Anatomy of the lungs and airways
The branching tree - 23 generations, trachea to alveolus
| Zone | Generations | Structure | Function |
|---|---|---|---|
| Conducting | 0-16 | Trachea -> bronchi -> bronchioles -> terminal bronchioles | No gas exchange - the anatomical dead space (~150 mL, ~2 mL/kg) |
| Transitional/respiratory | 17-23 | Respiratory bronchioles -> alveolar ducts -> alveolar sacs | Gas exchange |
- Cartilage is present in the trachea and bronchi (>1 mm diameter) and absent beyond the ~8th generation
- Bronchioles (<1 mm) have no cartilage and depend entirely on radial traction from the surrounding parenchyma for patency
- -> loss of elastic recoil (emphysema, ageing) -> small airway collapse on expiration -> air trapping. This is why emphysema causes airflow obstruction without any airway disease.
- Bronchus = cartilage + submucosal glands; bronchiole = neither
Lobes and fissures
- Right: 3 lobes (upper, middle, lower); oblique + horizontal fissures
- Left: 2 lobes + lingula; oblique fissure only
- 10 segments on the right, 8-9 on the left (segmental anatomy is the basis of lobectomy, segmentectomy and localising aspiration)
Key numbers
- Alveoli: ~300-500 million, total surface area ~70-100 m2 (a tennis court)
- Alveolar diameter ~0.2-0.3 mm; blood-gas barrier ~0.3 micrometres thick
- Total cross-sectional area increases exponentially with each generation
- Trachea ~2.5 cm2 -> terminal bronchioles ~180 cm2 -> alveoli ~10^4 cm2
- -> airflow velocity falls to near zero in the respiratory zone -> gas movement there is by diffusion, not bulk flow
- Most airway resistance (~80%) resides in airways >2 mm - the medium bronchi, not the trachea and not the bronchioles
- -> *the small airways are the "silent zone"* - substantial disease accumulates before spirometry changes
Why the right lung gets everything
- Right main bronchus: shorter (~2.5 cm), wider, and more vertical (~25 degrees vs ~45 degrees on the left)
- -> inhaled foreign bodies, aspiration and malpositioned endotracheal tubes go right
- Position determines the segment
- Supine aspiration -> posterior segment of the RUL, superior segment of the RLL
- Upright/sitting -> basal segments of the RLL
Blood supply - two circulations
| Pulmonary | Bronchial | |
|---|---|---|
| Source | RV | Systemic - aorta/intercostals |
| Pressure | Low (~25/8) | Systemic |
| Flow | Entire cardiac output | ~1-2% of cardiac output |
| Supplies | Gas exchange | Airway walls to the terminal bronchioles, pleura |
- Bronchial veins drain into pulmonary veins -> a physiological right-to-left shunt (~2-3%), the reason PaO2 never equals PAO2
- *Massive haemoptysis is almost always bronchial (systemic pressure) -> bronchial artery embolisation*, not pulmonary intervention
- Bronchial arteries hypertrophy in bronchiectasis, CF, aspergilloma and chronic TB
Lymphatics and nodal stations
- No lymphatics beyond the alveolar duct
- Drainage: intrapulmonary -> hilar -> mediastinal -> thoracic duct (left) / right lymphatic duct
- Nodal stations (IASLC map) drive lung cancer staging: N1 hilar/intrapulmonary, N2 ipsilateral mediastinal, N3 contralateral or supraclavicular
- N2 vs N3 is the difference between potentially resectable and unresectable
Innervation and cell types
- Parasympathetic (vagus, M3) -> bronchoconstriction, secretion - the target of ipratropium and tiotropium
- Sympathetic - little direct innervation; circulating adrenaline acts on beta-2 -> bronchodilation
- Sensory: vagal C-fibres and rapidly adapting receptors -> cough
- Cells: ciliated columnar (clearance), goblet + submucosal glands (mucus), club cells (bronchiolar, detoxification and progenitor), type I pneumocyte (95% of surface, gas exchange), type II pneumocyte (surfactant, progenitor for type I), alveolar macrophage
Nerves at risk
- Left recurrent laryngeal nerve loops under the aortic arch -> hoarseness from a left hilar/AP-window tumour
- Phrenic nerve (C3,4,5) runs anterior to the hilum -> diaphragm paralysis
- Sympathetic chain/stellate ganglion -> Horner syndrome; T1/C8 roots -> Pancoast tumour
- Thoracic duct -> chylothorax
Surface anatomy you use daily
- Trachea bifurcates at the sternal angle of Louis (T4/5) - the carina
- Oblique fissure follows the 6th rib anteriorly / T3 spinous process posteriorly
- Horizontal fissure at the 4th costal cartilage on the right
