Located in the ventrolateral medulla and provide excitatory synaptic input to the medullary inspiratory neurones. Stimulated by an increase in H+ concentration of the cereberal spinal fluid. Mainly from changes in PCO2. Central chemoreceptors account for 70 per cent of the increased ventilation upon increase in PCO2 (hypercapnia).Control of ventilation due to increased PCO2 Muscles produce more carbon dioxide, blood PCO2 will increase. A very small increase in arterial PCO2 causes a marked reflex increase in ventilation. Arterial PCO2 stabilised near 40mmHg. Carbon dioxide can diffuse across the membranes separating capillary blood and brain tissue thus causing an increase in brain extracellular fluid PCO2. This causes an increase in brain extracellular fluid H+ concentration stimulating central chemoreceptors. Central chemoreceptors stimulate medullary inspiratory neurons to increase ventilation. Holding the breath
A study carried out for the regulation of breathing showed that an increase of carbon dioxide led to an increase in ventilation. Subjects held their breath for a short while and compensatory hyperpnoea followed. Fig. 1 Stethograph tracing. Breath held for 30 seconds. At 20th expiration after breathing began again a sample of alveolar air was taken. CO2 = 4.77%
Fig 2. Breath held 130 seconds after 6 normal breaths of oxygen, at first arrow alveolar CO2 = 8.66%, o2 = 38.22%. At second arrow CO2 = 4.65%.
From the tracings it can be seen that although the alveolar CO2 pressure rose above normal while the breath was held, however, following hyperpnoea the CO2 pressure fell to below normal and only gradually rises to the normal again. The explanation for this is during the holding of breath, the blood becomes charged with the accumulation of CO2. This increase in PCO2 is sensed by the central chemoreceptors by the mechanism mentioned above causing a reflex increase in ventilation, hyperpnoea. After the breathing commences it...
Please join StudyMode to read the full document