Authors: John J Marini Samir Jaber
Publish Date: 2016/09/16
Volume: 42, Issue: 10, Pages: 1597-1600
Abstract
As currently implemented lung protective ventilation concentrates on certain static characteristics of the individual tidal cycle—tidal volume TV plateau pressure PEEP and recently on the difference between the latter two static values the driving pressure DP 1 The rationale for focusing on any of these has been based primarily on concept focused animal experiments and clinical data supporting their relative importance However the physical process that causes ventilatorinduced lung injury VILI has been difficult to pin down It is clear that mechanical forces lung pathoanatomy and nonventilatory characteristics each contribute Excessive stretch strain and tidal opening and closure may all be important but the precise mechanism through which they act remains unclear Dynamic characteristics—frequency flow rate strain rate—have recently been emphasized as key determinants of whether the ‘static’ variables inflict injury 2 In this issue Gattinoni and colleagues present an elegant and persuasive argument that energy delivered per unit time ‘power’ is a unifying entity into which most key ventilator settings and forces relevant to VILI can be channeled thus providing a “composite index” by which to translate this insight into clinical practice 3 As clearly stated by the authors themselves the mechanical power concept in the genesis of VILI is not new Rather the novelty of this work lies in proposing and validating a mathematical description of machine power responsive to the relative contributions of its bedsideadjustable components TV frequency ΔP aw PEEP IE flow This interesting and provocative proposal urges a potentially important conceptual shift in our thinking that deserves to be carefully examinedVentilators regulate either pressure or flow but not both simultaneously even in the dualcontrol modes available in some modern ventilators This restriction arises because the product of developed airway pressure force per unit area and the resulting delivered volume area–length product defines the energy cost of the breath to overcome resistance R and elastance 1/C Inflation is subject to the energy conservation law and therefore is constrained mathematically by a relationship known as the equation of motion of the respiratory system 4 The total inflation pressure P tot corresponding to any volume V above the fully relaxed value FRC must be accounted for in the sum of dissipated and conserved pressures usually approximated as P tot = flow × R + V/C + PEEPtot The energy expended during passive ventilation—the work of each tidal inflation—is the product of the proximal airway pressure and the volume change it produces 5 Power or energy load defined as work per unit time takes the number of energy cycles per minute breathing frequency f into accountThe proposition that delivered power relates directly to VILI has intuitive appeal Experimental studies have shown that although the peak magnitudes of tidal alveolar stresses and strains are very important other factors condition the resulting damage The excursion of tidal pressure DP appears to be more important than the maximum plateau pressure applied 1 and the frequency of potentially injurious cycling helps determine tissue damage 6 Flow rate and profile clinically adjustable variables often deemphasized in the lung protective strategy have also been shown to be influential even when plateau and driving pressures remain constant 2 7 Whether raising PEEP proves protective or deleterious has been thought to depend on its ability to recruit new units and whether DP or plateau pressure remains unchanged during the increaseThe alluring aspects of this ‘VILIPower’ hypothesis are several In accounting for key dynamic as well as static variables it lends mechanistic plausibility to the observation that DP is more influential than plateau pressure If damage resulted from excess power it would not depend exclusively on the maximal pressures achieved during the individual tidal cycle but rather on the entirety of the inspiratory pressure excursion DP and on the frequency of its application Moreover the power hypothesis builds upon the solid science that preceded it by integrating and assigning relative weights to machine settings which separately have been incriminated as contributors to VILI but individually cannot fully account for injury risk What is more these contributing components of the power equation can be quantified ranked and condensed into a single practical index with the potential to guide machine adjustments at the bedsideLike most provocative and insightful work questions regarding possible shortcomings and needed refinements come rather quickly to mind However attractive this concept might be it may need to be further polished before it can be relied upon to safely guide ventilation For example it is certainly true that the equation of motion accounts for the flows and pressures the ventilator generates relative to atmosphere and therefore determines the total work and energy that the ventilator must perform during a given inflation But airway pressure expands both the lung and chest wall and abnormal stiffness of the latter sometimes accounts for a sizeable fraction of the delivered pressure and work per cycle 8 What is more the local tissue tensions within the mechanically heterogeneous lung and by implication the unmeasured regional power relevant to microinjury may be affected by the force amplification that occurs in zones of stress focusing 9 This vital issue of lung heterogeneity is not readily quantified and clinicians at the bedside are left with what we can measure—the elements of the equation of motion Using transpulmonary pressure however would seem a logical and feasible option for calculating lung injury powerThere are other concerns Even though logically weighted not all components of the proposed power equation contribute to VILI in an obvious way For instance although flow magnitude and flow profile attack rate dP/dt relate to the aggressiveness of lung tissue expansion during inflation and may contribute to damage for that reason 2 7 it is difficult to link power dissipated in proximal airway resistance directly to noxious events at the alveolar levelRelationships of PEEP and driving pressure DP to energy imparted to the passive tissues of the respiratory system during a single inflation Flow resistive work performed by the machine is not illustrated Colored areas pressure × volume represent mechanical work a For a given tidal volume and DP an increase of PEEP from PEEP1 to PEEP2 increases inspiratory storage of energy rectangles while delivering similar incremental dynamic energy triangles The PEEPrelated energy stored during inflation along with its dynamic counterpart is then released during exhalation as it dissipates across the resistance of the circuit and exhalation valve allowing airway pressure to return to the PEEP level b A doubling of tidal volume and DP from the same PEEP level raises dynamic energy disproportionately to the tidal volume and driving pressure c During deflation some energy is retained by the lung as the remainder dissipates across the airways circuitry and exhalation valve Lenticularshaped areas quantify the energy retained at two PEEP levels with the same DP blue and green as well as the energy retained by doubling the tidal volume with the same PEEP
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