Are flashcards effective for the NBCRNA NCE?

Yes. Flashcards use active recall — retrieving an answer from memory — which research shows is one of the most effective ways to make information stick, especially in short sessions spread over several days. That matters for the high-volume pharmacology and physiology facts the NCE tests.

What topics do the CRNA flashcards cover?

All four NCE content areas: Basic Sciences, Equipment/Instrumentation/Technology, General Principles of Anesthesia (the largest area, including pharmacology, airway, regional, critical events, and professional/ethical/legal content), and Anesthesia for Surgical Procedures and Special Populations — plus exam logistics.

Do the flashcards include drug doses?

Yes, where they are high-yield — but anesthesia is high-stakes, so doses are presented with their concept and monitoring and are drawn from standard references. Always confirm any drug dose against the current FDA label and your institution's protocol before clinical use.

How should I study with these flashcards?

Mix the modes: flip to learn, type to test recall, match for speed, and quiz to check yourself. Spend the most time on General Principles of Anesthesia (35% of the NCE) and thread pharmacology throughout — it appears in every content area.

Are the CRNA flashcards free?

Yes — 100% free, all four study modes, no paywall and no sign-up.

Certified Registered Nurse Anesthetist — an APRN who provides the full spectrum of anesthesia care; certified by the NBCRNA.

National Certification Examination — the exam (administered by the NBCRNA) you pass to earn the CRNA credential.

National Board of Certification and Recertification for Nurse Anesthetists — owns the NCE, sets the content outline and passing standard.

Council on Accreditation of Nurse Anesthesia Educational Programs — accredits the programs candidates must graduate from (distinct from the NBCRNA, which certifies the individual).

American Association of Nurse Anesthesiology — the professional association; publishes practice standards (not the licensing or certifying body).

Variable-length computerized adaptive test (CAT) built on item response theory; 100–170 items (70–140 scored + 30 unscored pretest); 3-hour maximum.

NCE scored vs pretest

Minimum 100 items = 70 scored + 30 random unscored pretest; maximum 170 items (still 30 pretest).

Not allowed — questions are presented one at a time and you cannot return to or skip a previous question.

A single standard-set passing point on an ability scale (the same for every candidate) — there is no fixed passing percentage. Effective July 1, 2026, NBCRNA adjusted this standard to better reflect current professional knowledge and competencies.

Graduate of a COA-accredited program, current unrestricted RN license, and current ACLS and PALS at the time of application.

Doctoral entry to practice

Since January 1, 2022, every matriculating nurse-anesthesia student must enroll in a doctoral program (DNP/DNAP) — a COA standard.

Pass-the-NCE deadline

A candidate must pass the NCE within 2 years of program completion (up to 4 attempts in the first year).

Maintaining Anesthesia Certification — the NBCRNA recertification track: 60 Class A (MAC Ed) + 40 Class B (MAC Dev) credits per 4-year cycle; renew every 4 years.

CPC Assessment (legacy)

A 150-question, non–pass/fail assessment of the four core knowledge domains, taken once every 8 years; being transitioned to the MAC Check.

$ CO = SV \times HR $; normal $ \approx 4\text{–}8 $ L/min.

Stroke volume determinants

Preload, afterload, and contractility.

Increased ventricular preload (end-diastolic stretch) increases stroke volume, up to a point.

Ventricular end-diastolic volume/stretch; approximated by CVP (right) and PCWP/wedge (left).

The resistance the ventricle ejects against; LV afterload $ \approx $ systemic vascular resistance (SVR).

$ SVR = \frac{(MAP - CVP)}{CO} \times 80 $; normal $ \approx 800\text{–}1200 $ $ \text{dynes} \cdot \text{s} \cdot \text{cm}^{-5} $.

Mean arterial pressure (MAP)

$ MAP = DBP + \tfrac{1}{3}(SBP - DBP) $; or $ MAP = CO \times SVR $.

Ejection fraction (normal)

$ EF = SV/EDV \approx 55\text{–}70\% $.

Carotid sinus (CN IX) and aortic arch (CN X) sense rising BP, increasing parasympathetic and decreasing sympathetic outflow to lower HR and BP. Volatiles blunt it.

LV myocardium is perfused mainly during diastole; $ CPP_{coronary} = $ aortic diastolic pressure − LVEDP. Tachycardia is doubly harmful.

Cardiac conduction order

SA node (60–100 bpm) → AV node (delay) → bundle of His → right/left bundle branches → Purkinje fibers.

Oxyhemoglobin curve — right shift

Lower Hb–O₂ affinity (unloads O₂ to tissue): increased CO₂, temperature, 2,3-DPG, and decreased pH. Mnemonic: "CADET, face Right."

Oxyhemoglobin curve — left shift

Higher Hb–O₂ affinity (holds O₂): decreased CO₂, temperature, 2,3-DPG; increased pH; plus fetal hemoglobin, carboxyhemoglobin, and stored blood.

PaO₂ at which hemoglobin is 50% saturated; normal adult $ \approx 26.6\text{–}26.8 $ mmHg. A higher P50 = right shift.

Ventilation without perfusion (V without Q); anatomic (~2 mL/kg) + alveolar = physiologic dead space; normal $ V_D/V_T \approx 0.30\text{–}0.33 $.

Perfusion without ventilation (Q without V); causes hypoxemia that does NOT correct with 100% O₂ (key distinguishing feature).

Functional residual capacity (FRC)

Volume remaining after a normal expiration; the O₂ reservoir during apnea. Falls ~15–20% on induction and with obesity, pregnancy, and supine position.

Lung volume at which small airways begin to close; increases with age — when it exceeds FRC, atelectasis and shunt develop.

$ \dot{V}_E = V_T \times RR $ (tidal volume $ \times $ respiratory rate).

Tidal volume (normal)

$ \approx 6\text{–}8 $ mL/kg ideal body weight.

Alveolar gas equation

$ P_{A}O_2 = FiO_2(P_{atm} - P_{H_2O}) - \tfrac{PaCO_2}{R} $; room air at sea level $ \approx 100 $ mmHg. Normal A–a gradient 5–15 mmHg.

