April 10, 2020

REBEL Crit Cast Ep3.0: Airway Pressure Release Ventilation (APRV) Made Simple

Airway Pressure Release Ventilation (APRV) is a mode of ventilation that allows spontaneous breathing throughout the ventilation cycle.  It is a time-cycled mode of ventilation between two levels of positive airway pressure with the main time on the high level and a shorter period of time during the expiratory release to facilitate ventilation. This may not be a mode of ventilation many ED physicians are comfortable and have experience with and in this podcast Frank Lodeserto, MD reviews how to setup, titrate, and wean patients on this mode of ventilation.

REBEL Crit Cast Episode 3.0 – Airway Pressure Release Ventilation (APRV) Made Simple

Click here for Direct Download of Podcast

How it Works

Airway Pressure Release Ventilation (APRV) is essentially 2 levels of CPAP. There is a high CPAP pressure known as the Phigh, and that pressure is held for a longer than usual time known as the Thigh. After this time ends there is a release where the pressure is allowed to drop to a lower pressure known as the Plow. This pressure release is usually very brief, and this time is known as the Tlow. Essential this mode is also very similar to Pressure Control (PC) with an inverse ratio (Long inspiratory time and short expiratory time) as shown below. PC is triggered (trigger = determines when breath is delivered), time cycled (cycle = causes ventilator to switch from inspiration to exhalation), and pressure limited (limit = maximal value achieved during inspiration). Just like PC, APRV is also triggered by time, time cycled, and pressure limited. APRV like Pressure Control, also delivers a set pressure and your tidal volume will vary based on you patient’s compliance. The difference is that APRV has an open dynamic expiratory valve that allows for spontaneous respirations both during the Phigh (inspiratory phase) and Plow phases (expiratory phase).

APRV utilizes an open lung strategy where the Phigh is sustained over a long duration (Thigh) to recruit and maintain recruitment of atelecotatic alveoli. It is effective in oxygenation because it can deliver a high mean airway pressure (MAP). We often don’t think of mean airway pressures, but this is the most important determinant of oxygenation. We often say that PEEP and Fi02 are the major determinants of oxygenation and this is true as we spend majority of our inspiratory cycle in expiration. We spend 1/3 of inspiratory cycle at the higher peak inspiratory pressure (PIP) and 2/3 of our time (longer in obstructive lung disease) in expiration. So the average pressure in our airways is determined mostly by our PEEP. In APRV however, we sustain this very high pressure for a long period of time increasing our mean airway pressure (MAP).   The diagram below shows a conventional mechanical ventilation pressure graphic. As you can see, you only stay at this high inspiratory pressure for a shorter period of time compared to your expiratory pressure which is maintained twice as long.  This is why you often hear people say that PEEP is one of the most important parameters to control oxygenation.

(Image from Kevin Kuo, MD – Link is HERE)

Uses/Cautions:

  • Can be used safely in patients with acute lung injury, acute respiratory distress syndrome (ARDS), and profound atelectasis. Avoid in patients with obstructive lung disease (Asthma, COPD).

Setting up APRV:

APRV-TCAV (Time Controlled Adaptive Ventilation) from EMCrit Website [Link is HERE]

Adjusting APRV: Oxygenation & Ventilation

APRV Weaning:

  • Goal: Fi02 < 50%, patient awakening with spontaneously breathing, and lung injury resolving.
  • Start to decrease Phigh 1 – 2 cm H20 (DROP) and simultaneously increase Thigh 0.5 – 1 seconds (STRETCH). You dont need to change the Plow or Tlow. Increasing your Thigh will decrease the number of releases, so it’s important that your patient is awake and spontaneous breathing to help ventilate.
  • Continue to “drop & stretch” every 2 – 4 hours as tolerated by patients: stop if patient has increased work of breathing, tachypnea and /or desaturation, as they may have de-recruited (and developed atelectasis) with weaning
  • When the Phigh ~10 cmH20 and Thigh ~ 10 – 12 seconds, the patient is appropriate to consider switching to pressure support with PEEP in preparation for liberation from mechanical ventilation

Special Thanks to Joshua Vanhouten RT-ACCS

References:

