Pulmonary Function & Mechanics: Spirometry, Pressures, Laplace, V/Q, Airway Resistance

Quiet (eupneic) breathing
- Primary driver: diaphragm
- Contraction increases the longitudinal (vertical) dimension of the thoracic cavity.
- ↓ Intrapleural pressure → air flows in.
Exertional breathing
- Accessory inspiratory muscles (external intercostals, sternocleidomastoids, scalenes) become active.
- Lift & flare the ribs → ↑ antero-posterior (A–P) diameter of the thorax.
- Greater increase in thoracic volume = larger fall in intrapulmonary pressure.
Thoracic pressures mentioned
- Transcript cites a value of 760\;+\;4 (interpretable as atmospheric pressure 760 mm Hg plus 4 mm Hg positive intrapleural pressure in a pathologic state).
- A pressure rise to 764\;\text{mm Hg} inside the pleural space implies tension pneumothorax → mediastinal shift, lung collapse, and the clinical need for a chest tube.

Goal: Re-establish negative intrapleural pressure by allowing trapped air to exit.
Restores normal lung expansion & prevents further cardiopulmonary compromise.

Collins/wet spirometer
- Inverted air-filled bell floats on water inside a green cylinder.
- Bell connected to a pulley + lever + pen system; pen traces a volume–time graph on moving chart paper.
- Mouthpiece + nose-clip create a closed system: patient’s lungs ↔ tubing ↔ bell.
Graph interpretation
- Inspiration → bell descends (pen rises).
- Expiration → bell ascends (pen falls).

Tidal Volume (VT)
- Quiet breath in or out; graph shows small oscillations around baseline.
Inspiratory Reserve Volume (IRV)
- Extra air that can be inhaled after a normal inspiration.
- Calculated from tracing: \text{IRV}=2400\;\text{mL} for “Michael.”
Expiratory Reserve Volume (ERV)
- Extra air forcibly exhaled after a normal expiration.
- From tracing: \text{ERV}=2050\;\text{mL}.
Vital Capacity (VC)
- \text{VC}=VT+IRV+ERV
- Although VT value not explicitly stated in transcript, VC can be derived if VT known.
Additional volumes/capacities (not directly measured with closed spirometer): Residual Volume (RV), Total Lung Capacity (TLC).

Formula: P_{\text{collapse}} = \dfrac{2T}{r}
- P = collapsing (transmural) pressure
- T = surface tension
- r = radius of the alveolus
Transcript example
- "Large" alveolus with radius rL = 2rS (double the small).
- Assuming equal surface tension T:
- PL = \dfrac{2T}{2rS} = \dfrac{T}{r_S} = 3 (arbitrary units)
- PS = \dfrac{2T}{rS} = 6 (units)
- Conclusion: Smaller alveoli collapse more readily because P \propto 1/r.
Role of surfactant
- Reduces surface tension (T) proportionally more in small alveoli → equalizes pressures → prevents atelectasis.
- Transcript statement: “When we introduce surfactant … collapsing pressures decrease.”

Adequate gas exchange requires matching of alveolar ventilation (V̇A) with pulmonary capillary perfusion (Q̇).
Destruction or collapse of alveolar walls (e.g., emphysema, atelectasis) alters both V and Q, leading to V/Q mismatch.
- Destroyed alveoli → ↓ surface area, altered elastic recoil, potential airway collapse during expiration.

Airway radius (primary determinant per Poiseuille’s Law: R \propto \dfrac{1}{r^4}).
Lung volume: higher volumes pull airways open → ↓ Raw.
Smooth-muscle tone: β2-agonists relax, cholinergics constrict.
Mucus, edema, inflammation: narrow lumen → ↑ Raw.
Destruction of tethering alveolar walls (e.g., emphysema) → loss of radial traction → dynamic airway collapse.

Spirometry is a non-invasive, low-cost way to detect obstructive vs restrictive lung disease early.
Chest-tube placement is life-saving but invasive; requires sterile technique, analgesia, and informed consent.
Understanding surfuctant physiology informs neonatal care (exogenous surfactant for premature infants).
Recognition of V/Q mismatch guides triage in trauma, critical care, and anesthetic management.