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Airway Pressure Release Ventilation

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Airway Pressure Release Ventilation

Take home messages

  • APRV is an open lung method of invasive mechanical ventilation
  • Spontaneous breathing is encouraged
  • T low should be adjust to start the next breath at 75% peak expiratory flow rate

The idea

Take a deep breath in and hold it for five seconds.

While holding your breath in, add a few tiny little breaths on top.

Then exhale really fast, and immediately inhale as much as you can again.

Hold.

Repeat.

That's APRV.

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APRV is a pressure controlled mode that delivers nearly continuous positive pressure with time-cycled brief releases at a much lower pressure

What.

I know right? Normally we take a relatively smooth breath in and then immediately release it again, spending a greater amount of time in a state of exhalation rather than inhalation.

But if we're struggling to recruit a diseased hypoxic lung, letting it exhale and collapse down every breath is going to make oxygenation a lot harder.

Yes PEEP can help prevent this, but sometimes there's just not enough PEEP to go around.

Enter Airway Pressure Release Ventilation

APRV does precisely the opposite to conventional ventilation patterns, and the idea is keeping the lungs open, or fully inflated for as long as possible, to encourage oxygenation through nicely inflated alveoli, and avoiding having them collapse and derecruit after every breath.

It's essentially CPAP on steroids, or like ventilating a patient by repeatedly performing recruitment manoeuvres.

The brief and rapid exhalation is there to facilitate a bit of CO2 release, although usually these patients end up on some sort of 'permissive hypercapnia' protocol where we'll tolerate a respiratory acidosis if it means better oxygenation.

The other funky thing about APRV is that we try and get the patient to breathe spontaneously as well.

If done correctly, the patient will be taking little tidal breaths on top of the enormous inhale, venting out a little extra CO2 before the pressure gets released.

Catch me as I fall

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The patient's lungs need to be recruitable to benefit from APRV

Remember the key aim here is maintaining oxygenation in a recruitable lung, so what we want to avoid above all else is derecruitment and collapse of our hard-earned alveolar surface area.

But surely if we release the pressure to vent out CO2, the alveoli will all collapse and we'll be back to square one?

Exactly, so we set the next breath to kick in before the pressure drops to zero, thereby preventing alveolar collapse and maintaining recruitment.

Does it work?

Who knows.

In 1987, Stock et al. found that their array of artificially sleepy canine colleagues had much better arterial oxygen levels when ventilated with APRV than conventional techniques.

Since ten dogs with healthy lungs are eminently comparable to thousands of humans with profound respiratory failure from multiple different pathologies, we decided to crack on and use it in intensive care.

But hey - why not.

How to set it up

Forget tidal volumes, forget pressure support and say hello to:

P high

The highest level of pressure applied by the ventilator

  • It's different to Pinsp from conventional modes, because rather than applying this pressure to deliver a tidal volume, it's trying to hold the lungs open at this set pressure for a predetermined duration (T high)

T high

The amount of time spent at P high

  • 5 seconds is a sensible starting point

P low

The lowest pressure delivered by the ventilator

  • This is the pressure that the breath is 'released' to
  • Usually set to 0 cmH2O

T low

The time spent delivering the P low

  • Titrated such that the next breath starts to kick in before the actual airway pressure reaches the T low
  • If you look at the orange trace below, you'll see the pressure drops rapidly towards P low, but then jumps up again before reaching it, thereby maintaining some PEEP and preventing derecruitment

Here's a great graphic from deranged physiology

APRV with ventilator settings

The key parameter

Look at the green line above.

The exhaled flow starts really fast and rapidly slows down - you're trying to catch the point at which the flow is 75% of the peak expiratory flow rate.

You're trying to catch the exhalation just in time to deliver the next breath before the lungs start to collapse.

To do this you adjust the T low, such that the next inhalation starts when the expiratory flow is at 75% of its maximum.

If you wait any longer (until the flow is <75%) then you start derecruiting and the whole exercise is pointless.

Can you actually exhale any CO2?