Hypoxic pulmonary vasoconstriction

Alveolar hypoxia causes local pulmonary vasoconstriction that diverts blood to better-ventilated lung; volatile anesthetics inhibit it (relevant to one-lung ventilation).

Cerebral perfusion pressure (CPP)

$ CPP = MAP - ICP $ (or MAP − CVP, whichever is higher); normal $ \approx 60\text{–}80 $ mmHg.

Cerebral autoregulation

CBF held roughly constant over MAP $ \approx 50\text{–}150 $ mmHg; outside this range flow becomes pressure-passive.

CBF changes ~1–2 mL/100 g/min per 1 mmHg change in PaCO₂; hyperventilation transiently lowers CBF and ICP.

Volatile agents and the brain

Cerebral vasodilators that increase CBF and ICP while decreasing CMRO₂ ("uncoupling"); propofol/barbiturates lower CBF, CMRO₂, and ICP (coupled).

Monro-Kellie doctrine

The cranial vault is fixed: brain + blood + CSF is constant; an increase in one component raises ICP unless another decreases.

$ 5\text{–}15 $ mmHg; treat sustained values above ~20–22 mmHg.

$ \approx 50 $ mL/100 g/min (~15% of cardiac output); CMRO₂ $ \approx 3\text{–}3.8 $ mL O₂/100 g/min.

$ \approx 125 $ mL/min (~180 L/day); normal urine output $ \geq 0.5 $ mL/kg/hr.

$ \approx 20\text{–}25\% $ of cardiac output; the medulla is relatively hypoxic and vulnerable to ischemia.

