Dead Space

Dead space is the proportion of minute ventilation which does not participate in gas exchange.

Types of Dead Space

Dead space can be divided into:

  • Apparatus dead space
    Dead space from equipment, such as tubes ventilator circuitry. Some apparatus dead space may actually reduce total dead space, as an ETT bypasses the majority of anatomical dead space of the patient (nasopharynx).
  • Physiological dead space
    Dead space from the patient. Physiological dead space is divided into:
    • Anatomical dead space
      The volume of the conducting zone of the lung. Anatomical dead space is affected by:
      • Size and Age in the infant, falls to in the adult
      • Posture
        Decreases when supine.
      • Position of the neck and jaw
        Increased with neck extension.
      • Lung volumes
        Increases by ~20ml per litre of additional lung volume.
      • Airway calibre
        Bronchodilation increases airway diameter and therefore VD.
    • Pathological/Alveolar Dead Space
      Dead space caused by disease. Causes of pathological dead space include:
      • Erect posture
      • Decreased pulmonary artery pressure/impaired pulmonary blood flow
        • Hypovolaemia
        • RV failure/Increased RV afterload:
          • HPV
          • MI
        • PE
      • Increased alveolar pressure
        Increases West Zone 1 physiology.
      • COAD

Calculation of Dead Space

Two methods exist to allow dead space volumes to be calculated:

  • Physiological dead space may be measured with Bohr's method
  • Anatomical dead space may be measured by Fowler's method
  • Pathological dead space may be calculated by subtracting anatomical dead space (Fowler's method) from physiological dead space (Bohr's Method)

Fowler's Method

Fowler's Method is a single-breath nitrogen washout test, used to calculate anatomical dead space and closing capacity.


  • At the end of a normal tidal breath (at FRC) a vital-capacity breath of 100% oxygen is taken
  • The patient then exhales to RV
    Expired nitrogen concentration and volume is measured.
  • A plot of expired nitrogen concentration by volume is generated, producing a graph with four phases:
    • Phase 1 (Pure Dead Space)
      Gas from the anatomical dead space is expired. This contains 100% oxygen - no nitrogen is present.
    • Phase 2
      A mix of anatomical dead space and alveolar (lung units with short time constants) is expired. The midpoint of phase 2 (when area A = area B) is the volume of the anatomical dead space.
    • Phase 3
      Expired nitrogen reaches a plateau as just alveolar gas is exhaled (lung units with variable time constants).
    • Phase 4
      Sudden increase in nitrogen concentration, which indicates closing capacity. This increase occurs because:
      • Basal alveoli are more compliant than apical alveoli
      • Therefore, during inspiration basal alveoli inflate more than apical alveoli
        The single 100% oxygen breath therefore preferentially inflates the basal alveoli. At the end of the vital capacity breath, the oxygen concentration in basal alveoli is greater than that of apical alveoli.
      • In expiration, the process is reversed:
        • Basal alveoli preferentially exhale
        • At closing capacity, small basal airways close and now only apical alveoli (with a higher concentration of nitrogen) can exhale
        • Measured expired nitrogen concentration increases

Bohr's Method

Physiological dead space is measured using the Bohr equation. This calculates dead space as a ratio, or proportion of tidal volume:

The Bohr equation is based on the principle that all CO2 exhaled must come from ventilated alveoli.

Note that:

  • is the mixed-expired carbon dioxide
    Partial pressure of CO2 in an expired tidal breath.
  • The Bohr equation requires alveolar PCO2 to be measured
    As this is impractical, the Enghoff modification is typically used, which assumes that PACO2 ≈ PaCO2. The equation then becomes:
  • A normal value for physiological dead space during normal tidal breathing is 0.2-0.35

Physiological Consequences of Increased Dead Space

In dead space:

  • The V/Q ratio approaches infinity as alveolar perfusion falls
  • This results in a rise in PaCO2
  • In a spontaneously-ventilating individual, this stimulates the respiratory centre to increase minute ventilation to return alveolar ventilation (and therefore CO2) to normal
  • There is minimal effect on PaO2, as in pure dead space all blood is passing through ventilated alveoli and therefore undergoes gas exchange

Relationship between Alveolar Ventilation and PaCO2

Atmospheric air contains negligible CO2. As MV increases, PaCO2 will fall, as will the gradient for further CO2 diffusion. This can be expressed by the equation:

Note that this graph:

  • Describes the change in PaCO2 for a change in alveolar ventilation
    A doubling of alveolar ventilation will halve PaCO2.
  • Does not describe the change in ventilatory drive for a given change in PaCO2
    This is covered under removal of CO2.


Note that West Zone 1 (where PA > Pa > Pv) physiology is increased dead space.

The PaCO2-ETCO2 difference is a consequence of dead space, as dead space gas dilutes alveolar gas.


  1. Lumb A. Nunn's Applied Respiratory Physiology. 7th Edition. Elsevier. 2010.
  2. West J. Respiratory Physiology: The Essentials. 9th Edition. Lippincott Williams and Wilkins. 2011.
Last updated 2021-08-23

results matching ""

    No results matching ""