CFRN practice questions, each answer reasoned out

Insisting on a helipad overrides the pilot's weather decision; a stable ventilated patient can be managed on the ground until weather or ground transport allows.

The pilot owns go/no-go and weather decisions, and with a stable patient there is no medical reason to press on; the crew backs that call.

Scud running under lowering clouds is a known cause of controlled flight into terrain.

Pressing the pilot to continue for the patient's sake is the mission pressure behind many air medical crashes into weather.

A nasal tube can enter the cranial vault through a skull base fracture, which clear nasal fluid (CSF) suggests.

With midface fractures and CSF leak, the oral route avoids intracranial placement, and the tube vents gastric air before it expands at altitude.

Gastric air expands, not shrinks, as altitude increases.

A smaller nasal tube carries the same risk of passing through the fractured skull base.

Raising FiO2 to 1.0 does not loosen secretions; dry medical oxygen can make them thicker.

Deep suctioning every 15 minutes causes mucosal trauma and hypoxia and does not fix the dry air that causes the problem.

Routine saline instillation is not recommended; it causes desaturation and pushes bacteria deeper without thinning secretions.

Dry, cold aircraft air and bypassed upper airways thicken secretions; a heat and moisture exchanger restores humidity at the source.

Standard induction doses in shock cause hypotension or arrest because of slower drug distribution and less sympathetic reserve.

Cutting both doses gives slow, incomplete paralysis while still risking hypotension.

A reduced paralytic dose takes longer to work in a low-flow state, prolonging apnea and the risk of a poor first attempt.

In shock a smaller induction dose limits hypotension, while the paralytic dose is kept or raised because slower circulation delays its onset.

Visual indicators are easily missed in a dark, noisy, vibrating cabin, so muting audible alarms hides real events.

Disabling the apnea alarm removes the warning of a disconnection, which vibration and movement make more likely.

Limits widened to the maximum stop alarming for real deterioration.

Checking the patient first separates artifact from real change, and limits set for this patient cut nuisance alarms without hiding true events.

ACE inhibitor angioedema is bradykinin-driven, so epinephrine often fails, and departing without a secured airway risks obstruction in flight.

A nasopharyngeal airway cannot bypass progressive swelling of the tongue and larynx.

Antihistamines and steroids do not work on bradykinin-mediated swelling and do not protect the airway.

Progressive tongue and lip swelling with a muffled voice means airway compromise is coming; securing the airway on the ground avoids a crash airway in the aircraft.

An airway placed out of reach cannot be managed in flight, and pumps on the legs are unsecured projectiles.

The tube, airway and chest tube must stay reachable and monitors visible so problems are seen and fixed in a cramped cabin.

Pinning the chest tube side against the wall blocks access to the tube and the site.

The drainage unit must stay below the chest; placing it at the head lets fluid flow back into the pleural space.

Taking the patient off the ventilator and bagging separates a ventilator or circuit problem from a patient problem and supports oxygenation while the DOPE causes are checked.

Raising the alarm limit silences the warning without finding the cause of the high pressure.

Sedation and paralysis treat agitation or dyssynchrony, but they can hide a displaced tube, an obstruction or a pneumothorax.

Raising PEEP adds pressure before the cause is known and worsens a pneumothorax or air trapping.

A pressurized fixed-wing aircraft keeps cabin altitude low over a long distance, which limits the oxygen needed by a patient with refractory hypoxia.

Most rotorcraft are not pressurized, and 400 miles is beyond typical helicopter range.

An unpressurized fixed-wing aircraft at cruise altitude exposes the patient to hypoxic cabin altitudes.

An unpressurized helicopter cannot cover 400 miles efficiently, and altitude still lowers oxygen pressure.

Heat packs on the arms and legs cause vasodilation, which returns cold, acidotic blood to the core and can cause afterdrop and hypotension.

Blankets alone suit mild hypothermia with shivering; a non-shivering patient at 29 °C cannot generate enough heat.

Peritoneal lavage is invasive, not done in an aircraft, and is reserved for severe hypothermia or arrest.

At 29 °C with a pulse, active external warming of the trunk plus minimally invasive measures such as warmed IV fluids raise the temperature safely.

The communication center cannot help with an obstacle in the flight path in the next seconds.

Waiting for the pilot to ask loses time when an obstacle is close to the path.

A clear callout of the obstacle's clock position and distance gives the pilot the information needed to act at once.

The sterile cockpit rule restricts nonessential talk; it requires safety callouts, not silence.

Removing the tube eliminates the decompression a bowel obstruction needs, especially during a flight.

