Your FREE TMC Exam Flashcards 2026 – 200+ Cards

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

High pH (> 7.45) with a low PaCO2 (< 35 mm Hg) from hyperventilation (anxiety, pain, PE, hypoxia).

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

High pH (> 7.45) with a high HCO3 (> 26 mEq/L) — vomiting, diuretics, NG suction.

pH 7.35–7.45 · PaCO2 35–45 mm Hg · HCO3 22–26 mEq/L · PaO2 80–100 mm Hg · SaO2 95–100%.

1) pH (acidemia/alkalemia) → 2) PaCO2 vs HCO3 to find the cause → 3) assess compensation. The value moving with the pH is the primary cause.

The pH is back in the normal range while PaCO2 and HCO3 both stay abnormal — e.g., chronic respiratory acidosis in COPD with renal retention of HCO3.

PaO2 ÷ FiO2 (as a decimal). Berlin ARDS: 200–300 mild, 100–200 moderate, ≤ 100 severe (with PEEP ≥ 5).

80 ÷ 0.80 = 100 → severe ARDS. (90 ÷ 0.60 = 150 → moderate; 250 ÷ 0.50 = 500 → normal.)

Alveolar PO2 minus arterial PaO2. A widened gradient = a gas-exchange problem (V/Q mismatch, shunt, diffusion), not simple hypoventilation.

Respiratory rate × tidal volume. Example: 12 × 500 mL = 6,000 mL = 6 L/min.

(Tidal volume − dead space) × rate. Example: (600 − 150) × 10 = 4,500 mL = 4.5 L/min — only gas reaching the alveoli.

Hemoglobin bound to carbon monoxide; cannot carry O2. Pulse ox reads falsely normal — detect with CO-oximetry. Treat with 100% O2.

Hemoglobin with iron in the ferric (Fe3+) state; cannot bind O2. Causes cyanosis with SpO2 stuck near 85%; detected by CO-oximetry.

A normal square waveform with end-tidal CO2 ~35–45 mm Hg confirms the tube is in the trachea, not the esophagus.

A sudden rise in end-tidal CO2 signals return of spontaneous circulation as pulmonary blood flow is restored.

Fraction of FVC exhaled in the first second. Below ~0.70 = obstructive (asthma, COPD). Normal/high with low volumes = restrictive.

Rate ÷ tidal volume in liters. Below ~105 predicts weaning success; above 105 predicts failure (e.g., 32 ÷ 0.3 ≈ 107).

Inspiratory muscle strength, measured against an occluded airway. More negative than ~ −20 to −30 cm H2O favors weaning; −15 is inadequate.

Peak reflects airway resistance + compliance; plateau (inspiratory hold, no flow) reflects compliance only. The gap = airway resistance.

Trapped gas from incomplete exhalation (COPD/asthma, high rate). Found with an expiratory-hold; managed by lengthening expiratory time.

Volume of gas moved in one normal breath, ~5–8 mL/kg ideal body weight (about 500 mL in an adult). Set near 6 mL/kg IBW in lung-protective ventilation.

Maximum volume exhaled after a maximal inspiration (IRV + VT + ERV). Normal ~65–75 mL/kg; below ~10–15 mL/kg signals inadequate ventilatory reserve.

Volume remaining in the lungs after a normal exhalation (ERV + RV). PEEP and CPAP raise FRC; it falls in restrictive disease, ARDS, and obesity.

Gas remaining after a maximal exhalation; cannot be measured by simple spirometry (needs body plethysmography or gas dilution). Increased in air trapping/COPD.

Total volume after a maximal inspiration (~6 L). Decreased in restrictive disease; increased with hyperinflation in obstructive disease.

Conducting airways that hold gas but do no gas exchange, ~1 mL/lb of ideal body weight (~150 mL). Part of each breath that never reaches the alveoli.

Alveoli that are ventilated but not perfused (e.g., pulmonary embolism). Combined with anatomic dead space gives physiologic dead space.

