Pulmonary function testing: Pathological findings The last two episodes of this Chalk Talk series
focused on how spirometry and body plethysmography work.
This episode will discuss typical findings of these pulmonary function tests in obstruction,
hyperinflation, restriction, and mixed ventilatory defects.
Let’s begin with obstruction.
As a comparison, here’s a normal flow-volume loop.
An obstruction is the narrowing of the bronchi.
Airway narrowing leads to increased airflow resistance when breathing and, therefore,
to reduced FEV1 and FEV1:FVC values.
Airflow is depicted in the diagram on the y-axis, with obstruction indenting the curve.
In sole obstruction, lung volumes and, therefore, expansion on the x-axis remain unaltered.
This results in the characteristic concave shape.
The vital capacity, residual volume, and total lung capacity are within normal values in
obstruction.
Please keep in mind that lung diseases can't be diagnosed directly using pulmonary function
testing only.
Pulmonary function merely shows if the bronchi are narrowed.
In the case of obstruction, further examinations are required to find their cause.
The most common causes of obstruction, or more precisely of intrathoracic airway stenosis,
are chronic obstructive pulmonary disease, in short COPD, and bronchial asthma.
In COPD, repeated inhalation of toxic substances, such as cigarette smoke, destroys the ciliated
epithelium and leads to chronic inflammation of the bronchi.
During the course of the disease, the lung tissue is remodeled, ultimately leading to
irreversible obstruction.
In contrast, in asthma, certain stimuli induce an increased response of the bronchial system,
which manifests as bronchospasm and mucous membrane swelling.
Obstruction in asthma is, therefore, reversible.
This reversibility can be used as a criterion for differentiating between the two diseases.
To do so, a post-bronchodilator test is performed: The patient is administered a fast-acting
bronchodilator.
After administration, the bronchi are examined for dilation and whether the drug improves
pulmonary function.
If that’s the case, airway obstruction is reversible, and the diagnosis is most likely
asthma.
If the values don’t change, the irreversible obstruction is an indication of chronic obstructive
pulmonary disease.
However, in practice, it’s sometimes difficult to differentiate COPD from asthma.
This is because early-stage COPD can be partially reversible, and long-term asthma can become
chronic.
With body plethysmography, airway resistance can also be determined.
By measuring resistance at basal respiration, the obstruction can be objectified.
Now, here’s a diagram of a loop depicting physiological breathing.
As you can see, it’s quite steep.
In contrast, an obstruction shows a flatter curve, as more volume-dependent work is required
to generate the same airflow.
A potential effect of pronounced obstruction is hyperinflation of the lungs.
On rare occasions, this can also occur independently of an obstruction.
A characteristic of hyperinflation is the change in lung volumes: The vital capacity
decreases in favor of the residual volume.
In addition, the FEV1:FVC ratio is normal or decreased, depending on whether or not
there’s an additional obstruction.
Let’s look at an example with obstruction and, therefore, a reduced FEV1:FVC ratio:
The dark blue flow-volume loop depicts a typical finding in lung hyperinflation, whereas the
light blue loop shows a physiological finding.
In addition to curve indentation, which we already know from obstruction, a distinct
inflection point in the curve can be seen.
Do you have an idea of how this transpires?
This inflection point is caused by a sudden decrease in airflow during expiration.
To understand how this happens, let's take a step back and look at the processes involved
in physiological breathing: The elastic fibers of the lungs aren’t only responsible for
lung contraction during expiration.
At the same time, they also ensure that the walls of the bronchioles are pulled outward
and thereby kept open.
In the trachea and bronchi, this task is performed by the cartilage.
However, since there’s no cartilage in the bronchioles, the reduction of lung volume
during expiration would be transferred to the bronchioles without the elastic fibers.
With obstruction, constriction creates pressure in the bronchioles, which can lead to their
hyperinflation.
This destroys the surrounding lung tissue and elastic fibers.
Since the bronchioles are now no longer held open by the elastic fibers, they collapse
during expiration.
The resulting abrupt reduced airflow appears as a bend in the curve.
The bronchial collapse also hinders the complete expiration of the inhaled air.
This air remains trapped in the lungs.
Therefore, this state is also called air trapping.
During inspiration, the trapped air causes the alveoli to overextend.
In chronic overextension, the air space distal to the terminal bronchioles becomes irreversibly
dilated.
As a result, the alveolar walls and the gas exchange surface in the pulmonary capillaries
are destroyed, impairing gas exchange.
This condition is referred to as emphysema.
So, emphysema results from pulmonary hyperinflation.
In summary, the distinct inflection point in the flow-volume loop only represents collapse
of the small airways.
It provides no indication of whether the alveoli have been damaged already.
Accordingly, it would be premature to diagnose emphysema based on this feature in the curve.
To determine impaired gas exchange reliably, blood gases and diffusing capacity need to
be assessed.
Let’s go back to the curve in hyperinflation: We can see that it’s compressed on the right
because the trapped air increases the fraction of the lung volume that can’t participate
in ventilation.
This increased residual volume decreases the vital capacity.
This compression of the curve, therefore, shows air trapping.
The degree of hyperinflation can be seen from the ratio of residual volume to total lung
capacity.
If the total lung capacity remains normal, this is known as relative hyperinflation.
Here, as we’ve described, bronchial collapse occurs during expiration, and the time to
expire is shortened.
