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I. Upper Respiratory Tract
Structures: Nose, mouth, pharynx (nasopharynx, oropharynx, laryngopharynx), epiglottis,
larynx, trachea
Functions:
o Nose: warms, humidifies, filters air; contains turbinates; olfactory nerve (smell)
The inside of the nose is shaped into 3 passages by projections called
turbinates.
The turbinates increase the surface area of the nasal mucosa that warms and
moistens the air as it enters the nose.
o Pharynx: Subdivided into 3 parts: nasopharynx, oropharynx, and laryngopharynx.
Air moves through the oropharynx to the laryngopharynx. It then travels
through the epiglottis to the larynx before moving into the trachea.
o Epiglottis: prevents aspiration during swallowing
o Larynx: vocal cords, glottis (opening between cords)
o Trachea: U-Shaped cartilages keep the trachea open but allow the adjacent esophagus
to expand for swallowing, divides at carina → right/left main bronchi
5 inches (10 to 12 cm) long and 1 inch (1.5 to 2.5 cm) in diameter
o Carina: highly sensitive, stimulation → vigorous cough
II. Lower Respiratory Tract
Once air passes the carina, it is in the lower respiratory tract
Structures: bronchi, bronchioles, alveolar ducts, alveoli
Lungs:
o Right lung: 3 lobes
o Left lung: 2 lobes
Hilus: entry point for bronchi, vessels, nerves
Bronchi branching: lobar → segmental → subsegmental → bronchioles
o The right mainstem bronchus is shorter, wider, and straighter than the left mainstem
bronchus. That is why aspiration is more likely to occur in the right lung than in the left lung.
Bronchoconstriction vs. bronchodilation: airway diameter controlled by smooth muscle
Dead space (VD): ~150 mL of 500 mL tidal volume → no gas exchange
o The volume of air in the trachea and bronchi
Alveoli: ~300 million; interconnected by pores of Kohn (allow movement of air from alveolus to
alveolus); volume ~2500 mL; surface area = tennis court
o Primary site of gas exchange for O2 and CO
o Bacteria can move through pores of Kohn, spreading infection to previously uninfected
areas
Gas exchange: across alveolar–capillary membrane; impaired by pulmonary edema (excess
fluid fills the interstitial space and alveoli reducing gas exchange) III. Surfactant & Atelectasis
Surfactant: lipoprotein reducing alveolar surface tension, prevents collapse
o Reduces the amount of pressure needed to inflate the alveoli and makes them less
likely to collapse
o Sighing every 5 to 6 breaths stretches the alveoli and promotes surfactant secretion
Atelectasis: collapsed alveoli due to lack of surfactant
o Postoperative patient: At risk for atelectasis due to effects of anesthesia, decreased
mobility, and pain, which can alter breathing and lung expansion
Acute respiratory distress syndrome (ARDs): Lack of surfactant contributes to widespread
atelectasis and collapse of lung tissue IV. Blood Supply
Pulmonary circulation: right ventricle → pulmonary arteries (deoxygenated blood) → alveoli
(gas exchange) → pulmonary veins (oxygenated blood) → left atrium → left ventricle → systemic circulation
o Provides the lungs with blood that take part in gas exchange
o Venous blood is collected from capillary networks of the body and returned to the right
atrium by way of the superior and inferior vena cava.
Bronchial circulation: Does not take part in gas exchange but provides O2 to the bronchi and
other lung tissues, deoxygenated blood returns via azygos vein into the superior vena cava
o Starts with bronchial arteries
V. Chest Wall & Pleura
Shaped, supported, and protected by 24 ribs
Thoracic cage: ribs, sternum, mediastinum (separates lungs)
o Protects the lungs and heart from injury
Inspiration : active process; diaphragm contracts, external intercostals expand chest; negative intrathoracic pressure pulls air in Expiration : normally passive (elastic recoil); active when forced (abdominal & internal intercostal muscles). Return to their original size after being stretched or expanded. When intrathoracic pressure rises air moves out of the lungs. COPD/asthma : expiration becomes active due to airflow obstruction When dyspnea (shortness of breath) occurs, neck and shoulder muscles, and other accessory muscles of respiration, can aid the effort
- Compliance & Resistance
Compliance: Ease of lung expansion. The ability of the lungs to expand
o ↓ compliance (harder for lungs to inflate):
Conditions that increase fluids: Pulmonary edema, ARDs, pneumonia)
Conditions that make tissue less elastic: Pulmonary fibrosis, sarcoidosis
Conditions that restrict lung movements: Pleural effusion
o ↑ compliance: COPD (destruction of alveolar walls and loss of tissue elasticity)
Resistance: Any obstacle to airflow during inspiration and/or expiration. Airway diameter
decreases with asthma which increases resistance (treated with bronchodilators). Secretion exclude the airway increases resistance (treated with mucolytics or expectorants)
- Control of Respiration
Brainstem (medulla): primary control
Chemoreceptors:
o Receptors that respond to chemical composition changes (PaCO₂, pH)
Central Chemoreceptors
o Location: Medulla.
o Stimulus: Changes in hydrogen ion (H⁺) concentration (via PaCO₂ and cerebrospinal
fluid pH).
o Response:
↑ H⁺ (acidosis) → medulla increases respiratory rate & tidal volume (VT).
