Mechanics of Breathing

The mechanics of breathing describe the physical forces that move air in and out of the lungs — the interplay of pressures, compliance, surface tension, and resistance. This is a perennial NEET PG favourite because a handful of curves (compliance, pressure-volume loop) and one equation (Laplace) unlock most questions.

Overview: pressures that drive ventilation

Air flows down a pressure gradient. Four pressures must be kept straight:

Pressure	Definition	Typical value (quiet breathing)
Atmospheric (Patm)	Pressure outside the body	760 mmHg (reference 0)
Alveolar / intrapulmonary (Palv)	Pressure inside alveoli	0 at rest; −1 cmH₂O inspiration; +1 cmH₂O expiration
Intrapleural (Ppl)	Pressure in pleural cavity	−5 cmH₂O at FRC; −8 cmH₂O at end-inspiration
Transpulmonary (PL = Palv − Ppl)	Distending pressure across the lung wall	+5 cmH₂O at FRC (always positive)

The transpulmonary pressure is the true distending force keeping the lung open. Because Palv − Ppl stays positive, the lung is continuously stretched against its elastic recoil.

High-yield: Intrapleural pressure is always negative during normal quiet breathing. It becomes positive only during forced expiration (e.g., coughing, Valsalva, playing a wind instrument). Loss of negative intrapleural pressure (pneumothorax) collapses the lung.

The ventilatory cycle in flow →

1. Inspiration begins → diaphragm and external intercostals contract → thoracic volume rises.
2. Ppl becomes more negative (−5 → −8 cmH₂O) → transpulmonary pressure rises → lung expands.
3. Palv falls below atmospheric (−1 cmH₂O) → air flows in.
4. Inspiration ends → Palv = 0, lung volume maximal.
5. Expiration (passive at rest) → muscles relax → elastic recoil shrinks lung → Palv rises to +1 cmH₂O → air flows out.

Muscles of respiration

• Inspiration (quiet): diaphragm (≈70% of tidal volume), external intercostals. Diaphragm is supplied by the phrenic nerve (C3, C4, C5 — "C3,4,5 keep the diaphragm alive").
• Inspiration (forced): scalenes, sternocleidomastoid, pectoralis, serratus anterior — the accessory muscles.
• Expiration (quiet): passive, driven entirely by elastic recoil.
• Expiration (forced): internal intercostals and abdominal muscles (rectus abdominis, internal/external obliques, transversus abdominis).

High-yield: Quiet expiration is passive — no muscle does active work; the energy stored in elastic tissue during inspiration drives it. This is why work of breathing at rest is almost entirely inspiratory.

Compliance

Compliance (C) = ΔV / ΔP — the change in lung volume per unit change in distending (transpulmonary) pressure. It is the inverse of elastance/stiffness. A highly compliant lung distends easily; a stiff lung resists.

• Lung compliance ≈ 200 mL/cmH₂O
• Chest wall compliance ≈ 200 mL/cmH₂O
• Total (combined) compliance ≈ 100 mL/cmH₂O

Because lung and chest wall act in series, total compliance is lower than either component, given by:

1/C_total = 1/C_lung + 1/C_chest wall

Static vs dynamic compliance

• Static compliance is measured under conditions of no airflow (breath held) — reflects pure elastic properties of lung + chest wall.
• Dynamic compliance is measured during continuous breathing — influenced by airway resistance and is frequency-dependent.

High-yield: In normal lungs static ≈ dynamic compliance. In disease with heterogeneous time constants (e.g., asthma, early small-airway disease), dynamic compliance falls as respiratory rate rises ("frequency dependence of compliance") — fast units fill while slow units lag.

Compliance changes by disease — the most tested table

Condition	Compliance	Why
Emphysema	Increased	Destruction of elastic tissue (loss of recoil)
Old age (normal)	Increased	Reduced elastin
ARDS	Decreased	Alveolar oedema, surfactant loss, atelectasis
Pulmonary fibrosis	Decreased	Stiff, scarred interstitium
Pulmonary oedema / pneumonia	Decreased	Fluid-filled alveoli
Atelectasis / surfactant deficiency (NRDS)	Decreased	High surface tension, collapse
Kyphoscoliosis / obesity	Normal lung, ↓ chest-wall	Restricted chest expansion

High-yield: Emphysema = increased lung compliance (lung distends too easily, but recoil is lost → air trapping). ARDS and fibrosis = decreased compliance (stiff lungs). This single contrast is the favourite compliance MCQ.

A subtle point: in emphysema, although static compliance is high, dynamic compliance can fall at higher rates because of airway obstruction and prolonged time constants — the blurb's "increased dynamic compliance in emphysema" refers to the overall easy distensibility, but examiners may test the air-trapping consequence.