Volume change per unit pressure change, VT ÷ (plateau pressure − PEEP). Normal ~60–100 mL/cm H2O; low in ARDS, pneumonia, pulmonary edema.

Opposition to airflow, (peak − plateau pressure) ÷ flow. Rises with bronchospasm, secretions, kinked or small-bore ET tubes.

Sigmoid relationship of SaO2 to PaO2; a PaO2 of 60 corresponds to ~90% saturation (the steep upper-shoulder reference point).

Lower Hb-O2 affinity (unloads O2 to tissues) from acidosis, hypercapnia, fever, and increased 2,3-DPG. Mnemonic: "CADET, face Right."

Higher Hb-O2 affinity (holds O2) from alkalosis, hypocapnia, hypothermia, low 2,3-DPG, carboxyhemoglobin, and fetal hemoglobin.

Low arterial oxygen: mild PaO2 60–79, moderate 40–59, severe < 40 mm Hg on room air. Distinct from hypoxia (low tissue O2 delivery).

Hypoxemia that does not correct with increasing FiO2, indicating a large intrapulmonary shunt (ARDS); treated by recruiting alveoli with PEEP.

Blood passing perfused but unventilated alveoli (atelectasis, ARDS, pneumonia). Causes hypoxemia poorly responsive to oxygen; corrected with PEEP/recruitment.

Imbalance of ventilation to perfusion; the most common cause of hypoxemia. Low V/Q = shunt-like; high V/Q = dead-space-like. Usually responds to oxygen.

Na − (Cl + HCO3); normal 8–12 mEq/L. A high gap metabolic acidosis points to lactic acidosis, ketoacidosis, renal failure, or toxins.

Metabolic component of acid–base balance; normal ±2 mEq/L. A negative value (base deficit) indicates metabolic acidosis; positive indicates metabolic alkalosis.

O2 saturation of pulmonary artery blood (normal ~60–80%). A fall reflects worsening delivery or rising consumption (shock, anemia, hypoxemia).

(1.34 × Hb × SaO2) + (0.003 × PaO2). Hemoglobin-bound O2 dominates, so anemia drops content even when PaO2 and SaO2 look normal.

Diffusing capacity for carbon monoxide; reflects the alveolar-capillary membrane. Low in emphysema, fibrosis, anemia; high in alveolar hemorrhage and polycythemia.

Plots flow against volume in one cycle. A scooped expiratory limb = obstruction; flattened inspiratory/expiratory limbs = fixed upper-airway obstruction.

An increase in FEV1 of ≥ 12% and ≥ 200 mL after a bronchodilator indicates significant reversibility, characteristic of asthma.

Maximum flow during a forced exhalation; tracks asthma control. A drop from the patient's personal best signals worsening obstruction.

Provocation test for suspected asthma; a ≥ 20% fall in FEV1 at a low dose confirms airway hyperresponsiveness. Have a bronchodilator ready.

Measures distance walked and desaturation over 6 minutes to assess functional capacity and titrate oxygen in COPD and pulmonary hypertension.

The tip should sit 2–6 cm above the carina (~at the aortic knob, T4–T5). Too low = right mainstem intubation; pull back.

Diminished/absent left breath sounds, asymmetric chest rise, hypoxemia, and a tube tip past the carina on x-ray. Withdraw the tube.

Absent lung markings peripherally with a visible visceral pleural line; tension pneumothorax adds mediastinal shift away and a depressed hemidiaphragm.

Air-filled bronchi outlined by surrounding alveolar opacity, indicating consolidation such as pneumonia or ARDS.

Loss of a normal border on a chest film localizes a lesion; e.g., a lost right heart border places consolidation in the right middle lobe.

Short horizontal lines at the lung periphery from interstitial fluid, classically seen in pulmonary edema/heart failure.

Gram-positive diplococci suggest S. pneumoniae; gram-negative rods suggest Klebsiella/Pseudomonas; guides empiric antibiotic choice in pneumonia.

A systolic BP fall > 10 mm Hg on inspiration, seen in severe asthma, cardiac tamponade, and tension pneumothorax.