An open tube to vent or suction lets expanding gas escape, preventing distension and vomiting.

A clamped tube traps gastric air that expands during ascent, worsening distension and risking vomiting.

Instilling air adds gas that will expand at altitude.

A higher ultrafiltration rate does not clear hemolyzed blood and does not fix the circuit fault.

Returning hemolyzed blood gives the patient free hemoglobin and potassium.

Dark red-brown blood and effluent with pain and hypotension point to circuit hemolysis; stopping the pump without returning the blood avoids giving the patient hemolyzed blood.

Calcium treats citrate toxicity, not hemolysis, and continuing therapy keeps damaging cells.

Fuel vapor drifts downwind and fuel flows downhill, so this places the crew in the path of both.

Downwind puts the crew in the fuel vapor and smoke.

Upwind and uphill keeps the crew out of drifting vapor and away from fuel running downhill.

Downhill puts the crew where spilled fuel collects.

An unrestrained patient is thrown on impact; restraints stay on until the aircraft stops.

Sedation is not a safety step in the final seconds and takes time from bracing.

Loose equipment becomes a projectile on impact, and bracing reduces crew injury.

Unlatching the doors before touchdown risks ejection and structural failure on impact.

Vests are inflated outside the aircraft; an inflated vest traps a person inside a flooding, inverted cabin.

A vest inflated while strapped in floats the person up against the restraints and the ceiling.

Inflating as soon as the aircraft stops, while still inside, risks being pinned against the ceiling as the cabin fills.

Inflating before impact pins the wearer and blocks escape from the cabin.

Switching vasopressors abruptly when the bag runs out risks hypotension; the shortfall is preventable.

Lowering a vasopressor to stretch the supply drops BP in a patient who needs it.

Adding drug to a running bag changes the concentration unpredictably and is unsafe.

At 12 mcg/min the 50 mL left (0.8 mg) lasts about 66 minutes, short of the 90-minute flight, so a second prepared bag must come along.

Standard epinephrine every 3 minutes accumulates in a cold patient and is held or spaced until rewarming.

At 26 °C the heart often does not respond to defibrillation, and repeated shocks every 2 minutes offer little.

A hypothermic avalanche victim with a patent airway and normal potassium can survive long CPR, and ECMO rewarming gives the best chance.

ETCO2 below 10 mmHg is not a valid stopping rule in deep hypothermia, where metabolism and CO2 production are very low.

AHA's advice rests on trials that showed no survival benefit, not on the device's cost.

Large trials found no survival benefit when an ITD was added to conventional manual CPR, so AHA does not recommend it.

Placing an advanced airway does not change the trial result: with conventional CPR the ITD brought no survival benefit.

AHA rates the ITD with conventional CPR as no benefit (Class 3) after large trials found no survival gain, so it is not recommended.

100 mcg/mL is ten times the concentration actually made.

1 mg/mL is the undiluted concentration, ten times stronger than this mixture.

10 mcg/mL is right, but 5–10 mL gives 50–100 mcg, far too much for a push-dose bolus.

0.1 mg in 10 mL gives 10 mcg/mL; 0.5–2 mL delivers 5–20 mcg, the push-dose range.

A limb tourniquet cannot be placed above a wound at the inguinal crease.

Groin bleeding is junctional; a junctional tourniquet compresses the vessels where a limb tourniquet cannot reach.

Plain gauze without pressure is less effective than what already failed.

Elevation and vasopressors do not stop arterial bleeding and hide hemorrhagic shock.

Epinephrine treats bradycardia from other causes; hyperkalemic conduction block needs calcium first.

Albuterol shifts potassium but works slowly and does not protect the heart from a widening QRS right now.

Calcium stabilizes the membrane for only 30–60 minutes; with a wide QRS and bradycardia returning, it is repeated while shifting therapies and dialysis follow.

Normal saline does not stabilize the membrane or lower potassium in a patient awaiting dialysis.

A seizure during magnesium therapy is treated first with an additional 2 g IV magnesium over 5 minutes, since reflexes and breathing show no toxicity.

Phenytoin is less effective than magnesium for eclamptic seizures and is not the next step.

Calcium gluconate reverses magnesium toxicity; this patient has reflexes and a normal rate, so it would undo seizure prophylaxis.

Benzodiazepines are second line in eclampsia, used when magnesium fails or is contraindicated.

Traction on the head stretches the brachial plexus and can cause permanent nerve injury without freeing the shoulder.

When McRoberts and suprapubic pressure fail, delivering the posterior arm reduces the shoulder width and frees the impaction.

Pushing harder increases the impaction while the anterior shoulder stays stuck.