So, more air remains in the lungs than usual, and they become hyperinflated.
Hyperinflation initially occurs only during physical exertion but later also at rest.
Patients can initially counteract a relative, that is, less pronounced hyperinflation, through
pursed-lip breathing.
Here, the patient breathes in through the nose and out slowly through tightly pressed
lips.
This increases air pressure in the bronchi, preventing their collapse during expiration.
So, relative hyperinflation is the result of decreased air efflux caused by bronchial
collapse.
It depends on the respiratory rate and is initially reversible.
Therefore, it’s also referred to as dynamic hyperinflation.
In contrast, an increased total lung capacity is referred to as absolute hyperinflation.
In such cases, the flow-volume curve shifts to the left.
This, as well, is an effect caused by the loss of elastic fibers: Physiologically, elastic
fibers counteract lung expansion during inspiration.
In absolute hyperinflation, the lungs are, to an extent, "stretched out", and their total
volume is raised.
This is reflected by an increased total lung capacity.
Absolute hyperinflation is the result of the increased inflow of air caused by reduced
elastic recoiling during inspiration.
By the way, absolute hyperinflation is also termed static hyperinflation, because it’s
irreversible and independent of the respiratory rate.
Though in clinical practice, it’s difficult to differentiate between static and dynamic
hyperinflation.
Usually, both are found.
Both types are caused by the loss of elastic fibers in the lungs.
Finally, let's take a look at airway resistance in hyperinflation, where also a characteristic
finding can be seen.
The loop appears club-shaped.
In the lower part of the loop, which reflects expiration, the curve is distinctly widened
due to bronchial collapse.
The narrowed airways create increased airway resistance, against which only a limited airflow
can be generated.
This is also reflected by an indented curve.
Now, let’s move on to restrictive lung diseases.
Here, primarily lung expansion is limited, which reduces the lung volume.
As a result, the total lung capacity and vital capacity decrease, while the FEV1:FVC ratio
remains normal.
So, in restriction, there’s an absolute reduction in volume.
If we look at the image, we can see the light blue physiological curve and a red curve with
the characteristic shape of restriction.
Compared to the physiological curve, this curve is mainly narrowed on the x-axis in
restriction, which depicts the volume.
Since this indicates a reduced total lung volume, the total lung capacity is also decreased.
The right section of the curve is almost unchanged since restriction doesn’t impact the residual
volume.
Restriction of the lungs can be due to intrinsic or extrinsic causes.
The flow-volume loop even provides clues on the location of the cause: The curve depicted
here is characteristic of extrinsic causes.
With these, the vital capacity is decreased, but further progression of the curve resembles
the physiological finding.
Extrinsic causes can be a volume reduction due to external compression, such as in pneumothorax,
but also respiratory muscle weakness in neurological diseases.
These causes lead to decreased lung expansion.
In the case of intrinsic causes, the tissue has already been remodeled and is less distensible.
For example, in pulmonary fibrosis, the vital capacity decreases as a result of reduced
distensibility during inspiration.
In this respect, curve progression corresponds to that observed for extrinsic causes.
Also, in pulmonary fibrosis, there’s increased deflation of the lung during expiration, which
results from tissue stiffness.
Therefore, intrinsic causes usually show a curve with increased maximum airflow, or peak
expiratory flow, in short PEF.
So, now that you’ve become acquainted with findings in restrictive lung diseases, let’s
move onto the combination of restriction and obstruction.
Do you have an idea of what they could look like?
In clinical practice, patients often present with multiple impairments.
In mixed ventilatory defects, obstruction and restriction are present at the same time.
Now, we’ve already learned that the FEV1:FVC ratio is decreased in obstruction.
Due to restriction, the vital capacity reduces, and since it represents a true reduction in
lung volume, the total lung capacity also decreases.
So, what does the flow-volume loop look like here?
Well, in this case, the most obvious answer is the correct one: We need to combine the
individual findings just discussed.
For this, you can apply your newly acquired knowledge.
As a reference, we’ll first show you the physiological loop.
If you like, you can pause the video and think about the flow-volume loop for a mixed ventilatory
defect.
So, does your flow-volume loop look similar to this one?
If that’s the case, then great!
Now, let's look at the individual parts of the curve:
Here, the obstruction can also be seen as an indentation of the curve towards the Y-axis.
The curve takes on a concave shape.
If hyperinflation is also present, this shows as increased compression on the X-axis.
The curve is compressed on the right because the residual volume is increased at the expense
of the vital capacity.
In sole obstruction, the total lung capacity would be normal or even increased due to hyperinflation.
However, in mixed ventilatory defects, restriction is simultaneously present.
Therefore, there's an absolute decrease in the vital capacity.
This is depicted as compression on the left of the curve.
In contrast to hyperinflation on its own, the total lung capacity is also decreased.
This combination is often found in patients who’ve undergone surgery for lung cancer.
Removing lung tissue reduces the lung volume and results in restriction.
If COPD is simultaneously present, for example, due to smoking, this manifests as obstruction.
Pulmonary function testing then shows a combination of obstruction and restriction.
OK, so that was our overview of the most important pathological changes in pulmonary function
testing.
In the next episode, we’ll provide you with an interpretative strategy for pulmonary function
testing to quickly analyze clinical findings.