Also, another area which I remember discussing once with my professors was the - the Pathophysiology of rising lactate in sepsis. Apparently Elevated lactate in septic shock is not due to anaerobic metabolism, but rather due to due to endogenous epinephrine stimulating beta-2 receptors in the lungs. This can be read further read in Dr Paul Mariks works( the creator of Marik Protocol). Would love to hear your take on it, and perhaps a video in the future as well? Thank you for your time
Sepsis patients are often haemodynamically unstable, lactate production can increase as a result of inadequate DO2 from hypoperfusion. Other mechanisms for hyperlactataemia in sepsis include increased pyruvate production, release of lactate from lung parenchyma, decreased pyruvate dehydrogenase activity and decreased clearance of lactate.
Very informative lecture Sir. Thank for taking your time to teach budding doctors. I have a few points/doubts though - CRT is noted to be rather invaluable in adults. For one, the upper limit ranges from 2s in children to around 4.5s in elderly with the 3s for an average adult excluding other factors like temperature of the ED.
Also, at 15:00 you have mentioned that if you give a dextrose containing fluid, all of it will move to the extravascular compartment which isn't in line with my understanding - 5% dextrose contains 100% free water and following infusion will be distributed throughout the TBW; that is, two-thirds will pass into the intracellular compartment and one-third will be confined to the extracellular compartment; of the extracellular fluid one-third will remain intravascular, and the remaining two-thirds will be interstitial. So, Sir, what are your thoughts on this?
