Welcome! This series is an educational exercise to 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 email@example.com. The style of analysis
used here is that presented in my book "Clinical Acid-Base pHysiology".
Please consider the following clinical scenario and then
consider the question & discussions that follow.
Also: Answer to the question in Gas of the Week No 4 is now
A 74 year old lady was taken to her community
hospital by relatives because relatives said she was "pretty crook" (meaning
respiratory distress worsening over the previous 3 days & associated with fever). She
had a past history of severe chronic airway disease and continued to smoke heavily.
She was in significant respiratory distress with dyspnoea & peripheral cyanosis. She
was drowsy & confused. Chest examination revealed poor air entry and widespread
rhonchi. Resp rate 46/min, BP 120/80, temp 39.0°C. Urine testing was negative for
She was commenced on a high concentration of oxygen via a venturi mask and her colour
improved. She subsequently detoriorated so was intubated & ventilated and transferred
to the Intensive Care Unit at our hospital.
Blood gases & electrolytes were collected at various times.
Blood gases & Electrolyte Results
Results for Gas No
(temp corrected results for 38.8C)
(same results without temp
|After intubation &
ventilation on 100% oxygen
(not temp. corrected results)
|In Intensive Care
 How would you analyse the
initial set of results?
 Should blood gas results be 'temperature corrected'?
 Should we use pO2 or should we use SO2
as the best indicator of the adequacy of oxygenation in this patient? -Why?
Consultant (to Registrar)
How would you analyse the initial results? The are presented as two sets of
values: one temperature corrected and one not.
My initial quick scan reveals acidaemia, severe hypoventilation (in view of hypercapnia)
with adequate oxygenation.
Hypercapnia nearly always indicates
hypoventilation. The only exceptions of note are:
* Malignant hyperthermia particularly when ventilation is controlled
* Significant amounts of carbon dioxide present in the inspired gas.
Either of these 2 situations could
happen intraoperatively but this is not the situation here as the history excludes these
The other key thing the deserves comment
is that a pCO2 of 90mmHg is life-threatening because of the obligatorily
associated hypoxaemia if the patient is breathing room air. The pO2
here is quite high; too high to be breathing room air. The patient has arrived at hospital
in extremis and has been immediately commenced on oxygen (high FIO2)
so the gases were not collected on room air.
If the patient had been breathing room air with this arterial pCO2 level, what
would the arterial pO2 have been?
The alveolar pO2 can be calculated from the alveolar gas equation:
pAO2 = pIO2
where R is the respiratory exchange
ration (assume it is 0.8)
and pIO2 is inspired O2 concentration which = (pB
- pH20) x FIO2
Now substituting known values of 760mmHg
for barometric pressure (pB) and assuming room air (FIO2)
pAO2 = [(760 - 47)
x 0.21] - [87 / 0.8] = 41mmHg.
Now the arterial pO2 will be
lower than this even in health because of 'venous admixture'.
Before you go on, could you tell
me what you mean by 'venous admixture'?
This term is used in slightly different ways by different
people. I use the term to apply to the factors which cause the arterial pO2 to
be lower than than the alveolar pO2.
The assumption I make is the arterial pO2 is lower than alveolar pO2
because of the addition of mixed venous blood to the pulmonary end-capillary blood.
Pulmonary end-capillary blood has the same pO2 as that in the alveoli it is in
contact with because equilibrium is reached between the alveoli and pulmonary capillary
blood. Typically this equilibrium is reached in about one-third of the time (0.25 sec)
that the two are in contact (0.75 sec).
Now in reality of course the pO2 of the blood
causing this depression is rarely the the same as that in mixed venous blood, but we can calculate how much blood with
the composition of mixed venous blood would have to be added to cause the observed
depression in arterial pO2. This makes use of the shunt equation and the calculated value
for this 'virtual shunt' is referred to as the 'venous admixture'.
The two main contributors to venous admixture are:
* alveoli with low V/Q
* shunting (eg bronchial venous blood, thebesian blood draining into the left heart).
