In late sepsis, what typically happens to systemic vascular resistance (SVR)?

In late sepsis, systemic vascular resistance (SVR) typically decreases due to the physiological responses to infection and inflammation. Sepsis leads to a significant release of mediators such as cytokines, which cause widespread vasodilation. This vasodilatory response results in decreased resistance in the vascular system as blood vessels relax and widen, allowing for increased blood flow.

The decrease in SVR is a hallmark of septic shock, where even in the presence of low blood pressure, the vascular system becomes less resistant to blood flow, contributing to the overall management challenges in critically ill patients.

In contrast to this, the other scenarios where one might observe an increase, stability, or fluctuation in SVR are not characteristic of late sepsis; they tend to describe different physiological states or responses to other forms of shock or medical conditions. These responses ultimately fail to capture the distinct pathophysiological processes occurring during sepsis.