What is the role of gas exchange abnormalities in the etiology of hypoventilation syndromes?

Updated: Jul 22, 2021
  • Author: Jazeela Fayyaz, DO; Chief Editor: Guy W Soo Hoo, MD, MPH  more...
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The alveoli are perfused by venous blood flow from the pulmonary capillary bed and participate in gas exchange. This gas exchange includes delivery of oxygen to the capillary bed and elimination of carbon dioxide from the bloodstream. The continued removal of carbon dioxide from the blood is dependent on adequate ventilation.

The relationship between ventilation and PaCO2 can be expressed as PaCO2 = (k)(VCO2)/VA, in which VCO2 is the metabolic production of carbon dioxide (ie, venous carbon dioxide production), k is a constant, and VA is alveolar ventilation. Therefore, in alveolar hypoventilation, PaCO2 increases as the VA decreases. Because the alveolus is a limited space, an increase in PaCO2 leads to a decrease in oxygen, with resultant hypoxemia.

VA also can be reduced when an increase in physiologic dead-space ratio (ie, the dead-space gas volume-to-tidal gas volume [VD/VT] ratio) occurs. Physiologic dead space occurs when an increase in ventilation to poorly perfused alveoli occurs. An increase in physiologic dead space results in a ventilation-perfusion mismatch, which, in classic presentation, occurs in patients with COPD.

The effect of physiologic dead space on alveolar hypoventilation can be expressed in the equation PaCO2 = (k)(VCO2)/VE(1 - VD/VT), in which VE (ie, expired volume) is the total expired ventilation and 1 - VD/VT measures the portion of ventilation directly involved in gas exchange. An increase in the physiologic dead space without an augmentation in ventilation leads to alveolar hypoventilation and an increased PaCO2.

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