Thursday, March 9, 2017

"Come Alive (Dry Bones)" featuring Lauren Daigle - Live from the CentricWorship Retreat

Where is the army raised up to fight the government of Alberta about the failures in the continuing care system? Is there only Dr. Edward Redshaw and this stay at home mummy holding the GOA accountable? What the heck?

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I went to the Villa Marguerite but Rebecca was not very peppy.
I asked the nursing staff to set her up on the BiPAP and then I stayed from 1:30 to about 3:15 to wait out the time.
I was sleepy and so  I was dozing on a chair next to her.

She was a trifle better when I left to get the nursing staff to free her from the mask.
On the way home there were ten million cars on the Whitemud freeway.

When I got home I put the rice in the cooker as I want to make a stirfry with the limp broccoli and the mushrooms.

The sun is beating a froth of light outside my toasty writing room. I have a wall of green on one side where the geraniums are making a lattice of leaves.  I haven't watered them so they think it is extinction time and are producing blooms for the next generation of seeds.
Even my Canada Day cuttings are finally deciding to push out blooms.

I have another wall of posters. Most of them are odd pictures I have picked up at garage sales.  It's not as if I have any idea of art but I do know what I love.

Because I missed lunch I made do with some Red River cereal from days ago. It was reheated and mashed up and eaten.

Well I better go back to the lawsuit. I have so much information I begin to feel like a bank for continuing care information and carbon dioxide narcosis. Did you know that beyond a certain point of CO2 you begin to have auditory hallucinations? If you want to read further on this fascinating topic here is the reference:


The Diagnosis of Respiratory Failure Clinical recognition of alveolar hypoventilation may be difficult and the only certain method of diagnosis is the demonstration of a raised level of pCO2.
This is most conveniently achieved by analysis of arterial blood since the pCO2 of alveolar air and arterial blood are virtually identical. With practice, samples of arterial blood can be readily obtained by puncture of the brachial artery under local analgesia. Direct determination of both pCO2 and pO2 in arterial blood can be made by the bubble equilibration technique devised by Riley. This method has been extensively used in respiratory research but is technically too difficult for routine use in a biochemical laboratory. However, arterial pCO2 can be accurately estimated by an indirect method. Blood pH, pCO2 and total plasma CO2 content are related by the wellknown Henderson-Hasselbalch equation. If any two of these variables are known, then the third can be calculated. Thus, rearranging the equation: Total plasma CO2 content mM/L pCO2 = - 0.03 x (antilog blood pH - 6.09) + i

Total plasma CO2 content is measured by the manometric method of Van Slyke and Neill (1924) and blood pH with a glass electrode and pH meter. Practical details for measuring blood pH at body temperature are to be found in the papers of Wilson (1951), Severinghaus, Stupfel and Bradley (1956) and Wynn and Ludbrook (I957).

The Clinical Manifestations of Respiratory Failure The disturbances of blood gas tensions and in blood pH caused by respiratory failure have profound physiological effects on the brain, cerebral vessels, heart and lungs and are responsible for the appearance of certain characteristic signs and symptoms which may make a bed-side diagnosis of respiratory failure possible.

