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The Pleural Interface

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The Pleural Interface Thorax 1985;40:1-8 Thorax: first published as 10.1136/thx.40.1.1 on 1 January 1985. Downloaded from Editorial The pleural interface The pleural interface is a remarkable mechanical ised by the permeability of both pleural mem- coupling in the transmission of most of the work of branes.4 breathing from the chest wall and diaphragm to the To take gases first, the reason that the pleural lungs. It is remarkable in that the coupling is under interface is kept gas free was first realised by Rist tension and yet there is no adhesive force between and Strohl,5 who pointed out that the total tension of the pleurae, so that the two surfaces remain in close gases dissolved in venous blood is about 73 cm H2O apposition and able to slide over each other easily (54 mm Hg, 7*2 kPa) below that in arterial blood. If with no tendency for fluid or gases in adjacent tis- arterial blood is equilibrated with alveolar air, this sues to enter the potential cavity which their separa- represents a total blood-gas tension 73 cm H2O tion would create. At least, this is the case under below atmospheric-compared with any gas at the normal conditions. The basic physical and physiolog- interface, which would have an absolute pressure ical principles operating in normal circumstances only 5 cm H,O below atmospheric. This gives a driv- clearly need to be appreciated before we attempt to ing force of 68 cm H2O for resolving any rationalise pathological conditions. In this article pneumothorax. This simple calculation, however, attention is focused on the forces preventing fluid assumes that venous is the relevant total (Po2 + and gas accumulation, the lubrication of pleural Pco2+ PN2 + PH2o= 40 + 46 + 573 + 47 = 706 movement, and the possible role of the pleurae in mm Hg (or 5.3 + 6-1 + 76-4 + 6-3 = 94-1 kPa)), copyright. energy conservation during ventilation. especially when one side of the pleural interface is The detailed morphology of the pleural cavity in perfused by arterial blood and the other by venous. relation to the bony thorax is covered. in standard The deficit is unlikely, however, to be less than that texts of anatomy.' Essentially, these describe how found in subcutaneous tissue spaces, where the visceral pleura invests the lungs and interlobar implanted capsules permeable to all gases develop a http://thorax.bmj.com/ surfaces while the parietal pleura is thicker and partial vacuum measured as 41-48 mm Hg (5.5 - more easily separated2 from the walls of the three 6-4 kPa) in dogs6 and 79 mm Hg (10-5 kPa) in rab- intrathoracic surfaces which it lines-namely, costal, bits.' This is depicted graphically in figure 1. The mediastinal, and diaphragmatic. The physical nature inherent unsaturation of the adjacent tissue is ample of the interface will be discussed later but, histologi- to resolve a pneumothorax, just as it provides a driv- cally, each pleural surface appears as a uniform layer ing force for dissolving the bubbles produced by of flattened mesothelial cells, without a basement decompression that cause "the bends" in divers and membrane but resting on a layer of connective tissue aviators.7 The same driving force applies even after composed of collagen and elastic fibres. a pneumothorax may have been amplified (in vol- on September 28, 2021 by guest. Protected The reason that the coupling is under tension is ume) by gaseous anaesthetics-particularly nitrous that the chest wall tends to recoil outwards and the oxide.8 The physical chemistry has been described in lungs inwards, thus generating a negative pressure of detail elsewhere,7 but an inherent unsaturation about 5 cm H20 at the interface at rest (that is, at derived from the oxyhaemoglobin dissociation curve functional residual capacity). The variation of this and the relative solubilities of the metabolic gases partial vacuum during the respiratory cycle and with (02 + C02) becomes a driving force for dissolving age is discussed in detail in standard texts on pulmo- the inert gas present, which invariably becomes the nary mechanics.3 The presence of the partial vac- rate limiting component.9 The inherent unsaturation uum, however, raises the fundamental question of increases in step with the oxygen partial pressure in why fluid and gases dissolved in adjacent tissues do the inspired gas7 and this provides another reason not accumulate at the interface and eventually dis- for the recommended'0 administration of oxygen in rupt energy transmission. This question is emphas- cases of pneumothorax. This leaves the question of Address for reprint requests: Professor Brian A Hills, Department why the negative pressure at the pleural interface of Anesthesiology, University of Texas Medical School, Houston, does not cause the accumulation of fluid. Texas 77030, USA. Fluid shifts across the pleural interface are deter- 1 2 Thorax: first published as 10.1136/thx.40.1.1 on 1 January 1985. Downloaded from Atmosphere 'Alveolar' Arterial Venous (dry) air Blood Blood Cells Pleural Absolute 760' Interlace Pressure ..... .. : .:.:.