On room air, the typical (A-a)pO2 difference (or 'A-a gradient') is 5 to
15 mmHg. So with this very high pCO2 level, we would expect a pO2 of
about 30mmHg if the lungs were otherwise normal. This is why I said earlier that such a
high pCO2 is obligatorily associated with life-threatening hypoxaemia.
Of course, the lungs here are definitely not normal so if the pCO2 was that
high before arrival then the pO2 would have been much lower - this suggests
that the patient's ventilation has decreased since she was commenced on oxygen.
Now you said that this patient is 'hypoventilating' and yet the history is that she was
tachypnoeic (resp rate 44/min) and had significant respiratory effort. This doesn't sound
like hypoventilation does it?
That's an interesting point that I don't think I had realised before. We use the terms
hypo- & hyper-ventilation in 2 different ways:
 When clinically assessing a patient, 'hyperventilation' tends to refer to the amount
of effort the patient is making or perhaps more accurately the amount of ventilation per
minute; this is the minute volume of ventilation (MV).
 When we use the term 'hyperventilation' in acid-base physiology, we are referring to
the alveolar ventilation as this is what is important for pulmonary gas exchange. This is
related to MV as follows:
MV = [resp rate x (VD + VA)] where VD
is dead space volume & VA is alveolar volume.
If VD is increased, then a high MV could be associated with a low alveolar
In this particular case the clinical assessment is of much increased respiratory effort
but clearly the alveolar ventilation is much decreased. Perhaps hyperventilating in the
clinical sense of a high MV, but hypoventilating in the gas exchange sense of a low VA
- if this makes sense!
The equation that relates
arterial pCO2 to alveolar ventilation (and to the body's CO2
production (Vco2) ) is:
paCO2 = k.
(Vco2 / VA ) (where k is the proportionality constant)
Assuming Vco2 is constant,
then paCO2 and alveolar ventilation are inversely related. If paCO2 is
doubled then alveolar ventilation must have halved. It is the change in alveolar
ventilation that causes the change in arterial pCO2.
The other point I thing you are wanting
me to make is that the amount of respiratory effort by the patient as assessed clinically
gives a clue as to the cause of the alveolar hypoventilation.
If the cause is primarily pulmonary
(as in this case) then the elevated arterial pCO2
will stimulate the peripheral and central chemoreceptors resulting in stimulation of the
respiratory centre. This results in respiratory muscle activity to attempt to increase
alveolar ventilation and correct the hypercapnia.
If the cause is primarily central
depression (of the respiratory centre) such as
occurs with an overdose of opiates or barbiturates than there will be little respiratory
effort. This reduced respiratory effort is the cause of the hypercapnia.
So the amount of respiratory effort
gives a guide to the cause of the hypercapnia: central or pulmonary. This is useful to
know in some situations but in mostly you should know what is likely from the history or
even from just looking at the patient. Some cases are more complicated as a primarily
respiratory cause may be complicated by central depression from hypoxaemia and
You've made some good points. Now back to assessing the actual gas results. You have two
sets of results from the single initial sample: which do you use? -and why?
Well the patient's actual temperature is 38.8ºC. My initial thought is to use the gases
which give the actual values for the actual temperature. The patient's temperature is
entered into the blood gas machine before the analysis is done but I think the gases are
actually measured at 37ºC in the machine.
Yes that's right. The blood gas machine is thermostated to 37ºC and all measurements are
made at that temperature. The calomal reference electrode in the blood gas machine is very
temperature sensitive. Results for other temperatures are calculated using a formula which
is programmed into the blood gas machine.
It has been found experimentally that
the change in pH with temperature in a blood sample is almost linear. Anaerobic cooling of
a blood sample causes the pH to rise, so the pH is higher at a lower temperature (&
lower at a higher temperature).
A common formula for temperature correcting blood gas results uses the Rosenthal
correction factor. The Rosenthal factor is a change in pH of 0.015 pH units per degree
centigrade change in temperature.
