Lung compliance and resistance

9 min read Last updated April 8, 2026

Clinical relevance in anaesthesia/ICU

  • Ventilation pressures reflect both elastic load and resistive load: airway pressure = elastic (compliance) + resistive (flow × resistance) + PEEP
    • In volume control: rising peak pressure with stable plateau suggests increased resistance; rising plateau suggests reduced compliance
    • In pressure control: reduced tidal volume suggests reduced compliance and/or increased resistance (interpret with flow/pressure waveforms)
  • Dynamic hyperinflation/auto-PEEP occurs when expiratory time is insufficient for high resistance or high minute ventilation
    • Consequences: hypotension (↓ venous return), barotrauma, difficult triggering, CO2 retention
  • Recruitment and PEEP mainly affect compliance by changing aerated lung volume; bronchodilators mainly affect resistance
    • ARDS: low compliance; asthma/COPD: high resistance (often with increased compliance in emphysema)
  • ETT and circuit are major contributors to resistance, especially at high flows; humidification/secretions increase resistance
    • Small changes in ETT internal radius markedly change resistance (r^4 relationship in laminar flow)

Bedside patterns (ventilator pressures)

  • Peak pressure (Ppeak) reflects elastic + resistive components; plateau pressure (Pplat) reflects elastic component (and PEEP)
    • Ppeak − Pplat = resistive pressure (≈ flow × Raw)
    • Driving pressure = Pplat − PEEP (key for lung stress/strain and outcomes in ARDS)
  • If Ppeak rises but Pplat unchanged: think bronchospasm, secretions, kinked tube, biting, high flow, water in HME/circuit
    • If both Ppeak and Pplat rise: think reduced compliance (atelectasis, pulmonary oedema, pneumothorax, abdominal insufflation, obesity, chest wall rigidity)

Definitions and core equations

  • Compliance (C): change in volume per change in pressure
    • C = ΔV/ΔP (units: L·cmH2O−1 or mL·cmH2O−1)
    • Elastance (E) = 1/C (stiffness)
  • Resistance (R): pressure difference required to generate a given flow
    • R = ΔP/Flow (units: cmH2O·L−1·s)
    • Time constant (τ) = R × C (time to fill/empty a lung unit); 63% change in 1 τ, ~95% in 3 τ
  • Equation of motion (single-compartment model): Paw = (V/C) + (Flow × R) + PEEP (± inertance at high frequencies)
    • At zero flow (inspiratory hold), Paw ≈ Pplat = (V/C) + PEEP

Types of compliance and how they are measured

  • Static compliance (Cstat): measured at zero flow (inspiratory pause); reflects elastic properties of lung + chest wall
    • Cstat ≈ VT / (Pplat − PEEP) (if no intrinsic PEEP; otherwise use total PEEP)
  • Dynamic compliance (Cdyn): measured during flow; includes resistance and viscoelastic effects
    • Cdyn ≈ VT / (Ppeak − PEEP); falls with increased resistance and with reduced compliance
  • Lung vs chest wall compliance: total respiratory system compliance is lower than either component alone
    • 1/Crs = 1/CL + 1/Ccw (series relationship)
    • To separate, use oesophageal pressure as a surrogate for pleural pressure (transpulmonary pressure = Palv − Ppl)

Determinants of lung compliance

  • Elastic tissue: elastin/collagen framework; collagen limits overdistension at high volumes
  • Surface tension at the air–liquid interface is a major determinant; surfactant reduces surface tension and increases compliance
    • Laplace: P = 2T/r; without surfactant, small alveoli would require higher pressure and tend to collapse into larger alveoli
    • Surfactant effect is greater at low lung volumes (increases stability and reduces work of breathing)
  • Lung volume dependence: compliance is highest around FRC; lower at very low volumes (atelectasis) and very high volumes (overdistension)
  • Hysteresis: inflation and deflation pressure–volume curves differ due to surfactant dynamics and recruitment/derecruitment
    • For a given transpulmonary pressure, volume is greater on deflation than inflation