-. Recoil:5 l H20:47 Unsatura- Unsatura- 1 756 H20:47 tion: 54 tion:81 -91 t D .... .. ... .. C02:40 _ ,,~~~forcefor I 02:152 C02:40 H20:47 H20:47 : o n Partial pressure 02:100 C02:46 or 02:88 C02:(49) Gasi Tension 02:40 02:(10) m N2:608 . .** N2:573 N2:573 N2:573 Lz:7¶1 u u 0 . Conversion: Partial pressures in the diagram iri kPa Unsaturation 7.2 :10.8-12.1: copyright. H20 6.3 6.3 6.3 6.3 C02 5.3 5.3 6.1 ( 6.5) 02 20.3 13.3 11.7 5.3 ( 1.3) : http://thorax.bmj.com/ N2 81.1 76.4 76.4 76.4 76.4 Fig 1 The gas gradients for resorption ofa pneumothorax in which the gas is in the gaseous phase and the sum ofthe partial pressures must equal the absolute pressure (Dalton's law-which does not apply to the tensions ofgases dissolved in liquid or tissue). PLEURAL on September 28, 2021 by guest. Protected I E E i z e). co C: CL Fig 2 The hydrostatic and osmotic pressures providing the driving forces for the filtration offluid across the parietal pleura into the interface and the resorption ofthat fluid by the lung. Note that the resorptive capacity ofthe visceral pleura will be even greater than is indicated by the comparison ofdriving forces owing to its greater permeability to fluid. 3 Thorax: first published as 10.1136/thx.40.1.1 on 1 January 1985. Downloaded from mined by both hydrostatic and osmotic pressure less than 1.0 ml of fluid.4 '5 This is a very small quan- gradients as in most other places in the body. The tity for providing lubrication unless it is particularly fact that the chest wall and diaphragm are perfused evenly distributed as a layer separating the moving by systemic blood while the lung receives its blood surfaces. from the right side of the heart is a major factor Many attempts have been made to measure the responsible for the net flux of fluid from the parietal interpleural pressure at different points by inserting to the visceral pleura. This does not, however, balloons'6 or by titrating the external pressure until explain why fluid is prevented from accumulating at it returns the visceral pleura to its normal configura- the interface, which is below venous pressure. tion at sites where it has been exposed surgically.'7 Despite certain similarities in structure and activity, The results of these and other studies differ slightly the pleurae behave quite differently with respect to but all show that the differences in pleural pressure resorption and permeability in general." The hyd- recorded at various points are much less than the rostatic gradient from the systemic capillary bed in vertical head of fluid separating them. Thus the the chest wall (+ 30 mm Hg) to the pleural interface small volume of fluid is most unlikely to be present (-5 mm Hg) is relatively large at 35 mm Hg but the as a continuous liquid layer separating the pleurae to parietal pleura is relatively impermeable, limiting provide lubrication over the entire interface. Much the rate of filtration and producing almost protein analytical work'8 has been devoted to the relation- free filtrate. At least, at about 1l5% protein34 it ships between pleural pressure gradients, lung could produce a colloid osmotic pressure of 8 cm weight, and the configuration of the thoracic cavity H,O (6 mm Hg)3 or 5 mm Hg,4 to give an osmotic but, to a first approximation, they seem to conform gradient of 35 - 6 = 29 mm Hg) opposing the hyd- to the distribution which would be expected if the rostatic head of 35 mm Hg for a net gradient of 6 lung were replaced by a fluid of the same overall mm Hg. At the visceral pleura the same colloid density. Further evidence has been produced to osmotic pressure of 29 mm Hg is now tending to demonstrate the lack of continuity of the pleural drive fluid into pulmonary blood-or, more likely fluid and the way in which the pleurae are "pulled into the lymphatics-but is opposed by a hydrostatic into contact" by fluid removal'9 20 under the negative (venous-pleural) gradient of 11 + 5 = 16 mm Hg to pressures described above. copyright. give a net driving force for resorption of 13 mm Hg. The unique distribution of the negative pressure The relative pressure gradients are depicted in figure at the pleural interface provides the mechanism by 2.
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