Mental disturbance in respiratory failure varies with its severity. In mild cases the patient may be euphoric or mildly confused. More severe degrees of hypoxaemia and hypercapnia cause pro- gressive deterioration in mental function with visual and auditory hallucinations, delusions, stupor and finally coma. Although disturbed mental function is principally due to cerebral anoxia (Simpson, 1957), the effects of hyper- capnia and acidaemia on the brain should not be neglected. The effect of breathing Ioo per cent. oxygen shows that hypoxaemia is only one of the factors concerned since the patient in respiratory failure, although considerably improved, often remains confused and disorientated despite full saturation of the arterial blood with oxygen. If mental disturbance were solely due to hypoxaemia, an immediate return to mental clarity would be expected. Impaired memory is usual during a period of respiratory failure, even in the absence of obvious mental disturbance. After recovery from an acute respiratory infection, careful enquiry will often reveal that the patient has complete amnesia (lasting days or even a week or two) for the early phase of his illness, although at the time, he may have appeared alert and rational. Muscular twitching is another common neurological manifestation of respiratory failure. It consists of coarse, irregular, jerky movements of the fingers, arms and facial muscles and, less frequently of the trunk and legs. Similar movements have been observed in normal subjects exposed to severe anoxia. A low arterial pO2, high pCO2 and low pH all cause dilatation of the cerebral and retinal vessels, the volume of blood within the skull is increased and in consequence the C.S.F. pressure rises. In 12 emphysematous patients studied during respiratory infections (Westlake and Kaye, 1954), the C.S.F. pressure was above the upper limit of normal (200 mm.) in ten, and in five subjects it was over 350 mm. The highest pressure recorded was 600 mm. Raised intracranial pressure due to respiratory failure is frequently associated with a severe throbbing type of headache and in a few patients, frank papilloedema appears, with measurable swelling of the nerve head, gross dilatation of the retinal veins and flame-shaped haemorrhages. Papilloedema as a complication of emphysema was first described by Cameron (I933), and although some authors have attributed the phenomenon to raised venous pressure (Beaumont and Hearn, 1948), the work of Simpson (1948) leaves no doubt that the primary cause is cerebral vasodilatation consequent to respiratory failure, although in some cases raised jugular venous pressure may be a contributory factor. The combination of mental disturbance, headache and papilloedema may lead to an erroneous diagnosis of cerebral tumour as in the cases reported by Meadows (1947) and Conn et al. (1957). While respiratory failure causes cerebral vasodilatation, it has the opposite effect on the pulmonary arterioles and the pulmonary artery pressure rises (Whitaker, 1954). In patients with pre-existing hypertrophy of the right ventricle (cor pulmonale) the sudden increase in pulmonary artery pressure that occurs during acute respiratory infections frequently precipitates heart failure with dilatation of the right ventricle, the appearance of gallop rhythm (best heard over the xiphisternum), raised venous pressure and peripheral oedema(Stone et al., 1953; Fulton, 1953; Flint, 1954). The cardiac output is usually normal or even moderately raised (Ferrer et al., 1950; Mounsey et al., I952) and this, together with the vasodilator effect of hypoxaemia and hypercapnia on the small vessels of the limbs, is responsible for the warm extremities and bounding pulse present during episodes of congestive failure-in contrast to congestive failure in mitral stenosis, hypertension or ischaemic heart disease where the cardiac output is low and the extremities cold. As might be expected, congestive failure is most likely to occur when respiratory failure is severe. From Fig. i, it can be seen that of 1 patients with an arterial oxygen saturation below 55 per cent. and pCO2 above 70 mm., signs of heart failure were absent in only three.

Carbon Dioxide Narcosis In respiratory failure, there is a shift in the control of pulmonary ventilation from the medullary respiratory centre to the peripheral chemoreceptors of the carotid and aortic bodies. With rising arterial pCO2, the respiratory centre becomes less and less sensitive to the stimulus of carbon dioxide (Scott, 1920; Tenney, 1954; Prime and Westlake, 1954; Fishman et al., I955) and ventilation is increasingly maintained by the stimulus of hypoxaemia acting via the carotid and aortic chemoreceptors. Breathing high concentrations of oxygen abolishes the anoxic stimulus to breathing with the inevitable consequence that alveolar and arterial pCO2 levels are raised and arterial pH lowered still further. It is this phenomenon that is responsible for the development of carbon dioxide narcosis during oxygen therapy (Barach, 1935; Donald, I949; Comroe, Bahnson and Coates, 1950; Cohn, Carroll and Riley, 1954; Westlake, Simpson and Kaye, 1955; Sieker and Hickam, 1956). A typical example is illustrated in Fig. 2. The patient, a 62-year-old emphysematous man developed an acute pneumococcal bronchitis with moderately severe respiratory failure: oxygen saturation 64 per cent. (pO2 38 mm.), pCO2 72 mm. and pH. 7.26. On admission to hospital he was rational and orientated but within four hours of being placed in an oxygen tent he had lapsed into a semicomatose state with profuse sweating and coarse myoclonic jerking of the arms. Arterial blood showed that the pCO2 had risen to 105 mm. with fall in pH to 7.I3 (equivalent to the inhalation of 15 per cent. carbon dioxide by a normal subject). Over succeeding days, the arterial pH gradually returned toward normal values and the arterial pCO2 fell to 90 mm. Myoclonic jerking ceased and the patient regained consciousness but remained unduly drowsy. Throughout the period of oxygen therapy, the arterial blood remained fully saturated with oxygen. A broad correlation has been established between arterial pCO2, pH and mental state. Westlake, Simpson and Kaye (I955) found that mental disturbance was usually present when the arterial pH was less than 7.2 or the pCO2 above 100 mm., and coma when the pH fell below 7.1 or the pCO2 rose above 120 mm. Most patients were conscious and rational if the pH was above 7.3 or pCO2 less than 80 mm. These observations have been substantially confirmed by Sieker and Hickam (1956). They observed that there was usually no significant abnormality in mental state if the pCO2 was less than 90 mm. and the pH above 7.25. Semi-coma or coma were always observed when the pCO2 rose above I30 mm. and pH fell below 7.14. In general, the critical level for loss of consciousness in carbon dioxide intoxication is at a pH of 7.1-7.14 and pCO2 of I20-130 mm., although increased susceptibility to the narcotic action of carbon dioxide may be found in individual cases. Motor phenomena are common during carbon dioxide intoxication. They usually consist of fine tremors of the fingers, arms and facial muscles (Waters, 1937), but severe clonic movements of the limbs and generalized convulsions have been observed (Sieker and Hickam, 1956). The C.S.F. pressure often rises (Davies and Mackinnon, 1949; Westlake and Kaye, I954)-despite relief of anoxic cerebral vasodilatation-and papilloedema may make its first appearance during oxygen therapy. Carbon dioxide intoxication also causes tachy- cardia, sweating, skin vasodilatation and alterations in blood pressure. In the early stage the bloodpressure may rise, but more severe degrees of hypercapnia and acidaemia are usually associated with a profound fall in blood pressure. Prolonged narcosis frequently causes death from respiratory depression.
My entire reading program for the next few years will be on medical problems associated with respiratory failure. This sort of review explains many of the symptoms I am finding in the nursing notes.