Bulbous fingertips and loss of the nail-bed angle from chronic hypoxemia (cystic fibrosis, bronchiectasis, lung cancer, interstitial lung disease).

Recruitment of sternocleidomastoid and scalene muscles signaling increased work of breathing and impending respiratory failure.

Palpable vibration during speech; increased over consolidation (pneumonia) and decreased over pleural effusion or pneumothorax.

Discontinuous popping breath sounds from fluid or reopening alveoli — heard in pulmonary edema, pneumonia, and fibrosis.

High-pitched continuous musical sounds from narrowed airways; expiratory in asthma/COPD. Sudden silence ("silent chest") signals severe obstruction.

High-pitched inspiratory sound from upper-airway narrowing (croup, post-extubation edema, foreign body); treat with cool mist or racemic epinephrine.

A grating sound during inspiration and expiration from inflamed pleural surfaces (pleurisy, pulmonary embolism with infarction).

Scores eye, verbal, and motor responses from 3 to 15; ≤ 8 indicates an unprotected airway and the need to consider intubation.

Off the ventilator on oxygen, a PaCO2 rise to ≥ 60 mm Hg (or ≥ 20 above baseline) with no respiratory effort supports brain death.

VC > 10–15 mL/kg, spontaneous VT > 5 mL/kg, RR < 35, MIP more negative than −20, RSBI < 105 suggest readiness to wean.

Indicated for retained secretions with ineffective cough (cystic fibrosis, bronchiectasis, > ~25–30 mL sputum/day), not routine pneumonia.

Suggest for retained secretions or atelectasis unresponsive to therapy, foreign-body removal, hemoptysis evaluation, or specimen collection.

Indicated when frequent ABGs or continuous beat-to-beat blood-pressure monitoring is needed in unstable, ventilated patients.

Confirms collateral ulnar flow before radial arterial puncture; the hand should re-pink within ~5–15 seconds after releasing the ulnar artery.

Oxygen consumption ÷ arteriovenous O2 content difference. A low output widens the a−v O2 difference and lowers SvO2.

Right-heart preload, normal ~2–6 mm Hg. Elevated in fluid overload, right heart failure, cor pulmonale, tamponade, and tension pneumothorax.

Reflects left-atrial filling pressure, normal ~4–12 mm Hg. High (> 18) = cardiogenic pulmonary edema; normal/low with edema = ARDS.

Normal ~25/8 mm Hg (mean < 20). Elevated in pulmonary hypertension, PE, hypoxic vasoconstriction, and left heart failure.

Normal upright P waves with a rate > 100/min; in respiratory patients consider hypoxemia, hypercapnia, anxiety, fever, or beta-agonist effect.

Wide, early QRS complexes without a preceding P wave; often triggered by hypoxemia, hypokalemia, or acidosis — check oxygenation first.

Irregularly irregular rhythm with no discrete P waves; reduces cardiac output and is common in COPD, hypoxemia, and heart failure.

Right ventricular hypertrophy/failure from chronic lung disease and pulmonary hypertension; managed by correcting hypoxemia with oxygen.

Peaked T waves, widened QRS, and loss of P waves; can cause life-threatening arrhythmias, sometimes accompanying metabolic acidosis.

Rates newborn Appearance, Pulse, Grimace, Activity, Respiration 0–2 each at 1 and 5 minutes; 7–10 normal, 4–6 moderate distress, 0–3 needs resuscitation.

Grades neonatal respiratory distress (retractions, nasal flaring, grunting); a higher score means worse distress, opposite to Apgar.

Noninvasively trends PtcO2 and PtcCO2 through heated skin, mainly in neonates; rotate the site to prevent burns and recalibrate periodically.

Lecithin-to-sphingomyelin ratio in amniotic fluid; ≥ 2:1 indicates fetal lung maturity and low risk of respiratory distress syndrome.

Nasal cannula, simple mask, nonrebreather — supplies less than total inspiratory demand, so FiO2 varies with the breathing pattern.

Air-entrainment (Venturi) mask, high-flow nasal cannula — total flow meets/exceeds demand, giving a fixed, predictable FiO2.

