Your FREE CRNA Flashcards 2026 – 250+ Cards

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.

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.

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

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.

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.

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 $\approx 800\text{–}1200$ $\text{dynes} \cdot \text{s} \cdot \text{cm}^{-5}$.

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

$EF = SV/EDV \approx 55\text{–}70\%$.

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.

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

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

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).

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).

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

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

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

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

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.

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

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.

$pH = 6.1 + \log\frac{[HCO_3^-]}{0.03 \times PaCO_2}$.

Increased PaCO₂, decreased pH (hypoventilation); renal compensation raises HCO₃⁻ over days.

$AG = Na^+ - (Cl^- + HCO_3^-)$; normal $\approx 8\text{–}12$ mEq/L. High-gap causes: MUDPILES.

Expected respiratory compensation for metabolic acidosis: expected $PaCO_2 = 1.5\,[HCO_3^-] + 8 \pm 2$.

$3.5\text{–}5.0$ mEq/L; hyperkalemia → peaked T waves → widened QRS → sine wave.

$135\text{–}145$ mEq/L; rapid correction of hyponatremia risks osmotic demyelination.

Total body water $\approx 60\%$ of body weight; ICF ~40%, ECF ~20% (one-quarter of ECF is intravascular plasma).

Peaked T waves → widened QRS → sine wave; treat with calcium, insulin/glucose, bicarbonate, and beta-agonists.

What the body does to the drug: absorption, distribution, metabolism, excretion (ADME).

What the drug does to the body: receptor effect and dose-response.

$V_d = \frac{\text{amount of drug in body}}{\text{plasma concentration}}$; a large Vd indicates a lipophilic, tissue-bound drug. Loading dose $= V_d \times$ target concentration.

Volume of plasma cleared of drug per unit time; the main determinant of steady-state concentration (maintenance rate $=$ clearance $\times$ target concentration).

$t_{1/2} = \frac{0.693 \times V_d}{Cl}$; ~5 half-lives to reach steady state or eliminate ~97% of a drug.

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.

A constant FRACTION of drug is eliminated per unit time (most drugs).

A constant AMOUNT is eliminated per unit time (saturable enzymes): ethanol, phenytoin, high-dose aspirin.

Potency = dose needed for an effect (position of the curve, EC50); efficacy = maximal achievable effect (height of the curve).

A single bolus of propofol or thiopental wears off mainly by redistribution from the brain to muscle/fat, not by metabolism.

Binds without activating and shifts the dose-response curve to the right (surmountable) — e.g., naloxone, flumazenil, nondepolarizing NMBAs.

At constant temperature, $P \propto 1/V$ ($P_1V_1 = P_2V_2$) — estimates O₂ cylinder content.

At constant pressure, $V \propto T$ ($V_1/T_1 = V_2/T_2$).

At constant volume, $P \propto T$ — cylinder pressure rises if heated.

Total pressure = sum of the partial pressures of each gas in a mixture.

The amount of gas dissolved in a liquid is proportional to its partial pressure above the liquid (basis of blood:gas solubility).

Rate of gas diffusion $\propto 1/\sqrt{MW}$ — lighter gases diffuse faster.

Diffusion $\propto \frac{\text{area} \times \Delta\text{partial pressure}}{\text{membrane thickness}}$; thicker membranes (edema/fibrosis) slow diffusion.

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.

Occurs at high flow/large radii; flow $\propto \sqrt{\Delta P}$ and resistance depends on DENSITY (basis for Heliox in airway obstruction).

$Re = \frac{\rho v d}{\eta}$; $Re < \sim 2000$ = laminar, $> \sim 4000$ = turbulent.

Where gas velocity increases through a constriction, lateral pressure falls — entrains a second gas (nebulizers, jet ventilation).

Lower = faster onset/offset: desflurane 0.42 < nitrous oxide 0.46 < sevoflurane 0.65 < isoflurane 1.4.

Correlates with POTENCY (Meyer–Overton): higher oil:gas → lower MAC → more potent.

