How does apnea trigger the urge to breathe?

Question

I am thinking of writing about Obstructive Sleep Apnoea (UK spelling for apnea) out of interest in the condition (not a medical textbook).

During deep sleep, in persons with a narrow airway, the back of the tongue can fall back as muscles relax and obstruct the airway. As I understand it, when this happens, and airway is completely blocked so that breathing stops, the blood oxygen level (SpO2) falls over the next 1-2 minutes and the CO2 level rises until the brain detects that the CO2 level is too high (not that the O2 is too low, as I previously thought), and I believe it triggers the sympathetic nervous system to deliver adrenaline to the body, which, amongst other things, tends to wake one out of deep sleep into light sleep where breathing can occur again (until the body falls back into deep sleep again, where the problem happens again.

What I would like to know, is what is the mechanism by which this happens - how does the brain detect high CO2 or low blood oxygen and then trigger the response?

This Wikipedia page says:

the adrenal medulla produces a hormonal cascade that results in the secretion of catecholamines, especially norepinephrine and epinephrine.[4] The hormones estrogen, testosterone, and cortisol, as well as the neurotransmitters dopamine and serotonin, also affect how organisms react to stress.[5] The hormone osteocalcin might also play a part.[6][7]

so perhaps it is a function of the adrenal medulla? But I cannot find any reference to how it, or any other part of the brain, might detect high CO2 (or low O2).

Answer 1

Medulla is the part of brain which controls respiration. There is a special chemosensitive area in ventrolateral medulla which has chemoreceptors to detect increased CO2 or Hydrogen ions in brain fluid (CSF). similar chemoreceptors are also present in our carotid arteries and aorta. These chemoreceptors, when stimulated by their specific stimulus (CO2 in this case), initiate a series of neuronal firing (action potentials) to other parts of medulla which control respiratory muscles, so as to increase the respiratory rate. It also sends signals to Reticular activating system which causes arousal from sleep. Additionally, medulla also activates sympathetic nervous system (via neuronal firing) which cause release of catecholamines from nerve endings as well as from adrenal medulla. These hormones in return cause increase in blood pressure and heart rate. Additionally, the peripheral chemoreceptors (carotid and aortic) are also sensitive to hypoxemia (low pO2 in blood). I hope that clears your confusion.

REFERENCES: (This is a concised answer from alot of sources, main references are these)

1.Hall, J. E. (2015). Guyton and hall textbook of medical physiology (13th ed.). W B Saunders. (I am not sure if its available online, I used the hardcopy)

2. https://thorax.bmj.com/content/50/7/797?ijkey=cfa9ca75014668299646345b44e52a4966c52970&keytype2=tf_ipsecsha

3.https://thorax.bmj.com/content/59/2/159.full

4.https://physoc.onlinelibrary.wiley.com/doi/10.1113/jphysiol.2005.095968

5.https://med.libretexts.org/Bookshelves/Anatomy_and_Physiology/Anatomy_and_Physiology_(Boundless)/21%3A_Respiratory_System/21.10%3A_Respiration_Control/21.10C%3A_Chemoreceptor_Regulation_of_Breathing

6.https://www.researchgate.net/publication/320891657_Obesity_Cardiovascular_Disease_and_Sleep_Disorders_Insights_into_the_Rising_Epidemic

Answer 2

The term for "high CO2" is "partial CO2 pressure (PaCO2)". During hypoxemia -a condition that commonly occurs during apneas- arterial PaCO2 is increased, and arterial PaO2 decreased, which activates the chemoreceptor reflex.³ Chemoreceptors are special nerve cells that can detect changes in the chemical composition of the blood.

There are two kinds of respiratory chemoreceptors: the central chemoreceptors (CC) located in the brain that you mention in your question, and the peripheral or arterial chemoreceptors (PC), located in the bifurcation of the carotid artery. Both sense PaO2, PaCO2 and pH.

The PC are the main chemoreceptors to regulate respiratory activity.² The mechanism for detecting reductions in PO2 has yet to be identified.⁴

The CC detects changes in pH in the cerebrospinal fluid. With increased PaCO2, more CO2 will form carbonic acid (H2CO3) that lowers the pH. Thus, an increase in PaCO2 would stimulate chemoreceptors, which would increase alveolar ventilation.⁶

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1. 2017 - Carotid Body and Carotid Sinus -- General Information https://medicine.uiowa.edu/iowaprotocols/carotid-body-and-carotid-sinus-general-information
2. Iturriaga et al. 2016 - Carotid body chemoreceptors, sympathetic neural activation, and cardiometabolic disease https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768417/
3. Lindsey et al. 2018 - Carotid Bodies and the Integrated Cardiorespiratory Response to Hypoxia https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6088141
4. Ward et al. 2008 - Oxygen sensors in context https://www.sciencedirect.com/science/article/pii/S0005272807002496
5. Eugene et al. 2012 - Central Chemoreceptors: Locations and Functions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802370/ There are 15 references in the original text that I omitted for brevity.
6. Nattie et al. 2012 - Central Chemoreceptors: Locations and Functions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802370/

Inb4: I am a real human being and not an LLM