DR. SUSAN WILCOX: In this video, we will cover
mechanical ventilation and acute respiratory distress syndrome, or ARDS.
The first point to know is, what is ARDS?
Not all patients who present with severe hypoxemia have ARDS.
ARDS is defined by four major criteria.
First, it's an acute process.
It's not just an exacerbation of some chronic lung disease.
Second, there are bilateral patchy infiltrates.
This is why that first chest x-ray that showed a lobar pneumonia is not ARDS.
There has to be bilateral lung disease.
It cannot be fully explained by cardiogenic pulmonary edema.
Now, certainly, patients who have CHF can get ARDS.
But it cannot be fully explained by cardiogenic pulmonary edema.
And then, lastly, to define and quantify ARDS, we check the PaO2 to FiO2 ratio--
or the ratio of oxygen in the arterial blood
to the fraction of inspired oxygen. To do this adequately,
one needs to have the patient on at least 5 centimeters of water pressure.
Mild ARDS is defined as PaO2 to FiO2 ratio of less than 300.
Less than 200 is moderate, and less than 100 is severe.
It's important to quantify the degree of hypoxemia,
because this not only defines ARDS.
It also helps clinicians determine the prognosis for the patient.
As you might imagine, the worse the hypoxemia, the worse the outcomes are for these patients.
The principles of mechanical ventilation in ARDS
are fairly straightforward.
The whole idea is to prevent secondary lung injury.
The way we do that is keeping the patients on low tidal volume
ventilation with low pressures.
The first and most important rule is to put the patient on a low tidal volume
setting.
We target 4 to 8 milliliters per kilogram of predicted body weight.
Please keep in mind that predicted body weight is not
the same thing as a patient's actual body weight.
Based upon the patient's height and their biological sex.
We started the patient at 6 cc's per kilo of predicted body weight.
And we can titrate up or down as needed, depending
upon the patient's clinical response.
The next thing that we evaluate and monitor is the plateau pressure.
As we discussed in the physiology portion,
the plateau pressure is the pressure that we obtained when we stopped all
flow and let the pressures equilibrate.
It's really the pressure that the alveoli see.
We want to keep these pressures low to prevent
barotrauma or injury to the lungs.
The driving pressure is the difference between the plateau
pressure and the PEEP.
You can think about it as the pressure that it takes
to distend the alveoli for each breath.
Studies have shown that keeping the driving pressure less than 15
is associated with better outcomes in patients with ARDS.
Here's an example screen of somebody who has ARDS.
You can see at the bottom that the patient
is set on assist control, volume control ventilation
with a tidal volume of 340.
The patient is set at a respiratory rate of 34, a PEEP of 18,
and is on 100% FiO2.
To review, we want to check the peak inspiratory pressure and the plateau
pressure.
We perform a inspiratory hold, allowing us to see the plateau pressure.
In this example, as we saw in the prior video, the plateau pressures 38.
This pressure is extremely high.
And it's very concerning for lung-injurious ventilation.
The driving pressure is illustrated here as the change
between the PEEP and the plateau pressure,
or the pressure that's descending the alveoli.
The PEEP is the baseline pressure, the positive end-expiratory pressure.
It's the pressure that keeps the alveoli open and prevents atelectasis.
This is a great example of why it's so important to keep the patient on lung
protective ventilation and not do secondary harm.
These are excellent images taken for Dr. Malhotra's publication
in The New England Journal, in 2007.
Here we see rat lungs that have been ventilated with 20 minutes of lung
injurious ventilation.
High tidal volume, high pressure ventilation.
You go from having normal lungs, normal architecture,
to boggy, distended, hemorrhagic lungs within just a few minutes.
And if you look at the electron microscopy view,
you can see that the lungs are actually shredded.
Doing the high tidal volume, high pressure ventilation
tears up the lungs.
And what happens here is that you may not see it acutely,
but this leads to cytokine release.
The cytokine released results in multi-organ system failure days
to weeks later, and results in the patient's death.
This is why lung protective ventilation is so critically
important in patients who have ARDS.
Here's another example of a ventilator screen,
illustrating the principles of lung protective ventilation.
Somebody who is being ventilated at a tidal volume of 330,
which for this person--
we can see at the bottom-- is 6.35 milliliters per kilogram
of their predicted body weight.
They are on 18 of PEEP, with 100% FiO2.
And they're at 22 breaths per minute.
The peak pressure here is 36.
Because it's higher than 30, we now have to be concerned
that perhaps the plateau pressure is also higher than 30.
The way to do this is to perform an inspiratory hold.
Here's an example of the inspiratory hold
being performed on this very patient.