Your FREE CRNA Flashcards 2026 – 250+ Cards

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CRNA Flashcards

CRNA: Certified Registered Nurse Anesthetist — an APRN who provides the full spectrum of anesthesia care; certified by the NBCRNA.
NCE: National Certification Examination — the exam (administered by the NBCRNA) you pass to earn the CRNA credential.
NBCRNA: National Board of Certification and Recertification for Nurse Anesthetists — owns the NCE, sets the content outline and passing standard.
COA: Council on Accreditation of Nurse Anesthesia Educational Programs — accredits the programs candidates must graduate from (distinct from the NBCRNA, which certifies the individual).
AANA: American Association of Nurse Anesthesiology — the professional association; publishes practice standards (not the licensing or certifying body).
NCE format: Variable-length computerized adaptive test (CAT) built on item response theory; 100–170 items (70–140 scored + 30 unscored pretest); 3-hour maximum.
NCE scored vs pretest: Minimum 100 items = 70 scored + 30 random unscored pretest; maximum 170 items (still 30 pretest).
NCE back-tracking: Not allowed — questions are presented one at a time and you cannot return to or skip a previous question.
NCE passing standard: A single standard-set passing point on an ability scale (the same for every candidate) — there is no fixed passing percentage. Effective July 1, 2026, NBCRNA adjusted this standard to better reflect current professional knowledge and competencies.
NCE eligibility: Graduate of a COA-accredited program, current unrestricted RN license, and current ACLS and PALS at the time of application.
Doctoral entry to practice: Since January 1, 2022, every matriculating nurse-anesthesia student must enroll in a doctoral program (DNP/DNAP) — a COA standard.
Pass-the-NCE deadline: A candidate must pass the NCE within 2 years of program completion (up to 4 attempts in the first year).
MAC Program (recert): Maintaining Anesthesia Certification — the NBCRNA recertification track: 60 Class A (MAC Ed) + 40 Class B (MAC Dev) credits per 4-year cycle; renew every 4 years.
CPC Assessment (legacy): A 150-question, non–pass/fail assessment of the four core knowledge domains, taken once every 8 years; being transitioned to the MAC Check.
Cardiac output (CO): $CO = SV \times HR$ ; normal $\approx 4\text{–}8$ L/min.
Stroke volume determinants: Preload, afterload, and contractility.
Frank-Starling law: Increased ventricular preload (end-diastolic stretch) increases stroke volume, up to a point.
Preload: Ventricular end-diastolic volume/stretch; approximated by CVP (right) and PCWP/wedge (left).
Afterload: The resistance the ventricle ejects against; LV afterload $\approx$ systemic vascular resistance (SVR).
SVR formula: $SVR = \frac{(MAP - CVP)}{CO} \times 80$ ; normal $\approx 800\text{–}1200$ $\text{dynes} \cdot \text{s} \cdot \text{cm}^{-5}$ .
Mean arterial pressure (MAP): $MAP = DBP + \tfrac{1}{3}(SBP - DBP)$ ; or $MAP = CO \times SVR$ .
Ejection fraction (normal): $EF = SV/EDV \approx 55\text{–}70\%$ .
Baroreceptor reflex: Carotid sinus (CN IX) and aortic arch (CN X) sense rising BP, increasing parasympathetic and decreasing sympathetic outflow to lower HR and BP. Volatiles blunt it.
Coronary perfusion: LV myocardium is perfused mainly during diastole; $CPP_{coronary} =$ aortic diastolic pressure − LVEDP. Tachycardia is doubly harmful.
Cardiac conduction order: SA node (60–100 bpm) → AV node (delay) → bundle of His → right/left bundle branches → Purkinje fibers.
Oxyhemoglobin curve — right shift: Lower Hb–O₂ affinity (unloads O₂ to tissue): increased CO₂, temperature, 2,3-DPG, and decreased pH. Mnemonic: "CADET, face Right."
Oxyhemoglobin curve — left shift: Higher Hb–O₂ affinity (holds O₂): decreased CO₂, temperature, 2,3-DPG; increased pH; plus fetal hemoglobin, carboxyhemoglobin, and stored blood.
P50: PaO₂ at which hemoglobin is 50% saturated; normal adult $\approx 26.6\text{–}26.8$ mmHg. A higher P50 = right shift.
Dead space: Ventilation without perfusion (V without Q); anatomic (~2 mL/kg) + alveolar = physiologic dead space; normal $V_D/V_T \approx 0.30\text{–}0.33$ .
Shunt: Perfusion without ventilation (Q without V); causes hypoxemia that does NOT correct with 100% O₂ (key distinguishing feature).
Functional residual capacity (FRC): Volume remaining after a normal expiration; the O₂ reservoir during apnea. Falls ~15–20% on induction and with obesity, pregnancy, and supine position.
Closing capacity: Lung volume at which small airways begin to close; increases with age — when it exceeds FRC, atelectasis and shunt develop.
Minute ventilation: $\dot{V}_E = V_T \times RR$ (tidal volume $\times$ respiratory rate).
Tidal volume (normal): $\approx 6\text{–}8$ mL/kg ideal body weight.
Alveolar gas equation: $P_{A}O_2 = FiO_2(P_{atm} - P_{H_2O}) - \tfrac{PaCO_2}{R}$ ; room air at sea level $\approx 100$ mmHg. Normal A–a gradient 5–15 mmHg.
Hypoxic pulmonary vasoconstriction: Alveolar hypoxia causes local pulmonary vasoconstriction that diverts blood to better-ventilated lung; volatile anesthetics inhibit it (relevant to one-lung ventilation).
Cerebral perfusion pressure (CPP): $CPP = MAP - ICP$ (or MAP − CVP, whichever is higher); normal $\approx 60\text{–}80$ mmHg.
Cerebral autoregulation: CBF held roughly constant over MAP $\approx 50\text{–}150$ mmHg; outside this range flow becomes pressure-passive.
CBF and PaCO₂: CBF changes ~1–2 mL/100 g/min per 1 mmHg change in PaCO₂; hyperventilation transiently lowers CBF and ICP.
Volatile agents and the brain: Cerebral vasodilators that increase CBF and ICP while decreasing CMRO₂ ("uncoupling"); propofol/barbiturates lower CBF, CMRO₂, and ICP (coupled).
Monro-Kellie doctrine: The cranial vault is fixed: brain + blood + CSF is constant; an increase in one component raises ICP unless another decreases.
Normal ICP: $5\text{–}15$ mmHg; treat sustained values above ~20–22 mmHg.
CBF (normal): $\approx 50$ mL/100 g/min (~15% of cardiac output); CMRO₂ $\approx 3\text{–}3.8$ mL O₂/100 g/min.
GFR (normal): $\approx 125$ mL/min (~180 L/day); normal urine output $\geq 0.5$ mL/kg/hr.
Renal blood flow: $\approx 20\text{–}25\%$ of cardiac output; the medulla is relatively hypoxic and vulnerable to ischemia.
Henderson-Hasselbalch: $pH = 6.1 + \log\frac{[HCO_3^-]}{0.03 \times PaCO_2}$ .
Respiratory acidosis: Increased PaCO₂, decreased pH (hypoventilation); renal compensation raises HCO₃⁻ over days.
Anion gap: $AG = Na^+ - (Cl^- + HCO_3^-)$ ; normal $\approx 8\text{–}12$ mEq/L. High-gap causes: MUDPILES.
Winter's formula: Expected respiratory compensation for metabolic acidosis: expected $PaCO_2 = 1.5\,[HCO_3^-] + 8 \pm 2$ .
Normal serum K⁺: $3.5\text{–}5.0$ mEq/L; hyperkalemia → peaked T waves → widened QRS → sine wave.
Normal serum Na⁺: $135\text{–}145$ mEq/L; rapid correction of hyponatremia risks osmotic demyelination.