Determinants of airway resistance

  • Major site: medium-sized bronchi; small airways contribute less in health but dominate in disease (asthma/COPD)
  • Flow regime: laminar vs turbulent
    • Laminar (Poiseuille): R ∝ (η × L) / r^4; ΔP ∝ Flow
    • Turbulent: ΔP ∝ Flow^2; promoted by high flow, large airways, branching, ETT, secretions
    • Reynolds number Re = (ρ × v × d) / η; turbulence more likely when Re > ~2000
  • Lung volume: airway calibre increases with lung volume due to radial traction; resistance falls as lung volume rises
  • Autonomic tone and mediators: parasympathetic (M3) bronchoconstriction; β2 bronchodilation; histamine/leukotrienes constrict
  • Dynamic airway compression in forced expiration: equal pressure point moves distally with low elastic recoil (emphysema) → flow limitation

Work of breathing and clinical interpretation

  • Work of breathing has elastic work (overcoming elastance) and resistive work (overcoming resistance); both increase total work
    • Restrictive disease: ↑ elastic work; obstructive disease: ↑ resistive work (especially during expiration)
  • Breathing pattern: high resistance favours slow, deep breaths; low compliance favours rapid, shallow breaths (minimises work)

Typical values and patterns

  • Approximate adult respiratory system compliance (intubated, supine): ~50–100 mL·cmH2O−1 (varies with size, posture, anaesthesia)
  • Airway resistance: ~1–2 cmH2O·L−1·s in awake, lower airways; higher when intubated (ETT adds substantial resistance)
  • Disease patterns
    • ARDS/pulmonary oedema/fibrosis: ↓ compliance (↑ elastance), often relatively normal resistance unless bronchospasm/secretions
    • Asthma: markedly ↑ resistance; compliance may be normal or increased (hyperinflation); dynamic hyperinflation common
    • Emphysema: ↑ lung compliance (loss of recoil) but expiratory flow limitation due to airway collapse; resistance may be increased in small airways
Define lung compliance and airway resistance. Give units and clinical significance.

Start with definitions, then link to ventilator pressures and work of breathing.

  • Compliance: C = ΔV/ΔP (mL·cmH2O−1); describes distensibility (inverse of elastance)
  • Resistance: R = ΔP/Flow (cmH2O·L−1·s); describes pressure needed to generate flow
  • Clinical significance: determines work of breathing and ventilator pressures; separates causes of high airway pressure into compliance vs resistance problems
How do you distinguish reduced compliance from increased resistance on a ventilator? Include key pressures and a stepwise approach.

Use peak, plateau, PEEP, and the inspiratory hold manoeuvre.

  • Measure Ppeak and perform inspiratory pause to obtain Pplat (zero flow)
  • If Ppeak ↑ with Pplat unchanged: increased resistance (bronchospasm, secretions, kink/biting, ETT obstruction, high flow, HME blockage)
  • If both Ppeak and Pplat ↑: reduced compliance (atelectasis, pulmonary oedema/ARDS, pneumothorax, abdominal insufflation, obesity, chest wall rigidity)
  • Quantify: resistive pressure = Ppeak − Pplat; driving pressure = Pplat − PEEP (or total PEEP if auto-PEEP)
Explain static vs dynamic compliance. How are they calculated and what do they represent?

Static is measured at zero flow; dynamic includes resistive component.

  • Static compliance: Cstat ≈ VT/(Pplat − PEEP); reflects elastic properties of lung + chest wall
  • Dynamic compliance: Cdyn ≈ VT/(Ppeak − PEEP); includes resistance and viscoelasticity; falls with bronchospasm and with stiff lungs
  • If Cdyn falls but Cstat unchanged, suspect increased resistance
A ventilated patient has VT 500 mL, Ppeak 35 cmH2O, Pplat 25 cmH2O, PEEP 5 cmH2O. Calculate (i) Cstat (ii) resistive pressure (iii) driving pressure. Interpret.

Show calculations clearly and interpret pattern.

  • Cstat = VT/(Pplat − PEEP) = 0.5 L/(25−5) = 0.5/20 = 0.025 L·cmH2O−1 = 25 mL·cmH2O−1 (low compliance)
  • Resistive pressure = Ppeak − Pplat = 35−25 = 10 cmH2O (moderate resistive component)
  • Driving pressure = Pplat − PEEP = 25−5 = 20 cmH2O (high; suggests significant lung stress if ARDS)
  • Interpretation: predominant problem is reduced compliance (low Cstat) with some increased resistance; consider atelectasis/ARDS/oedema plus ETT/secretions/bronchospasm
Describe the pressure–volume (P–V) curve of the lung, including hysteresis and the effect of surfactant.

Mention recruitment, surface tension, and differences between inflation/deflation limbs.

