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Certified Respiratory Therapist — the NBRC entry-level credential earned by passing the TMC Exam at the low cut score.

Registered Respiratory Therapist — earned by passing the TMC at the high cut score AND passing the Clinical Simulation Examination (CSE).

Therapist Multiple-Choice Examination — 160 items (140 scored + 20 pretest) in 3 hours; one exam, two cut scores (CRT low, RRT-eligibility high).

Low cut earns the CRT; high cut earns the CRT plus eligibility for the CSE toward the RRT.

Commission on Accreditation for Respiratory Care — accredits the degree programs whose graduates are eligible to sit NBRC exams.

pH (direction) → PaCO2 (respiratory) → HCO3 (metabolic) → match the value moving with the pH → assess compensation.

7.35–7.45; below is acidemia, above is alkalemia.

35–45 mm Hg; high = respiratory acidosis driver, low = respiratory alkalosis driver.

22–26 mEq/L; low = metabolic acidosis driver, high = metabolic alkalosis driver.

Low pH (< 7.35) with a high PaCO2 (> 45) from hypoventilation — COPD, sedation, neuromuscular weakness.

High pH (> 7.45) with a low PaCO2 (< 35) from hyperventilation — anxiety, pain, pulmonary embolism, hypoxia.

Low pH (< 7.35) with a low HCO3 (< 22) — DKA, lactic acidosis, renal failure, diarrhea.

High pH (> 7.45) with a high HCO3 (> 26) — vomiting, diuretics, nasogastric suction.

Acute = high PaCO2 with a near-normal HCO3 (no compensation); chronic = high HCO3 pulling pH toward normal (COPD baseline).

Acute (uncompensated) respiratory acidosis — low pH, high PaCO2, near-normal HCO3.

Na − (Cl + HCO3), normally ~8–12 mEq/L; a high gap signals unmeasured acids (ketoacids, lactate).

140 − (100 + 10) = 30 — a high-anion-gap metabolic acidosis (e.g., DKA).

Expected PaCO2 for a metabolic acidosis ≈ 1.5 × HCO3 + 8 (±2); checks adequate respiratory compensation.

1.5 × 14 + 8 = 29 mm Hg — the expected PaCO2 if the lungs are compensating appropriately.

Near-normal pH (e.g., 7.38) with a high PaCO2 (60) and a high HCO3 (35) — the stable COPD pattern.

PaO2 ÷ FiO2 (decimal); Berlin ARDS severity — 200–300 mild, 100–200 moderate, ≤100 severe (PEEP ≥ 5).

60 ÷ 0.60 = 100 — moderate-to-severe oxygenation impairment.

Alveolar PO2 minus arterial PaO2; normal with hypoxemia = hypoventilation, widened = gas-exchange problem (V/Q mismatch, shunt, diffusion).

Points to pure alveolar hypoventilation — a ventilation (CO2) problem, not a gas-exchange defect.

Hemoglobin bound to carbon monoxide; can't carry O2 and is missed by pulse oximetry (falsely normal SpO2) — use CO-oximetry.

100% oxygen by nonrebreather to speed CO elimination; hyperbaric oxygen in severe cases.

Ferric (Fe3+) hemoglobin that can't bind oxygen; cyanosis with SpO2 stuck near 85% that doesn't improve on O2 — detect by CO-oximetry.

About 1–2% is a normal baseline in a healthy nonsmoker; higher in smokers.

Continuous exhaled-CO2 measurement; a normal square waveform after intubation confirms tracheal placement.

Indicates return of spontaneous circulation as pulmonary blood flow is restored.

A widened gap between end-tidal CO2 (e.g., 30) and arterial PaCO2 (e.g., 42), as in pulmonary embolism.

Fraction of FVC exhaled in 1 second; below ~0.70 defines an obstructive pattern (asthma or COPD).

Reduced FEV1/FVC ratio with a normal or increased total lung capacity (air trapping).

Normal or high FEV1/FVC ratio but a reduced total lung capacity — confirm with lung volumes.

FEV1 improves ≥12% AND ≥200 mL after a bronchodilator (reversible obstruction = asthma).

Single-breath diffusing capacity; low when gas-exchange surface is lost (emphysema, interstitial, pulmonary vascular disease).

Low in emphysema (alveolar wall destruction) but normal or high in asthma — helps separate the two.

Volume of gas left in the lungs after a normal resting exhalation (ERV + RV).

Indicates air trapping and hyperinflation from obstructive disease.

Air-filled bronchi outlined within consolidated (fluid-filled) alveoli on a chest film.

Absent breath sounds, tracheal deviation away from the affected side, hypotension — a respiratory emergency.

Discontinuous popping sounds at end-inspiration, as in pulmonary edema or fibrosis.

Wheezes are high-pitched and musical; rhonchi are low-pitched, snore-like, and often clear with secretion mobilization.

High-pitched crowing heard mainly on inspiration, localizing to upper-airway obstruction (e.g., epiglottitis, post-extubation edema).

