Пікірлер

• 
  @gagankumarMD3 күн бұрын

  Slide @ 9:36 : There is typo. Please read SaO2 as SpO2.

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  @lien32125 күн бұрын

  I thought HbS shifts the OHDC to the right whilst HbF shifts the curve to the left thus will affect the SaO2 but not the SpO2.

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  @gagankumarMD3 күн бұрын

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

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  @lien32126 күн бұрын

  I’m lost, where does the 0.2ml/l come from? Where is this curve (oxygen consumption vs minute ventilation) from?

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  @gagankumarMD3 күн бұрын

  @ 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.

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  @lien32123 күн бұрын

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

• 
  @karldrago198213 күн бұрын

  Can you do a video on management of AKI

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  @gagankumarMD12 күн бұрын

  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....

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  @karldrago198213 күн бұрын

  Super sir

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  @934729741713 күн бұрын

  Sir kindly do a video on heart lung interactions and fluid responsiveness

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  @gagankumarMD12 күн бұрын

  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/

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  @934729741711 күн бұрын

  @@gagankumarMD thank you sir

• 
  @vbuche13 күн бұрын

  Made really complicated

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  @gagankumarMD12 күн бұрын

  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.

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  @vbuche14 күн бұрын

  ABG is not that complicated, we made it very simple. Interested??

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  @gagankumarMD13 күн бұрын

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

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  @vbuche14 күн бұрын

  Good well illustrated But you made it really complicated with lot of mistakes

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  @gagankumarMD13 күн бұрын

  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 ?

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  @My_Roblox_Life27 күн бұрын

  Very nice even though i didn’t watch it and just came here to comment this 😁

• 
  @HikketX2Ай бұрын

  Amazing video, the way you explained this made this so simple for me. Thank you!!

• 
  @nsas955Ай бұрын

  it is difficult especially the formula regarging increase of plasma by addin N/S.

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  @gagankumarMDАй бұрын

  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.

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  @karldrago1982Ай бұрын

  Very informative sir...u deserve a million views...keep making great contents

• 
  @jyothijo4131Ай бұрын

  Sir can you please upload the pdf of this lecture

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  @gagankumarMDАй бұрын

  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.

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  @gagankumarMD2 ай бұрын

  This is the situation: Before albumin infusion: @ of filtration = @ of lymphatic return. After albumin infusion : decrease @ of filtration but lymphatic return is still the same. So net influx into vascular compartment. But after sometime, lymphatic flow will slow down as well and again @ of filtration = @ of lymphatic return.

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  @gagankumarMD2 ай бұрын

  Life of WBC is 2-3 days after activation while RBC is about 120 days. So @ 4:35, you can see deformed RBC but all old WBC should be disintegrated. Any WBCs, if present are 'active' and suggest infection.

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  @kaze123ckr2 ай бұрын

  5:51 In here, you mentioned Na reaching DCT and proximal collecting duct stimulates RAAS, and subsequently causing hypokalemia. However, RAAS actually turned off if macula densa sensed larged sodium (increased GFR). The reason why RAAS was activated is that loss of Na in NaHCO3 would lead to intracascular depletion, and subsequently activate RAAS, and further causing potassium loss.

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  @kaze123ckr2 ай бұрын

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

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  @dipanjanchatterjee56212 ай бұрын

  Thank you so much for elaborating UAG so specifically and so nicely and so smoothly.

• 
  @gagankumarMD2 ай бұрын

  You are so welcome!

• 
  @HowardAndersonIII-ke2hz2 ай бұрын

  👍🏽👍🏽👍🏽

• 
  @NonstopNeuron2 ай бұрын

  Hi Ganga Kumar, It's Vipul from Nonstop Neuron. Thanks for your comment on my channel. I visited your website but could not find an email address to contact you.

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  @kaze123ckr2 ай бұрын

  6:29 If urine output increase giving the condition of same urine osmolarity, you should drink less water or else will worsened hyponatremia. My question is if a patient was in a state of high ADH (= high urine osmolarity） They should be less urine produced right？ （anti diuresis) So if urine amount increase, probably their urine osmolarity (ADH) was decreasing simultaneously. You start to pee out free water. Your serum sodium will rise. In this discussion, to maintain serum sodium constant. If urine output increase, you need to drink more water to maintain serum sodium constant.

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  @gagankumarMD2 ай бұрын

  you are very intuitive. I agree with your assessment.

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  @Dr_hamad2 ай бұрын

  If patient came to ER and suffering from vomiting , headache, dizziness , fatigue and unusual gait from three days . No medical history except taking antidepressants for two months. We found his sodium 122 and potassium 3.2 , shall we give him 3% hypertonic saline immediately?

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  @gagankumarMD2 ай бұрын

  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.

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  @Dr_hamad2 ай бұрын

  @@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 ?

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  @AhmedYousif-cr6fi2 ай бұрын

  Thank you for this wonderful lecture

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  @amidoc91882 ай бұрын

  Best channel I encountered! Love your work! Researched about you , got that you did audiology course after MS here in AIIMS, then switched to internal med! Such a demanding journey and giving back to the community for so many years! Pranam!

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  @gagankumarMD2 ай бұрын

  Thanks and welcome

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  @amidoc91882 ай бұрын

  Very good explanation! Not for nurses only, but medical students too! Very clear and concise!

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  @gagankumarMD2 ай бұрын

  thanks . . .

