He is what I know: First the endotoxin (Lipid A) activates the alternative pathway leading to the generation of C3a and C5a whick are anaphalatoxins. These stimulate the mast cells to releawse Histamine and other chemical mediators. Histamine increases the membrane permeability of the venules and vasodilates arterioles. vasodilation leads to: 1. decreased PVR/SVR (arteriole dilation) this would mean decreased BP and increased VR and resultant increased preload. this increased preload would lead to increased CO and SV. 2. vasodialtion of skin vessels lead to increased blood flow and warm skin. This is different than the other two shocks which exhibit cold skin.
Remember endotoxins damage endothelium directly leading to synthesis of prostacylin and Nitric oxide which are vasodilators too.
The other shocks cardiogenic and hypovolemic, all you need to do is recall the response to a decreased BP. decreased effective blood volume---> decreased BP, that's decreased baroreceptor streches--> incrseased sympathetic outflow and decreased PANS outflow. Sympathetic has three important actions: 1. at the heart (b1), 2. at the arterioles (a1) and 3. at the JGA in the kidney (b1) where you get renin release.
differentiating the shocks:
septic versus the other two(cardio and hypovolemic): in septic the patient has warm skin the other two cold skin.
Hypovolemic vs cardio: use the LVEDV/P. since in cardiogenic the heart failed(systolic dysfunction), you would expect an increase in LVEDV. that's you have so much volume in the LV that's not been ejected. in Hypovolemic shock the LVEDV is decreased b/c you had volume loss which lead to decreased preload.
don't forget the mixed venous oxygen content which is increased in spetic and decreased in the other two.
you can easly figure out what happens to CO in all three cases. gl.
Bottomline: if you know your ANS physio then this becomes much easier.