Fundal pressure drives the shoulder harder against the pubic bone and worsens the impaction.

Evening hours are a period of relatively good alertness, well before the overnight low.

Late morning is near peak alertness.

Early morning hours after 0600 bring rising alertness, not the circadian low.

The circadian low falls between about 0200 and 0600, when alertness and performance are lowest.

With no fire and rotors still turning, the crew stays belted until the pilot signals that it is safe to exit.

Removing the patient while the rotors turn exposes everyone to the blades.

Exiting while the rotors are turning risks a blade strike.

The ELT signals the crash to rescuers and should stay on.

Loading first lets the patient bleed during the move and flight.

More gauze over a soaked dressing does not stop arterial bleeding.

A tourniquet above the wound stops life-threatening bleeding immediately, before the patient is moved.

Crystalloid replaces volume while the bleeding continues and dilutes clotting factors.

BIS is not routine on an aircraft and does not show the drug's hemodynamic effect.

Fentanyl reduces sympathetic tone; in a trauma patient this can unmask hypovolemia and drop BP, so BP and heart rate are watched closely.

The patient is ventilated, so respiratory depression is not the main concern.

Pupil size changes with opioids but is a poor measure of sedation and misleads in head injury.

Ketorolac impairs platelet function and kidney blood flow in a bleeding patient.

Meperidine has a neurotoxic metabolite and is no longer recommended for acute pain.

Fentanyl has fast onset and little histamine release, so it is the most hemodynamically stable choice for a patient in hemorrhagic shock.

Morphine releases histamine and causes vasodilation and hypotension in a patient who is already bleeding.

Infusing four units of plasma before departure delays transport and does not reliably reverse apixaban.

Hemorrhagic shock needs blood and rapid surgical control; reversal is arranged without delaying transport.

Waiting for anti-factor Xa levels delays definitive care while the patient bleeds.

Idarucizumab reverses dabigatran, not apixaban.

A Heimlich valve lets air escape one way; it must be unclamped and venting, as trapped air expands on ascent.

A Heimlich valve is not connected to high suction, which can damage lung tissue.

Emptying the bag records output but does not prevent an in-flight pneumothorax.

Clamping the tubing stops air from escaping and risks tension pneumothorax as gas expands at altitude.

Crystalloid resuscitation does not create a gas space that expands on ascent.

Recent penetrating chest trauma can leave a small pneumothorax that expands as the aircraft climbs and becomes a tension pneumothorax.

Controlled hypertension does not create a gas-expansion risk.

An old healed appendectomy leaves no trapped gas.

CPAP by mask cannot open a wired jaw and pushes vomit into the airway.

Ondansetron and nasal suctioning do not clear vomit behind wired teeth.

Suctioning between the teeth cannot remove enough vomit to protect the airway.

Cutting the fixation wires or bands opens the mouth so vomit can be cleared and the airway managed.

Oxygen targets are not tied to altitude; hypoxemia drives sickling in acute chest syndrome at any altitude.

An 88–92% target applies to chronic hypercapnic lung disease, not to acute chest syndrome, where hypoxemia drives more sickling.

Keeping SpO2 at 95% or above, or at the patient's baseline, limits hypoxia-driven sickling in acute chest syndrome.

Oxygen toxicity is not a concern at these levels, and an SpO2 of 85% causes more sickling.

An approved defibrillator is tested to discharge safely with the aircraft systems running, and survival from VT falls with every minute without a shock, so the crew shocks in flight.

Delaying the first shock for 20 minutes of CPR gives up the main treatment for pulseless VT.

A precautionary landing costs minutes of pulseless time; an approved device does not require the aircraft to be on the ground.

Approved devices do not need the avionics turned off, and the crew would lose communication with the pilot during an emergency.

A bright headlamp throws glare across the cabin and windscreen and can wipe out the pilot's night adaptation.

Light aimed forward reflects off the windscreen into the pilot's field of view.

Even a brief bright cabin light can wipe out the pilot's dark adaptation or flood night vision goggles.

A low, shielded light lets the nurse work without glare reaching the windscreen or the pilot's night-adapted eyes and night vision goggles.

A shorter traction device keeps the femur out to length, controlling pain and bleeding, while fitting inside the aircraft.

A pillow splint does not hold the femur out to length, so pain, bleeding and muscle spasm increase.

Angling the splint loses traction alignment and moves the fracture ends.

Without traction the thigh muscles shorten the femur, increasing pain, bleeding and nerve injury.

Verbal de-escalation cannot be relied on in a loud cabin, and an uncontrolled patient endangers the aircraft.