Low-flow; roughly 24–44% at 1–6 L/min (about 4% FiO2 per liter), varying with the patient's breathing pattern.

Reservoir bag + one-way valves; ~60–80% O2 at 10–15 L/min. Keep the bag from fully collapsing — raise the flow if it does.

High-flow device that delivers a precise FiO2 (24–50%) set by the jet size and entrainment ports, regardless of breathing pattern.

Obstruction or stiffness: secretions/mucus plug, kinked or bitten tube, bronchospasm, falling compliance, pneumothorax, coughing.

Leak or disconnection: circuit disconnect, underinflated ET cuff, loose connection, ruptured cuff or chest-tube leak.

Two-point calibration: expose the sensor to room air (21%) and to 100% O2. A galvanic cell reading low on room air signals a depleted fuel cell.

Plots blood-gas control results over time to detect trends and shifts (e.g., six points on one side of the mean = a systematic shift).

Multirule QC system that distinguishes random from systematic error and decides whether to accept or reject a run. A result > 3 SD (1-3s rule) rejects the run.

Critical → sterilize; semicritical (mucous membranes) → high-level disinfection; noncritical (intact skin) → low/intermediate disinfection.

Contacts oral mucosa → semicritical under Spaulding → requires high-level disinfection between patients.

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

Droplet (surgical mask): influenza, pertussis. Contact (gown/gloves): MRSA, C. difficile.

Galvanic (fuel cell) self-powered, slower; polarographic (Clark) needs a battery, faster response. Calibrate both to 21% and 100% O2.

Unreliable with poor perfusion, motion, nail polish, carboxyhemoglobin (falsely high), and methemoglobin (drifts toward 85%). Confirm with CO-oximetry.

Phase I baseline (dead space), II rising upstroke, III alveolar plateau, then inspiratory downstroke. End of plateau = end-tidal CO2.

A sloped, blunted upstroke on capnography indicates bronchospasm or obstruction (asthma, COPD); flattens after effective bronchodilation.

A notch in the capnogram plateau showing spontaneous effort against the ventilator as paralytic wears off — reassess sedation/neuromuscular blockade.

Measures gas flow (and integrates to volume) via a pressure drop across a fixed resistance; condensation or secretions cause inaccurate readings.

A handheld vane device that measures exhaled tidal and minute volume at the bedside; reads inaccurately at very low or very high flows.

Heats the ventilator circuit to prevent condensation ("rainout") that can cause auto-triggering, inaccurate volumes, and false alarms.

Acts as a one-way valve; continuous bubbling signals an air leak, and tidaling (fluid rising/falling with breathing) confirms patency.

Bubbling in the water-seal chamber indicates an air leak — check connections first; if persistent, suspect a bronchopleural leak.

Adds water vapor to dry gas for low-flow oxygen above ~4 L/min; a popping pressure-relief valve signals downstream obstruction or kinked tubing.

Delivers warmed, fully saturated gas (target ~37 °C, 100% relative humidity at the airway) for intubated patients to prevent mucosal drying.

A passive "artificial nose" that recycles exhaled heat and moisture; avoid with thick secretions, hemoptysis, or large air leaks (increases dead space).

Pneumatic jet nebulizer driven at 6–8 L/min that aerosolizes medication; tapping the cup and proper fill volume reduce dead-volume waste.

A holding chamber slows aerosol and reduces oropharyngeal deposition, improving delivery for patients with poor hand-breath coordination.

Uses a vibrating piezoelectric crystal to make a dense aerosol; can deliver large water volumes for sputum induction but may cause bronchospasm.

Particles 1–5 microns deposit in the lower airways; larger particles impact in the upper airway, smaller ones are exhaled.

A pressure-based flowmeter that reads accurately regardless of position but over-reads flow if there is downstream obstruction.

A gravity-dependent, back-pressure-compensated flowmeter; must stay upright to read accurately. A stuck float signals a contaminated tube.