Surface tension and surfactant

The alveolar air-liquid interface generates surface tension that tends to collapse alveoli. Surface tension accounts for roughly two-thirds of the lung's elastic recoil; tissue elastin accounts for the rest. A lung inflated with saline (no air-liquid interface) is far more compliant than one inflated with air — the classic demonstration that surface tension dominates recoil.

Surfactant

Pulmonary surfactant is secreted by type II pneumocytes. Its main component is the phospholipid dipalmitoylphosphatidylcholine (DPPC / lecithin), plus surfactant proteins SP-A, B, C, D.

Functions:

• Reduces surface tension → increases compliance, reduces work of breathing.
• Increases alveolar stability (prevents collapse of small alveoli — see Laplace below).
• Keeps alveoli dry (lowers the transudation force pulling fluid into alveoli).
• Variable surface-tension lowering: surfactant molecules pack densely when the alveolus is small (tension drops most then) and spread out when large — stabilising both ends of the size range.

High-yield: Surfactant is produced by type II pneumocytes from about the 24th–28th week of gestation, with mature levels by ~35 weeks. Deficiency causes Neonatal Respiratory Distress Syndrome (Hyaline Membrane Disease) — decreased compliance, atelectasis, increased work of breathing.

High-yield: Lecithin : Sphingomyelin (L:S) ratio ≥ 2:1 in amniotic fluid indicates lung maturity. The presence of phosphatidylglycerol (PG) is the most reliable single marker. Antenatal corticosteroids (betamethasone/dexamethasone) accelerate surfactant production.

Laplace's law and alveolar stability

For a sphere (alveolus) with a single liquid surface:

P = 2T / r

where P = collapsing pressure, T = surface tension, r = radius. (For a bubble with two surfaces it is 4T/r, but the alveolus is modelled with one air-liquid interface → 2T/r.)

The instability problem: If surface tension (T) were constant, a smaller alveolus (smaller r) would generate a higher collapsing pressure and empty into a connected larger alveolus → progressive collapse of small units.

Surfactant solves this: because surfactant lowers T more in smaller alveoli (molecules packed densely) and less in larger ones, it equalises pressures across alveoli of different sizes → prevents the small-alveolus collapse and keeps alveoli stable.

High-yield: Laplace = P = 2T/r. Smaller radius → larger collapsing pressure → tendency to collapse. Surfactant's radius-dependent reduction in surface tension is what keeps small and large alveoli stable simultaneously.

Airway resistance

Resistance to airflow obeys an analogue of Ohm's law:

Resistance (R) = Driving pressure (Palv − Patm) / Airflow

Airflow in airways is governed by Poiseuille's law, in which resistance is inversely proportional to the fourth power of the radius:

R ∝ 8ηL / πr⁴

Hence halving the radius increases resistance 16-fold — radius is overwhelmingly the dominant variable.

Where is most resistance? (counter-intuitive favourite)

High-yield: The site of highest airway resistance is the medium-sized bronchi (segmental/lobar bronchi, generations ~2–5), NOT the small bronchioles. Although each small bronchiole is narrow, their enormous total cross-sectional area in parallel makes their collective resistance very low. This is why small-airway disease can be clinically silent early ("silent zone").

Determinants of airway resistance

Factor	Effect on resistance
Lung volume ↑	Resistance ↓ (radial traction by surrounding parenchyma widens airways)
Bronchial smooth muscle	Parasympathetic (vagal, ACh, muscarinic) → bronchoconstriction ↑ R; Sympathetic (β₂, adrenaline) → bronchodilation ↓ R
CO₂ in airways	↑ CO₂ → bronchodilation; ↓ CO₂ → bronchoconstriction
Mucus, oedema, secretions	↑ R
Loss of elastic recoil (emphysema)	↑ R (dynamic airway collapse on expiration)
Density/viscosity of gas	Heliox (low density) ↓ turbulent resistance

Dynamic compression of airways: During forced expiration, intrapleural pressure becomes positive and compresses airways downstream of the equal pressure point (EPP). In emphysema, loss of elastic recoil moves the EPP toward the alveoli, causing premature small-airway collapse and air trapping — the basis of expiratory flow limitation.

Work of breathing

Work of breathing (WOB) is the energy expended to move air and overcome resistive and elastic forces. It has two principal components:

1. Elastic (compliance) work — to expand the lung and chest wall against elastic recoil and surface tension.
2. Resistive (non-elastic) work — to overcome airway resistance + tissue viscous resistance.

