Your FREE FP-C Flashcards 2026 – 200+ Cards

Coordinated use of all people, information, and equipment to make safe decisions and manage workload; flattens the authority gradient so anyone can speak up.

A personal fitness-for-duty check: Illness, Medication, Stress, Alcohol, Fatigue, Emotion.

The self-imposed stressors a crew member can control: Drugs, Exhaustion, Alcohol, Tobacco, Hypoglycemia (or Hypoxia).

Roughly 100 × 100 ft, level, firm, free of obstructions/wires/debris; approach from the front in the pilot's view, never the tail rotor or uphill side.

Hot, high, humid air thins the air and reduces lift — most dangerous on takeoff when the payload is heaviest. The pilot has final authority to abort.

Commission on Accreditation of Medical Transport Systems — voluntary accreditation standards for transport safety, staffing, and quality.

Mark an LZ with lights at the corners (no light pointed up at the aircraft); avoid white lights that flood the cockpit and ruin the pilot's night vision.

Approach a helicopter from the front in the pilot's view; the tail rotor is nearly invisible and lethal. On sloped ground, approach from the downhill side.

A rule prohibiting non-essential conversation and activity during critical phases of flight (takeoff, landing, low altitude) to reduce crew distraction.

A safety culture where the full crew must agree to accept a flight, but any single member may decline or abort it without question or penalty.

An airworthy aircraft flown into ground, water, or obstacles, usually from loss of situational awareness in poor weather/visibility — a leading HEMS fatality cause.

Unintended entry into instrument meteorological conditions (loss of visual references); the protocol is to climb, level the wings, and transition to instruments.

Sequentially calling programs after one declines a flight for weather — a dangerous practice; weather turn-downs should be shared transparently between programs.

Image-intensifying goggles that amplify ambient light to improve obstacle/terrain detection on night flights; reduce CFIT risk but narrow the field of view.

Treat all blood and body fluids as infectious: hand hygiene, gloves/gown/mask/eye protection as indicated, and safe sharps handling on every patient.

Carried for a forced landing in remote terrain: signaling, shelter, water, fire, first aid; the priority after a survivable crash is to stay with the aircraft.

Fixed-wing suits long-range (>150–250 mi), pressurized, weather-tolerant flights; rotor-wing suits short scene/interfacility runs and can land near the patient.

Sustained cabin noise can exceed 90–100 dB, masking auscultation and alarms; protect hearing and rely on capnography and monitors over breath sounds.

Total aircraft weight and its center of gravity must stay within limits; patient, crew, fuel, and equipment all count and can force off-loading of supplies.

P₁V₁ = P₂V₂ — as pressure falls on ascent, trapped gas EXPANDS (pneumothorax, GI gas, ET cuff, IABP balloon, air splints). The highest-yield FP-C gas law.

Total pressure = sum of the partial pressures. At altitude total pressure drops, so the partial pressure of O₂ falls and the patient becomes hypoxic at the same FiO₂.

Dissolved gas is proportional to its partial pressure. As pressure falls, dissolved nitrogen leaves solution — the basis of decompression sickness.

A gas diffuses faster the lighter it is (rate ∝ 1/√MW). Governs alveolar gas exchange across the respiratory membrane.

Low partial pressure of inspired O₂ — the default hypoxia of altitude (Dalton's law). Treat with supplemental O₂ or a lower cabin altitude.

Reduced O₂-carrying capacity (anemia, hemorrhage, CO poisoning). CO poisoning gives a falsely high SpO₂; treat with high-flow O₂.

The cells cannot use delivered oxygen — classically cyanide or hydrogen-sulfide poisoning. Treat with the antidote (e.g., hydroxocobalamin for cyanide).

CO binds hemoglobin with ~200–250× the affinity of O₂; SpO₂ reads falsely high. Detect with CO-oximetry; treat with 100% O₂ (consider hyperbaric).

The interval from a sudden loss of cabin oxygen until a person can no longer take corrective action; it shortens sharply as altitude rises.

