Causes of Pulmonary Edema
Pulmonary edema occurs when fluid accumulation in the lungs exceeds the capacity for fluid removal, primarily due to imbalances in Starling forces (hydrostatic and oncotic pressure gradients) and/or increased capillary permeability. 1
Primary Mechanisms
1. Hydrostatic Pulmonary Edema
- Increased hydrostatic pressure gradient
- Left heart failure (most common cause)
- Mitral stenosis/regurgitation
- Volume overload
- Increased pulmonary venous pressure
- Iatrogenic fluid administration
2. Permeability Pulmonary Edema
- Increased capillary permeability
- Acute lung injury/ARDS
- Sepsis
- Pneumonia
- Inhalation injuries
- Trauma
- Drug toxicity
3. Mixed Mechanism Pulmonary Edema
- Combined hydrostatic and permeability factors
- Common in critically ill patients
Starling Forces and Fluid Balance
The movement of fluid across the pulmonary capillary membrane is governed by Starling's equation, which describes the balance between:
- Hydrostatic pressure gradient - pushes fluid out of vessels
- Oncotic pressure gradient - pulls fluid into vessels
- Capillary permeability - determines ease of fluid movement
- Lymphatic drainage capacity - removes excess fluid 1
When fluid deposition exceeds the capacity of the lungs to remove fluid (primarily via lymphatic flow), extravascular water accumulates, first as interstitial edema and then as alveolar edema. 1, 2
Pathophysiological Mechanisms in Detail
Cardiogenic Pulmonary Edema
- Left ventricular failure increases left atrial and pulmonary venous pressures
- Elevated hydrostatic pressure drives fluid into the interstitium
- Often associated with:
- Increased systemic vascular resistance
- Insufficient systolic/diastolic myocardial reserve
- Redistribution of fluid rather than total body fluid excess 3
Non-cardiogenic Pulmonary Edema (ARDS)
- Characterized by diffuse alveolar damage
- Inflammatory mediators damage the alveolar-capillary membrane
- Increased permeability allows protein-rich fluid to leak into alveoli
- Surfactant dysfunction further worsens alveolar collapse
- Progresses through exudative, fibroproliferative, and fibrotic phases 1
High-Altitude Pulmonary Edema
- Hypoxia-induced pulmonary vasoconstriction
- Uneven hypoxic pulmonary vasoconstriction
- Increased capillary pressure in non-constricted areas
- Stress failure of pulmonary capillaries 4
Clinical Implications
Pulmonary edema presents with:
- Dyspnea, tachypnea
- Crackles, wheezing
- Decreased lung compliance
- Hypoxemia due to ventilation-perfusion mismatch and shunt
- Radiographic findings of interstitial or alveolar infiltrates 2, 5
In acute pulmonary edema, treatment focuses on:
- Improving oxygenation
- Reducing hydrostatic pressure (diuretics, vasodilators)
- Addressing the underlying cause
- In cardiogenic edema: intravenous furosemide (40-80 mg) 6
- In permeability edema: lung-protective ventilation strategies
Important Considerations
- Pulmonary edema in ARDS often requires mechanical ventilation with PEEP to recruit collapsed alveoli
- Excessive fluid administration can worsen pulmonary edema, especially in patients with increased capillary permeability
- Monitoring pulmonary artery pressure may be indicated in cases where the etiology is unclear 1
- Therapeutic thoracentesis in pleural effusions should be limited to 1-1.5L to prevent re-expansion pulmonary edema 1
Remember that pulmonary edema represents a final common pathway for multiple disease processes, and identifying the underlying cause is essential for appropriate management.