WOB curve logic →

• Slow, deep breathing → ↑ elastic work, ↓ resistive work.
• Rapid, shallow breathing → ↓ elastic work, ↑ resistive work.
• The body automatically selects the respiratory rate that minimises total work for a given alveolar ventilation.

High-yield: In restrictive disease (↓ compliance, e.g., fibrosis, ARDS) patients minimise work by breathing rapid and shallow. In obstructive disease (↑ resistance, e.g., COPD, asthma) patients breathe slow and deep to reduce resistive work.

At rest, WOB consumes only ~2–3% of total body O₂ consumption; in severe lung disease it can exceed 30%, contributing to respiratory muscle fatigue.

The pressure–volume loop and hysteresis

When lung volume is plotted against transpulmonary pressure during a breath, the inflation and deflation limbs do not coincide — this separation is hysteresis, caused mainly by surface-tension behaviour of surfactant (more pressure needed to recruit collapsed alveoli on inflation than to keep them open on deflation).

• The slope of the P–V curve = compliance.
• A flatter slope (shifted right/down) = decreased compliance (fibrosis, ARDS).
• A steeper slope (shifted up/left) = increased compliance (emphysema).

High-yield: Hysteresis of the lung pressure-volume loop is primarily due to surface tension / surfactant, demonstrated by its near-disappearance in saline-filled lungs.

Functional residual capacity (FRC) — the balance point

FRC is the volume at end of quiet expiration, where the inward elastic recoil of the lung exactly balances the outward recoil of the chest wall, and intrapleural pressure is −5 cmH₂O.

• FRC increases in emphysema (loss of recoil, air trapping → barrel chest, hyperinflation).
• FRC decreases in restrictive disease, obesity, and supine posture.

Key differentials / contrasts

Feature	Obstructive (COPD/emphysema/asthma)	Restrictive (fibrosis/ARDS)
Compliance	Increased (emphysema)	Decreased
Airway resistance	Increased	Normal/low
FRC, RV, TLC	Increased	Decreased
FEV₁/FVC ratio	Decreased (<0.7)	Normal or increased
Breathing pattern	Slow, deep	Rapid, shallow
Elastic recoil	Decreased (emphysema)	Increased

Recently asked / exam angle

• "Site of maximum airway resistance" → medium-sized bronchi (not terminal bronchioles).
• "Compliance in emphysema" → increased; "compliance in ARDS / fibrosis / RDS" → decreased.
• "Laplace's law for alveoli" → P = 2T/r; small alveolus tends to collapse without surfactant.
• "Main component of surfactant" → dipalmitoylphosphatidylcholine (DPPC); secreted by type II pneumocytes.
• "Intrapleural pressure during quiet breathing is always..." → negative.
• "Major component of resting work of breathing" → overcoming elastic/compliance (inspiratory) work; expiration is passive.
• "Hysteresis is due to" → surface tension/surfactant.
• "L:S ratio for lung maturity" → ≥ 2:1; PG most reliable.
• "Nerve supplying diaphragm" → phrenic (C3,4,5).
• "Transpulmonary pressure = " → Palv − Ppl, always positive at FRC.
• Numerical/graph items: identifying the compliance slope on a P–V loop, or calculating combined compliance from 1/C_total = 1/C_L + 1/C_cw.

Rapid revision

1. Transpulmonary pressure = Palv − Ppl; it is always positive and keeps the lung distended.
2. Intrapleural pressure is −5 cmH₂O at FRC, −8 at end-inspiration; always negative in quiet breathing.
3. Quiet expiration is passive, powered by elastic recoil; quiet inspiration uses diaphragm + external intercostals.
4. Compliance = ΔV/ΔP; total (~100 mL/cmH₂O) is lower than lung or chest-wall alone (~200 each).
5. Emphysema → ↑ compliance; ARDS, fibrosis, RDS, oedema → ↓ compliance.
6. Surfactant = DPPC from type II pneumocytes; lowers surface tension, raises compliance, stabilises alveoli, keeps them dry.
7. Laplace: P = 2T/r — smaller alveolus has higher collapse pressure; surfactant equalises this.
8. Surface tension accounts for ~2/3 of elastic recoil; saline-filled lung has no hysteresis.
9. Highest airway resistance = medium-sized bronchi, not bronchioles (huge parallel cross-section makes bronchioles low-resistance).
10. Resistance ∝ 1/r⁴ (Poiseuille); resistance falls as lung volume rises (radial traction).
11. Restrictive disease → rapid, shallow breathing; obstructive → slow, deep to minimise work.
12. FRC = point where lung inward recoil balances chest-wall outward recoil; ↑ in emphysema, ↓ in restriction.