Yes actually, quite a bit:

  • You can reasonably get around 50 litres per minute expiratory flow
  • If T low is 0.5 then you're looking at just over 400ml 'tidal volume' before the next breath in
  • If you're doing 12-16 of these per minute, the minute ventilation is around 5 litres per minute - not unreasonable

If you add in some spontaneous breathing as well, you can actually get some pretty effective CO2 clearance.

A neat trick is to see what minute ventilation is needed to achieve a suitable PaCO2 before starting APRV, and then aim to establish this minute ventilation once APRV has been commenced.

75% appears to be the sweet spot of getting enough CO2 out without allowing too much alveolar collapse.

When to use it

Clearly you're not going to take your freshly intubated pneumonia patient and whack them straight onto APRV - you're going to try some normal stuff first.

The question to be asking yourself is:

"Is this patient recruitable, and do I think lots of recruitment manoeuvres will help their oxygenation?"

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APRV is worth a try if the PaO2/FiO2 ratio is less than 13 kPa and the patient has recruitable lungs

Indications

  • Proning has failed
  • Low tidal volume ventilation has failed
  • Recruitable ARDS
  • Recruitable multi-focal pneumonia

What are the intended benefits of APRV?

  • Improved gas exchange
  • Maintenance of alveolar recruitment, particularly in dependent areas
  • Reduced left ventricular afterload (via reduced transmural pressure)
  • Encourage respiratory muscle activity and avoid muscle wasting
  • Reduced sedation

What are the downsides?

Nothing we do is without risk of harm, and APRV is the same.

Lung damage

  • We're not completely sure, but there might be an increased risk of barotrauma
  • You're not really controlling how big the tidal volumes are, so they can end up being uncomfortably large
  • Atelectotrauma can still occur if T low is longer than 0.2 seconds, because there will be at least some derecruitment and collapse
  • Bronchopleural fistulae will almost certainly get worse

In the wonderful words of Dr Yartsev:

"There is a higher risk of pneumothorax and pneumomediastinum...perhaps partly due to the fact that these patients are awake and therefore free to cough violently while on a PEEP of 30".

Cardiovascular instability

  • We normally like dry lungs for ARDS, but APRV requires a decent amount of filling if you're not going to squish the vena cavae shut and completely mess with the venous return
  • Patients with pulmonary hypertension and right heart failure are going to have a seriously hard time with APRV, hence it's a fairly strong contraindication

They need to be breathing

Without the added benefit of the spontaneous breathing on top, APRV is just inverse ratio ventilation.

  • If the patient is sedated heavily enough to be apnoeic, or paralysed, then APRV loses rather a lot of its value
  • Spontaneous breathing can also be quite hard work, and consume a lot of oxygen in its own right
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It's nice to keep pressures below 30, but in reality we have no idea how these numbers relate to actual lung trauma in real life, so prioritise oxygenation over some hypothetical pressure limit.

Contraindications

There aren't any absolute contraindications to APRV really.

Relative contraindications

  • Restrictive lung disease
  • Severe cardiovascular instability - particularly hypovolaemia, or pulmonary hypertension with a bad right ventricle
  • Bronchospasm
  • Bronchopleural fistula
  • Pneumothorax (without a chest drain in)
  • Recent lung surgery

Traumatic brain injury and raised intracranial pressure have often been cited as relative contraindications to APRV but it may actually be the case that the benefit of improved oxygenation outweighs any potential harm by theoretical increases in ICP.

Probably best to only do this in a specialist centre with ICP monitoring in situ.

What settings should I start on?

Whatever your consultant has told you to, however if you've boldly decided to initiate APRV by yourself, then the following are some sensible starting numbers:

  • FiO2 100% - the patient is already hypoxic and you can wean this down
  • P high - set to current plateau pressure
  • T high - set to 5 seconds
  • P low - set to 0 cmH2O*
  • T low - set to 0.5 seconds

Then check that the T low is sufficiently short that the expiratory flow is being stopped at around 75% of peak flow.

This usually involves some scrolling with a clicky dial on the ventilator screen and looking at the graph.

If you don't immediately know what we're referring to, then you probably shouldn't be initiating APRV by yourself just yet.

