{"id":849,"date":"2025-04-05T06:00:28","date_gmt":"2025-04-05T06:00:28","guid":{"rendered":"https:\/\/perfusfind.com\/ic\/?p=849"},"modified":"2025-04-04T18:38:08","modified_gmt":"2025-04-04T18:38:08","slug":"first-stabilize-and-then-gradually-recruit-a-paradigm-shift-in-protective-mechanical-ventilation-for-acute-lung-injury","status":"publish","type":"post","link":"https:\/\/perfusfind.com\/ic\/index.php\/2025\/04\/05\/first-stabilize-and-then-gradually-recruit-a-paradigm-shift-in-protective-mechanical-ventilation-for-acute-lung-injury\/","title":{"rendered":"First Stabilize and then Gradually Recruit: A Paradigm Shift in Protective Mechanical Ventilation for Acute Lung Injury"},"content":{"rendered":"
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Summary of \u201cFirst Stabilize and then Gradually Recruit: A Paradigm Shift in Protective Mechanical Ventilation for Acute Lung Injury\u201d<\/strong> Citation<\/strong>: Nieman GF, Kaczka DW, Andrews PL, et al. J Clin Med<\/em>. 2023;12(14):4633. doi:10.3390\/jcm12144633<\/p>\n<\/blockquote>\n

Abstract<\/strong> The article introduces a new paradigm in mechanical ventilation for acute lung injury, emphasizing a \u201cStabilize Lung Approach\u201d (SLA) over traditional methods. Unlike the protective lung approach (PLA) or open lung approach (OLA), which either limit tidal volume or aggressively recruit lung tissue, the SLA uses Time-Controlled Adaptive Ventilation (TCAV) to first stabilize alveoli with a brief expiratory phase, then gradually recruit collapsed tissue over time. This strategy aims to halt ventilator-induced lung injury (VILI) by preventing repetitive alveolar collapse and expansion (RACE), reducing stress concentrators, and enabling personalized, physiology-based care.<\/p>\n

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Graphical Abstract<\/figcaption><\/figure>\n

Key Points<\/strong><\/p>\n

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  1. \n

    Heterogeneity of ARDS<\/strong>: ARDS involves regionally varied injury that causes a mismatch in alveolar opening and collapse time constants, making lungs vulnerable to RACE and progressive atelectasis, contributing to VILI.<\/p>\n<\/li>\n

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    Limitations of PLA and OLA<\/strong>: While the PLA protects against overdistension using low tidal volumes, it may permit ongoing atelectasis. OLA attempts early recruitment but has failed to significantly reduce mortality due to inadequate or transient lung opening.<\/p>\n<\/li>\n

  3. \n

    VILI Vortex Concept<\/strong>: The progressive loss of functional lung due to injury and collapse leads to overdistension of the remaining tissue, perpetuating a cycle of worsening injury\u2014a “VILI vortex.”<\/p>\n<\/li>\n

  4. \n

    Stabilize Lung Approach (SLA)<\/strong>: SLA reverses the OLA sequence by immediately stabilizing the lung with brief exhalation time (TLow \u2264 0.5s), minimizing collapse, then slowly recruiting lung tissue during extended inspiratory phases (THigh).<\/p>\n<\/li>\n

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    Time-Controlled Adaptive Ventilation (TCAV)<\/strong>: TCAV is a method of setting APRV where the brief expiratory phase prevents collapse and the extended inspiratory phase gradually opens the lung, providing both lung protection and recruitment.<\/p>\n<\/li>\n

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    Physiology-Based Personalization<\/strong>: TCAV adapts to the patient\u2019s lung compliance (CRS), using the slope of the expiratory flow curve to set TLow, ensuring ventilation parameters match individual pathophysiology.<\/p>\n<\/li>\n

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    Alveolar Stability and Recruitment<\/strong>: Animal studies show that TCAV maintains alveolar stability and reduces histologic injury better than traditional high PEEP, even at higher VTs.<\/p>\n<\/li>\n

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    Mechanical Power Efficiency<\/strong>: The CPAP phase during TCAV allows continued alveolar recruitment without increasing airway pressure, thus minimizing mechanical power\u2014one of the drivers of VILI.<\/p>\n<\/li>\n

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    Inflate-and-Brake Ratchet Model<\/strong>: The breath-by-breath mechanism of TCAV is likened to a ratchet, with the brief release phase acting as a brake to prevent re-collapse, progressively increasing open lung volume.<\/p>\n<\/li>\n

  10. \n

    Paradigm Shift in ARDS Management<\/strong>: The authors advocate for replacing open-lung-first strategies with a stabilize-then-recruit model, grounded in the dynamic pathophysiology of ARDS and supported by translational, animal, and clinical data.<\/p>\n<\/li>\n<\/ol>\n