↓ H⁺ (alkalosis) → opposite effect (slows respiration).
o Mechanism: CO₂ + H₂O → H₂CO₃ → dissociates to H⁺ → lowers CSF pH → stimulates
breathing.
Peripheral chemoreceptors
o Location: Carotid bodies (at bifurcation of common carotid arteries). Aortic bodies
(above & below aortic arch).
o Stimulus:
↓ PaO₂
↓ pH
↑ PaCO₂
o Response: Stimulate respiratory center to increase ventilation.
COPD consideration:
o COPD = chronically elevated PaCO₂.
o Central chemoreceptors become less sensitive to CO₂.
o Ventilation maintained mainly by hypoxic drive (peripheral chemoreceptors
responding to low PaO₂).
Mechanical receptors:
o Irritant receptors:
Found in conducting airways.
Sensitive to inhaled particles/aerosols.
Trigger cough reflex.
o Stretch receptors:
Located in smooth muscle of airways.
Control respiration by preventing overinflation.
Responsible for Hering-Breuer reflex → inhibits inspiration as lungs inflate.
o Juxtacapillary (J) receptors:
Found in alveolar capillaries.
Stimulated by ↑ pulmonary capillary pressure.
Cause rapid, shallow breathing (tachypnea) , e.g., in pulmonary edema.
VII. Respiratory Defense Mechanisms
Air filtration: nasal hairs, increased air turbulence (due to abrupt changes in direction of airflow
that occur as air moves through the nasopharynx and larynx)
o Most large particles (greater than 5 μm) are less dangerous because they are removed
in the nasopharynx or bronchi and do not reach the alveoli
Mucociliary clearance: 100 mL mucus/day
o Also called the mucociliary escalator, responsible for the movement of mucus
o Secretory immunoglobulin A (IgA) in the mucus helps protect against bacteria and
viruses
o Dehydration, smoking, inhaling high O2 concentrations, infection, and drugs, such as
atropine, anesthetics, alcohol, or cocaine, impair ciliary action
IX. Assessment of Respiratory System A. Subjective Data
History: upper/lower respiratory issues, allergies, family history (Box 27.1 Genetic Risk Alert:
CF, α1-antitrypsin deficiency, asthma, COPD risk)
o Ask about asthma, COPD, pneumonia, and TB
o Ask the patient with allergies about possible precipitating factors or triggers, such as
medications, pollen, smoke, mold, or pet exposure
Medications: inhalers, ACE inhibitors (cough), O2 therapy
o Ask about the dose (if known), frequency, length of time taken, side effects, and the
reason for taking the medication
o Cough is a common side effect of angiotensin-converting enzyme (ACE) inhibitors
o Include the patient’s cognitive and physical ability related to using O2 and any
metered-dose inhalers.
Surgeries/treatments: intubation, chest physiotherapy
o Determine if the patient has ever been intubated because of a respiratory problem.
1. Change in Health Status
Ask about perceived changes over days, months, or years.
COPD: lung function declines slowly; patients may not notice due to activity modification.
Acute changes (e.g., infection): sudden dyspnea, decreased exercise tolerance.
Asthma: symptoms may worsen with exercise, mold, temperature changes, or pollution.
2. Course of Illness
Determine onset, type of symptoms, and aggravating/relieving factors.
Patients with chronic disease often report changes in existing symptoms (not new ones).
Example: Increased SOB or purulent sputum may suggest acute COPD exacerbation.
3. Cough Assessment
Identify quality:
o Loose = secretions
o Dry/hacking = airway irritation/obstruction
o Harsh/barky = upper airway obstruction (e.g., subglottic edema)
Assess strength of cough (can secretions be cleared?).
Productive vs. nonproductive.
Acute vs. chronic (chronic = >3 weeks).
Ask about cough pattern: regular, paroxysmal, time-related, activity-related, weather-related,
triggers (talking, deep breathing).
Identify relief measures tried (Rx or OTC).
4. Sputum Characteristics (if productive cough)
Evaluate: amount, color, consistency, odor.
Quantify daily volume; note changes.
Normal: clear/whitish.
Smokers: clear to gray, sometimes brown specks.
COPD: whitish/yellow, especially in morning.