Diameter-Index and Pin-Index Safety Systems prevent connecting gas equipment to the wrong gas source — a safeguard against gas mix-ups.

Minutes remaining = (gauge psi × 0.28 cylinder factor) ÷ flow in L/min. A full O2 E-cylinder holds ~625 L at ~2,200 psi.

Uses molecular sieve beds (zeolite) to deliver ~90–95% O2 at low flows for home use; output purity drops if the sieve fails or at high flow.

Placed on the expiratory limb to protect the ventilator and environment; a wet or clogged filter raises resistance and triggers high-pressure alarms.

Run before connecting a patient to verify circuit integrity, alarm function, and sensor calibration; a failed leak test means find and fix the leak first.

Sterilization destroys all microbes including spores (autoclave, ethylene oxide); disinfection kills most pathogens but not all spores.

A chemical agent used for high-level disinfection of semicritical equipment (e.g., bronchoscopes); requires adequate soak time and thorough rinsing.

Treat all blood and body fluids as infectious: hand hygiene plus gloves, gown, mask, and eye protection based on anticipated exposure.

Elevate the head of bed 30–45°, daily sedation and extubation-readiness assessment, oral care, and DVT/stress-ulcer prophylaxis to lower VAP risk.

Allows suctioning without disconnecting the patient, preserving PEEP and reducing exposure/contamination in high-FiO2 or infectious patients.

Adjust display sweep speed and amplitude to read ventilator graphics correctly; misreading a flat or compressed trace can mask auto-PEEP or asynchrony.

Run low, normal, and high control levels to validate analyzer accuracy across the clinical range before reporting patient results.

Keep 20–30 cm H2O — seals the airway without exceeding tracheal capillary pressure. Above 30 risks mucosal ischemia (remove air).

Intact gag and cough (airway protection) with the underlying cause of failure resolved — not just good vitals or numbers.

No leak when the cuff is deflated suggests laryngeal edema and a risk of post-extubation stridor; treat with racemic epinephrine.

New trach + sudden dyspnea + can't pass a suction catheter → remove the inner cannula first to check for a mucus plug.

Every breath — patient- or machine-triggered — is delivered at the full set tidal volume or pressure; the most support, rests the muscles.

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

Augments each spontaneous breath with a set inspiratory pressure and cycles to expiration when inspiratory flow falls.

Low tidal volume ~6 mL/kg of ideal body weight with plateau pressure < 30 cm H2O to limit volutrauma and barotrauma.

70 kg × 6 mL/kg = 420 mL — start ARDS ventilation near this volume, set by ideal body weight, not actual weight.

Deliberately tolerating an elevated PaCO2 to protect the lung with low tidal volumes, as long as the pH stays within the protocol limit.

Short-acting beta-2 agonist; rapidly relaxes bronchial smooth muscle — first-line for acute bronchospasm (asthma, COPD).

Short-acting anticholinergic bronchodilator that blocks muscarinic receptors; slower onset, often combined with albuterol.

Reduces upper-airway swelling by mucosal vasoconstriction — used for croup and post-extubation stridor.

Mucolytic (DNase) that thins the sticky DNA-rich sputum of cystic fibrosis, improving airway clearance.

Positions the affected lung segment uppermost so gravity drains secretions toward the larger central airways for clearance.

Incentive spirometry: alert, cooperative patient takes slow deep breaths. IPPB: for patients who can't take an adequate deep breath on their own.

Indicated for a resting room-air PaO2 ≤ 55 mm Hg (or SaO2 ≤ 88%), or ≤ 59 mm Hg with cor pulmonale, edema, or hematocrit > 55%.

Continuous positive airway pressure for spontaneously breathing patients; raises FRC to improve oxygenation in atelectasis, OSA, and cardiogenic edema.

Noninvasive ventilation with separate IPAP and EPAP levels; the IPAP–EPAP difference (pressure support) drives ventilation in COPD exacerbation.

First-line for COPD exacerbation with respiratory acidosis and for cardiogenic pulmonary edema; avoid with apnea, shock, or inability to protect the airway.

