Pulmonology
Respiratory System
Lungs, alveoli, and breathing — gas exchange across 70 m² of membrane
The respiratory system delivers oxygen and removes CO2 through ventilation, gas exchange, and pulmonary perfusion. Air passes through nose, pharynx, larynx, trachea, then 23 generations of branching airways, ending at ~480 million alveoli with combined surface area ~70 m². Gas exchange occurs across the alveolar-capillary membrane (~0.5 μm thick). Inspiration is active (diaphragm and external intercostals); expiration is passive at rest (elastic recoil). Surfactant (DPPC, made by type II pneumocytes) reduces surface tension preventing alveolar collapse. Control is via brainstem (medullary respiratory centers, pre-Bötzinger), with peripheral chemoreceptors (carotid/aortic bodies) sensing PaO2 and central chemoreceptors sensing CSF pH (PaCO2). Disease spans obstruction (asthma, COPD), restriction (fibrosis), gas exchange (PE, ARDS), and ventilation (NMD).
- Alveoli~480 million; ~70 m² surface area
- Tidal volume~500 mL at rest (6-8 mL/kg)
- Membrane thickness~0.5 μm (alveolar-capillary)
- SurfactantDPPC, made by type II pneumocytes
- Generations23 (trachea to alveolar sacs)
- V/Q ratio (normal)~0.8 overall (varies regionally)
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Why the respiratory system matters
- Asthma and COPD. 250 million asthma cases, COPD is 3rd leading cause of death globally.
- Pneumonia. Common community and hospital infection; major mortality cause.
- Acute respiratory failure. Recognition and ventilation strategy save lives.
- Pulmonary embolism. Common, lethal, treatable — diagnosis requires high suspicion.
- Anesthesia. Pre-oxygenation, intubation, ventilation strategies underpin every surgery.
- Smoking cessation. Single highest-impact preventive intervention in adult medicine.
- Pandemic preparedness. COVID-19 highlighted ventilator and ICU capacity limits.
Common misconceptions
- Resistance is highest in smallest airways. Highest in medium bronchi; total cross-section grows distally.
- Hypoxic drive is the main respiratory drive. CO2/pH dominates normally; hypoxia matters in chronic CO2 retainers.
- All hypoxemia improves with O2. Shunt physiology resists O2 supplementation.
- Higher tidal volume is better. Lung-protective ventilation (6 mL/kg) reduces ARDS mortality.
- FEV1 measures restriction. FEV1/FVC ratio defines obstruction; absolute FEV1 doesn't distinguish.
- Pulse ox 95% rules out PE. Many PE patients have normal SpO2; A-a gradient and clinical suspicion needed.
Frequently asked questions
How does breathing happen mechanically?
Inspiration: diaphragm contracts (descends 1-10 cm), external intercostals lift ribs, thoracic volume increases, intrapleural pressure drops to -7 cmH2O, alveolar pressure becomes subatmospheric, air flows in. Expiration: muscles relax, elastic recoil of lungs and chest wall reduces volume, alveolar pressure becomes positive, air flows out. Forced expiration uses internal intercostals and abdominal muscles. Compliance (∆V/∆P) reflects lung distensibility — decreased in fibrosis, ARDS; increased in emphysema. Resistance is highest in medium bronchi (counter-intuitive — total cross-section grows distally).
How does gas exchange work at the alveolus?
Alveolar PO2 ~100 mmHg; pulmonary capillary PO2 ~40 mmHg — O2 diffuses down gradient. CO2 has higher diffusivity (smaller, more soluble) so even though gradient is smaller (~6 mmHg), exchange is efficient. Equilibration occurs in ~0.25 sec — much faster than transit time (~0.75 sec at rest), giving reserve for exercise. Diffusion limited only in severe disease (DLCO measures this). Membrane: alveolar epithelium (type I pneumocyte), basement membrane, capillary endothelium. Total thickness ~0.5 μm.
What is V/Q mismatch?
Ventilation-perfusion ratio. Normal global V/Q ~0.8 (ventilation 4 L/min, perfusion 5 L/min). Regional variation: apex V/Q ~3 (over-ventilated, under-perfused), base V/Q ~0.6. V/Q = 0 (shunt): perfusion without ventilation — pneumonia, atelectasis, ARDS; doesn't improve with O2. V/Q = ∞ (dead space): ventilation without perfusion — PE, low cardiac output. Treatment differs: shunt needs PEEP/recruitment, dead space needs perfusion restoration. A-a gradient distinguishes hypoxemia mechanisms.
What's the role of surfactant?
Lipid-protein mixture (~90% phospholipid — DPPC predominant, surfactant proteins SP-A/B/C/D) made by type II pneumocytes. Reduces surface tension at air-liquid interface, preventing alveolar collapse (Laplace's law: pressure to keep open = 2T/r — small alveoli would collapse without surfactant). Production begins ~26 weeks; sufficient ~35 weeks. Premature birth → infant respiratory distress syndrome (RDS) — treated with exogenous surfactant (Survanta, Curosurf) and antenatal corticosteroids accelerate fetal production. Adult ARDS also has surfactant dysfunction.
How is breathing controlled?
Medullary respiratory centers (dorsal — inspiratory rhythm; ventral — expiratory) generate respiration. Pre-Bötzinger complex is the rhythm generator. Pontine centers (apneustic, pneumotaxic) modulate rate and depth. Inputs: central chemoreceptors (in medulla, sense CSF H+ from PaCO2 — most powerful drive), peripheral chemoreceptors (carotid/aortic bodies sense low PaO2 < 60), stretch receptors (Hering-Breuer reflex — prevents over-inflation). PaCO2 normally drives breathing; in chronic CO2 retainers (severe COPD), hypoxia becomes the main drive — relevant to O2 therapy targets.
What's the difference between obstructive and restrictive disease?
Obstructive (asthma, COPD, bronchiectasis, CF): airway narrowing causes air trapping. PFTs: reduced FEV1/FVC < 0.7, increased TLC and RV, reduced FEV1. Bronchodilator response > 12% suggests asthma. Restrictive (fibrosis, neuromuscular, chest wall, severe obesity): can't inflate lungs fully. PFTs: normal FEV1/FVC, reduced TLC, FVC, FEV1 proportionally. DLCO low in interstitial disease, normal in extrapulmonary. Mixed disease occurs (e.g., fibrosis + emphysema).
What is ARDS?
Acute respiratory distress syndrome — non-cardiogenic pulmonary edema due to inflammatory injury to alveolar-capillary membrane. Berlin definition: acute onset (< 7 days), bilateral infiltrates, no cardiac cause, hypoxemia (PaO2/FiO2 < 300 mild, < 200 moderate, < 100 severe). Causes: sepsis, pneumonia, aspiration, trauma, transfusion, pancreatitis, COVID-19. Pathology: diffuse alveolar damage with hyaline membranes, edema, inflammation. Treatment: lung-protective ventilation (6 mL/kg ideal body weight, plateau pressure < 30 cmH2O), prone positioning, conservative fluids, ECMO in severe cases. Mortality 30-40%.