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
      3.3ml.kg^-1 in the infant, falls to 2.2ml.kg^-1 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 V_D.
      
  • 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.
      • PEEP
    • 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 volume.

Method:

• 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.
    • 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
    • Onset of phase 4 indicates the point at which closing capacity is reached
    • The volume exhaled between phase 4 commencing and reaching RV is the closing volume
      This can be combined with a measurement of RV to quantify the closing capacity.

Bohr's Method

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

${V_D \over V_T} = {V_T - V_A \over V_T}$

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

${V_D \over V_T} = {PA_{CO_2} - P\bar{E}_{CO_2} \over PA_{CO_2}}$

Note that:

• $P\bar{E}_{CO_2}$ 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:
  ${V_D \over V_T} = {Pa_{CO_2} - P\bar{E}_{CO_2} \over Pa_{CO_2}}$
• 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:
$PaCO_2 \propto {1 \over \dot{V}_A}$

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.

Footnotes

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.

References

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.