Concerning changes:
o Color change → possible complications.
o Consistency: thick, thin, frothy, pink-tinged (possible pulmonary edema).
o Odor: foul = infection.
Ask if sputum varies with position (↑ lying down) or activity.
5. Hemoptysis (blood in sputum)
Ranges: streaks → massive bleeding.
Differentiate from hematemesis (vomiting blood).
Causes: pneumonia, TB, lung cancer, severe bronchiectasis.
Dyspnea scale: Modified Borg Scale (0–10)
1. Breathing & Airway History
Ask about history of breathing difficulties.
Wheezing = airway obstruction (asthma, foreign body, emphysema).
Family exposure to TB.
2. Smoking & Environmental Exposure
Smoking = most important risk factor for COPD & lung cancer.
Ask about all forms of tobacco use (cigarettes, cigars, pipes, chewing tobacco, e-cigs, hookah).
Assess exposure to secondhand smoke.
Explore quit attempts and methods used.
Document smoking history in pack-years.
Ask about places lived/traveled → TB risk (immigration, prisons, shelters, HIV, IV drug use).
Risk factors for fungal infections: soil, bird/rodent feces, polluted water, immunocompromised.
Effect on family, work, and social life.
Impact of meds, O₂ therapy, special routines (e.g., cystic fibrosis pulmonary hygiene).
Occupational exposures: fumes, toxins, asbestos, coal, silica.
Hobbies: woodworking, pottery, animal exposure → triggers.
Asthma: hyperreactive airways triggered by smoke/fumes/chemicals.
11. Sexuality–Reproductive Pattern
Breathing difficulties may affect intimacy.
Discuss positions/strategies to reduce dyspnea.
Encourage pulmonary hygiene before sexual activity.
May need O₂ therapy during intercourse.
12. Coping–Stress Tolerance Pattern
Dyspnea ↔ anxiety = vicious cycle, leads to deconditioning & isolation.
Assess frequency of leaving home and social activity.
Pulmonary rehab/support groups may help.
Chronic illness = prolonged stress → assess coping strategies.
B. Objective Data Nose
Inspect for patency, inflammation, deformities, symmetry, discharge.
Test airflow by occluding each nostril.
With speculum/light:
o Mucosa → pink, moist, no edema/exudate/bleeding.
o Septum → check deviation, perforation, bleeding (mild deviation = normal).
o Turbinates → inspect for polyps (from chronic irritation/allergies).
Discharge:
o Purulent/malodorous = foreign body.
o Watery = allergies or CSF leak.
o Bloody = trauma/dryness.
o Thick = infection.
Mouth & Pharynx
Inspect oral mucosa: color, lesions, masses, gums, dentition.
Tongue → symmetry, lesions.
Pharynx → smooth, moist, no exudate, ulcerations, swelling, or postnasal drip.
Tonsils → assess color, symmetry, enlargement.
Gag reflex → test CN IX (glossopharyngeal) & CN X (vagus).
Neck
Inspect symmetry, swelling, tenderness.
Palpate lymph nodes systematically (ears → skull base → mandible → midline).
Normal: small, mobile, nontender (“shotty nodes”).
Abnormal: tender, hard, fixed nodes.
Manifestations of Inadequate Oxygenation System Early Late Cardiovascu lar Dysrhythmias, mild HTN, tachycardia Dysrhythmias, hypotension, cyanosis, cool/clammy skin CNS Restlessness, irritability, apprehension, confusion/lethargy Confusion/lethargy, combativeness, coma Respiratory Dyspnea on exertion, tachypnea Dyspnea at rest, pauses between words, accessory muscle use, retractions Other Diaphoresis, fatigue, ↓ urine output Same as early (progresses) Thorax & Lungs General Exam Setup
Use warm, well-lit room, ensure privacy.
Expose chest; start with posterior chest (less interference from breast tissue).
Posterior exam: patient leans forward, arms folded.
Anterior exam: upright or semi-Fowler’s (30°); may lean forward for support.
Inspection
Look for signs of distress: tachypnea, accessory muscle use.
Chest shape/symmetry:
o Normal AP:transverse ratio = 1:2.
o Barrel chest = aging or hyperinflation.
o Sternum abnormalities: pectus carinatum (protrusion), pectus excavatum
(indentation).
o Spinal curvatures affecting breathing: kyphosis, scoliosis, kyphoscoliosis.
o Bronchovesicular : medium pitch, I:E = 1:1, heard between scapulae & 1st/2nd ICS
anteriorly.
o Vesicular : soft, low-pitched, rustling, I:E = 3:1, heard over most lung fields.
10. Normal vs. Abnormal Findings Normal
Clear vesicular sounds, equal expansion, no accessory muscle use
Abnormal
Crackles
o Fine: short, high-pitched, just before end of inspiration (atelectasis, early HF,
pulmonary fibrosis, pneumonia, edema).
o Coarse: loud, low-pitched, bubbling/snoring, inspiration &/or expiration
(pneumonia, pulmonary edema, COPD, HF).
