10 free Paramedic practice questions: Critical Care Concepts

The heart rate of 124 with a soft blood pressure: A heart rate of 124 with a blood pressure of 98/60 shows up in a large PE from right heart strain and obstructive shock, and it shows up just as easily in a dehydrated, acidotic patient, so it fits both causes and sorts neither.

The respiratory rate of 32 with clear lungs: A respiratory rate of 32 with clear, equal lung sounds is the shared presentation that put both diagnoses on the table, Kussmaul breathing in metabolic acidosis and compensatory tachypnea in PE, so it cannot be the finding that separates them.

The end-tidal carbon dioxide of 17 mmHg: An end-tidal carbon dioxide of 17 mmHg with a rectangular waveform confirms hyperventilation in both conditions, PE through dead space and acidosis through compensation, but a low number here never tells you which mechanism produced it.

The tube has migrated into the right mainstem bronchus: A tube slipping into the right mainstem bronchus is a real complication, usually presenting with rising peak airway pressure and breath sounds heard on the right but diminished on the left. Nothing in this stem reports unequal breath sounds or a pressure change, and mainstem migration shifts the gradient slowly, not in a two-breath collapse from 38 mmHg to 9 mmHg; that mismatch points to circulation, not tube position.

The patient has developed worsening bronchospasm: Worsening bronchospasm is real when airway resistance rises, and on a capnogram it slurs the upstroke into a shark fin shape while usually raising the number as air trapping builds. This waveform kept its clean rectangular shape and the value fell instead, the opposite pattern, so bronchospasm does not fit here.

The tidal volume setting has become too large: An oversized tidal volume can wash out carbon dioxide, but it does so gradually over several breaths as minute ventilation rises, and the vignette states the set rate and volume never changed. A two-breath fall to 9 mmHg is too abrupt for a ventilator setting problem and points to a circulation failure instead.

The patient's measured weight of 140 kg: Nearly every other drug and device you use is set from the weight on the scale, so reaching for 140 kg is the trained habit. Measured weight is the number that causes the harm here. It reflects tissue the lungs never gained, and using it hands you a dangerously large breath.

The average of measured weight and ideal body weight: Splitting the difference feels like the cautious answer when two numbers sit that far apart. Averaging still carries part of the error forward, and there is no such method. The calculation uses height and sex, full stop.

The weight the patient reports carrying a year ago: A patient who has gained recently might sound like a better match to the lungs they had, which is the reasoning here. A remembered weight from a year ago is still a scale weight, and a less reliable one. Lung capacity did not change when the number did.

Increase the rate to clear the rising carbon dioxide: Rising carbon dioxide in status asthmaticus is expected and usually tolerated through permissive hypercapnia, so speeding the rate to blow it off looks reasonable, but the pressure of 84/56 only recovered once exhalation was allowed to finish, showing air trapping, not ventilation, is the problem; a faster rate shortens expiratory time and rebuilds the same trap that just dropped the pressure.

Increase the positive end-expiratory pressure setting: Extra PEEP is the fix for atelectasis or refractory hypoxemia from shunting, not for a patient whose pressure only climbed back up when the circuit was opened and pressure released; adding PEEP raises intrathoracic pressure again and recreates the same obstruction to venous return that just caused the hypotension.

Increase the tidal volume and leave the rate unchanged: A bigger tidal volume is used to fix hypoventilation from an inadequate breath, but this patient already cannot exhale the volume he's getting, evidenced by the pressure recovering only after passive exhalation was allowed; a larger volume still must exit the same narrowed airways and worsens the trapping that dropped his pressure.

Obtain a plateau pressure with an inspiratory hold: Obtaining a plateau pressure with an inspiratory hold separates high airway resistance from low compliance once a patient is stable on the vent, reading pressure at end-inspiration. With the SpO₂ already falling, running that measurement first delays the action that restores oxygenation, so it waits until after you bag the patient by hand.

Silence the alarm and raise the oxygen concentration: Silencing the alarm and raising the oxygen concentration is the reflex when the alarm feels like the problem, but the alarm is only reporting the high pressure, not causing it, and more oxygen does nothing for the falling SpO₂ if air isn't reaching the alveoli. This treats the warning, not the obstruction, displacement, or pneumothorax behind it.

Increase the inspiratory flow rate on the ventilator: Increasing the inspiratory flow rate is a real fix for flow starvation and patient-ventilator asynchrony, adjusted through the machine's settings. It assumes the ventilator itself is the source of the trouble, which you haven't established yet, and turning that dial while the chest is hard to ventilate wastes time better spent bagging the patient by hand.

