Metabolic mechanisms compensate for respiratory disturbances.

If the complex motor respiratory system [not necessarily the lungs] get injured, then the kidneys and the rest of the body will have to work harder in order to compensate. Please read about the Renal compensation for a primary respiratory disturbance:  ” Here, the kidney alters excretion of acid (excrete an acid, gain a base; retain an acid, excrete a base) in response to primary respiratory disturbances. This begins within hours of an acute respiratory disturbance, but take several days (3-5 days) to take full effect.

This happened to Paula at birth, when her airways were blocked by meconium and she needed life saving manoeuvres. Whether her respiratory defect or injury today is acquired or genetic makes no difference to Paula. It means that any future load on the respiratory system, such that it is, will require some form of resuscitation once more. this is why it is important to screen for such injuries. And it only takes one minute and a stop watch, first aid style, to measure respiratory rate and I’m sure we could measure minute volume using portable medical tools if we wanted to. So what is stopping us now that we realize that people like Paula do not know that they have this kind of injury limiting their defence against significant retention of carbon dioxide??

Paula and I don’t get it.

Paula is like the naked mole rat…..The naked mole rat cannot exist physiologically; and yet it does exist, very well thank you. There is a lot of science to learn from this!

Isn’t anyone out there interested in science???

Or are they only interested in what has been found in textbooks that do not include new and provocative findings, pushing the envelope of knowledge and benefitting mankind [or at least patients like Paula].

  • Correction of a primary respiratory acid-base abnormality usually requires medical or surgical intervention of the primary problem causing the acid-base disturbance, e.g. surgical relief of a collapsed trachea that is causing a primary respiratory acidosis (this is because the lungs cannot correct themselves, but need help to do so). Once the collapsed trachea is resolved, the lungs can rapidly blow off accumulated carbon dioxide.from

In Paula’s case, as well as others with exacerbation of an acquired or congenital primary respiratory motor problem affecting how people breathe, will cause a primary respiratory acidosis requiring supportive medical care. But doctors have not figured this out yet. Why? Because they have forgotten the wide range of breathing rates and depths seen in the normal healthy adult population.

In Paula’s case, what would happen if she developed an acute kidney injury? Well, her kidney would not be able to compensate for her respiratory defect any longer and she would be in immediate trouble.

Hypercapnia also may have metabolic and endocrine effects. At high levels of PCO2, constriction of the renal afferent arteriole may cause acute kidney injury and a decrease in urine output. Hypercapnia may cause increased sodium and water retention, as well as hyperkalemia. The anterior pituitary may be stimulated by increased CO2, leading to increased ACTH secretion.4 Hypoventilation Meredith L. Daly VMD, DACVECC, in Small Animal Critical Care Medicine (Second Edition), 2015

This is what we think happened when Paula suddenly got sick and confused.

Acute kidney injury can have many different causes. The National Kidney Foundation explains that Decreased blood flow  can slow blood flow to your kidneys and cause AKI.

Paula had cool, pale even blue feet and hands, indicating the decreased blood flow due to vasoconstriction. The most likely explanation for her prolonged vasoconstriction is as a reaction to her mild endogenous hypothermia, but this doesn’t rule out the body trying to prevent and contain hidden bleeding in the brain and body. The consequences of acute kidney failure in a person with too slow breathing at rest is unknown and needs to be thought out. It is likely that slowed breathing at rest makes it harder to maintain normal body temperature or to produce fever.

Signs and symptoms of acute kidney injury differ depending on the cause and may include: Paula had me put the symptoms she remembers in BOLD.

  • Too little urine leaving the body
  • Swelling in legs, ankles, and around the eyes
  • Fatigue or tiredness
  • Shortness of breath [unable to talk more than a few words; unaware of sensation regarding any disturbance to breathing due to neural [we assume] damage incurred at birth]
  • Confusion
  • Nausea
  • Seizures or coma in severe cases
  • Chest pain or pressure.

In some cases, AKI causes no symptoms and is only found through other tests done by your healthcare provider.

The National Kidney Foundation also gives us a clue as to why acute kidney inhere attacks re-occur later on; [especially, one would think, if respiratory rate and volume is already compromised in health], ” After having AKI, your chances are higher for other health problems (such as kidney disease, stroke, heart disease) or having AKI again in the future. The chances for developing kidney disease and kidney failure increase every time AKI occurs. To protect yourself, you should follow up with your healthcare provider to keep track of your kidney function and recovery. The best ways to lower your chances of having kidney damage and to save kidney function are to prevent acute kidney injury or to find and treat it as early as possible.

So patients like Paula should be monitored carefully for AKI during their entire lives, because the risk of another kidney attack is increased after the first, and it is likely that Paula will not be able to communicate properly if it happens again….Should she become mentally confused again or begin to look “like a psychiatric” patient, doctors should get an arterial blood gas test to check for hypercapnia repsiratory failure, as well as acute kidney injury requiring supportive medical treatment; something these patients will not get in a psychiatric hospital…..until the psychiatric culture begins to change, upon realizing that they have never considered the possibility of injured patients requiring outpatient or inpatient critical care during reversible failure of a second organ.

Welcome to the 21st Century folks!


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