Increased ventilation does not always mean hyperventilation. Hyperventilation is defined by a decrease in Paco2 from the normal value, implying excess Va for the given Vco2. Therefore, the effectiveness of ventilation can be judged by the Paco2 at any given metabolic rate. For example, if Va is doubled, Paco2 is halved, regardless of the exact values for either variable. The most important thing to remember about the alveolar ventilation equation is that Va and Paco2 (or Paco2) are inversely related for any given metabolic rate. In practice, arterial Pco2 is substituted for alveolar Pco2 because the two values are equal in normal lungs and an arterial blood sample is usually taken to measure arterial Po2 for evaluating gas exchange. Va = (V co2/Paco2 )K, where K is a constant (= 0.863) to convert Fco2 to Pco2 in mm Hg, and Vco2 in mLsTPD/min to Va in LBTPs/min. The alveolar ventilation equation is obtained by substituting Paco2 for Faco2 and rearranging the Fick equation: Fico2 is nearly zero, so the inspired terms can be dropped. (V co2) = (V aFaco2)-(V iFico2), where Vco2 is the difference between the CO2 expired from the alveoli and the amount of CO2 inspired to the alveoli. The Fick equation (see Chapter 18) defines CO2 elimination from the lungs (Vco2) as:
10) but gas exchange principles can be used to obtain a more direct measure of the effective, or functional, alveolar ventilation.Īlveolar Ventilation Equation Predicts Paco2 Anatomic dead space can be measured with the single breath method (see Chapter 18, Fig. Va = /R(Vt - Vd), where Va is alveolar ventilation, fR is respiratory frequency, Vt is tidal volume, and Vd is anatomic dead space. As described in Chapter 18, anatomic dead space reduces the fraction of the tidal volume that reaches the alveoli: Ventilation is the first step in the O2 cascade, and the level of alveolar ventilation (Va) is the most important physiologic factor determining arterial Po2 for any given inspired Po2 and level of O2 demand (Vo2) in healthy lungs.
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