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Welcome! This is the first in a series of discussions which provide practice in interpreting blood gas results in a clinical context. Most of the case scenarios will have an emphasis on Anaesthetic or Intensive Care practice but interesting gas results on other patients that I come across may be included. Most of the results are ones you could typically come across in your daily practice so the emphasis is not on finding strange or extreme results though some unusual results may be included. Perhaps you have come across an 'interesting gas' - please feel free to send this along to me at firstname.lastname@example.org. The method of analysis used here is that presented in my Acid-Base text.
Please consider the following clinical scenario and then consider the question & discussions that follow.
 How would you analyse these results?
Consultant (to Registrar)
These are the 3 possibilities or patterns that I am checking for. In this case: the pCO2 is low (32mmHg as compared to a normal value of 40mmHg) and the bicarbonate at 25mmol/l is close to the normal value of 24mmol/l. I would consider this then to match the third pattern. A low pCO2 with a normal bicarbonate: this means the alkalosis I detected in step 1 is a respiratory alkalosis and not a metabolic alkalosis. With a metabolic alkalosis, the bicarbonate would be increased but it is still in the normal range here.
3. Clues : The other results reported on the blood gas machine are all within the reference range. The recent preoperative results are all normal and the anion gap is also normal at 10mmol/l. So there is nothing here that alerts a suspicion of anything else.
4. Compensation for an acute respiratory alkalosis is assessed using the 2 for 10 rule ie I would expect the plasma bicarbonate to decrease by 2mmol/l for every 10mmHg decrease in pCO2. So at 32mmHg - this is close to a 10mmHg decrease so the bicarbonate should decrease by almost 2 from the standard normal value of 24mmol/l - that is, to 22mmol/l. Now at 25 mmol/l it is slightly higher then I would predict so it looks like there is indeed a mild metabolic alkalosis present. This is small but explains why the pH is a little higher than expected for a pCO2 of 32mmHg. I hadn't considered this much in step 2 as I was comparing the actual value against the 'normal' value of 24mmol/l but I should have been comparing the 'actual' value against the 'expected value' of 22mmol/l.
5. So the diagnosis I would make is a respiratory alkalosis and a mild metabolic alkalosis as well.
6. Confirmation: For this particular acid-base situation there is really no reason to look for confirmation in other biochemistry results
The pO2 doesnt tell me anything about the acid-base status, only about the amount of oxygen in the arterial blood.
Of course, other results provide useful supportive information. As you know, I have for example used the electrolyte and other biochemical results to check the acid-base results. This is useful because certain acid-base disorders cause changes in these and can help me make the diagnosis. For example, if a metabolic acidosis was present, then I would use the anion gap to differentiate the types of metabolic acidosis.
But there is also the 5 for 10 rule for a chronic respiratory alkalosis.
Why didnt you use this other rule instead? If you had then you would have predicted a bicarbonate result of (24 minus 5) or 19mmol/l - this then is quite different from the actual bicarbonate result of 25mmol/l and would give good evidence that a more marked metabolic alkalosis was present.
The 3 components of this analysis are:
Initial Clinical Assessment
i. From the history, examination &
initial investigations, you can make a clinical decision about what is the most likely
Secondly: Make an Acid-Base Diagnosis
Finally: Make a Clinical Diagnosis
& act upon it.
The 3 components are:
What you did was incomplete as you only carried out the middle step of making an acid-base diagnosis.
So would you like to try again using this more complete approach?
Firstly: The Clinical Assessment.
A supratentorial tumour grows within the fixed volume cranial cavity but ICP does not initially rise because of compensatory processes, particularly CSF translocation (ie the tumour grows and CSF moves out into the spinal subarachnoid space and the ventricles become smaller). Oedema surrounding the tumour also contributes.
A posterior fossa tumour can obstruct CSF drainage in the narrower confines of the posterior fossa and cause raised ICP. This can occur earlier (as the space is smaller) and as the problem is obstruction then the ventricles are large, rather than small.
In this patient I know that there is little clinical evidence of raised pressure (eg no vomiting or papilloedema, but there is a headache) and the MRI & CT scans do not show obstruction as the ventricles are normal in size. Additionally the patient is on dexamethasone which reduces oedema surrounding a cerebral tumour. The patient is also on ranitidine so even if vomiting were present then there is little chance of a significant metabolic acidosis occurring. The preoperative electrolyte profile shows a normal bicarbonate which is against the presence of any significant metabolic disorder.
She is talking normally and is not mentally obtunded. There is no clinical evidence of respiratory depression so no suspicion of a respiratory acid-base disorder.
Overall, there is no preoperative evidence of a pre-existing acid-base disorder.
At the time of collection of the gases, the patient is anaesthetised, paralysed and ventilated with a pCO2 of 29mmHg and stable haemodynamics. As the patient was in good cardiorespiratory health I would expect the arterial pCO2 to be higher then this, perhaps by 2 to 8mmHg. I usually work on an expectation of 5mmHg based on an old study I think by Nunn. So possibly an arterial pCO2 of about 34mmHg or so. This would lead me to expect that the arterial blood gas would show a respiratory alkalosis, and it would be acute and mild.
