Step II MV02 question

[MyNameIsAlex]

i understand why MVO2 is decreased in hypovolemic/hemorrhagic/etc shock

but why
is MVO2 normal in septic shock>??

 

[Doc176]

Well I'm not entirely sure but I probably read in Goljan that MVO2 is normal in septic shock secondary to arteriolar dilatation specially the ones in the muscles so most of the oxygen is being channeled rapidly to the veins so MVO2 is normal and that the tissues are not getting enough oxygen due the rapid flow

Please correct me someone if this is wrong

 

[turkeyjerky]

Well I'm not entirely sure but I probably read in Goljan that MVO2 is normal in septic shock secondary to arteriolar dilatation specially the ones in the muscles so most of the oxygen is being channeled rapidly to the veins so MVO2 is normal and that the tissues are not getting enough oxygen due the rapid flow

Please correct me someone if this is wrong

I'm not sure if goljan's really reliable on this one. With sepsis, the SVO2 can either be high or low ( or normal). There are two main issues in sepsis on this regard: 1. there is abnormal vasodilation in less metabollicaly active vascular beds, these function as sort of a AV shunt; 2. there is a cellular problem (likely at the mitochondrial level) in the use of O2 for energy production--this leads to cellular dysoxia in the presence of normal tissue oxygenation, this is likely the more important principle in the big picture.

So, in early sepsis, the SVO2 will be high and the patient will be warm. CO is high due to the vasodilation, but cells can't use the O2 available to them (thus the lactate rises). As an aside, the actual VO2 might be normal due to the O2 consuming effects of the respiratory burst.

In late sepsis, CO actually falls, the vessels clamp down and the SVO2 is low. This is bad.