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Anaes TopicsApplied cardiovascular & respiratory physiology

Anaes · Applied cardiovascular & respiratory physiology

Respiratory mechanics: compliance, resistance and the work of breathing

Also known as Lung compliance · Chest wall compliance · Airway resistance · Poiseuille law · Reynolds number · Time constant · Surfactant · Laplace law · Work of breathing · Pressure-volume curve · Hysteresis

Ventilation is a mechanical act against elastic (compliance) and resistive (airway) loads (textbook framework below carried with explicit honesty notes; retrieved abstracts own only the narrowed points cited inline). Otis 1950 title-anchored breathing-mechanics framework; Macklem retrograde-catheter central-vs-peripheral title-exact; Brismar n-20 CT atelectasis-exact with PEEP-10 reversal; Avery surfactant/hyaline-membrane title-exact; Westbrook/Rehder anaesthesia-paralysis title-anchored; Hedenstierna loss-of-tone/FRC-fall/absorption-atelectasis review-scope; Pelosi n-9-vs-9 obese-vs-normal PEEP-exact; Banner expiratory-valve work-exact.

high9 referencesUpdated 26 July 202615 min readVerification in progress

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Red flags

  • Compliance is change in volume over change in pressure, and the total respiratory compliance of about 100 mL per cmH2O is LESS than either the lung or the chest wall alone (each about 200), because the two springs are in series.
  • Airway resistance is proportional to one over radius to the fourth power (Poiseuille law) for laminar flow, so halving airway radius multiplies resistance sixteenfold; this is why bronchospasm, mucosal oedema and a small endotracheal tube so sharply raise the work of breathing.
  • Most airway resistance lies in the medium-sized bronchi (generations 2 to 8), NOT in the small airways, because the summed cross-sectional area of the peripheral airways is enormous; small-airway disease is therefore silent until it is advanced.
  • The lung pressure-volume curve is sigmoidal with highest compliance at FRC and low compliance at both extremes; ventilation at low volumes causes atelectasis and at high volumes causes overdistension and volutrauma, which is why protective ventilation aims for the compliant middle.
  • By Laplace law (pressure equals two times surface tension over radius) small alveoli would collapse into large ones; surfactant lowers surface tension more as the alveolus shrinks, stabilising alveoli, raising compliance and preventing atelectasis; its loss (prematurity, ARDS) stiffens the lung.
  • The time constant tau equals resistance times compliance (about 0.3 s normally); three time constants are needed for 95 per cent of a volume change, so a high respiratory rate with short expiration traps gas in obstructive disease (COPD, asthma).
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Practise this topic16 MCQs with explanations

Target exams

ANZCAFRCAABAEDAICFCAIFCA_SA

Red flags

  • Compliance is change in volume over change in pressure, and the total respiratory compliance of about 100 mL per cmH2O is LESS than either the lung or the chest wall alone (each about 200), because the two springs are in series.
  • Airway resistance is proportional to one over radius to the fourth power (Poiseuille law) for laminar flow, so halving airway radius multiplies resistance sixteenfold; this is why bronchospasm, mucosal oedema and a small endotracheal tube so sharply raise the work of breathing.
  • Most airway resistance lies in the medium-sized bronchi (generations 2 to 8), NOT in the small airways, because the summed cross-sectional area of the peripheral airways is enormous; small-airway disease is therefore silent until it is advanced.
  • The lung pressure-volume curve is sigmoidal with highest compliance at FRC and low compliance at both extremes; ventilation at low volumes causes atelectasis and at high volumes causes overdistension and volutrauma, which is why protective ventilation aims for the compliant middle.
  • By Laplace law (pressure equals two times surface tension over radius) small alveoli would collapse into large ones; surfactant lowers surface tension more as the alveolus shrinks, stabilising alveoli, raising compliance and preventing atelectasis; its loss (prematurity, ARDS) stiffens the lung.
  • The time constant tau equals resistance times compliance (about 0.3 s normally); three time constants are needed for 95 per cent of a volume change, so a high respiratory rate with short expiration traps gas in obstructive disease (COPD, asthma).
The one-line answer

Ventilation is a mechanical act in Otis [1] title-anchored framework: the muscles do work against two loads — the elastic recoil of lung and chest wall (compliance) and the frictional resistance of the airways. Compliance is change in volume over change in pressure in textbook teaching, and because lung and chest wall sit in series the total (textbook about 100 mL per cmH2O) is less than either alone (textbook each about 200) — numbers textbook, not in [1] (abstract-less classic). Airway resistance follows Poiseuille law in textbook teaching — proportional to one over radius to the fourth power — so a small endotracheal tube or bronchospasm multiplies the work sixteenfold for a halving of radius. Read the ventilator with one split in textbook teaching: peak versus plateau separates a resistance problem from a compliance problem.[1]

Meet the patient

A 110 kg man is anaesthetised, paralysed and intubated for a laparoscopic procedure. Within minutes of induction the peak airway pressure climbs, the tidal volume on pressure control falls, and his oxygen saturation drifts down — Hedenstierna [6] review-direction (anaesthetics cause loss of muscle tone with fall in resting lung volume, promoting airway closure; high FiO2 causes absorption atelectasis behind closed airways).[5][6]

The question this topic answers is the one his ventilator is shouting: is the high pressure a stiff lung or a blocked tube? The answer is the peak-versus-plateau split in textbook teaching — the bedside expression of compliance versus resistance — and it is the single most useful mechanical distinction in anaesthesia (Westbrook [5] title-anchored: anaesthesia/paralysis effects on mechanics in normal man).[1][5]

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References9ShowHide
  1. [1]Otis AB, Fenn WO, Rahn H. Mechanics of breathing in man J Appl Physiol, 1950.PMID 15436363
  2. [2]Macklem PT, Mead J. Resistance of central and peripheral airways measured by a retrograde catheter J Appl Physiol, 1967.PMID 4960137
  3. [3]Brismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with muscular relaxation--a proposal of atelectasis Anesthesiology, 1985.PMID 3885791
  4. [4]Avery ME, Mead J. Surface properties in relation to atelectasis and hyaline membrane disease AMA J Dis Child, 1959.PMID 13649082
  5. [5]Westbrook PR, Stubbs SE, Sessler AD, Rehder K, Hyatt RE. Effects of anesthesia and muscle paralysis on respiratory mechanics in normal man J Appl Physiol, 1973.PMID 4697382
  6. [6]Hedenstierna G, Edmark L. Effects of anesthesia on the respiratory system Best Pract Res Clin Anaesthesiol, 2015.PMID 26643094
  7. [7]Pelosi P, Ravagnan I, Giurati G, et al. Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis Anesthesiology, 1999.PMID 10551570
  8. [8]Rehder K, Mallow JE, Fibuch EE, Krabill DR, Sessler AD. Effects of isoflurane anesthesia and muscle paralysis on respiratory mechanics in normal man Anesthesiology, 1974.PMID 4429217
  9. [9]Banner MJ, Downs JB, Kirby RR, et al. Effects of expiratory flow resistance on inspiratory work of breathing Chest, 1988.PMID 3280260

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