Arterial PaCO2 and end-tidal PCO2

Briefly describe the potential causes of a difference between measured end-tidal and arterial partial pressure of carbon dioxide (03B11) (96B7)

What is the end tidal CO2? How does it differ from arterial CO2 tension and the mixed expired CO2 tension? What factors influence its value? (1995)

End-tidal PCO2

End-tidal PCO2 is the partial pressure of CO2 at the end of expiration during tidal breathing.

=> ASSUMED to be representative of alveolar gas

=> It is lower than 'ideal' alveolar PCO2, because the almost CO2-free gas from alveolar dead space dilutes and lower the end-tidal PCO2.

Mixed expired PCO2 is the partial pressure of CO2 in the expired gas during a tidal breath.

=> It is much lower in PCO2 because the CO2-free gas from anatomical dead space dilutes even more.

Arterial PaCO2 and 'ideal' alveolar PCO2

 

Shunt of 10% will cause an alveolar-arterial PCO2 gradient of about 0.7mmHg.

=> Thus by convention, arterial and "ideal" alveolar PCO2 values are taken to be identical.

Normal PaCO2 = 38.3mmHg +/- 7.5mmHg (95% limits, 2 standard deviation.)

Difference between arterial PaCO2 and end-tidal PCO2

In a healthy person breathing room air, the difference between arterial PaCO2 and end-tidal PCO2 is small.

=> end-tidal PCO2 is about 2~5mmHg lower

The size of this difference is a simple index of the amount of alveolar dead space.

=> as the alveolar dead space volume increases, more relatively CO2-free gas mixes in with gases from better perfused units, thus lowering the end-tidal PCO2

=> Because PaCO2 is usually very close to PCO2 of the perfused alveoli, increased alveolar dead space would lower the end-tidal PCO2 and increase the difference between that and arterial PaCO2.

Alveolar dead space

Alveolar dead space is the part of the inspired gas which passes through the anatomical dead space to mix with gas at the alveolar level, but does not participate in gas exchange. (i.e. infinite V/Q)

Basically it is the difference between physiological dead space and anatomical dead space.

Factors influencing alveolar dead space

• Low cardiac output can increase alveolar dead space (increasing West's zone 1)
• Pulmonary embolism

Measurement error

Difference between end-tidal CO2 and PaCO2 could also be due to:

• sampling error
• calibration error
• leaks or occulsion in sampling lines
• difficulty in obtaining a true end-tidal CO2
  => delayed alveolar emptying with slow rise of expired CO2, leading to failure to obtain a true plateau.

 

 

Additional notes

Factors influencing PaCO2

Arterial PaCO2 is influenced by:

1. Alveolar PACO2
2. Shunts (effects of venous admixture)
3. V/Q scatter (effects of venous admixture and CO2-free alveolar dead space gas)

In turn, alveolar PACO2 is influenced by:

1. Barometric pressure
2. Inspired CO2 concentration
3. CO2 output/production
4. Alveolar ventilation, via
   - tidal volume,
   - dead space,
   - respiratory frequency

(PACO2 is INVERSELY proportional to ventilation.)

 

Examiner's comment

• Require an explanation of alveolar dead space
• Factors relating to measurement:
  - sampling site
  - calibration
  - accuracy of measurement
  - leaks, occulsion
• delayed alveolar emptying with slow rise of expired CO2, leading to failure to obtain a true plateau
• Common error: incorrect use of Bohr equation, with substitution of end tidal for mixed expiratory partial pressure of carbon dioxide. This was used to quantify alveolar dead space. Nunn has modified the equation to obtain alveolar dead space/alveolar volume ratio by using end tidal CO2.
• Common error: failure to appreciate that normally arterial, alveolar, and end tidal partial pressure of CO2 are generally considered to have the same value. Normal healthy awake subjects have no alveolar dead space, and no arterial end tidal differences in regional pressures of CO2.
• Common error: failure to mention measurement-related factors