  • Then wean the sedation and reverse any paralysis and get them breathing
  • Allow for 'permissive' hypercapnia, as long as pH remains above 7.25
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Any time you adjust anything on the ventilator, you need to reassess whether you're still cutting off the expiratory flow at 75% of peak flow.

*Some advise that P low should be around 5 cmH2O to reduce sudden pressure changes in the lung, however this hasn't been widely adopted yet.

Then sit back and try to be comfortable with the fact that your I:E ratio is now around 9:1.

Tweaking and Troubleshooting

The PaO2 is too high

  • Reduced FiO2
  • Once FiO2 40-50%, reduce P-high

Same as weaning PEEP and FiO2 in conventional ventilatory modes.

The PaO2 is too low

  • Increase FiO2
  • Increase P high by 2
  • Increase T high by 0.5 seconds
  • If T high already >10, maybe reduce T low by 0.2s

The PaCo2 is too high

  • Reduce sedation to encourage spontaneous breathing
  • You can also use automatic tube compensation on many vents but this is more technical
  • Reduce T-high by 0.2 s (but not lower than 3 seconds)
  • Check HME filter and circuit
  • Maybe increase P high to reduce dead space

This one is probably the trickiest one to fix

The PaCO2 is too low

  • Check blood pressure is adequate and this isn't due to hypoperfusion
  • Increase T high by 0.2 s
  • Decrease P high if oxygenation will allow

Drop and Stretch

Once APRV is working and the patient is starting to improve, you can think about 'dropping and stretching'.

This basically means reducing the P high and increasing the T high in a gradual trend towards continuous, normal level CPAP, with the patient breathing away spontaneously.

drop and stretch method of APRV weaning
Image credit

How to do it

  • Reduce the FiO2 gradually to 40%
  • Reduce P high by 2 every couple of hours, as oxygenation allows
  • Once P high is at 20 cmH2O, increase T high by 2 seconds
  • Every time you drop P high by 2, increase T high by 2
  • You'll end up with a spontaneously breathing patient on CPAP of 10 at 40% oxygen

Well done you.

If you're not quite able to get all the way down this ladder, once P high is around 15 cmH2O, you can switch back over to standard pressure support ventilation, with the PEEP set at 15 and about 5-10 cmH2O of pressure support on top.

Then wean as normal.

If you're interested in the research

Tell me about the pigs

So a study was done with a bunch of pigs in three groups:

  • Induced sepsis and started on APRV 1 hour later
  • Induced sepsis and started on ARDSnet lung protective ventilation (LPV) once mild ARDS criteria met (PF ratio <40 kPa)
  • Control group with no sepsis, ventilated at 10ml/kg tidal volume

What they found:

  • The LPV group had reduced surfactant and worse looking histology than the APRV group
  • The lung tissue in the APRV group actually looked pretty good at post mortem (as well as dead pig lung can look I guess)

It looked like APRV might actually help prevent ARDS in the first place.

This is both interesting and probably not examinable.

Human studies

Most of the research done on APRV was before the ARDSnet trial.

This makes it harder to work out which of the two is better, however it seems:

What about tummy time?

Those of you who worked on ICU during the golden months of 2020 and 2021 will be fairly familiar with proning for severe hypoxia, but how does it compare to APRV?

    If you like APRV and someone is telling you you're wrong, send them this

    APRV
    APRV.pdf
    5 MB
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    Useful Tweets and Resources

    References and Further Reading

    Airway Pressure Release Ventilation (APRV) for ARDS
    APRV has never come up in the CICM exams, and may never come up, because it would be unfair to test the candidates on something even the examiners themselves have little understanding of. It is a promising but poorly researched strategy that maximises alveolar recruitment and embodies the main principles of open-lung ventilation for ARDS.
    Deranged PhysiologyAlex Yartsev
    Airway Pressure Release Ventilation (APRV)
    Airway pressure release ventilation (APRV) is inverse ratio, pressure controlled, intermittent mandatory ventilation with unrestricted spontaneous breathingbased on the Open Lung Approach To Ventilation first described by Stock et al 1987
    Life in the Fast Lane • LITFLChris Nickson

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