  1. Zhou Y et al.  Early Application of Airway Pressure Release Ventilation may Reduce the Duration of Mechanical Ventilation in Acute Respiratory Distress Syndrome. Intensive Care Medicine 2017. PMID:28936695
  2. Habashi NM et al. Other Approaches to Open-Lung Ventilation: Airway Pressure Release Ventilation. Crit Care Med 2005. PMID:15753733

For More Thoughts on This Topic Checkout:

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter: @srrezaie)

Cite this article as: Frank Lodeserto MD, "REBEL Crit Cast Ep3.0: Airway Pressure Release Ventilation (APRV) Made Simple", REBEL EM blog, April 10, 2020. Available at: https://rebelem.com/rebel-crit-cast-ep3-0-airway-pressure-release-ventilation-aprv-made-simple/.
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Frank Lodeserto MD

Associate Professor, Geisinger Commonwealth School of Medicine Program Director, Critical Care Fellowship Adult & Pediatric Critical Care Geisinger Medical Center Janet Weis Children’s Hospital Danville, PA
5 Comments
  • MP
    Posted at 12:29h, 10 April Reply

    how come the patient inspirations are registered as increase in Paw? the flow is negative, why wouldn’t the breaths decrease from the Paw if they are negative pressure/native breaths?

    • Salim Rezaie
      Posted at 12:47h, 10 April Reply

      Great question…from Frank –> They are spontaneous breaths but taken at a high airway pressures (Phigh). The Maw pressure would oscillate slightly higher and lower than 30 with breaths. So for example if Phigh set at 30 and spontaneous breaths you would see small changes in the pressure waveform (i.e. Above and below 30).
      The flow may be negative but the pressure will still remain overall positive.

  • John Jones M.D.
    Posted at 04:29h, 12 April Reply

    DON’T TLDR THIS
    READ AND COMMENT
    SAVE LIVES
    THANK YOU!

    Gary F Nieman (https://www.researchgate.net/profile/Gary_Nieman) has been working on the pathophysiology and treatment of ARDS for over 35 years at SUNY and pioneered this really cool version of APRV called TCAV, that’s basically extra gentle and a meta-analysis showed benefit in ARDS. He runs a physiology lab that has created some extremely practical literature on lung physiology, surfactant, and invasive as well as noninvasive ventilation (I have never seen better lung physiology figures).

    All of the RebelEM info has been very helpful lately with COVID (https://rebelem.com/covid-19-hypoxemia-a-better-and-still-safe-way/), so was wondering, has anyone tried APRV with seemingly better outcomes? From a physiology perspective it seems like a better idea… also if that works maybe TCAV could be a good idea as well?

    TCAV Protocol listed here:
    Link: https://www.researchgate.net/post/Would_it_be_possible_to_get_a_copy_of_this_protocol
    “Attached is the protocol that Ben Daxon uses at the Mayo Clinic. I’m a basic scientistn [at SUNY] and don’t treat patients so I don’t have a clinical protocol but Ben has worked and studied with us so he knows how to run the TCAV protocol. My guess is that the attached is a good clinical protocol.
    GF APRV 8-29-2018.pdf”

    Acute lung injury: how to stabilize a broken lung
    November 2018 Critical Care
    DOI: 10.1186/s13054-018-2051-8
    Why APRV/TCAV works so well, and how the same concept can also be applied to CPAP.
    Focuses on avoiding ventilator-induced lung injury (VILI).

    Mechanical Ventilation Lessons Learned From Alveolar Micromechanics
    March 2020 Frontiers in Physiology
    DOI: 10.3389/fphys.2020.00233

    Surfactant delivery in rat lungs: Comparing 3D geometrical simulation model with experimental instillation
    October 2019
    DOI: 10.1371/journal.pcbi.1007408
    Describes why initial surfactant trials failed in adults and how to fix it.

