How can Paula be alive with a respiratory rate of only 3 breaths per minute?

Does she have a respiratory acid base disorder? Her routine blood tests and her 02 [pulse oximetry] are normal, very good in fact. Her lung function is great. Her respiratory rate is not. How can this be? She has decreased ventilation and is completely well.

Does Paula have an “ integrated whole body host response‘ to decreased ventilation that we are not aware exists and do not understand? What happens if Paula’s breathing is impeded?

Paula has the same decreased ventilation when ill with infection and viruses. That is not normal; ventilation should increase with the stress of physical illness. Yet in Paula, it does not.

Under conditions of health and under conditions of illness, Paula is unaware of her decreased ventilation and it is not very visible.

When Paula is sick, she has signs of sympathetic activation which does not increase her breathing rate. When she is sick, she has no interest in food or drink, perhaps to slow down the metabolism of fats and carbohydrate to lower the formation of CO2. This approach [even if it is a coordinated and integrated host response] cannot last forever.

Respiratory acidosis

From Wikipedia, the free encyclopedia

Respiratory acidosis is a state in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood’s pH (a condition generally called acidosis).

Carbon dioxide is produced continuously as the body’s cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia). The increase in PaCO2 in turn decreases the HCO3/PaCO2 ratio and decreases pH.

Physiological response

Mechanism

Metabolism rapidly generates a large quantity of volatile acid (H2CO3) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO2. The CO2 combines with H2O to form carbonic acid (H2CO3). The lungs normally excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of CO2 can cause a respiratory acid-base disorder. The PaCO2 is maintained within a range of 35–45 mm Hg in normal states.

Alveolar ventilation is under the control of the respiratory center, which is located in the pons and the medulla. Ventilation is influenced and regulated by chemoreceptors for PaCO2, PaO2, and pH located in the brainstem, and in the aortic and carotid bodies as well as by neural impulses from lung stretch receptors and impulses from the cerebral cortex. Failure of ventilation quickly increases the PaCO2

To understand our ongoing ideas and discussions on mind and loss of mind and the role of PCO2 in the blood and hypercapnia,   please look at our post on     *** a Potential two Step Marker for Bipolar Depressive Illness [to start] and our post on      *** How to Save a Manic Depressive Life.

1] https://ofsoundmind.life/2020/11/09/we-have-a-2-step-marker-for-bipolar-illness/ We have a potential new 2 step biomarker for bipolar illness. Ventilatory issues and [hidden] hypercapnia can cause specific patterns of “odd behaviour”, mood and locomotor activity.    

AND

2]  https://ofsoundmind.life/2020/11/11/how-to-save-a-manic-depressives-life/

At the very least!

Paula and I have identified a ventilatory injury/defect in that I can be most clearly identified in the  depressive stage of manic depressive insanity.  Kraepelin seems to have identified the same injury/defect over 100+ years ago. This is what is guiding us to new research to connect the dots. It is a lot of fun. It is something that scientists can follow up on. And we think this will make a huge difference in the new updated understanding of the reversible syndrome of bipolar illness and its treatment. this is how we have gotten to learn about adenosine and its ability to inhibit respiration rate in the face of hypercapnia.

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