Waiting until airborne to sedate means a combative patient is loaded unsecured and treated in a cramped, moving cabin.

A combative patient can strike the crew or controls in a confined cabin, so chemical sedation and restraint are completed on the ground.

Restraints without sedation leave a fighting patient straining against straps in a confined cabin, where the airway and the crew are both at risk.

Blankets inside the isolette block the warm airflow around the neonate and hide the chest from view.

Heat lost during loading in a cold cabin is hard to regain in a 1.2-kg infant.

A prewarmed isolette kept on aircraft power gives a warm environment from the first minute and saves the battery for the moves between vehicles.

Maximum settings risk hyperthermia; the isolette is set to keep a normal temperature, not maximum heat.

Rotor noise drowns out sound, so a device that displays the fetal heart rate, or feeds it into the headset, gives a usable reading.

Movement shows the fetus is alive but does not give the heart rate.

A fetoscope depends on hearing heart tones, which cabin noise makes impossible.

A tocodynamometer records uterine contractions, not the fetal heart rate.

Body heat keeps the bags near body temperature, so small boluses for hypotension do not chill the patient.

Fluid at freezing outdoor temperature lowers the core temperature of a patient already at risk of hypothermia.

The cargo area is as cold as the outside air, and the bags may freeze there.

Running fluid wide open wastes a limited supply and floods the patient with cold fluid.

Restraints increase agitation and delirium and are a last resort for safety, not a treatment.

Rotor noise cuts the patient off from voices; a headset lets the crew reorient and reassure the patient, the first step in managing delirium.

Benzodiazepines worsen delirium in older adults and add respiratory depression.

A 5-mg dose is far above the low starting dose for an older adult and treats distress that reorientation can often relieve.

Rotor noise makes auscultation unreliable, so it cannot confirm the tube position in flight.

Waiting until arrival leaves a displaced tube undetected for the whole flight.

Desaturation is a late sign; a dislodged tube can go unnoticed for minutes after preoxygenation.

Every transfer can pull or push the tube, so its depth at the teeth and the capnography waveform are checked after each move; breath sounds are useless in the cabin.

Dropping PEEP collapses recruited alveoli and causes the derecruitment the step is meant to prevent.

A bag without a PEEP valve lets the lungs collapse between breaths, and fast bagging adds barotrauma and auto-PEEP.

Extra oxygen delays desaturation but does not stop alveoli from collapsing when the circuit is opened.

Clamping the endotracheal tube during the brief disconnection keeps airway pressure in the lungs, so recruited alveoli do not collapse when PEEP is lost.

The hull's fixed pressure difference, not the climb rate, limits cabin altitude, so a slower climb cannot hold a sea-level cabin at the usual cruise altitude.

The pressure difference the hull can hold is fixed, so the cabin cannot be kept at sea level at the usual cruising altitude.

The cabin can only be held so far above outside pressure, so a sea-level cabin means flying lower, where the aircraft burns more fuel, flies slower and may need a fuel stop.

Climbing higher lowers outside pressure and makes a sea-level cabin harder, not easier, to hold.

The cylinder holds a fixed amount of gas; altitude does not create more usable oxygen.

A pneumatic ventilator draws extra oxygen to run its valves, so the supply runs out sooner than minute ventilation alone predicts.

PEEP is a pressure, not a volume of gas used, so it does not add to oxygen consumption this way.

Minute ventilation misses the device's own consumption, a common reason cylinders run dry early.

A standard rate cuts minute ventilation sharply and causes a sudden fall in pH.

Salicylate patients rely on hyperventilation to offset the acidosis; lower ventilation after intubation lets pH fall and pushes more salicylate into the brain.

Bicarbonate is part of treatment, alkalinizing the blood and urine to keep salicylate out of the brain and speed its excretion.

Permissive hypercapnia worsens the acidemia that drives salicylate into tissues.

Covering a patient who cannot sweat traps more heat.

The rise comes from heat gain and blocked sweating, not a fever, so an antipyretic does little.

Physostigmine reverses delirium in selected cases; it is not the first treatment for heat gain in a hot cabin.

Anticholinergic toxicity blocks sweating, so heat from a hot cabin cannot be shed; removing the heat and cooling externally treat the rise.

A high cord injury cuts sympathetic control of skin vessels and shivering below the lesion, so body temperature drifts toward the cabin temperature.

CT showed no other injury, and a hidden bleed would show tachycardia and hypotension, not isolated cooling.

Dysreflexia causes hypertension and sweating above the lesion, usually weeks later, and is triggered by a noxious stimulus.

Altitude does not lower metabolic rate enough to cool a patient this quickly.