Hypoxia, barometric (dysbarism), thermal (~2 °C drop per 1,000 ft), decreased humidity, noise, vibration, fatigue, G-forces, spatial disorientation, flicker vertigo.

At constant pressure, gas volume is directly proportional to absolute temperature (V₁/T₁ = V₂/T₂). A cold cabin shrinks trapped gas; warming re-expands it.

At constant volume, gas pressure is directly proportional to absolute temperature (P₁/T₁ = P₂/T₂). Relevant to fixed-volume cylinders heating or cooling.

Gas transfer across a membrane rises with surface area and pressure gradient and falls with membrane thickness — impaired by pulmonary edema or fibrosis at altitude.

Inadequate blood flow despite adequate oxygenation — shock, cardiac arrest, G-forces, or tourniquet. The tissue is oxygen-starved from poor perfusion, not low PaO₂.

A synonym for time of useful consciousness — the usable interval after an oxygen-supply loss before a crew member cannot perform corrective tasks.

A compensatory response to hypoxia producing respiratory alkalosis with tingling, dizziness, and tetany; mimics hypoxia and must be distinguished from it.

Pain or injury when gas in body cavities expands on ascent — barotitis media, barosinusitis, barodontalgia, GI distension. Boyle's law in the patient.

Decompression sickness: nitrogen leaving solution as pressure falls (Henry's law), causing the bends, the chokes, or neurologic deficits. Treat with 100% O₂ and recompression.

Capping cabin altitude (often near sea level) to limit gas expansion and hypoxia in patients with pneumothorax, recent eye/GI surgery, or air emboli.

Disorientation, nausea, or even seizure from rotor blades chopping sunlight at low frequency; mitigated by looking away or shielding the eyes.

An inability to correctly sense aircraft position/motion relative to the earth, especially without a visual horizon; trust the instruments over body sensations.

Troposphere (surface to ~36,000 ft, where weather and aeromedical flight occur), then stratosphere; ~80% of air mass is in the troposphere.

Physiologic zone (sea level–10,000 ft, well tolerated), physiologically deficient zone (10,000–50,000 ft, O₂ needed), space-equivalent zone (>50,000 ft).

Tooth pain on ascent when gas trapped under a filling or in a cavity expands; a form of trapped-gas dysbarism.

Pressurized/heated cabin air is very dry, causing mucosal drying, thickened secretions, and insensible fluid loss; humidify O₂ and protect the cornea.

Preparation, Preoxygenation, Pretreatment, Paralysis with induction, Positioning, Placement with proof, Post-intubation management.

Continuous end-tidal CO₂ — the gold standard for confirming and monitoring ET tube placement in the noisy, moving cabin where breath sounds are unreliable.

Major burns/crush >24–72 h old, denervation, prolonged immobility, and hyperkalemia (lethal K⁺ efflux from receptor upregulation). Use rocuronium instead.

Encapsulates and rapidly reverses aminosteroid nondepolarizing paralytics (rocuronium, vecuronium).

Dissociative agent that supports blood pressure and bronchodilates — good for shock or asthma; preserves airway reflexes.

Hemodynamically stable induction agent; a single dose can transiently suppress adrenal cortisol synthesis (debated in sepsis).

Passed under the epiglottis in a Grade III view (only epiglottis seen); the ET tube is then railroaded over it. Confirm with tracheal clicks/hold-up.

Backward, Upward, Rightward Pressure on the thyroid cartilage to bring an anterior glottis into the laryngoscopic view (external laryngeal manipulation).

Causes of sudden decline in a ventilated patient: Displacement, Obstruction, Pneumothorax (expands at altitude), Equipment failure. Check capnography first.

PaO₂ ÷ FiO₂ — grades oxygenation. Berlin ARDS: 200–300 mild, 100–200 moderate, ≤100 severe. PaO₂ 80 on FiO₂ 1.0 = P/F 80 (severe).

