[Pulmonary and hemodynamic changes in endotoxic shock]

With help of an endotoxin-infusion-model an endotoxic shock was induced. It was possible with the demonstrated parameters to display in different ways the pulmonary and hemodynamic changes. The pathophysiology of the pulmonary hemodynamic was characterized by a marked rise in the difference of the alveolar-arterial oxygen partial pressure, of the pulmonary resistance and of the intrapulmonary right to left shunt immediately at the beginning of the experiment. The influence on the hemodynamic changes of the systemic circulation was manifested at a later time and was characterized by a hypodynamic change in the circulation. Essential pathognomonic signs were, besides the reduction in cardiac output and the increase in total peripheral resistance a continuous decrease in colloid osmotic pressure. Measurement of PaO2 and PaCO2 plays an important role in the overall clinical diagnosis of septic shock. In this experiment this reduction reflects however much less the true measure of the disturbed respiratory-hemodynamic function than the above mentioned findings and the metabolic changes. Here the lactate level of blood is a more meaningful indicator of disturbed cell function. The hemodynamic, hematological and x-ray findings are confirmed by light- and electron microscope findings. Here a characteristic train of events can be demonstrated some of which were typified by capillary endothelial damage, fluid- and cell permeation into the interstitium, intravascular thrombosis and the consequences of cell hypoxia. The differential consideration of the results of the experiment gives an early indication of the further trend as regards those animals which died early and those which survived. Only by early diagnosis with corresponding therapy can the prognosis of endotoxic shock be improved.