DR. SUSAN R. WILCOX: In this video, we're
going to discuss the physiology of mechanical ventilation.
The purpose of this video is not to provide a comprehensive review
of all pulmonary pathophysiology.
The goal here is to hit the highlights of physiology
that are relevant to taking care of a critically ill patient at the bedside.
The first concept to review is ventilation perfusion matching.
What this means is that the ventilation or the oxygen delivery and CO2 removal
are adequate for the body's needs.
This is indicated here by this figure that we'll
use repeatedly throughout the video.
Unfortunately, a lot of our patients in critical illness
do not have adequate ventilation perfusion matching.
One of the most common causes of hypoxemia in critically ill patients,
especially those with COVID-19 is shunt.
When we say shunt what we mean is that there
are parts of the lungs that are not being adequately ventilated,
although blood is still going to those areas.
The classic example is an intracardiac shunt.
This is an anatomic defect that leads to some
of the blood bypassing appropriate oxygenation and ventilation.
What then occurs is that the oxygenated blood, that goes through the lungs
normally, mixes with the deoxygenated blood and leads to overall hypoxemia.
While this is an extreme example, we see this very commonly within the lungs
themselves.
A great example is atelectasis.
So if a part of the lung is decompressed and not participating in gas exchange,
it still is receiving perfusion and that can lead to hypoxemia.
Similarly, parts of the lungs that are filled with edema or other infiltrates
will have the same effect.
When we look at a patient's lungs who have ARDS,
we see a lot of heterogeneity.
Here in this x-ray, we see a profound example of that.
We see areas up here that have normal ventilation perfusion
and are participating relatively regularly in the process.
There is a large area over here of profound edema and consolidation
and infiltrate.
And then, you can imagine that there are parts
of the bases that have atelectasis.
And so while I have an example here of gross areas of normal edematous
and atelectotic parts of the lung, recognize that in an individual patient
this will vary.
And it often can happen on a more micro level as opposed to the macro level
that I'm using here as an example.
Another major concept in the pathophysiology of hypoxemia
is derecruitment.
When we say derecruitment what we're talking about
is atelectasis on a grand scale.
We have patients who come in, they have negative inspiratory force.
They're participating in negative pressure ventilation, which
is a very efficient way of ventilating.
We will sedate them, relax them, intubate them,
put them on the ventilator, and they will profoundly derecruit.
If we lie them flat, and then their lungs,
which are boggy and heavy with edema with infiltrates,
will then collapse upon themselves.
It also gets worse, because the heart will compress the lungs as well,
the abdominal contents come up and compress
the inferior portion of the lungs.
And this isn't just a schematic.
You can see here, this is the CT scan image of someone who is laid flat.
And you can see the heart actually causing the compression,
causing derecruitment behind it.
Another key concept is hypoxemic vasoconstriction.
So when you have a lung unit that for whatever
reason is not participating in adequate gas exchange, what can occur
is that the body will try to correct for that by minimizing
the perfusion to that lung.
So there will be constriction leading to decreased perfusion of these bad lung
units.
This happens all the time.
We all have areas of ventilation perfusion
on a daily basis, which is normal.
And our body is able to use compensatory mechanisms to optimize our ventilation
perfusion matching.
But when a patient gets critically ill, sometimes those mechanisms
are overwhelmed, and it doesn't work.
Another concept to think about for pulmonary pathophysiology
is the normal physiology of carbon dioxide removal.
Here, in this example, we see carbon dioxide
coming in, and then being ventilated off.
This process is very efficient.
And so the major determinant in CO2 removal
is just the amount of gas that's moved through the lungs.
We quantify this when we're talking about mechanical ventilation
as the minute ventilation.
That's the tidal volume times the breaths per minute.
I have it illustrated here by showing the volume in the lungs
and thinking about how many times a minute it's moving in and out.
Considering pulmonary mechanics is very important,
and we don't often think about it in cases where we're not
talking about mechanical ventilation.
In this example here, we have at the top a normal set of lungs and airways.
However, some of our patients can have resistance problems.
Resistance means resistance to flow.
You have to have airflow to have resistance.
And you can see, here in this example, might
represent somebody who has asthma, would be a great example of somebody
who has a resistance problem.
Conversely, there are patients who have compliance problems.
Their airways are fine, they have no problem with flow,
but the lungs themselves are stiff, they're edematous,
they don't inflate very easily.
Those are patients who have a compliance problem.
You can also see compliance problems in patients
who have a large chest wall, heavy abdominal contents,
intra abdominal hypertension, anything in the pulmonary system
that creates that heaviness in the lungs or the chest wall
will lead to a compliance problem.
We can use the ventilator to help us determine
whether a patient has more of a resistance problem,
or a compliance problem, or sometimes both.
The ventilator will give us a lot of information
about the pulmonary mechanics.
The first point to look at is the peak inspiratory pressure.
The peak inspiratory pressure is the top pressure for any breath.
That's why it's called the peak.
When we're talking about the peak inspiratory pressure,
we're looking at factors that involve both resistance and compliance alike.
Compliance is measured by the plateau pressure.
Plateau pressure is determined by doing an inspiratory hold.