Low tidal volumes ~6 mL/kg ideal body weight in ARDS, PEEP titrated to oxygenation, limit plateau pressure; allow long expiration in asthma/COPD.

Near-simultaneous administration of a potent induction agent and a paralytic to create optimal intubating conditions while minimizing aspiration risk.

Procedural sedation (often ketamine) to allow effective preoxygenation/denitrogenation in an uncooperative hypoxic patient before giving the paralytic.

High-flow nasal O₂ (e.g., 15 L/min) left on during the apneic period of RSI to extend safe apnea time and delay desaturation.

Replacing alveolar nitrogen with oxygen before RSI to build an O₂ reservoir; aim for end-tidal O₂ high / SpO₂ 100% for maximal safe apnea time.

Depolarizing paralytic, ~1.5 mg/kg IV; onset ~45–60 s, duration ~6–10 min. Watch for hyperkalemia, malignant hyperthermia, and bradycardia in children.

Nondepolarizing aminosteroid paralytic, ~1.0–1.2 mg/kg IV for RSI; onset ~45–60 s, duration ~30–60 min; reversible with sugammadex.

Laryngoscopic view: I = full glottis, II = partial glottis/arytenoids, III = epiglottis only, IV = neither glottis nor epiglottis. Higher grade = harder intubation.

Predicts a difficult airway: Look externally, Evaluate 3-3-2, Mallampati, Obstruction, Neck mobility.

A hypermetabolic crisis triggered by succinylcholine or volatile agents: rising EtCO₂, rigidity, hyperthermia, acidosis. Treat with dantrolene and cooling.

The tube advanced too far enters the more vertical right bronchus — unilateral (right) breath sounds, left collapse, hypoxia. Withdraw the tube and reconfirm.

The rescue airway for 'can't intubate, can't oxygenate': incise the cricothyroid membrane and place a tube. The definitive failed-airway maneuver in adults.

Provides analgesia and sedation while preserving airway reflexes and respiratory drive; useful for post-intubation sedation and procedural pain.

A potent short-acting synthetic opioid (~1–2 mcg/kg) for analgesia and RSI pretreatment; can blunt the sympathetic response but may cause chest-wall rigidity at high doses.

A rapid-onset, short-acting sedative-hypnotic for sedation/induction; causes dose-dependent hypotension and respiratory depression — caution in shock.

A paralyzed but inadequately sedated patient who is conscious and in distress; always pair paralytics with adequate ongoing analgesia and sedation.

Visualization of oropharyngeal structures (I = full soft palate/uvula to IV = hard palate only) predicting intubation difficulty; higher class = harder view.

Pressure maintained at end-expiration to keep alveoli open, improving oxygenation and reducing atelectrauma; excessive PEEP raises intrathoracic pressure and drops preload.

Alveolar distending pressure measured on an inspiratory hold; keep <30 cmH₂O in ARDS to limit barotrauma/volutrauma.

The maximum airway pressure during inspiration; a high peak with a normal plateau points to airway resistance (kink, bronchospasm, secretions, mucus plug).

Air trapping from incomplete exhalation in obstructive disease, causing rising pressures and hypotension; treat by disconnecting the circuit and prolonging expiratory time.

Accepting an elevated PaCO₂ and lower pH to keep tidal volumes/pressures lung-protective in ARDS or severe asthma; avoid in raised ICP.

Set to ~6 mL/kg of ideal (not actual) body weight in ARDS; calculate IBW from height, not the patient's measured weight.

Inspiratory-to-expiratory time ratio (normal ~1:2). Lengthen expiration (1:3–1:5) in obstructive disease to prevent air trapping and auto-PEEP.

A set inspiratory pressure delivers a variable tidal volume; limits peak pressure but tidal volume falls if compliance worsens — monitor minute ventilation.

A set tidal volume delivers a variable pressure; guarantees minute ventilation but airway pressures rise as compliance falls — monitor plateau pressure.

Low tidal volume (~6 mL/kg IBW), plateau <30, higher PEEP, permissive hypercapnia, and prone positioning; targets oxygenation while limiting ventilator-induced lung injury.