Prevents attaching the wrong gas CYLINDER to the yoke via a unique two-pin geometry per gas.

Prevents misconnection of PIPELINE hoses via gas-specific threaded diameters.

Full ~1900–2200 psi, ~625–660 L; stored as a gas, so pressure falls linearly with content (a half-full cylinder reads ~1000 psi).

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.

$\approx 50$ psi (the primary working source); cylinder regulators reduce to ~45 psi so the pipeline is used preferentially.

Pressure-sensing device that shuts off/reduces N₂O if O₂ SUPPLY PRESSURE falls — it does NOT detect a crossed pipeline or low O₂ concentration.

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.

The only true last-line defense against a hypoxic mixture — placed in the inspiratory limb, downstream of all mechanical safety devices.

Positioned downstream (closest to the common outlet) so a leak in an upstream flowmeter is least likely to cause a hypoxic mixture.

Splits flow and recombines streams to deliver the dialed concentration (sevo, iso); temperature-compensated; delivers constant PARTIAL PRESSURE despite altitude.

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).

Delivers ~35–75 L/min of pure O₂, bypassing the vaporizers; hazards are barotrauma and dilution/awareness.

Confirm a backup means of ventilation (a self-inflating/Ambu bag) is available — you must always be able to ventilate if the machine fails.

Allows rebreathing after CO₂ absorption; uses two unidirectional valves, a CO₂ absorber, an APL valve, and a reservoir bag.

$\ce{CO2 + H2O -> H2CO3}$; then $\ce{H2CO3 + Ca(OH)2 -> CaCO3 + H2O}$ + heat (exothermic).

A nephrotoxic degradation product of SEVOFLURANE with desiccated strong-base absorbents; mitigate with adequate fresh-gas flow and KOH/NaOH-free absorbents.

Produced when DESICCATED absorbent degrades volatiles — worst with desflurane/isoflurane; classic Monday-morning first case after gas was left flowing.

Most efficient for SPONTANEOUS ventilation.

Most efficient for CONTROLLED ventilation; the Bain is a coaxial D (fresh gas runs inside the expiratory tube).

Confirms inner-tube integrity of a Bain circuit before use (a disconnected inner tube causes massive rebreathing).

The safe ventilator design — it fails to refill and collapses on a disconnect, giving an obvious visual alarm.

A malfunctioning scavenging system can transmit excessive positive (barotrauma) or negative pressure to the patient's airway.

Continuous evaluation of oxygenation, ventilation, circulation, and temperature during every anesthetic, with a qualified provider present.

$\approx 35\text{–}45$ mmHg; the gold-standard, fastest confirmation of correct ETT placement.

Phase I above zero = rebreathing (incompetent valve, exhausted absorbent, inadequate fresh-gas flow).

A sloped upstroke with loss of plateau = expiratory obstruction (bronchospasm, COPD, kinked ETT).

A flatline = esophageal intubation, circuit disconnect, complete obstruction, or cardiac arrest.

A notch in the plateau = a spontaneous breath during mechanical ventilation (returning/inadequate neuromuscular blockade).

Uses two wavelengths (red 660 nm, infrared 940 nm) and the Beer–Lambert law on the pulsatile arterial signal.

Drives the SpO₂ reading toward ~85% regardless of the true saturation.

Falsely HIGH/normal SpO₂ — the pulse oximeter cannot distinguish COHb from oxyhemoglobin, masking CO poisoning.

Best for detecting P waves/dysrhythmias and inferior-wall (RCA) ischemia.

Best single lead for detecting anterolateral (LV) ischemia (LAD/circumflex).

Sluggish trace, lost dicrotic notch → falsely low systolic; caused by air bubbles, clots, kinks.

Overshoot/ringing → falsely high systolic; caused by stiff tubing or catheter whip.

Zero at the phlebostatic axis (4th intercostal space, mid-axillary line, $\approx$ right atrium); use the external auditory meatus for the sitting craniotomy.

Atrial contraction; lost in atrial fibrillation, large "cannon a waves" in AV dissociation/complete heart block.