We stop all flow, so there is no resistance.
And what's left behind is a measure of the compliance.
This is illustrated here in this diagram.
So looking at the tracing on the ventilator,
we can see that at initiation of a breath
we have an alveolus above that is sitting there with no flow,
sitting there at rest.
The breath starts and air rushes into the small airway and the alveolus.
This leads to a flow issue.
We check a plateau pressure by doing an inspiratory hold, all flow stops.
With the inspiratory hold, we're then able to measure the pressure
within the alveolus.
This is the plateau pressure.
Then, with exhalation, we again have a factor of flow.
Here's an example on the ventilator itself.
We can see here a peak inspiratory pressure, also known as a PIP,
which is the maximum pressure that is received during the breath.
In this example, the peak inspiratory pressure is a little over 50,
so it is extremely high.
When we perform an inspiratory hold and there is a plateau pressure obtained.
The plateau pressure in this example is 38.
This is also an extremely high plateau pressure.
We'd like to target a plateau of 30 or less, the lower the better.
Thinking about compliance, it's important to understand
the relationship between pressure and volume.
When we have a ventilator, we can set a control variable.
We can either set a pressure or we can set a volume.
But whichever one we set, we're going to receive
the other as a conditional variable.
If you set a pressure, you're going to receive a volume on the ventilator.
And if you set a volume, you will receive a pressure.
The relationship between these two is what
we refer to as the compliance, the change in volume
divided by the change in pressure.
So you can imagine that if a patient has poor compliance in their lungs,
they have stiff lungs that are difficult to expand,
it's going to take a lot of pressure to get even a small tidal volume.
Understanding this concept is very helpful in thinking
about the ventilator later.
Another key concept is to think about air trapping.
Air trapping is a major problem for many patients on the ventilator.
The concept behind air trapping is that when a patient is exhaling,
they have not fully exhaled when the next breath comes.
You can imagine that over time that pressure and a volume
will accumulate within the respiratory system
and will lead to increasing distension, increasing pressure,
and can have significant hemodynamic and respiratory compromise.
Please note that the illustration that I show here
is not any wave form that you'll ever see on the ventilator.
It's rather just being shown for illustrative purposes.
Here is a conceptual idea of what we see within the lungs.
Note that this is again not necessarily something
that we would look at to look for air trapping,
but it does explain the concept behind it.
This patient has bad COPD.
Her lungs are very expanded, her diaphragms are flattened,
and you can even see that her mediastinum is
relatively small and compressed due to all of that trapped air, all the air
pressure, within her intrathoracic cavity.
To quantify the air trapping, we perform an expiratory hold.
Just like we performed an inspiratory hold to look at the plateau pressure,
performing an expiratory hold allows us to measure the pressures in the system
when all flow stops.
So what we can do is press on the ventilator,
the expiratory pause button, or the expiratory hold button,
called different things on different ventilators,
and the pressure that's left behind will show us the auto PEEP
or also known as the intrinsic PEEP.
Again, they are the same thing.
Intrinsic PEEP or auto PEEP are synonyms.
In this example, the patient has an intrinsic PEEP measured at 1.6,
also known as auto peep of 1.6.
This means that the pressure that's left behind in the system
after the patient is exhaling is 1.6 centimeters of water.
So this is a small number.
We don't usually worry until that pressure starts to get over 5,
and certainly we worry when it gets over 10.
The last thing to consider is the effect that positive pressure ventilation
has on hemodynamics.
Certainly, patients who come in and are intubated
are given sedatives, given neuromuscular blockade, and that
can lead to a loss of adrenergic tone, and patients
can have hypotension from that alone.
The positive pressure also has its own independent effects.
It impacts the right ventricle and the left ventricle slightly differently.
And understanding that will help you apply these effects
to your patient's physiology.
First, considering the right ventricle.
When you intubate a patient and put them a positive pressure ventilation,
that positive pressure will decrease the preload to the right heart.
That's indicated there by the white and blue arrowheads,
that increased pressure decreases venous return.
However, it'll increase the after load on the right ventricle.
And this is sometimes a little bit of a tricky concept to understand.
What occurs is that with positive pressure ventilation,
the alveoli will become distended, as shown in the inset here.
This leads to a crimping of the small capillaries,
and that increases the pulmonary vascular resistance overall.
So increasing the pulmonary vascular resistance
increases the after load on the right ventricle.
This is why a patient who comes in, in right ventricular failure
and gets intubated often deteriorates precipitously with that intubation.
Conversely, the left ventricle has some different effects.
Similar to the right ventricle, it does result
in decreased preload when the patient is placed on positive pressure
ventilation.
However, it also decreases the after load to the left ventricle.
This is a function of the transmural pressure,
being illustrated here by the red and white arrows and the black arrows.
The positive pressure shown by the black arrows
decreases the transmural pressure, that transmural gradient, and that
leads to a decrease in the after load.
This is why sometimes putting a patient on positive pressure ventilation
can be advantageous for somebody who presents in left ventricular failure.
So this has been a very brief review of the physiology needed to take care
of patients on mechanical ventilation.
For further details, please refer to the written works accompanying this video.