Triggered by obstruction, biting, kinked tube, bronchospasm, secretions, pneumothorax, or falling compliance; work the DOPE differential immediately.

Triggered by a circuit leak, disconnection, cuff leak, or extubation; reconnect/inspect the circuit and reassess the airway.

Tidal volume × respiratory rate; the primary determinant of CO₂ clearance. Raise rate or volume to lower PaCO₂.

Compliance is lung/chest distensibility (low in ARDS, edema, pneumothorax); resistance opposes flow (high in asthma, kinks, secretions). They drive different alarms.

Arterial CO₂ normally runs ~2–5 mmHg above end-tidal; a widening gap signals dead-space ventilation (low cardiac output, PE) or sampling problems.

High PaCO₂ with low pH from hypoventilation (sedation, obstruction, fatigue); correct by increasing minute ventilation (rate or tidal volume).

Low PaCO₂ with high pH from hyperventilation (pain, anxiety, hypoxia, over-ventilation); reduce minute ventilation and treat the underlying drive.

IV isotonic fluids FIRST (profound volume depletion), then an insulin infusion, then potassium. Hold insulin if K⁺ is below 3.3 mEq/L.

Early cultures, broad-spectrum antibiotics within the hour, balanced fluids (~30 mL/kg then dynamic measures), norepinephrine to MAP ≥65 mmHg.

Blanching, coolness, and pain at a peripheral pressor site = risk of tissue ischemia/necrosis. Stop the infusion, secure new access, reassess the limb.

First-line vasopressor for septic and most distributive shock (~0.01–3 mcg/kg/min); strong α with some β₁ — raises MAP via vasoconstriction with modest inotropy.

A potent α/β agonist drip (~0.01–0.5 mcg/kg/min) for refractory shock, anaphylaxis, or bradycardia; boosts inotropy, chronotropy, and vascular tone.

A non-catecholamine vasoconstrictor (fixed ~0.03–0.04 units/min) added to norepinephrine in septic shock; acts on V1 receptors independent of adrenergic tone.

A β₁ inotrope (~2–20 mcg/kg/min) that raises cardiac output in cardiogenic shock/heart failure; can drop blood pressure via β₂ vasodilation.

A pure α₁ vasoconstrictor that raises blood pressure with reflex bradycardia; useful when tachycardia must be avoided but offers no inotropy.

Approximately diastolic + ⅓ (systolic − diastolic); the perfusion pressure of most organs. Target ≥65 mmHg in shock, higher in known hypertension/TBI.

IM epinephrine 0.3–0.5 mg (1:1,000) into the lateral thigh is first-line; add airway management, fluids, antihistamines, steroids, and an epi drip if refractory.

Vasodilation/maldistribution lowers SVR (sepsis, anaphylaxis, neurogenic); warm, well-perfused skin early. Treat with fluids and vasopressors.

A mechanical block to flow — tamponade, tension pneumothorax, or massive PE; fix the obstruction (pericardiocentesis, decompression, thrombolysis), not just give fluid.

Glucocorticoid deficiency causing refractory hypotension, hyponatremia, and hyperkalemia; treat with IV hydrocortisone, fluids, and dextrose.

Severe hyperthyroidism: hyperthermia, tachyarrhythmia, agitation. Treat with beta-blockade, thionamides, iodine (after thionamide), and steroids; cool aggressively.

Decompensated hypothyroidism: hypothermia, bradycardia, hypotension, altered mentation. Treat with IV levothyroxine, steroids, and careful warming.

IV calcium to stabilize the membrane, then insulin + dextrose and beta-agonists to shift K⁺ intracellularly, plus removal (diuresis, dialysis); calcium does not lower K⁺.

Na⁺ − (Cl⁻ + HCO₃⁻), normal ~8–12. A high gap (MUDPILES) signals added acid — ketones, lactate, toxins; a normal gap suggests bicarbonate loss.

