Tap any sentence or table row to start listening from there. Education only — local protocols and medical direction override.
Airway & Respiratory Diseases — Causes, Findings & Treatments
Prepared for Chase Westbrook • NREMT-Paramedic review • Builds on Jones & Bartlett Paramedic Ch 16 (Airway Management) & Ch 17 (Respiratory Emergencies, pp 1094–1148)
Disclaimer: Education only. Local protocols and medical direction override everything here; doses are typical adult teaching doses (pediatric noted where relevant), not standing orders.
How to use: Each row gives the cause (what is going wrong + common triggers/risk factors), the signs & symptoms (what the patient tells you + what you find), treatment, and the trap the exam likes. "p ####" = Ch 17 page cited in your Ch 17 quiz feedback. Breathing patterns and breath sounds (Kussmaul, Cheyne-Stokes, stridor vs wheeze vs crackles, etc.) are covered in detail in your Abnormal Breathing Patterns study guide; drug mechanisms are in your Ch 13 Drug Study Sheet.
1. Upper Airway Diseases (above the glottis / larynx / trachea) — think STRIDOR, voice change, drooling
| Disease | Cause (pathophysiology • triggers / risk factors) | Signs & Symptoms (patient reports • exam findings) | Prehospital treatment | Pitfalls / exam traps |
|---|---|---|---|---|
| Croup (laryngotracheobronchitis) | Viral (parainfluenza most common) inflammation & edema of the larynx/subglottic trachea → narrowed airway below the cords. Risk: age ~6 mo–3 yr; fall/winter; often worse at night; follows a cold | Reports: cold for 1–2 days, then barking ("seal-like") cough, hoarse voice, often worse at night. Exam: inspiratory stridor, low-grade fever, retractions; usually nontoxic appearing. X-ray (hospital): steeple sign | Keep child calm on caregiver's lap; position of comfort. Blow-by or humidified O2 as tolerated. Severe/stridor at rest: nebulized epinephrine (racemic or 1 mg/mL L-epi) and dexamethasone per protocol. Transport | Don't agitate (crying worsens obstruction) — no tongue blade, no unnecessary IVs. Rebound after neb epi is possible → transport even if improved. Stridor at rest, lethargy, cyanosis = severe |
| Epiglottitis (supraglottitis) | Bacterial infection → rapid swelling of the epiglottis/supraglottic tissues that can completely obstruct the airway. Classic cause Haemophilus influenzae type b — now rare in children due to Hib vaccine (p 1132); now seen more in adults and unvaccinated kids; also strep/staph | Reports: sudden high fever, very sore throat, painful swallowing, muffled ("hot potato") voice. Exam: drooling, tripod position, toxic appearance, soft stridor; usually little or no cough | Leave in position of comfort with caregiver; calm, quiet transport; blow-by/high-flow O2 as tolerated; notify hospital early. If complete obstruction: BVM ventilation (often works) → advanced airway/surgical airway per protocol | Never look in the mouth or use a tongue blade — can trigger laryngospasm/complete obstruction. Don't lay supine. Avoid IVs/agitation. High fever + drooling + no barking cough ≠ croup |
| Bacterial tracheitis | Bacterial (often Staph aureus) infection of the trachea, usually secondary to a viral croup-like illness → thick purulent secretions/membranes that can plug the trachea. Risk: young children | Reports: croup-like illness that suddenly worsens. Exam: high fever, toxic appearance, stridor, brassy cough, copious secretions; does not improve with nebulized epinephrine | High-flow O2 as tolerated; position of comfort; suction visible secretions gently; rapid transport; ventilate with BVM if failing (high resistance from secretions) | Think of it when "croup" looks toxic or fails neb epi. Can obstruct suddenly; prepare for difficult ventilation |
| Peritonsillar abscess | Pus collection beside a tonsil, usually a complication of tonsillitis/strep pharyngitis. Risk: teens & young adults | Reports: severe one-sided sore throat, pain on swallowing, ear pain, fever. Exam: muffled "hot potato" voice, trismus (can't open jaw), drooling, uvula pushed to the opposite side, swollen tonsil | Position of comfort (upright), O2 if hypoxic or distressed, suction as needed, transport; analgesia per protocol | Usually not an airway emergency, but watch for spread/swelling; trismus makes airway management difficult |
| Retropharyngeal abscess | Infection of lymph nodes behind the pharynx (after URI or penetrating injury, e.g., fall with stick in mouth). Risk: mostly children <5 yr | Reports: fever, sore throat, painful swallowing, neck stiffness / refuses to move neck. Exam: drooling, muffled voice, stridor, neck swelling, toxic look | As for epiglottitis: calm, position of comfort, O2, no oral exam, rapid transport | Can mimic meningitis (stiff neck) or epiglottitis; abscess can rupture into the airway |