Predicts intubation difficulty by visible oropharyngeal structures; Class I favorable, Class III–IV potentially difficult.

Assigned at 1 and 5 minutes after birth (with continued scoring if the neonate is depressed).

Trapped intrinsic PEEP from incomplete exhalation; total PEEP minus set PEEP on an expiratory-hold maneuver.

12 − 5 = 7 cm H2O of auto-PEEP — reduce it by lengthening expiratory time.

Tidal volume ÷ (peak pressure − PEEP); e.g., 500 mL ÷ (30 − 5) = 20 mL/cm H2O.

Measured during an inspiratory hold (no flow); reflects compliance and is kept < 30 cm H2O to limit lung injury.

An objective marker of functional exercise capacity; terminate and assess the patient for severe dyspnea or desaturation.

Peaked T waves, a widened QRS, and a flattened P wave — a can't-miss electrolyte emergency.

Cannula, simple mask, nonrebreather — flow is below total inspiratory demand, so FiO2 varies with the breathing pattern.

Venturi mask, high-flow nasal cannula — flow meets or exceeds demand, giving a fixed, predictable FiO2.

Roughly 4% per liter from 1–6 L/min (~24–44% FiO2); a low-flow, variable device.

Sets a precise FiO2 by jet size and entrainment ports; raising the set FiO2 LOWERS total flow (less entrainment).

At a high set FiO2 the lower total flow may not meet a febrile, tachypneic patient's demand — entrains extra room air.

Heated, humidified gas up to ~60 L/min; flushes nasopharyngeal dead space and adds a small PEEP-like effect.

Flow is too low — raise it until the reservoir bag stays partially inflated.

A stationary unit delivers at least roughly 90% oxygen; it is electrically powered, so loss of power halts output.

Minutes = cylinder factor × gauge pressure (psig) ÷ flow (L/min); H factor ≈ 3.14, E factor ≈ 0.28.

(3.14 × 2200) ÷ 8 ≈ 860 minutes of oxygen available.

(0.28 × 1200) ÷ 5 ≈ 67 minutes — adequate for a 45-minute transport with a small margin.

Change a cylinder at about 200–500 psig rather than running it to empty.

Float sits downstream of the needle valve, so a downstream restriction does not falsely lower the flow reading.

Position-independent (works in any orientation), making it ideal for transport; reads pressure, not true flow against a restriction.

Read the flow at the top flat surface of the float.

Verify FiO2 downstream in the delivered gas; a blender reading 1.0 across the range is faulty — remove it from service.

Enter sterile tissue or the bloodstream (surgical instruments) — must be STERILIZED.

Contact mucous membranes or non-intact skin (reusable laryngoscope blade) — at least HIGH-LEVEL DISINFECTION.

Touch only intact skin (BP cuff, ventilator surface) — LOW- or intermediate-level disinfection.

Negative-pressure room + fit-tested N95 for pathogens in small droplet nuclei — tuberculosis, measles, varicella.

A surgical mask for larger respiratory droplets — influenza, pertussis.

Gown and gloves for spread by touch — MRSA, C. difficile.

Place in a negative-pressure airborne infection isolation room and wear a fit-tested N95 or higher.

Gown, then respirator (mask), then eye protection, then gloves.

Perform hand hygiene immediately after doffing gloves and gown.

Head of bed 30–45°, sedation interruption, oral care, and stress-ulcer plus VTE prophylaxis as appropriate.

Suction without disconnecting the circuit — less contamination and less loss of PEEP/oxygenation.

Sets both the offset (zero) and the slope of each electrode across the measuring range.

Plots daily quality-control values around the mean to spot shifts and trends in analyzer performance.

A shift is an abrupt jump to one side of the mean (new reagent lot); a trend is a gradual drift (aging electrode).

Hold patient results, troubleshoot and correct the analyzer, then repeat the control before reporting.

Results are tightly grouped (reproducible) but consistently off the true value — a calibration problem.

The oxygen channel reads erroneously when the semipermeable membrane through which O2 diffuses to the cathode is damaged.

One puff at a time with a slow, deep inhalation; inhaling too fast triggers the spacer's flow whistle.

A quick, forceful, deep inhalation creates the turbulence that disperses the powder; keep it dry (moisture clumps it).

May fail because severe bronchospasm lowers inspiratory flow below what the device needs to aerosolize the dose.

Use the lowest flow that keeps SpO2 in the ordered target range (commonly 92–96%), correcting tissue hypoxia.

Oxygen corrects the hypoxemia but does not fix the inadequate ventilation — address the cause (e.g., reverse sedation, support ventilation).

Switch to a higher-concentration device such as a mask system rather than pushing cannula flow higher.

About 0.24 (24%) using the common low-flow estimation rule.

A fast, shallow breathing pattern dilutes low-flow oxygen with more room air, lowering the delivered FiO2.

