Why Closing Volume Increases in Left Ventricular Failure
Closing volume increases in left ventricular failure because elevated left ventricular end-diastolic pressure (LVEDP) transmits backward to the pulmonary circulation, causing increased pulmonary venous and capillary pressures that lead to small airway closure at higher lung volumes, particularly in dependent lung regions.
Pathophysiologic Mechanism
Backward Transmission of Elevated Filling Pressures
Left ventricular failure elevates LV diastolic pressure, which directly transmits to the left atrium and pulmonary veins, increasing pulmonary capillary wedge pressure 1.
This backward pressure transmission occurs whether the LV failure is systolic (reduced ejection fraction) or diastolic (impaired relaxation and increased stiffness) in nature 2, 3.
In systolic dysfunction, impaired emptying increases end-systolic volume, which elevates end-diastolic pressure even when the ventricle attempts to fill 2.
In diastolic dysfunction with preserved ejection fraction, the stiff, non-compliant ventricle requires elevated filling pressures to achieve adequate cardiac output, directly causing pulmonary congestion 3.
Pulmonary Vascular and Interstitial Effects
Elevated pulmonary venous pressure causes fluid transudation into the pulmonary interstitium and alveolar spaces, creating peribronchial edema that compresses small airways 4.
Chronic LV failure produces profound pulmonary remodeling with vascular fibrosis, increased muscularization of pulmonary vessels, and leukocyte infiltration that further compromises small airway mechanics 4.
The increased interstitial fluid volume and peribronchial cuffing reduce the tethering forces that normally keep small airways open during expiration 1.
Regional Lung Effects
Dependent lung zones experience higher pulmonary venous pressures due to gravitational effects, causing preferential small airway closure in these regions at higher lung volumes 1.
When regional pleural and interstitial pressures exceed pulmonary arterial pressure (West zone 1 conditions), airway closure occurs even earlier in the expiratory cycle 1.
The combination of increased closing volume and reduced functional residual capacity creates ventilation-perfusion mismatch and hypoxemia 1.
Clinical Implications
Distinguishing Features
Patients with LV failure and elevated closing volume typically present with orthopnea and paroxysmal nocturnal dyspnea, as recumbency worsens the dependent zone airway closure 1, 2.
Physical examination may reveal basilar crackles from small airway reopening during inspiration, though this finding can be absent in chronic compensated states 1.
Pulmonary function testing demonstrates increased closing volume and reduced expiratory reserve volume, with the closing capacity potentially exceeding functional residual capacity during tidal breathing 1.
Management Considerations
Reducing LV filling pressures with diuretics directly decreases pulmonary venous pressure and improves small airway mechanics 2, 5.
Treating the underlying cause of LV dysfunction (ischemia, hypertension, valvular disease) addresses the root pathophysiology rather than just the pulmonary consequences 1, 5.
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 1.
Common Pitfalls
Do not attribute increased closing volume solely to intrinsic lung disease without evaluating for LV dysfunction, as heart failure is a common and treatable cause 2, 4.
Avoid aggressive diuresis that causes intravascular volume depletion while interstitial edema persists, as this reduces cardiac output without fully resolving airway closure 6.
Recognize that chronic LV failure causes permanent pulmonary remodeling with fibrosis that may not fully reverse even after successful treatment of the cardiac dysfunction 4.