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Free NREMT practice questionsFree Paramedic practice questions · Medical/Obstetrics/Gynecology

7 free Paramedic practice questions: Critical Care Concepts

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.

Work through all 7, then move on to the next topic. When you want the full picture, the free Paramedic diagnostic covers every topic in one sitting. No account needed for any of it.

Question 1 of 7

A 46-year-old patient reports difficulty breathing that has worsened over the past day. Breathing is deep and regular at a rate of 32, and lung sounds are clear and equal in all fields. The vital signs are BP 98/60, P 124, R 32, and SpO₂ 99% on room air, with EtCO₂ 17 mmHg and a rectangular waveform. Which finding most strongly separates a metabolic cause from a pulmonary embolism here?

Show the answer and rationale

Correct answer · The oxygen saturation of 99% on room air

This patient's deep, regular breathing at 32 is Kussmaul breathing from a metabolic acidosis. The SpO₂ of 99% on room air is what separates a metabolic cause from a pulmonary embolism. A saturation that high tells you the alveoli are exchanging gas normally. A pulmonary embolism blocks blood flow to alveoli that are still getting air. The blocked flow creates dead space, where air reaches the alveoli but blood does not. This mismatch between air and blood flow drops the saturation, and extra oxygen does not fix the low saturation well. A metabolic acidosis leaves the lungs alone. The body breathes deep and fast to blow off carbon dioxide and buffer the acid. Gas exchange stays normal, so the saturation stays normal. A normal saturation on room air points you toward a metabolic acidosis, and then you look for its cause.

Why the others are wrong

The heart rate of 124 with a soft blood pressure: A heart rate of 124 with a blood pressure of 98/60 fits a large pulmonary embolism straining the right side of the heart. The same vital signs show up in a patient who is dehydrated and acidotic. Vital signs that fit both causes cannot separate them.

The respiratory rate of 32 with clear lungs: A respiratory rate of 32 with clear, equal lung sounds is why both causes are possible here. In metabolic acidosis, the fast, deep rate is Kussmaul breathing. With a pulmonary embolism, the body breathes fast to compensate. A finding both causes share cannot tell them apart.

The end-tidal carbon dioxide of 17 mmHg: An end-tidal CO₂ of 17 with a rectangular waveform shows the patient is blowing off extra carbon dioxide. A pulmonary embolism lowers the end-tidal CO₂ through dead space. With a metabolic acidosis, the number drops from the fast breathing that compensates for the acid. The low number does not tell you which problem caused it.

Question 2 of 7

An intubated 58-year-old patient is being ventilated on a transport ventilator at a set rate of 12. The capnogram has held a rectangular shape at 38 mmHg for the past 20 minutes. Over two breaths the EtCO₂ falls to 9 mmHg while the waveform keeps its rectangular shape, the set rate is unchanged, and the circuit is intact and cycling normally. Which problem does this change point to?

Show the answer and rationale

Correct answer · The patient has lost effective circulation

This patient has lost effective circulation. The EtCO₂ fell from 38 mmHg to 9 mmHg over two breaths. The waveform kept its rectangular shape, the ventilator rate stayed at 12, and the circuit is intact. Carbon dioxide only reaches the alveoli when blood carries it there from the tissues. The ventilator and the circuit are working the same as before. When the carbon dioxide suddenly drops out, blood flow through the lungs has collapsed. Cardiac arrest, a massive pulmonary embolism, or profound shock can cause that collapse. Stop adjusting the ventilator and check a pulse right away. You are dealing with a perfusion failure, not an airway problem.

Why the others are wrong

The tube has migrated into the right mainstem bronchus: A tube that slips into the right mainstem bronchus usually raises the peak airway pressure. You would hear breath sounds on the right and diminished breath sounds on the left. Nothing in this question mentions unequal breath sounds or a pressure change. Mainstem migration also changes the EtCO₂ slowly, not with a drop from 38 mmHg to 9 mmHg in two breaths.

The patient has developed worsening bronchospasm: Worsening bronchospasm happens when airway resistance rises. On the capnogram, the upstroke slurs into a shark fin shape, and the number usually goes up as air gets trapped. This waveform stayed rectangular, and the number fell.

The tidal volume setting has become too large: A tidal volume that is too large can wash out carbon dioxide. The EtCO₂ falls gradually over several breaths as the minute ventilation rises. In this question the set rate is unchanged and the circuit is cycling normally. A drop to 9 mmHg in two breaths is too abrupt for a ventilator setting problem.

Question 3 of 7

A 44-year-old patient who weighs 140 kg and stands 165 cm tall has been intubated for acute respiratory failure and is being placed on a transport ventilator. The crew is setting the initial tidal volume. On which weight should that setting be based?

