Gas exchange is the prime function of the lung. The pulmonary circulation moves the pulmonary blood into close association with the alveoli (at the blood-gas barrier) so that gas exchange is facilitated. The flow involved is large as the pulmonary blood flow is equal to the cardiac output. Efficient gas exchange is facilitated because the blood-gas membrane is thin with a large surface area. At any moment, the pulmonary capillary blood volume is about 80 mls.
The key features of the pulmonary microcirculation are:
The Starling equation can be applied to the pulmonary microcirculation in the same way as any other capillary bed.
Typical values for the Starling’s Forces in Pulmonary Capillaries
Capillary hydrostatic pressure (Pc) is 13 mmHg (arteriolar end) to 6 mmHg (venous end) but variable because of the hydrostatic effects of gravity esp in the erect lung.
• Interstitial hydrostatic pressure (Pi) - Variable but ranges from zero to slightly negative.
• Capillary oncotic pressure = 25 mmHg (Same as in systemic capillaries)
• Interstitial oncotic pressure = 17 mmHg (This is estimated from measurements on lung lymph)
The interstitial oncotic pressure is high indicating significant leak of protein (mostly albumin) across the thin capillary walls under normal circumstances. The reflection coefficient has been estimated at about 0.5
Considering the typical values and allowing for the reflection coefficient, it can be estimated that the net oncotic gradient is small but favours reabsorption.
The capillaries are called ‘intra-alveolar vessels’ and the presssure they are exposed to is close to alveolar pressure (which has an average value of zero). However, actual measurements of pressure in the alveolar interstitium have found slightly negative pressures ( eg -2 mmHg). Closer to the hilum, the interstitial pressures become more negative and this favours flow of fluid from the alveolar intersitium into the pulmonary lymphatics.
The capillary hydrostatic pressure is variable because of the effects of gravity. Consider: The erect lung is basically suspended in a gravitational field so the pressure in the vessels at the base of the lung is higher than the pressure at the apex. The pressure difference is equivalent to the height of a static water column from the base to the apex. The distance involved is about 30 cms so the pressure difference is 30 cms H2O which is about 23 mmHg. If the typical pulmonary artery pressure is 25/8 then it is apparent that the pressure is just adequate for perfusion of the apex of the erect lung.
The pulmonary circuit has a low resistance and about half of this resistance is due to the pulmonary capillaries which have no muscle in their walls. The capillary hydrostatic pressure is quickly affected by changes in pulmonary artery pressure and left atrial pressure without much protective buffering.
The balance of Starling forces in the lung is generally stated as favouring reabsorption because of the clinical fact that the lungs are generally ‘dry’ and clearly need to be to facilitate gas exchange. Under normal conditions, there is a small net outward movement of fluid. This is estimated as equal to the pulmonary lymph flow rate. The flow is usually small (eg 10 to 20 mls/min) which is only about 2% of the pulmonary blood flow. So despite the net outward hydrostatic pressure gradient and the high reflection coefficient which limits the effectiveness of the oncotic pressure in opposing outward fluid movement, the measured low lymph flow means that the balance of forces is clearly to minimise loss of fluid into the interstitium.
The large surface area and thin capillary walls which assist efficient gas exchange also facilitate filtration from the capillaries to the interstitium. The interstitial fluid move towards the hilum along the spaces beside the vessels and the airways. The interstitial hydrostatic pressure probably becomes more negative as the hilum is approached. The excess filtrate is removed by the pulmonary lymphatics. Lymphatic flow is promoted by the rhythmic external compression that occurs during the ventilatory cycle and by the presence of one way valves.
The Starling equation is not very useful clinically because it is not possible to measure all six of the unknown values. In particular, bedside determination of the interstitial hydrostatic & oncotic pressures and the reflection coefficient is not possible. The clinician is limited to assessments based on plasma protein concentration (as index of capillary oncotic pressure) and values obtainable from use of a pulmonary artery catheter (eg wedge pressure as estimate of left atrial pressure & mean pulmonary venous pressure). A clinical examination and a chest xray are much more useful in assessing & monitoring pulmonary oedema.
For pulmonary oedema to occur, excess fluid must first accumulate in the interstitium (interstitial oedema), then must move into the alveoli (alveolar flooding). The lung is relatively resistant to the onset of pulmonary oedema and this is usually ascribed to several safety factors:
These safety mechanisms are quite effective especially in preventing pulmonary oedema associated with rises in capillary hydrostatic pressure. It has been estimated that the capillary hydrostatic pressure can rise to three times normal before alveolar flooding occurs. Surfactant assists in the prevention of alveolar flooding also.