In a patient with severe mitral stenosis, the pulmonary capillary wedge pressure (PCWP) is 28 mmHg. At this pressure, the most likely respiratory finding is:
- A Pulmonary oedema; PCWP exceeds the oncotic pressure (~25 mmHg), causing net Starling filtration of fluid into alveoli ✓
- B Compensatory hyperventilation reducing PaCO2 to expand alveolar PO2 without pulmonary oedema
- C Pleural effusion only, because lymphatic drainage prevents alveolar flooding below 35 mmHg
- D Pulmonary haemosiderosis; haemoglobin is filtered across high-pressure capillaries chronically
Explanation
According to the Starling-Landis equation for capillary fluid exchange, the balance between hydrostatic and oncotic forces determines net fluid movement. Normal pulmonary capillary hydrostatic pressure is 7–12 mmHg, well below plasma oncotic pressure (~25 mmHg), keeping alveoli dry. When PCWP exceeds plasma oncotic pressure (~25 mmHg), net outward hydrostatic force exceeds the inward oncotic force, causing protein-poor fluid to accumulate in the interstitium and then the alveoli (pulmonary oedema). At PCWP 28 mmHg, pulmonary oedema occurs. Initially, interstitial oedema develops (perivascular cuffing, Kerley B lines), and with further rise, alveolar flooding follows. Option D (pulmonary haemosiderosis) does occur in chronic severe mitral stenosis but is a long-term consequence, not the acute respiratory finding at PCWP 28 mmHg.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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