How respiratory system mechanics may help in minimising ventilator-induced lung injury in ARDS patients

Abstract

The main supportive therapy in acute respiratory distress syndrome patients is mechanical ventilation. As with any therapy, mechanical ventilation has sideeffects, and may induce lung injury (ventilator-induced lung injury (VILI)/ventilatorassociated lung injury). The mechanical factors responsible for VILI are thought to be related to tidal recruitment/derecruitment of previously collapsed alveoli and/or pulmonary overdistension.The volume/pressure (V/P) curve of the respiratory system in patients as well as in animal models of acute lung injury (ALI) has a characteristic sigmoid shape, with a lower inflection point (LIP) corresponding to the pressure/end-expiratory volume required to initiate recruitment of collapsed alveoli, and an upper inflection point (UIP) corresponding to the pressure/end inspiratory volume at which alveolar overdistension occurs. "Protective" ventilatory approaches have therefore set out to minimise mechanical injury by using the V/P curve to individualise positive end-expiratory pressure (PEEP) (PEEP above the LIP) and tidal volume (by setting end-inspiratory V/P below the UIP) since a large number of experimental studies correlate P/V curves to histological and biological manifestations of VILI and two randomised trials showed that protective ventilatory strategy individually tailored to the P/V curve minimised pulmonary and systemic inflammation and decreased mortality in patients with ALI.However, despite the fact that several studies have: 1) proposed new techniques to perform pressure/volume curves at the bedside, 2) confirmed that the lower inflection point and upper inflection point correspond to computed tomography scan evidence of atelectasis and overdistension, and 3) demonstrated the ability of the pressure/volume curve to estimate alveolar recruitment with positive end-expiratory pressure, no large studies have assessed whether such measurement can be performed in all intensive care units as a monitoring tool to orient ventilator therapy. Preliminary experimental and clinical studies show that the shape of the dynamic inspiratory pressure/time profile during constant flow inflation (stress index), allows prediction of a ventilatory strategy that minimises the occurrence of ventilator-induced lung injury. Eur Respir J 2003; 22: Suppl. 42, 15s-21s.

Impact of mechanical ventilation on the pathophysiology of progressive acute lung injury

“…Thus the ability to personalize the mechanical breath to the lung pathology of each patient remains a significant clinical problem. The "Open Lung" strategy attempts to personalize the mechanical breath by optimally setting PEEP following a recruitment maneuver (RM) based on physiological parameters that include best dynamic tidal compliance (125), best Pa O 2 (18), best stress index (126), and upper and lower infection points (6). Although the approach is sound in principle, it has multiple problems: 1) it is not preemptive and sufficient lung damage has already occurred necessitating an RM; 2) there can be negative side effects so RMs cannot be conducted very often; 3) because RMs can be applied so infrequently the lung may recollapse resulting in heterogeneous ventilation; and 4) alveoli may become more unstable Fig.…”

Non-pulmonary factors strongly influence the stress index

“…As an aid to accomplishing safe ventilation, a mathematical parameter, the stress index (SI), has been suggested as a relatively simple way to characterize the profile of the PV relationship of the respiratory system [2][3][4]. The attractive rationale is as follows: under conditions of constant airflow, delivered volume is directly proportional to time elapsed since inflation onset, so that the airway pressure tracing obtained under passive conditions is analogous to a quasi-static PV curve.…”

Respiratory system dynamical mechanical properties: modeling in time and frequency domain

“…Secondly, the singlecompartment model (Eq. 8) assumes that Rrs and Ers are linear and that the only forces opposing lung inflation are the resistive and the elastic pressures, thus neglecting viscoelastic and inertial properties, as well as ventilatory nonhomogeneities (Terragni et al 2003). Thirdly, respiratory muscle tone must be suppressed or at least decreased for the estimation of the passive Rrs and Ers by Eq.…”