Body water (60-40-20 rule): Total body water $\approx 60\%$ of body weight; ICF ~40%, ECF ~20% (one-quarter of ECF is intravascular plasma).
Hyperkalemia ECG: Peaked T waves → widened QRS → sine wave; treat with calcium, insulin/glucose, bicarbonate, and beta-agonists.
Pharmacokinetics: What the body does to the drug: absorption, distribution, metabolism, excretion (ADME).
Pharmacodynamics: What the drug does to the body: receptor effect and dose-response.
Volume of distribution (Vd): $V_d = \frac{\text{amount of drug in body}}{\text{plasma concentration}}$ ; a large Vd indicates a lipophilic, tissue-bound drug. Loading dose $= V_d \times$ target concentration.
Clearance: Volume of plasma cleared of drug per unit time; the main determinant of steady-state concentration (maintenance rate $=$ clearance $\times$ target concentration).
Elimination half-life: $t_{1/2} = \frac{0.693 \times V_d}{Cl}$ ; ~5 half-lives to reach steady state or eliminate ~97% of a drug.
Context-sensitive half-time: Time for plasma concentration to fall 50% after STOPPING a continuous infusion; lengthens with infusion duration for most drugs — but stays flat (~3–4 min) for remifentanil.
First-order kinetics: A constant FRACTION of drug is eliminated per unit time (most drugs).
Zero-order kinetics: A constant AMOUNT is eliminated per unit time (saturable enzymes): ethanol, phenytoin, high-dose aspirin.
Potency vs efficacy: Potency = dose needed for an effect (position of the curve, EC50); efficacy = maximal achievable effect (height of the curve).
Redistribution: A single bolus of propofol or thiopental wears off mainly by redistribution from the brain to muscle/fat, not by metabolism.
Competitive antagonist: Binds without activating and shifts the dose-response curve to the right (surmountable) — e.g., naloxone, flumazenil, nondepolarizing NMBAs.
Boyle's law: At constant temperature, $P \propto 1/V$ ( $P_1V_1 = P_2V_2$ ) — estimates O₂ cylinder content.
Charles's law: At constant pressure, $V \propto T$ ( $V_1/T_1 = V_2/T_2$ ).
Gay-Lussac's law: At constant volume, $P \propto T$ — cylinder pressure rises if heated.
Dalton's law: Total pressure = sum of the partial pressures of each gas in a mixture.
Henry's law: The amount of gas dissolved in a liquid is proportional to its partial pressure above the liquid (basis of blood:gas solubility).
Graham's law: Rate of gas diffusion $\propto 1/\sqrt{MW}$ — lighter gases diffuse faster.
Fick's law of diffusion: Diffusion $\propto \frac{\text{area} \times \Delta\text{partial pressure}}{\text{membrane thickness}}$ ; thicker membranes (edema/fibrosis) slow diffusion.
Poiseuille's law: Laminar flow $Q = \frac{\pi \Delta P\, r^4}{8 \eta L}$ — flow is proportional to the FOURTH power of the radius; resistance depends on viscosity.
Turbulent flow: Occurs at high flow/large radii; flow $\propto \sqrt{\Delta P}$ and resistance depends on DENSITY (basis for Heliox in airway obstruction).
Reynolds number: $Re = \frac{\rho v d}{\eta}$ ; $Re < \sim 2000$ = laminar, $> \sim 4000$ = turbulent.
Bernoulli / Venturi effect: Where gas velocity increases through a constriction, lateral pressure falls — entrains a second gas (nebulizers, jet ventilation).
Blood:gas coefficient: Lower = faster onset/offset: desflurane 0.42 < nitrous oxide 0.46 < sevoflurane 0.65 < isoflurane 1.4.
Oil:gas coefficient: Correlates with POTENCY (Meyer–Overton): higher oil:gas → lower MAC → more potent.
Pin Index Safety System (PISS): Prevents attaching the wrong gas CYLINDER to the yoke via a unique two-pin geometry per gas.
Diameter Index Safety System (DISS): Prevents misconnection of PIPELINE hoses via gas-specific threaded diameters.
E-cylinder O₂: Full ~1900–2200 psi, ~625–660 L; stored as a gas, so pressure falls linearly with content (a half-full cylinder reads ~1000 psi).
E-cylinder N₂O: Full ~745 psi, ~1590 L; stored as a liquid, so the gauge stays ~745 psi until the liquid is gone — weigh the cylinder to estimate contents.
Pipeline pressure: $\approx 50$ psi (the primary working source); cylinder regulators reduce to ~45 psi so the pipeline is used preferentially.
Oxygen fail-safe: Pressure-sensing device that shuts off/reduces N₂O if O₂ SUPPLY PRESSURE falls — it does NOT detect a crossed pipeline or low O₂ concentration.
Oxygen proportioning system: Links O₂ and N₂O flow controls to guarantee a minimum FiO₂ (~25%): Datex-Ohmeda Link-25 or Dräger ORMC. Cannot prevent a crossed pipeline or a third gas.
Oxygen analyzer: The only true last-line defense against a hypoxic mixture — placed in the inspiratory limb, downstream of all mechanical safety devices.
O₂ flowmeter position: Positioned downstream (closest to the common outlet) so a leak in an upstream flowmeter is least likely to cause a hypoxic mixture.
Variable-bypass vaporizer: Splits flow and recombines streams to deliver the dialed concentration (sevo, iso); temperature-compensated; delivers constant PARTIAL PRESSURE despite altitude.
Desflurane Tec 6 vaporizer: Heated (~39°C) and pressurized because desflurane boils ~22.8°C; delivers a constant % — so at altitude its partial pressure FALLS (dial up at altitude).
Oxygen flush valve: Delivers ~35–75 L/min of pure O₂, bypassing the vaporizers; hazards are barotrauma and dilution/awareness.
First machine checkout item: Confirm a backup means of ventilation (a self-inflating/Ambu bag) is available — you must always be able to ventilate if the machine fails.
Circle system: Allows rebreathing after CO₂ absorption; uses two unidirectional valves, a CO₂ absorber, an APL valve, and a reservoir bag.
CO₂ absorbent reaction: $\ce{CO2 + H2O -> H2CO3}$ ; then $\ce{H2CO3 + Ca(OH)2 -> CaCO3 + H2O}$ + heat (exothermic).
Compound A: A nephrotoxic degradation product of SEVOFLURANE with desiccated strong-base absorbents; mitigate with adequate fresh-gas flow and KOH/NaOH-free absorbents.
Carbon monoxide (absorbent): Produced when DESICCATED absorbent degrades volatiles — worst with desflurane/isoflurane; classic Monday-morning first case after gas was left flowing.
Mapleson A (Magill): Most efficient for SPONTANEOUS ventilation.
Mapleson D / Bain: Most efficient for CONTROLLED ventilation; the Bain is a coaxial D (fresh gas runs inside the expiratory tube).
Pethick test: Confirms inner-tube integrity of a Bain circuit before use (a disconnected inner tube causes massive rebreathing).
Ascending bellows: The safe ventilator design — it fails to refill and collapses on a disconnect, giving an obvious visual alarm.
Scavenging hazard: A malfunctioning scavenging system can transmit excessive positive (barotrauma) or negative pressure to the patient's airway.
ASA standard monitors: Continuous evaluation of oxygenation, ventilation, circulation, and temperature during every anesthetic, with a qualified provider present.
