10 free AEMT practice questions: Ventilation and Oxygenation Support

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.

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.

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.

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 bag-valve-mask: 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.

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: Some students carry a blanket rule that a patient with COPD gets low flow no matter what the saturation reads. 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.

Continue the NRB unchanged and reassess again in five minutes: Repeating an intervention that has already failed to correct the hypoxia delays the escalation this patient needs.

Switch to a nasal cannula, which delivers a lower oxygen concentration: A nasal cannula delivers less oxygen than an NRB and would be a downgrade, not an escalation, for persistent hypoxia.

Withhold further intervention, since the patient is still breathing on their own: Adequate spontaneous breathing does not rule out inadequate oxygenation; the persistently low saturation despite maximal passive oxygen is the finding that drives escalation.

The patient is deteriorating and bronchospasm is worsening: Worsening bronchospasm would trend toward reduced air movement and a quieter or absent wheeze, not a louder one paired with subjective and capnographic improvement.

The louder wheeze indicates the treatment failed and a repeat dose is contraindicated: A louder wheeze here reflects improved air movement, so it does not indicate treatment failure.

The change is unrelated to the treatment and should be disregarded: The change directly follows the bronchodilator and correlates with two other objective/subjective improvement markers, so it should not be disregarded.

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 crackles 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.

Increase the CPAP pressure setting to further reduce the work of breathing: Increasing the pressure would worsen the reduction in venous return and further lower the blood pressure.

Continue CPAP unchanged, since a pressure drop is an expected and desirable response: A pressure drop after starting CPAP is a recognized complication to act on, not an expected or desirable therapeutic response.

Immediately give a rapid isotonic fluid bolus without reassessing first: Fluid may eventually be appropriate, but the immediate step is reassessment of the patient's response to CPAP before choosing a next intervention, not an unassessed bolus in a pulmonary edema patient.

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.