Abstract
The major complication of post-thoracic surgery is a severe disturbance of lung extravascular water that is the main cause of morbidity and mortality and therefore still represents an unmet medical challenge. Accordingly, the need to devise novel therapies ought to go through a more thorough understanding of the pathophysiological mechanisms. This review presents an updated description of the time evolution of this process providing the pathophysiological reason for its explosive development. Despite various names (“idiopathic edema”, acute lung injury -ALI, atelectasis, ARDS), a common patho-physiological pathway can be traced for respiratory dysfunction in post-operative thoracic surgery. We will present the evidence for the loss of control on the volume of extravascular lung water from the new perspective of the derangement and disorganization of interstitial proteoglycans, a family of link molecules controlling microvascular permeability and mechanical stability of the extravascular matrix. We analyze in detail specific conditions of lung water disturbance pertaining to cardiac surgery, lung transplant and lung resection surgery. In particular, we will discuss the functional link between lung edema formation and increase in pulmonary vascular resistances, and wish to develop the concept that pulmonary hypertension and right ventricle overload ought to be regarded as the consequence of a decrease in vascular bed reflecting microvessels compression in the edematous tissue both in the acute phase as well as in the fibro-proliferative repair process.
Highlights
Cardiac and lung pathology are strictly related as they impact reciprocally on the respective organ function
In this article we will consider the cardiopulmonary consequences of post-thoracic surgery from the new perspective of the disorganization/ fragmentation of the lung extracellular matrix as an important cofactor causing the severe alteration of lung fluid balance
The preservation of lung architecture during conservation has been considered an important cofactor against ischemia-reperfusion injury, re-establishment of optimal lung geometry has been recommended by maintaining lungs inflated during preservation on the account that changes in alveolar architecture caused by atelectasis expose the lungs to inhomogeneous parenchymal and shear stress distribution that may favor an increase in microvascular permeability on reperfusion [39]
Summary
Cardiac and lung pathology are strictly related as they impact reciprocally on the respective organ function. Severe complications of post-thoracic surgery are acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) referred on clinical basis as primary respiratory dysfunction. These pathologies, being commonly interpreted as the inflammation induced injury on the vascular endothelium and alveolar epithelium, still represent an unmet medical challenge. In this article we will consider the cardiopulmonary consequences of post-thoracic surgery from the new perspective of the disorganization/ fragmentation of the lung extracellular matrix as an important cofactor causing the severe alteration of lung fluid balance
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