Capnography (EtCO₂ normal): $\approx 35\text{–}45$ mmHg; the gold-standard, fastest confirmation of correct ETT placement.
Capnograph — rising baseline: Phase I above zero = rebreathing (incompetent valve, exhausted absorbent, inadequate fresh-gas flow).
Capnograph — shark-fin: A sloped upstroke with loss of plateau = expiratory obstruction (bronchospasm, COPD, kinked ETT).
Capnograph — sudden loss: A flatline = esophageal intubation, circuit disconnect, complete obstruction, or cardiac arrest.
Capnograph — curare cleft: A notch in the plateau = a spontaneous breath during mechanical ventilation (returning/inadequate neuromuscular blockade).
Pulse oximetry principle: Uses two wavelengths (red 660 nm, infrared 940 nm) and the Beer–Lambert law on the pulsatile arterial signal.
Methemoglobin and SpO₂: Drives the SpO₂ reading toward ~85% regardless of the true saturation.
Carboxyhemoglobin and SpO₂: Falsely HIGH/normal SpO₂ — the pulse oximeter cannot distinguish COHb from oxyhemoglobin, masking CO poisoning.
ECG lead II: Best for detecting P waves/dysrhythmias and inferior-wall (RCA) ischemia.
ECG lead V5: Best single lead for detecting anterolateral (LV) ischemia (LAD/circumflex).
Arterial line — overdamped: Sluggish trace, lost dicrotic notch → falsely low systolic; caused by air bubbles, clots, kinks.
Arterial line — underdamped: Overshoot/ringing → falsely high systolic; caused by stiff tubing or catheter whip.
Transducer leveling: Zero at the phlebostatic axis (4th intercostal space, mid-axillary line, $\approx$ right atrium); use the external auditory meatus for the sitting craniotomy.
CVP a wave: Atrial contraction; lost in atrial fibrillation, large "cannon a waves" in AV dissociation/complete heart block.
CVP v wave: Atrial filling against a closed tricuspid valve; large v waves occur in tricuspid regurgitation.
BIS monitor: Processed EEG (0–100); target 40–60 for general anesthesia. Ketamine and N₂O may keep BIS falsely high.
Train-of-four (TOF): Four stimuli at 2 Hz over 2 seconds; the TOF ratio (T4/T1) quantifies nondepolarizing block recovery.
TOF count and block depth: 0 twitches = deep block; 1–2 twitches = adequate surgical relaxation; 4 with no fade = recovery.
Adequate reversal (TOF ratio): A TOF ratio $\geq 0.9$ indicates acceptable recovery; quantitative monitoring is needed to confirm it.
Post-tetanic count (PTC): Used to gauge DEEP block when the TOF count is 0; fewer post-tetanic twitches = deeper block.
Phase I block (sux): Sustained response to tetanus, NO fade, NO post-tetanic facilitation; potentiated (not reversed) by anticholinesterases.
Phase II block: Develops with high/repeated succinylcholine; shows fade and post-tetanic facilitation like a nondepolarizing block.
Core temperature sites: Best: pulmonary artery (gold standard), distal esophagus, nasopharynx, tympanic membrane.
Macintosh blade: Curved; tip into the vallecula to indirectly lift the epiglottis (more room for tube passage).
Miller blade: Straight; lifts the epiglottis directly — preferred in infants (long, floppy epiglottis).
LMA (supraglottic airway): Seats over the glottis; does NOT protect against aspiration; a key rescue device in the difficult-airway algorithm.
Video laryngoscope: Camera at the blade tip gives an around-the-corner view; often needs a rigid stylet (the "see it but can't pass it" pitfall).
Flexible fiberoptic intubation: Gold standard for the anticipated difficult / awake airway and the unstable cervical spine.
Bougie: An introducer railroaded into the trachea when only the epiglottis is seen; "tracheal clicks" confirm placement.
Cricothyrotomy: Emergency surgical/needle airway for the "cannot intubate, cannot oxygenate" (CICO) situation.
ETT cuff pressure: Maintain $20\text{–}30$ cmH₂O; above ~30 cmH₂O impairs tracheal mucosal perfusion. N₂O diffuses in and raises cuff pressure.
Pediatric ETT size (uncuffed): $\text{ID (mm)} = \frac{\text{age}}{4} + 4$ for children older than 2 years.
MAC: Minimum alveolar concentration preventing movement to surgical incision in 50% of patients — an ED50 and the index of inhaled-agent potency.
MAC of sevoflurane: $\approx 2.0\%$ in oxygen.
MAC of desflurane: $\approx 6.0\%$ .
MAC of isoflurane: $\approx 1.15\text{–}1.2\%$ .
MAC of nitrous oxide: $\approx 104\%$ — cannot reach 1 MAC alone at 1 atmosphere, so it is used as an adjunct.
MAC additivity: MAC values are additive: 0.5 MAC sevoflurane + 0.5 MAC N₂O $\approx$ 1 MAC.
Second gas effect: High-volume uptake of N₂O concentrates a co-administered volatile, speeding its onset.
Concentration effect: A higher inspired concentration speeds the rise of the alveolar concentration (FA/FI).
Diffusion hypoxia: On stopping N₂O, it pours into the alveoli and dilutes O₂ — give 100% O₂ for 3–5 minutes at emergence.
MAC-awake: $\approx 0.3\text{–}0.5$ MAC — the concentration at which consciousness is lost/regained.
Factors that DECREASE MAC: Increasing age, hypothermia, pregnancy, opioids/sedatives, α2-agonists, acute alcohol, hyponatremia.
Factors that INCREASE MAC: Hyperthermia, chronic alcohol use, acute amphetamine/cocaine, hypernatremia.
Volatile agents and MH: All volatile anesthetics are malignant-hyperthermia triggers; nitrous oxide is essentially a non-trigger.
Sevoflurane: Nonpungent → ideal for inhalational (mask) induction; forms Compound A with desiccated absorbents.
Desflurane: Lowest blood:gas (fastest emergence) but pungent (airway irritation); rapid increases cause sympathetic stimulation; needs the heated Tec 6.
Nitrous oxide cautions: Diffuses into air-filled spaces (avoid in pneumothorax, bowel obstruction, middle-ear/retinal-gas surgery); inactivates vitamin B₁₂.
Propofol: GABA-A agonist; induction $\approx 1.5\text{–}2.5$ mg/kg IV; lowers BP (vasodilation), antiemetic, pain on injection.
Propofol infusion syndrome: Prolonged high-dose infusion → metabolic acidosis, rhabdomyolysis, lipemia, cardiac failure.
Etomidate: GABA-A modulator; $\approx 0.2\text{–}0.3$ mg/kg; hemodynamically stable but causes adrenal suppression (11-β-hydroxylase) and myoclonus.
Ketamine: NMDA-receptor antagonist; $\approx 1\text{–}2$ mg/kg IV; sympathomimetic, bronchodilator, analgesic; emergence reactions; dissociative anesthesia.
Ketamine mechanism: A noncompetitive NMDA-receptor antagonist producing dissociative anesthesia.
Dexmedetomidine: Central α2-agonist; sedation/analgesia with minimal respiratory depression; causes bradycardia and hypotension.
Midazolam: Benzodiazepine (GABA-A); anxiolysis and anterograde amnesia; reversed by flumazenil.
Thiopental: Barbiturate (GABA-A); contraindicated in porphyria; cerebroprotective (lowers CMRO₂/CBF).
Fentanyl: Potency $\approx 100\times$ morphine; fast onset, ~30–60 min by redistribution; intraop bolus ~1–3 mcg/kg. CSHT rises with prolonged infusion.
Sufentanil: The most potent opioid in common use ( $\approx 1000\times$ morphine).
