Role of cardiopulmonary interactions in development of ventilator-induced lung injury—Experimental evidence and clinical Implications

Abstract

Ventilator-induced lung injury (VILI) impacts outcomes in ARDS and optimization of ventilatory strategies improves survival. Decades of research has identified various mechanisms of VILI, largely focusing on airspace forces of plateau pressure, tidal volume and driving pressure. Experimental evidence indicates the role of adverse cardiopulmonary interaction during mechanical ventilation, contributing to VILI genesis mostly by modulating pulmonary vascular dynamics. Under passive mechanical ventilation, high transpulmonary pressure increases afterload on right heart while high pleural pressure reduces the RV preload. Together, they can result in swings of pulmonary vascular flow and pressure. Altered vascular flow and pressure result in increased vascular shearing and wall tension, in turn causing direct microvascular injury accompanied with permeability to water, proteins and cells. Moreover, abrupt decreases in airway pressure, may result in sudden overperfusion of the lung and result in similar microvascular injury, especially when the endothelium is stretched or primed at high positive end-expiratory pressure. Microvascular injury is universal in VILI models and presumed in the diagnosis of ARDS; preventing such microvascular injury can reduce VILI and impact outcomes in ARDS. Consequently, developing cardiovascular targets to reduce macro and microvascular stressors in the pulmonary circulation can potentially reduce VILI. This paper reviews the role of cardiopulmonary interaction in VILI genesis.

Prognostic value of oxygen saturation index trajectory phenotypes on ICU mortality in mechanically ventilated patients: a multi-database retrospective cohort study

“…The present data also supported this finding, indicating that the association between OSI values and mortality was mediated by ARDS. Critically ill patients with ARDS experienced a decline in pulmonary compliance and an increase in nonaerated compartments, potentially making them more susceptible to VILI [ 71 , 72 ]. Previous studies have also demonstrated that ARDS patients with higher OSI values exhibited higher mortality, which was further validated in the present study [ 5 , 20 , 73 ].…”

The place of positive end expiratory pressure in ventilator-induced lung injury generation

“…Higher levels of PEEP increase the pulmonary vascular resistance that governs right ventricular (RV) afterload, while simultaneously raising pleural and central venous pressures to impede systemic venous return and limit right ventricular preload [27,28 ▪ ]. Without compensatory recruitment of the vascular bed, raising PEEP augments PVR and the ejection impedance confronting the afterload-sensitive RV, especially in the setting of ARDS [28 ▪ ]. Indeed, cor pulmonale has been reported to occur in approximately one quarter of such patients with acute lung injury [29].…”

“…Higher levels of PEEP not only raise PVR but also increase the vascular pressure gradient across the alveolus, with the potential to modulate alveolar stress and strain. A greater microvascular pressure difference predisposes to edema formation, and under certain ventilatory conditions, a heightened vascular gradient also augments endothelial shear and promotes the expression of VILI [28 ▪ ,31]. Small animal experiments demonstrate that when tidal airway pressures are high, raising precapillary vascular pressures or lowering postcapillary pressures dramatically worsen erythrocyte extravasation and other histologic signs of rupture of the blood-gas barrier.…”