What is the physiological consequence of a significant increase in dead space ventilation on arterial PaCO2, assuming constant carbon dioxide production?

A significant increase in dead space ventilation, assuming constant carbon dioxide production, results in an increase in arterial PaCO2 (partial pressure of carbon dioxide in arterial blood). Dead space ventilation refers to the portion of each breath that does not participate in gas exchange. This includes anatomical dead space (the volume of the conducting airways, such as the trachea and bronchi, where no gas exchange occurs) and alveolar dead space (alveoli that are ventilated but not perfused with blood, meaning they receive air but no blood flow for gas exchange). Because dead space ventilation does not contribute to carbon dioxide removal from the blood, an increase in dead space means that a larger portion of each breath is ineffective at eliminating CO2. If carbon dioxide production remains constant (meaning the body is producing the same amount of CO2), but a smaller proportion of each breath is involved in gas exchange due to increased dead space, CO2 will accumulate in the arterial blood. The body will try to compensate for this by increasing minute ventilation (the total volume of air breathed in one minute), which is calculated by multiplying tidal volume (the volume of air inhaled or exhaled in a single breath) by respiratory rate (the number of breaths per minute). However, if minute ventilation cannot adequately compensate for the increased dead space, PaCO2 will rise, leading to hypercapnia (elevated levels of carbon dioxide in the blood).