The pH here is 7.215 at 37ºC. Using the Rosenthal correction factor, then it will be
lower by (1.8 x 0.015) at 38.8ºC:
pH (at 38.8ºC) = 7.215 - [(38.8 -37.0) x 0.015] = 7.188
So the machine at the referring hospital
is using the Rosenthal correction factor.
Similarly, there are formulas in the machine's programming to temperature correct the pO2
and the pCO2. The [HCO3] is calculated from the pH and the pCO2
using the Henderson-Hasselbach equation.
The thing I'm a bit unsure about is how the pO2 and the pCO2 values
can actually change with change in temperature. This is all happening in a closed system
where there is no contact between the blood sample and the ambient air. So how can the gas
values change? There is no entry of any O2 or CO2 from outside so
the gas content of the sample cannot change. So how can the pO2 and the pCO2
in the sample change? Now I know the reported values change but is this a 'real'
Yes, I think that is not well understood by a lot of people. The way to find the answer
though is to have a clear understanding of what the 'partial pressure' values mean. We are
taught about using pO2 and pCO2 and become familiar with this but
what does the partial pressure values really mean?
Well, they tell you the 'tension' of the gas present in the solution and this tells you
how much of the particular gas is present.
You say 'how much' so you are referring to content. Well, consider this: if the pO2
of a blood sample was doubled from 100mmHg to 200mmHg, does the oxygen content also
No, because the vast majority of the oxygen present is combined to haemoglobin (Hb) and at
a pO2 of 100mmHg the Hb is essentially fully saturated so doubling pO2
from 100 to 200mmHg does not result in a doubling in total oxygen content. The saturated
Hb cannot carry more.
I should clarify: what I meant was that
the partial pressure of the gas in the solution tells you the amount dissolved in
the solution. If the pO2 increased from 100 to 200mmHg, then the amount (or
content) present as dissolved oxygen will indeed be doubled (even though the total amount
present would not be). The same is true for all gases: if the amount of gas dissolved in a
solution doubles, then the partial pressure of that gas doubles.
Good. What is the basis of our universal practice of referring to the amount of a gas
dissolved in a solution in terms of 'partial pressure' (in mmHg or in kPa) rather then
using the actual amount (in mls/dl) present.
This is just Henry's Law.
This says that "at equilibrium, the
amount of gas dissolved in a liquid is proportional to the partial pressure of gas at the
surface of the liquid" (One proviso is that this does not refer to gases which
are infinitely miscible in the liquid.) The formula we derive from Henry's law is:
Amount of gas dissolved = k x partial
(where k is the proportionality
Now the value of 'k' is very important
as it is a measure of how soluble the gas is in the liquid. If k is high, the gas is more
soluble. If k is low, then the gas is said to be less soluble. The value of k is different
for different gases. This proportionality constant is important then for that reason and
is referred to as the 'solubility coefficient' for the particular gas in the
particular liquid. For example, the solubility coefficient for oxygen in water is 0.003
Dissolved O2 = 0.003 x
If pO2 is in mmHg, then
this will give you the amount of oxygen dissolved in mls O2 per mmHg per 100mls
So how much oxygen is dissolved in arterial blood when the pO2 is 100mmHg?
Amount dissolved = 0.003 x 100 = 0.3 mls O2 /dl of blood.
What is the physiological significance of this?
Under normal conditions, the amount of oxygen carried as dissolved oxygen is very small
(in comparison to the amount carried on Hb). This is a direct consequence of the very
low solubility of oxygen in water. The way that this problem is overcome in the body
is by using a specific oxygen carrying protein. Haemoglobin at a concentration of 15 g/dl
can carry about 20mls of oxygen per dl of blood. This is over 60 times the amount of
dissolved oxygen in the same volume of blood at a pO2 of 100mmHg.
Under normal conditions, dissolved
oxygen is not an important transport form for delivering oxygen to the tissues. Dissolved
oxygen accounts for less than 2% of the normal 1,000 mls of oxygen delivered to the
tissues per minute.
So dissolved oxygen is not important in the body then?