Low bicarbonate with low pH from acid gain or bicarbonate loss; the lungs compensate by blowing off CO₂ (Kussmaul respirations). Treat the cause.

High bicarbonate with high pH from acid loss (vomiting, NG suction) or diuretics; the lungs compensate by hypoventilating. Often chloride-responsive.

A falling serial lactate indicates improving perfusion and is a resuscitation endpoint in shock; a rising lactate signals ongoing anaerobic metabolism.

The metabolic component of an ABG; a large base deficit reflects significant metabolic acidosis and correlates with shock severity and transfusion need.

Expected PaCO₂ = 1.5 × HCO₃⁻ + 8 (±2) in metabolic acidosis; if measured CO₂ differs, a second respiratory acid-base disorder is present.

Cholinergic excess (SLUDGE/DUMBELS) from acetylcholinesterase inhibition; treat with high-dose atropine titrated to secretions plus pralidoxime (2-PAM).

Histotoxic hypoxia with high lactate and a narrowed arteriovenous O₂ gap; classic in enclosed-space fires. Antidote is hydroxocobalamin (or the nitrite/thiosulfate kit).

Wide QRS, terminal R in aVR, hypotension, seizures, anticholinergic signs; give sodium bicarbonate for QRS widening and ventricular dysrhythmias.

Bradycardia and hypotension; treat with high-dose glucagon, atropine, calcium, pressors, and high-dose insulin-euglycemia therapy.

Bradycardia, hypotension, and hyperglycemia; treat with IV calcium, high-dose insulin-euglycemia therapy, pressors, glucagon, and consider lipid emulsion.

A mixed respiratory alkalosis and high-anion-gap metabolic acidosis with tinnitus and hyperthermia; alkalinize urine with bicarbonate and consider dialysis. Do NOT intubate casually — apnea worsens acidosis.

Delayed hepatotoxicity plotted on the Rumack-Matthew nomogram; the antidote N-acetylcysteine is most effective within ~8 hours of ingestion.

Respiratory depression, miosis, and decreased mentation; support ventilation and titrate naloxone to restore breathing without precipitating full withdrawal.

Methanol and ethylene glycol cause a high-anion-gap acidosis with an osmolar gap; treat with fomepizole (or ethanol) and hemodialysis.

Core temperature >40 °C with CNS dysfunction; cool rapidly (evaporative or cold-water immersion) and support organs. Antipyretics do not work for environmental heat stroke.

Handle gently, rewarm actively, and remember 'not dead until warm and dead'; defibrillation and many drugs are ineffective until core temperature rises.

An inhaled bronchodilator for asthma/COPD bronchospasm; also shifts potassium intracellularly as an adjunct in hyperkalemia.

Eye (1–4) + Verbal (1–5) + Motor (1–6) = 3 to 15. GCS ≤8 generally means secure the airway. Lowest possible score is 3.

Hypertension with a widening pulse pressure, bradycardia, and irregular respirations — a late sign of raised ICP and impending herniation.

Prevent secondary injury: avoid hypoxia and hypotension, head up ~30° and midline, maintain normocapnia (no routine hyperventilation).

Focal deficit from arterial occlusion; permissive hypertension supports the penumbra, give thrombolytics within the window if eligible, and avoid hypoglycemia/hyperthermia.

Bleeding into brain/subarachnoid space; control blood pressure to a target, reverse anticoagulation, manage ICP, and avoid thrombolytics. CT distinguishes it from ischemic stroke.

CPP = MAP − ICP; maintain roughly 60–70 mmHg to perfuse the injured brain. Both hypotension and high ICP starve the brain of flow.

A blown (fixed, dilated) pupil, posturing, and Cushing's triad signal herniation; permit brief targeted hyperventilation and hyperosmolar therapy as a bridge.

Hypertonic saline or mannitol to draw water out of brain tissue and lower ICP; mannitol also acts as an osmotic diuretic — watch volume status and sodium.

