In the lungs, what is meant by the term ‘dead space’?

The air inspired during a normal breath V_T is divided into:

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  Alveolar volume V_A, the volume of air which reaches perfused alveoli.

  
  
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  Dead space V_D, the volume of inspired air that plays no part in gas exchange; that is, the air remaining in either the conducting airways or non-perfused alveoli.

Mathematically:

What are the different types of dead space?

Dead space is classified as ‘anatomical’, ‘alveolar’ or ‘physiological’:

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  Anatomical dead space VDAnat is the volume of the upper airways and first 16 generations of the tracheobronchial tree, which form the conducting airways (see Chapters 6 and 7).

  
  
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  Alveolar dead space VDAnat is the total volume of the ventilated alveoli that are unable to take part in gas exchange due to insufficient perfusion (i.e. due to V̇/Q̇ mismatch; see Chapter 15).

  
  
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  Physiological dead space VDPhys is the total dead space; that is, the sum of anatomical and alveolar dead space:

  
  
  VDPhys=VDAnat+VDAlv
  
  

What factors affect anatomical dead space? How is anatomical dead space measured?

VDAnat is measured using Fowler’s method (see p. 47). Typical VDAnat is 150 mL for a 70‑kg man; that is, approximately 2 mL/kg, or around a third of the normal V_T (7 mL/kg). VDAnat may be altered by a number of factors:

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  Size of patient: VDAnat increases as the size of the lungs increases.

  
  
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  Lung volume: at high lung volumes, radial traction on the airway walls increases airway diameter, thus increasing VDAnat.

  
  
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  Posture: lung volume decreases in the supine position, which reduces airway diameter and therefore reduces VDAnat.

  
  
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  Bronchoconstriction reduces airway diameter: VDAnat therefore decreases.

  
  
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  Bronchodilatation increases airway diameter: VDAnat therefore increases.

How is alveolar dead space measured and what factors affect it?

Alveolar dead space cannot be measured directly. As VDPhys=VDAnat+VDAlv, the alveolar dead space can be calculated if VDPhys and VDAnat are known. VDPhys is measured using the Bohr equation (see p. 48) and VDAnat is measured using Fowler’s method. In normal lungs, VDAlv is negligible as alveolar ventilation and perfusion are well matched. However, VDAlv may increase as a result of:

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  Upright posture. Owing to the effect of gravity, blood only just perfuses the lung apices (i.e. West zone 2 – see Chapter 16). The apical alveoli are well ventilated but not adequately perfused, which increases VDAlv.

  
  
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  Low pulmonary artery pressure; for example, as a result of reduced right ventricular output. Like upright posture, this leads to insufficient perfusion of the lung apices, a high V̇/Q̇ ratio and thus an increase in VDAlv.

  
  
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  Positive end-expiratory pressure and positive pressure ventilation both increase alveolar pressure. In the lung apices, the increase in alveolar pressure causes compression of the pulmonary capillaries, reducing alveolar perfusion. This is West zone 1 (see Chapter 16). In addition, the increase in intrathoracic pressure reduces venous return to the right ventricle, which in turn reduces pulmonary artery pressure. Both effects increase VDAlv.

  
  
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  Pulmonary artery obstruction by an embolus (arising from thrombus, gas, fat or amniotic fluid) results in the downstream alveoli being ventilated but not perfused, thus increasing VDAlv.

  
  
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  Chronic obstructive pulmonary disease. The associated destruction of alveolar septa results in enlarged air spaces. The surface area available for gas exchange is therefore reduced. Much of the air entering the enlarged airspaces cannot participate in gas exchange, which results in an increase in VDAlv.