The reasons why PaCO2 rises are often misunderstood. This is explained in detail in Chapter 2. To summarise:
• "CO2 retention" is the phenomenon that occurs with uncontrolled oxygen therapy in patients with chronic hypoxaemia (for example, some patients with COPD).
• Hypercapnic respiratory failure - or ventilatory failure - has nothing to do with oxygen therapy. Ventilatory capacity is the amount of spontaneous ventilation that can be maintained without the development of respiratory muscle fatigue. Normally ventilatory capacity matches demand. Hypercapnic respiratory failure results from either a reduction in ventilatory capacity or an increase in ventilatory demand - or both.
Metabolism rapidly generates acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO2. This combines with water to form carbonic acid. The lungs excrete the volatile fraction through ventilation. Ventilation is influenced and regulated by chemoreceptors for PaCO2, PaO2, and pH located in the brainstem as well as by neural impulses from lung stretch receptors and impulses from the cerebral cortex. PaCO2 is determined by the balance between CO2 production and its removal via alveolar ventilation. This can be expressed by the equation:
PaCO2 - VcoJVa where Vco2 is the rate of delivery of CO2 to the alveoli by capillary blood and Va is the rate of removal of CO2 by alveolar ventilation.
CO2 production is increased in hypermetabolic states and by infusions of sodium bicarbonate. At a constant rate of carbon dioxide production, PaCO2 is determined by the level of alveolar ventilation. A decrease in alveolar ventilation can result either from reduced minute ventilation or increased dead space.
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