Nurse interview questions

I trust the subtle signs and escalate assessment before the vitals crash, because deterioration shows in trend and behavior first.

• New confusion, restlessness, or a climbing respiratory rate often precede a pressure drop by an hour.
• I widen the picture: recheck a full set, look at urine output, skin mottling, and the last few hours of trend, not one snapshot.
• If two systems are drifting the same direction I call the rapid response or the provider early rather than waiting for a hard number.

I check the patient before I chase the tracing, because how they tolerate the rhythm decides the urgency.

• Are they symptomatic: chest pain, hypotension, short of breath, altered? Unstable means I prep for synchronized cardioversion and call the provider now.
• Stable, I get a 12-lead, confirm it is new onset, review potassium and magnesium, and anticipate rate control like diltiazem.
• I note onset time, since anticoagulation and cardioversion decisions hinge on whether it started under or over 48 hours ago.

When in doubt with a wide-complex tachycardia, I treat it as ventricular tachycardia until proven otherwise, because that assumption is the safe one.

• I look at the patient first: a pulse and stability change everything versus a pulseless rhythm that means starting CPR and defibrillation.
• History tips me off: prior MI or heart failure makes VT far more likely than SVT with aberrancy.
• I get a 12-lead and the provider fast, but I never delay treating an unstable patient to win the ECG debate.

A single monitor lead can hint at ST changes, but I confirm with a proper 12-lead because monitor leads miss and distort ST segments.

• ST elevation across contiguous leads with reciprocal depression is the pattern that makes me move, along with the patient's symptoms.
• Correct electrode placement matters: a misplaced V lead or limb lead reversal can fake or hide elevation, so I verify positions before I call it.
• I treat it as time-critical: 12-lead, provider, aspirin, and door-to-balloon clock, not a wait-and-watch.

I go to the patient first and separate a resistance problem from a compliance problem, because that split points straight to the cause.

• High peak with normal plateau means airway resistance: kinked tube, secretions needing suction, biting, or bronchospasm.
• High peak with high plateau means the lung got stiffer: pneumothorax, worsening edema, or ARDS, and that needs the provider fast.
• I never just silence it; I assess breath sounds, suction if indicated, and check the tubing and patient before touching settings.

I look for the whole picture that the underlying problem is resolving, not just one good number, before we pull the tube.

• The reason for intubation should be improving, they should be awake enough to protect the airway with a decent cough and gag.
• Minimal support: low FiO2 and PEEP, stable gases, and a spontaneous breathing trial they tolerate without tiring out.
• I watch the rapid shallow breathing index and their work of breathing, and I keep reintubation gear ready in case the trial fails.

That is an uncompensated respiratory acidosis, and the CO2 tells me this is a ventilation problem to fix at the source.

• pH is low, CO2 is high, bicarb is near normal, so the lungs are not blowing off enough CO2 and the kidneys have not compensated yet.
• I check why: sedation, fatigue, secretions, worsening COPD, or inadequate ventilator support, and I look at the patient's rate and effort.
• I act on the cause: support ventilation, reverse oversedation, suction, or adjust vent settings, then recheck a gas to confirm the trend.

I titrate to the ordered MAP, not a single blood pressure reading, and I watch the whole patient while I do it.

• I run it through a central line when possible and check the site often, because extravasation of a vasopressor causes tissue necrosis.
• I titrate in small steps against the MAP, reassess perfusion signs like urine output, mentation, and lactate, not just the number on the screen.
• I never stop it abruptly; I wean as the patient improves and keep fluids and the source of sepsis in the picture, since pressors alone do not fix the cause.

I follow the protocol but I anchor on the anion gap closing, not just the glucose falling, because that is what says DKA is resolving.

• I check point-of-care glucose hourly and titrate per protocol, and I watch potassium hard since insulin drives it into cells and it can crash.
• When glucose hits around 200 I expect to add dextrose so I can keep insulin running to close the gap without going hypoglycemic.
• I do not stop the drip until the gap normalizes and overlap with subcutaneous insulin, or the ketoacidosis rebounds.

I stop and think about bleeding risk first, then follow the nomogram, because a critical aPTT means the patient is over-anticoagulated.

• I hold or reduce the infusion per the weight-based protocol, assess for active bleeding, and recheck the aPTT at the protocol interval.
• I look for the cause: a bolus that was too large, a rate error, or the wrong lab draw timing off the same line as the infusion.
• For a serious bleed I escalate immediately and have protamine on the radar, and I document the hold and the provider notification.

