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The Cardiopulmonary Effects of Hypercapnia

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Intensive Care Medicine
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Abstract

Carbon dioxide (CO2) is a product of oxidative metabolism in humans. The arterial CO2 partial pressure (PO2) can be represented by equation (1):

$$ PO_2 = K \cdot \left( {VCO_2 /V_A } \right) + PiCO_2 $$
(1)

where K is a proportion constant, VCO2 the CO2 production, VA the alveolar ventilation, and PCO2 is the inhaled CO2. Aveolar ventilation (VA) is a component of the total ventilation (VT) minus the dead space ventilation (VD), which is VA = VT - VD or:

$$ V_A = V_T \left( {1 - V_D /V_T } \right) $$
(2)

therefore, by combining equations 1 and 2, the following equation results:

$$ PCO_2 = K \cdot VCO_2 /V_T \left( {1 - V_D /V_T } \right) + PiCO_2 $$
(3)

Consistent with this equation, we can identify four causes for hypercapnia: A) increased CO2 production (VCO2); B) hypoventilation (increased value of 1/VT); C) increased dead space ventilation (VD); and D) increased inhaled CO2 (PiCO2) [1].

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Manca, T., Welch, L.C., Sznajder, J.I. (2008). The Cardiopulmonary Effects of Hypercapnia. In: Vincent, JL. (eds) Intensive Care Medicine. Springer, New York, NY. https://doi.org/10.1007/978-0-387-77383-4_26

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  • DOI: https://doi.org/10.1007/978-0-387-77383-4_26

  • Publisher Name: Springer, New York, NY

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