aliases:
- septic shock
- 败血性休克
Prerequisite Knowledge
Coagulation mechanism 凝血机制笔记
Mechanism
The outer membrane of Gram-negative bacteria contains endotoxins, mostly large-volume lipopolysaccharides.
- Directly damages vascular endothelial cells, initiating the release of vasodilators such as NO.
- Activates the complement system, stimulating mast cells to release histamine, causing vasodilation.
- Activates the immune system, including macrophages and neutrophils, which release pro-inflammatory cytokines (tumor necrosis factor, interleukins, etc.), stimulating vascular endothelial cells to release more pro-inflammatory cytokines (platelet-activating factor, reactive oxygen species, etc.), damaging the endothelium, increasing vascular permeability, leading to vascular leakage.
- Endothelial cells release FⅢ (tissue factor), which enhances coagulation. Meanwhile, anticoagulant factors have already been heavily consumed (used up in the early stage of sepsis), resulting in an overall hypercoagulable state in the microcirculation, causing vascular occlusion and further reducing perfusion.
In summary, vascular resistance decreases, blood rushes through rapidly, and oxygen may be shunted back to the lungs before release, resulting in increased peripheral vascular blood flow, which does not cause coldness but may even cause heat (warm shock).
Vasodilation + increased vascular permeability + microcirculatory obstruction lead to reduced blood perfusion of vital organs (such as renal units).