Pulmonary oedema: a review.

Abstract

Pulmonary oedema results from derangement of a normal physiological process which is continuously producing and removing extravascular lung water according to principles stated by Starling’s equation of fluid flow across semipermeable membranes. The parameters in Starling’s equation cannot all be measured. However, experiments have suggested that increased pulmonary capillary hydrostatic pressure forces fluid extravascularly, diluting the colloid osmotic pressure of tissue fluids and increasing the hydrostatic pressure of lung tissue fluids. Once these reserves and the ability of pulmonary lymphatics to remove lung water are overcome, pulmonary oedema results. This oedema can also result from reduced colloid osmotic pressure in the pulmonary capillaries and increased capillary permeability, even at low pulmonary capillary hydrostatic pressure. Perhaps because of the reserve created by colloid osmotic pressure of tissue fluids, hydrostatic pressure of lung tissue fluids and lymphatic drainage, pulmonary oedema accumulates at a slow rate initially, and at a much more rapid rate in later stages of oedema development. The rate of oedema formation may also relate to damage to the lung created by interstitial oedema, which opens the barrier to a later stage of alveolar oedema. While lung compliance is reduced with each successive increase in oedema formation, increased shunting and hypoxaemia do not result until alveolar oedema is present, in normal lung. The diagnosis of pulmonary oedema is best made by searching for causes of oedema and by chest radiographs. The management of pulmonary oedema must begin with maintenance of oxygenation of blood. This can best be achieved by applying continuous positive pressure ventilation (CPPV). CPPV does not remove lung water (in fact it may slightly increase it), but it does improve oxygenation by ventilating alveoli that were previously filled with fluid. The improved oxygenation buys time, so that therapy directed at the cause of pulmonary oedema (Starling’s law) can be applied. Since current knowledge is inadequate we do not know how to reverse an increased capillary permeability, other than by removing its cause; or how to reduce tissue colloid osmotic pressure, or to increase the hydrostatic pressure of lung tissue fluids or the intracapillary colloid osmotic pressure or the lymphatic flow of fluid. This leaves only increasing intracapillary colloid osmotic pressure or decreasing pulmonary capillary hydrostatic pressure as the means available to reduce pulmonary oedema. In the face of a non-compliant left ventricle colloid infusions may be dangerous, as the attendant increase in blood volume may increase pulmonary capillary hydrostatic pressure and worsen pulmonary oedema. If increased capillary permeability is the cause of pulmonary oedema, colloids might leak extravascularly and draw fluid with them. Therefore the most important therapy in pulmonary oedema, regardless of cause, is to reduce pulmonary capillary hydrostatic pressure. Depending on the cause of pulmonary oedema and the associated cardiac output, pul monary capillary hydrostatic pressure may be decreased by reducing left ventricular preload, increasing myocardial contractility, reducing left ventricular after-load or some combination of these. The anaesthetic implications are that Starling reserves are large and pulmonary oedema should not occur in the normal patient. In the patient with pulmonary oedema or reduced cardio-pulmonary reserve preoperatively, every effort must be made to optimize Starling’s forces before undertaking an anaesthetic in these life threatening situations.