PaCO2 Equation

I’ve previously written about the alveolar gas equation and oxygen delivery equation, both of which deal with the physiologic process of oxygenation. Now I want to discuss the important relationship between alveolar ventilation (VA), carbon dioxide production (VCO₂), and alveolar carbon dioxide tension (PACO₂). For this explanation, PACO₂ roughly approximates arterial carbon dioxide tension (PaCO₂) if ventilation/perfusion (V/Q) mismatch is minimal.

Assuming a normal PaCO₂ is 35 – 45 mmHg, the equation above shows that an elevated PaCO₂ (hypercapnia) results from decreased VA (respiratory depression, oversedation, muscle fatigue, or dead space ventilation). An important consideration is that increased VCO₂ is handled well by an intact respiratory system. For example, your PaCO₂ remains relatively stable when you exercise since your increased VCO₂ during exertion is matched with an increased VA. Therefore, an increased VCO₂ is not traditionally considered a cause of hypercapnia in otherwise healthy patients.

Looking at the curve, patients who are already hypercarbic (high PaCO₂) and proceed to have a drop in their VA as shown by the purple arrow will have a much more significant increase in PaCO₂ than if the patient has a normal PaCO₂ with the same reduction in alveolar ventilation (green arrow). But, again, this is simply due to movement along the steeper portion of the curve.

Clinically, if you see a patient “panting” with rapid, deep breaths, this might NOT be hyperventilation. Instead, this might be compensation for an underlying process increasing carbon dioxide production. Therefore, sedating these patients to calm them down might be detrimental (reduce VA) and throw them into hypercarbic failure.

Hypercarbia and hypocarbia have significant physiologic implications ranging from vascular autoregulation to acid-base status, so it’s important to remember the PaCO₂ equation when considering a patient’s ventilation.

Drop me a comment below with questions! 🙂