| Ludwig's angina | Rapidly spreading cellulitis of the floor of the mouth/submandibular space, usually from an infected lower molar (dental) infection. Risk: poor dentition, diabetes, immune compromise | Reports: tooth pain, fever, neck/jaw pain, trouble swallowing or talking. Exam: firm "woody" swelling under the jaw, tongue pushed up and back, drooling, trismus, muffled voice, stridor | Upright position of comfort, high-flow O2, suction, rapid transport, early notification; advanced airway only per protocol by most experienced provider (anatomy is distorted); prepare for surgical airway | Can progress to complete obstruction in hours. Supine position and paralytics can lose the airway. Expect a very difficult intubation |
| Foreign body airway obstruction (FBAO) | Object (food, toy, coin) lodged in the upper airway. Risk: toddlers, elderly, dentures, alcohol, stroke/dysphagia, eating while talking/laughing | Reports/history: sudden choking while eating/playing. Exam — partial: coughing, can speak, stridor/wheeze. Complete: can't speak/cough/breathe, universal choking sign, cyanosis, → unconscious | Partial w/ good air exchange: encourage coughing, don't interfere, O2, transport. Complete (conscious): abdominal thrusts (chest thrusts if pregnant/obese; infant 5 back slaps + 5 chest thrusts). Unconscious: CPR, look in mouth before breaths; direct laryngoscopy + Magill forceps removal | No blind finger sweeps. Sudden wheeze or stridor in a toddler with no fever = foreign body until proven otherwise ("all that wheezes is not asthma"). An object below the cords may need BVM/intubation to push past |
| Anaphylaxis / allergic angioedema | IgE-mediated release of histamine & other mediators → vasodilation, capillary leak, bronchospasm and swelling of lips/tongue/larynx. Triggers: foods (nuts, shellfish), insect stings, drugs (antibiotics, NSAIDs), latex | Reports: itching, throat tightness, "lump in throat," trouble swallowing/breathing, sense of doom, GI upset. Exam: hives/flushing, lip/tongue swelling, hoarseness, stridor and/or wheeze, tachycardia, hypotension | IM epinephrine first (1 mg/mL, 0.3–0.5 mg adult, 0.01 mg/kg peds, anterolateral thigh; repeat q5–15 min per protocol). High-flow O2, airway management, IV fluid bolus for hypotension, albuterol for wheeze, then adjuncts (diphenhydramine, H2 blocker, steroid) per protocol | Antihistamines/steroids don't replace epi. Hoarseness/stridor = early airway swelling — prepare early (smaller tube, surgical airway). Watch for biphasic reaction; patients on beta blockers may resist epi (glucagon per protocol) |
| ACE-inhibitor angioedema (and hereditary angioedema) | Bradykinin-mediated (not histamine) swelling of deep tissues. Caused by ACE-inhibitor ("-pril") drugs — can occur months to years after starting. Hereditary angioedema = inherited C1-esterase inhibitor deficiency. Risk: ACE-I use, more common in Black patients | Reports: swelling of tongue/lips/face, trouble swallowing or speaking; often no itching. Exam: asymmetric tongue/lip swelling, drooling, voice change, stridor; usually no hives, often normal BP | Position of comfort (upright), O2, suction, rapid transport with early notification; epinephrine/antihistamines/steroids may be tried per protocol but often help little; prepare for difficult airway (awake/fiberoptic/surgical airway at hospital) | Responds poorly to epi/antihistamines because it isn't histamine-mediated. Ask about "-pril" meds. Tongue swelling can make BVM and intubation extremely difficult |
| Airway burns / inhalation injury (thermal) | Superheated air/steam damages the supraglottic airway (the upper airway cools air, protecting the lungs; steam can injure lower). Edema builds over minutes–hours. Risk: enclosed-space fire, explosion, steam | Reports: hoarseness, sore throat, cough, trouble swallowing. Exam: facial burns, singed nasal hairs/eyebrows, soot in mouth/nose, carbonaceous sputum, voice change, stridor, wheeze | Remove from source; high-flow O2 by NRB (humidified if available); assess for CO/cyanide (enclosed space); early advanced airway per protocol if stridor/hoarseness progressing; rapid transport to burn center | Stridor or hoarseness after a fire = impending obstruction; the airway gets worse, not better — intervene early. Normal SpO2 doesn't rule out CO |
| Laryngeal / tracheal trauma & swelling | Blunt (dashboard, clothesline, strangulation, hanging) or penetrating neck injury → fracture, hematoma, or edema of larynx/trachea; also laryngospasm | Reports: neck pain, voice change, pain swallowing, coughing blood. Exam: hoarseness, stridor, subcutaneous emphysema, loss of thyroid cartilage landmarks, bruising, hemoptysis | Spinal motion restriction as indicated, high-flow O2, suction, gentle ventilation; advanced airway per protocol (avoid blind techniques; be ready for surgical airway — cricothyrotomy may be contraindicated if larynx is fractured); rapid transport | Positive-pressure ventilation can worsen subQ air/disruption. A patient who can talk now may obstruct later — monitor voice and stridor |
