10 free Paramedic practice questions: Sepsis and Septic Shock

As a maintenance drip only, with the pressure watched closely: A slow drip is tempting as a compromise between doing nothing and doing harm. Maintenance rates do not move an intravascular deficit, so the patient stays underfilled while the clock runs.

As a full 30 mL/kg bolus run in as fast as the line allows: The standard volume is tempting because it is the number quoted for sepsis everywhere. Pushed into a failing heart without reassessment it fills the lungs, and the patient trades one problem for another.

Not at all, moving straight to a vasopressor instead: Skipping fluid is tempting because the crackles make every drop feel dangerous. Heart failure patients get smaller volumes, not zero, and a vasopressor squeezing an empty tank does not fix the volume deficit underneath.

Give another 30 mL/kg of isotonic crystalloid: More fluid is tempting because the first round is the standard and the lungs are still clear. Once an adequate volume has gone in and the pressure has not followed, the remaining problem is vascular tone, and tone does not respond to volume.

Start a dopamine infusion titrated to the pressure: Dopamine is tempting because it is a familiar pressor that many services still carry. At an equivalent degree of pressure support it produces more tachydysrhythmia than norepinephrine, which is why norepinephrine is first line here.

Give push-dose epinephrine every 2 minutes during transport: Push-dose epinephrine is tempting because it works fast and is easy to prepare. It is a bridge for a short gap, not a substitute for an infusion in a patient whose hypotension is going to persist for the whole trip.

A heart rate of 128 rather than a normal heart rate: A heart rate of 128 fits bleeding perfectly well. Tachycardia is the body compensating for poor perfusion, and it does that no matter which mechanism caused the poor perfusion.

Flat neck veins rather than distended neck veins: Flat neck veins are real and they matter, but they point at both candidates at once. Bleeding empties the system and sepsis enlarges the container, and either one leaves the neck veins flat.

A systolic pressure of 82 rather than a normal pressure: A systolic of 82 is exactly what significant blood loss produces. The number tells you the patient is in shock, which you already knew, and it does not tell you which kind.

A capillary refill of 4 seconds: Delayed capillary refill tells you perfusion is poor, which is true in both conditions. It confirms shock without telling you which container problem you are looking at.

A systolic pressure of 80: A systolic of 80 is the definition of the problem, not the discriminator. Septic shock reaches that number just as readily as neurogenic shock does.

A respiratory rate of 24: A rate of 24 fits sepsis better than neurogenic shock, since a septic patient is often breathing fast to compensate for acidosis. Choosing it moves you toward sepsis, not away from it.

One liter of isotonic crystalloid run wide open without interruption: A liter is in the right neighborhood for a first increment, so the volume is not the error. Running it wide open without interruption throws away the reassessment that tells you when to stop.

A single 250 mL bolus, then transport with no further fluid: A 250 mL increment is a legitimate way to titrate fluid where protocol calls for small steps. Stopping there in a hypotensive septic patient leaves most of the weight-based volume ungiven.

Fluid withheld until the systolic pressure falls below 70: Waiting for a systolic below 70 waits for compensation to fail completely. A systolic of 84 with suspected sepsis is already the point at which weight-based fluid is indicated.

Add a second line and run fluid through both sites at once: A second line gives you faster delivery and a backup route, which is worth having. Doubling the rate of delivery is the opposite of what new crackles are asking for.

Increase the fluid rate so the pressure comes up faster: Raising the rate is the instinct when the pressure is still low, and the pressure probably is still low. Pushing harder against a chest that is already filling makes the oxygenation worse without improving perfusion.

Continue the same fluid rate and recheck the lungs at the hospital: Continuing at the same rate treats the crackles as background noise. They are the one finding that tells you the next increment will land in the lungs rather than the circulation.

Beta-2 stimulation that relaxes bronchial smooth muscle: Beta-2 opens airways, which is the property you want in bronchospasm. Nothing about it addresses a dilated vascular bed, and norepinephrine has little beta-2 activity to offer anyway.

Beta-1 stimulation that raises heart rate and contractile force: Beta-1 raises rate and force, and norepinephrine does carry some. The problem left after adequate fluid is not a weak pump, it is a vascular bed that will not hold pressure around the volume already given.

Dopaminergic dilation that preserves renal and mesenteric flow: Dopaminergic effects dilate renal and mesenteric beds, and preserving kidney flow sounds appealing in a septic patient. Dilation is the wrong direction entirely when the problem is that everything is already dilated.

Sedate without a paralytic to slow the respiratory rate down: Sedation without paralysis feels like the gentler option, and it avoids the tube. Slowing the rate is the specific harm you are trying to avoid, since the rate is doing necessary work.

Begin positive pressure ventilation at 20 breaths per minute: Positive pressure at 20 breaths per minute delivers less minute volume than the patient is generating alone, so the carbon dioxide climbs. It also raises chest pressure in an underfilled patient and cuts venous return.

Perform rapid sequence intubation before the rate climbs further: Intubating early to get ahead of a deteriorating airway is sound thinking in many presentations. Here it removes the respiratory compensation that is holding the pH survivable while simultaneously dropping the preload.

Ventilate to an EtCO₂ target of 45 mmHg to correct the low value: Driving toward a normal-looking EtCO₂ treats the number as the goal. The low value reflects the acidosis and the perfusion state, and ventilating down to a normal reading means underventilating the patient.

Ventilate at 8 breaths per minute with a large tidal volume: Eight breaths with a large tidal volume attempts to recover the volume through depth. Large volumes injure septic lungs, and the minute volume still falls far short of what the patient was generating.

Ventilate at 10 breaths per minute to allow full exhalation: Ten breaths per minute is a reasonable default in most intubated adults, and allowing full exhalation matters in obstructive disease. Here it delivers roughly a third of the minute volume this patient needed to stay compensated.

Perform rapid sequence intubation to protect the airway: Intubating because the rate is high removes the patient's own compensation for the metabolic acidosis, and induction plus positive-pressure ventilation can produce peri-intubation collapse in a volume-depleted septic patient; resuscitation comes first.

Assist ventilations with a BVM: Breath sounds are clear with no increased work of breathing, so there is no indication that ventilation is inadequate, substituting assisted ventilation for an effective compensatory drive removes that compensation the same way intubation would.

Administer a sedative to reduce the respiratory rate: A sedative blunts the same compensatory respiratory drive that is keeping the metabolic acidosis compensated, and it does nothing to correct the volume depletion and hypotension actually driving the tachypnea.