Ventilation / Perfusion Distributions and Gas Exchange

 

 

 

This is a computer simulation of mammalian gas exchange.  Its purpose is to provide an easy way to play around with and thereby discover the relative importance of the major factors determining arterial blood gas composition.  These factors are:

 

1.      the distribution of fractional ventilation and perfusion in the lung  (V/Q)

2.      the composition of the mixed venous blood 

3.      the inspired oxygen  fraction  (FiO2)

4.      the overall O2 uptake and CO2 output required by the body

5.      the cardiac output and minute ventilation

 

These are some of the assumptions present in the model:

 

1.      Gas exchange is modeled as a parallel model of  ventilation and perfusion.  The model looks like this:

 

Graph

 

2.      Because of this arrangement, the arterial composition is a perfusion weighted average of the end-capillary O2 and CO2 contents.  Similarly, the mixed expired PO2 and PCO2 are ventilation weighted averages of the alveolar PO2 and PCO2 of the compartments.

 

3.      Gas exchange is steady-state and complete equilibration of the alveolar gas and capillary blood occurs  (ie there is no diffusion impairment).  The compartment compositions are computed by solving the coupled non-linear equations of mass balance for O2, CO2, and N2.

 

4.      An 11 compartment model is used.  Each compartment has a specified V/Q ratio and you determine the fractional bloodflow of each compartment when you start the simulation.  The V/Q ratios are roughly equally spaced on a log scale to cover the range of useful values.

 

 

 

Two simulations are provided.  The first (VAQ.htm) allows you to specify the V/Q distribution and the mixed venous composition and then compute the arterial composition.  The second simulation (VO2.htm)  is more complex.  It allows you to specify the V/Q distribution, the cardiac output, and the total O2 consumption (VO2) and CO2 production (VCO2) required by the body.  The program then finds the appropriate mixed venous composition and the arterial and mixed expired compositions.

 

If you would like to, feel free to review the quantitative physiology of arterial blood gases here.

 

Here are some simple observations you should investigate:

  1. Holding the V/Q distribution,VO2,  and VCO2 fixed, increase the cardiac output.  Why does minute ventilation rise ? 
  2. What happens to venous admixture as cardiac output rises in the above scenario  ?  Why ?  What about physiologic deadspace ?
  3. What happens to physiologic deadspace as shunt is increased ?  Why does minute ventilation fall ?
  4. What happens to venous admixture as you increase perfusion of high V/Q areas ?
  5. What happens to the difference between venous admixture and shunt (V/Q= 0) as FiO2 increases ?  Why ?
  6. Watch what happens to the mixed venous composition and ABGs when VO2 is increased (as in fever) in the presence and absence of V/Q inhomogeneity.  You've seen this in the ICU.
  7. What is the effect of anemia on the mixed venous and arterial compositions in the presence and absence of V/Q inhomogeneity.  Notice the magnitude of the effect.  What is the mechanism ?

 

 

Click here for VAQ.htm

 

Click here for VO2.htm

 

 

If you would like to study the code or mathematics behind these simulations, please visit with me.   You can send junk mail to nojunk@siumed.edu    If you'd like to send email, substitute kkapitan for nojunk in the previous address.

 

                                                                        Kent S Kapitan, MD