2. Lower Airway & Lung Diseases — think WHEEZE (bronchioles), CRACKLES (alveoli), diminished sounds (pleura)
2A. Obstructive airway diseases (asthma & COPD)
| Disease | Cause (pathophysiology • triggers / risk factors) | Signs & Symptoms (patient reports • exam findings) | Prehospital treatment | Pitfalls / exam traps |
|---|---|---|---|---|
| Asthma | Reversible airway obstruction from 3 parts: bronchospasm + mucus plugging + airway edema/inflammation. Triggers: allergens, cold air, exercise, URI, smoke, stress, aspirin/NSAIDs | Reports: SOB, chest tightness, cough (often at night), "inhaler isn't working." Exam: expiratory wheezing, prolonged expiration, tachypnea, accessory muscles, tripod, short phrases; silent chest = no air movement = exhaustion | Position upright, O2 to SpO2 target, albuterol neb (± ipratropium), steroid (methylprednisolone/dexamethasone) per protocol; severe: magnesium, IM epinephrine per protocol. Anxious, tachypneic but still breathing: CPAP per protocol (p 1128) | Bronchodilators fix the spasm only — mucus & edema need steroids/time. A quiet chest or improving-sounding wheeze with ↓LOC is worsening, not better. Prior ICU/intubation = high-risk patient (p 1128) |
| Status asthmaticus | Severe, prolonged attack that does not break with usual treatment (repeated bronchodilators) → air trapping, fatigue, hypercapnia | Reports: unable to speak more than 1–2 words. Exam: exhaustion, diaphoresis, ↓LOC, cyanosis, silent chest, pulsus paradoxus, rising ETCO2, falling RR | High-flow O2, continuous albuterol + ipratropium, IV steroid, magnesium 2 g IV, IM epinephrine per protocol; assist ventilations with slow rate and long exhalation; advanced airway/ventilator per protocol; rapid transport | True emergency — can progress to arrest. Auto-PEEP: fast BVM rates trap air → hypotension/pneumothorax/arrest. Slowing RR with ↓LOC = respiratory failure |
| COPD — emphysema | Destruction of alveolar walls → loss of elastic recoil, air trapping, ↓gas-exchange surface. Mostly cigarette smoking; also alpha-1 antitrypsin deficiency. Progressive & irreversible | Reports: chronic, progressive dyspnea on exertion, weight loss. Exam: thin ("pink puffer"), barrel chest (from air trapping, p 1137), pursed-lip breathing, prolonged expiration, diminished breath sounds, tripod, accessory muscles | Position of comfort first (p 1131); O2 titrated to ~88–92%; bronchodilators for exacerbation (see below) | Barrel chest is air trapping, not muscle (p 1137). Pursed lips create their own back pressure (natural PEEP) — encourage it |
| COPD — chronic bronchitis | Chronic inflammation → enlarged mucus glands, excess mucus, impaired cilia, airway narrowing. Defined by productive cough ≥3 months/yr for 2 consecutive years. Smoking, pollutants | Reports: chronic productive cough, frequent chest infections. Exam: often overweight, cyanotic ("blue bloater"), rhonchi, wheeze; signs of right heart failure (JVD, peripheral edema) | O2 to ~88–92%, bronchodilators, position of comfort, suction/cough support; treat as COPD exacerbation | Antitussives (cough suppressors) can worsen bronchitis — they stop the cough that clears mucus (p 1116). Right-sided HF (cor pulmonale): JVD, hepatojugular reflux, edema → O2, don't fluid-load (p 1140) |
| COPD exacerbation (acute) | Acute worsening of chronic disease, typically triggered by environmental changes — weather, inhaled triggers (p 1139) — and infections; also med/O2 noncompliance | Reports: worse SOB over hours–days, more sputum or change in color. Exam: tachypnea, wheeze/rhonchi, accessory muscles, tripod, pursed lips, ↓SpO2, tachycardia, ↑ETCO2 | Position of comfort, O2 (don't withhold — titrate to ~88–92%), albuterol + ipratropium, steroid per protocol; CPAP if alert, breathing spontaneously and protecting airway; assist ventilations if RR/depth fall (p 1140) | Never withhold O2 out of hypoxic-drive fear — hypoxia kills faster; just titrate. Fever + productive cough + localized rhonchi in a COPD pt = think pneumonia (p 1140) |
| End-stage COPD | Advanced, irreversible lung destruction → chronic respiratory failure, often cor pulmonale, wasting. Repeated EMS calls, home O2 | Reports: constant dyspnea, family worn out. Exam: emaciated, on home O2, ↓LOC, inadequate breathing, cyanosis, tripod/fatigue | Assist ventilations if breathing inadequately and contact medical control; respect a valid DNR/POLST — if not produced, begin care (p 1140) | Don't wait for paperwork to start ventilations; don't jump to aggressive intubation without direction. Discuss goals of care with family/OLMC |
2B. Infectious & pediatric lung diseases
| Disease | Cause (pathophysiology • triggers / risk factors) | Signs & Symptoms (patient reports • exam findings) | Prehospital treatment | Pitfalls / exam traps |
|---|---|---|---|---|
