Not all raised lactate is sepsis or hypoperfusion! Watch this video to learn about the Lactate Map and a killer acronym to help you avoid missing the important causes of elevated lactate
This information here should be provided to everyone who works in acute medicine. Thank you very much for your efforts. As an ICU expert, i understand the importance of this information.
Monitoring of Co-factor thiamine is helpful for patients before infusion of pharmaceutical lactate Crystalloidals giving negative feedback inhibition hyperventilation.
Thank you so much sir, I came to learn more about raise lactate after learning about a patient that was given fluid due to raise lactate, and subsequently went into fluid overload. Your explanation has made life easy. Thank you
Doctors killed my mom in the ICU ,she most likely had thiamine deficiency that caused most her problems from all the diabetic drugs causes B1 deficiency and eventually heart failure, enlarged heart etc.....doctors overload her with IV 10 different drugs: dopamine, potassium, magnesium, etc.....AND ONLY 100mg of thiamine 3 times a day. In the studies I've read it say must be doses of 1500mg a day or higher to have benefits in 4 days pacient can be discharged from hospital,also it mentioned Vitamin C as well together with thiamine IT WILL STOP THE PROGRESSION OF SEPSIS!!!!!! for all the doctors out there, if you have to break the rules of the hospitals protocol of treatments to save people's lives THEN YOU MUST DO IT!!! MY mon died because the lack of knowledge of those doctors out there.MOST OF THEM DONT READ RESEARCH and every day kill people because don't want to break rules of hospitals base treatment THAT DOESN'T WORK FOR MOST PEOPLE AND SOME DRIE BECAUSE OF THIS. IF THE BODY IS SICK THE OBVIOUS IS LACK OF CERTAIN NUTRIENTS.
From non science background you made me understand it so beautifully. It will be great if some one can tell me how can we have enough oxygen for pyruvate to go towards PDH than Acetyl CoA. I see extreme high lactate in my OAT report
Important to note that in inborn errors of metabolism, the treatment is often glucose infusion.. this causes elevated lactate, and in this case it is just the response to treatment.
Dear Dr. Read, Thanks for this excellent video. Can you make any recommendations on further key papers/reviews on lactate metabolism in ICU patients - as a supplement to your video. Thank you.
1. Marik PE, Bellomo R. Lactate clearance as a target of therapy in sepsis: A flawed paradigm. OA Critical Care. 2013;1(1). 2. Jansen TC, van Bommel J, Bakker J. Blood lactate monitoring in critically ill patients: A systematic health technology assessment*. Critical Care Medicine. 2009 Oct;37(10):2827-39.
Great video thank you. How long can the elevated lactate go on for if it was due to salbutamol please? If the salbutamol use has stopped. Could it last months (tingling in fingers on outbreath for example)?
So basically you f you don’t eat sugar before or after a workout you won’t have a response from pyruvate? No pain? I think this is true because when I eat keto and workout no pain. But it’s f I eat a carbohydrate rich meal after. Workout there is pain.
My son 3.5months old he have Lactate plasma issue 10.7 . Now he is not able to speak🗣 and he is not identifying if say anything he is not able to understand. My docter said it is genetic problem come from mother she said it is not curable. Please suggest it is curable? What steps we need to take to improve my baby
mrmeach1967 check this out! “Magnesium plays an important role in oxidative metabolism. The conversion of thiamine to its active triphosphate form is reliant on magnesium as a cofactor.9-11 Thiamine pyrophosphate, in conjunction with pyruvate dehydrogenase, is critical in the metabolism of pyruvate to acetyl coenzyme A for entrance into the citric acid cycle.12 In the absence of magnesium, disrupted oxidative phosphorylation shifts toward anaerobic metabolism, resulting in lactic acid production.” www.ncbi.nlm.nih.gov/pmc/articles/PMC4909152/
Things have moved on since the pyruvate goes to Acetyl CoA under aerobic circumstances and to lactate in anaerobic conditions hypothesis. There is no oxygen demand for either pathway and no way for oxygen to switch metabolism from one to the other. All pyruvate is now thought to be converted to lactate in the cytosol. This shuttles between cells as needed for energy transfer (see lactate shuttle theory). Lactate that enters the mitochondrial intramembrane space is converted back to pyruvate and then on to Acetyl CoA. Elevated lactate does not signify ischaemia or hypoxia, it signifies a "stressed" metabolism with glycolytic production of lactate exceeding intracellular clearance. If lactate somehow was linked to hypoxia then it would rise under hypoxic conditions and conversely one would find hypoxia where there is high lactate. The former is not seen in Everest submitters who had normal lactates despite SpO2 of as low as 30% and the latter is not seen intracellularly in volunteer athlete's thigh muscles after exercise to failure.
