform is improving, so the louder sound reflects more air moving through opening airways, not less; treating this louder wheeze alone as failure ignores the two corroborating findings and would wrongly block a needed repeat dose.

The change is unrelated to the treatment and should be disregarded: The wheeze changed immediately after nebulized albuterol and lines up with the patient's subjective report and the capnography trend, so this is a treatment effect to track, not noise to dismiss.

Question 8 of 10

A 60-year-old patient reports sudden onset of difficulty breathing and sharp pleuritic chest pain that began at rest, two weeks after knee replacement surgery. Lung sounds are clear and equal bilaterally. The pulse oximeter reads 88% despite high-concentration oxygen. Capnography shows a low EtCO₂ with a normal waveform shape in a tachypneic patient. Which condition is most consistent with this presentation?

Show the answer and rationale

Correct answer · Pulmonary embolism

Split sudden difficulty breathing into the causes that change the lung sounds and the causes that do not. This patient's lungs are clear and equal, which throws out most of the airway and fluid causes in one move. Two weeks out from a knee replacement is the risk factor that matters: immobility after lower-extremity surgery is how a deep vein thrombosis forms, and a piece of that clot lodging in the pulmonary circulation blocks blood flow to alveoli that are still being ventilated. That is why the oxygen barely helps: the alveoli are fine, the blood is not reaching them, and it is why capnography shows a low EtCO2 with a normal waveform shape in a patient who is breathing fast: she is ventilating dead space, moving air past capillaries with no perfusion to unload CO2 into. Clear lungs plus hypoxia that ignores high-concentration oxygen plus a low number with a preserved waveform shape is the clinching combination.

Why the others are wrong

Asthma exacerbation: Asthma is the right call when the patient has audible wheezing, a prolonged expiratory phase, and a capnogram with the classic shark-fin upslope from uneven emptying of obstructed airways. Here the lung sounds are clear and equal and the waveform shape is normal, so there is no bronchoconstriction to hear or to see on the capnogram. Asthma also tends to trap CO2 and drive EtCO2 up as the patient tires, rather than down while the waveform stays square.

Bacterial pneumonia: Pneumonia fits the patient who has been building fever, a productive cough, and focal rhonchi or diminished sounds over a day or two, because it takes time to consolidate a lobe. This onset was sudden and at rest, and the lung sounds are clear and equal bilaterally: an infection dense enough to drag a saturation down to 88% would be audible. Pulmonary embolism is the sudden-onset, clear-lung version of hypoxia, which is what this question describes.

Cardiogenic pulmonary edema: the answer when the left ventricle backs fluid up into the alveoli: crackles from the bases upward, orthopnea, often a heart-failure history. Fluid in the alveoli is loud, and clear, equal breath sounds are the single finding that rules it out here. The pleuritic pain and the postoperative immobility both point back toward a clot rather than a failing pump.

Question 9 of 10

An AEMT applies CPAP to a patient in cardiogenic pulmonary edema. Two minutes later, the patient's blood pressure has dropped from 158/92 mmHg to 96/60 mmHg, and the patient appears more lethargic. What should the AEMT do?

Show the answer and rationale

Correct answer · Reassess perfusion, and remove CPAP if hypotension or mental status decline persist

The blood pressure drop from 158/92 to 96/60 paired with new lethargy is the finding that decides this. CPAP raises intrathoracic pressure, which reduces preload and venous return to the right heart, dropping cardiac output and cerebral perfusion, and this effect intensifies as pressure rises. The AEMT's job is to keep reassessing perfusion and mental status after each CPAP adjustment; if the hypotension or lethargy does not resolve, CPAP has to come off or be turned down before it causes a bigger perfusion failure than the pulmonary edema itself.

Why the others are wrong

Increase the CPAP pressure setting to further reduce the work of breathing: This treats CPAP as a dial to turn up whenever breathing looks labored, but here the problem is the pressure already applied is dropping venous return, so more pressure drives the blood pressure and mental status down further.

Continue CPAP unchanged, since a pressure drop is an expected and desirable response: A blood pressure fall to 96/60 with lethargy is not the goal of CPAP, it is a hemodynamic complication from reduced preload that has to be caught and corrected, not tolerated as normal.

Immediately give a rapid isotonic fluid bolus without reassessing first: A fluid bolus may end up being the right call for preload-dependent hypotension, but giving it before reassessing skips the step of confirming CPAP is the cause and whether removing it alone resolves the drop, and a rapid isotonic bolus also risks worsening pulmonary edema in a cardiogenic failure patient.

Question 10 of 10

A 79-year-old patient has had three days of fever, chills, and a cough productive of thick sputum, with difficulty breathing that has worsened today. Rhonchi are heard in the right lower lung field only, and the remaining lung fields are clear. There is no jugular venous distention and no swelling of the ankles. The T is 102.4°F. The vital signs are BP 118/70, P 110, R 26, and SpO₂ 90% on room air. Which condition is most consistent with this presentation?

Show the answer and rationale

Correct answer · Bacterial pneumonia

Three days of fever and chills with a cough producing thick sputum is an infectious time course, not a cardiac or vascular one. The clinching finding is where the abnormal sound lives: rhonchi in the right lower field only, with every other field clear. Infection consolidates a segment of lung, so it produces localized findings, while pressure-driven and airway-driven causes of difficulty breathing act on both lungs at once. The temperature of 102.4°F is the finding that nothing else on this list explains at all. The hypoxia at 90% comes from blood flowing past alveoli that are filled with inflammatory debris instead of air, so it never picks up oxygen.

Why the others are wrong

Cardiogenic pulmonary edema: right for the patient whose left heart is failing and backing pressure up into the lungs: crackles in both bases, jugular venous distention, pedal edema, often orthopnea and a known heart failure history. This question specifically states there is no jugular venous distention and no ankle swelling, and the abnormal sounds are confined to one side. Both conditions fill alveoli with fluid, but the key's fluid is infectious exudate in one lobe with a fever driving it, and back-pressure edema does not produce a temperature of 102.4°F.

Pulmonary embolism: right for sudden difficulty breathing with clear lungs, often pleuritic chest pain and hypoxia out of proportion to the exam, in a patient with a risk factor such as recent immobility, surgery, or a known clot. Here the onset was gradual over three days and the cough is productive of thick sputum, neither of which a clot causes. Both give tachycardia and hypoxia, but the key accounts for the fever and the focal rhonchi, and a clot accounts for neither.

Asthma exacerbation: right for wheezing heard throughout both lung fields, produced by diffuse bronchoconstriction, usually with a known asthma history and an identifiable trigger. Obstruction is a whole-airway problem, so it cannot confine itself to one lower lobe while the rest of the chest stays clear. That pattern argues directly against it. Asthma also does not cause fever or purulent sputum, which are the two findings the key is built on.

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