Hyperventilation (ie increased alveolar ventilation) is the mechanism responsible for the lowered arterial pCO2 in ALL cases of respiratory alkalosis.
This low arterial pCO2 will be sensed by the central and peripheral chemoreceptors and the hyperventilation will be inhibited unless the patientís ventilation is controlled.
Causes of Respiratory Alkalosis
1. Central Causes (direct action via respiratory centre)
2. Hypoxaemia (act via peripheral chemoreceptors)
3. Pulmonary Causes (act via intrapulmonary receptors)
4. Iatrogenic (act directly on ventilation)
Hyperventilation is the mechanism in all of the situations in the above list & indeed in all cases.
Theoretically, a decreased carbon dioxide production could result in respiratory alkalosis if alveolar ventilation remained fixed. But this would not occur in a normal person because any drop in arterial pCO2 would reflexly cause a decreased ventilation (via chemoreceptor inhibitory input into the respiratory centre).
About the only situation where maybe a decrease in CO2 production could be the mechanism of respiratory alkalosis would be in an intubated patient on fixed ventilation during Anaesthesia or in Intensive Care Unit and where the CO2 production was low due to hypothermia and decreased metabolic rate. However, even in such a circumstance, this mechanism is usually referred to as 'excessive controlled ventilation' (which it is relative to the amount of CO2 production). So the answer to the question posed must be no.