Positive end-expiratory pressure that keeps alveoli open, raises FRC, and improves oxygenation in ARDS; excess PEEP lowers cardiac output and risks barotrauma.

The PEEP that gives the best oxygenation and compliance with the least hemodynamic compromise; titrate by oxygenation, compliance, and blood pressure.

Delivers a set inspiratory pressure with a decelerating flow; tidal volume varies with compliance and resistance, so monitor VT closely.

Delivers a guaranteed tidal volume with a fixed flow; airway pressure varies with compliance and resistance, so watch the peak/plateau pressures.

A dual-control mode that targets a set tidal volume at the lowest pressure, adjusting inspiratory pressure breath to breath as compliance changes.

Prolonged high CPAP with brief timed releases; recruits collapsed alveoli in ARDS while allowing spontaneous breathing.

Delivers very small tidal volumes at high rates around a constant mean airway pressure; a lung-protective rescue mode in severe neonatal/ARDS hypoxemia.

Normal ~1:2 to 1:3; lengthen expiration (e.g., 1:4) for obstructive air trapping, and consider inverse ratio to improve oxygenation in ARDS.

Flow triggering (sensing a flow change) generally requires less patient effort than pressure triggering; sensitivity set ~1–3 L/min or −1 to −2 cm H2O.

To lower PaCO2, increase minute ventilation by raising the respiratory rate or tidal volume (staying lung-protective).

To raise PaO2/SpO2, increase FiO2 and/or PEEP; once FiO2 exceeds ~0.60, raise PEEP to recruit alveoli and limit oxygen toxicity.

Prolonged FiO2 > 0.50–0.60 can cause absorption atelectasis and alveolar injury; use the lowest FiO2 maintaining adequate oxygenation.

Mismatch between patient effort and ventilator delivery (double-triggering, flow starvation, auto-PEEP); fix by adjusting flow, trigger, or sedation, not just paralysis.

Improves V/Q matching and oxygenation in moderate-to-severe ARDS; guidelines support ≥ 12–16 hours prone per session for sustained benefit.

A brief trial on minimal support (low PSV or T-piece) to test readiness to extubate; failure shows as tachypnea, distress, desaturation, or hemodynamic change.

Near-simultaneous sedative and paralytic for emergent intubation in patients at aspiration risk; have suction, bag-mask, and rescue airways ready.

Slight neck flexion with head extension aligns the oral, pharyngeal, and laryngeal axes to optimize the view for intubation in adults.

Holds the tongue forward to maintain an airway in an unconscious patient; in an awake patient it triggers gagging or vomiting — use a nasopharyngeal airway instead.

A supraglottic device for ventilation when bag-mask is difficult or intubation fails; it does not fully protect against aspiration.

Typical internal diameter 7.0–8.0 mm for women and 8.0–9.0 mm for men; larger bore lowers airflow resistance and eases bronchoscopy and secretion clearance.

Uncuffed tube size ≈ (age ÷ 4) + 4 mm; e.g., a 4-year-old needs roughly a 5.0 mm internal-diameter tube.

Pre-oxygenate, limit each pass to ≤ 15 seconds, apply suction only on withdrawal, and keep adult vacuum about −100 to −150 mm Hg.

Outer diameter should be less than half the ET tube's internal diameter; size in French ≈ (ET tube ID × 2) to limit airway pressure drop.

Hypoxemia, vagally mediated bradycardia, dysrhythmias, mucosal trauma, atelectasis, and raised intracranial pressure — preoxygenate and limit duration.

Clean or replace the inner cannula and stoma regularly; keep an obturator and a spare tube of the same and a smaller size at the bedside.

A one-way valve on a tracheostomy that lets air exit through the upper airway for speech; the cuff must be deflated before placement to avoid suffocation.

Delivers heated, humidified gas up to 60 L/min with a precise FiO2; washes out dead space and provides a small PEEP effect in hypoxemic respiratory failure.

A helium-oxygen mix that is less dense than air, lowering resistance through narrowed airways in severe asthma and upper-airway obstruction; flowmeters need a correction factor.

