What causes pulmonary congestion?

From the Guidelines

Pulmonary congestion is primarily caused by left-sided heart failure, which leads to increased pressure in the pulmonary veins and capillaries, as supported by the most recent study 1. When the left ventricle cannot effectively pump blood out to the body, pressure backs up into the left atrium and then into the pulmonary circulation. This increased hydrostatic pressure forces fluid from the capillaries into the lung tissue and alveoli, resulting in pulmonary edema.

Key Causes of Pulmonary Congestion

• Left-sided heart failure, which is the most common cause, as it leads to increased pressure in the pulmonary veins and capillaries 1
• Mitral valve disease, which impedes blood flow from the left atrium to the left ventricle
• Acute myocardial infarction, which reduces left ventricular function
• Severe hypertension, which increases afterload on the heart
• Fluid overload from kidney failure or excessive IV fluids
• Non-cardiac causes such as acute respiratory distress syndrome, high-altitude pulmonary edema, and certain toxins that damage the alveolar-capillary membrane The fundamental mechanism involves an imbalance between hydrostatic and oncotic pressures in the pulmonary circulation, leading to fluid accumulation in the lungs and the characteristic symptoms of shortness of breath, cough, and in severe cases, pink frothy sputum.

Pathophysiology of Pulmonary Congestion

• The inability to control and maintain water-ion homeostasis, mediated mainly by neurohormonal drive and impaired kidney function, is a central disturbance in heart failure that results in water and sodium retention and/or volume shifts, leading to clinically overt congestion 1
• Activation of the sympathetic nervous system, renin–angiotensin–aldosterone system, proinflammatory pathways, as well as non-osmotic vasopressin release and peripheral resistance to natriuretic peptides, all of which increase sodium avidity and facilitate congestion development 1

From the FDA Drug Label

Furosemide is indicated in adults and pediatric patients for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome Furosemide is indicated as adjunctive therapy in acute pulmonary edema.

The cause of pulmonary congestion is not directly stated in the label, but it can be inferred that congestive heart failure is a condition associated with edema and pulmonary edema, which may lead to pulmonary congestion.

• Congestive heart failure is a potential cause of pulmonary congestion.
• The label does not provide a direct answer to the question of what causes pulmonary congestion, but it suggests a link between congestive heart failure and pulmonary edema 2.

From the Research

Causes of Pulmonary Congestion

Pulmonary congestion is a complex condition that can arise from various factors, including:

• Cardiac pressure and/or volume overload, which plays a central role in the pathophysiology, presentation, and prognosis of heart failure (HF) 3
• Increased blood volumes in the heart and lungs, such as pulmonary and heart blood volumes (Vp and Vh, respectively) and extravascular lung water (EVLW), which can lead to reduced lung function and spirometric measures 4
• Engorgement of the bronchial circulatory bed, which may contribute to pulmonary function abnormalities and symptoms such as orthopnea and exertional dyspnea in HF patients 5
• Passive pulmonary congestion, which can occur in acute myocardial infarction and lead to hypoxemia and functional disturbance of the lung 6
• Elevated left ventricular (LV) filling pressures, which can result in hemodynamic congestion and have deleterious effects on the heart and lungs, even in the absence of clinical congestion 7

Key Factors Contributing to Pulmonary Congestion

Some key factors that contribute to pulmonary congestion include:

• Increased cardiac filling pressures 3, 4, 7
• Expanded blood volumes in the heart and lungs 4
• Engorgement of the bronchial circulatory bed 5
• Decreased lung function and spirometric measures 4
• Hypoxemia and functional disturbance of the lung 6
• Hemodynamic congestion, which can occur days or weeks before clinical congestion develops 7