Ventilating Obstructed Lungs

There are two major references for the data contained in this post which have been linked here:

Mechanical Ventilation of the Severe Asthmatic Patient
Managing Initial Mechanical Ventilation in the ED

A summary of the ventilation of the patient with obstructive lung disease patient is below:

Setting up the ventilator for the Obstructed Lung

The problem with obstructive lungs that need ventilation

We often think of asthma (and COPD) as a problem of getting air out, however by the time the patient presents with a need for invasive airway management and ventilation, the problem also becomes one of getting air in.

One of the big challenges with ventilating the patient with obstructive pathology, is that simply placing an ETT and placing the patient on mechanical ventilation does nothing to help the patient, in fact, forcing more air, under more pressure is more likely to increase the danger to the patient and possibly worsen the condition.

OK, so what do I do then?

Let’s say we do get to the point where the patient with an obstructive lung pathology needs to be ventilated… first of all, what does this look like?

If the above symptoms progress despite maximal therapy, then the patient may need to be escalated to airway management and invasive ventilation.

There are some things you should already have considered and have already tried to prevent this downward spiral of trapping of air and increasing pressure:

The fix here is NOT to push more air into the chest, rather to ventilate in a way that limits the pressure buildup within the chest, and thus decreases the risk of hypotension, hypoxia and death. The whole aim of intubating this patient for ventilation is to maximize the expiatory time and decrease the pressure buildup within the thorax, to buy time for the medications you are still administering to work.

The aims of mechanical ventilation are:

Let’s have a look at the physiology and pathophysiology associated with the acute exacerbation of asthma/COPD leading to air trapping (this is a fairly complicated explanation that is summarized below).

How does a normal lung work to inflate and deflate?

Normally, the brain senses an increase in the concentration of CO2 in the system through chemoreceptors located in the arch of the aorta, the carotid bodies, and measuring CSF at the medulla oblongata.

This increase leads to stimulation of the respiratory center, increasing rate and volume of ventilation (to increase the minute volume).

Messages are sent down the phrenic nerve (that innervates the diaphragm) and other nerves that innervate the intercostal muscles to contract these muscles, making the volume inside the thorax larger, and the pressure inside the thorax lower.

This causes a rush of air into the lungs from the outside, in an attempt to equalize the pressure, and the lungs fill with air. As can be seen this is an active process as the pressure within the thorax needs to be decreased by increasing the volume of space within to allow for air movement.

In the patient who is trapping air, this is really difficult as the resting pressure within the thorax is already a lot higher when compared to the normal patient above, this results in a resting positive pressure within the thorax. In order to get air to move, this patient still needs to create a negative pressure but because their starting point is much higher, the patient needs to work much harder to move the same amount of air.

Often the patient with bronchospasm or air trapping will have a prolonged expiratory phase, but as they struggle more and more with increasing pressure, the expiration may not always come to an end before the hypoxia and air hunger drives the next breath. The patient is not yet finished breathing out, when they are triggered by their brains to take a new breath in, and more air is inevitably trapped.

Normal lungs at end of expiration

In this image you can see that in order to generate a negative pressure to pull air into the lungs, the patient will need to contract some muscle. Let’s say a hypothetical pressure of -4cmH20 is needed for a normal tidal volume.

Obstructed lungs at end of expiration

In this image you can see that in order to generate a
negative pressure to pull air into the lungs, the patient will need to contract muscle a lot harder to get to a -4CmH20 This patient needs to overcome the 5cmH20 positive pressure in his lungs and exert a negative pressure of 4cmH20 before the lungs will fill with air.

The trick comes in here, that even if we were able to (and we are to an extent), decrease how hard the patient has to work to move air (by increasing the external pressure of the air that moves into the lungs by blowing it in under pressure), this doesn’t really solve the problem. It only buys a little time, after which; the pressure inside the thorax will still be larger (due to air being blown in and still trapped by the bronchoconstriction) than the external pressure.

The pressure being used to assist the patient will need to be increased again to allow for some air movement. This can be only be done to a certain limit, as the chest wall can only expand to a point. Once the pressure driving the air in reaches equilibrium with the pressure trapped, there is no way that air can move in the lungs. This is when the patient often arrests or ends up with a “Silent Chest” when there is not enough pressure generated to move air into the lungs.

These patients arrest for a few reasons:

The image to the right shows the effect of massive expiratory pressure on the smaller airways, resulting in collapse, leading to an increase in trapping:

As if all the other stuff we have already covered is not enough… We also need to be careful about ending up in a situation where hyperoxia occurs (where we administer too much oxygen). This is a problem as the hypoxic vasoconstriction in the pulmonary circuit actually helps to maximize perfusion to the areas that are better ventilated and will begin to decrease if there is too much oxygen administered, and resulting in a worsening V/Q mismatch.

Hypoxic vasoconstriction diverts blood from those lung units most affected by bronschospastic ventilation failure, thereby maintaing a good V/Q match.

Hyperoxia contributes oxygen to poorly ventilated bronschspastic regions, and degrades the V/Q matching by “stealing” blood from well ventilated regions.

If all we are going to do is intubate the patient so we can force air under greater pressure into the lungs, we are not helping the patient at all. If your vent settings are such that we can minimise the pressure, and maximize the expiration, whilst allowing the medication we are still administering time to work, then we will be able to actually assist this patient.

Right…so we are at the point where we need to intubate and ventilate this patient… HELP!

Some things we have to get right from the start:

Ventilator Settings:

Anticipate that there will be a MUCH higher PaCO2 level than you might be comfortable with as a result of the slower respiratory rate and lower tidal volume. This will have to be accepted for the period whilst the patient is still trapping pressure. Permissive hypercapnia is the term used to describe this where you may have to accept PaCO2 levels that are very high. Provided the pH doesn’t drop below 7.2, this is considered to be safe.

If the patient’s condition is complicated by RICP (or some other disease process where CO2 level maintenance should be within strict norms) then this is not the best approach to take.

Affecting Expiratory Time

Some things we have to get right from the start:

Normal ventilation of a patient. All the settings on the right and all the monitored results in the grey block. Take note of the peak pressure, the I:E ratio and the inspiratory time.

When we adjust just the I:E time by decreasing the inspiratory time, we adjust the I:E ratio. BUT the actual expiratory time has only increased by 0.4 of second. Also notice what happened to the PIP when we made the inspiratory time shorter.