Abstract des Autors

Mechanical stimuli (such as pulmonary distension and collapse, reaching respiratory centre through vagus afferent fibres) and chemical stimuli (such as reduction of oxygen and increase of CO2 both in alveolar air and in blood, with consequent increasing stimuli on respiratory centres) all together cooperate to interrupt voluntary apnoea. Anoxaemia itself has a depressive action on respiratory centre, but through chemoceptors it also increases its activity. A more important chemical action is made by the increase of CO2, which stimulates the respiratory centre, both directly and for reflex action. During voluntary apnoea, the 3 phases of alveolar air blood, and venous blood, regarding both O2 and CO2 turnover, tend to balance until when no more gas-exchanges take place between the phases. Such a process goes on until the anoxia and hypercapnia chemical stimuli are enough to stop voluntary apnoea (break-point). When underwater divers go very deep, a progressive reduction of pulmonary volume takes place, with an increase of both O2 and CO2 density, and partial pressure. When they come up, pulmonary volumes return normal, total pressure becomes 1 ATA again, and O2-CO2 partial pressures decrease. Sudden drop of PO2 could be a risk of anoxia and syncope. Verf.-Referat