Arterial (middle meningeal) bleed with a lucid interval then rapid decline; a biconvex/lens-shaped CT collection that does not cross suture lines.

Venous (bridging-vein) bleed forming a crescent-shaped collection that crosses suture lines; common in the elderly and on anticoagulants, often slower onset.

Continuous or recurrent seizures ≥5 minutes without recovery; treat with a benzodiazepine first, then a second-line agent (levetiracetam, fosphenytoin, valproate).

From spinal cord injury above ~T6: hypotension WITH bradycardia and warm, dry skin from lost sympathetic tone. Treat with fluids, vasopressors, and atropine for bradycardia.

Transient loss of all reflexes and motor/sensory function below a cord injury; distinct from neurogenic shock, which is a hemodynamic state.

In injuries above T6, a noxious stimulus below the lesion triggers severe hypertension with bradycardia and a pounding headache; relieve the trigger (often a full bladder).

The Full Outline of UnResponsiveness coma scale (eye, motor, brainstem, respiration); usable in intubated patients where GCS verbal scoring fails.

Usually a right coronary artery occlusion. Obtain a right-sided ECG (V4R) for RV infarct — it is preload-dependent, so AVOID nitroglycerin.

Tall R waves + ST depression with upright T waves in V1–V3 (mirror image). Confirm with posterior leads V7, V8, V9 and treat as a STEMI.

1 mV = 10 mm of vertical deflection at standard calibration; verify the calibration pulse before judging amplitudes.

Less than 120 ms (under three small boxes). At or above 120 ms is a wide complex — bundle branch block or ventricular origin.

Inflates in diastole (augments coronary perfusion) and deflates in systole (reduces afterload). The air-filled balloon is affected by altitude (Boyle's law).

Left anterior descending occlusion; large myocardium at risk with high risk of pump failure and cardiogenic shock. ST elevation in the precordial leads.

Left circumflex or diagonal occlusion; ST elevation in the lateral leads. Often paired with anterior or inferior territory involvement.

Deeply inverted or biphasic T waves in V2–V3 during pain-free intervals — signals critical proximal LAD stenosis and impending anterior MI; avoid stress testing.

Identifies STEMI in the presence of LBBB or a paced rhythm: concordant ST elevation ≥1 mm, concordant ST depression in V1–V3, or excessively discordant ST elevation.

Peaked T waves → flattened P waves and widened QRS → sine wave → asystole/VF. Stabilize the myocardium with IV calcium first.

Flattened T waves, ST depression, and prominent U waves; predisposes to ventricular ectopy and torsades — replace potassium (and magnesium).

Polymorphic VT with a twisting axis on a prolonged QT; treat with IV magnesium sulfate, correct electrolytes, and overdrive pace if recurrent.

Treat as VT until proven otherwise; consider amiodarone or procainamide. Avoid AV-nodal blockers (e.g., calcium-channel blockers) if VT is possible.

300 mg IV/IO for refractory VF/pulseless VT after defibrillation, with a 150 mg repeat. A maintenance infusion follows return of circulation.

6 mg rapid IV push (then 12 mg) for stable, regular, narrow-complex SVT; causes a brief asystolic pause. Ineffective for atrial fibrillation/flutter.

A shock timed to the R wave for unstable tachycardias with a pulse (AF, flutter, SVT, monomorphic VT) to avoid the vulnerable T-wave R-on-T period.

Atropine 1 mg IV (repeat to 3 mg max); if refractory, transcutaneous pacing or epinephrine/dopamine infusion. Atropine is ineffective for high-grade AV blocks.

Pump failure: high preload, low cardiac output, cool skin. Support with inotropes (dobutamine), pressors as needed, and mechanical support (IABP, Impella).

Hypotension, muffled heart sounds, and JVD; pulsus paradoxus and low voltage/electrical alternans on ECG. Definitive relief is pericardiocentesis.

A continuous-flow pump producing little/no pulse — auscultate for a hum and use MAP via Doppler/arterial line, not SpO₂ or a cuff. Never stop the controller.

