Maybe you won't read this op but you are a great help to me and I'm grateful for your existence , I'm a first year resident in the er and I wait for each video of yours Please never stop uploading
I truly do read every comment and try to respond to most! I am really happy to hear this from you and glad to know that I have been able to help in some way. Wishing you all the best in your residency and beyond. I will certainly keep them coming! :)
OPC poisoning is very common here in rural area of Bangladesh. I have seen and also managed many many cases with Atropine. As you stated from minimal to very high dosages is used.
@@ICUAdvantage This potentially could go into your next medication 2PAM for the Organophosphate poisoning. As a Paramedic / Haz-Medic we utilize atropine in the field , but getting them to your hospital to get to 2PAM on board will help reduce the amount of atropine that the ICU would have to give. As the organophosphate breaks down the acetylcholinesterase. Fun fact it could take the body one month to produce acetylcholinesterase if you don’t get the 2PAM administer in time.
Wow, thank you so much for the support and the kind words! I do appreciate you spreading the word and it will be interesting to see where things continue to grow to in the future!
Thanks Eddie so much, please continue on this serie of "critical care medications", really liked you've mentioned the organophosphate poisoning, we have it here commonly in my country "Sudan" Best Regards!
Thanks for sharing Ahmed! Interesting to hear about organophosphate poisoning! I've had a few people chime in that in their area they DO see it, so I'm glad I decided to include it in the video. Glad you liked the video and def plan to keep up the series!
Glad you liked it! And how interesting! I figured, given this audience that people had probably seen this, but I certainly never have. The closest was my chemical weapons training in the Army! haha
You misspelled hypocalcemia when referencing potential adverse effects, did you mean to say hypokalemia? Not trying to nitpick, I promise. I LOVE your videos, they’re getting me through paramedic school! I write down what you say and use them as notes for studying, that’s the only reason I am asking for clarification. Thank you for all of your videos!
I came here mainly because I'm studying for ACLS recertification and I didn't understand why we aren't supposed to give Atropin for symptomatic bradycardia caused by 2°degree Type 2 and complete heart block. But I think I understand it now. It's not harmful to give but it's basically not effective because the conduction doesn't even go past the AV node, hence is not being affected by Atropin. I hope I understood this correctly? Thank you for a great explanation of Atropin.
Awesome, thanks David! So funny, because someone just left a comment saying it was "stupid" haha. I appreciate the feedback! I personally really like it.
The AHA ACLS bradycardia algorithm lists an individual dose of Atropine as 0.5 mg, although I’ve only ever seen 1 mg syringes in code carts. Any insight on this?
2020 AHA updated recommendation to 1mg. It used to be 0.5 ever since I knew it until then. cpr.heart.org/-/media/cpr-files/cpr-guidelines-files/algorithms/algorithmacls_bradycardia_200612.pdf
Correct me if I'm wrong. Was this the med that you need to flush immediately after administering because if it didn't reach the heart within 15sec it will not have an effect? I can't remember if I've watched it here but it did stick on my mind when I knew about that.TIA
Any thoughts or comments on atropine and norepi induced bradycardia? Also, I was always taught a slow push of atropine can cause reflex bradycardia. Is that true?
Low dose atropine can cause bradycardia but these vagal effects are far outweighed with larger doses, hence why you shouldn't slow push. I hadn't heard of it for norepinephrine though.
