Acute pulmonary oedema: cardiogenic vs non-cardiogenic differentiation

^[30]

The pathophysiology — hydrostatic forces vs permeability leak

Acute pulmonary oedema develops when fluid accumulates in the interstitium and alveoli faster than lymphatics can clear it. The Starling equation governs transcapillary fluid flux: net filtration = the hydraulic pressure pushing fluid OUT minus the oncotic pressure pulling it BACK, multiplied by the capillary permeability coefficient. Two fundamentally different insults disturb this balance, producing the two phenotypes.^[30]

In cardiogenic (hydrostatic) oedema, left-sided filling pressures rise — left atrial pressure (LAP) → pulmonary venous pressure → capillary hydrostatic pressure (Pc). Once Pc exceeds plasma oncotic pressure and interstitial pressure, fluid is pushed across an INTACT alveolar–capillary membrane into the interstitium, then into the alveoli. The fluid is a TRANSUDATE (protein-poor), and the membrane architecture is preserved — which is why the lung recovers rapidly once pressure is relieved. Fein found that when pulmonary capillary wedge pressure was less than 20 mmHg, the oedema-fluid-to-plasma protein ratio exceeded 0.6, whereas the mean ratio in cardiogenic oedema was 0.46.^[28]

In non-cardiogenic (permeability) oedema, an insult — sepsis, pneumonia, aspiration, major trauma, pancreatitis, massive transfusion — destroys the integrity of the alveolar–capillary membrane. Endothelial and epithelial injury, neutrophil activation, cytokine surge and loss of surfactant produce a leaky barrier. Fluid AND protein pour into the interstitium and alveoli at a NORMAL or LOW pulmonary capillary pressure. The fluid is a protein-rich EXUDATE. This is the ARDS lung — stiff, heavy, non-compliant permeability oedema. The Berlin definition grades hypoxaemia as mild (200 mmHg < PaO2/FiO2 ≤ 300 mmHg), moderate (100 mmHg < PaO2/FiO2 ≤ 200 mmHg), and severe (PaO2/FiO2 ≤ 100 mmHg); empirical evaluation associated these stages with mortality of 27%, 32%, and 45%. AECC (1994) described ARDS as nonhydrostatic pulmonary oedema.^{[16] [17]}

The crucial implication at the bedside: lowering the pressure (diuresis, CPAP/NIV) can reverse hydrostatic oedema, but does NOT seal an ARDS membrane. 3CPO: faster 1-hour physiology with NIV vs oxygen, without a 7-day mortality difference. ARDS demands treatment of the cause, lung-protective ventilation to avoid further injury, and time for the membrane to heal. ^{[30] [18]}

References31ShowHide

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