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I appreciate that!

O2 and CO2 are small molecules and can diffuse across any membrane easily. CO2 is 20 times more diffusible so you see tissue hypoxia first. So O2 and CO2 will be carried back via venous blood. Note that lymphatic flow is very slow (~5ml/min from entire body). SO hypoxemia results mostly from decreased flow to the tissues rather than low filtration. Glucose is interesting as it does not crosses cell membrane easily and needs glucose transporters. but glucose can diffuse between the endothelial cells. This is the main way glucose enters tissue. There is some convective component to it which will depend on filtration rate but that seems to be not that important. check out this reference : Maeda, A., Himeno, Y., Ikebuchi, M. et al. Regulation of the glucose supply from capillary to tissue examined by developing a capillary model. J Physiol Sci 68, 355-367 (2018). In short, the oxygen/CO2/ glucose delivery is not hampered by low filtrate but will be hampered by low perfusion. Things that will be hampered will be transport of large molecules and immune cell migration.

@@gagankumarMDThank you!

You're welcome!

thanks for having a good eye... On the slide in the 9:36 to 9:56 time should all be SpO2 instead of SaO2.

@ 7:56 : 0.2ml of every 1L of oxygen is used by respiratory muscles under normal conditions. Its the green dot on the graph. This graph is taken from Nunn's respiratory physiology.

@@gagankumarMD thx…btw, your videos are amazing!

please watch my videos on creatinine.. once you understand how and why creatinine rises. you should be able to find what would really work in AKI....

certainly... I am going to finish these topics first and then go from there... if you want to read about it - this is the best material that is out there : heart-lung.org/

@@gagankumarMD thank you sir

i am glad that you could understand the complexities of multiple acid base issues going on in one patient. In pediatric intensivist world, you don't usually see such type of complex ABGs where patients have COPD and CHF together where patients are on diuretics. it becomes easy to misinterpret these as shown in the example. I hope there was an easier method but i could not find any. The first step in learning is to know that a problem exists and know what the limitations of interpretations are. If you do have a simpler method, please comment on your method so we all can learn.

certainly... if you could send me the references for the methods, I would certainly appreciate.

thank you for the comment. If you could point the errors, i would gladly correct them. Interpreting ABG in patients with chronic compensation is certainly a challenge. if you have a simpler method ..why not ?

you can simply take ratio of Intravascular : total ECF compartment for any person to give you a rough idea. e.g. if intravascular volume is 3L (you can not take the cellular compartment in intravascular compartment) and interstitium is 12L; about 3/(3+12) of amount given should remain intravascular. but things are more complicated than this as we will see in further lectures. once you understand these fluid movements you will figure out more novel ways to treat your patient.

i usually dont make a pdf. but you will find everything in this article : Metabolic Alkalosis Pathogenesis,Diagnosis, and Treatment: Core Curriculum 2022. Catherine Do, Pamela C. Vasquez, and Manoocher Soleiman. Am J Kidney Dis. 80(4):536-551. you can find links to other articles in the description.

So in a state where RAAS is activated, if you supply with NaHCO3 load, Na will be reabsorbded and potassium will lose more.

You are so welcome!

you are very intuitive. I agree with your assessment.

this would be a difficult question to answer as the literature is scarce with regard to your patient in question. Usually this level of sodium should not cause such a degree of symptoms. Likely dehydration and low volume status are confounding the symptoms. I would be a bit cautious in using 3%, however, if your rise in Na is within the range, it should be ok. note that 150cc of 3% will bring Na up by 1-2 points, so using some to increase Na by few points should not be cause of concern. you will certainly find docs on both side of spectrum - some will, some wont. No good evidence based answer for this one.

@@gagankumarMD Thank you for your response, do you think the patient will improve after fluid restriction 1L daily and increased salt intake for 2 weeks ?

Thanks and welcome

thanks . . .

I agree... i subscribe to them as well...I have gotten in touch with them.. hopefully they will reply.

Glad it was helpful!

Thank you.

you are right. In a true SIADH : ADH are inappropriately high so your urine concentration (osmolality) is high. SIADH is a euvolemic state. So RAAS doesnt gets stimulated so no Aldosterone. So normal Urine Sodium. in low stimulation of baroreceptor (true hypovolemia, CHF, cirrhosis etc.): ADH is actually appropriately high. So urine osmolality is high. And RAAS is stimulated as well. so low urine sodium. Note that urine osmolality depends on "addition" or "removal" of water, rather than the solutes !!!

Hi thank you for your replied! In CHF、Cirrhosis, ADH is appropriately high. But RAAS was also simultaneously activated. When ADH high urine osmarity will be elevated, I think so do urine sodium concentration. When RAAS activated，,due to reabsorption of sodiu, urine sodium concentration will be low. I am wondering just like this situation, is urine sodium concentration good for evaluating whether RAAS is being activated? Or aldosterone effect on lowering urine sodium concentration is just protent than ADH elevating urine osmolarity and sodium concentration ???

I hope i could put all the lectures in one long one lecture and don't have to self reference. but try to focus on references as well. They are the real Promo SM, I want to promote.

I am really sorry to hear that . . . this channel is not really for medical advice but for people in medical field to know underlying pathophysiology and use this knowledge to understand how to help them. If you are in medical field, i would suggest you go through the CHF and diuresis series and read the references. There is a good CHF guidelines by AHA which is freely available. I do suggest that you start with that.

Glad you like them!

its total osmoles in 150 cc of 3%. = 1027 x150/1000 ~ 154