Effect of lung inflation on pulmonary vascular resistance by arterial and venous occlusion

Abstract

To explain the changes in pulmonary vascular resistance (PVR) with positive- and negative-pressure inflation (PPI and NPI, respectively), we studied their effects in isolated canine left lower lobes perfused at constant flow rate. The venous pressure was kept constant relative to atmospheric pressure during lung inflation. The total arteriovenous pressure drop (delta Pt) was partitioned with the arterial and venous occlusion technique into pressure drops across arterial and venous segments (large indistensible extra-alveolar vessels) and a middle segment (small distensible extra-alveolar and alveolar vessels). PPI caused a curvilinear increase in delta Pt due to a large Starling resistance effect in the alveolar vessels associated with a small volume-dependent increase in the resistance of alveolar and extra-alveolar vessels. NPI caused an initial decrease in delta Pt due to reduction in the resistance of extra-alveolar vessels followed by an increase in delta Pt due to a volume-dependent increase in the resistance of all vessels. In conclusion, we provided for the first time evidence that lung inflation results in a volume-dependent increase in the resistance of both alveolar and extra-alveolar vessels. The data suggest that while the volume-related changes in PVR are identical with PPI and NPI, there are pressure-related changes that can be different between the two modes of inflation.

Interactions between pulmonary hemodynamics and lung mechanics

“…However, these previous studies addressed either the pulmonary vascular or the lung mechanical changes, their simultaneous alterations have not been characterized. In contrast with the consistent data obtained for PPLI, the findings on pulmonary hemodynamic changes during NPLI are still controversial [13,15,18,23] mainly due to the inconsistency in the measurement of pulmonary vascular pressures.…”

“…Whereas one study demonstrated a monotonic decrease in Rv during NPLI [18] others have documented a mild drop in Rv, followed by gradual increases at high lung volumes [13,15,23]. All these previous studies characterized the pulmonary vascular and lung mechanical changes under steady-state conditions, the mechanical changes in these compartments during dynamic inflation-deflation maneuvers remain unknown.…”

“…Positive-pressure lung inflation (PPLI), commonly applied to maintain gas exchange during mechanical ventilation, is far from being physiological and results in a number of side-effects, originating from the high positive intrathoracic pressures that may subsequently worsen pre-existing pulmonary lesions. PPLI may jeopardize the pulmonary hemodynamic conditions, mainly via compression of the pulmonary vessels [12][13][14][15][16][17]. These adverse pulmonary hemodynamic effects do not exist during normal breathing, since negative-pressure lung inflation (NPLI) generated by a negative pressure around the lungs exerts a different pressure gradient across the pulmonary vascular wall that generates a radial traction on the vessels as the lung parenchyma expands [18].…”

“…These adverse pulmonary hemodynamic effects do not exist during normal breathing, since negative-pressure lung inflation (NPLI) generated by a negative pressure around the lungs exerts a different pressure gradient across the pulmonary vascular wall that generates a radial traction on the vessels as the lung parenchyma expands [18]. There is a consensus in the literature that PPLI decreases the airway resistance (Raw), alters the viscoelastic properties of the lungs [19][20][21] and increases the pulmonary vascular resistance (Rv) [12,13,[15][16][17][18]22]. However, these previous studies addressed either the pulmonary vascular or the lung mechanical changes, their simultaneous alterations have not been characterized.…”

“…The underlying physiological phenomena have been well established and may involve the compression of the intra-alveolar vessels by the increased positive pressure leading to compression and distortion of the capillaries, in addition to the elongation of intra-and extra-alveolar vessels [12][13][14][15][16][17].…”