Wednesday, March 15, 2017

-RESPIRATORY FAILURE AND CARBON DIOXIDE NARCOSIS By E. KEITH WESTLAKE, M.A., M.D., M.R.C.P. Senior Medical Registrar, Middlesex Hospital---------My feeling is that the system-especially in continuing care is not experienced in respiratory care or problems. In any case, I have reviewed the litany of these problems over and over again with folks and at least I have a good handle on problems that other folks consider-to be nothing at all--such as day time drowsiness, confusion, decreased oxygen saturations, mood change, memory problems (can't remember what she ate for example), talking to her Teddy Bears, using language she doesn't normally use, the lying in bed like a limp rag, the failure to have the bed upright so she can breathe easier, the lack of BIPAP when she is lying on the bed, the tippiness even with a walker that increases fall propensity--all these symptoms are well known to staff because they write these things down but now why aren't they diagnosing carbon dioxide buildup? Who knows? I will go out for supper. I will enjoy my steak, potato and salad. I will put away the lawsuit and think about the future. The future where I talk to the judge and the public about the continuing care system and the system wide failures in the care of a defenceless handicapped woman who was blamed for a lack of compliance to BIPAP use that she could not follow because guess what? The system was broken and could not figure out that she didn't have the technical ability to tell the system that without proper therapeutic oversight and proper supports in place --a severely handicapped person is set up to fail.