We can see here that the plateau pressure, which is provided here
in this inset screen, is 32.
This is higher than ideal pressure of 30 that we're targeting.
So the next step is to take this volume down.
We know that the patient's set on 6.35 milliliters per kilogram.
I would recommend taking this down to 5 milliliters per kilogram.
Then reassessing to see if we can get that plateau pressure
down to 30 or below.
PEEP is the next thing to discuss.
PEEP is wonderful in ARDS, and it's especially
important in patients with COVID-19.
We're finding that these patients, in general, are very PEEP responsive.
PEEP increases oxygenation.
First, by increasing the mean airway pressure,
it increases the pressure in the overall system.
And you can see that illustrated here, by how it lifts up the entire waveform.
The other thing that PEEP does is help prevent and treat
atelectasis and derecruitment.
So in a patient who has ARDS, there are going
to be many areas of atelectasis, of derecruited lung,
illustrated here by the blue shading on this chest x-ray.
When patients have an increase in PEEP, they
go from having atelectasis, hopefully, to an optimal state.
But we don't want to over-distend them.
So the goal at the bedside is to find the optimal PEEP where the patient's
sitting in the optimal space.
But not atelectatic nor over-distended.
The over-distension is a very real risk, and if you over-distend the lungs,
there are a few things that can happen.
Not only can it result in barotrauma, which seems obvious,
but it can also result in hemodynamic compromise.
This is why with PEEP, more is not always
necessarily better as we're thinking about ventilating patients with ARDS.
We also have to be cognizant of their minute ventilation.
As we saw in the physiology video, minute ventilation
is equivalent to the tidal volume times the breaths per minute.
As we decrease a patient's tidal volume, we usually
need to increase the respiratory rate
to keep them at a fairly comparable minute ventilation.
We can certainly allow patients to have permissive hypercapnia,
or allow the CO2 to rise above what we would normally
consider to be an acceptable range.
However, when patients have evidence of right ventricular
strain or pulmonary hypertension, we do have
to be cognizant that having an increase in CO2
can, at times, be somewhat deleterious.
Therefore, most authors recommend that we not let the pH fall below around
7.2-7.25, if we're using a permissive hypercapnia strategy.
Trying to increase the respiratory rate to optimize the CO2 is a better move.
And permissive hypercapnia should be reserved, if that's not sufficient.
Here's another example of a patient being ventilated with ARDS.
We can see that this person is set on a tidal volume of 400
milliliters, a respiratory rate of 30--
trying to maintain that high minute ventilation, a PEEP of 18 keeping high
mean airway pressure.
It's keeping the patient well recruited.
And it's still set on 100% FiO2.
If we look at the values that we're receiving,
the patient has a peak pressure of 47.
This is extremely high and a very concerning level.
The plateau pressure has been checked here.
We can see that it's 43.
43 is far above 30.
And, again, this is a very concerning finding.
We can try to bring down the tidal volume
to bring that plateau pressure down, That's a pretty big jump from 43
down to 30.
When we see levels like this, we start to think
that we might need to do some more invasive treatments
and have another plan.
At this point, expert consultation is most definitely warranted.
When we're treating a patient with optimized mechanical ventilation
and they continue to over-breathe the vent,
we might need to provide neuromuscular blockade.
Previously, we used to recommend giving neuromuscular blockade for almost
all cases of moderate to severe ARDS.
But recently there was a study that was published
that showed that there was no difference in patients
who were randomized to receive neuromuscular blockade or who were not.
The concern is that patients who are dyssynchronous with the vent
will have ongoing lung-injurious ventilation, even though they
are set at appropriate tidal volumes.
Here's an example of someone who was set at 380,
yet this person has significant air hunger
and is pulling tidal volumes in the 800-range--
as we can see here on the ventilator screen.
Another clue that this person is dyssynchronous with the ventilator
is to look at the wave forms.
Rather than having smooth regularized wave forms,
we can see that they're jagged and irregular.
If this patient is well sedated, but they
continue to be dyssynchronous with the ventilator,
this is a great time to add neuromuscular blockade
to improve ventilator synchrony.
Another move to improve oxygenation is to provide a recruitment maneuver.
So recruiting maneuvers can be provided in multiple different ways.
A recent study randomized patients to receiving recruitment maneuvers
with a stepwise PEEP approach.
In that approach, they started off with a PEEP of 25, then 35, and then 45.
Resulting in total pressures of 60 centimeters of water pressure.
This is an extremely high level of pressure and large jumps in the PEEP.
In that study, patients who were randomized to that treatment
had worse outcomes.
Many of us, therefore, recommend a more gentle approach to recruit maneuvers.