Remifentanil: Ultra-short opioid metabolized by nonspecific plasma esterases; context-sensitive half-time stays ~3–5 min regardless of infusion duration.
Morphine: Active metabolite morphine-6-glucuronide accumulates in renal failure; causes histamine release.
Meperidine: Treats postoperative shivering; metabolite normeperidine causes seizures; avoid with MAOIs (serotonin syndrome).
Naloxone: Opioid antagonist; reverses respiratory depression but is short-acting (re-narcotization risk).
Opioid side effects: Respiratory depression, miosis, bradycardia, constipation, pruritus, nausea, and chest-wall rigidity with rapid high doses.
Succinylcholine: Depolarizing NMBA $\approx 1\text{–}1.5$ mg/kg IV; fastest onset (~30–60 s), shortest duration (~5–10 min).
Succinylcholine mechanism: Binds and activates the nicotinic ACh receptor → sustained depolarization → fasciculations then flaccid paralysis (Phase I).
Succinylcholine contraindications: Hyperkalemia-risk states (burns/crush/denervation older than ~24–48 h, prolonged immobility), MH history, myopathies, pseudocholinesterase deficiency.
Succinylcholine side effects: Hyperkalemia, MH trigger, bradycardia, myalgias, and increased ICP, intraocular, and intragastric pressure.
Pseudocholinesterase deficiency: Prolongs succinylcholine paralysis; a dibucaine number ~20 indicates the homozygous atypical enzyme.
Rocuronium: Nondepolarizing aminosteroid; $\approx 0.6$ mg/kg to intubate, $\approx 1.2$ mg/kg for RSI; reversible by sugammadex.
Vecuronium: Nondepolarizing aminosteroid; intermediate duration; no histamine release; reversible by sugammadex.
Cisatracurium: Nondepolarizing benzylisoquinolinium cleared by Hofmann elimination (organ-independent) — ideal in renal/hepatic failure.
Nondepolarizer mechanism: Competitive antagonists at the ACh receptor; block shows fade on TOF/tetanus and post-tetanic potentiation; potentiated by volatiles, aminoglycosides, and magnesium.
Neostigmine: Acetylcholinesterase inhibitor; $\approx 0.04\text{–}0.07$ mg/kg; give with glycopyrrolate; has a ceiling (needs some twitches present).
Sugammadex: γ-cyclodextrin that encapsulates rocuronium/vecuronium; $\approx 2$ mg/kg (moderate block), 4 mg/kg (deep), 16 mg/kg (immediate). Binds hormonal contraceptives.
Sugammadex mechanism: Encapsulates aminosteroid NMBAs in plasma, creating a gradient that pulls them off the receptor; renally excreted.
Edrophonium: Short-acting cholinesterase inhibitor paired with atropine (matched onset).
Local anesthetic mechanism: Block voltage-gated sodium channels from the intracellular side, preventing action-potential propagation.
Esters vs amides: Esters (one "i"): plasma-cholinesterase metabolism, PABA allergy risk. Amides (two "i"s): hepatic metabolism, rare true allergy.
LA onset and pKa: The closer the pKa is to physiologic pH, the larger the non-ionized fraction and the faster the onset; acidotic/infected tissue blocks poorly.
LA potency and duration: Potency tracks lipid solubility; duration tracks protein binding (epinephrine prolongs duration and reduces absorption).
Lidocaine max dose: $\approx 4.5$ mg/kg plain, $\approx 7$ mg/kg with epinephrine.
Bupivacaine: Long-acting amide; the most CARDIOTOXIC local anesthetic (avid Na-channel binding); max $\approx 2.5\text{–}3$ mg/kg.
Ropivacaine: Long-acting amide; less cardiotoxic than bupivacaine (S-enantiomer); good sensory-motor differential.
LAST — signs: CNS first (perioral numbness, tinnitus, seizures), then cardiovascular collapse.
LAST — treatment: 20% lipid emulsion ( $\approx 1.5$ mL/kg bolus then 0.25 mL/kg/min), airway/100% O₂, benzodiazepines for seizures, reduced-dose epinephrine, avoid vasopressin.
Mallampati classification: Class I: soft palate, fauces, uvula, pillars; II: uvula; III: soft palate + base of uvula; IV: hard palate only. Higher class predicts harder intubation.
LEMON assessment: Look externally, Evaluate 3-3-2, Mallampati, Obstruction, Neck mobility — predicts a difficult airway.
3-3-2 rule: 3 fingers mouth opening, 3 fingers chin-to-hyoid, 2 fingers hyoid-to-thyroid notch.
Preoxygenation goal: Denitrogenate the FRC to extend safe apnea time; target end-tidal O₂ above ~90%.
Rapid sequence induction (RSI): Preoxygenate → rapid induction agent + fast paralytic (sux or high-dose roc) → intubate without (or with limited) mask ventilation; for aspiration risk.
ASA Physical Status I: A normal healthy patient.
ASA II: Mild systemic disease (controlled HTN/DM, smoker, pregnancy, obesity).
ASA III: Severe systemic disease with substantive limitation (poorly controlled DM/HTN, COPD, stable CAD).
ASA IV: Severe systemic disease that is a constant threat to life (recent MI, sepsis).
ASA V: Moribund patient not expected to survive without the operation (ruptured AAA).
ASA VI: A brain-dead patient whose organs are being procured.
ASA "E" modifier: Emergency — appended to any ASA class.
NPO — clear liquids: 2 hours.
NPO — breast milk: 4 hours.
NPO — formula / light meal: 6 hours.
NPO — fatty/heavy meal: 8 hours.
4-2-1 maintenance fluid rule: 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 above 20.
Crystalloid vs colloid: Crystalloids (LR, NS) distribute to the extracellular fluid (~3:1 replacement); colloids (albumin) stay intravascular longer.
Massive transfusion ratio: Balanced ~1:1:1 PRBC : FFP : platelets; watch citrate (hypocalcemia), hyperkalemia, and hypothermia.
PRBC effect: Each unit raises hemoglobin by ~1 g/dL in an average adult.
Citrate toxicity: Citrate in stored blood chelates calcium → hypocalcemia (hypotension, prolonged QT); treat with calcium.
OR fire triad: Oxidizer (O₂/N₂O) + ignition (cautery/laser) + fuel (drapes, prep, ETT); minimize O₂ in a shared airway.
TIVA: Total intravenous anesthesia (e.g., propofol + remifentanil); useful when volatiles are contraindicated (MH risk).
Monitored anesthesia care (MAC): A sedation continuum (light/moderate/deep) with a provider monitoring the patient.
Four ethical principles: Autonomy, beneficence, nonmaleficence, justice (plus veracity and fidelity).
Informed consent elements: Capacity, disclosure, understanding, voluntariness.
DNR in the OR: Not automatically suspended — "required reconsideration": discuss and clarify the DNR's intraoperative status before surgery.
Negligence (4 D's): Duty, Dereliction (breach), Direct causation, Damages — all four are required to prove malpractice.
Standard of care: What a reasonably prudent, similarly trained provider would do under the same circumstances.
Res ipsa loquitur: "The thing speaks for itself" — an injury that does not occur without negligence (e.g., a retained sponge).
Captain of the ship: An older doctrine (largely abandoned) holding the surgeon liable for everyone in the OR; CRNAs are accountable for their own practice.
Just culture: Console human error, coach at-risk behavior, and discipline reckless behavior — keyed to the behavior, not the outcome.
