What are the causes of pulmonary edema?

Causes of Pulmonary Edema

Pulmonary edema develops through two fundamental mechanisms: cardiogenic causes driven by elevated hydrostatic pressure from cardiac dysfunction, and non-cardiogenic causes driven by increased capillary permeability from inflammatory injury. 1

Cardiogenic Causes (Elevated Hydrostatic Pressure)

The primary pathophysiology involves elevated left ventricular filling pressures that transmit backward into pulmonary capillaries, forcing fluid into the interstitium and alveoli when hydrostatic pressure exceeds oncotic pressure. 1

Specific Cardiac Etiologies:

• Acute myocardial infarction or injury creates sudden ventricular dysfunction with elevated pulmonary capillary wedge pressure (PCWP >18 mmHg), driving fluid from intravascular space into lung tissue 1

• Decompensated heart failure from any cause results in inadequate cardiac output with compensatory fluid retention and elevated filling pressures 1

• Valvular disease, particularly aortic stenosis and mitral regurgitation, creates pressure or volume overload that transmits backward into pulmonary veins 1

• Cardiac arrhythmias such as supraventricular tachycardia impair ventricular filling or reduce cardiac output, leading to pulmonary congestion 1

• Cardiomyopathy of any etiology increases capillary hydrostatic pressure through impaired ventricular function 2

• Pericardial disease restricts cardiac filling and elevates venous pressures 2

Non-Cardiogenic Causes (Increased Capillary Permeability)

Inflammatory mediators increase capillary permeability by causing endothelial cell contraction and disruption, creating gaps that allow protein-rich fluid to leak into interstitium and alveoli. 1, 3

Specific Non-Cardiogenic Etiologies:

• Sepsis and ARDS represent prototypical causes where inflammatory mediators eliminate the protective oncotic gradient, allowing protein-rich fluid accumulation in alveoli 1

• Diffuse alveolar damage progresses through exudative, fibroproliferative, and fibrotic phases with hyaline membrane formation 1, 3

• Pneumonia can progress to ARDS when severe, with 28-33% of septic patients meeting ARDS criteria at clinical presentation 3

• Smoke inhalation causes direct toxic injury to alveolar-capillary membrane 4

• High-altitude exposure causes pulmonary edema in 40-60% of mountaineers through mechanisms including subclinical edema and increased cough-receptor sensitivity 2

• Neurogenic causes including epilepsy, brain trauma, and electrocution 5

• Upper airway obstruction such as laryngeal paralysis or strangulation creates low alveolar pressure 5

• Drug-induced lung injury including vaping-induced injury requires withholding the causative agent 2

• Pulmonary embolism causes cough and edema in nearly half of documented cases 2

Additional Contributing Factors:

• Renal failure increases capillary hydrostatic pressure through volume overload 2

• Cirrhosis with portal hypertension elevates hydrostatic pressure 2

• Decreased plasma oncotic pressure from hypoalbuminemia 4

• Iatrogenic second hits including excessive fluid administration, blood product transfusions, and injurious mechanical ventilation aggravate existing lung injury 2

Critical Diagnostic Distinction:

The fundamental clinical task is distinguishing cardiogenic (elevated cardiac filling pressures) from non-cardiogenic (normal pressures with increased permeability) causes. 1

• Pulmonary artery catheterization definitively measures PCWP: >18 mmHg suggests cardiogenic, <18 mmHg suggests non-cardiogenic 2, 1

• Echocardiography objectively assesses ventricular function, wall motion abnormalities, and valvular disease 1

• B-natriuretic peptide or NT-proBNP elevation suggests cardiac etiology, though obesity and renal failure affect levels 1

• Radiographic patterns differ: cardiogenic shows symmetric "batwing" pattern with vascular pedicle widening, while non-cardiogenic shows patchy widespread opacities without fluid overload signs 3