Thread by @Thind888

1/ ncbi.nlm.nih.gov/pubmed/30985210

Thought provoking study. The oversimplistic view of sepsis we're taught is that it's a vasodilatory state with high cardiac output and high ScVO2.

Sure enough, ScVO2 was >70 in 65% of the cases in this study with likely optimal cardiac output.

2/ Interestingly, lactate levels were highest at extremes of ScVO2.
Question. Why is there tissue hypoxia inspite of high ScVO2?
Answer - microcirculatory dysfunction (especially shunting) +/- mitochondrial dysfunction. The authors describe this as 'oxygen use impairment'.

3/ Macrocirculatory optimization (fluids, inotropes) will have little benefit, if at all, in this situation. E.g. Consider a patient with lactate = 10, cardiac index = 4.2, and ScVO2 = 92. Obvious microcirculatory dysfunction here; fluids won't help. *cough* ?vitamin C?* *cough*

4/ 35% of the patients had ScVO2 < 65%. These patients have 'macrocirculatory oxygen transport defect'. But isn't this is contrary to traditional teaching?
Q. What explains low ScVO2 (and likely inadequate cardiac output) in sepsis.
Answer - Multiple potential reasons -

5a/ (i) Inadequate venous return - from (a) venous pooling from venodilation: vasopressors may help, or (b) true intravascular volume depletion due to capillary leak: volume needed.
(ii) Dynamic LV outflow obstruction - DLVOTO from SAM or dynamic IVO from severe LV underfilling.

5b/ (PMID: 26082197). These patients typically have severe impairment of venous return. Rx: fluids, beta-blockers, avoid inotropes.
(iii) Severe septic cardiomyopathy with adequate MCFP but severely impaired inotropy. This is rare. Rx - inotropes and ensure preload optimization.

6/ Bottomline - Sepsis is a heterogenous condition with multiple phenotypes. Hyperlactatemia does not equal fluid therapy. Pay attention to ScVO2. #POCUS can help in defining the macrocirculatory state. There is a dire need of robust therapies that improve the microcirculation.