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    Acute respiratory distress syndrome (ARDS) tetrad of pathologic components [18<\/strong><\/a>]. Pulmonary surfactant forms a complete monolayer (blue layer) on the alveolar walls. Pulmonary capillaries (red ovals) run through the alveolar walls. ARDS is a syndrome and can be caused by multiple mechanisms, including severe trauma, hemorrhagic shock, sepsis, and viral or bacterial pneumonia (including that caused by SARS-CoV-2). These injuries initiate systemic inflammatory response syndrome (SIRS), increasing microvascular permeability and causing Endothelial Leakage<\/em> of plasma (black arrows) from the pulmonary capillaries (red ovals). The increased permeability allows pulmonary edema to move into the alveolus (Endothelial Leakage<\/em>\u2014tan edema blebs and black arrows) [19<\/strong><\/a>]. As edema expands, the monolayer is disrupted, causing Surfactant Deactivation<\/em> (blue surfactant sluffed into the alveolus). If unchecked, pulmonary edema will eventually flood the entire alveoli (Alveolar Edema<\/em>\u2014tan area within alveolus) [20<\/strong><\/a>]. Improperly set mechanical ventilation can exacerbate surfactant disruption [21<\/strong><\/a>] initially caused by edema leaking into the alveolus (Surfactant Deactivation<\/em>). High alveolar surface tension can independently increase edema [22<\/strong><\/a>], setting up a vicious cycle of increased vascular permeability \u2192 alveolar flooding \u2192 improper mechanical ventilation \u2192 surfactant deactivation \u2192 elevated alveolar surface tension \u2192 more edema. Alveoli flood in a heterogeneous manner such that there are edema-filled alveoli directly adjacent to air-filled alveoli. The stress of ventilation is concentrated in areas between collapsed or flooded and open alveoli and is known as a stress multiplier. These locations are subjected to stress failure, as alveolar walls are bent toward the edema-filled alveolus (Alveolar Edema<\/em>\u2014green arrow) [23<\/strong><\/a>]. Alveolar Edema<\/em> will eventually cause CO2 retention and hypoxemia, necessitating the use of mechanical ventilation; however, if inappropriately set, this can cause an unintentional ventilator-induced lung injury (VILI). The mechanisms of VILI include stress multipliers causing volutrauma in adjacent inflated alveoli (green arrow) [23<\/strong><\/a>,24<\/strong><\/a>,25<\/strong><\/a>,26<\/strong><\/a>] and unstable alveoli that collapse and reopen with every breath (Repetitive Alveolar Collapse and Expansion\u2014RACE<\/em>), causing atelectrauma. Both volutrauma and atelectrauma exacerbate endothelial leak (Endothelial Leakage<\/em>), accelerating lung damage. Reproduced from Reference [18<\/strong><\/a>], under terms of the Creative Commons Attribution 4.0 International License.<\/figcaption><\/figure>\n
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    Pressure\/Time and Flow\/Time curves for the mechanical breath profile (MBP) generated by the ARDSnet method to set and adjust the Volume Assist-Control (VAC) and airway pressure release ventilation (APRV) mode, set using the time-controlled adaptive ventilation (TCAV) method. The MBP contains all airway pressures, volumes, flows, rates, and the time they are applied at both inspiration and expiration. (A<\/strong>) Pressure\/Time and Flow\/Time curves for the MBP generated with the VAC mode. Key features of the VAC mode include an inspiratory\/expiratory ratio of 1:3, generating a short inspiratory and long expiratory time. There is no extended plateau pressure, so peak inspiratory pressure is very brief. A set positive end-expiratory pressure (Set-PEEP) and FiO2 adjusted using oxygenation as the trigger for change [27<\/strong><\/a>]. (B<\/strong>) Pressure\/Time and Flow\/Time curves for the MBP generated with the TCAV method to set and adjust the APRV mode. Key features include an inspiratory\/expiratory ratio of ~12:1, generating a long inspiratory and short expiratory time. The continuous positive airway pressure (CPAP) Phase is ~90% of each breath. A tidal volume (VT), which is measured as the volume of gas released (VR) during the Release Phase (brown arrow), is not set but is influenced by changes in, (i) respiratory system compliance (CRS), (ii) the CPAP Phase pressure, and (iii) the duration of the Release Phase. The Release Phase is determined by the Slope of the Expiratory Flow Curve (SlopeEF, red arrow), which is a breath-to-breath measure of CRS. The lower the CRS, the faster the lung recoil, the steeper the SlopeEF, and the shorter the Release Phase, further reducing VT. Thus, the VT will always be low in a non-compliant injured lung and will increase in size only when the lung recruits and CRS increases. Since a change in CRS directs the Release Phase duration, which in turn adjusts the VT and the time-controlled PEEP (TC-PEEP), the TCAV method is both personalized<\/em> and adaptive<\/em> as the patient\u2019s lung becomes better or worse: small VT and higher TC-PEEP in the injured lung and larger VT and lower TC-PEEP in the normal lung, always keeping the Driving Pressure (\u2206P = Vt\/CRS) in the safe range. Reproduced from Reference [30<\/strong><\/a>], under terms of the Creative Commons Attribution 4.0 International License.<\/figcaption><\/figure>\n

    Conclusion<\/strong> The traditional PLA and OLA have failed to meaningfully reduce ARDS mortality over the past two decades. TCAV, as part of a \u201cStabilize Lung Approach,\u201d offers a physiology-based, personalized strategy that addresses the root pathophysiology of ARDS\u2014regional alveolar instability. By stabilizing alveoli first and gradually recruiting tissue over time, TCAV may significantly reduce VILI and improve outcomes in patients with ARDS.<\/p>\n