Now: the putting it all together phase:
Making a Clinical Diagnosis.
paCO2 = k . VCO2 / VA
where VCO2 is body CO2 production per minute, VA is alveolar ventilation & k represents the proportionality constant. So theoretically a decreased CO2 production could also be a cause of a low arterial pCO2 but in practice this is virtually never the case.
Excessive vasoconstriction is avoided as this could compromise cerebral oxygenation and could lead to postoperative increased cerebral blood flow. This is because compensation would occur with a lowered brain interstitial fluid bicarbonate which would start returning the brain ISF pH towards normal. At the end of the operation then, a normal arterial pCO2 would result in an an increase in cerebral blood flow (and in intracranial pressure). The decreased brain ISF pH due to the normal arterial pCO2 will now stimulate the respiratory centre and this will counteract the effect. However, postoperatively, respiration may be depressed by the residual effects of the anaesthetic agents and by opioids so this increased ventilation response may be obtunded.
Now the situation with expired gas is that it can be considered to be a mixture of this alveolar gas from these perfused alveoli COMBINED with the gas that comes from any unperfused alveoli. Such unperfused alveoli are of course known as the alveolar dead space and the pCO2 composition of this gas is virtually zero. So the mixing of gas from perfused alveoli (pCO2 = paCO2) with gas from the alveolar dead space (pCO2 = 0) results in a lowering of the end-tidal pCO2. (It is at the end of expiration that the gas from the different alveoli mix, so an end-tidal sample contains the mixture of these gases).
The net result is that end-tidal pCO2 is lower than arterial pCO2. In healthy young people (who have little alveolar dead space) the (a-ET)pCO2 gradient is small, typically 2 to 5 mmHg. Under general anaesthesia the gradient may increase and may be as much as 5 to 10mmHg. In any case, there is variability and many of our patients are not healthy so it could be higher then this. If there is hypotension then the amount of non-perfused areas of the lung (or areas of high V/Q ratio) may increase.
So, the practical implication of all this is that we monitor endtidal pCO2 continuously but calibrate and check against intermittent arterial pCO2 sampling because it is the arterial pCO2 that we are aiming to reduce (to cause cerebral vasoconstriction) in certain neurosurgical cases.
The size of the (a-ET)pCO2 gradient is an index of the amount of alveolar dead space. The gradient increases (eg to >15mmHg) in situations where the amount of alveolar dead space is increased. The most particularly important clinical situations are with pulmonary embolism (acute situation) and ventilation of pulmonary bullae (chronic situation). Indeed with a large pulmonary embolism, the amount of alveolar dead space can be very large indeed!
But I have to pull you up on one thing: you say that the pCO2 of gas from unperfused alveoli (alveolar dead space) is zero - Are you sure about that? Really sure?
CO2 is delivered to the lungs in the pulmonary arterial blood and is evolved into only those alveoli that are perfused. However, if you mean that there is some perfusion of this alveolar dead space then it is really a situation of high V/Q ratio rather then alveolar dead space (V/Q of infinity). If this is what you are implying then it really isnt true alveolar dead space so I would say you are mistaken.
Alternatively, there will of course be some metabolism in the pneumocytes lining the unperfused alveoli and in their walls as well so there will be a very small local CO2 production. I think this would be so small that it would not account for any significant pCO2 level in the alveolar dead space.
So my answer is Im sure: if they are NOT perfused then they absolutely cannot take part in gas exchange so there cannot be any CO2 evolved into them, and local CO2 production is too small to be considered.
Also, I must admit I had heard that you asked one of the other registrars this question last week so I took the precaution of looking it up as an extra check before I came along today. For example, in Anesthesia Review by Michelle Bowman-Howard (Lippincott Williams & Wilkins, published 2000) on p115 she says The pETCO2 of dead space is zero. And on p249 of Physiology 3rd edition by Bullock, Boyle & Wang (Williams & Wilkins, 1995) it has a diagram (fig 18-12) of an alveolus labelled Alveolar dead space which has the actual gas values in the alveolus indicated: pO2 150mmHg (the same as in humidified inspired gas) and pCO2 of 0 mmHg just as I said.
BUT, you are indeed quite wrong. However, I think you can work it out yourself, because this requires an understanding at a very simple level and not memorising without understanding, or complex analysis or looking something up in a book. Ill give you a clue, though a somewhat cryptic one: Many many years ago when I was a child we used to sing a little ditty, which as I recall included words something like this:
Blood goes round and round, air goes in and out . . . etc
The words may not be completely correct (it has been many years) but the principle is clear.
The above is a hypothetical dialogue which is presented for educational purposes.
© Kerry Brandis, 2001
Last updated Sunday, 04 August 2002 12:53 PM EST