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 patient’s ventilation is controlled.
Causes of Respiratory Alkalosis
1. Central Causes (direct action via respiratory centre)
Head Injury
Stroke
Anxiety-hyperventilation syndrome (psychogenic)
Other 'supra-tentorial' causes (pain, fear, stress, voluntary)
Various drugs (eg analeptics, propanidid, salicylate intoxication)
Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients
with chronic liver disease)
2. Hypoxaemia (act via peripheral chemoreceptors)
Respiratory stimulation via peripheral chemoreceptors
3. Pulmonary Causes (act via intrapulmonary receptors)
Pulmonary Embolism
Pneumonia
Asthma
Pulmonary oedema (all types)
4. Iatrogenic (act directly on ventilation)
Excessive controlled ventilation
Can a decreased CO2 production cause respiratory alkalosis?
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.