Asian Journal of Research in Cardiovascular Diseases

Background: the first manifestations of cardiogenic pulmonary edema include hemodynamic pulmonary congestion and high capillary pressure. This causes fluid to flow from the capillaries into the interstitium and alveolar spaces. High capillary pressure can also cause blockage, increasing the inability to penetrate and transfer fluid to the interstitium and alveoli. The fluids in the alveoli alter the properties of the surfactant and increase local stress. This can lead to the formation of additional edema and atelectasis due to inactive gas exchange. Patients with gait obstruction have elevated levels of surfactant protein B, and these levels often remain high after initial clinical development. Routine clinical examination may not identify patients with increased extravascular fluid in the lungs; pulmonary ultrasound can easily detect pulmonary edema in patients with severe degeneration and in patients at risk of caries. Serial pulmonary ultrasound studies can help identify patients with cardiogenic pulmonary edema and identify small populations that need additional treatment. Conventional treatment for cardiogenic pulmonary edema generally includes diuresis, post-exercise load reduction, and, in some cases, irregular air supply to reduce respiratory function and improve oxygen uptake. Patients with persistent symptoms, abnormal chest x-rays, and resistance to diuretics may benefit from other treatment options. These may include beta agonists and pentoxifylline, which allow further investigation in patients with cardiogenic pulmonary edema.

Conclusion: Unfortunately, despite the right treatment, the effects of cardiogenic pulmonary edema / heart failure are very serious. There is no cure for this disease, and the important thing is to prevent this condition in the first place.