Lung Zones (West)
| Zone | Location | PA vs Pa vs Pv | Flow |
|---|---|---|---|
| Zone 1 | Apex | PA > Pa > Pv | No flow; dead space; ↑ in hypovolemia, PPV |
| Zone 2 | Middle | Pa > PA > Pv | Intermittent (Starling resistor) |
| Zone 3 | Base | Pa > Pv > PA | Continuous; best V/Q; most flow |
V/Q mismatch: V/Q >1 = dead space (Zone 1; embolism). V/Q <1 = shunt-like (Zone 3; pneumonia). True shunt: hypoxemia does NOT correct with 100% O2. V/Q mismatch: hypoxemia DOES correct with supplemental O2.
Gross Anatomy
Right lung: 3 lobes (upper, middle, lower), 10 bronchopulmonary segments, shorter/wider main bronchus (aspirated objects go RIGHT). Left lung: 2 lobes (upper/lower), 8-9 segments, cardiac notch + lingula.
Pleura
- Visceral pleura — on lung surface; no pain fibers
- Parietal pleura — lines thorax/diaphragm; somatic pain fibers
- Pleural space — negative pressure (-5 cmH2O); 10-20 mL fluid normally
Tension pneumothorax: tracheal deviation AWAY from affected side, decreased breath sounds, JVD, hypotension. Needle decompression at 2nd ICS MCL; then chest tube at 4th-5th ICS anterior axillary line.
Airways
| Segment | Cartilage | Epithelium | Notes |
|---|---|---|---|
| Trachea | C-shaped rings | Pseudostratified ciliated columnar | Carina at T4-5; R bronchus ~25° (aspirations go R) |
| Main bronchi | Complete rings | Pseudostratified ciliated | Right: shorter, wider, more vertical |
| Lobar/Segmental bronchi | Plates | Ciliated columnar | 3R lobar, 2L lobar |
| Terminal bronchioles | None (muscle only) | Simple ciliated columnar | Last conducting airway; NO gas exchange |
| Respiratory bronchioles | None | Cuboidal; Club cells | First gas exchange unit |
| Alveoli | None | Type I + II pneumocytes | Primary gas exchange; ~500 million |
Microscopic Anatomy
Pneumocytes
| Cell | % Surface | Function |
|---|---|---|
| Type I | ~95% | Gas exchange; thin squamous; cannot replicate |
| Type II | ~5% | Surfactant (lamellar bodies); repair/replicate after injury; cuboidal |
Surfactant
- Main component: DPPC (dipalmitoylphosphatidylcholine)
- Produced by Type II cells; secreted ~28+ weeks gestation
- Reduces alveolar surface tension → prevents collapse on expiration
Neonatal RDS (IRDS): premature infants lack surfactant → ground-glass opacities; grunting, flaring, retractions. Prevention: maternal betamethasone. Treatment: exogenous surfactant. L/S ratio >2 = fetal lung maturity.
Alveolar macrophages — phagocytose debris; become "heart failure cells" (hemosiderin-laden) in pulmonary edema. Club (Clara) cells — in terminal/respiratory bronchioles; detoxify inhaled toxins; no cilia.
Pulmonary Vasculature
Low-pressure (~25/8 mmHg), high-flow system. Pulmonary arteries carry deoxygenated blood; pulmonary veins carry oxygenated blood (4 veins → LA). Bronchial arteries (from thoracic aorta) supply airway walls and pleura.
Hypoxic Pulmonary Vasoconstriction (HPV)
Local alveolar hypoxia → vasoconstriction of pulmonary arterioles → diverts blood to better-ventilated areas → improves V/Q matching. OPPOSITE of systemic circulation response to hypoxia.
Pulmonary arterial hypertension (PAH): mean PA pressure >20 mmHg. Group 1 (idiopathic/heritable): BMPR2 mutation. Symptoms: exertional dyspnea, syncope, right heart failure. Tx: PDE5i, ERA, prostacyclins.
Embryology
Lungs develop from ventral foregut endoderm (laryngotracheal groove) at ~week 4-5.
| Stage | Weeks | Key Development |
|---|---|---|
| Embryonic | 0-7 | Tracheal bud; lobar bronchi |
| Pseudoglandular | 7-17 | Conducting airways form; no gas exchange |
| Canalicular | 16-25 | Acini form; vascularization; limited viability |
| Terminal sac/Saccular | 24-36 | Primitive alveoli; surfactant begins ~28 wks |
| Alveolar | 36 wks - 8 yr | Mature alveoli form; most postnatal |
Tracheoesophageal fistula (TEF): most common = esophageal atresia + distal TEF (Type C, 85%). 3 Cs: Coughing, Choking, Cyanosis with first feeds. Polyhydramnios in utero. Treat with surgical repair within first days of life.
Clinical Pearls
| Condition | Key Features | Pearl |
|---|---|---|
| COPD/Emphysema | Centriacinar (smoking); panacinar (A1AT) | Barrel chest; ↓DLCO; pursed-lip breathing |
| Asthma | Reversible obstruction; eosinophils; Charcot-Leyden | Samter triad: ASA + nasal polyps + asthma |
| Pulmonary embolism | Pleuritic chest pain, dyspnea, hypoxia | Westermark sign; Hampton hump; ↑D-dimer |
| Sarcoidosis | Non-caseating granulomas; bilateral hilar LAD | ↑ACE; Lofgren syndrome = good prognosis |
| IPF | UIP pattern; honeycombing; basal peripheral | Velcro crackles; no steroid response; ↓FVC |
| ARDS | Diffuse alveolar damage; bilateral infiltrates | P/F ratio <300; lung-protective ventilation 6 mL/kg |
PFT interpretation: FEV1/FVC <0.7 = obstructive. Normal FEV1/FVC + ↓FVC = restrictive. ↓DLCO: emphysema (alveolar destruction), ILD (thickened membrane), anemia. Normal DLCO in asthma between attacks.