A catheter-mounted axial-flow pump that draws blood from the LV and ejects it into the aorta, directly unloading the ventricle in cardiogenic shock.

Early inflation closes the aortic valve prematurely; late deflation increases afterload. Augmentation should appear at the dicrotic notch on the arterial waveform.

Tearing pain, a pulse/blood-pressure differential between arms, possible new murmur. Lower heart rate (esmolol) before vasodilators; control shear force, not just BP.

Obstructive shock with hypotension, acute right-heart strain (S1Q3T3, RBBB), and hypoxia; consider systemic thrombolytics if no contraindication.

Hypothermia + acidosis + coagulopathy — each worsens the others. Add hypocalcemia for the 'trauma diamond.' Break it with damage-control resuscitation.

Permissive hypotension, warmed balanced blood products, aggressive warming, calcium replacement, and early TXA — not large-volume cold crystalloid.

Head/neck 9%, each arm 9%, anterior trunk 18%, posterior trunk 18%, each leg 18%, perineum 1%. The patient's palm ≈ 1% TBSA for scattered burns.

4 mL × weight (kg) × %TBSA of Lactated Ringer's over 24 h. Half in the first 8 h (from the time of the burn), half over the next 16 h; titrate to urine output.

Hypotension, JVD, absent breath sounds, late tracheal deviation. Needle decompression then chest tube; pleural air EXPANDS at altitude (Boyle's law).

From burn over-resuscitation ('fluid creep'): tense abdomen, rising airway pressures, falling urine output, hypotension. Titrate fluids to urine output to prevent it.

Appearance, Pulse, Grimace, Activity, Respiration — each 0–2 (max 10), at 1 and 5 minutes. Describes the newborn but does NOT direct resuscitation.

Ventilation, not compressions. PPV if apneic or HR <100; compressions (3:1) only if HR <60 after effective PPV; epinephrine (UVC) if HR stays <60.

After ~20 weeks the gravid uterus compresses the aorta and IVC when supine. Relieve with left lateral tilt or manual uterine displacement.

New hypertension with proteinuria (or end-organ signs) after 20 weeks; risks seizure and stroke. Control blood pressure (labetalol/hydralazine) and prevent seizures.

Preeclampsia plus seizures; magnesium sulfate is first-line for treatment and prophylaxis. Definitive treatment is delivery of the fetus.

Seizure prophylaxis/treatment in preeclampsia/eclampsia; monitor for toxicity (loss of reflexes, respiratory depression). The antidote is IV calcium gluconate.

Hemolysis, Elevated Liver enzymes, Low Platelets — a severe preeclampsia variant with right-upper-quadrant pain; the definitive treatment is delivery.

Premature placental separation: painful vaginal bleeding, a rigid/tender uterus, and fetal distress; bleeding may be concealed. A maternal-fetal emergency.

A placenta overlying the cervical os causing painless bright-red bleeding; avoid any vaginal/digital exam and prepare for cesarean delivery.

Most often uterine atony; manage with fundal massage and uterotonics (oxytocin, then methylergonovine/misoprostol/TXA) plus blood products.

The umbilical cord presents ahead of the fetus, compressing its blood supply; elevate the presenting part off the cord, knee-chest position, and expedite cesarean.

The fetal shoulder lodges behind the pubic symphysis after head delivery; relieve with McRoberts positioning and suprapubic (not fundal) pressure.

Meconium-stained fluid with a non-vigorous newborn; routine intrapartum suctioning is no longer recommended — prioritize effective ventilation if depressed.

Newborns lose heat fast (high surface area, thin skin); dry, warm, cover the head, and use skin-to-skin or a transport isolette. Cold stress worsens acidosis and hypoglycemia.

Failure of the fetal circulation to transition, with right-to-left shunting and refractory hypoxia; manage oxygenation, minimize stimulation, and consider iNO.

The preferred rapid vascular access for neonatal resuscitation; used for epinephrine and volume when the heart rate stays <60 despite effective ventilation.

