Thank you for joining us.
We're going to go ahead and do a sample problem here to see if you can understand what you
might need to do on a ventilator given a specific situation.
Let's say that you were covering a patient who was in AC mode.
You would see this.
You'd see AC 12, that means twelve breaths per minute, tidal volume 400, FIO2 of 40 percent
and a peep of 5.
Let's say that the blood gas results were 7.26, 60, 55, 26.
For those of you who don't know, this is the Ph.
That's a little low.
This is the PCO2.
That's a little high.
This is the PO2.
That's low.
This is the bicarb.
For those of you who don't know how to interpret these, please look at our medical acid based
lectures.
The Ph is low.
The PCO2 is high.
Because these are going in opposite directions, this has to be a respiratory disorder.
Because the Ph is low, it's a respiratory acidosis.
We're under-ventilating here most likely.
Also, the PO2 is low, as well, so we're under-oxygenating.
What things could we do to these vent settings to improve this patient's blood gas?
Let's assume that this patient is sedated.
When I say that, that should clue you into the fact that if the patient's AC is set at
12, that means they're actually probably breathing at 12.
That's important because if they're not sedated and they're set at an AC of 12, they could
be breathing at 16 or 20 because they're controlling the rate.
If you sedated them with Morphine or Ativan or Versed or some other sedative, then their
respiratory center may not be functioning and they may be what we call riding the vent.
When they're riding the vent, they're sedated and their AC is at 12.
Now, if I were to drop this rate, they would probably follow it down or of course if I
were to increase the rate, they would follow it up.
Now, the opposite is true if they're not being sedated.
Let's say that they're not being sedated, that their AC backup rate is set at 12, but
they're breathing at, let's just say, 18.
If they're breathing at 18 and I increase the AC rate from 12 to 14, am I really doing
any change?
No, I'm increasing the backup rate, but because they're breathing well above the backup rate,
that is not going to have any effect of the blood gas.
What I'm telling you here in this case, is that they are sedated and they are what we
call riding the ventilator, so they're at an AC of 12 and they're actually breathing
at respiratory rate, or what we call a spontaneous respiratory rate, of 12.
What could we do to improve ventilation and oxygenation?
Based on our previous discussion, you know that we could increase the AC to 14 or 16.
Okay.
You could also use odd numbers, but we just like to use even numbers because it's just
easier for some reason.
Tidal volume doesn't need to be 400.
400 could be a little bit low.
We could go up to 500.
Those are 2 changes that we could make, which would improve the Ph and reduce the PCO2.
Now, let's look at our FIO2.
It's a 40 percent, and our PO2 is pretty low at 55.
The PEEP is 5.
There's a lot of things we can do.
We can change either the FIO2 or we can change the PEEP.
If this patient's blood pressure is marginal, I'm probably not going to want to increase
the PEEP.
As we told you before, the reason why we don't want to increase the PEEP is because increased
PEEP increases intrathoracic pressure.
Intrathoracic pressure increases the pressure in the right atrium.
Increasing the pressure in the right atrium decreases venous return, and as you know,
decreased venous return reduces cardiac output which reduces blood pressure.
I.E.
increase peep decreases blood pressure, usually.
If the blood pressure is marginal, I'd probably want to go with increasing the FIO2 on the
ventilator to improve our oxygenation.
Now, on the other hand if this patient is a congestive heart failure patient on the
ventilator, then we have plenty of venous return coming back to the heart and probably
some pulmonary edema in the alveoli.
Increasing the peep to 10 in that case may actually be beneficial because that increased
and expiratory pressure is going to push that pulmonary edema out of the alveolus.
It's going to increase the right atrial pressure, push back that fluid that's congesting it,
and allow the heart to work at a better efficiency.
You can see here that depending on the clinical situation you may want to choose one versus
the other.
We're going to sort of get into some special circumstances here coming up.
I wanted to show you that as a possibility so we were to get a blood gas later 7.40,
40, 80, 26.
Okay, so now you know how to adjust vent settings.
Let's us look at a couple of special cases here.
Let's look at a thing called ARDS.
Now, what is ARDS?
ARDS is adult respiratory distress syndrome, or acute respiratory distress syndrome.
Used to be known as adult, but it's acute respiratory distress syndrome.
This is an inflammatory condition which affects the lungs diffusely and you can see it after
any type of infection.
I'm talking urinary tract infection, pneumonia, aspiration, terrible ARDS.
Here is basically what happens.
The lungs become very stiff, so the compliance of the lungs drops.
Because of that you'll see elevated plateau pressures.
Sometimes you'll get pneumothoraces in the lungs.
Here's the key, though.
You get a restrictive lung physiology, the lungs become very, very stiff.
Also, in the alveoli, there is a lot of hyaline membrane that gets deposited.
As a result, if you were to look microscopically at the alveoli level, they would be filled
with fluid and they would be collapsed.
