TRANSVASCULAR FLUID AND PROTEIN DYNAMICS IN THE LUNG FOLLOWING HEMORRHAGIC SHOCK

Abstract

Although many factors have been implicated in the development of the syndrome of post traumatic pulmonary insufficiency, the role of hemorrhagic shock remains in doubt [2]. Several groups have reported hemorrhagic and congestive changes in the lungs of dogs after treatment for hemorrhagic shock [3, 231, but the documentation of any functional pulmonary deterioration has been less impressive [3, 171. A universal finding in post traumatic respiratory insufficiency is an increase in pulmonary extra-vascular water which may appear as either interstitial and/or alveolar pulmonary edema [16]. The most frequently recognized cause of increased pulmonary extra-vascular water is an elevation of pulmonary microvascular pressure due to left ventricular failure. When pulmonary edema occurs in the absence of cardiac failure, it is usually ascribed to either an increase in permeability of the lung capillaries to fluid and protein [19] or to a severe decrease in plasma colloid pressure with altered microvascular driving forces in the Starling Equation of transcapillary exchange which has been shown to apply to the lung [ll]. Some studies have suggested that an increase in pulmonary capillary permeability occurs as a result of hemorrhagic shock [6, 141, while others have failed to observe any changes in the protein transport properties of the pulmonary capillary following a period of hemorrhagic shock [5,9].