| Pneumonia | Infection (bacterial, viral, fungal) of the lung parenchyma → alveoli fill with fluid/pus (consolidation) → V/Q mismatch, hypoxia. Risk: elderly, COPD, immune compromise, nursing homes, recent illness | Reports: fever, chills, productive cough (colored sputum), pleuritic chest pain, malaise; elderly may only be confused. Exam: crackles/rhonchi (often localized), ↓breath sounds over consolidation, tachypnea, tachycardia, hypoxia | O2 to target, position of comfort, monitor for sepsis (fluids per protocol), assist ventilation if failing; bronchodilator only if wheezing from coexisting COPD/asthma | Bronchodilators don't treat pneumonia. Can lead to sepsis/septic shock. Elderly may be afebrile. Wear a mask (droplet precautions) |
| Aspiration pneumonia / pneumonitis | Inhalation of stomach contents, saliva, food, or fluid → chemical injury (acid) ± infection, often right lower lobe. Risk: ↓LOC (alcohol, OD, seizure, stroke), dysphagia, vomiting, poor gag | Reports/history: vomiting or choking episode, unresponsive period. Exam: cough, wheeze, crackles/rhonchi, hypoxia, fever later | Suction, recovery position or airway protection, O2, ventilate if needed; advanced airway if unable to protect airway per protocol | Prevent it: suction ready, avoid gastric distention with BVM (slow, low-volume breaths), elevate head when possible |
| Bronchiolitis / RSV (peds) | Viral (RSV most common) inflammation of the bronchioles with mucus & edema. Risk: infants <2 yr (esp. <3 months), premature birth, congenital heart/lung disease; winter | Reports: runny nose & cough for a few days, poor feeding, fewer wet diapers, apnea in young infants. Exam: wheezing, crackles, tachypnea, nasal flaring, retractions, grunting, hypoxia | Nasal suctioning (big help in infants), O2/humidified O2 to target, position of comfort, monitor for apnea, assist ventilations if failing; bronchodilator only if protocol allows a trial | Infant wheezing is often bronchiolitis, not asthma — albuterol often doesn't help. Watch for fatigue and apnea |
| Pertussis (whooping cough) | Bacterial infection (Bordetella pertussis) of the airway; highly contagious via droplets. Risk: unvaccinated/under-vaccinated infants & children; waning adult immunity | Reports: cold-like start, then coughing fits for weeks, vomiting after cough. Exam: paroxysmal cough followed by inspiratory "whoop"; infants may have apnea/cyanosis instead of whoop; between fits may look well | O2, suction, position of comfort, monitor/support breathing (apnea in infants); transport | Droplet precautions (mask on you and the patient). Infants are at highest risk of death. Report per local public-health rules |
| Tuberculosis (TB) & other airborne/droplet infections | TB = Mycobacterium tuberculosis, spread by airborne droplet nuclei; often latent, reactivates. Risk: HIV/immune compromise, homeless shelters, prisons, travel/immigration from endemic areas. (Also influenza, COVID-19, measles etc.) | Reports: chronic cough (>2–3 wk), hemoptysis, night sweats, weight loss, fever, fatigue. Exam: cough, sometimes crackles; may look chronically ill | Supportive: O2 to target, position of comfort; N95/fit-tested respirator for you, surgical mask on patient (if tolerated), ventilate the ambulance (exhaust fan/windows); notify receiving facility | PPE is the key exam point: airborne = N95 (not just a surgical mask). Report exposures per your agency's exposure plan |
| Cystic fibrosis (CF) | Genetic (inherited) disorder → thick, sticky mucus in lungs (and pancreas) → airway plugging, chronic infection, bronchiectasis. Diagnosed in childhood | Reports: chronic productive cough, frequent lung infections, poor weight gain/GI problems, known CF history. Exam: crackles/rhonchi/wheeze, clubbing, hypoxia; possible hemoptysis or pneumothorax | O2 to target, position of comfort, suction, bronchodilators per protocol if wheezing; consider pneumothorax with sudden worsening; transport (often to their CF center if feasible) | Patient/family are usually experts on their own disease — use their care plan. Sudden pain + dyspnea in CF = possible pneumothorax |
2C. Fluid, vascular & alveolar problems
| Disease | Cause (pathophysiology • triggers / risk factors) | Signs & Symptoms (patient reports • exam findings) | Prehospital treatment | Pitfalls / exam traps |
|---|---|---|---|---|
| Pulmonary edema — cardiogenic (CHF) | Left ventricle fails → back-pressure into pulmonary veins → fluid leaks into interstitium/alveoli. Triggers: MI/ischemia, hypertension crisis, missed meds/dialysis, high salt intake, dysrhythmia | Reports: SOB, orthopnea, paroxysmal nocturnal dyspnea, needs to sit up. Exam: crackles (may progress to pink frothy sputum), wheeze ("cardiac asthma"), JVD, edema, hypertension common, diaphoresis | Sit upright, O2, CPAP if alert, breathing spontaneously & protecting airway; nitroglycerin only if BP allows (and no PDE-5 use) per protocol; 12-lead; IV access. If deteriorating on CPAP (↑RR, ↓SpO2, ↓LOC): remove CPAP, BVM, prepare to intubate (p 1127) | Wheezes can be cardiac — all that wheezes is not asthma. No nitro if hypotensive. Don't give fluid boluses. CPAP can drop BP — monitor |
