Many of the patients in this series required vasopressor therapy during the course of septic shock. It could be argued that the hemodynamic and myocardial changes found are related in part to the use of vasopressors. There are no differences in the data and subsequent conclusions, however, in the mean initial hemodynamic findings, the right ventricular or left ventricular ejection fractions, or the right ventricular or left ventricular volumes if one analyzes only the subset of patients not receiving vasopressor therapy (n = 22). Therefore, the entire patient group studied is presented herein.
More of the nonsurvivors than the survivors required mechanical ventilation and positive end-expiratory pressure, especially on the final study. It would be expected that the effects of increased positive end- expiratory pressure would be to increase pulmonary artery pressures and thereby increase right ventricular end-diastolic volume and decrease right ventricular ejection fraction. Initially, however, the survivors tended to have a lower right ventricular ejection fraction than the nonsurvivors, and the nonsurvivors did not have a significant change in either right ventricular ejection fraction or end-diastolic volume index from initial to final studies. Thus, it is unlikely that the changes in mechanical ventilation account for the differences in right ventricular function between survivors and nonsurvivors.
The mechanism by which myocardial depression is produced in humans with septic shock has been the subject of intense investigation. Studies of coronary sinus blood flow have demonstrated that myocardial perfusion is not significantly compromised in patients with septic shock. The presence of a circulating humoral factor is believed by many to be the major cause of myocardial depression in septic shock. In vitro studies have provided convincing evidence that this is the case. In this model, a spontaneously beating rat heart cell culture was used as an in vitro assay of myocardial performance to evaluate patients’ serum samples for the presence of a circulating substance that depressed myocardial cell extent and velocity of shortening. Serum samples from patients in the acute phase of septic shock produced a significant decrease in the extent and velocity of myocardial cell contractility. Serum samples from control groups or from patients who had recovered from septic shock did not produce significant changes in extent or velocity of contraction. The degree of depression produced in vitro correlated with the depression of left ventricular ejection fraction found in vivo. The global, biventricular dysfunction seen in the group of patients with septic shock in this study is consistent with the theory that a circulating myocardial depressant substance affects the performance of both the right and left ventricles. kamagra soft tabs
Myocardial dysfunction in septic shock remains a common and important clinical problem. It is hoped that a better understanding of the effects of septic shock on the myocardium will lead to more effective treatment of patients with this highly lethal syndrome.