  • P–V curve is sigmoidal: low compliance at low volumes (recruitment), highest around mid-volumes, low compliance at high volumes (overdistension)
  • Hysteresis: for the same pressure, volume is greater on deflation than inflation due to surfactant behaviour and recruitment/derecruitment
  • Surfactant reduces surface tension (T), lowering opening pressures and increasing compliance, especially at low lung volumes
Use Laplace’s law to explain alveolar stability and the role of surfactant.

State the equation and apply it to different radii.

  • Laplace: P = 2T/r; with constant T, smaller alveoli (smaller r) would require higher pressure and tend to empty into larger alveoli
  • Surfactant reduces T and does so more at smaller radii (higher concentration), equalising pressures and preventing collapse (atelectasis)
  • Clinical links: neonatal RDS (surfactant deficiency) → low compliance, atelectasis, high work of breathing
Explain Poiseuille’s law and its limitations in the airway. How does endotracheal tube size affect resistance?

Differentiate laminar vs turbulent flow and highlight r^4 dependence.

  • Poiseuille (laminar): R = 8ηL/(πr^4); therefore small decreases in radius markedly increase resistance
  • Limitations: much airway flow is transitional/turbulent, especially in large airways and through ETT; then ΔP ∝ Flow^2
  • ETT: smaller internal diameter and secretions increase resistance; higher inspiratory flow rates disproportionately increase pressure requirements
Define the time constant and explain its importance in mechanical ventilation, including auto-PEEP.

Link R and C to filling/emptying and to heterogeneous lung units.

  • Time constant τ = R × C; describes how quickly a lung unit fills/empties (63% in 1 τ, ~95% in 3 τ)
  • High R (asthma/COPD) or high C (emphysema) → long τ → slow emptying → air trapping if expiratory time insufficient
  • Auto-PEEP increases end-expiratory alveolar pressure, increases work to trigger breaths, and can cause hypotension/barotrauma
A patient with severe asthma on volume control develops hypotension and rising Ppeak. Pplat is unchanged. What is happening and how would you manage ventilator settings?

Recognise increased resistance and dynamic hyperinflation; prioritise expiratory time and permissive hypercapnia.

  • Pattern suggests increased resistance (bronchospasm/ETT obstruction) with dynamic hyperinflation causing raised intrathoracic pressure and hypotension
  • Immediate checks: exclude kink/biting, suction ETT, check HME/circuit, consider pneumothorax if sudden deterioration
  • Ventilation strategy: reduce minute ventilation and allow longer expiration (↓ RR, ↑ I:E to 1:3–1:5, reduce inspiratory flow time, accept permissive hypercapnia)
  • Treat cause: bronchodilators, steroids, magnesium; consider deepening anaesthesia; consider paralysis if severe asynchrony
Explain why compliance falls in ARDS and how PEEP can improve oxygenation but may worsen compliance at high levels.

Discuss reduced aerated lung volume (“baby lung”), recruitment, and overdistension.

  • ARDS: alveolar flooding, collapse, and inflammation reduce aerated lung volume and increase elastance → low compliance
  • PEEP can recruit collapsed units, increase FRC, improve V/Q matching and compliance (on the recruitment limb)
  • Excess PEEP overdistends already open units, increasing elastance and worsening compliance; also risks barotrauma and reduced venous return
How do lung volume and radial traction affect airway resistance? Apply this to anaesthesia and atelectasis.

Link reduced FRC under anaesthesia to increased resistance and closure.

  • As lung volume increases, radial traction splints airways open → airway calibre increases → resistance decreases
  • Under anaesthesia: reduced FRC and atelectasis reduce traction → increased resistance and airway closure, especially in dependent regions
  • Clinical implication: PEEP and recruitment can reduce resistance by restoring volume/traction as well as improving compliance
Describe dynamic airway compression and the equal pressure point. Why is expiration flow-limited in emphysema?

Use pressure gradients from alveoli to mouth during forced expiration.

  • During forced expiration, pleural pressure rises; airway pressure falls along the airway towards the mouth due to resistive losses
  • Equal pressure point: location where airway pressure equals pleural pressure; beyond this point, transmural pressure becomes negative and airway narrows/collapses
  • Emphysema: reduced elastic recoil lowers alveolar pressure driving force, moving equal pressure point distally into smaller, non-cartilaginous airways → early collapse and flow limitation

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