A selective pulmonary vasodilator that improves oxygenation in persistent pulmonary hypertension of the newborn and refractory ARDS; wean slowly to avoid rebound.

Instilled into the airway of premature neonates with respiratory distress syndrome to lower surface tension; monitor for transient desaturation during instillation.

The R-isomer short-acting beta-2 agonist; bronchodilates with potentially fewer tachycardia/tremor side effects than racemic albuterol.

Long-acting beta-2 agonists (LABAs) for maintenance bronchodilation; never used as monotherapy in asthma — combine with an inhaled corticosteroid.

A long-acting anticholinergic (LAMA) for maintenance bronchodilation in COPD; not a rescue medication for acute bronchospasm.

Anti-inflammatory controllers (budesonide, fluticasone) for persistent asthma; rinse the mouth after use to prevent oral thrush and dysphonia.

Oral or IV steroids (prednisone, methylprednisolone) reduce airway inflammation in asthma and COPD exacerbations over hours, not minutes.

A mucolytic that breaks disulfide bonds to thin secretions; its sulfur odor and irritant effect can trigger bronchospasm, so pretreat with a bronchodilator.

A mast-cell stabilizer used prophylactically for asthma (including exercise-induced); it has no role in treating an acute attack.

Inhaled antibiotic for Pneumocystis pneumonia prophylaxis; deliver in a negative-pressure room with a filtered nebulizer to protect staff.

An inhaled aminoglycoside antibiotic for chronic Pseudomonas in cystic fibrosis; delivers high airway concentrations with low systemic toxicity.

IV adjunct in severe asthma exacerbations that relaxes bronchial smooth muscle when standard bronchodilators and steroids are insufficient.

Intramuscular epinephrine is the first-line treatment for anaphylaxis with bronchospasm and hypotension; give early into the anterolateral thigh.

A life-threatening emergency: immediate needle decompression (2nd intercostal space, midclavicular line) followed by chest-tube placement.

30:2 for one or two rescuers without an advanced airway; with an advanced airway, give continuous compressions and one breath every 6 seconds.

Rate 100–120/min, depth ≥ 2 inches (5 cm) in adults, full recoil, and minimal interruptions for the best perfusion during CPR.

Shock ventricular fibrillation and pulseless ventricular tachycardia; do not shock asystole or pulseless electrical activity (treat with CPR and epinephrine).

1 mg IV/IO every 3–5 minutes during cardiac arrest to improve coronary and cerebral perfusion through vasoconstriction.

An antiarrhythmic given for shock-refractory VF/pulseless VT: 300 mg IV/IO first dose, then 150 mg if needed.

After return of spontaneous circulation, titrate FiO2 to keep SpO2 ~92–98% and avoid hyperoxia, which worsens reperfusion injury.

Delivers near-100% O2 with a reservoir at 10–15 L/min; ventilate ~10–12/min in adults, watching for visible chest rise.

30:2 for a single rescuer and 15:2 for two rescuers in infants and children; compression depth about one-third the chest's AP diameter.

Warm, dry, stimulate, and position; if apneic or HR < 100, start positive-pressure ventilation, and begin compressions if HR < 60 despite effective PPV.

Viral subglottic edema causing a barking cough and stridor; treat with cool humidified mist, racemic epinephrine, and corticosteroids.

Acute supraglottic swelling (drooling, tripod posture); avoid agitating the child or examining the throat, and prepare for controlled intubation in the OR.

A technique that creates back-pressure to splint airways open, slowing exhalation and reducing air trapping and dyspnea in COPD.

Exhaling against resistance keeps airways open and moves secretions centrally; flutter/Acapella devices add oscillation for airway clearance.

An inflatable vest that vibrates the chest to loosen secretions in cystic fibrosis and bronchiectasis without manual chest physiotherapy.

A structured program of exercise training, education, and breathing techniques that improves dyspnea, exercise tolerance, and quality of life in COPD.

The single most effective intervention to slow COPD progression; combine behavioral support with nicotine replacement or pharmacotherapy.