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    In patients with acute respiratory distress syndrome (ARDS), the evolution of ventilator-induced lung injury (VILI) can be described as an ever-shrinking normal \u2018baby\u2019 lung, resulting in a \u2018VILI Vortex\u2019. A ventilation strategy that does not prevent progressive lung collapse fuels the VILI Vortex. If unchecked, lung injury will progress into severe ARDS, at which point rescue methods such as extracorporeal membrane oxygenation (ECMO) may be necessary. In order to circumvent this VILI Vortex, methods to quickly stabilize and then gradually reopen collapsed lung tissue must be developed. We hypothesize that a stabilize the lung approach (SLA) that first stabilizes alveoli and then gradually reopens collapsed tissue can be accomplished using the time-controlled adaptive ventilation (TCAV) method to set and adjust the airway pressure release ventilation (APRV) mode. If our hypothesis is correct, this will be a paradigm shift in the way medicine is practiced from open-the-lung first<\/em> and stabilize-the-lung second<\/em> using the Open Lung Approach (OLA) to reversing this order of treatment (stabilize and then gradually recruit<\/em>) using the Stabilize Lung Approach. Reproduced from Reference [64<\/strong><\/a>], under terms of the Creative Commons Attribution 4.0 International License.<\/figcaption><\/figure>\n
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    The impact of expiratory and inspiratory time on alveolar collapse and recruitment. ((A<\/strong>) Top<\/strong>) A graph of the tracheal tidal volume (tVT, dotted line) measured by the ventilator, and subpleural alveolar tidal volume (aVT, solid line) measured using in vivo microscopy at three Release Phase durations: (a) Prolonged, (b) Moderate, and (c) Very Brief. Both tVT and aVT decrease as the Release Phase is shortened. Alveolar tidal volume is very small (c 0.02%\u2014solid line) with a very brief Release Phase (green box), even with a large tVT (12 cc\/kg\u2014dashed line) [105<\/strong><\/a>]. A large alveolar tidal volume (aVT\u2014solid line) is a direct measurement of repetitive alveolar collapse and expansion (RACE). ((A<\/strong>) Bottom<\/strong>) Subpleural alveoli (Blue circles) measured using in vivo microscopy during the CPAP Phase and Release Phase using the APRV mode. With a prolonged Release Phase (a, b), alveoli collapsed and did not all reinflate during the CPAP Phase (large white areas between blue alveoli). With a brief Release Phase set by the TCAV method (c\u2014green box), alveoli were open and stable (i.e., no RACE) throughout the ventilatory cycle (green box, blue alveoli fill the photomicrographs at both the CPAP and Release phases). With Permission [105<\/strong><\/a>]. ((B<\/strong>) Top<\/strong>) A graph showing whole lung and alveolar recruitment over time with static applied pressure. The Percent Recruitment\/Time curve following 40 cmH2O airway pressure on both subpleural alveoli (black line) and the gross lung surface (gray line). Following the application of airway pressure, there was a very slight delay in opening, followed by short rapid recruitment, and then continual recruitment as long as the airway pressure was applied. With Permission [81<\/strong><\/a>]. ((B<\/strong>) bottom<\/strong>) In vivo microscopy showing progressive subpleural alveoli recruitment (circled in black) (Video S3<\/strong><\/a>) and the progressive recruitment of lung tissue (red tissue turning pink) (Video S4<\/strong><\/a>) over 40 s at a constant airway pressure. Lung tissue and alveoli demonstrate viscoelastic behavior and continue to recruit throughout the CPAP Phase without an increase in airway pressure [81<\/strong><\/a>]. With an extended CPAP Phase set by the TCAV method (yellow box), alveoli (black circles) and lung tissue (red tissue turning pink) are gradually and continually recruited over 40 s without an increase in airway pressure (green box). (C<\/strong>) Ventilator monitor showing Pressure\/ Flow and Volume\/Time curves set using the TCAV method. The very short Release Phase stabilizes alveoli, preventing collapse (green boxes). The extended CPAP Phase recruits alveoli for the entire time the pressure is applied (yellow boxes). Subpleural alveoli were filmed using in vivo microscopy and color-coded blue using computer image analysis. Alveolar tidal volume was measured as the percent change (%) in the area of the photomicrograph occupied by alveoli (blue) from inspiration to expiration [105<\/strong><\/a>]. Percent Recruitment for alveoli was measured as the percent of the photomicrograph occupied by inflated alveoli and, for the whole lung, the percent of the entire lung surface occupied by inflated (pink) tissue.<\/figcaption><\/figure>\n
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    ACCESS FULL ARTICLE HERE<\/a><\/p>\n<\/blockquote>\n

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    First Stabilize and then Gradually Recruit: A Paradigm Shift in Protective Mechanical Ventilation for Acute Lung Injury<\/figcaption><\/figure>\n
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    Watch the following video on “Science and Clinical Research of APRV using TCAV” by Gary Nieman<\/a><\/p>\n