Show the answer and rationale

Correct answer · The ideal body weight calculated from height and sex

Base the tidal volume on the ideal body weight from height and sex. Lungs do not grow when a patient gains weight. Lung size follows the size of the skeleton. That's why the lung-protective tidal volume comes from ideal body weight, and ideal body weight comes from height and sex. This patient is 165 cm tall and weighs 140 kg. If you set the volume from the 140 kg, each breath can be close to double what these lungs hold. Breaths that big overstretch the alveoli and injure them with every cycle. Going too small is not safe either, because small breaths waste more of each breath on dead space.

Why the others are wrong

The patient's measured weight of 140 kg: Most drugs and devices you use are set from the weight on the scale, which is 140 kg here. For a ventilator, the measured weight is the number that causes harm. The extra weight is tissue the lungs never gained. Using 140 kg gives this patient a dangerously large breath.

The average of measured weight and ideal body weight: Averaging the two weights looks careful when they are that far apart. The average still carries part of the error forward. No ventilator method averages the weights. The calculation uses height and sex only.

The weight the patient reports carrying a year ago: A weight from a year ago is still a scale weight, and a less reliable one than today's. This patient's lungs did not change size when the weight changed. Only height and sex set the ideal body weight.

Question 4 of 7

An intubated 34-year-old patient with a severe asthma exacerbation is on a transport ventilator at a set rate of 20. The vital signs are BP 84/56, P 132, R 20, and SpO₂ 90% on the ventilator. Breath sounds are equal and the trachea is midline. The crew disconnects the circuit, allows full passive exhalation, and the blood pressure improves immediately. Which ventilator change is most appropriate before reconnecting?

Show the answer and rationale

Correct answer · Lower the rate and lengthen the expiratory time

This patient has breath stacking, also called dynamic hyperinflation, from a severe asthma attack. The blood pressure is 84/56, and it came back up the moment the crew disconnected the circuit and let the patient fully exhale. The narrowed airways cannot empty before the ventilator gives the next breath. Air gets trapped in the chest, and the pressure inside the chest climbs. That pressure squeezes the vena cava, so less blood gets back to the heart and the cardiac output drops. This is obstructive shock from trapped air, not from blood loss. If you reconnect at the same rate of 20, the air traps again within seconds. Lower the rate and lengthen the expiratory time. The narrowed airways then have time to empty before the next breath. The carbon dioxide will run higher, and the blood pressure stays up.

Why the others are wrong

Increase the rate to clear the rising carbon dioxide: A rising carbon dioxide level is expected in a severe asthma attack, and it is usually tolerated. That is called permissive hypercapnia. The blood pressure only recovered once the patient could finish exhaling, so trapped air is the problem here. A faster rate shortens the time to exhale and traps even more air.

Increase the positive end-expiratory pressure setting: More PEEP is the fix for collapsed alveoli or a low oxygen level that will not come up. This patient's blood pressure climbed back only when the circuit was opened and the pressure was let off. Adding PEEP puts pressure back into the chest and blocks blood return to the heart again.

Increase the tidal volume and leave the rate unchanged: A bigger tidal volume helps a patient whose breaths are too small. This patient already cannot get out the volume being given now. You know that because the pressure came back only after passive exhalation. A larger breath still has to leave through the same narrowed airways, and it makes the trapping worse.

Question 5 of 7

An intubated patient on a transport ventilator suddenly becomes difficult to ventilate. The high pressure alarm is sounding and the SpO₂ is falling. Which action should be taken first?

Show the answer and rationale

Correct answer · Disconnect the ventilator and ventilate by hand with a BVM

Disconnect the ventilator and ventilate the patient by hand with a bag-valve mask. The high pressure alarm is sounding and the SpO₂ is falling, so gas exchange is failing right now. The problem is either in the tube and lungs or in the ventilator and circuit. Taking the ventilator off is the only way to tell which one. If the bag stays tight and hard to squeeze, think about a displaced tube, a blocked tube or airway, or a pneumothorax. If the bag moves air easily, the ventilator or the circuit is the problem. Bagging by hand gets oxygen into the patient right away and shows you where the problem is.

Why the others are wrong

Obtain a plateau pressure with an inspiratory hold: A plateau pressure with an inspiratory hold reads the pressure at the end of inspiration. On a patient who is stable on the ventilator, a plateau pressure helps you tell high airway resistance from low compliance, which means stiff lungs. This patient's SpO₂ is already falling. Measuring the plateau pressure first delays the step that gets oxygen in. The measurement waits until after you bag the patient by hand.