Sympathetic over-stimulation would be ↑epi/norepi rather than ACh (which is more *para*sympathetic). If you're in sympathetic over-stimulation, you want to activate the parasympathetic system to counter act this; ego, ↑ACh ↓AChase
@@marinal2705 Mechanisms of Myofascial Pain M. Saleet Jafri www.ncbi.nlm.nih.gov/pmc/articles/PMC4285362/ Psychological stress results in an increase of certain hormones and increase of sympathetic neural stimulation. It is believed that the increase in hormones and sympathetic stimulation during this condition leads to increase in release of acetylcholine at the neuromuscular junction contributing to the contraction of the motor units involved in a trigger point [53]. This and other mechanisms that initiate a myofascial trigger point must feed into the mechanisms for their persistence described in the next section The persistence of myofascial trigger points requires a self-sustaining positive feed-forward process. Simons presented the integrated hypothesis for myofascial trigger points to offer an explanation The persistence of myofascial trigger points requires a self-sustaining positive feed-forward process. Simons presented the integrated hypothesis for myofascial trigger points to offer an explanation [4]. The integrated hypothesis is a six-link chain that starts with step (1): the abnormal release of acetylcholine. This triggers step (2): increased muscle fiber tension which is seen as the taut band found in a myofascial trigger point. The taut band is thought to constrict blood flow that leads to step (3): local hypoxia. The reduced oxygen disrupts mitochondrial energy metabolism reducing ATP and leads to step (4): tissue distress and step (5): the release of sensitizing substances. These sensitizing substances lead to pain by activation of nociceptors (pain receptors) and also lead to step (6): autonomic modulation that then potentiates step (1): abnormal acetylcholine release. More recently this hypothesis has been expanded by Gerwin and coworkers [53]. It suggests more specific details of the feedback loop. For example, sympathetic nervous system activity augments acetylcholine release as well as the local hypoperfusion caused by the muscle contraction. The resulting ischemia/hypoxia leads to acidification (decreased pH). Experiments have shown that injections of acidic saline of pH 4 can cause muscle pain through activation of muscle pain receptors called acid-sensing ion channels (ASIC3) [54, 55]. While this low pH is much lower than that seen during ischemia, a smaller physiological decrease in pH has been shown to activate ASIC3 channels [56]. The prolonged ischemia/hypoxia also leads to muscle injury resulting in the release of potassium, bradykinins, cytokines, ATP, and substance P which might stimulate nociceptors in the muscle [53, 57]. The end result is the tenderness and pain observed with myofascial trigger points accompanied by calcitonin gene-related peptide (CGRP). Depolarization of nociceptive neurons causes the release of CGRP [58]. CGRP inhibits acetylcholine esterase and upregulates the amount of acetylcholine receptors and release of acetylcholine. This nonquantal spontaneous acetylcholine release at the motor end plate as a result of CGRP is termed as acetylcholine leakage [59]. This differs from the other modes of acetylcholine release such as simulation induced multiquantal release resulting in an end plate potential (EPP) and spontaneous quantal releases resulting in a miniature end plate potential (MEPP) [59]. The theory also postulates CGRP release from nerve terminals with the same targets. Furthermore, a decrease in pH can also cause an increase in acetylcholine release [60]. The result is increased acetylcholine in the nerve terminal, synaptic cleft, and increased motor endplate potentials resulting in more contraction [61, 62]. The model also suggests that psychological stress also increases acetylcholine release into the neuromuscular junction.
Hello This might seems out to topic question. May I know what is the software you use to write these notes we see on screen? Would you kindly tell me the name please? Thank you so much!
So I just use Qucktime to record my screen and then write on a blank Adobe Photoshop project. I screencast to an iPad with Astropad Audio and then use the Apple Pencil to do the writing. Blue Yeti microphone to record the audio.
@@ICUAdvantage Just trying to satisfy the algorithm. I really appreciate the work you've done with these videos. I'd love to see you produce one for "Bedside Intubation" - when it happens, why, and moreover the equipment that an RN should be expected to procure from an airway cart. I think this would be extremely helpful for newer ICU nurses as it is something that happens with regularity in this milieu.
![BRASIL vs. URUGUAY [1-1] | RESUMEN | ELIMINATORIAS SUDAMERICANAS | FECHA 12](http://i.ytimg.com/vi/-hWBAuxF1eY/mqdefault.jpg)
Maybe you won't read this op but you are a great help to me and I'm grateful for your existence , I'm a first year resident in the er and I wait for each video of yours
Please never stop uploading
I truly do read every comment and try to respond to most! I am really happy to hear this from you and glad to know that I have been able to help in some way. Wishing you all the best in your residency and beyond. I will certainly keep them coming! :)
OPC poisoning is very common here in rural area of Bangladesh. I have seen and also managed many many cases with Atropine. As you stated from minimal to very high dosages is used.