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  @josetrujillo7382 ай бұрын

  It would be awesome to see these concepts and explained in an animated type of presentation: similar to “nonstop neuron”

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  @gagankumarMD2 ай бұрын

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

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  @angelicamaedelacruz6163 ай бұрын

  Thank you so much for making this topic so chewable. This really made me understand the topic instead of memorizing the table of the difference in RTA type II vs Type I. 🎉

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  @gagankumarMD2 ай бұрын

  Glad it was helpful!

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  @mahmoudkareem15943 ай бұрын

  Great and most familiar explanation 🙏😘

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  @andreipopescu16903 ай бұрын

  Excellent review! Your work is much appreciated. All your lectures are very good!

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  @karldrago19823 ай бұрын

  Thank you sir...i have seen all of ur video🙏

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  @gagankumarMD3 ай бұрын

  Thank you.

• 
  @gagankumarMD3 ай бұрын

  This took me quite sometime to make. Hope you learn something new from it as I have.

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  @kaze123ckr3 ай бұрын

  I finally understand it !!!

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  @kaze123ckr3 ай бұрын

  9:45 Hey!thanks for your informative video I have a question on Since Urine sodium were assessed using concentration. Low ECV as a stimulus of both ADH and Aldosterone Aldosterone will decrease the urine sodium loss, and reflective as low urine sodium concentration Simultaneously, ADH effect will decrease free water loss, and increase the urine sodium concentration. So I think in some situations like in a true SIADH patient ADH are too high and the concurrent low ECV status and the activation of Aldosterone cannot be found or masked by High ADH if we using urine sodium concentration I don’t know if my thinking process is correct?

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  @gagankumarMD3 ай бұрын

  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 !!!

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  @kaze123ckr3 ай бұрын

  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 ???

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  @Lucas-en3jw3 ай бұрын

  'Promo SM'

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  @gagankumarMD3 ай бұрын

  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.

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  @karldrago19823 ай бұрын

  Super presentation sir

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  @karldrago19824 ай бұрын

  Good video sir…very informative

• 
  @navanirman14 ай бұрын

  ❤❤❤

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  @ajaytangoo31904 ай бұрын

  Sir my grandfather is diagnosing with RHF and he has too much fluid accumulation in his body...(like moderate ascities and pitting edema) Doc prescribed initial dose of lasix 40 mg morning and 20 mg evening IV along with spironolactone 25mg for 5 days and that time his urine output is normal...however it works earlier stage and his ascities improved Then again he got same situation again and doc suggested same dosage but it didn't work out, so he increase the dose 40 mg bd for 5 days but things dont work out .... He hasn't any improvements . And now doctor again increase the dose to 60 - 40 mg BD and still there's no significant changes.... What's the problem? Can you please assist me with this

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  @gagankumarMD4 ай бұрын

  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.

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  @gagankumarMD4 ай бұрын

  I have revised this version to make it more clear.

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  @user-jy4fs2yu6c5 ай бұрын

  great video! as usual. I am an M4 student interested in nephrocritical care. THESE ARE GREAT!

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  @gagankumarMD4 ай бұрын

  Glad you like them!

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  @5omethingsBetterThanNothing5 ай бұрын

  sir you are very helpful and very brght. thank you

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  @touseefbeig9155 ай бұрын

  . Thankyou for this sir.

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  @harishpawar68435 ай бұрын

  154 meq for 3% ns is wrong. It should be 514

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  @gagankumarMD5 ай бұрын

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

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  @anuraj426 ай бұрын

  I have two queries, for a patient in ACMV all the spontaneous respirations will be fully assisted by the ventilator, so is it important to set the RR high in a tachonoeic patient ? Second query is what happens to the I E ratio when the RR is increased or decreased ? Will it change or remain the same ?

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  @gagankumarMD6 ай бұрын

  This video is for the initial settings only. When you intubate your patients, most doctors will use paralytic. This is the time where you try to match the tachypnea. once the paralytic wears off, and patient is triggering the vent at higher rates than set rate, he will get TV at his respiratory rate. Watch - "how to optimize Flows & RR" to further adjust the RR in these patients. this video will answer your second question as well. kzread.info/dash/bejne/nYmlx66zadHVacY.html kzread.info/dash/bejne/fplpq8aGfdOtkag.html

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  @GebrehiwetGebregergs7 ай бұрын

  thanks for you lecture

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  @happyman76097 ай бұрын

  This is one of the best basic video I needed , thank you so much :)

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  @gagankumarMD7 ай бұрын

  thanks.. please watch the pulse oximetry for more details.... i have just outlined those in this lecture.

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  @Dr_hamad7 ай бұрын

  If patient serum sodium level 122 and potassium level 3 we gave him hypertonic saline in icu his sodium level to 138 in 2 days is that correct way ? Or considering as overcorrectin !?

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  @gagankumarMD7 ай бұрын

  usually reserve hypertonic saline for low sodiums. once you cross 120, fluid restriction may be sufficient. but to answer your question, it is not overcorrection if it slowly goes from 122 to 138. if it is 124 next daya nd 138 on second, it will be overcorrection.

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  @glksivakaran8 ай бұрын

  Thank you sir

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  @glksivakaran8 ай бұрын

  Thank so much sir from uk 🇬🇧

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  @sauravsah86268 ай бұрын

  Thank you very much sir...helped me understand a lot that why not to give 0.9 % NS in hyponatremia using normal calculations...and specially why it works sometimes..

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  @gagankumarMD8 ай бұрын

  You are most welcome