A passenger who knows how to stay belted, use the headset and get out in an emergency does not become a hazard to the crew, the child or the aircraft.

Passengers are escorted to and from the aircraft by a crew member, approaching from the front in the pilot's view and never near the tail rotor.

Without a headset the parent cannot hear instructions or warnings and is exposed to damaging noise.

A child held on a lap is torn loose in a crash or hard landing; the child stays secured to the stretcher.

Fistula bleeding comes from a high-flow arterialized vessel; firm pressure held over the puncture for 10–15 minutes stops most bleeding and keeps the access usable.

A tourniquet is the fallback when pressure fails, because it can clot off the patient's dialysis access.

Elevation alone does not stop bleeding under arterial pressure in a patient who is already hypotensive.

Blind clamping crushes the vessel and can destroy the access.

SIADH does not fit a volume-depleted, hyperglycemic patient whose sodium is rising as glucose falls.

The sodium is rising, not falling, and the low value at departure was caused by hyperglycemia, not true hyponatremia.

The corrected sodium has not changed, so this is not true overcorrection, and stopping fluids would harm a volume-depleted patient.

As glucose falls, water moves back into cells and the measured sodium rises; corrected for glucose it stays near 137 mEq/L, so the change is expected.

Plasma is not given for an INR without bleeding; it adds volume and hides the INR trend the transplant team uses.

Lactulose is a cirrhosis treatment; it does not address acute liver failure and can cause distension and dehydration.

A failing liver cannot release or make glucose, so hypoglycemia recurs quickly; a continuous dextrose infusion with hourly checks prevents it en route.

Sedatives worsen encephalopathy and hide a falling level of consciousness, the main warning sign of cerebral edema.

A normal PaCO2 is not the goal here; the current settings are causing a pH of 7.58.

A larger tidal volume adds ventilation and breath stacking, the opposite of what this alkalemic COPD patient needs.

A chronic CO2 retainer has a high bicarbonate, so bringing PaCO2 to a normal 38 mmHg causes severe alkalemia; the rate is reduced so PaCO2 rises toward the patient's usual level.

More ventilation worsens an already dangerous alkalemia and adds air trapping in COPD.

After several days of Guillain-Barré weakness, denervated muscle develops extra acetylcholine receptors, and succinylcholine can cause a lethal rise in potassium.

Etomidate is a hemodynamically stable induction agent with no special risk in Guillain-Barré.

A nondepolarizing agent is the safer paralytic in neuromuscular disease, at a reduced dose because of sensitivity.

Post-intubation sedation is needed; midazolam has no particular hazard here beyond the usual hypotension watch.

Urine output helps with monitoring but does not change the next hour of resuscitation.

Spinal restriction is applied when indicated, but it does not address hemorrhagic shock without adequate access.

A 22-gauge line cannot deliver blood at the rate this hypotensive patient needs, and access is much harder in a moving aircraft, so large-bore or IO access comes before departure.

Repeat imaging delays transfer to definitive care without changing management.

Breath sounds are unreliable in the cabin; waveform capnography confirms the tube without stopping CPR.

A video laryngoscope lets the operator see the cords and pass the tube while the device keeps compressing, with at most a pause of a few seconds.

A 30-second pause drops coronary perfusion pressure, which takes many compressions to rebuild.

Delaying the airway by a fixed number of cycles is not a rule; the aim is placement without long pauses.

Glucose falls faster than ketones clear, so once it falls below 250 mg/dL dextrose is added and insulin continues until the anion gap closes and ketones clear.

Stopping the drip while the gap is still open lets ketoacidosis rebound; the transition waits until DKA has resolved.

A bolus treats hypoglycemia that is not present, and stopping insulin leaves the ketosis untreated.

A higher rate speeds the fall in glucose toward hypoglycemia without clearing ketones safely.

The red color comes from the drug itself, not from hemolysis, and does not mean red cells are breaking down.

Hydroxocobalamin colors skin, urine and plasma red and interferes with colorimetric lab assays, so the receiving team must know it was given before trusting chemistry results.

A transient BP rise is an expected effect of hydroxocobalamin and is not a reason to stop it.

A second dose is given only if the patient's response warrants it; it is not routinely scheduled.

Rolling the patient twists the unstable ring and can restart bleeding; the backboard adds nothing a scoop does not.

Each log-roll moves the fracture and can break up clot in the pelvic veins, so a scoop stretcher lifts the patient in one move and keeps the injured ring still.

Repeated pelvic springing moves the fragments and dislodges clot; stability is checked once, gently, if at all.

Flexing the hips moves the pelvic fragments and can widen the fracture.