Right. Lung-function tests: the volumes.
So the capacity of the lung can also be measured.
How big are the lungs? And this is really
mainly important to identify people who have
shrunken lungs – that happens in pulmonary
fibrosis. So they have reduced total lung
capacity. But it’s also useful in obstructive
airways disease. Because obstructive airways
disease – whether it’s COPD or ongoing
severe asthma – causes an increase in the
residual volume. And as the volume of the
lung is dictated by the residual volume as
well as you vital capacity, then the total
lung capacity will go up in these patients.
So you get this paradoxical situation where
patients with airways disease – such as
COPD – will have low vital capacity but
high lung volumes. And that’s largely because
they’ve got residual volume increases. They
have air trapping in their lungs and that
makes their lungs bigger than they should
So what do we mean by air trapping? Well,
essentially as you breathe out, you generate
a positive pressure. And that squeezes the
air out of the lungs. But it also squeezes
the tubes taking the air out of the lungs
– the bronchial tree. And if the bronchi
are compressed by that positive pressure,
then air flow’s going to be limited. And
in patients who have airways disease, the
problem here is that, on inspiration, they
can breathe in relatively freely but, on expiration,
the obstruction is made worse by this positive
pressure. And you get a degree of air trapping
with every breath. And that slowly but surely
inflates the lungs and leaves them operating
with a high residual volume. And this is particularly
pronounced in emphysema because the alveolar
destruction that occurs in emphysema allows
the airways to collapse when faced with this
positive pressure on expiration. That’s
called dynamic airways collapse.
So we can use flow volume loops to give a
little bit more information about how the
patient’s air flow is changing during the
inspiratory and expiration cycles. They’re
quite complex. They give distinctive patterns
with different diseases. And so they’re
especially useful in emphysema and in patients
with upper airways obstruction.
I’ll show you the pictures that we might
get in those circumstances. So, on the left,
we have somebody with emphysema. So in expiration,
we do get this dynamic airways collapse. And
how that is presented in this is that the
flow on expiration is initially rapid and
then, suddenly, there’s a fall. And that’s
due to the dynamic airways collapse. And that’s
followed by a long tail or slow, low air flow
expiration. If you have an obstruction to
the major airways – so a tracheal tumour
for example – then you get this distinct
squared-off appearance to the flow volume
loop. And that can be very helpful in identifying
these patients who are otherwise hard to identify.
So the lung-function tests we’ve described
so far describe the volumes of the lung and
how much air you’re able to shift during
inspiration and expiration and the rate with
which you shift that.
What they don’t measure is how easy it is
for oxygen to get from the alveoli into the
blood. And to measure that we use the transfer
This is measured by inhaling a low concentration
of carbon monoxide and then measuring how
much carbon monoxide is exhaled. And the difference
between the two is a factor that reflects
how efficient oxygen transfer will be across
the alveolar membrane into the pulmonary capillaries.
There are two factors we measure: one is the
DLCO – which is the absolute factor. But
the problem with that is that, if you remove
somebody’s left lung and left them with
just one lung, you’re going to halve the
transfer factor because you’ve halved the
surface area which they have for oxygen diffusion
or carbon monoxide diffusion. So you need
to adjust the transfer factor for the alveolar
volume. And that’s called KCO. And that’s
the transfer factor divided by alveolar volume.
And that reflects how efficient oxygen transfer
will be per units of lung. And using that
parameter, you can identify patients who actually
seem to have lung disease as opposed to just
decreased lung volume.
There are a variety of factors that affect
transfer factor but these fall into the following
categories. One is the alveolar surface area.
So if you reduce the alveolar surface area
then you’re going to reduce the transfer
factor. And that can happen after a lung resection,
as we just discussed, but it also occurs in
emphysema characteristically where the alveoli
destruction decreases the surface area available
for gas exchange.
If you increase the alveolar barrier thickness
– and that occurs in interstitial lung disease
– then you will reduce the ability of oxygen
to cross that barrier. So that is also another
cause of a low transfer factor.
But transfer factors critically depend on
blood supply to the lung. And if you reduce
the blood supply to the lung, then it will
go down. And that occurs in pulmonary emboli,
pulmonary hypertension and also right-to-left
It’s also critically dependent on the ability
of that oxygen to pick up oxygen and that
requires haemoglobin. So the transfer factor
is low in patients who are anaemic.
Cardiac function also is relevant of him.
So mitral valve disease, pulmonary oedema
etc. will also affect the transfer factor.
So we can actually measure how much oxygen
is present in the blood. And we do two measurements
for that: one is the oxygen saturation which
measures how saturated the haemoglobin is
with oxygen. Low saturation = low oxygen availability.
High saturation = good oxygen availability.
In general, people should have saturations
of 95 to 99%. Because of the steepness of
the oxygen saturation curve, as you become
more hypoxic and the saturation falls to 90%,
you get a lot of fluctuation in the values
here. So, although in patients who have 95%+
the saturation remains relatively stable,
when you get down below 90% they often fluctuate
3 or 4%. It’s a very useful test because
it’s non-invasive and you can use it actually
continuously to monitor how patients are doing.
And it’s also useful not just in acute circumstances
but also for the monitoring of patients who
may be developing respiratory failure due
to chronic lung disease. It’s inaccurate
if the patient has poor peripheral perfusion
– if they’ve got cold fingers – and
there’s thick nail varnish on as it measures
through the nailbed itself.
The other measure of oxygen are blood gases.
And what that measures is how much oxygen
is dissolved in the blood. But in addition
to that, it gives you other parameters which
are very important: it gives you the carbon
dioxide level dissolved in the blood, it gives
you the pH and it gives you bicarbonate and
the base excess. So it’s very useful in
identifying acid-base problems as well and
problems with excretion of CO2 – hypoventilation.
So we use blood gases to see whether somebody
has type-I or type-II respiratory failure.
That is either hypoxia with no increase in
the carbon dioxide or somebody with hypercapnia.
And if they have type-II respiratory failure,
we need to know whether they have acidosis
with that or not. And it’s also used when
acid-base disorders may be present.