Atrial filling against a closed tricuspid valve; large v waves occur in tricuspid regurgitation.

Processed EEG (0–100); target 40–60 for general anesthesia. Ketamine and N₂O may keep BIS falsely high.

Four stimuli at 2 Hz over 2 seconds; the TOF ratio (T4/T1) quantifies nondepolarizing block recovery.

0 twitches = deep block; 1–2 twitches = adequate surgical relaxation; 4 with no fade = recovery.

A TOF ratio $\geq 0.9$ indicates acceptable recovery; quantitative monitoring is needed to confirm it.

Used to gauge DEEP block when the TOF count is 0; fewer post-tetanic twitches = deeper block.

Sustained response to tetanus, NO fade, NO post-tetanic facilitation; potentiated (not reversed) by anticholinesterases.

Develops with high/repeated succinylcholine; shows fade and post-tetanic facilitation like a nondepolarizing block.

Best: pulmonary artery (gold standard), distal esophagus, nasopharynx, tympanic membrane.

Curved; tip into the vallecula to indirectly lift the epiglottis (more room for tube passage).

Straight; lifts the epiglottis directly — preferred in infants (long, floppy epiglottis).

Seats over the glottis; does NOT protect against aspiration; a key rescue device in the difficult-airway algorithm.

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).

Gold standard for the anticipated difficult / awake airway and the unstable cervical spine.

An introducer railroaded into the trachea when only the epiglottis is seen; "tracheal clicks" confirm placement.

Emergency surgical/needle airway for the "cannot intubate, cannot oxygenate" (CICO) situation.

Maintain $20\text{–}30$ cmH₂O; above ~30 cmH₂O impairs tracheal mucosal perfusion. N₂O diffuses in and raises cuff pressure.

$\text{ID (mm)} = \frac{\text{age}}{4} + 4$ for children older than 2 years.

Minimum alveolar concentration preventing movement to surgical incision in 50% of patients — an ED50 and the index of inhaled-agent potency.

$\approx 2.0\%$ in oxygen.

$\approx 6.0\%$.

$\approx 1.15\text{–}1.2\%$.

$\approx 104\%$ — cannot reach 1 MAC alone at 1 atmosphere, so it is used as an adjunct.

MAC values are additive: 0.5 MAC sevoflurane + 0.5 MAC N₂O $\approx$ 1 MAC.

High-volume uptake of N₂O concentrates a co-administered volatile, speeding its onset.

A higher inspired concentration speeds the rise of the alveolar concentration (FA/FI).

On stopping N₂O, it pours into the alveoli and dilutes O₂ — give 100% O₂ for 3–5 minutes at emergence.

$\approx 0.3\text{–}0.5$ MAC — the concentration at which consciousness is lost/regained.

Increasing age, hypothermia, pregnancy, opioids/sedatives, α2-agonists, acute alcohol, hyponatremia.

Hyperthermia, chronic alcohol use, acute amphetamine/cocaine, hypernatremia.

All volatile anesthetics are malignant-hyperthermia triggers; nitrous oxide is essentially a non-trigger.

Nonpungent → ideal for inhalational (mask) induction; forms Compound A with desiccated absorbents.

Lowest blood:gas (fastest emergence) but pungent (airway irritation); rapid increases cause sympathetic stimulation; needs the heated Tec 6.

Diffuses into air-filled spaces (avoid in pneumothorax, bowel obstruction, middle-ear/retinal-gas surgery); inactivates vitamin B₁₂.

GABA-A agonist; induction $\approx 1.5\text{–}2.5$ mg/kg IV; lowers BP (vasodilation), antiemetic, pain on injection.

Prolonged high-dose infusion → metabolic acidosis, rhabdomyolysis, lipemia, cardiac failure.

GABA-A modulator; $\approx 0.2\text{–}0.3$ mg/kg; hemodynamically stable but causes adrenal suppression (11-β-hydroxylase) and myoclonus.

NMDA-receptor antagonist; $\approx 1\text{–}2$ mg/kg IV; sympathomimetic, bronchodilator, analgesic; emergence reactions; dissociative anesthesia.

