Letters to researchers suggesting simpler, more basic reasons why they are finding what they are finding

Could simply measuring respiratory rate [as a start] at rest in unmedicated people suffering from major depression with psychomotor retardation  lead to the reason [eg hypercapnia] why you [the researcher] found …………….[fill in the blanks eg, cortical glial damage, essential hypertension, visual changes, etc….]………… in your studies?

Please look at the evolution of our discoveries as we examine how and why Paula may have had a debilitating episode of major depression. and [ and manic reactions to  medication after one year].  Paula remember what happened very well, now that she is fine. She now remembers what she could not retain for more than a few seconds when she was ill and incapacitated. Wow! How can that be?

I discuss in some of the earlier blogs how to try to replicate [or not] some of Kraepelin’s conclusions based on his basic measurements of basic vital signs- respiratory rate at rest, blood pressure, heart rate [and signs] and body temperature.  he seems to describe a response to ventilatory failure and possible hypercapnia and reduction of need for oxygen, in order to maintain baseline homeostasis, even at the cost of higher functioning of the brain [and mind.  The loss of the connection between having a thought and speaking or acting on the thought is unpleasant but it does keep you pretty immobile….and this lack of locomotor activity will lower body temperature [[as Kraepelin notes when he looks at the pattern of vital signs in his unmedicated patients in the depressive stage] and the reduced awareness of hunger or thirst or any other bodily needs ]urinating or defecating-which are also inhibited] will also allow the autonomic nervous system to reflexibly monitor and control all body functions and hormonal release in order to keep the patient upright [helps breathing] and able to follow others if necessary [helpful in order to follow the crowd in an emergency] and maintain homeostasis and metabolism well enough to keep the patient alive for a long time, allowing for possible reversible of this condition.  And Kraepelin noted spontaneous recovery of most of the vital signs [except normal range of respiratory rate] and baseline mental status [although without treatments it might take decades of illness and lost time and lost living and sometimes outright cardiorespiratory collapse and death, in these mostly young and healthy people, in what should be the prime of their lives. 

I am interested in the motor aspect of breathing and its disturbance.Doctors and researchers do not often measure ventilatory rates at rest and tidal volume and minute ventilation [in ambulatory patients, no matter how mentally confused they may be or how bad they feel]] .yet the skeletal muscle/nerve system moving air in and out of the body is susceptible to injury at any time during one’s lifetime, perhaps especially during difficult birth conditions.
I have learnt recently that physiologists of the 1940’s were aware that the range of respiratory rates at rest is very wide; from as low as 3-5 breaths per minute to as high as 30 in healthy adults.Modern doctors do not measure respiratory rates and tidal volumes and have forgotten this.   [they have begun to look at respiratory rates in hospitalized patients recently because they are realizing abnormal rates can predict physiological deterioration]. 
It seems to me that those at either extreme of this range of breathing rates are at risk of ventilatory failure [with normal lungs] during difficult respiratory conditions due to illness, injury, or exposure to higher levels of CO2 in the air.
My friend Paula is one of these people. We found out at a basic first aid class 20 years ago that her average respiratory rate at rest during health is 3-5 breaths per minute. She had no idea. Neither did anyone else. It does not show at all. 
 We have gotten her tested this year and her average tidal volume is 750-850ml which is larger than average and her minute ventilation is adequate for good health. 
Paula is prone to ventilatory hypercapnic failure, we think, and was misdiagnosed with major depression during an attack she had after several minor viral illnesses, loss of weight due to loss of appetite, exposure to a workplace that was overcrowded, poorly ventilated and rundown and old and mouldy and also after the hormonal changes of menopause. [estrogen and breathing seem to be related].
Paula became quietly mentally confused for over a year, had very high blood pressure, a fast heart rate with intermittent arrhythmias and murmurs, mild hypothermia and cold pale extremities .  Her breathing rate remained depressed.  We think that she could not maintain her larger tidal volume because she was weakened by illness and exposure.  She normally uses abdominal muscles to help push air out so that she can take more air in, albeit slowly and this takes sustained effort for each and every breath. .
Hypercapnia can cause cerebral hyper-perfusion and increased intracranial pressure and often arterial blood pressure is raised to preserve cerebral blood flow.  This is what we think happened. 
Yet no one but I knew this and no one would listen because she looked depressed and no one measured her basic vital signs, especially not breathing rate or minute ventilation. They just jumped to conclusions due to stereotyped behavior and appearance.
Paula’s  routine blood tests were normal because ventilatory failure with normal lungs may not affect these blood tests.  Even arterial blood gas tests may be preserved in ventilatory failure with normal lungs until late in the process.   Or perhaps ABG tests might have shown a higher level of PaCO2.   No one ordered this test either so we missed the chance to investigate.   No one except both of us knew how cognitively impaired she was. Her depression was in retrospect, most likely a sensation of dyspnea- difficulty breathing, a sensation known to often be invisible like pain, and known to be unbearable and very distressing [same for major depression apparently]..Paula was very distressed, very cognitively impaired and could not speak more than 2-3 words before feeling short of breath [which is not visible with depressed breathing].  She did not recognize this sensation as having to do with her breathing.
When healthy, she is also not aware of her depressed breathing and active exhaling- she thought she was normal and that breathing was supposed to take a lot of effort.
All to say, I do not know why researchers and doctors interested in autonomic nervous system injuries do not measure respiratory rate , blood pressure, heart rate and body temperature to see the pattern at rest, and to look for abnormal patterns.
When Paula recovered finally, all her vital signs returned to normal, including her cognitive ability and mood- except of course, for her depressed breathing, which seems to be a nonprogressive permanent injury. She probably sustained this injury during her difficult birth and successful resuscitation. 
Over 100 years ago, a famous doctor-Dr Emile Kraepelin, found depressed breathing rates in bipolar patients in the depressive stages.  Like Paula, when reversibly quietly delirious-which is what depressive insanity is, we think, the depressed breathing was accompanied by high blood pressure, fast heart rate, arrhythmias, murmurs, mild hypothermia and cold pale extremities.  We think that these patients must have had intracranial hypertension which when it worsened resulted in manic signs.  In mania breathing became irregular , Kraepelin reported, and patients had intermittent bradycardia lower but still raised blood pressure and ruddy red faces, and hyperthermia.    No medications existed then.   Kraepelin followed these patients for decades and was intrigued because even after years of depression and mania [or chronic hypo and hyper locomotor subtypes of metabolic dysfunction and delirium, we think] most patients spontaneously remitted and went home , and regained their baseline mental status.  Kraepelin was hopeful that treatments of the future would speed up their recovery and prevent relapse.
Unfortunately, after Kraepelin, no one bothered to measure the vital signs of these or any other delrious or demented patients to look for abnormal vital signs and treatable conditions [with modern supportive medical care of course- availible today].
So I hope you will look into depressed ventilatory rates at rest [or chronically high ventilatory rates at rest] and their limitations during difficult breathing conditions and the risk of respiratory failure and metabolic dysfunction that is hidden until unmasked by measurement and a little thought.
I think that abnormal and rigid breathing rates and limited ability to compensate for respiratory acidosis or alkalosis is common, either due to a respiratory nonprogressive injury or defect or due to aging and becoming physically weaker and having increased difficulty moving air in and out of even healthy lungs.

And I think that this might explain the changes to vision, and to essential hypertension, glial damage and more…….

Simply see if depressed ventilation at rest is linked to your [researchers] findings and provide an essential new [old] hypothesis same as Kraepelin proposed. ……..It is that simple


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