There are two types of pulmonary edema, cardiogenic and noncardiogenic. We will discuss cardiogenic pulmonary edema here. Cardiogenic pulmonary edema refers to the accumulation of fluid in the lungs, specifically in the alveoli and the interstitial spaces between the alveoli and pulmonary capillaries. This accumulation of fluid can impair gas exchange and lead to respiratory distress. Cardiogenic pulmonary edema is pulmonary edema caused by acute uncompensated heart failure.

Acute uncompensated heart failure is typically due to left ventricular failure. Several conditions can cause acute uncompensated heart failure beyond cardiac origins including but not limited to fluid overload, primary severe hypertension, severe renal artery disease, or secondary hypertension due to renal artery stenosis.

Cardiogenic pulmonary edema is a fluid overload problem and is due to a sudden elevation in the hydrostatic pressure of the pulmonary capillaries. Increased pressure forces or pushes fluid out of the capillaries and into the interstitial spaces and alveoli. Injury to the pulmonary capillary endothelium can increase its permeability, enlarging the tiny spaces between the cells of the capillary membranes. These spaces are now large enough to let proteins and fluid to leak out of the capillaries and accumulate in the interstitial spaces and alveoli. Causes of increased capillary permeability include infections (such as pneumonia), inhalation of toxic gases, and acute respiratory distress syndrome (ARDS). Reduction in plasma oncotic pressure due to conditions such as hypoalbuminemia (low levels of albumin in the blood), liver disease, or protein-losing conditions can impair fluid reabsorption from the interstitial spaces, leading to edema formation. Decreased colloid osmotic forces pull fluid from one space to another. When a patient has a condition like congestive heart failure, the heart’s inability to adequately pump blood forward leads to increased pressure in the pulmonary circulation. This can cause fluid to back up into the lungs, resulting in pulmonary edema.

Your patient will have dyspnea, complain of a wet cough with pink-tinged sputum, and you may hear crackles in the bases on auscultation. If your patient has significant hypoxia, they will need to be intubated and placed on a ventilator while diuresis occurs. When they are intubated pink-tinged frothy sputum often erupts out of the endotracheal tube.

Overall, the pathophysiology of pulmonary edema involves a complex interplay of hemodynamic, inflammatory, and neurohumoral factors leading to fluid accumulation within the lungs. Treatment strategies typically target the underlying cause while also addressing the symptoms and consequences of pulmonary edema, such as oxygen therapy, diuretics, and in severe cases, mechanical ventilation.

References

Nathani, A., Jones, C., Ghamande, S. A., & Jones, S. F. (2021). Unilateral pulmonary edema and acute severe mitral regurgitation associated with operatively repaired aortic coarctation. Baylor University Medical Center Proceedings, 34(2), 289–290. https://doi-org.proxy.mul.missouri.edu/10.1080/08998280.2020.1860441

Pilgrim, A. (2023). Acute Pulmonary Edema and NSTEMI. Journal of Education & Teaching in Emergency Medicine (JETem), 8(3), 1–32. https://doi-org.proxy.mul.missouri.edu/10.21980/J8CW67

Zanza, C., Saglietti, F., Tesauro, M., Longhitano, Y., Savioli, G., Balzanelli, M. G., Romenskaya, T., Cofone, L., Pindinello, I., Racca, G., & Racca, F. (2023). Cardiogenic Pulmonary Edema in Emergency Medicine. Advances in Respiratory Medicine (MDPI), 91(5), 445–463. https://doi-org.proxy.mul.missouri.edu/10.3390/arm91050034