I'm a respiratory doc with teaching responsibilities. I have had a copy of West's Pathophysiology since the first edition. Many, if not all of my pulmonary. Lectures in Pulmonary PathophysiologyJohn B. West MD, PhD. Jump to A description of the lectures and why they were developed can be seen here PDF. (c) >>> page 1 of 8 PDF File: de5 West's Pulmonary Pathophysiology By John B. West, Andrew M. Luks.
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The Role of Inflammatory and Oxidative Lung Injury in the Setting of Acute Heart Failure Severe inflammatory insult to the pulmonary capillary endothelium and the alveolar epithelium, leading to barrier dysfunction and high permeability pulmonary edema formation, plays a pivotal role in the pathophysiology of acute lung injury and its most severe manifestation, acute respiratory distress syndrome ARDS.
However, there is increasing evidence to suggest that hydrostatic lung injury in the setting of AHF is related to lung inflammation. Furthermore, prolonged blood-gas barrier dysfunction after acute cardiogenic pulmonary edema may be related to pulmonary parenchymal inflammation.
Lung inflammation may be part of the repair mechanism after pulmonary hydrostatic injury.
On the other hand, lung inflammation in the setting of AHF may be a direct response to mechanical stress of the pulmonary microcirculation.
Pulmonary endothelium can transduce the mechanical signal into a biological response by inducing several intracellular signaling pathways, which may result in increased inflammatory cytokine production, macrophage activation, acute inflammation, and barrier dysfunction.
Oxidative stress plays an important role in blood-gas barrier compromise, either by direct oxidative damage to basic cellular components of the barrier or through the activation of redox-sensitive signaling pathways leading to apoptosis and inflammation. Inflammatory and oxidative lung injury may play a significant pathophysiological role in HF decompensation by further damaging the alveolar-capillary barrier and increasing its permeability.
As a consequence, the pulmonary capillary hydrostatic pressure threshold for pulmonary fluid accumulation decreases. This parameter could account for the vulnerability of AHF patients to recurrences. So far, access to this fluid has been based on bronchoalveolar lavage, which is an invasive technique requiring bronchoscopy and may influence the levels of airway inflammation.
Consequently, there is limited information from a small number of patients with cardiogenic pulmonary edema requiring mechanical ventilation. EBC has emerged as a potential tool in the study of the alveolar epithelial lining fluid.
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