Am I reading the below quote from the other forum correctly? It seems to be saying the centrals are triggered by having O2 levels above what's needed so the body simply doesn't take a breath. Makes sense if the APAP doesn't raise pressure for them, but why then, are they considered a bad thing?
Quote from
The Other Forum:
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Finally (whew, for now I think!) here is how high pressures cause central apneas. I am really out of time and have to get back to my life. But if you want confirmation, do a literature review here, PubMed, or ask any competent physician accredited in sleep disorders:
The major signal to breath is a rise in carbon dioxide levels. CO2 and H+ concentration (which refers to pH and related to the level of CO2) levels in cerebral spinal fluid are detected by a chemoreceptor in the brain’s medulla called the Central Chemoreceptor. Additionally, an increase in blood CO2 is detected by the Peripheral Chemoreceptors located in the aorta and carotid arteries (called the aorta and carotid bodies). The peripheral chemoreceptors also detect O2 levels.
If a CPAP pressure is too high, then CO2 is literally “blown off” and the signal to the brain to breath is removed until either the oxygen level drops to a trigger level or the CO2 level rises again. Here are the blood levels (called the Threshold) that trigger the response to breath:
The threshold pO2 for activation is 60 - 80 mmHg with normal arterial pO2 about 95 mmHg. Any elevation of pCO2 above a normal value of 40 mmHg, or a decrease in pH below 7.4 causes chemoreceptor firing.
Vicki
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