Thank you for sharing! I wondered how prevalent it would be in some rural communities.
@@ICUAdvantage This potentially could go into your next medication 2PAM for the Organophosphate poisoning. As a Paramedic / Haz-Medic we utilize atropine in the field , but getting them to your hospital to get to 2PAM on board will help reduce the amount of atropine that the ICU would have to give. As the organophosphate breaks down the acetylcholinesterase. Fun fact it could take the body one month to produce acetylcholinesterase if you don’t get the 2PAM administer in time.
Starting a CVICU rotation as a 4th year medical student next week so this series has been huge for me. Thanks so much for your work!
Just finished my critical care flex in nursing school... I can't describe how valuable your videos are.
This is so great to hear Juan! Happy to have been able to help!
Genuinely my favorite youtuber. You will reach 1million subscribers in no time. Have been telling everyone about you
Wow, thank you so much for the support and the kind words! I do appreciate you spreading the word and it will be interesting to see where things continue to grow to in the future!
Continue this series more
I am certainly planning to keep this going each week for a while!
More videos like this please! Very helpful as a deeper dive on ACLS medications and others used in critical care
Awesome to hear this feedback Alex. I will certainly keep this series going for a while each week!
Thanks Eddie so much, please continue on this serie of "critical care medications", really liked you've mentioned the organophosphate poisoning, we have it here commonly in my country "Sudan"
Best Regards!
Thanks for sharing Ahmed! Interesting to hear about organophosphate poisoning! I've had a few people chime in that in their area they DO see it, so I'm glad I decided to include it in the video. Glad you liked the video and def plan to keep up the series!
Love your explanation! Clear and concise. Thank you!! I've seen a few organophosphate poisonings as a mode of suicide.
Glad you liked it! And how interesting! I figured, given this audience that people had probably seen this, but I certainly never have. The closest was my chemical weapons training in the Army! haha
@7:00 I’m so happy you said it! Paramedics around the country are stoked about it lmao.
Woohoo!
You misspelled hypocalcemia when referencing potential adverse effects, did you mean to say hypokalemia? Not trying to nitpick, I promise. I LOVE your videos, they’re getting me through paramedic school! I write down what you say and use them as notes for studying, that’s the only reason I am asking for clarification. Thank you for all of your videos!
Thank you for this refresher. I really do enjoy your videos! So keep them coming!!
Great to hear Marqell. I will certainly keep making them!
Thank you so much! It’s very simplified and easy to understand. ✔️👍
Truly my pleasure. Glad you liked it!
Great content as always! I have seen many organophosphate poisonings here in Sri Lanka, accidental and suicidal!
Interesting! Glad you enjoyed it.
I came here mainly because I'm studying for ACLS recertification and I didn't understand why we aren't supposed to give Atropin for symptomatic bradycardia caused by 2°degree Type 2 and complete heart block. But I think I understand it now. It's not harmful to give but it's basically not effective because the conduction doesn't even go past the AV node, hence is not being affected by Atropin. I hope I understood this correctly? Thank you for a great explanation of Atropin.
Exactly! Not harmful, just completely useless. I've still seen it ordered to be given "just in case" but truly pointless.
@@ICUAdvantage Thank you so much!! And in the meantime I passed the ACLS. 👍🙂
@@yasmine4754 YAY! Congrats!!
@@ICUAdvantage Haha, thanks to your videos! 😂
This is awesome, thank you!!
Happy to hear this!!
Love & respect from India.
Very cool! Thank you!
I Love your videos man! helping me out with paramedics!!!
Thank you soo much Sir , Grateful for This Videos 🤗🥰
Truly happy to be able to help!
Thank you ❤🎉
Great greater and greatest , lectures on icu advantage 🙏. Keep it up
Really glad you liked it!