- Lung apex projects 2-3 cm above the clavicle -> vulnerable in subclavian line insertion and supraclavicular nerve blocks
- Safe triangle for chest drain insertion: lateral border of pectoralis major, anterior border of latissimus dorsi, a line at the level of the nipple, apex below the axilla - ~5th intercostal space, mid-axillary line, over the upper border of the rib (neurovascular bundle runs inferiorly)
Radiology
- Silhouette sign localises pathology by which border is lost
- Right heart border -> RML; left heart border -> lingula; hemidiaphragm -> lower lobe; aortic knuckle -> apicoposterior LUL
- Collapse patterns (generations of exam questions)
- LLL: "sail sign" behind the heart, double left heart border, loss of the medial hemidiaphragm
- RUL: elevated horizontal fissure, Golden S sign if from a central mass
- RML: loss of the right heart border, preserved hemidiaphragm
- Whole lung: opacification with tracheal and mediastinal shift TOWARD the collapse (vs a large effusion, which pushes AWAY)
- Hila: left hilum is 1-2 cm higher than the right - if not, something is pulling or pushing
Bronchoscopic anatomy
- Orientation to the carina, then RUL (the first branch, taking off laterally and early), bronchus intermedius, RML, RLL; left main -> LUL/lingula and LLL
- Know it to sample the right segment and to interpret the report
Where anatomy changes what you do
- Aspiration: image the dependent segment for the patient's posture; a normal CXR early does not exclude it
- Foreign body: rigid bronchoscopy; suspect a right-sided obstruction with unilateral wheeze and air trapping
- Endotracheal tube too deep -> right main bronchus intubation -> left lung collapse + right-sided hyperinflation; tip should be ~4-5 cm above the carina, mid-trachea on CXR
- Massive haemoptysis
- Bad lung DOWN (lateral decubitus) to protect the good lung; secure the airway; bronchial artery embolisation
- Chest drain in the safe triangle; ultrasound-guided for effusion
- Lobar collapse: bronchoscopy to look for an endobronchial lesion, with washings +/- biopsy; physiotherapy and mucolytics for mucus plugging
- Lung cancer staging: EBUS-TBNA samples stations 2, 4, 7, 10, 11; mediastinoscopy and EUS complement it - the N2/N3 distinction determines resectability
- Lobectomy vs segmentectomy planned on segmental anatomy and calculated ppoFEV1/ppoDLCO (segments removed / 19 total)
Clinical correlates
- Aspiration pneumonia and lung abscess - posterior RUL and superior RLL when supine
- Right main bronchus intubation and foreign body aspiration
- Pancoast (superior sulcus) tumour - Horner syndrome, C8/T1 wasting, shoulder pain
- Recurrent laryngeal nerve palsy from left hilar/mediastinal disease
- Bronchiectasis and cystic fibrosis - bronchial artery hypertrophy, massive haemoptysis
- Congenital: tracheo-oesophageal fistula, bronchogenic cyst, pulmonary sequestration (systemic arterial supply), congenital lobar emphysema, tracheal bronchus ("pig bronchus")
- Situs inversus and primary ciliary dyskinesia (Kartagener)
- Pneumothorax from apical blebs; iatrogenic from subclavian access and supraclavicular blocks
- Chylothorax after thoracic duct injury (oesophagectomy, lymphoma)
Development and decline
- Alveolarisation continues until ~2-8 years of age - childhood insults (prematurity, ventilation, severe infection, smoke exposure) permanently reduce the alveolar number and set a lower lifetime FEV1 peak
- Peak lung function is reached at ~20-25 years, then declines
- Two routes to COPD: an accelerated decline, or a low peak never attained - roughly half of COPD arises from the latter
- Airway remodelling in chronic asthma -> fixed airflow obstruction (basement membrane thickening, smooth muscle hypertrophy, goblet cell hyperplasia)
- Emphysema destroys the alveolar attachments that hold bronchioles open -> the obstruction is a loss of tethering, not airway narrowing
- Bronchiectasis: permanent bronchial dilatation with loss of cartilage and elastic tissue -> a vicious cycle of impaired clearance -> infection -> inflammation -> more damage
- The lung has limited regenerative capacity in adults: type II pneumocytes repopulate type I cells after injury, but destroyed alveolar architecture does not regrow
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