| High-altitude pulmonary edema (HAPE) | Noncardiogenic edema from hypoxic pulmonary vasoconstriction at altitude (usually >~2,500 m / 8,000 ft). Risk: rapid ascent, exertion, prior HAPE, cold | Reports: decreased exercise tolerance, dry cough → productive (may be pink/frothy), SOB at rest. Exam: crackles, tachypnea, tachycardia, cyanosis, low SpO2 for altitude; often 2–4 days after arrival | Descent (definitive), O2, minimize exertion, keep warm; CPAP/portable hyperbaric bag per protocol | Descent is the treatment — don't delay for testing. Can coexist with high-altitude cerebral edema (ataxia, AMS) |
| ARDS (acute respiratory distress syndrome) | Diffuse noncardiogenic alveolar-capillary injury → protein-rich fluid leaks into alveoli → stiff, noncompliant lungs, severe hypoxia. Causes: sepsis, pneumonia, aspiration, major trauma, burns/inhalation, near-drowning, pancreatitis | Reports: worsening SOB hours–days after the injury/illness. Exam: severe tachypnea, diffuse crackles, hypoxia refractory to high-flow O2, ↑work of breathing; often already in ICU (interfacility) | High-flow O2, PEEP (CPAP/ventilator) per protocol, ventilator management on interfacility transfers per orders (low tidal volumes), treat underlying cause | Stiff lungs → high airway pressures with BVM; risk of barotrauma. Not fluid overload — don't treat with diuretics/nitro reflexively |
| Pulmonary embolism (PE) | Blood clot (usually from a DVT in leg/pelvis) blocks a pulmonary artery → ventilated lung that isn't perfused (dead space) → hypoxia, right heart strain. Risk: immobility, recent surgery/long travel, cancer, pregnancy/postpartum, estrogen/birth control, smoking, prior clots | Reports: sudden dyspnea, pleuritic chest pain, cough, possible hemoptysis, anxiety, leg pain/swelling. Exam: tachycardia, tachypnea, clear lungs, hypoxia that doesn't fully correct with O2, JVD/hypotension if massive; syncope; cardiac arrest (PEA) | High-flow O2, position of comfort, IV access, cardiac monitor/12-lead, fluids/pressors cautiously for hypotension per protocol, rapid transport to facility capable of thrombolysis | Clear lungs + sudden dyspnea + hypoxia not fixed by O2 = think PE. Bronchodilators/CPAP don't fix it. Massive PE can cause PEA arrest |
2D. Pleural space & conditions outside the lung parenchyma
| Disease | Cause (pathophysiology • triggers / risk factors) | Signs & Symptoms (patient reports • exam findings) | Prehospital treatment | Pitfalls / exam traps |
|---|---|---|---|---|
| Spontaneous pneumothorax | Rupture of a small surface bleb → air enters the pleural space → partial lung collapse without trauma. Risk: tall, thin young males, smokers, COPD/emphysema, CF, Marfan syndrome; can occur with exertion or at rest | Reports: sudden sharp pleuritic chest pain (one side) and dyspnea. Exam: diminished breath sounds on affected side (often apex), tachypnea, mild hypoxia; subQ emphysema possible | Position of comfort, high-flow O2 and transport (p 1144); IV, monitor. Needle decompression only if it becomes tension | Don't decompress a simple pneumothorax (p 1144). Positive pressure (BVM, CPAP) can convert it to tension — avoid unless needed; reassess often |
| Tension pneumothorax | One-way valve lets air into the pleural space without escape → pressure collapses lung, shifts mediastinum, kinks great vessels → ↓venous return → obstructive shock. Causes: trauma, positive-pressure ventilation, untreated pneumothorax | Reports: severe, worsening SOB, anxiety. Exam: absent breath sounds one side, hypotension, tachycardia, JVD, increasing difficulty bagging (↑resistance), hypoxia; tracheal deviation is a late sign | Needle decompression of affected side per protocol (2nd ICS midclavicular or 4th–5th ICS anterior/midaxillary line), high-flow O2, ventilatory support, rapid transport; reassess (needle can clog/kink) | Don't wait for tracheal deviation. Suspect in a ventilated patient who suddenly becomes hard to bag and hypotensive |
| Pleural effusion | Fluid collects in the pleural space (outside the lung) → compresses lung. Causes: CHF, pneumonia, cancer, renal/liver failure, TB | Reports: gradually increasing dyspnea, worse lying flat, pleuritic or dull chest pain, cough. Exam: diminished/absent breath sounds at the bases (dependent), dullness to percussion, tachypnea; friction rub possible | Upright position of comfort, O2 to target, transport (definitive tx = thoracentesis in hospital) | Crackles are not typical — the fluid is outside the lung, so sounds are just diminished. Don't confuse with pneumothorax (sudden onset, apex) |
