Which component of mechanical power is most important in causing VILI?

Marini, John J.; Rocco, Patricia R. M.

doi:10.1186/s13054-020-2747-4

Cited by 36 publications

(40 citation statements)

References 15 publications

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“…Our findings in this study thus build upon our previous work examining the association of mechanical power and outcomes among patients with ARDS [ 15 ]. It has been previously suggested that mechanical power, which encompasses additional ventilatory parameters such as rate, is able to capture repetitive force in a way that static measures are not [ 15 , 20 , 21 ]. In our previous work, we demonstrated that mechanical power added additional mortality prediction over other measures of force [ 15 ].…”

Section: Discussionmentioning

confidence: 99%

On the Transition from Control Modes to Spontaneous Modes during ECMO

Stephens

Mitchell

Overton

et al. 2021

JCM

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The transition from control modes to spontaneous modes is ubiquitous for mechanically ventilated patients yet there is little data describing the changes and patterns that occur to breathing during this transition for patients on ECMO. We identified high fidelity data among a diverse cohort of 419 mechanically ventilated patients on ECMO. We examined every ventilator change, describing the differences in >30,000 sets of original ventilator observations, focused around the time of transition from control modes to spontaneous modes. We performed multivariate regression with mixed effects, clustered by patient, to examine changes in ventilator characteristics within patients, including a subset among patients with low compliance (<30 milliliters (mL)/centimeters water (cmH2O)). We found that during the transition to spontaneous modes among patients with low compliance, patients exhibited greater tidal volumes (471 mL (364,585) vs. 425 mL (320,527); p < 0.0001), higher respiratory rate (23 breaths per minute (bpm) (18,28) vs. 18 bpm (14,23); p = 0.003), greater mechanical power (elastic component) (0.08 mL/(cmH2O × minute) (0.05,0.12) vs. 0.05 mL/(cmH2O × minute) (0.02,0.09); p < 0.0001) (range 0 to 1.4), and lower positive end expiratory pressure (PEEP) (6 cmH2O (5,8) vs. 10 cmH2O (8,11); p < 0.0001). For patients on control modes, the combination of increased tidal volume and increased respiratory rate was temporally associated with significantly low partial pressure of arterial oxygen (PaO2)/fraction of inspired oxygen (FiO2) ratio (p < 0.0001). These changes in ventilator parameters warrant prospective study, as they may be associated with worsened lung injury.

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Section: Discussionmentioning

confidence: 99%

On the Transition from Control Modes to Spontaneous Modes during ECMO

Stephens

Mitchell

Overton

et al. 2021

JCM

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“…Recent work has made clear that surpassing minimum thresholds for tidal stress and strain may be required to initiating lung injury in healthy as well as pre-injured lungs [4,11] and that both static and dynamic stresses impact the actual strains experienced at the cellular level [7]. Micromechanical amplifiers of stress include geometric heterogeneity within the parenchyma, differential viscoelastance and rates of parenchymal expansion, and progressive loading due to dropout of weaker stress-bearing matrix fibrils as tidal cycling proceeds (If unrelieved or interrupted, the latter process may eventuate catastrophic alveolar barrier breakdown.).…”

Section: Mechanical Forcesmentioning

confidence: 99%

“…A series of ongoing studies have demonstrated that each individual element of tidal energy and power, even PEEP, contributes to tissue damage (albeit with different potency and effect) if it is applied above the aforementioned injury threshold [8,11]. With that proviso, total power-the product of minute ventilation with the sum of flow resistive, tidal expansive, and baseline pressuresis a single integrating variable with the potential to track VILI risk [11,12]. Predictably, duration of a damaging ventilation pattern influences eventual injury expression.…”

Section: Mechanical Forcesmentioning

confidence: 99%

What have we learned from animal models of ventilator-induced lung injury?

Rocco

Marini

2020

Intensive Care Med

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Despite its obvious benefits, mechanical ventilation can inflict pulmonary structural damage [1] and destabilize hemodynamics [2]. Deleterious effects of mechanical ventilation-collectively known as ventilator-induced lung injury (VILI)-include inflammatory infiltration and vascular permeability, hyaline membrane formation, and pulmonary edema [3]. Interactive mechanical forces prompt biophysical, biochemical, and biomolecular alterations that ultimately lead to VILI [4]. Repeated nonphysiological stretching of lung tissue can release inflammatory mediators, alter gene expression, and either upregulate or downregulate synthesis of several extracellular matrix proteins [5]. Therefore, understanding the physiological and biological consequences of mechanical ventilation and becoming familiar with logical clinical strategies intended to prevent and minimize lung damage are important clinical goals. These cannot be studied directly at the bedside for obvious ethical and logistical reasons. Yet, over the past two decades, the experimental laboratory has provided the needed guidance to develop approaches and equipment modifications essential to VILI prevention. Animal models continue to elucidate mechanisms underlying the complex pathophysiology of VILI, aiding immeasurably in developing preventative and therapeutic approaches. Important factors upon which to focus when selecting an animal model of VILI include availability, cost, public opinion regarding the conduct of animal research (e.g., feelings toward dogs or primates compared to rodents), the number of animals that should be used,

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“…Quite reasonably, it has been suggested that, for any individual patient, excessive strain per inflation cycle may be a co-requisite with size-normalized power for damage to occur. 13 In other words, a threshold of stress/strain (sharp or indistinct) may need to be crossed before the applied energy contributes to injury. If that presumption proves true, it follows that, during each breath, some of the delivered inflation energy would not contribute to damage; rather, only the energy that crosses the critical stress/strain boundary would do so (Fig.…”

Section: How Important Is Stretch?mentioning

confidence: 99%

“…9,20,21 For example, it might be argued that only energy that relates to driving pressure or total elastic pressure {ie, the product of volume and absolute alveolar pressure, or (V T Â [DP + PEEP])} would best track lung stretch and VILI risk. 13 Alternatively, the total kinetic energy applied in excess of PEEP {ie, the product of volume and the sum of DP + P res . ie, (V T Â [DP + P res ])} might hold equal interest regarding the potential to generate inflamma- tory changes.…”

Section: Cautions Regarding the Threshold-partitioned Modelmentioning

confidence: 99%

Estimating the Damaging Power of High-Stress Ventilation

2020

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Redirection of our clinical attention from the pressures and volumes of the individual cycle to the broader and more inclusive considerations of energy load and power has untapped potential to reduce iatrogenic risk from ventilation (ie, ventilator-induced lung injury). Power is the product of breathing frequency and inflation energy per breath. Yet, while feasible to calculate at the bedside, measuring total power may not prove to be precise enough for accurate prediction of ventilator-induced lung injury, even if normalized to lung capacity (ie, specific power). The same power value can be reached by a multitude of frequency and tidal volume combinations, not all of which carry equal risk of damage. If some arbitrary level of alveolar pressure were accepted as a sharply defined hazard boundary, a rather straightforward geometric analysis theoretically would allow partitioning of overall tidal energy into components above and below a damage threshold. In this discussion, we introduce the concept of quantitative power partitioning and illustrate how tidal energy and power might be deconstructed into their key parts.

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Which component of mechanical power is most important in causing VILI?

Cited by 36 publications

References 15 publications

On the Transition from Control Modes to Spontaneous Modes during ECMO

On the Transition from Control Modes to Spontaneous Modes during ECMO

What have we learned from animal models of ventilator-induced lung injury?

Estimating the Damaging Power of High-Stress Ventilation

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