Hemodynamic Alterations Following Miliary Pulmonary Embolization in Relation to the Pathogenesis of the Consequent Diffuse Edema

Abstract

In an effort to further elucidate the pathogenesis of the severe, diffuse lung edema attendant upon unilobar miliary pulmonary embolization with starch, serial recordings of several hemodynamic variables were made during the course of the procedure. Of the animals studied, some were embolized without prior medication while the remainder were pretreated with a variety of drugs, some of which depressed edema formation to varying degrees. A small group of the control preparations were injected into the right ventricle, giving rise to a disseminated, rather than to a localized, starch distribution (without edema formation). Of the pressures measured, only the left atrial pressure remained essentially unchanged during the entire course of the procedure, both in the control and the premedicated groups. This serves to effectively exclude left ventricular failure as the cause of the edema formation in our experiments. Both pulmonary arterial wedge and pulmonary venous pressures exhibited a modest rise after embolization, the peak values of which did not exceed even the lower values for plasma oncotic pressure. Similar increments were recorded in both control and pretreated groups, regardless of whether edema had or had not formed. In the light of these findings, it is unlikely that the capillary hydrostatic pressure alterations reflected by the pressure changes could be held primarily responsible for the edema, although they may possibly play an ancillary role in its initiation and/or perpetuation. If the edema formation is independent of the capillary hydrostatic pressure changes produced by the starch, other mechanisms must be considered, particularly a primary alteration of the permeability of the pulmonary capillaries. In the light of our previous deduction on the basis of other data to the effect that a neurogenic or neuro-humoral mechanism may be involved, it is concluded that the neurogenic or neuro-humoral mechanism may act to regulate capillary permeability.