I never assume two drips can share a lumen; I verify compatibility before I let them run together, because a precipitate or reaction can be fatal.

• I check an IV compatibility reference for each pair and keep incompatible or continuous critical drips on dedicated lumens.
• Vasoactives get priority on the central line, and I avoid piggybacking anything that would bolus a pressor when I flush.
• I map out my lines deliberately and label them, so a rate change or a new med does not accidentally interrupt a titrated pressor.

I treat high-alert meds with hard stops, because these are the drugs where one error does real harm.

• Independent double-check with another nurse on the drug, dose, rate, and pump settings before it runs.
• IV potassium is never pushed; it goes as a controlled infusion at a safe rate on a pump, with cardiac monitoring for faster rates.
• I confirm the indication against the actual lab, check renal function and urine output, and recheck the level after to guide the next dose.

I start with a focused clinical question and real evidence, not a hunch, because that is what moves a practice change past opinion.

• I frame it as PICO: the population, the intervention, the comparison, and the outcome I want to improve.
• I appraise the strength of the evidence, favoring systematic reviews and strong guidelines over a single study or a vendor claim.
• I pilot the change with the team, measure a real outcome before and after, and bring it to shared governance so it sticks instead of fading.

I go back to the bundle and audit whether we are actually doing every element every time, because CLABSI rates climb when compliance slips.

• Daily review of line necessity is the highest-yield step: the safest central line is the one that comes out.
• I reinforce sterile insertion, chlorhexidine skin prep, scrubbing the hub, and clean dressings with a change date that is honored.
• I make it data-driven: audit real practice, feed the numbers back to staff, and coach at the bedside instead of just posting a policy.

This is a medical emergency, and I move on cardiac stabilization first because the peaked T waves mean the heart is at risk right now.

• I get the patient on the monitor, call the provider, and anticipate IV calcium to protect the myocardium, which does not lower potassium but buys time.
• Then shift it into cells: insulin with dextrose, and albuterol, while I prepare to remove it with a binder or dialysis for the real fix.
• I check for a hemolyzed sample but I never assume it is falsely high with ECG changes present, and I recheck a level after treatment.

I correct hyponatremia slowly and deliberately, because raising sodium too fast can cause permanent brain injury from osmotic demyelination.

• The limit is a modest rise over 24 hours; overcorrection is the danger, not just the low number itself.
• I look at symptoms and volume status, since severe symptoms like seizures change the urgency and may warrant hypertonic saline carefully.
• I trend sodium frequently, watch for a too-rapid climb, and involve the provider to slow correction if it is rising faster than the target.

A rising lactate tells me there is tissue hypoperfusion even if the blood pressure still looks okay, so I take it as an early warning.

• A lactate over the threshold pushes me toward the sepsis bundle: cultures, broad antibiotics fast, and fluid resuscitation.
• I trend it: clearing lactate after treatment is a good sign, while a rising lactate despite fluids says the patient is not responding and needs escalation.
• I read it in context, since seizures, ischemia, or certain drugs raise lactate too, but with infection signs I treat it as sepsis until proven otherwise.

I stage by the deepest tissue visible, because the stage drives the treatment and the documentation.

• Stage 1 is intact skin with non-blanchable redness; stage 2 is partial-thickness with an open shallow wound; stage 3 reaches fat; stage 4 exposes muscle, bone, or tendon.
• It is unstageable when slough or eschar covers the base so I cannot see the depth; I document it as unstageable rather than guessing a number.
• Deep tissue injury looks like intact maroon or purple skin and can deteriorate fast, so I flag it early and offload pressure immediately.

I assess the stoma's color, output, and the skin around it every shift, because those three tell me whether it is healthy.

• A healthy stoma is beefy red and moist; a dusky, purple, or black stoma signals ischemia and I escalate immediately.
• High output over the concerning threshold puts the patient at risk for dehydration and electrolyte loss, so I track intake, output, and labs.
• I protect the peristomal skin with a proper barrier and good fit, since leakage and breakdown are common and painful complications.

I activate early on a trend, not a single crashing number, because sepsis is far more survivable when we catch it before shock.

• Two or more warning signs together, fever with a rising heart rate and respiratory rate, new confusion, or a falling pressure, trigger me to call.
• I do not wait for permission: I start the bundle I can, cultures, fluids, oxygen, get IV access, and have the antibiotic timeline ready.
• I give a clean handoff to the responding team so they can act in the first minutes, since time to antibiotics drives the outcome.