Increase the positive end-expiratory pressure: Positive end-expiratory pressure recruits alveoli to fix oxygenation, and this patient's SpO₂ of 97% with equal breath sounds and normal pressures gives you nothing to recruit.

Increase the fraction of inspired oxygen: A higher fraction of inspired oxygen treats hypoxemia, not the retained carbon dioxide driving this acidosis, and an SpO₂ of 97% shows oxygenation was never the problem.

Reduce the tidal volume and accept the pH: Dropping tidal volume and tolerating the pH is permissive hypercapnia, a real strategy for lung-protective ventilation when airway pressures are high and you're fighting ARDS-type lung injury; this patient's airway pressures are normal and nothing points to that picture, so shrinking the breath only lowers minute ventilation further, pushes the PaCO₂ higher, and drives the pH down instead of fixing it.

Accept the saturation and continue the current settings: Accepting 86% treats the number as fixed when a proven, untried lever (PEEP) is still available, so this leaves the patient hypoxic on purpose instead of correcting the shunt.

Increase the tidal volume to recruit more alveoli: Increasing tidal volume looks like more recruitment, but the volume is already set to the lung-protective target for ideal body weight, and pushing it higher with a plateau already at 22 cm H₂O risks volutrauma while doing nothing for the collapsed alveoli driving the shunt.

Increase the respiratory rate to improve oxygen delivery: A faster rate raises minute ventilation, but the EtCO₂ of 41 mmHg with a normal waveform shows ventilation isn't the failing job here, so adding breaths doesn't reopen collapsed alveolar units.

Falling compliance from developing pulmonary edema: Pulmonary edema is a real transport complication, fluid moving into the alveoli stiffens the lung and shows up as a rising peak with a rising plateau, since both track compliance and climb by roughly the same amount together. That is not what happened here: the plateau held flat at 20 cm H₂O while only the peak rose, which points to the pathway narrowing rather than the lung stiffening.

Overdistension from an excessive tidal volume: Excessive tidal volume overdistends alveoli and drives the plateau pressure up along with the peak, because overdistension is a compliance problem measured at zero flow. The plateau's staying at 20 cm H₂O rules that out directly.

A tension pneumothorax on the right side: A tension pneumothorax raises both peak and plateau pressure and drops the blood pressure with unilateral absent breath sounds, none of which appear here, since sounds are equal, the trachea is midline, and the pressure is stable.

Give corticosteroids to limit the chemical lung injury: Corticosteroids get chosen because gastric acid does chemically burn the alveolar lining, but trials of steroid use after witnessed aspiration show no improvement in oxygenation, so a drug that doesn't clear fluid or open alveoli won't move the SpO2 off 87%.

Instill sterile water through the tube and suction it back: Instilling sterile water and suctioning it back is legitimate for loosening thick, tenacious mucus plugs, and it can look tempting since suctioning already returned material from the tube, but the alveoli here are flooded with gastric acid, not blocked by mucus, so more fluid worsens the chemical injury and interrupts ventilation instead of fixing the shunt behind the 87% saturation.

Start antibiotics before signs of pneumonia develop: Antibiotics belong to an aspiration pneumonia that develops later, marked by fever, a new infiltrate, or purulent sputum, not to the acute hypoxia in front of you now; starting them here treats an infection that hasn't happened and does nothing for the SpO2 of 87%.

Increase the rate to lower the carbon dioxide: A rising rate seems like the fix for tachycardia, but the EtCO2 of 38 mmHg on a clean rectangular waveform already shows ventilation is adequate, so this treats a breathing problem the numbers don't support instead of the sedation gap behind the vital signs.

Check the tube depth and withdraw it 2 cm: Withdrawing the tube fits a picture of a mainstem intubation, where breath sounds go unequal and airway pressures climb, but this patient has equal breath sounds and unchanged pressures, so pulling a tube that capnography and lung sounds confirm is well placed only risks losing the airway.

Give a repeat dose of the paralytic agent: Repeating the paralytic looks right when tachycardia and hypertension suggest the block is wearing off, since rocuronium can run shorter than etomidate's sedation, but the ventilator cycles normally and pressures stay unchanged, showing no fight against the tube; the tearing eyes and autonomic surge signal awareness, not resistance. Deepening the block masks those reflexes without restoring the missing sedation.