What are the causes of pulmonary congestion?

Causes of Pulmonary Congestion

Pulmonary congestion results primarily from elevated left ventricular filling pressures that cause backward transmission of pressure into the pulmonary circulation, leading to fluid accumulation in the pulmonary interstitium and alveoli. 1

Primary Cardiac Mechanisms

Left Heart Dysfunction

• Left ventricular systolic or diastolic dysfunction is the most common cause, impairing the ventricle's ability to fill with or eject blood, which elevates left ventricular end-diastolic pressure and subsequently pulmonary capillary wedge pressure 1
• Acute decompensated heart failure in patients with known heart failure history represents the most frequent presentation, characterized by worsening symptoms of congestion 1
• De novo acute heart failure occurs in patients without prior heart failure history, presenting with new-onset pulmonary congestion 1

Valvular Heart Disease

• Mitral stenosis or regurgitation directly elevates left atrial pressure, causing pulmonary venous hypertension and increased lymphatic pressures (manifesting as Kerley B lines) 1
• Aortic stenosis or regurgitation increases left ventricular afterload or volume overload, leading to elevated filling pressures 1

Other Cardiac Causes

• Acute coronary syndrome with myocardial ischemia or infarction impairs ventricular function acutely 1
• Acute myocarditis causes inflammatory myocardial injury with troponin elevation and ventricular dysfunction 1
• Congenital heart defects can lead to volume or pressure overload 1

Vascular and Hemodynamic Mechanisms

Fluid Redistribution

• Acute increase in systemic vascular resistance superimposed on insufficient myocardial reserve causes fluid shift from the intravascular compartment into pulmonary interstitium and alveoli, even without total body fluid accumulation 2, 3
• Reduced venous capacitance increases preload while increased arterial stiffness elevates afterload, redistributing fluid to the lungs 3
• This redistribution mechanism explains why many patients develop pulmonary edema with minimal weight change 3

Pulmonary Vascular Disease

• Pulmonary veno-occlusive disease (PVOD) or pulmonary capillary hemangiomatosis causes post-capillary obstruction with risk of severe pulmonary edema when treated with pulmonary arterial hypertension therapies 1
• Pulmonary hypertension due to left heart disease develops from passive backward pressure transmission, potentially complicated by superimposed pulmonary vasoconstriction and vascular remodeling 1

Right Heart Contribution

Venous Congestion

• Right ventricular dysfunction worsens systemic venous congestion and decreases venous return, perpetuating the cycle of congestion 1, 4
• Elevated right atrial pressure reduces the renal perfusion gradient, contributing to cardiorenal syndrome and further fluid retention 5, 4
• Systemic venous congestion decreases venous return to right heart chambers while simultaneously increasing left filling pressures through ventricular interdependence 1

Neurohormonal and Inflammatory Mechanisms

Compensatory System Activation

• Renin-angiotensin-aldosterone system activation causes vasoconstriction, fluid retention, and sodium reabsorption in response to decreased cardiac output 1, 4
• Sympathetic nervous system activation increases sodium reabsorption and perpetuates the congestion cycle 4
• Sustained hemodynamic congestion activates neurohormones causing subendocardial ischemia, myocardial necrosis/apoptosis, and secondary mitral regurgitation 5

Bronchial Circulation Contribution

• Bronchial vascular engorgement may occur from increased flow or blood volume stasis due to high cardiac filling pressures, leading to thickened bronchial mucosa and reduced airway compliance 6
• This mechanism potentially contributes to "cardiac asthma," orthopnea, and exertional dyspnea characteristic of heart failure 6

Precipitating Factors

Acute Triggers

• Respiratory infection as a precipitant factor is associated with higher in-hospital mortality (>4%) in acute heart failure patients 1
• Non-adherence with diuretic therapy or excessive fluid/salt intake can trigger decompensation, though recent data suggest this is less common than previously thought 3
• Acute coronary syndrome precipitates pulmonary congestion through acute myocardial dysfunction 1

Important Clinical Caveats

• Hemodynamic congestion precedes clinical congestion by days to weeks, representing the "tip of the iceberg" of underlying hemodynamic abnormalities 5
• Physical examination has limited sensitivity (58%) for detecting elevated pulmonary capillary wedge pressure ≥22 mmHg, meaning absence of rales does not exclude significant congestion 1, 5
• Pulmonary congestion can occur with normal or reduced left ventricular ejection fraction, emphasizing that diastolic dysfunction alone is sufficient 1
• One in four patients have disproportionate elevation of right-sided versus left-sided pressures, making isolated assessment of pulmonary congestion insufficient 5