Wheezes: continuous high-pitched musical, mainly on expiration (asthma, COPD,
obstruction).
Stridor: loud, crowing sound (croup, epiglottitis, foreign body, post-extubation
edema).
Pleural friction rub: grating, creaking, both inspiration & expiration, no change with
cough (pleurisy, pneumonia, infarct).
Absent breath sounds: pneumothorax, pleural effusion, obstruction, large
atelectasis, pneumonectomy.
Voice changes:
o Bronchophony/whispered pectoriloquy: clearer words (pneumonia).
o Egophony: “E” sounds like “A” (pneumonia, effusion).
Inspection
Abdominal paradox: inward abdomen on inspiration → severe distress.
Accessory muscle use/retractions: COPD, asthma, secretion retention; severe
distress/hypoxemia.
↑ AP diameter (barrel chest): COPD, asthma, CF, hyperinflation, aging.
Clubbing: bulbous fingertips → chronic hypoxemia, lung cancer, CF, bronchiectasis.
Cyanosis: late hypoxemia; bluish lips, conjunctiva.
Kussmaul respirations: rapid, deep, fruity odor → metabolic acidosis.
Pursed-lip breathing: COPD/asthma; helps slow exhalation.
Splinting: ↓ tidal volume due to pain (surgery, trauma, pleurisy).
Tachypnea (>20/min): fever, anxiety, hypoxemia, restrictive disease.
Tripod position: leaning forward with arms supported → COPD, asthma, pulmonary
edema, severe distress. Asthma Exacerbation
Inspection: Prolonged expiration, tripod position, pursed-lip breathing.
Palpation: ↓ chest movement.
Percussion: Hyperresonant.
Auscultation: Wheezes; ↓ breath sounds (ominous if very diminished).
Atelectasis
Inspection: Usually no change unless large area involved.
Palpation:
o Small: no change.
o Large: ↓ movement, ↓ fremitus.
Percussion: Dull over affected area.
Auscultation: Fine crackles (may clear with deep breaths); absent if large.
COPD
Inspection: Barrel chest, cyanosis, tripod position, accessory muscle use.
Palpation: ↓ movement.
Percussion: Hyperresonant; dull if consolidation present.
Auscultation: Crackles, wheezes, distant (quiet) breath sounds.
Pleural Effusion
Inspection: Tachypnea, accessory muscle use.
Palpation:
o ↑ movement/fremitus above effusion.
o Absent fremitus over effusion.
Percussion: Dull.
Auscultation: ↓ or absent breath sounds over effusion; egophony above effusion.
Pneumonia
Inspection: Tachypnea, accessory muscle use, cyanosis/duskiness.
After VATS: Chest tube management, monitor breath sounds, encourage deep breathing. Mediastinoscopy
Before: Consent, prep for OR and general anesthesia.
After: Monitor as for bronchoscopy.
Exercise & Pulmonary Testing Exercise Testing
Before: Ensure patient wears comfortable shoes.
During: Encourage holding handlebars, walk as quickly as possible.
Pulmonary Function Tests (PFTs)
Before: Avoid mealtime, no bronchodilators for 6 hr, assess for distress.
During: Assess for distress.
After: Monitor distress, provide rest.
Radiology Chest X-ray
Before: Undress to waist, gown, remove metal objects.
CT Scan
Before: Check renal function & shellfish/iodine allergy, NPO 4 hr if contrast used.
During: Warn about flushed/warm feeling, patient must remain still.
After: Encourage fluids to prevent renal issues.
MRI
Before: Check pregnancy, allergies, renal function. Remove metal objects/patches, assess for
implanted devices or staples, claustrophobia (offer antianxiety meds). May need fasting.
During: Remain still.
PET Scan
Before: Obtain IV access, NPO 4 hr (except water/meds), hold glucose IV, check glucose (60–
140 mg/dL).
During: Remain still.
After: Encourage fluids to excrete tracer.
Pulmonary Angiogram
Before: Assess contrast allergy, NPO 6–12 hr, give sedative.
After: Monitor site (pressure dressing), BP, pulse, distal circulation, use compression device,
encourage fluids. Ventilation–Perfusion (V/Q) Scan
Same as chest x-ray prep.
After: No special precautions (radioactivity dissipates quickly).
6-Minute Walk Test
During: Monitor SpO₂ and tolerance; allow rests as needed.
Thoracentesis
Before: Explain procedure, obtain consent.
During: Position upright leaning on overbed table, feet supported, instruct not to talk/cough.
After: Monitor for hypoxia, pneumothorax, check breath sounds, encourage deep breaths, send
specimens promptly.