Silence the alarm and raise the oxygen concentration: The alarm is only reporting the high pressure. Silencing the alarm does nothing about what is causing the high pressure, like a blocked tube, a displaced tube, or a pneumothorax. Raising the oxygen does not help the falling SpO₂ if air is not reaching the alveoli.

Increase the inspiratory flow rate on the ventilator: Increasing the inspiratory flow rate is a real fix for flow starvation and for a patient who is out of sync with the ventilator. Changing a ventilator setting assumes the ventilator is the source of the trouble. You have not ruled out the tube and the lungs yet. Changing the flow rate while the chest is hard to ventilate wastes time you should spend bagging the patient by hand.

Question 6 of 7

A patient who vomited during a seizure has been intubated. Suctioning through the tube returns gastric contents, and the SpO₂ stays at 87% on 100% oxygen. Breath sounds are equal, the trachea is midline, and the vital signs are BP 132/80, P 118, R 16 on the ventilator, with EtCO₂ 44 mmHg. Which management approach is most appropriate?

Show the answer and rationale

Correct answer · Continue suctioning and apply positive end-expiratory pressure

Keep suctioning and add PEEP. The SpO₂ stays at 87% on 100% oxygen. A saturation that low on 100% oxygen means blood is passing alveoli that are not exchanging gas. This is called a shunt. A shunt is not a ventilation problem, and more oxygen will not fix a shunt. Aspirated stomach acid destroys surfactant and floods the alveoli with fluid. The oxygen you deliver to the airway never reaches the blood in those capillaries. Suctioning removes the fluid you can reach. PEEP holds the flooded, collapsing alveoli open so the blood flowing past them can pick up oxygen.

Why the others are wrong

Give corticosteroids to limit the chemical lung injury: Gastric acid does chemically burn the alveolar lining, and corticosteroids are aimed at that burn. Studies of steroids after witnessed aspiration show no improvement in oxygenation. Steroids do not clear fluid or open alveoli, so steroids will not move the SpO₂ off 87%.

Instill sterile water through the tube and suction it back: Instilling sterile water and suctioning it back is used to loosen thick mucus plugs. These alveoli are flooded with gastric acid, not blocked by mucus. More fluid makes the chemical injury worse and interrupts ventilation.

Start antibiotics before signs of pneumonia develop: Antibiotics are for aspiration pneumonia, which develops later with fever, a new infiltrate, or purulent sputum. This patient's problem right now is acute hypoxia. Starting antibiotics treats an infection that has not happened and does nothing for the SpO₂ of 87%.

Question 7 of 7

Twelve minutes after an intubation facilitated by etomidate and rocuronium, a patient becomes tachycardic and hypertensive with tearing eyes. The SpO₂ is 98%, EtCO₂ is 38 mmHg with a rectangular waveform, breath sounds are equal, airway pressures are unchanged, and the ventilator is cycling normally. Which action is most appropriate?

Show the answer and rationale

Correct answer · Give sedation and analgesia per protocol

This patient is awake and aware while still paralyzed, and needs sedation and analgesia now. Twelve minutes after the intubation, the patient became tachycardic and hypertensive with tearing eyes. Every airway and ventilator number is normal. The SpO₂ is 98%, the EtCO₂ is 38 mmHg on a rectangular waveform, and breath sounds are equal. Airway pressures are unchanged and the ventilator is cycling normally. Etomidate is short acting, and its sedation has worn off. Rocuronium's paralysis lasts far longer. A paralytic has no sedative or pain relieving effect at all. The fast heart rate, the high blood pressure, and the tearing are the signs of a patient who is awake but cannot move or communicate. Give sedation and analgesia per protocol now. Keep redosing on schedule for as long as the paralysis lasts.

Why the others are wrong

Increase the rate to lower the carbon dioxide: Raising the rate lowers carbon dioxide, which helps when the carbon dioxide is high. An EtCO₂ of 38 mmHg on a clean rectangular waveform is normal, so ventilation is fine. Turning up the rate treats a breathing problem this patient does not have.

Check the tube depth and withdraw it 2 cm: Pulling the tube back fixes a tube that went too deep into the right mainstem bronchus. A right mainstem tube diminishes the breath sounds on the left. This patient has equal breath sounds and unchanged airway pressures. Withdrawing a well placed tube only risks losing the airway.

Give a repeat dose of the paralytic agent: More paralytic fits a patient whose paralysis is wearing off and who is fighting the ventilator. The ventilator is cycling normally and the pressures are unchanged, so this patient is not fighting the tube. Rocuronium is still working this early. The tearing and the jump in heart rate and blood pressure mean the patient is aware. A paralytic has no sedative effect, so more paralytic leaves the patient awake and paralyzed.

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