In a patient with acute left ventricular failure, pulmonary oedema develops when pulmonary capillary wedge pressure (PCWP) exceeds which threshold, and what is the primary protective mechanism that delays oedema at moderately elevated pressures?

• A Pulmonary oedema begins when PCWP exceeds ~25–28 mmHg; at lower elevations (18–25 mmHg), increased lymphatic drainage from pulmonary lymphatics provides the primary safety valve, removing excess interstitial fluid before alveolar flooding ✓
• B Pulmonary oedema begins when PCWP exceeds 18 mmHg; plasma protein oncotic pressure provides no protection because pulmonary capillary permeability is high
• C Pulmonary oedema begins when PCWP exceeds 40 mmHg; the primary protection is hypoxic pulmonary vasoconstriction diverting blood away from waterlogged areas
• D Pulmonary oedema begins when PCWP exceeds 12 mmHg; the primary protection is surfactant preventing water entry into alveoli regardless of hydrostatic pressure

Explanation

Normal PCWP is 6–12 mmHg. Pulmonary oedema clinically appears when PCWP exceeds ~25–28 mmHg (once Starling forces and safety factors are overwhelmed). Between 18–25 mmHg (Stage II), increased lymphatic flow—the primary safety mechanism—removes up to 10× normal fluid from the interstitium, delaying alveolar flooding. Plasma oncotic pressure (~25 mmHg) also opposes filtration. Once PCWP exceeds 25–28 mmHg, Starling forces favour net filtration exceeding lymphatic capacity, and alveolar flooding (pulmonary oedema) begins. Option B incorrectly states oedema at 18 mmHg; 18 mmHg is the threshold for mild interstitial oedema, not frank alveolar oedema. Surfactant prevents collapse, not fluid entry.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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