Brilliantly explained
Glad you liked it!
You are awesome Eddie! Thanks!😀
Wow thank you Becky!!
very helpful for step 1!
Thanks a lot !❤
If wish plz u could make all the emergency drug videos
I do have plans to dedicate a whole video to just those at some point in the future.
Great work 👏👍
Thank you so much 😀
Excellent video!
Thank you teacher
Great content
Thank you thank you!!!
You are very welcome Renee!
Really helpful 💞 Thank you so much!
Very useful and practical thanks
Happy to hear this!
We carry kits with atropine on the ambulance for crew use in case we are exposed
I am about to be assigned in the SDU/CCU and I really find your videos useful! I'm binge-watching all of it now :) Thank you!
Great music in the beginning 👌
Awesome, thanks David! So funny, because someone just left a comment saying it was "stupid" haha. I appreciate the feedback! I personally really like it.
Perfect thank you
I take Lomotil aka diphenoxylate/atropine to help with crohns symptoms. Why does this drug contain atropine? What is the purpose?
Very informative.
Glad to hear it!
Thank You 🙌🙌🔥🔥📺
You're welcome!
Well explained. Thanks.
Glad it was helpful!
Thank you!
Welcome!
Great info as always
I appreciate that!
Thanks
Welcome
Thanks you so informative
Glad it was helpful!
Can you please tell me what software you use to make these videos 📹
Nice information
Thanks! Hope to keep this med series going for a while each week.
more meds pls!!
Yes, I do have more planned
The AHA ACLS bradycardia algorithm lists an individual dose of Atropine as 0.5 mg, although I’ve only ever seen 1 mg syringes in code carts. Any insight on this?
2020 AHA updated recommendation to 1mg. It used to be 0.5 ever since I knew it until then.
cpr.heart.org/-/media/cpr-files/cpr-guidelines-files/algorithms/algorithmacls_bradycardia_200612.pdf
2020 guidelines changed to 1mg instead of 0.5mg ... our favourite youtuber is updated already.
Thank you so much for your all videos.Can you do one on nitroglycerin?
Great suggestion! I'll add it to the todo list!
Thank you very much sir
Very informative as usual ... :*
And thank you as always!
One day we used atropin as an infusion for a patient who got poisoned with a chemical liquid
Correct me if I'm wrong. Was this the med that you need to flush immediately after administering because if it didn't reach the heart within 15sec it will not have an effect? I can't remember if I've watched it here but it did stick on my mind when I knew about that.TIA
You are thinking of adenosine
@@ICUAdvantage thank you! I dunno why atropine stuck on my mind. Maybe because they both start at letter A.haha
@@synergistex7088 I figured that's what happened!
Any thoughts or comments on atropine and norepi induced bradycardia? Also, I was always taught a slow push of atropine can cause reflex bradycardia. Is that true?
Low dose atropine can cause bradycardia but these vagal effects are far outweighed with larger doses, hence why you shouldn't slow push. I hadn't heard of it for norepinephrine though.
If someone is in sympathetic over stimulation and too much acetylcholine wouldnt they want LESS acetylcholine and more acetylcholinesterase?