    Time-controlled adaptive ventilation (TCAV) accelerates simulated mucus clearance via increased expiratory flow rate
    November 2019
    DOI: 10.1186/s40635-019-0250-5
    Results show traditional ventilation does not clear mucus (rate was 0 in all groups), but TCAV does actually clear it (2-8cm/min in all groups wow!), quickly and steadily moves it proximally like it should. The concept is this: as long as your vent settings have a higher expiratory flow rate than an inspiratory flow rate mucus will move up and out of the bronchial tree and trachea. Since inspiration is prolonged to gently open alveoli (slow flow rate), and expiration is quick to keep alveoli open and assisted (fast flow rate, just not less than half a second according to their data because need to allow expiration to actually occur of course).

    Related thoughts on Humidified air:
    On a related note, and I’m not sure if RebelEM has any ideas here, humidity is obviously very important as well, since without adequate humidity the mucus dries, cilia are damaged, and innate immunity cannot function to remove pathogens and debris up and out the respiratory tract (source list at bottom inside this link https://www.globenewswire.com/news-release/2020/03/13/2000488/0/en/Humidity-helps-in-the-fight-against-COVID-19-virologists-report.html). I also personally see this logically that as a result of overly dry air, more debris will remain in in the airway and likely increase the odds as well of superinfection or hospital acquired infection. The longer the patients mucus is not functioning properly the longer this remains a risk (also surfactant blocks pathogens as well so that is another issue as well for patients with surfactant layer disruption). I just wrote this as an idea regarding how humidity complements any ventilation method that supports mucus flow, and also how there have been many anecdotal reports of COVID patients who seem to find humidified air to be extremely helpful, perhaps even more than one would expect from just a therapeutic effect, perhaps it has recovery benefit as well- so maybe we should consider it more as an actual intervention, since many of our interventions dry the airway (intubation blocks off the nasopharynx and blocks natural humidification and warming of the air, hence humidity being added. Also high flow devices without humidity can dry out, as well. Even mask wearing with HFNC also boosts humidity around the face, while also blocking the aerosolization of the virus as covered by RebelEM previously.

    We have all seen the data reflecting lower spread in countries that had widespread facemask use, which contains the aerosol spread as RebelEM discussed, and now attention is being placed on wearing even surgical or cloth masks to prevent spread especially for the general public. Perhaps it also helps since it is trapping the humidity close the the face (anyone that has ever worn a face mask or stood in surgery knows this) which moistens the airway of the wearer and promotes the mucociliary clearance and transport of virus out of the airway (sources at bottom of this link as well https://www.globenewswire.com/news-release/2020/03/13/2000488/0/en/Humidity-helps-in-the-fight-against-COVID-19-virologists-report.html)

    Link to their project:
    https://www.researchgate.net/project/Time-Controlled-Adaptive-Ventilation-TCAV-Protocol-to-Reduce-the-Incidence-of-ARDS

    I just wanted to post in case Rebel EM found it worthy of discussion at some point. If these things can save lives people should know. I don’t need credit or a publication, I just want the word out. There are other very useful studies that are putting things together as well if you look across disciplines, look at the immune response beginning to be detailed by the immunology and virology communities, look at the post mortem lung path reports, look at the two brief POCUS ultrasound videos from Case Western that will train you in a heartbeat and its easy to track the B-lines, read the RebelEM COVID anticoagulation discussion, EVMS guide, ACE-2 receptor locations, SARS-1 pathophysiology…. if you look at it across disciplines you will see the common themes emerge …

    KEEP IT UP REBEL EM!

    • Salim Rezaie
      Posted at 13:56h, 12 April Reply

      Hello John,
      Appreciate you sharing these thoughts. Don’t worry, I read all of it. There are many now shifting to APRV-TCAV mode of ventilation as the initial strategy. It seems to make the most sense of what we have available thus far. Agree with many of your points from a clinical perspective and TY for taking the time to share all of this info. We actually just put a podcast out on APRV done by Frank Lodeserto, MD as a primer for many who may not feel comfortable or may not know about the that mode of ventilation. We always appreciate the opportunity in our community to have discussion and healthy debate for one common goal of the most benefit for the most people possible. Stay safe and wash your hands a lot.

      Salim

  • SARS-CoV-2 literature review April 2 – April 10, 2020
    Posted at 07:02h, 12 April Reply

    […] RebelEM covered these useful posts:Trying Not to Intubate Early & Why ARDSnet may be wrong and Airway Pressure Release Ventilation (APRV) Made Simple. […]

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