Mechanisms controlling the volume of pleural fluid and extravascular lung water

Abstract

Pleural and interstitial lung fluid volumes are strictly controlled and maintained at the minimum thanks to the ability of lymphatics to match the increase in filtration rate. In the pleural cavity, fluid accumulation is easily accommodated by retraction of lung and chest wall (high compliance of the pleural space); the increase of lymph flow per unit increase in pleural fluid volume is high due to the great extension of the parietal lymphatic. However, for the lung interstitium, the increase in lymph flow to match increased filtration does not need to be so great. In fact, increased filtration only causes a minor increase in extravascular water volume (,10%) due to a marked increase in interstitial pulmonary pressure (low compliance of the extracellular matrix) which, in turn, buffers further filtration. Accordingly, a less extended lymphatic network is needed. The efficiency of lymphatic control is achieved through a high lymphatic conductance in the pleural fluid and through a low interstitial compliance for the lung interstitium. Fluid volume in both compartments is so strictly controlled that it is difficult to detect initial deviations from the physiological state; thus, a great physiological advantage turns to be a disadvantage on a clinical basis as it prevents an early diagnosis of developing disease.

Pathophysiology of Extravascular Water in the Pleural Cavity and in the Lung Interstitium After Lung Thoracic Surgery

“…This ensures, in turn, a high efficiency of the gas diffusion. Similarly to the pleural fluid, also lung interstitial fluid is kept at a subatmospheric pressure (also ~ -10 cmH 2 O, Fig.4) due to the powerful draining action of lymphatics in face of a very low microvascular permeability (Miserocchi, 2009). The latter feature allows to keep microvascular filtration as low as 1· 10 -4 ml/cm 2 in 24h.…”

“…Pleural lymphatics act as efficient regulators of pleural liquid volume avoiding hydrothorax formation by increasing the draining flow (up to ~ 20 fold) in proportion to the increase in filtration rate (Miserocchi, 2009). As a matter of fact, for a tenfold increase in filtration rate, the volume of the pleural fluid would only be hardly doubled (Miserocchi, 2009).…”

“…As a matter of fact, for a tenfold increase in filtration rate, the volume of the pleural fluid would only be hardly doubled (Miserocchi, 2009). Any increase in pleural fluid filtration can in principle easily accumulate in the chest due to the opposite retraction of the lung and chest wall (Fig.…”

“…The volume of the extravascular water is strictly controlled so that the lung appears quite resistant to the development of edema. In fact, at least three mechanisms cooperate to allow only minimal variations in extravascular water volume relative to the steady state condition (Miserocchi, 2009). First, the glycosaminoglycan chains of PGs can bind excess water to form gel-like structures; this results in an increase in the steric hindrance of proteoglycans and corresponding decrease in the porosity of the basement membrane and thus also in microvascular permeability.…”

“…Second, the assembly of large matrix PGs within the extracellular matrix provides low tissue compliance and this represents an important "tissue safety factor" against the development of edema. In fact, a minor increase in extravascular water in response to increased microvascular filtration, causes a marked increase in interstitial pressure (e.g., from ~ -10 to ~ 5 cmH 2 O) (Miserocchi, 2009) that buffers further filtration. Third, arteriolar vasoconstriction represents an important reflex to avoid or actually decrease capillary pressure when filtration is increased due to an increase in microvascular permeability (Negrini, 1995, Rivolta et al, 2011.…”