Ever since Heymans elucidated the controlling role of the carotid bodies in the reflex governing ventilation, researchers have puzzled over the seeming paradox presented by the action of hydrogen sulfide on the nervous system. While the dominant effect is a depression of function, manifested as a paralysis of ventilation and loss of the sense of smell, the neural receptors of the carotid and aortic bodies appear stimulated. The immediate effect of sublethal doses of H2S is on these receptors, resulting in hyperpnea. The paper resolves the paradox by examining the described effect in the light of the cellular mechanism of action of H2S. This poison most rapidly affects the intracellular mitochondical enzyme cytochrome oxidase, interfering with the transfer of electrons and hydrogen ions to oxygen, thus blocking oxidative metabolism. The chemosensors associated with ventilatory control are primarily sensitive to partial pressure (pO2) of oxygen in blood flowing through the carotid sinuses and the aortic arch. Normally hyperpnea is instigated with the pO2 falls into the 60-30 mm Hg range. Halting oxidative metabolism through H2S poisoning has the same effect as a decrease in oxygen supply, so that hyperpnea is the initial response of sublethal H2S intoxication.