Alveolar Ventilation and Gas Diffusion

Hello :) in this post we'll continue onto the next topic in our respiratory section of Veterinary Physiology 1 by looking at alveolar ventilation and gas diffusion. We'll consider the different types of ventilation and how to calculate alveolar ventilation as well as the effects of deadspace on ventilation. I'll also explain the concept of expiratory flow rate respiration and how it relates to the dynamic compression of airways. We'll also look at the partial pressures of oxygen and carbon dioxide and the three factors which influence these pressures in alveolar gas. We'll finish off by discussing the effects of hyper- and hypoventilation and ventilation/perfusion mismatch.

Respiratory Ventilation

Ventilation rates can be defined differently depending on which part of the lung we are considering.

• Minute Ventilation : this is the total volume of air entering the lung per minute. This can be calculated using the following equation:

    VE = VT x f  where VT= tidal volume and f= respiratory frequency

• Deadspace ventilation: the volume of air that is inspired per minute that does not take part in gas exchange. An increase in the amount of deadspace makes it more difficult to breathe. This is because the animal has to breathe harder to receive enough oxygen. It can be calculated using the following equation:
  

  VD = VT x f   where VT= tidal volume and f= respiratory frequency 

  There are 3 types of deadspace:
  
  1. Anatomical Deadspace: this refers to the conducting airways that do not participate in gas exchange. For example, the trachea, bronchi and bronchioles.
  2. Alveolar Deadspace: this refers to the ventilated alveoli that do not receive a blood supply and thus cannot participate in gas exchange. This is normally quite a small amount. 
  3. Equipment of Mechanical Deadspace: this is associated with respiratory equipment and is therefore not normally a consideration. For example ET tubes, face masks and tubing increase the amount of deadspace because they provide an extension of the trachea.
• Alveolar Ventilation: this is the volume of air that reaches the alveoli per minute, it does take part in gas exchange. This can be calculated using the following calculation:
  

  VE = VE - VD

  
  Expiratory Flow Limitation (EFL) and Dynamic Compression of Airways 
  
  
  During the early stages of respiration, the flow rate is effort-dependent. However, as the amount of air remaining in the lungs is low, expiration becomes effort independent. In other words, no matter how hard you try you can't change the rate at which you exhale towards the end of expiration. This is known as expiratory flow limitation (EFL). You can experience this by inhaling as much as you can and then exhaling as hard as possible and note the force of air movement against your hand. Now try and increase that flow rate at low lung volumes by trying to breathe harder. You'll notice that you can't control the flow rate at low lung volumes.
  
  Now, EFL is due to a what's called Dynamic Airway Compression. At low lung levels the pressure outside the airways is greater than the pressure inside the airways and this results in airway collapse. This can be illustrated in the diagram below which is from this website :
  
  

  

  Expiratory Flow Limitation

  During forced exhalation the driving force for expiratory flow decreases closer to the mouth. There is a pressure gradient along the length of the airway towards the mouth. This gradient will be high in the alveoli because the intra alveolar pressure is higher than the atmospheric pressure and will gradually decrease until it reaches the mouth where the pressure will be similar to atmospheric pressure. Along the airway there comes a point during forced exhalation where the pressure in the airway is equal to the pressure that is surrounding the airway. This is known as the Equal Pressure Point (EPP). The airways beyond the EPP (closer to the mouth) are compressed because the pressure outside the airway is greater than the pressure inside the airway. In these airways the expiratory flow is now independent of effort. ie the flow can't be increased no matter how hard you exhale. This is because the airway has narrowed and this increases resistance which limits flow. 
  
  Normally the EPP occurs in airways that contain cartilage and so the airways do not collapse. However, the position of the EPP is not static and will move during pulmonary disease. Pulmonary disease causes an increase in airway resistance and thus a pressure drop in the airways. This causes the EPP to move closer to the alveoli. If the EPP occurs in airways with no cartilage the airways collapse and 'premature airway collapse occurs'.
  
  Partial Pressures
  
  Dalton's law states that the total pressure of a mixture of gases is a sum of the partial pressures exerted by each gas. A partial pressure is the pressure exerted by an individual gas in a mixture. It is the proportion of total air pressure contributed by that gas.
  
  
  
  The partial pressures in alveolar gas are different to those in the atmosphere. This is because gas exchange occurs continuously between alveoli and blood as well as the fact that alveolar air is saturated with water. Water affects partial pressures by decreasing the partial pressure contributions of the other gases. In addition, atmospheric air mixes with dead space gas in the alveoli and this causes an increased concentration of CO₂ and a decreased concentration of O₂. In alveoli, the partial pressure of oxygen is 100mmHg while the partial pressure of carbon dioxide is 40mmHg. In atmospheric air, the partial pressure of oxygen is 160mmHg while the partial pressure of carbon dioxide is 0.3mmHg.  
  
  
  In systemic arteries, which carry oxygenated blood around the body, the pO2 is 100mmHg while pCO2 is 40mmHg. In systemic veins, which carry deoxygenated blood around the body, the pO2 is 40mmHg while the pCO2 is 45mmHg.
  
  
  The Effects of Hyper-and Hypoventilation
  
  
  During hyperventilation an animal is basically breathing too much for what the cells require. In other words, the alveolar ventilation exceeds the demand of tissues. This means that excess CO2 is removed and excess O2 is inspired for the body’s requirement. This causes the partial pressure of carbon dioxide to decrease below 40mmHg and the partial pressure of O2 to increase above 100mmHg in the alveoli and blood.
  
  
  During hypoventilation, an animal is basically breathing too little for what its cells require. Ie. Alveolar ventilation is insufficient to meet tissue demands. The cells continue to produce CO2 and consume O2 but the ventilation is unable to remove and replace these gases. This causes pCO2 to increase above 40mmHg and pO2 to decrease below 100mmHg in the alveoli and blood.  
   

Factors Affecting Diffusion 

As you know, oxygen and carbon dioxide diffuse along a partial pressure gradient. There are a few factors which affect this diffusion:

• Magnitude of Partial Pressure Gradient: i.e the differences in pressure between two places
• Surface Area: the area available for diffusion
• Diffusion Constant: CO2 has a higher diffusion constant than O2 and so diffuses 20x more rapidly. 

The rate of diffusion is inversely proportional to the thickness of the membrane.

Ventilation/ Perfusion Mismatch 

Ventilation refers to the flow of air to alveoli while perfusion refers to the blood flow to that area. Ventilation must match perfusion to ensure that an adequate pO2 and pCO2 are in the blood leaving the alveoli. 

A decreased ventilation, which may be caused by a disease such as Heaves in horses, results in the adequate perfusion of poorly ventilated alveoli. This causes the amount of oxygen to decrease and the amount of carbon dioxide to increase in the arterial blood surrounding the alveoli. This causes the vasoconstriction of smooth muscle in the pulmonary arterioles which leads to an increase in resistance and a decrease in perfusion to that area. In addition, bronchodilation may occur which will decrease resistance and increase ventilation to the area.    

A decrease in perfusion, which may be caused by a pulmonary thromboembolism, results in the adequate perfusion of well ventilated alveoli. This effectively increases alveolar deadspace. This results in brochoconstriction to reduce airflow to the regions with poor ventilation.