Holds the tongue forward and acts as a bite block in a patient with NO gag reflex; provokes gagging if the gag is intact.

Can push the epiglottis down and worsen the obstruction.

Better tolerated by a conscious/semiconscious patient and serves as a conduit for nasotracheal suctioning.

The tip stimulates the larynx/hypopharynx, causing gagging and coughing — withdraw it slightly.

Capnography (square waveform) is most reliable; equal bilateral breath sounds, no epigastric sound, and a confirming chest film.

Should sit about 2–6 cm above the carina.

20–30 cm H2O — high enough to seal, low enough to avoid tracheal mucosal ischemia.

Below range — add air to bring it into the 20–30 cm H2O window (prevents leaks and aspiration).

Above range — remove air; pressure above tracheal capillary perfusion can cause ischemia.

Seals at a lower pressure over a larger contact area, reducing focal mucosal injury.

About −100 to −150 mm Hg; higher risks mucosal trauma and atelectasis.

Withdraw the catheter and reoxygenate the patient before any further attempt.

Generally discouraged — it can cause desaturation and does not reliably thin secretions.

May read low despite correct tracheal placement because low pulmonary blood flow reduces delivered CO2.

Progressive gastric distension, absent breath sounds, and no CO2 waveform.

Every breath delivers the full set volume/pressure — maximum support; the mode for a patient with no respiratory drive.

Synchronized mandatory breaths plus the patient's own spontaneous breaths in between (often with pressure support).

Patient triggers every breath; a set inspiratory pressure augments it and the breath cycles off as flow falls.

Obstruction or stiffness — secretions, a kinked/bitten tube, bronchospasm, falling compliance, pneumothorax.

A leak or disconnection — circuit disconnect, underinflated cuff, loose connection, cuff rupture.

Pressure held at end-exhalation to keep alveoli open and improve oxygenation, letting you lower the FiO2.

Reduced venous return → lower cardiac output and blood pressure (hypotension after a PEEP increase); also barotrauma.

The level that maximizes oxygenation and compliance without overdistension or hemodynamic compromise.

Improved oxygenation from recruited alveoli allows reducing FiO2 (e.g., 0.80 → 0.50) to limit oxygen toxicity.

One continuous pressure throughout the breath; splints alveoli and the upper airway but does not actively assist ventilation.

Cardiogenic pulmonary edema and obstructive sleep apnea — keeps alveoli and the airway open.

A higher inspiratory (IPAP) and lower expiratory (EPAP) pressure; the IPAP–EPAP difference is pressure support.

Widen the IPAP–EPAP gap (raise IPAP) to increase tidal volume and minute ventilation.

Raise EPAP — it recruits alveoli like PEEP.

Set for a patient at risk of hypoventilation so the device delivers breaths if the patient's effort fails.

Low-level pressure support or CPAP to test readiness; abort for tachycardia, desaturation, or distress.

A daily spontaneous breathing trial liberates patients faster than gradually reducing support over many days.

Passed SBT, stable, oxygenating on minimal support, AND able to protect the airway (intact gag and cough).

No leak when the cuff is deflated suggests laryngeal edema and risk of post-extubation stridor.

Short-acting beta-2 agonist that rapidly relaxes bronchial smooth muscle — first-line for acute bronchospasm.

An option when racemic albuterol causes marked tachycardia; the active R-isomer of albuterol.

Short-acting anticholinergic bronchodilator; slower onset than albuterol and often combined with it.

A long-acting anticholinergic (LAMA) for once-daily COPD maintenance bronchodilation.

Constricts upper-airway mucosal vessels to shrink swelling — croup and post-extubation stridor; watch for rebound.

Recombinant DNase that cleaves DNA-rich cystic-fibrosis sputum; give a bronchodilator first.

A mucolytic that breaks mucus disulfide bonds; can trigger bronchospasm, so it is often paired with a bronchodilator.

Draws water osmotically into the airway to improve secretion clearance.

A low-density helium-oxygen mix that cuts turbulent flow and the work of breathing in severe airway obstruction.

80/20 is less dense and more effective; benefit shrinks as the oxygen fraction (and density) rises.

A selective pulmonary vasodilator; monitor methemoglobin and nitrogen-dioxide (NO2) byproduct.

Slow, sustained maximal inspirations by an alert, cooperative patient — high-yield after upper-abdominal or thoracic surgery.

IPPB (positive pressure) is for patients who cannot take an adequate deep breath on their own.

Positions the affected lung segment uppermost so gravity drains secretions; schedule before meals or 1–2 h after.

Avoid head-down (Trendelenburg) positions, which can further raise intracranial pressure.

Positive-expiratory-pressure and oscillatory devices splint airways open and mobilize mucus.

Mobilizes secretions for patients who cannot tolerate manual chest physiotherapy.

A brief sustained high pressure reopens collapsed alveoli in ARDS; follow with adequate PEEP to keep them open.

Hypotension from reduced venous return — stop the maneuver if blood pressure drops.