Lung Mechanics: Compliance, Resistance and the Pressure-Volume Loop

Two numbers that describe a lung

Breathing mechanics reduce to two physical properties borrowed straight from engineering: compliance, how much the lung's volume changes for a given change in pressure (the inverse of stiffness), and resistance, how much pressure it takes to push air through the airways at a given flow rate.

C = delta V / delta P     compliance   (mL per cmH2O)   -- how stretchy
R = delta P / flow        resistance    (cmH2O per L/s)  -- how narrow the airways are

time constant  tau = R * C   -- how long the lung takes to (de)inflate toward equilibrium

The pressure-volume loop

Plot lung volume against the pressure driving it through one breath and you get a pressure-volume (P-V) loop: inspiration traces one path as volume rises with pressure, expiration traces a slightly different path back down. The two paths do not overlap exactly — the loop has area, called hysteresis — because part of the pressure during inspiration goes into overcoming resistive and surface-tension forces that are not simply recovered on the way out. The slope of the loop over its more linear middle section is a direct visual read of compliance: a steep, wide loop means a very stretchy lung (large ΔV for small ΔP), a flat loop means a stiff one.

COPD: too compliant, too resistive

Chronic obstructive pulmonary disease destroys alveolar walls (emphysema) and narrows and inflames airways (chronic bronchitis), producing the opposite problem in each parameter: the alveolar tissue loses its elastic recoil, so compliance rises — the lung becomes floppier and over-distends easily — while damaged, mucus-narrowed airways sharply raise resistance, especially on exhalation, since airways are compressed further by the very effort of breathing out forcefully. The combination — easy to inflate, hard to empty — produces air trapping and hyperinflation: each breath starts from a higher resting volume than the last because there was not enough time to exhale fully before the next inspiration began, driven by an abnormally long time constant τ = RC.

ARDS: the opposite failure mode

Acute respiratory distress syndrome moves the same two numbers in the other direction. Inflammatory fluid floods the alveoli and inactivates surfactant, so alveoli that would normally resist collapsing under surface tension instead collapse readily and the tissue becomes stiff — compliance falls sharply — while airway resistance is often relatively less affected. Low compliance means every millilitre of tidal volume needs disproportionately more driving pressure, so ARDS ventilation strategy centres on protective low tidal volumes (around 6 mL/kg of predicted body weight) plus enough positive end-expiratory pressure (PEEP) to keep alveoli from collapsing at the end of each breath, because pushing a normal tidal volume into a stiff, injured lung at high pressure can itself tear the tissue further.

Why the time constant matters clinically

τ = RC sets how quickly a lung unit equilibrates to a change in driving pressure; a single time constant lets roughly 63% of the pressure change happen, and about five time constants gets you close to full equilibration. In a healthy lung all regions share a similar τ, so ventilation is roughly uniform. In diseased lungs, different regions can have wildly different local R and C (some airways more obstructed than others, some alveoli stiffer than others), giving each region its own time constant — fast-filling regions finish inspiration early and start to empty while slow regions are still filling, which is exactly the mismatched, uneven ventilation that makes obstructive and restrictive lung disease inefficient at gas exchange even when total minute ventilation looks adequate on a monitor.

Frequently asked questions

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