TEFRA medical direction: The 7 steps an anesthesiologist must meet to medically direct $\leq 4$ concurrent CRNA cases.
QZ modifier: Billing modifier for a CRNA service WITHOUT medical direction (nondirected).
QX modifier: Billing modifier for a CRNA service WITH medical direction by a physician.
Medicare opt-out: A state's governor may opt out of the federal physician-supervision requirement for CRNAs (state law still governs).
Provider substance use disorder: Anesthesia is a high-risk specialty; the most-diverted agents are fentanyl/opioids and propofol; the first sign is sometimes death. Witness all wastage.
Levels of evidence: Strongest: systematic review/meta-analysis of RCTs > RCT > cohort > case-control > case series > expert opinion.
Sensitivity vs specificity: High sensitivity, when Negative, rules OUT (SnNout); high specificity, when Positive, rules IN (SpPin).
Malignant hyperthermia: A hypermetabolic crisis from volatile agents/succinylcholine in RYR1-susceptible patients.
MH — earliest sign: An unexplained, rapidly rising EtCO₂ unresponsive to increased ventilation (hyperthermia is a LATE sign).
MH — treatment: Stop triggers, hyperventilate with 100% O₂, give dantrolene 2.5 mg/kg IV (repeat up to ~10 mg/kg), cool, and treat hyperkalemia/acidosis/arrhythmias.
Dantrolene mechanism: Inhibits the ryanodine (RYR1) receptor, blocking calcium release from the sarcoplasmic reticulum.
Anaphylaxis — intraop: Hypotension and bronchospasm; the #1 perioperative cause is neuromuscular blockers; first-line treatment is epinephrine.
Laryngospasm: Reflex glottic closure (often light anesthesia/emergence); treat with positive-pressure O₂, jaw thrust (Larson's point), deepen, and low-dose succinylcholine if severe.
Bronchospasm: Wheeze, rising peak pressures, upsloping capnograph; deepen anesthesia, give an inhaled β2-agonist, and epinephrine if severe.
Intraoperative awareness: Explicit recall under general anesthesia; risk with TIVA, paralysis, and light anesthesia; reduce with end-tidal agent monitoring and BIS.
PONV — Apfel score: Female sex, nonsmoker, history of PONV/motion sickness, and postoperative opioids; manage with multimodal antiemetics.
Spinal anesthesia: A single injection into the subarachnoid/intrathecal space (below L1–L2 in adults); small dose, fast dense block.
Conus medullaris: The spinal cord ends ~L1–L2 in adults (L3 in infants); place neuraxial needles below this level.
Tuffier's line: The intercristal line connecting the iliac crests; crosses ~the L4 body / L4–L5 interspace.
Neuraxial needle layers: Skin → subcutaneous fat → supraspinous ligament → interspinous ligament → ligamentum flavum → epidural space → dura → arachnoid → CSF.
Spinal baricity: Hyperbaric solutions sink to dependent regions and follow gravity/patient position to set block height.
Spinal complications: Hypotension (sympathectomy), bradycardia (high block, T1–T4), high/total spinal, PDPH, and urinary retention.
Post-dural-puncture headache: A positional headache (worse upright) from a CSF leak; treat conservatively, then with an epidural blood patch.
Epidural anesthesia: A catheter in the epidural (potential) space identified by loss of resistance; titratable, slower onset, larger volume than spinal.
Epidural test dose: ~3 mL lidocaine with epinephrine 1:200,000; a rising HR suggests intravascular placement, a rapid dense block suggests intrathecal.
Interscalene block: For shoulder surgery; causes ~100% ipsilateral phrenic nerve palsy — avoid in severe respiratory disease.
Supraclavicular block: The "spinal of the arm"; main risk is pneumothorax (proximity to the pleura).
Axillary block: For forearm/hand surgery; often spares the musculocutaneous nerve (it leaves the plexus early).
Dermatome — T4: The nipple line; the target sensory level for cesarean section and upper-abdominal surgery.
Dermatome — T10: The umbilicus; the target level for TURP and labor analgesia.
One-lung ventilation: Lung isolation with a double-lumen tube or bronchial blocker; manage hypoxemia with CPAP to the nondependent lung and PEEP to the dependent lung.
Cardiopulmonary bypass — heparin: Full heparinization before cannulation, target ACT > ~400–480 s; reverse with protamine (~1 mg per 100 units heparin).
Cardioplegia: A high-potassium solution that arrests the heart in diastole to minimize myocardial O₂ demand.
Venous air embolism: Risk in sitting craniotomy; signs are a sudden drop in EtCO₂ and a "mill-wheel" murmur; place in left-lateral head-down (Durant) position and aspirate via a right-atrial catheter.
Neuroanesthesia — ICP: Lower ICP with transient hyperventilation, head-up neutral positioning, mannitol/hypertonic saline; maintain CPP.
Pregnancy physiology: Increased cardiac output and blood volume, decreased FRC, increased O₂ consumption and aspiration risk, dilutional anemia, MAC down ~30–40%.
Aortocaval compression: After ~20 weeks the supine gravid uterus compresses the IVC/aorta → hypotension; prevent with left uterine displacement.
Preeclampsia: New hypertension with proteinuria after 20 weeks; magnesium for seizure prophylaxis — watch Mg toxicity (loss of DTRs, respiratory depression).
Magnesium toxicity treatment: IV calcium gluconate or calcium chloride.
Postpartum hemorrhage — 4 Ts: Tone (atony, most common), Trauma, Tissue, Thrombin; uterotonics: oxytocin (first line), methylergonovine, carboprost, misoprostol.
Methylergonovine caution: Contraindicated in hypertension/preeclampsia (vasoconstriction).
Carboprost caution: Contraindicated in asthma (bronchospasm).
Pediatric airway: Larger head/tongue, a more cephalad larynx (C3–C4), the cricoid as the narrowest point (classic), and a large floppy epiglottis.
Pediatric physiology: Higher O₂ consumption + lower FRC → rapid desaturation; heart-rate-dependent cardiac output, so bradycardia is poorly tolerated.
Geriatric anesthesia: Decreased MAC, decreased organ reserve, increased drug sensitivity, and a risk of postoperative cognitive dysfunction — reduce and titrate doses.
Obesity airway: Increased difficult mask/intubation risk and reduced FRC → rapid desaturation; use the ramped position and preoxygenate well.
Obesity drug dosing: Succinylcholine by total body weight; propofol induction and nondepolarizing NMBAs by lean/ideal body weight.
Trauma anesthesia: Assume full stomach, cervical-spine injury, hypovolemia, and difficult airway; use RSI with in-line stabilization and balanced 1:1:1 transfusion with early TXA.
Lethal triad (trauma): Hypothermia, acidosis, and coagulopathy — prevent during damage-control resuscitation.
TRALI: Transfusion-related acute lung injury — the leading cause of transfusion-related mortality; non-cardiogenic pulmonary edema within 6 hours.
Acute hemolytic reaction: From ABO incompatibility (clerical error); under anesthesia may show only hypotension, hemoglobinuria, and diffuse oozing — stop the transfusion.

