Pathophysiology of Closing Volume in Left Ventricular Failure

Mechanism of Increased Closing Volume

Left ventricular failure elevates LV diastolic pressure, which directly transmits to the left atrium and pulmonary veins, increasing pulmonary capillary wedge pressure, as stated by the American Heart Association 1, 2.
Dependent lung zones experience higher pulmonary venous pressures due to gravitational effects, causing preferential small airway closure in these regions at higher lung volumes, according to the European Society of Intensive Care Medicine 2.
The combination of increased closing volume and reduced functional residual capacity creates ventilation-perfusion mismatch and hypoxemia, as reported by the American Thoracic Society 2.

Patients with LV failure and elevated closing volume typically present with orthopnea and paroxysmal nocturnal dyspnea, as recumbency worsens the dependent zone airway closure, as noted by the American College of Cardiology 1.
Physical examination may reveal basilar crackles from small airway reopening during inspiration, though this finding can be absent in chronic compensated states, as stated by the American Heart Association 3.

Treating the underlying cause of LV dysfunction (ischemia, hypertension, valvular disease) addresses the root pathophysiology rather than just the pulmonary consequences, as recommended by the American College of Cardiology 4, 1.
In acute decompensated heart failure with severe pulmonary congestion, positive pressure ventilation can temporarily improve closing volume by increasing functional residual capacity above closing capacity, as suggested by the European Society of Intensive Care Medicine 2.