Sympathetic over-stimulation would be ↑epi/norepi rather than ACh (which is more *para*sympathetic). If you're in sympathetic over-stimulation, you want to activate the parasympathetic system to counter act this; ego, ↑ACh ↓AChase
@@marinal2705
Mechanisms of Myofascial Pain
M. Saleet Jafri
www.ncbi.nlm.nih.gov/pmc/articles/PMC4285362/
Psychological stress results in an increase of certain hormones and increase of sympathetic neural stimulation. It is believed that the increase in hormones and sympathetic stimulation during this condition leads to increase in release of acetylcholine at the neuromuscular junction contributing to the contraction of the motor units involved in a trigger point [53]. This and other mechanisms that initiate a myofascial trigger point must feed into the mechanisms for their persistence described in the next section
The persistence of myofascial trigger points requires a self-sustaining positive feed-forward process. Simons presented the integrated hypothesis for myofascial trigger points to offer an explanation
The persistence of myofascial trigger points requires a self-sustaining positive feed-forward process. Simons presented the integrated hypothesis for myofascial trigger points to offer an explanation [4]. The integrated hypothesis is a six-link chain that starts with step (1): the abnormal release of acetylcholine. This triggers step (2): increased muscle fiber tension which is seen as the taut band found in a myofascial trigger point. The taut band is thought to constrict blood flow that leads to step (3): local hypoxia. The reduced oxygen disrupts mitochondrial energy metabolism reducing ATP and leads to step (4): tissue distress and step (5): the release of sensitizing substances. These sensitizing substances lead to pain by activation of nociceptors (pain receptors) and also lead to step (6): autonomic modulation that then potentiates step (1): abnormal acetylcholine release.
More recently this hypothesis has been expanded by Gerwin and coworkers [53]. It suggests more specific details of the feedback loop. For example, sympathetic nervous system activity augments acetylcholine release as well as the local hypoperfusion caused by the muscle contraction. The resulting ischemia/hypoxia leads to acidification (decreased pH). Experiments have shown that injections of acidic saline of pH 4 can cause muscle pain through activation of muscle pain receptors called acid-sensing ion channels (ASIC3) [54, 55]. While this low pH is much lower than that seen during ischemia, a smaller physiological decrease in pH has been shown to activate ASIC3 channels [56]. The prolonged ischemia/hypoxia also leads to muscle injury resulting in the release of potassium, bradykinins, cytokines, ATP, and substance P which might stimulate nociceptors in the muscle [53, 57]. The end result is the tenderness and pain observed with myofascial trigger points accompanied by calcitonin gene-related peptide (CGRP). Depolarization of nociceptive neurons causes the release of CGRP [58]. CGRP inhibits acetylcholine esterase and upregulates the amount of acetylcholine receptors and release of acetylcholine. This nonquantal spontaneous acetylcholine release at the motor end plate as a result of CGRP is termed as acetylcholine leakage [59]. This differs from the other modes of acetylcholine release such as simulation induced multiquantal release resulting in an end plate potential (EPP) and spontaneous quantal releases resulting in a miniature end plate potential (MEPP) [59]. The theory also postulates CGRP release from nerve terminals with the same targets. Furthermore, a decrease in pH can also cause an increase in acetylcholine release [60]. The result is increased acetylcholine in the nerve terminal, synaptic cleft, and increased motor endplate potentials resulting in more contraction [61, 62]. The model also suggests that psychological stress also increases acetylcholine release into the neuromuscular junction.
Hello
This might seems out to topic question. May I know what is the software you use to write these notes we see on screen? Would you kindly tell me the name please? Thank you so much!
So I just use Qucktime to record my screen and then write on a blank Adobe Photoshop project. I screencast to an iPad with Astropad Audio and then use the Apple Pencil to do the writing. Blue Yeti microphone to record the audio.
❤❤❤
do a video about swan catheters?
Yes, I do have that one on the todo list!
Can you bolus Atropine 600mcg in 1ml IV or does it need to be diluted?
I'm not sure. I've only ever administered it in the 1mg/10ml syringe
What secretions do you mean that the parasympathetic increases?
And why do we need to block them with Atropine if the problem is an ACLS algorithm problem?
Oral and respiratory secretions.
The blocking of secretions is related to the use for paralytic reversal and not for ACLS. 2 different uses.
Piosion patient uses of atropine duration of treatment, patient mentility loss and chenge behaviour why are
comment
Thanks
@@ICUAdvantage Just trying to satisfy the algorithm. I really appreciate the work you've done with these videos. I'd love to see you produce one for "Bedside Intubation" - when it happens, why, and moreover the equipment that an RN should be expected to procure from an airway cart. I think this would be extremely helpful for newer ICU nurses as it is something that happens with regularity in this milieu.
Well explained. Thank you
Thank you so much!