Energetics and the Root Mechanical Cause for Ventilator-induced Lung Injury.

<zdoi;10.1097/ALN.0000000000002203> Anesthesiology, V 128 • No 6 1062 June 2018 S INCE the discovery that acute lung injury could be worsened by unwise choices for mechanical ventilation, investigators have sought the mechanisms and clinical parameters that initiate such damage (ventilator-induced lung injury). 1 Our understanding has progressed from simply confining tidal volumes to fixed guideline values to limiting the plateau and driving pressures of the tidal cycle. But damage requires energy and ventilator-induced lung injury is not caused by single deep inflations. Recent attention has logically (if somewhat belatedly) turned toward better defining the place of ventilation frequency and cumulative energy load delivered to the lung over the span of multiple cycles.2 Such loading has been described as “power,” a variable related to exposure intensity that quantifies energy imparted per minute and includes all mechanical factors shown experimentally to influence ventilator-induced lung injury. The root mechanical cause that initiates ventilator-induced lung injury at the tissue level, however, remains elusive. Laboratory work reported by Santos et al. in this issue of A NESTHESIOLOGY3 helps enlighten by demonstrating that tidal pressures and power have overlapping influence on development of biomarker-detected inflammation and histologic changes. Fundamental concepts of physics must be applied at the micro level to put these observations into perspective. As an analogy to electricity, pressure corresponds to voltage, flow to amperage, and their product, the within cycle inflation power, the wattage. Over the span of multiple cycles occurring within a fixed time period, cumulative energy load (“power,” as defined previously3) is analogous to the kilowatt-hour. Although actual tissue tensions cannot be directly measured, lung stresses relate loosely to transpulmonary pressure. Strain is the stress-related elongation of structural microelements from their relaxed states.4 Because compliance more closely parallels the number of aeratable lung units than their individual recoil properties, the stress increment that occurs during tidal inflation is reflected in the driving pressure—plateau minus positive end-expiratory pressure (PEEP), numerically equivalent to the quotient of tidal volume and respiratory system compliance.5 Transpulmonary driving pressure may be the most important measurable variable of the individual cycle that determines the propensity for lung injury. However, its associated risk is conditioned by the pressure range over which it operates, i.e., there exists a pressure “threshold” for causing damage.6 Peak tissue stresses are encountered at end inspiration and early expiration. Although seldom considered, abrupt release of stored energy at the onset of exhalation accentuates viscoelastic drag, adding to potentially damaging tissue distortion. Static variables of the individual tidal cycle such as PEEP, plateau, and driving pressures cannot of themselves fully explain propensity to injure. Forces in static balance do not expend damaging energy. To perform mechanical work, unbalanced forces must move the object in the direction of their net action. Therefore, it is not PEEP, plateau, or even the difference between these two static tidal variables that counts, but the dynamic process of moving from one to the other. This kinetic mechanical energy of inflation can deform and damage, dissipate as heat against friction, or transition to stored potential energy. As a tightly conserved “zero sum” quantity, tidal mechanical energy must be accounted for among these categories with no overlaps. Total machine energy imparted to the respiratory system during a breath is the product of the applied airway pressure and resulting volume change—the area of the corresponding airway pressure volume plot (fig. 1). Energy input concentrates in inverse proportion to the capacity of the “baby lung” to receive it. The three pressure components influencing energy are resistive, tidal elastic (driving pressure), and PEEP. Resistive energy spent in moving gas and deforming tissue against frictional forces is not stored, but converts to heat. Some fraction of the relatively high resistive energy losses that occur Energetics and the Root Mechanical Cause for Ventilator-induced Lung Injury