In the inter-war period, many medical investigators who studied the hyperventilation syndrome (HVS) had already questioned the chemosensitivity to CO2 in HVS patients, without being able to explore it for all intents and purposes.~It was subsequently observed that although HVS is not systematically linked to manifest resting hypocapnia, it is nevertheless systematically correlated with significant variability and complexity of ventilation.~This is consistent with the observations of an increased plant gain in HVS, to be related to an increased loop gain (due to instability of controller gain feedback).~On the other hand, some authors already noted that, when capnia is chronically compromised in HVS, it can be greatly altered by small, transient and barely perceptible increases in VE: a 10% increase in VE could indeed halve PetCO2, while a sigh would be able to decrease PetCO2 by up to 15mmHg.~More recently, teh assumption was made that peripheral chemosensitivity may be impaired in HVS patients.~For all these considerations, it seems reasonable to investigate central and peripheral chemosensitivities in identified HVS subjects on the basis of an objective test, such as the induced hyperventilation test.
For almost a century, many hypotheses have converged on the idea of altered chemosensitivity in patients suffering from hyperventilation syndrome (HVS).~Given the evolution of current technical equipment and the ability to maximise true positives in HVS ( using the revised hyperventilation provocation test), it seems reasonable to investigate central and peripheral chemosensitivities in HVS subjects.