An Overview of the Updates of Management of Pulmonary Edema: Narrative Review

Abstract

The development of abrupt respiratory failure linked to fluid buildup in the lung's alveolar spaces due to an elevated heart-filling pressure is known as pulmonary oedema. Pulmonary oedema can result from any cardiac condition marked by a rise in left ventricular pressure. Long-term high capillary pressure can potentially break down the barrier, resulting in increased fluid transfer and permeability into the alveoli and atelectasis and oedema. Numerous variables, such as dysregulated inflammation, strong leukocyte infiltration, activation of procoagulant processes, cell death, and mechanical stress, contribute to the disruption of the alveolar-epithelial barrier. In order to properly treat patients with pulmonary oedema, a thorough medical history and a physical examination are necessary to assess the condition's symptoms and possible causes. In the interim, second-level diagnostic procedures such as echocardiography, chest radiograph, natriuretic peptide level, and pulmonary ultrasonography should be performed. To determine the best course of treatment for these patients, it is imperative to identify the unique pulmonary oedema phenotype. Early in the course of treating this illness, non-invasive ventilation should be taken into consideration. For pulmonary congestion, diuretics and vasodilators are employed. Vasopressors and inotropes are sometimes needed to address hypoperfusion. Additional strategies (i.e., beta-agonists and pentoxifylline) may be beneficial for patients with diuretic resistance and chronic symptoms. The pathogenesis, clinical manifestation, and therapy of pulmonary oedema are reviewed in this publication.