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By Career EmployerUpdated Jun 18, 2026

250+ free CRNA flashcards — 4 ways to study

CRNA Flashcard of the Day

The classic card. Do you know this one?

Click Study Flashcards above to open the flashcard hub — hundreds of CRNA cards you can flip, match, type, or quiz yourself on. Every card is drawn from the four NBCRNA NCE content areas, so you study exactly what the National Certification Examination tests.^[1] Pair them with our free practice test and study guide.

CRNA Flashcard Study Modes

Most flashcard sites give you one thing: a card to flip. Ours has four modes so you can both learn the material and prove you know it — the difference between recognizing an answer and recalling it under pressure.

Flip (Study) — the classic card. Flip term ↔ definition, shuffle the deck, and mark each card “Got it” or “Still learning.”
Match (Game) — a timed game: pair each term to its definition as fast as you can. Great for cementing facts like MAC values and isolation precautions.
Type (Recall) — read the definition and type the term. Typing forces true active recall instead of passive recognition.
Quiz (Test) — multiple-choice questions generated from the cards, so you can self-test exactly like exam day.

Free CRNA flashcards from Career Employer — active recall for the NBCRNA National Certification Examination

Why Flashcards Work for the NBCRNA NCE

Flashcards aren’t busywork — they’re built on active recall: pulling an answer out of memory strengthens it far more than re-reading notes. Pair that with spacing — short sessions across several days rather than one cram — and you retain more in less time.

That matters on the NCE, where pharmacology facts (MAC values, NMBA and reversal dosing, opioid potency), physiology constants, and equipment safety must be instantly available. Used alongside our practice test and study guide, flashcards turn review time into measurable progress.

CRNA Flashcards by Content Area

The cards are organized by the four NBCRNA NCE content areas. Weight your study toward the heaviest one — General Principles of Anesthesia is over a third of the exam — and thread pharmacology throughout, since it appears in every area:^[1]

NCE content areas and weighting
NBCRNA NCE content area	% of exam
General Principles of Anesthesia	35%
Surgical Procedures & Special Populations	25%
Basic Sciences	20%
Equipment, Instrumentation & Technology	20%

How to Get the Most Out of These Flashcards

Start early, review daily. Begin flashcards as you cover each content area, not the week before — a few minutes a day beats one marathon session.
Use Type and Quiz, not just Flip. Recognizing the right answer is easy; recalling and choosing it is the real test.
Drill your weakest area. Pick a single content-area deck and grind it until the Match time drops and the Quiz score climbs.
Mirror the exam weighting. Spend the most time on General Principles of Anesthesia — it is 35% of the NCE.
Verify every dose. Anesthesia is high-stakes; confirm any drug dose against the current FDA label and your institution’s protocol before clinical use.
Then prove it. When the cards feel easy, confirm with our practice test — aim for steady mastery before exam day.

CRNA Flashcards FAQ

Hundreds of free CRNA flashcards, organized across the four NBCRNA NCE content areas plus exam logistics. They're free to use with no account required.

References

1.National Board of Certification and Recertification for Nurse Anesthetists. “NCE Content Outline (effective for exams on or after 1/2/2024).” NBCRNA.com. ↑
2.National Board of Certification and Recertification for Nurse Anesthetists. “NCE Resources (Handbook & Format).” NBCRNA.com. ↑
3.Malignant Hyperthermia Association of the United States. “Managing an MH Crisis & MH Triggers.” MHAUS.org. ↑
4.American Society of Anesthesiologists. “ASA Physical Status Classification System.” ASAHQ.org. ↑

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