Thats a trick question because the answer is this:
Dissolved oxygen is vitally
important in the body. It is the form of oxygen that diffuses from the capillaries
to the cells. It is the form of oxygen that reacts with cytochrome oxidase at the end of
the electron transport chain in the mitochondria. This is what permits oxidative
phosphorylation to continue. This reaction in mitochondria accounts for about 80% of the
body's use of oxygen. (The many oxidases in the body account for much of the rest.)
Dissolved oxygen is not particularly
important in the transport of oxygen in arterial blood. It is this one circumstance where
its low solubility (& consequent small amount dissolved) is a physiological problem
which is overcome by the presence of haemoglobin. Don't generalise to say that it is not
important in the body though. It is only not very important in transport of the blood
under normal conditions of [Hb] & cardiac output.
Now back to Henry's Law because we still
haven't answered the question about how the partial pressure of a gas in solution can
change even though the dissolved gas content does not. This is what you were trying
The key thing to remember is that because of the Henry's law proportionality, you can
refer to gases using the gas phase concept of partial pressures as an indicator of the
amount dissolved in the liquid even though this does not actually indicate the actual
amount dissolved. The gas is present in a dissolved form; it is not there as a gas which
can be measured by its partial pressure. The partial pressure refers to amount of the gas
in the gas phase which would be in equilibrium with that amount of dissolved gas if
they were in contact.
The amount of oxygen dissolved in water (or blood) at
a partial pressure of say 50mmHg is different from the amount of CO2 dissolved at the same partial
pressure. The actual amount present is different because the two gases have different
solubility coefficients. We can say that if the partial pressure of each were to double
then the amount of each gas dissolved would be doubled but the dissolved amounts of each
gas are different. (The additional confusing thing about these two gases is that there are
other forms of carriage for each present as well. This affects the total amount present
but we are only considering the dissolved content.)
The key thing that links the partial pressure (in the gas
phase) to the amount of dissolved gas (in the liquid) is the proportionality constant 'k'.
This is the 'solubility coefficient'. The final key fact to know is that this 'constant'
is not constant!. It is temperature dependent and this provides the answer to your
So the partial pressure of the gas in the liquid
can change even though the dissolved amount of gas does not. It is the value of the
solubility coefficient that changes. In this patient then, the pCO2 of 95.7mmHg
represents the same amount of dissolved CO2 as the pCO2 of 86.9mmHg
at 37ºC. The partial pressure changes but the amount
present doesn't. This makes sense then as in a closed system, the total amount dissolved
must be a constant but if the solubility coefficient changes value with temperature than
the partial pressure must change (because it is equal to the product of 'k' & the
The way we use Henry's law to indicate the amount of gas
dissolved in a liquid is essentially an agreed 'convention'. We could have all agreed to
only speak of the actual amount present but we didn't. This convention is undoubtedly
The lack of understanding of what this is all about
has lead to a couple of other absurd situations. For example, the somewhat common practice
of referring to the pH2O in a blood sample as being 47mmHg (at 37ºC) is quite annoying. Many texts do
this. But how can water be dissolved in water??? Granted that this is absurd then it is
quite silly to refer to a dissolved pH2O. The use of pH2O in
this way is really to do with saturated vapour pressure and not Henry's law. It is not an
indicator of the amount of H20 dissolved in the blood sample which is what this Henry's law convention is
Similarly there is no reason why the sum of all the
partial pressures of dissolved gases must add up to 760mmHg. Clearly they never can if the
pH2O is not added in. Again this is a misuse of another gas law: Dalton's law of
partial pressures. This law refers only to the gas phase. The misapplication of Dalton's
law to liquids is what makes the use of a pH2O value necessary. Perhaps then you could say it is a 'convention'
also. Simpler to just say it is wrong.
This then also applies to the use of the
Henderson-Hasselbach equation. The change in the pCO2 doesn't alter the
calculated pH because the term in the denominator is the dissolved CO2 (ie: k x
pCO2) and this doesn't change despite the change in pCO2.