Croup: barking cough, gradual, can lie back (racemic epinephrine + dexamethasone). Epiglottitis: abrupt fever, drooling, tripod — keep calm, don't instrument the airway.

4 mL/kg/hr for the first 10 kg + 2 mL/kg/hr for the next 10 kg + 1 mL/kg/hr for each kg over 20. A 25 kg child = 40 + 20 + 5 = 65 mL/hr.

A length-based (crown-to-heel) tape that estimates a child's weight and gives weight-based drug doses and equipment sizes when the weight is unknown.

First shock 2 J/kg, escalating to 4 J/kg and higher on subsequent shocks. Hypoglycemia: ~0.5 g/kg dextrose (5 mL/kg of D10).

A rapid 'from-the-doorway' evaluation of Appearance, Work of Breathing, and Circulation to the skin to categorize the sick child before hands-on assessment.

Children maintain blood pressure with tachycardia and vasoconstriction; hypotension is a LATE, ominous sign. Treat early with 20 mL/kg isotonic boluses.

Large occiput and tongue, anterior/higher larynx, narrowest at the cricoid, short trachea; position with shoulder roll and beware right-mainstem with deep tubes.

A rapid alternative when IV access fails — most drugs/fluids can be given IO; proximal tibia is common. Confirm placement and watch for extravasation.

Viral (RSV) lower-airway infection in infants with wheezing and respiratory distress; care is supportive (suction, oxygen, hydration) — bronchodilators are often unhelpful.

0.01 mg/kg IV/IO of 1:10,000 every 3–5 minutes during cardiac arrest; the leading pediatric arrest cause is respiratory, so prioritize oxygenation and ventilation.

Consider atropine (~0.02 mg/kg) before RSI in young children to blunt the vagal bradycardia of laryngoscopy and succinylcholine.

Injuries inconsistent with the history or developmental stage, patterned marks, or delayed care; mandated reporting and a careful, non-confrontational transport.

Use a length-based tape (Broselow) or a formula when no scale is available; weight-based dosing/equipment errors are a major pediatric safety risk.

Assault = creating reasonable apprehension of imminent harmful/offensive contact (no touch). Battery = actual unconsented physical contact.

Unilaterally ending the provider-patient relationship without consent and without transferring care to an equal or higher level of provider.

Limits CPR if arrest occurs; does NOT bar comfort/supportive care and does NOT become void during transport. Honor a valid order.

The principle obligating the crew to honor a competent, fully informed patient's refusal of care — even when the crew disagrees with the choice.

A physician's order does not expand a paramedic's certified scope; decline the out-of-scope act, explain the limit, and find an alternative within scope.

Ground and Air Medical qUality in Transport — standardized quality-improvement metrics that benchmark transport program performance.

Distinguishes human error and at-risk behavior (coach/console) from reckless behavior (discipline), encouraging non-punitive reporting of near-misses.

Federal law requiring a medical screening exam and stabilization before transfer; an unstable patient may be transferred only when the benefits outweigh the risks.

A lawful interfacility transfer requires accepting facility/physician, qualified personnel and equipment for the patient's needs, and sending of records.

A competent patient must understand the nature, risks, benefits, and alternatives of care before agreeing; documentation of the discussion is essential.

Consent presumed for an unconscious or incapacitated patient with an emergent, life-threatening condition, on the basis that a reasonable person would agree.

Duty, breach of that duty, causation (the breach caused harm), and damages. All four must be present for a malpractice claim to succeed.

Federal protection of patient health information; share protected information only for treatment, payment, operations, or as legally required.

Online (direct, real-time physician) vs offline (protocols/standing orders) medical direction governing the crew's clinical decisions.

Match patient acuity, time/distance, weather, and aircraft capability; the safest appropriate transport — sometimes ground — outweighs raw speed.

Critical Incident Stress Management supports crews after traumatic calls; recognize acute stress and burnout as fitness-for-duty issues, not weakness.