| Lung cancer | Malignant tumor growth in lung tissue → airway obstruction, effusion, bleeding, collapse. Risk: smoking (#1), radon, asbestos, secondhand smoke, occupational exposures | Reports: chronic cough, hemoptysis, weight loss, chest pain, hoarseness, fatigue, recurrent pneumonia; may have known diagnosis/chemo. Exam: wheeze (localized), ↓breath sounds (effusion), hypoxia, cachexia | O2 to target, position of comfort, suction for hemoptysis (affected side down if massive bleeding and side known), pain management; respect DNR/hospice plans | Massive hemoptysis is an airway emergency. Ask about advance directives and the goals of care |
2E. Toxic inhalation & other causes
| Disease | Cause (pathophysiology • triggers / risk factors) | Signs & Symptoms (patient reports • exam findings) | Prehospital treatment | Pitfalls / exam traps |
|---|---|---|---|---|
| Toxic inhalation (irritant gases) | Inhaled chemicals injure the airway. Water-soluble gases (e.g., ammonia, chlorine to a degree) dissolve in moist upper airway → fast upper-airway burns/edema. Low water-solubility gases (e.g., phosgene, nitrogen dioxide) reach the alveoli → delayed pulmonary edema (hours). Sources: industrial, farming (silo gas), household mixes (bleach + ammonia), fires | Reports: burning eyes/nose/throat, cough, chest tightness, SOB. Exam: tearing, hoarseness, stridor (upper), wheeze; with phosgene may initially seem fine → crackles/pulmonary edema hours later | Scene safety/hazmat first: remove from exposure only if trained and protected, decontaminate. High-flow O2 (humidified), bronchodilators for wheeze, airway management, CPAP for edema per protocol; transport even if minimal symptoms after phosgene-type exposure | Don't become a patient. Delayed onset with phosgene — early lack of symptoms is false reassurance; recommend transport/observation |
| Carbon monoxide (CO) poisoning | CO binds hemoglobin ~200–250× more tightly than O2 → ↓O2 delivery & cellular hypoxia. Sources: fires, faulty furnaces/heaters, generators/vehicles in enclosed spaces, charcoal grills indoors | Reports: headache, nausea, dizziness, flu-like illness affecting several people/pets in the same house (better away from home). Exam: confusion, ↓LOC, chest pain/dysrhythmias, seizures, syncope; "cherry red" skin is a late, unreliable sign | Remove from source; 100% O2 via NRB (or BVM/CPAP) regardless of SpO2; SpCO monitor (CO-oximetry) if available; consider hyperbaric center (LOC change, pregnancy, high levels) per protocol | Standard pulse oximetry reads falsely normal (can't tell COHb from oxyhemoglobin). Pregnant patients/fetus at high risk. Check the crew's own exposure |
| Cyanide poisoning | Cyanide blocks cytochrome oxidase → cells can't use O2 (cellular asphyxia) → lactic acidosis. Sources: smoke from burning plastics/synthetics (enclosed-space fires), industrial exposures, some suicides | Reports: headache, dizziness, anxiety, SOB, nausea; bitter almond odor (not detectable by all). Exam: ↓LOC, seizures, tachypnea → apnea, hypotension, dysrhythmias, cardiac arrest; SpO2 may be normal | Remove from source, 100% O2, airway/ventilatory support; hydroxocobalamin (Cyanokit) 5 g IV over ~15 min adult per protocol; treat seizures/hypotension | Suspect it with CO in any enclosed-space fire victim with ↓LOC, hypotension, or arrest. Hydroxocobalamin turns skin/urine red |
| Hyperventilation syndrome | Anxiety/panic-driven over-breathing → blows off CO2 (respiratory alkalosis) → ↓ionized calcium effects. Diagnosis of exclusion — only after ruling out serious causes | Reports: anxiety, SOB, numbness/tingling around mouth & fingers, lightheadedness, chest tightness. Exam: tachypnea, carpopedal spasm, normal SpO2, low ETCO2 | Calm, reassuring coaching; O2 if any doubt or hypoxia; check glucose, SpO2, ECG; transport per protocol | Never have the patient rebreathe into a paper bag or NRB without O2. Hyperventilation is also a sign of PE, DKA (Kussmaul), asthma, MI, sepsis, toxins (e.g., aspirin) — rule those out first |
3. Treatment Toolbox
3A. Oxygen devices, flow rates & SpO2 targets
| Device / target | Flow rate | Approx. FiO2 | Use it for / notes |
|---|---|---|---|
| Nasal cannula | 1–6 L/min | ~24–44% | Mild hypoxia, COPD titration; >6 L/min dries mucosa without much gain (standard teaching) |
| Simple face mask | 6–10 L/min | ~35–60% | Moderate hypoxia; ≥6 L/min to flush exhaled CO2 |
| Nonrebreathing mask (NRB) | 10–15 L/min (bag stays inflated) | Up to ~90% | Severe hypoxia, CO poisoning, trauma; patient must be breathing adequately |
| Venturi mask | Per adapter | 24–50% (precise) | When precise FiO2 needed (COPD) — where carried |
| Blow-by / humidified O2 | Per protocol | Variable | Peds who won't tolerate a mask (croup, epiglottitis); humidification soothes upper airway |
| BVM with reservoir | 15 L/min | Near 100% | Inadequate or absent breathing; apnea |
| CPAP | Per device (start ~5 cm H2O, titrate to ~10 per protocol) | Adjustable | See CPAP row below |