I notice in the 2 results that the [HCO3] is the same in both. But if the pH
has changed, and the (k x pCO2) term is constant, then if [HCO3] is
constant, the pKa must have changed.
Yes, that is so. Just to summarise the effects of
temperature on a closed system:
pH increases with decrease in temperature (and the
reverse with an increase in temperature). The amount is estimated using the Rosenthal
pCO2 decreases with a decrease in
temperature. This is because gases are more soluble at a lower temperature due to a lower
kinetic energy and thus less tendency to escape from solution. So if the total CO2 content
is constant as is true for this closed system, the pCO2 decreases (and
the solubility coefficient rises)
[HCO3 ] is constant with changes in temperature.
pKa increases with a decrease in temperature
pO2 decreases with a decrease in temperature for reasons as for
pCO2. There is an additional factor here as the haemoglobin oxygen dissociation
curve shifts to the left with a decrease in temperature - this means Hb has a higher
oxygen affinity at a lower temperature. These 2 factors (increased solubility &
increased Hb affinity) make for a more complex situation then with CO2. If pO2
is high the Hb is already fully saturated and the change in affinity won't have much
effect. At lower pO2 levels, the increased affinity means some of the dissolved
oxygen will bind to Hb causing a decrease in pO2. This is additional to the
decrease in pO2 that occurs with the increased solubility of O2 at
the lower temperature. Total oxygen content does not change.
These changes I'm talking about here are what's happening
in the closed system of a blood-gas syringe and in the blood gas machine. In the patient
at a temperature other than 37C, other effects are important. For example a decreased
oxygen consumption and a decreased CO2 production occur with hypothermia (in
the absence of shivering).
Anyway, back to the patient. These are the changes
occurring with the change in temperature but are they clinically important?
Well I have to say no in this case. The pO2 & the pCO2 are different at the two temperatures but not
enough to make any clinical difference. The patient is grossly hypercapnic but the
obligatory hypoxaemia has been able to be overcome by administering high oxygen
concentrations. The patient is in extremis though and deteriorated despite oxygen. She
required intubation and ventilation. The deterioration was possibly due to central
depression by the hypercapnia, the lessening of hypoxic drive following oxygen
administration or simply exhaustion, or probably all of these factors.
The situation with temperature changes in blood gas values is more marked with quite
hypothermic patients (eg if cooled to 20 to 28ºC while on cardiopulmonary bypass). Maybe
the use of temperature corrected values would be more appropriate then. However, I
understand that the current recommendation is to not temperature correct the values even
at these temperatures.
Yes. This is the alpha-stat approach (which we don't
have time to discuss here today). One problem with temperature correction of gas results
is that we have no reference range for temperatures other than 37ºC. So how can we
interpret what is normal or abnormal at a temperature different from 37ºC?
Temperature correction is necessary in some situations (eg to correctly determine the
endtidal-arterial pCO2 difference).
In this patient then, please analyse the initial non-temperature corrected results for me.
Clearly a severe respiratory acidosis is present. The
electrolyte results are not presented for this time.
If this was an acute respiratory acidosis, the 1 for 10 rule would apply. This predicts a
[HCO3] of 28.5mmol/l. I think 90mmHg is about the limit for experimental
confirmation of the expected amount that bicarbonate changes. By and large, [HCO3]
will always be below 30mmol/l if due to an acute respiratory acidosis alone.
I think this is clearly the wrong approach in this patient. This is an acute infective
exacerbation of COAD and has been present for 3 days by the history. It would be useful to
review any recent electrolyte results to see if 'total CO2' was elevated as
this would provide evidence of chronic CO2 retention. Renal compensation is
well under way I would say so the 'rule of thumb' for a chronic respiratory acidosis is
the one to use. The 4 for 10 rule says the [HCO3] increase by 4mmol/l for each
10mmHg chronic elevation in pCO2 and this takes say 3 or more days to reach its maximum. A
pCO2 predicts a [HCO3] of (24 + 18) = 42mmol/l.
