Cardiogenic Pulmonary Edema in Emergency Medicine

Highlights What are the main findings? Cardiogenic pulmonary edema is the most common cause of respiratory failure and results from increased cardiac filling pressure and alveolar-epithelial barrier breakdown due to factors like inflammation, leukocyte infiltration, procoagulant processes, and ion channel modification by reactive oxygen and nitrogen species. Rapid evaluation of the patient with cardiogenic pulmonary edema and appropriate treatment are necessary to reduce mortality and morbidity. What is the implication of the main finding? Bedside tests, especially ultrasound, help us to quickly identify and to understand the need of amine support. Optimal therapy for patients with cardiogenic pulmonary edema hinges on precise phenotypic identification and etiological assessment, with early consideration of non-invasive ventilation and diuretics. Hypoperfusion necessitates inotropes and, at times, vasopressors, while individuals exhibiting persistent symptoms and diuretic resistance may benefit from vasodilators and additional therapeutic strategies, including beta-agonists, underscoring the need for further studies to explore medical interventions in mitigating pulmonary damage in CPE patients.Highlights What are the main findings? Cardiogenic pulmonary edema is the most common cause of respiratory failure and results from increased cardiac filling pressure and alveolar-epithelial barrier breakdown due to factors like inflammation, leukocyte infiltration, procoagulant processes, and ion channel modification by reactive oxygen and nitrogen species. Rapid evaluation of the patient with cardiogenic pulmonary edema and appropriate treatment are necessary to reduce mortality and morbidity. What is the implication of the main finding? Bedside tests, especially ultrasound, help us to quickly identify and to understand the need of amine support. Optimal therapy for patients with cardiogenic pulmonary edema hinges on precise phenotypic identification and etiological assessment, with early consideration of non-invasive ventilation and diuretics. Hypoperfusion necessitates inotropes and, at times, vasopressors, while individuals exhibiting persistent symptoms and diuretic resistance may benefit from vasodilators and additional therapeutic strategies, including beta-agonists, underscoring the need for further studies to explore medical interventions in mitigating pulmonary damage in CPE patients.Abstract Cardiogenic pulmonary edema (CPE) is characterized by the development of acute respiratory failure associated with the accumulation of fluid in the lung's alveolar spaces due to an elevated cardiac filling pressure. All cardiac diseases, characterized by an increasing pressure in the left side of the heart, can cause CPE. High capillary pressure for an extended period can also cause barrier disruption, which implies increased permeability and fluid transfer into the alveoli, leading to edema and atelectasis. The breakdown of the alveolar-epithelial barrier is a consequence of multiple factors that include dysregulated inflammation, intense leukocyte infiltration, activation of procoagulant processes, cell death, and mechanical stretch. Reactive oxygen and nitrogen species (RONS) can modify or damage ion channels, such as epithelial sodium channels, which alters fluid balance. Some studies claim that these patients may have higher levels of surfactant protein B in the bloodstream. The correct approach to patients with CPE should include a detailed medical history and a physical examination to evaluate signs and symptoms of CPE as well as potential causes. Second-level diagnostic tests, such as pulmonary ultrasound, natriuretic peptide level, chest radiograph, and echocardiogram, should occur in the meantime. The identification of the specific CPE phenotype is essential to set the most appropriate therapy for these patients. Non-invasive ventilation (NIV) should be considered early in the treatment of this disease. Diuretics and vasodilators are used for pulmonary congestion. Hypoperfusion requires treatment with inotropes and occasionally vasopressors. Patients with persistent symptoms and diuretic resistance might benefit from additional approaches (i.e., beta-agonists and pentoxifylline). This paper reviews the pathophysiology, clinical presentation, and management of CPE.