The idea behind a recruit maneuver is simple.
We want to recruit that atelectatic lung to improve surface area
and improve the areas for gas exchange.
There are some risks, however.
The high levels of pressure can lead to over-distension
of the good areas of the lung.
And that can crimp the capillaries, leading to transient hypoxemia.
Usually this is only short-lived.
And will stop as soon as the patient is placed back
on a lower level of pressure.
The more concerning finding is that a patient who has some right ventricular
dysfunction at baseline-- or especially in light of the ARDS--
may be particularly susceptible to hemodynamic consequences
with a recruitment maneuver.
The increasing pressure in the inter-thoracic system
can lead to decrease in venous return and increase of pulmonary vascular
resistance, and acute right heart failure and decompensation.
This is why we recommend instead a more judicious approach
to increasing the PEEP.
At our institution, we use a stepwise PEEP gradation
of about 2 to 3 centimeters of water, held for approximately five breaths
before increasing to the next level.
By using this slow stepwise level, we are
able to recruit the lungs gently and reduce the risk of having
some hemodynamic perturbations.
If at any point while performing a recruitment maneuver the patient starts
to become unstable, decreases their blood pressure,
we will stop, reassess, and likely put the patient
back down to a lower PEEP level.
A recruitment maneuver should never be done
without the full team aware and ready to respond if there is any deterioration.
For further information about recruitment maneuvers,
please see the written materials.
These patients have derecruitment as a major cause of their hypoxemia.
As we showed in the physiology video, lying a patient flat
can lead to the posterior surface area becoming
compressed and atelectatic derecruited.
To improve this, we can prone patients.
It appears that patients with COVID-19 do especially well with proning.
What happens with proning is we take the weight off
of that large surface area of the back of the lungs.
And move it to the front, which is a smaller surface area.
Additionally, this improves pulmonary mechanics,
allows better lung expansion.
And it takes the weight of the heart off of the back of the lungs
and puts it into the front of the chest.
Studies have shown significant improvements in oxygenation,
and also improvements in mortality with proning.
Therefore, many are recommending an early proning strategy
for patients with COVID-19.
Pulmonary vasodilators are another method to improve oxygenation.
The way they work is by improving V/Q matching.
So in the first column here, we have two different sets of lung units.
At the top, we have a lung unit that is ineffective.
It's not participating in gas exchange.
The lung unit at the bottom is working well and it has excellent V/Q matching.
When we instill a pulmonary vasodilator--
an inhaled pulmonary veins vasodilator, it
doesn't go to the lung units that are ineffective due to the pathology.
However, it will go to the effective lung units and cause vasodilation.
By this mechanism, it redirects blood flow to the good lung units.
Thereby, improving V/Q matching.
What we see is an improvement in oxygenation.
Unfortunately, inhaled pulmonary vasodilators
have never been shown to improve mortality.
They do possibly have a role, however.
Inhaled pulmonary vasodilators can be used to help transport a patient,
say for ECMO evaluation or to get them to a tertiary care center.
They can be very useful as a bridge to other therapies
or to wait for other therapies to take effect.
In COVID-19, we are recommending against the use of inhaled epoprostenol
as a pulmonary vasodilator.
The reason why is that it requires frequent ventilator circuit changes,
and we don't want to do anything that can increase
the aerosolization of the virus.
Another example of a patient with severe ARDS.
We have a patient here who's set on tidal volume of 380,
a respiratory rate of 24, a PEEP of 10, and an FiO2 of 90%.
Looking at the patient's pulmonary mechanics,
they have a peak pressure of 45, with a plateau of 37.
Plateau of 37 is, again, far too high and greater than the 30
that we are targeting.
We could try to bring down the tidal volume from 380
to see if we can get down closer to a 4 cc's per kilo of predicted body
weight strategy.
This may help get us down to a plateau pressure of less than 30.
However, it's not clear that it necessarily will.
When we have pressures that are this high
and we're having difficulty oxygenating or ventilating
without performing lung-injurious ventilation,
a typical considerations is ECMO.
In the time of COVID-19, the role of ECMO is very much in question.
The idea behind veno-venous ECMO has really been to allow the lungs to rest.
We will provide the patient oxygenation, CO2 removal,
without having to use lung-injurious ventilation,
and give the patient some time.
This was used with some success in patients who
had the H1N1 epidemic many years ago.
However, the role in COVID is still very much in question.
Patients with COVID-19 are requiring prolonged mechanical ventilation.
And those who've been placed on ECMO have not yet
shown to have good outcomes.
As such, the role in this epidemic is still to be determined.
That concludes the video on mechanical ventilation in ARDS.
For further information, please refer to the written materials.