Abstract
BackgroundAcute respiratory distress syndrome causes a heterogeneous lung injury with normal and acutely injured lung tissue in the same lung. Improperly adjusted mechanical ventilation can exacerbate ARDS causing a secondary ventilator-induced lung injury (VILI). We hypothesized that a peak airway pressure of 40 cmH2O (static strain) alone would not cause additional injury in either the normal or acutely injured lung tissue unless combined with high tidal volume (dynamic strain).MethodsPigs were anesthetized, and heterogeneous acute lung injury (ALI) was created by Tween instillation via a bronchoscope to both diaphragmatic lung lobes. Tissue in all other lobes was normal. Airway pressure release ventilation was used to precisely regulate time and pressure at both inspiration and expiration. Animals were separated into two groups: (1) over-distension + high dynamic strain (OD + HDS, n = 6) and (2) over-distension + low dynamic strain (OD + LDS, n = 6). OD was caused by setting the inspiratory pressure at 40 cmH2O and dynamic strain was modified by changing the expiratory duration, which varied the tidal volume. Animals were ventilated for 6 h recording hemodynamics, lung function, and inflammatory mediators followed by an extensive necropsy.ResultsIn normal tissue (NT), OD + LDS caused minimal histologic damage and a significant reduction in BALF total protein (p < 0.05) and MMP-9 activity (p < 0.05), as compared with OD + HDS. In acutely injured tissue (ALIT), OD + LDS resulted in reduced histologic injury and pulmonary edema (p < 0.05), as compared with OD + HDS.ConclusionsBoth NT and ALIT are resistant to VILI caused by OD alone, but when combined with a HDS, significant tissue injury develops.
Highlights
Acute respiratory distress syndrome causes a heterogeneous lung injury with normal and acutely injured lung tissue in the same lung
There was no significant difference between groups in cardiac output (CO), mean arterial pressure (MAP), central venous pressure (CVP), arterial pH, serum lactate, or the volume of fluids and norepinephrine given (p > 0.05; Table 1)
There was a significant increase in end-expiratory pressure (EEP) (12.9[2.7] vs 3.0[1.2] cmH2O) and PaO2/FiO2 ratio (P/F) ratio (333.0[156] vs 162.0[124]) in the OD + low dynamic strain (LDS) group as compared with the OD + high dynamic strain (HDS) group
Summary
Acute respiratory distress syndrome causes a heterogeneous lung injury with normal and acutely injured lung tissue in the same lung. Mechanical ventilation is a double-edged sword: necessary for respiratory support, when set improperly, it can cause a secondary ventilator-induced lung injury (VILI) that can exacerbate ARDS mortality [3]. Alveoli share walls with neighboring alveoli; this interdependent design equalizes airway pressure between adjacent alveoli, minimizing both collapse and overdistension (OD), as long as all alveoli are open and homogeneously ventilated [6]. This system is dependent on lung volume (decreased resistance in collateral channels with increase in lung volume) and largely defeated in conditions when lung volume is below functional residual capacity (FRC) [7]
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