part 2. 6.7.25 in class Pulmonary Anatomy & Physiology – Detailed Lecture Notes

Roll-Call & Context

• Brief attendance at start: Destiny, Nicole, Nancy, Perronina, Eggers present; Samantha absent.
• Transition immediately into lecture on lungs & alveoli.

Alveolus: Definition & Core Functions

• An alveolus (plural “alveoli”): terminal air sac; primary site of pulmonary gas exchange.
• Gas exchange driven by simple diffusion of $O<em>2$ & $CO</em>2$ across the respiratory membrane.

Cellular Composition of the Alveolar Wall

• THREE principal cell types
  • Type I alveolar cells (Type I pneumocytes)
  • Simple squamous epithelium; extremely thin.
  • Provide >95 % of alveolar surface area; nuclei bulge slightly into lumen.
  • Type II alveolar cells (Type II pneumocytes / septal cells)
  • Cuboidal; scattered among Type I cells.
  • Synthesize & secrete pulmonary surfactant (blue layer on model).
  • Capable of mitosis → can replace both Type I & Type II cells after injury.
  • Alveolar macrophages (dust cells)
  • Part of reticulo-endothelial system; free-roaming on inner alveolar surface.
  • Phagocytose dust, smoke particles, bacteria, viruses, carbon pigment, etc.

Pulmonary Surfactant

• Chemically a “surface-active substance” (detergent-like phospholipid-protein mix).
• Function: ↓ alveolar surface tension.
  • Analogy: dropping dish soap into a pot of water eliminates surface film → ripples form; same principle inside alveolus.
• Physiological benefit
  • Prevents alveolar collapse (atelectasis) at end-expiration.
  • Facilitates reinflation if walls temporarily adhere.
• Neonatal relevance
  • Premature neonates—statistically more often African-American—may have insufficient Type II maturity ⇒ inadequate surfactant.
  • First breath must inflate lungs + individual alveoli; lack of surfactant keeps walls stuck → large portions non-functional.
  • Consequences
  • ↓ gas-exchange surface ⇒ hypoxemia $\big(\text{low }O_2\text{ in blood}\big)$.
  • Rapid progression to hypoxia $\big(\text{cellular }O_2\text{ starvation}\big)$; infant turns blue (cyanosis).
  • Management
  • Incubator, possible endotracheal intubation & mechanical ventilation.
  • Supplemental $O_2$.
  • MOST IMPORTANT: aerosolized/artificial surfactant instilled through ETT; “a couple of puffs” often reverses cyanosis almost instantly.
  • Historical note: 1980s Russian clinical trials pioneered large-scale synthetic surfactant use.

Reticulo-Endothelial (Mononuclear Phagocyte) System Examples

• Epidermis → Langerhans cells.
• CNS → microglia.
• Lung → alveolar macrophages.
• More to be discussed in later lectures.

Respiratory Membrane: Microscopic Anatomy & Diffusion Path

• Composite thickness = “respiratory membrane.”
  1. Thin cytoplasm of Type I pneumocyte.
  2. Shared basement membrane (fused basal laminae of epithelium & capillary endothelium).
  3. Capillary endothelial cell layer (simple squamous).
• Total thickness ~0.5 µm in healthy lung; minimal barrier for diffusion.
• Direction of gas flow
  • $O_2$: alveolus → blood.
  • $CO_2$: blood → alveolus.
• Health of membrane directly proportional to diffusion efficiency.

Additional Microscopic Details

• Alveolar pores (pores of Kohn): tiny openings between adjacent alveoli permitting collateral ventilation and pressure equilibration.
• In histology slides/models: multiple adjoining alveoli with intervening pores visualized.

Gross Anatomy of the Lungs

• Right lung
  • 3 lobes: superior, middle, inferior.
  • Fissures: horizontal & oblique.
• Left lung
  • 2 lobes (not detailed here but implied).
• Surfaces & landmarks (apply to both lungs unless specified)
  • Apex projects into supraclavicular fossa; auscultated above clavicle.
  • Base rests on concave diaphragm surface.
  • Costal surfaces: anterior, lateral, posterior—lie against ribs.
  • Mediastinal surface (medial): faces mediastinum; contains hilum.
• Hilum / Root of lung
  • Bundle of entering/exiting structures: primary bronchus, pulmonary arteries, pulmonary veins, lymphatics, autonomic nerves.
  • Hilar lymph nodes (green on model) frequently enlarge (hilar lymphadenopathy) in infections (pneumonia, TB, etc.).

Pleura & Pleural Cavity (Review from A&P I)

• Serous membrane with two continuous sheets
  • Visceral pleura: adherent to lung surface; reflects at hilum.
  • Parietal pleura: lines thoracic wall, diaphragm, mediastinum.
• Pleural cavity: potential space w/ thin film of serous fluid → lubrication, ↓ friction, prevents mechanical wear.

Intrapleural Pressure & Lung Inflation Mechanics

• Intrapleural pressure (IPP) is negative relative to atmospheric: $P<em>{pl} < P</em>{atm}$.
  • “Negative” behaves like suction, keeping visceral pleura (and thus lung) adherent to thoracic wall → lungs remain partially inflated even at end-expiration.
• Conceptual contrast
  • Positive pressure = pushing.
  • Negative pressure = sucking.

Pneumothorax & Atelectasis

• Penetrating chest wound introduces air → pleural cavity ⇒ pressures equalize.
  • Presence of air in pleural space = pneumothorax ($\text{pneumo-} = \text{air}$).
• Loss of negative IPP → affected lung recoils & collapses.
  • Collapse of lung tissue = atelectasis.
• Demonstrated on model: intact side vs. collapsed side image.

Dual Blood Supply of the Lungs

1. Pulmonary circulation
   • Pulmonary trunk → pulmonary arteries → alveolar capillaries → pulmonary veins → left atrium.
2. Bronchial (systemic) circulation
   • Thoracic aorta → bronchial arteries → oxygenate & nourish lung tissue (bronchi, connective tissue, pleura).
   • Bronchial veins return deoxygenated blood; some drains into pulmonary veins.

• Analogy: like liver’s dual supply (hepatic artery + portal vein).

Pathology Highlights

• Lung cancer specimen shown
  • Normal tissue vs. yellowish malignant mass.
  • Heavy smoke deposition (blackened parenchyma) visible in smoker’s lung.
• Mesothelioma
  • Malignancy of pleura; can invade underlying lung.
  • Mentioned as separate entity but related to asbestos exposure in other contexts.

Laboratory / Model Handling Notes

• Student groups formed (4 groups of 3) to work with anatomical models.
• Models available
  • Large lung–bronchial tree plaques; alternate model with removable lungs & heart.
  • Bronchial tree standalone model.
• Handling instructions
  • Do not write on laminated cards; return intact.
  • Larynx on model: to open, insert finger, gently move laterally, then lift superiorly; reverse to close—avoid breaking studs.
  • Cheat-sheet index provided linking cards ⇄ models.
• Additional props: paranasal sinus plaques; multiple anatomical parts supplied per group.

These notes consolidate every concept, example, analogy, clinical correlation, structural detail, and procedural instruction mentioned in the lecture, providing a stand-alone study resource.