| SpO2 targets | — | — | Most patients: ≥94% (typically 94–99%), avoid unnecessary hyperoxia. COPD/chronic CO2 retainers: ~88–92% (still give O2 — don't withhold). CO poisoning: 100% O2 regardless of SpO2. The more hypoxic the patient, the faster they desaturate (p 1120) |
3B. Ventilation support: CPAP & BVM
| Tool | Indications | Contraindications / when to stop | Key points |
|---|---|---|---|
| CPAP | Moderate–severe distress from pulmonary edema, COPD exacerbation, asthma (per protocol), near-drowning; patient alert, breathing spontaneously, can follow commands and protect own airway | Apnea/inadequate breathing, ↓LOC/can't protect airway, vomiting, hypotension, suspected pneumothorax or chest trauma, facial trauma/can't seal mask, recent upper GI/facial surgery (per protocol) | Splints alveoli open, pushes fluid out, ↓work of breathing; can ↓BP (↓venous return). Remove and switch to BVM if deteriorating (↑RR, ↓SpO2, ↓LOC) (p 1127). Coach anxious patients |
| BVM ventilation | Inadequate rate/depth, apnea, failing CPAP, ↓LOC with poor ventilation (e.g., end-stage COPD, opioid OD — ventilate first, then naloxone, p 1101) | None when the patient needs it; adjust technique | Adult 1 breath q6 s (10/min); infant/child 1 breath q2–3 s (20–30/min) (AHA 2020). Just enough volume for chest rise, over ~1 s. Severe obstruction (asthma/COPD): slower rate, allow full exhalation to prevent auto-PEEP (air trapping → ↓BP, barotrauma, arrest). Watch ETCO2 |
3C. Typical teaching medications (adult unless noted — per protocol)
| Medication | What it does | Use in airway disease | Typical teaching dose (per protocol) |
|---|---|---|---|
| Albuterol | Beta-2 agonist → bronchodilation | Asthma, COPD, anaphylaxis wheeze; trial in bronchiolitis only if protocol allows | 2.5 mg neb (repeat or continuous per protocol); MDI 4–8 puffs with spacer |
| Ipratropium (Atrovent) | Anticholinergic → bronchodilation, ↓secretions | Add to albuterol in moderate–severe asthma/COPD (often as DuoNeb) | 0.5 mg neb (often up to ×3 in first hour) |
| Methylprednisolone (Solu-Medrol) / Dexamethasone | Corticosteroid → ↓airway inflammation & edema (onset hours) | Asthma, COPD exacerbation, anaphylaxis adjunct, croup (dexamethasone) | Methylpred 125 mg IV (adult); dexamethasone dose varies widely by protocol (croup: ~0.6 mg/kg PO/IM/IV, max ~10–16 mg) |
| Magnesium sulfate | Smooth-muscle relaxant → bronchodilation | Severe/refractory asthma (status asthmaticus) | 2 g IV over 15–20 min; watch for hypotension, ↓reflexes, respiratory depression |
| Epinephrine IM (1 mg/mL) | Alpha + beta agonist → vasoconstriction, bronchodilation, ↓swelling | Anaphylaxis (first-line); severe asthma unresponsive to nebs per protocol | 0.3–0.5 mg IM anterolateral thigh (peds 0.01 mg/kg, max 0.3–0.5 mg); repeat q5–15 min |
| Nebulized epinephrine (racemic 2.25% or L-epi 1 mg/mL) | Alpha vasoconstriction → shrinks subglottic edema | Croup with stridor at rest; upper-airway swelling per protocol | Racemic: 0.5 mL of 2.25% in 3 mL NS. L-epi (peds): 0.5 mL/kg of 1 mg/mL, max 5 mL. Watch for rebound — transport |
| Nitroglycerin | Venodilator (high dose arterial) → ↓preload/afterload | Cardiogenic pulmonary edema (with CPAP) | 0.4 mg SL q5 min only if BP allows (SBP threshold per protocol) and no PDE-5 inhibitor use (sildenafil/vardenafil 24 h, tadalafil 48 h) |
| Hydroxocobalamin (Cyanokit) | Binds cyanide → cyanocobalamin (excreted) | Suspected cyanide poisoning (smoke inhalation) | 5 g IV over ~15 min (adult) per protocol |
4. Upper vs Lower Airway — Quick Compare
| Feature | Upper airway problem | Lower airway problem |
|---|---|---|
| Key sound | Stridor — high-pitched, mostly inspiratory (above/at cords) | Wheeze — musical, mostly expiratory (bronchioles); crackles (fluid in alveoli); rhonchi (mucus in larger airways); diminished sounds (pleural air/fluid) |
| Voice / swallowing | Hoarse, muffled "hot potato" voice; drooling, painful swallowing | Voice normal but speaks in short phrases (dyspnea) |
| Cough | Barking (croup), brassy (tracheitis), little/no cough (epiglottitis) | Productive (pneumonia, bronchitis), dry/nocturnal (asthma), paroxysmal "whoop" (pertussis), pink frothy (pulmonary edema) |
| Position | Upright/tripod with neck extended ("sniffing"), refuses to lie down | Tripod, upright; orthopnea in CHF |
| Main dangers | Sudden complete obstruction; agitation or exam can trigger it | Fatigue → respiratory failure; air trapping/auto-PEEP; hypoxia |
| Main tools | Calm, position of comfort, O2 as tolerated, neb epi (croup), IM epi (anaphylaxis), BVM, advanced/surgical airway | Bronchodilators (spasm only), steroids, magnesium, CPAP, nitro (CHF), slow BVM with full exhalation |
Red flags — impending respiratory failure / arrest
Altered mental status: anxiety/restlessness → confusion, drowsiness, combativeness (hypoxia/hypercapnia).