A noncompetitive NMDA-receptor antagonist producing dissociative anesthesia.

Central α2-agonist; sedation/analgesia with minimal respiratory depression; causes bradycardia and hypotension.

Benzodiazepine (GABA-A); anxiolysis and anterograde amnesia; reversed by flumazenil.

Barbiturate (GABA-A); contraindicated in porphyria; cerebroprotective (lowers CMRO₂/CBF).

Potency $\approx 100\times$ morphine; fast onset, ~30–60 min by redistribution; intraop bolus ~1–3 mcg/kg. CSHT rises with prolonged infusion.

The most potent opioid in common use ($\approx 1000\times$ morphine).

Ultra-short opioid metabolized by nonspecific plasma esterases; context-sensitive half-time stays ~3–5 min regardless of infusion duration.

Active metabolite morphine-6-glucuronide accumulates in renal failure; causes histamine release.

Treats postoperative shivering; metabolite normeperidine causes seizures; avoid with MAOIs (serotonin syndrome).

Opioid antagonist; reverses respiratory depression but is short-acting (re-narcotization risk).

Respiratory depression, miosis, bradycardia, constipation, pruritus, nausea, and chest-wall rigidity with rapid high doses.

Depolarizing NMBA $\approx 1\text{–}1.5$ mg/kg IV; fastest onset (~30–60 s), shortest duration (~5–10 min).

Binds and activates the nicotinic ACh receptor → sustained depolarization → fasciculations then flaccid paralysis (Phase I).

Hyperkalemia-risk states (burns/crush/denervation older than ~24–48 h, prolonged immobility), MH history, myopathies, pseudocholinesterase deficiency.

Hyperkalemia, MH trigger, bradycardia, myalgias, and increased ICP, intraocular, and intragastric pressure.

Prolongs succinylcholine paralysis; a dibucaine number ~20 indicates the homozygous atypical enzyme.

Nondepolarizing aminosteroid; $\approx 0.6$ mg/kg to intubate, $\approx 1.2$ mg/kg for RSI; reversible by sugammadex.

Nondepolarizing aminosteroid; intermediate duration; no histamine release; reversible by sugammadex.

Nondepolarizing benzylisoquinolinium cleared by Hofmann elimination (organ-independent) — ideal in renal/hepatic failure.

Competitive antagonists at the ACh receptor; block shows fade on TOF/tetanus and post-tetanic potentiation; potentiated by volatiles, aminoglycosides, and magnesium.

Acetylcholinesterase inhibitor; $\approx 0.04\text{–}0.07$ mg/kg; give with glycopyrrolate; has a ceiling (needs some twitches present).

γ-cyclodextrin that encapsulates rocuronium/vecuronium; $\approx 2$ mg/kg (moderate block), 4 mg/kg (deep), 16 mg/kg (immediate). Binds hormonal contraceptives.

Encapsulates aminosteroid NMBAs in plasma, creating a gradient that pulls them off the receptor; renally excreted.

Short-acting cholinesterase inhibitor paired with atropine (matched onset).

Block voltage-gated sodium channels from the intracellular side, preventing action-potential propagation.

Esters (one "i"): plasma-cholinesterase metabolism, PABA allergy risk. Amides (two "i"s): hepatic metabolism, rare true allergy.

The closer the pKa is to physiologic pH, the larger the non-ionized fraction and the faster the onset; acidotic/infected tissue blocks poorly.

Potency tracks lipid solubility; duration tracks protein binding (epinephrine prolongs duration and reduces absorption).

$\approx 4.5$ mg/kg plain, $\approx 7$ mg/kg with epinephrine.

Long-acting amide; the most CARDIOTOXIC local anesthetic (avid Na-channel binding); max $\approx 2.5\text{–}3$ mg/kg.

Long-acting amide; less cardiotoxic than bupivacaine (S-enantiomer); good sensory-motor differential.

CNS first (perioral numbness, tinnitus, seizures), then cardiovascular collapse.

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.