Usually what happens when Rebecca is going into carbon dioxide narcosis is that family informs the system and the system does what it can. I have taken Rebecca to Medicentres and emergency in the past because I don't think the system -at least the continuing care system has the respiratory expertise needed to promptly deal with respiratory emergencies. After all we aren't talking here about a cold. We're talking about the breath of life and death.
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Julie Ali
 feeling happy.
22 mins
I am still in 2010 reading up on the many hospital visits and the preliminary and post nursing notes.
The past is a sort of cereal that I am pouring out into a bowl with the cold milk of the present.
It's doubtful that any of the problems that Rebecca experienced have been solved anywhere in the system.
Why? Well if you don't review data you can't learn from files can you?
Right now I have decided to take a small coffee break. Older boy had a massage and is off to do a movie. Younger boy is slaving away at NAIT.
Tonight we will go out for supper. I don't know where. Older boy is the sort of kid who enjoys life unlike his Puritan mother and so he will make a reservation somewhere and we will eat out. Usually I eat out at a restaurant once a year -and only with older boy.
Older boy is only here for a short time so I have to work on his income taxes tomorrow after he has gone to visit Dr. Kurji.
Dr. Kurji is such a nice dentist. She is keeping both the boys on and she has told us her clinic will keep kids full cycle and not dump them at a certain age as the other paediatric dentist was about to do.
I do not know how Rebecca is doing. I have left her care to the folks at the Villa Marguerite after telling them about the symptoms of carbon dioxide narcosis that I have detected. As is usual for the system they usually do what the system wants to do rather than the blood gas that will confirm carbon dioxide narcosis.
When I have the time tomorrow I will check up on her. Her GP is supposed to be seeing her. I have had Rebecca see facility GPs in the past and what usually happened is that I went to the Medicentre with her and got her diagnosis to give to the facility doctor so that her pneumonia for example could be treated. It's troubling that a stay at home mum has to do the oversight of the system but there you go.
Where was I? I am now in September 2010 where yet again on Sept 27, 2010 I have discovered through a Medicentre that Rebecca has pneumonia. In a previous incident on July 6, 2010 I had taken Rebecca to the Medicentre for a similar diagnosis and meanwhile in the future --in 2013 after the Grey Nuns Hospital dumps her out of ICU on August 21, 2013-- without the least bit of interest in her possible infection--dad has to pick her up and take her to the UAH and then she ends up in the RAH ICU.
Currently I have about 23 emergency, hospital and EMS visits. I am swimming in data. I can't understand these system wide failures. I see everyone blaming the resident who has had cognitive testing to demonstrate memory, attention and follow through problems and yet no one decided to say -hey -maybe we should set up a compliance program? Maybe when she is confused and asking for pain killers this is an indication of respiratory problems that need attention? Maybe someone in the system understands carbon dioxide narcosis? ? ???
If not let me again post the carbon dioxide narcosis paper to indicate that the auditory hallucinations are not psychiatric problems but due to carbon dioxide excess and perhaps low oxygen levels.
https://www.ncbi.nlm.nih.gov/…/P…/pdf/postmedj00494-0004.pdf
RESPIRATORY FAILURE AND
CARBON DIOXIDE NARCOSIS
By E. KEITH WESTLAKE, M.A., M.D., M.R.C.P.
Senior Medical Registrar, Middlesex Hospital
The Clinical Manifestations of Respiratory Failure
The disturbances of blood gas tensions and in
blood pH caused by respiratory failure have pro- found 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 degreesof 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 respi- ratory 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 vaso- dilatation, 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
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.
Many of the features of respiratory failure are illustrated by the following case history: A 63- year-old log sawyer was admitted to hospital on January I2, I955. Apart from a chronic 'smoker's'
cough with scanty mucoid sputum he had been in good health until 1943, when he had a severe attack of acute bronchitis. Since then he had been subject to repeated exacerbations of winter
bronchitis with purulent sputum, headache and
wheeziness. In 195i, he noticed moderate exertional
dyspnoea but this was not severe enough to interfere with his work. On January 3, I955, after walking home in a gale, he felt ill and retired to bed. Subsequently his sputum became purulent and he complained of anorexia, wheeziness, insomina and severe throbbing headaches. On January 7, I955, his practitioner prescribed a four-day course of aureomycin (o.25 g. six-hourly) but despite this he continued to deteriorate, and on
January 9, 1955, was disorientated with rambling speech and hallucinations.
On admission three days later he appeared critically ill. There was
deep cyanosis of the lips and nail beds, the neck
veins were engorged to the angle of the jaw and he
was unable to give any coherent history. Examination
of the fundi showed dilated, tortuous veins
with some blurring of the disc margins but no
retinal haemorrhages. Heart sounds were normal
with a regular tachycardia, rate Ioo. Blood
pressure I 5/55. Mild sacral oedema was present. Respirations were shallow and rapid and on auscultation of the chest coarse rales were audible at both bases with generalized inspiratory and
expiratory rhonchi. The resting ventilation was
6.25 litres per minute (respiratory rate 40 x tidal
air I56 ml.). Analysis of arterial blood confirmed
the clinical diagnosis of severe respiratory failure:
oxygen saturation 44 per cent. (PO2 26 mm.), pCO2 raised to 88 mm. (more than twice normal) and pH reduced to 7.24 (normal range 7.36-7.44). A chest radiograph showed considerable cardiac
enlargement but the lung fields were clear.
Treatment with oxygen, antibiotics, bronchodilators,
nikethamide and corticotrophin resulted
in rapid recovery from respiratory failure and disappearance
of the signs of right heart failure.
Studies on recovery showed that the arterial blood
was still mildly unsaturated (02 saturation 9I.4 per cent.), but that the pCO2 (44 mm.) and pH (7.42) had returned to normal. The resting ventilation was again 6.2 litres per minute but the larger tidal
air (310 ml.) now provided adequate alveolar
ventilation. He subsequently returned to work
and has remained in good health.
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 develop- metnt 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 pneu- mococcal 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 blood
pressure 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 feeling is that the system-especially in continuing care is not experienced in respiratory care or problems. In any case, I have reviewed the litany of these problems over and over again with folks and at least I have a good handle on problems that other folks consider-to be nothing at all--such as day time drowsiness, confusion, decreased oxygen saturations, mood change, memory problems (can't remember what she ate for example), talking to her Teddy Bears, using language she doesn't normally use, the lying in bed like a limp rag, the failure to have the bed upright so she can breathe easier, the lack of BIPAP when she is lying on the bed, the tippiness even with a walker that increases fall propensity--all these symptoms are well known to staff because they write these things down but now why aren't they diagnosing carbon dioxide buildup? Who knows?
I will go out for supper. I will enjoy my steak, potato and salad. I will put away the lawsuit and think about the future. The future where I talk to the judge and the public about the continuing care system and the system wide failures in the care of a defenceless handicapped woman who was blamed for a lack of compliance to BIPAP use that she could not follow because guess what? The system was broken and could not figure out that she didn't have the technical ability to tell the system that without proper therapeutic oversight and proper supports in place --a severely handicapped person is set up to fail.

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