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I, hopefully temporarily, moved the following section here, because it is in need of discussion:
The peripheral chemoreceptor's input is usually secondary to CO2 central chemoreceptors in healthy patients, but becomes the primary driver of ventilation in individuals who suffer from chronic hypercapnia (such as emphysema). Non-responsive hypercapnia can induce a tolerance mechanism within the cerebrospinal fluid, effectively negating carbon dioxide as a ventilation stimulus. In major cases this can prevent the use of general anaesthesia, as the carotid body is unable to communicate with the central nervous system sufficiently to stimulate breathing during recovery.
The confusing is that, if basically the carotid body senses oxygen and the central nervous system senses carbon dioxide, then it makes perfect sense that the CNS starts to negate carbon dioxide as a ventilation stimulus during prolonged hypercapnia. However, the last sentence rather says that it is the peripheral receptors, i.e. oxygen sensors, or rather their communication with the CNS, that become nonfunctional during hypercapnia. So, before reinsertion, where is really the problem located? Mikael Häggström 12:56, 7 October 2007 (UTC)