Class I: soft palate, fauces, uvula, pillars; II: uvula; III: soft palate + base of uvula; IV: hard palate only. Higher class predicts harder intubation.

Look externally, Evaluate 3-3-2, Mallampati, Obstruction, Neck mobility — predicts a difficult airway.

3 fingers mouth opening, 3 fingers chin-to-hyoid, 2 fingers hyoid-to-thyroid notch.

Denitrogenate the FRC to extend safe apnea time; target end-tidal O₂ above ~90%.

Preoxygenate → rapid induction agent + fast paralytic (sux or high-dose roc) → intubate without (or with limited) mask ventilation; for aspiration risk.

A normal healthy patient.

Mild systemic disease (controlled HTN/DM, smoker, pregnancy, obesity).

Severe systemic disease with substantive limitation (poorly controlled DM/HTN, COPD, stable CAD).

Severe systemic disease that is a constant threat to life (recent MI, sepsis).

Moribund patient not expected to survive without the operation (ruptured AAA).

A brain-dead patient whose organs are being procured.

Emergency — appended to any ASA class.

2 hours.

4 hours.

6 hours.

8 hours.

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.

Crystalloids (LR, NS) distribute to the extracellular fluid (~3:1 replacement); colloids (albumin) stay intravascular longer.

Balanced ~1:1:1 PRBC : FFP : platelets; watch citrate (hypocalcemia), hyperkalemia, and hypothermia.

Each unit raises hemoglobin by ~1 g/dL in an average adult.

Citrate in stored blood chelates calcium → hypocalcemia (hypotension, prolonged QT); treat with calcium.

Oxidizer (O₂/N₂O) + ignition (cautery/laser) + fuel (drapes, prep, ETT); minimize O₂ in a shared airway.

Total intravenous anesthesia (e.g., propofol + remifentanil); useful when volatiles are contraindicated (MH risk).

A sedation continuum (light/moderate/deep) with a provider monitoring the patient.

Autonomy, beneficence, nonmaleficence, justice (plus veracity and fidelity).

Capacity, disclosure, understanding, voluntariness.

Not automatically suspended — "required reconsideration": discuss and clarify the DNR's intraoperative status before surgery.

Duty, Dereliction (breach), Direct causation, Damages — all four are required to prove malpractice.

What a reasonably prudent, similarly trained provider would do under the same circumstances.

"The thing speaks for itself" — an injury that does not occur without negligence (e.g., a retained sponge).

An older doctrine (largely abandoned) holding the surgeon liable for everyone in the OR; CRNAs are accountable for their own practice.

Console human error, coach at-risk behavior, and discipline reckless behavior — keyed to the behavior, not the outcome.

The 7 steps an anesthesiologist must meet to medically direct $\leq 4$ concurrent CRNA cases.

Billing modifier for a CRNA service WITHOUT medical direction (nondirected).

Billing modifier for a CRNA service WITH medical direction by a physician.

A state's governor may opt out of the federal physician-supervision requirement for CRNAs (state law still governs).

Anesthesia is a high-risk specialty; the most-diverted agents are fentanyl/opioids and propofol; the first sign is sometimes death. Witness all wastage.

Strongest: systematic review/meta-analysis of RCTs > RCT > cohort > case-control > case series > expert opinion.

High sensitivity, when Negative, rules OUT (SnNout); high specificity, when Positive, rules IN (SpPin).

A hypermetabolic crisis from volatile agents/succinylcholine in RYR1-susceptible patients.

An unexplained, rapidly rising EtCO₂ unresponsive to increased ventilation (hyperthermia is a LATE sign).

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.

Inhibits the ryanodine (RYR1) receptor, blocking calcium release from the sarcoplasmic reticulum.

Hypotension and bronchospasm; the #1 perioperative cause is neuromuscular blockers; first-line treatment is epinephrine.

Reflex glottic closure (often light anesthesia/emergence); treat with positive-pressure O₂, jaw thrust (Larson's point), deepen, and low-dose succinylcholine if severe.