Now the problem is, is that they had found in research studies that when they ventilated
these people with high tidal volumes, it was opening up and closing these alveoli.
Opening up, closing.
Every single time the patient took a breath in and out, they would open up and close,
and that let to one thing and one thing only.
That was inflammation.
That they believed led to death.
They had idea.
They said let's go ahead and do something different.
Let's do something called the open lung model.
The open lung model was this.
Let's go ahead and stint open as many alveoli as we possibly can using high levels of peep.
Okay, we're talking peep around 12, 14 ... It just depended on how much the oxygen was diminished
by.
The lower the oxygen levels were, the higher levels of peep that they used.
They felt that is the oxygen was low that these alveoli needed to be recruited.
More they needed to be recruited, the more peep they added.
As they added this peep, they were able to open up these alveoli.
Now, with these alveoli open, they didn't want them to derecruit.
In other words, these didn't want them to close.
What they did was they had just tiny tidal volumes.
The key here is high PEEP, low tidal volume.
What I mean by low tidal volume, I'm talking 6 to 8 milliliters per kilogram ideal body
weight.
By the way, ideal body weight is measured by your height.
You measure somebody's height and that converts into what their ideal body weight is in kilograms.
Once you know what that is, multiply it by 6 to 8, and that's the range of tidal volume
that you should be using.
We're talking usually in the 4 to 500 hundred range.
Okay?
When they did this type of strategy with ARDS, they found that survival improved.
Mortality went down.
They were able to affect change.
That is the standard of care now with ARDS.
If you have ARDS in a patient, you want to make sure that you're using low tidal volumes
and increasing your PEEP for recruitment.
Okay, let's talk about the other special case, COPD.
Completely, completely different problem.
The compliance of the lung in COPD is actually high, but the problem here is that these airways
are obstructed, and so it's very hard to get the air out.
As a result of that, air gets trapped, and because air gets trapped, the key there is
that you have very long expiratory phases.
Now, the key with this is, these patients that come in typically have high CO2 levels.
The temptation there is when you see a high CO2 level, it's to do what?
It's to increase the respiratory rate and to increase the tidal volume.
When you do that, you're increasing the amount of air in the lungs, and it takes longer for
that air to get out.
You need more time for that air to come out, otherwise you're going to stack another breath
on top of the old one.
If you're increasing the respiratory rate, you're not allowing more time.
In fact, you're allowing less time for that air to come out.
Think about it this way.
If the respiratory rate that you set on a patient is 12, how much time do you have for
a complete breath cycle?
You have 5 seconds because 12 goes into 60 seconds 5 times for 5 seconds.
Let's say you set the rate to 15.
How many seconds do you have then?
4 seconds.
You can see that by increasing the rate here from 12 to 15, you chopped off an entire second
per breath to get that air out.
They key here is, normally when somebody takes a breath in, it's usually one third, two thirds,
in terms of inhalation and exhalation.
Okay?
What we can do in COPD is we can actually affect the time it takes to take a breath
in.
This is called the inspiratory flow rate.
Typically it's around 60 liters per minute.
Now, in patients with COPD, what do we want to do with the inspiratory flow rate?
We would love for that air to get in very quickly so that we could have more time for
exhalation.
In other words, we want to decrease the inspiratory time by increasing the inspiratory flow rate.
In other words, get the air in quickly so you can have the rest of your 5 seconds to
have the air come out.
My recommendation for inspiratory flow rates and indeed the society's recommendation, is
they should usually be around 80 to 100.
If you can get the air in quickly, you have more time for that air to come out.
Avoid the temptation to increase the respiratory rate because you make actually make the carbon
dioxide worse by increasing the respiratory rate or the tidal volume.
The strategy that I would employ in somebody with COPD is make sure that the inspiratory
flow rate is high.
Make sure they're getting very good bronchodilators, and look at the flow volume loops on the ventilator.
Make sure that flow is returning back to 0 before the next breath goes in because if
flow is not returning back to 0 before the next breath is being initiated or air is going
in, then you must be getting breath stacking.
If you get breath stacking, you can hyperinflate, and if you hyperinflate, you will increase
the intrathoracic pressure to be very high which is going to increase cardiac output
and the patient will code because their blood pressure will go down very low.
By the way, the treatment for that is to simply disconnect the patient from the ventilator
so they have time to exhale and get all that air out.
That is COPD.
That is a special case.
We could talk a long time about that, but I think we have discussed the basics here
over the last few lectures.
We've talked about what the ventilator is.
We've talked about what the endotracheal tube is, what it looks like, what its purpose is,
what the different modes are, what kind of alarms there are, the peak pressure, the plateau
pressure, and how to affect change on a ventilator using the venting, and now finally a couple
of special cases.
I would practice these things.
Read up more about it, and we can talk a little bit more about specific cases and the ventilator
in future lectures.
I think this is a good basic introduction to what the terms mean and what to do on the
ventilator.
Thanks once again for joining us.