Silent chest or disappearing wheeze with no improvement in distress = no air moving.
Slowing respiratory rate or shallow breathing in a tired patient ("getting better" with ↓LOC is getting worse) → assist ventilations (p 1140).
Can't speak more than 1–2 words, tripod, accessory muscles, retractions, nasal flaring, grunting/head bobbing (peds), paradoxical/seesaw breathing.
SpO2 falling despite O2 (or <90% on high flow), cyanosis, rising ETCO2 (or very low ETCO2 with poor ventilation).
Stridor at rest, drooling, voice change, inability to swallow — upper airway closing.
Bradycardia in a hypoxic patient (especially children) = imminent arrest.
Deterioration on CPAP (↑RR, ↓SpO2, ↓LOC) → remove CPAP, BVM, prepare advanced airway (p 1127).
5. Rapid-Recall Flashcards
| Question | Answer |
|---|---|
| Which vaccine made epiglottitis rare in children, and what must you never do in suspected epiglottitis? | Hib (Haemophilus influenzae type b) vaccine (p 1132). Never look in the mouth or use a tongue blade — it can trigger complete obstruction. |
| What are the 3 components of an asthma attack, and which one do bronchodilators treat? | Bronchospasm, mucus, and airway edema/inflammation. Bronchodilators treat only the bronchospasm; steroids treat inflammation. |
| Severe asthmatic with a prior ICU intubation, anxious and tachypneic, inhaler not helping — best next step? | Apply CPAP, transport immediately, and start vascular access en route (p 1128). |
| COPD is characterized by…? And what typically triggers an exacerbation? | Progressive, irreversible changes in lung structure and function (p 1137). Exacerbations are usually triggered by environmental changes — weather or inhaled triggers (p 1139). |
| What causes the barrel chest in emphysema? | Air trapping in the lungs (p 1137). |
| Emphysema patient, SpO2 76% on home O2, pursed lips — first action? | Place her in a position that makes breathing easier (p 1131), then titrate O2 (target ~88–92%), bronchodilators. |
| Emphysema patient on NRB: RR and depth are now decreasing. What do you do? | Begin assisting ventilations with a BVM and 100% O2 (p 1140). Don't remove O2 out of hypoxic-drive fear. |
| Chronic bronchitis patient with diffuse rhonchi who recently started an OTC cough suppressor — likely cause of distress? | The antitussive — suppressing the cough lets mucus build up (p 1116). |
| COPD patient with fever, chills, productive cough, and left lower-lobe rhonchi? | Pneumonia (p 1140) — bronchodilators don't treat it. |
| Pulmonary edema patient on CPAP: RR rising, SpO2 falls from 90% to 84%. Next step? | Remove CPAP, assist ventilations with BVM, prepare to intubate (p 1127). |
| Young woman with sudden pleuritic chest pain, dyspnea, SpO2 93%, ↓breath sounds right upper lobe — treatment? | High-flow O2 and transport (p 1144). Needle decompression only if signs of tension (hypotension, JVD, absent sounds). |
| Sudden dyspnea, clear lungs, tachycardia, SpO2 won't rise with O2, recent long flight? | Pulmonary embolism — O2, IV, monitor, rapid transport. |
| Why can a CO-poisoned patient show SpO2 98%? | Standard pulse oximeters can't distinguish carboxyhemoglobin from oxyhemoglobin. Give 100% O2 regardless; use SpCO if available. |
| Child with barking cough, stridor at rest, steeple sign — treatment? | Keep calm with caregiver, humidified/blow-by O2, nebulized epinephrine and dexamethasone per protocol; transport (watch for rebound). |
| Why slow the BVM rate in severe asthma? | To allow full exhalation and prevent auto-PEEP (air trapping → hypotension, pneumothorax, arrest). |