Once I have done my daily dose of review of the medical file I will go and write poetry. It is best to do the hard stuff first since no will be around to help me as I go through the process of a lawsuit. I still do not have the Health Quality Audit done in October 2014 that Alberta Health has not given me. I don't know why they won't give me this information since they have given me the CCHSS standards audit with the many non-compliances that was done in January 2015.  AHS has not given me the respiratory review of the facility either. Maybe the AHS review of the respiratory services was not very thorough?  Maybe the folks at AHS simply go have coffee and fart around instead of providing us with deliverables? There are so few of us holding government accountable.  But at least I am not alone. Here is Dr. Redshaw beating on the same drum:

From: Edward Redshaw <
Date: Fri, Feb 24, 2017 at 11:55 AM
Subject: Long-Term Care
Cc:, >,,,,, ,,, Advocate Seniors <>

Dear Honourable Premier:

Re: "We're not out of the woods yet, far from it,", Ceci says.

Honourable Ceci says "Operating expenses in the health ministry are forecast to be $284 million more than budgeted, due partly to growth in the number of physicians".

I do believe that in light of the past actions of the Health Minister and Alberta Health Services in providing extreme preferential treatment to physicians (acute care) that the word "partly" in the foregoing should more accurately read "primarily".

This would be in keeping with the fact that acute care in Alberta is funded 35% more that the national average while continuing care is funded 21% less than the national average. This could even be worse now.

 Based on my personal observations the quality of care provided by overworked, overwhelmed care workers in long-term care facilities is on the decline. This is primarily the result of your funding system currently in place.

Sadly, the Health Minister and Alberta Health Services has conscienceless cut this to the bone. It is obvious that with the now established "Level System" human souls entering the Long-Term Care Level are regarded as a disposable liability.

Even though your government will definitely be replaced in the next election you have, unfortunately, set in place a system that will be continued by Alberta Health Services into the next government.

I recently received through FOIP 264 pages of minutes from Continuing Care Meetings for the period May 2015 to August 2016. It is of interest to note the conspicuous absence of the Health Minister and the AHS CEO from these meetings. Further, there is no mention of Long-Term Care problems in these meetings. It is obvious that these meetings provide little more than an outlet for AHS and anything in regards to long-term care is like rearranging chairs on the deck of the Titanic. Personally it is my belief that these meetings provide a coffee break opportunity and an excuse to get out of the office.

This communication, like all those preceding it, will be just an exercise in frustration in communication attempts with your government. You and your Health Minister and AHS will blindly ignore the current disastrous Long-Term Care situation and carry on happily with your other vote buying projects.

Dr. Edward S. Redshaw.

Sent from my iPhone

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