This topic is for some reason the subject of one frequently repeated question. Notable duplicates include the following:
- Question 6.4 from the first paper of 2013 (a detailed discussion is carried out here)
- Question 22.2 from the second paper of 2011
- Question 6.4 from the first paper of 2011
- Question 24 from the first paper of 2010
- Question 18 from the first paper of 2007
Mechanisms responsible for lactic acidosis in sepsis
- Endogenous catecholamine release and use of catecholamine inotropes
- Circulatory failure due to hypoxia and hypotension
- Microvascular shunting
- Inhibition of pyruvate dehydrogenase (PDH) by endotoxin
- Coexistent liver disease
- Slowed hepatic blood flow, impairing clearance
So the lactate in sepsis is raised. What of it?
The college seems to favour this concept as an exam topic. It has come up repeatedly in the past papers. It seems important for the trainees to understand that in septic shock the lactate elevation is not purely a feature of tissue hypoperfusion, but rather the outcome of complex metabolic changes.
The mechanism of lactate elevation in sepsis is discussed in greater detail in a chapter dedicated to these metabolic changes. Instead of revisiting that elaborate explanation, I will instead produce some references, and this confusing flowchart diagram:
There, now that's all clear.