Wheeze, rising peak pressures, upsloping capnograph; deepen anesthesia, give an inhaled β2-agonist, and epinephrine if severe.

Explicit recall under general anesthesia; risk with TIVA, paralysis, and light anesthesia; reduce with end-tidal agent monitoring and BIS.

Female sex, nonsmoker, history of PONV/motion sickness, and postoperative opioids; manage with multimodal antiemetics.

A single injection into the subarachnoid/intrathecal space (below L1–L2 in adults); small dose, fast dense block.

The spinal cord ends ~L1–L2 in adults (L3 in infants); place neuraxial needles below this level.

The intercristal line connecting the iliac crests; crosses ~the L4 body / L4–L5 interspace.

Skin → subcutaneous fat → supraspinous ligament → interspinous ligament → ligamentum flavum → epidural space → dura → arachnoid → CSF.

Hyperbaric solutions sink to dependent regions and follow gravity/patient position to set block height.

Hypotension (sympathectomy), bradycardia (high block, T1–T4), high/total spinal, PDPH, and urinary retention.

A positional headache (worse upright) from a CSF leak; treat conservatively, then with an epidural blood patch.

A catheter in the epidural (potential) space identified by loss of resistance; titratable, slower onset, larger volume than spinal.

~3 mL lidocaine with epinephrine 1:200,000; a rising HR suggests intravascular placement, a rapid dense block suggests intrathecal.

For shoulder surgery; causes ~100% ipsilateral phrenic nerve palsy — avoid in severe respiratory disease.

The "spinal of the arm"; main risk is pneumothorax (proximity to the pleura).

For forearm/hand surgery; often spares the musculocutaneous nerve (it leaves the plexus early).

The nipple line; the target sensory level for cesarean section and upper-abdominal surgery.

The umbilicus; the target level for TURP and labor analgesia.

Lung isolation with a double-lumen tube or bronchial blocker; manage hypoxemia with CPAP to the nondependent lung and PEEP to the dependent lung.

Full heparinization before cannulation, target ACT > ~400–480 s; reverse with protamine (~1 mg per 100 units heparin).

A high-potassium solution that arrests the heart in diastole to minimize myocardial O₂ demand.

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.

Lower ICP with transient hyperventilation, head-up neutral positioning, mannitol/hypertonic saline; maintain CPP.

Increased cardiac output and blood volume, decreased FRC, increased O₂ consumption and aspiration risk, dilutional anemia, MAC down ~30–40%.

After ~20 weeks the supine gravid uterus compresses the IVC/aorta → hypotension; prevent with left uterine displacement.

New hypertension with proteinuria after 20 weeks; magnesium for seizure prophylaxis — watch Mg toxicity (loss of DTRs, respiratory depression).

IV calcium gluconate or calcium chloride.

Tone (atony, most common), Trauma, Tissue, Thrombin; uterotonics: oxytocin (first line), methylergonovine, carboprost, misoprostol.

Contraindicated in hypertension/preeclampsia (vasoconstriction).

Contraindicated in asthma (bronchospasm).

Larger head/tongue, a more cephalad larynx (C3–C4), the cricoid as the narrowest point (classic), and a large floppy epiglottis.

Higher O₂ consumption + lower FRC → rapid desaturation; heart-rate-dependent cardiac output, so bradycardia is poorly tolerated.

Decreased MAC, decreased organ reserve, increased drug sensitivity, and a risk of postoperative cognitive dysfunction — reduce and titrate doses.

Increased difficult mask/intubation risk and reduced FRC → rapid desaturation; use the ramped position and preoxygenate well.

Succinylcholine by total body weight; propofol induction and nondepolarizing NMBAs by lean/ideal body weight.

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.

Hypothermia, acidosis, and coagulopathy — prevent during damage-control resuscitation.

Transfusion-related acute lung injury — the leading cause of transfusion-related mortality; non-cardiogenic pulmonary edema within 6 hours.

From ABO incompatibility (clerical error); under anesthesia may show only hypotension, hemoglobinuria, and diffuse oozing — stop the transfusion.