10 free Paramedic practice questions: Cardiogenic Shock and Decompensated Heart Failure

An allergic reaction to the CPAP mask material: An allergic reaction fits the fact that a device-related complication has occurred, but the question gives no hives, wheezing beyond the existing pulmonary edema, or facial or airway swelling to support anaphylaxis.

Resolution of the underlying pulmonary edema: Improved breathing sounds like the underlying heart failure has resolved, but pulmonary edema does not resolve within minutes, and the timing of the blood pressure drop matches a known effect of CPAP rather than resolution of disease.

Peak effect of a home antihypertensive medication taken earlier: A home medication is an easy thing to blame the change on, but the question gives no history of an antihypertensive medication, and the timing tied directly to CPAP use is a far stronger explanation.

Increased venous return that restores adequate cardiac preload: CPAP does affect hemodynamics, but in the opposite direction this option describes: raising intrathoracic pressure decreases venous return and lowers preload, which is actually beneficial in a fluid-overloaded left ventricle. That drop in preload helps cardiac performance, but the oxygenation improvement you're asked about comes from alveolar recruitment, not from restored venous return.

Relaxation of coronary artery smooth muscle that increases myocardial blood flow: This describes nitroglycerin, which relaxes vascular smooth muscle to dilate veins and coronary arteries and lower preload and afterload; nothing in the question points to a nitrate, and CPAP has no direct action on coronary smooth muscle.

Increased systemic vascular resistance that raises alveolar perfusion pressure: CPAP does not raise systemic vascular resistance, and raising SVR would increase afterload on a failing ventricle and worsen the pulmonary edema rather than improve alveolar perfusion pressure.

The narrow gap between the systolic and diastolic pressures: A narrowing pulse pressure shows up in tamponade, and it shows up in plenty of other low output states including a tension pneumothorax. It supports the picture without separating the two.

The heart rate of 132 alongside a systolic pressure of 84: A fast rate with a low pressure is the shock response itself. Every cause of obstructive shock produces it.

The distended neck veins in a hypotensive patient: Distended neck veins are the finding the two conditions share. Both raise the pressure the heart has to fill against, so both fill the neck veins.

The sudden onset of difficulty breathing at rest: Sudden onset should raise your suspicion for an embolism, but acute pulmonary edema can also build over minutes in a patient who was fine at dinner. Onset speed narrows your thinking without settling it.

The oxygen saturation of 86% on room air: Hypoxia is expected in a massive embolism and in pulmonary edema alike. The saturation tells you the patient needs oxygen now, not which side of the lung the problem sits on.

The heart rate above 130 with a systolic in the 70s: That rate and that pressure tell you the patient is in shock, which you already knew from looking at the patient. A finding that shows up in every category on the list cannot tell you which category you are in.

An early pneumonia settling into both bases: Two weeks of a changing body in a 68-year-old does invite an infectious explanation, and a tender right upper abdomen can read that way too. Pneumonia gives you a fever, a productive cough, and sounds in the affected lobe, and nothing here points to infection. Swollen ankles with full neck veins are a circulation finding rather than a lung finding.

Volume depletion from two weeks of poor intake: Shoes that stopped fitting is a two-week story, and two-week stories in older patients are often about eating and drinking less. A depleted patient has flat neck veins, because there is not enough volume to fill them. Distended neck veins and pitting edema say the volume is present and stuck in the wrong place.

Left-sided failure backing fluid into the lungs: You have the right organ here and the wrong side of it, which is the closest miss available. Left-sided failure puts the fluid in the alveoli, so you would hear crackles. This chest is clear in every field, which is the finding that sends you to the other side of the heart.

A single large bolus of isotonic fluid run wide open: You are right that this patient needs volume, so the direction is correct. Running it wide open takes away the reassessment that titration is built around, and there is still a left ventricle that can flood if you overshoot.

Sublingual nitroglycerin to open the vessels: Nitroglycerin drops preload by design, which is the single thing this ventricle cannot afford. Giving it to a patient in this pattern is the classic way to turn a soft pressure into a profound crash.

Supine positioning with the legs raised and nothing else: Raising the legs is harmless and it does move a little volume centrally, but it is not enough on its own for a pressure in the 80s, and it is not the treatment the pattern calls for.

Assist breathing with a BVM at 20 breaths per minute: A saturation of 84% with a rate of 34 is a patient who looks like someone should be breathing for them, and that read is worth having. The patient is alert, cooperative, and generating breaths without help, so the ability to do the work has not been lost. Positive pressure ventilation is where you go when that changes, not while the patient can still drive it.

Lay the patient supine and run a 500 mL fluid bolus: A systolic of 98 is low enough to pull you toward fluid, and laying a hypotensive patient flat is the reflex from every other kind of shock. Both halves are wrong for this patient. Fluid adds to a chest that is already flooded, and laying the patient flat takes away the gravity that is currently keeping some of that fluid out of the upper lungs.

Place an NRB at 15 liters per minute and transport: High flow oxygen is a reasonable first move while you set up, but it only offers a richer gas to breathe across a membrane that is soaked. Pressure is what moves the fluid, and pressure is what is missing.

Deepen sedation to stop the patient fighting the machine: Nothing here says the patient is fighting the ventilator, and sedatives lower blood pressure on their own. You would be adding a second cause of hypotension on top of the one you created.

Increase the set respiratory rate to 20: A faster rate moves more carbon dioxide, and carbon dioxide is not what changed. More breaths per minute also means more time spent at positive pressure, which pushes the blood pressure further down.

Decompress the left chest with a needle: Needle decompression is for a tension pneumothorax, and this patient has neither of its findings. Equal breath sounds with a midline trachea take that off the table before you reach for a needle.

The rising pulse is anxiety from the mask: A mask can make anyone anxious, so it is a fair thought. Anxiety does not cool the fingertips and slow capillary refill, and those two findings make this a perfusion trend rather than an emotional one.

The patient is responding well to the treatment: Only one number improved, and two got worse. A rising pulse with cooling skin is a patient working harder to hold the same ground, which is not the same as responding well.

The CPAP is no longer reaching the alveoli: The saturation rose from 88% to 91%, which means pressure is reaching the alveoli and doing what it is supposed to do. The lungs are the part of this picture that improved.

Administer a large-volume normal saline bolus: Hypotension and tachycardia alone often point toward hypovolemic shock, where a fluid bolus is the standard fix. Bilateral crackles and jugular venous distension, plus the note that volume status is not in question, rule that out here: the ventricle is failing, not empty, and a large bolus only floods lungs already backing up.

Withhold treatment until a 12-lead ECG is obtained: Obtaining a 12-lead helps find an infarct or dysrhythmia behind the pump failure, but this patient already shows hypotension and cool mottled skin from hypoperfusion, and withholding treatment for diagnostics delays the vasoactive support that needs to start now.

Administer a high-dose diuretic to reduce total body fluid: Crackles from pulmonary congestion make diuresis tempting, but lowering intravascular volume further in a patient who is already hypotensive drops perfusion pressure and worsens the shock instead of treating the pump failure causing it.