The actual [HCO3] of 33.8mmol/l is lower than this. The 2 possibilities to
* A coexistent lactic acidosis (or other metabolic acidosis) is present
* Insufficient time has elapsed for maximum compensation
Now you need to apply the 'So what' test.
OK then. The 'So what' test means to assess the
clinical significance of something. In effect to say 'so what does this mean for the
patient'. The test result is never an end in itself and should not be ignored.
So what does this mean? My clinical assessment suggests that this patient has had several
days of illness but it is very unlikely she has survived for 3 days with a pCO2
of 86mmHg at home because as discussed earlier this pCO2 means a severe hypoxaemia with
pO2 of less then 30mmHg. More likely is that she has had slowly worsening gas exchange but
mostly with a pCO2 lower than 86mmHg. A [HCO3] of about
34mmHg would be full compensation for a pCO2 of about 65mmHg: this would allow a more tolerable pO2 level.
The lactate level was measured with the next set of gases 2.5 hours later after
intubation. The value of 2.7mmol/l excludes a significant lactic acidosis and this is
consistent with the above scenario. The anion gap is low and there is no clinical or
biochemical evidence of another cause of metabolic acidosis (such as renal failure,
You mention the phrase 'full compensation' in your
response. Is this what you mean?
Actually no, that was a mistake. The body's
compensation for an acid-base disorder is virtually never 'full' in the sense of enough to
return the pH to the normal range. So we should avoid the phrase 'full compensation'. What
I meant was 'maximal compensation'. I understand this is a common error.
I think you explanation is very plausible. It would indeed be
unlikely that a person ill with a pCO2 of almost 90mmHg would be just sitting around at home for so long. The
obligatorily associated severe hypoxaemia would be fatal.
Extremely high pCO2 values (say
>100mmHg) occur only in patients receiving a high inspired oxygen concentration if only
because they would undoubtedly be dead from hypoxia if breathing room air.
Another point to make is that a severe lactic acidosis is much more likely with poor
perfusion than with hypoxaemia. The various autoregulatory changes allow the tissues to
cope better with a low pO2
than with a low perfusion.
Is it better to use SaO2 or paO2 as an indicator of
the adequacy of oxygenation in this patient?
Well I tend to use paO2
as the indicator of 'oxygenation'. This is a more sensitive indicator of the lung's
ability to add oxygen to the blood when the inspired oxygen concentration is high. For
example, if the patient is breathing 100% oxygen and her paO2
is 100mmHg and saturation is 98% then there is a major defect in oxygenation but the
saturation value is high and insensitive to this defect. If paO2
is low, then SaO2 will also be low and either could
On the other hand, looking at it from the tissues point of view, it is the 'oxygen flux'
(tissue oxygen delivery per minute) that is most important. The key factors then are
cardiac output, SaO2 and [Hb]. The proviso here is that
there are not significant quantities of abnormal haemoglobins present (eg HbCO, metHb) as
these do not carry oxygen. The ABGs at 0310hrs exclude this problem in this patient.
If there was a
large amount of say HbCO present, then the SaO2
of the Hb would be normal but its oxygen carrying capacity would be severely reduced. In
that case, SaO2 would be a poor indicator of the
adequacy of tissue oxygen delivery.
In general, paO2 is a good indicator of oxygenation
if considering pulmonary function, but SaO2
is generally a better indicator of tissue oxygen delivery (assuming of course that cardiac
output & [Hb] are adequate).
But how can haemoglobin saturation be normal if a
substantial percentage is in the form of carboxyhaemoglobin?
The oxygen flux equation says:
Oxygen delivery/min = [ CO x [Hb]
x SaO2 x 1.34 ] + [ 0.003
If a lot of HbCO were present, oxygen flux must be decreased and the only way this can be
accounted for in the equation is by a decrease in SaO2. So how can the SaO2 be normal?
I see your point but nevertheless you are wrong. Have
a think about it and we'll discuss it next week.
What mistake has the registrar made?
Email me if you think you have worked out the
the correct answer.
The above is a purely hypothetical dialogue which is presented for
All material ©
Kerry Brandis, 2002