Great video Failing to compensate for a metabolic acidosis=implies hypercapnic failure, often occurring with a normal (or occasionally low) Pco2 (important not to miss) This mean Mixed Acidosis . In case of DKA patient, If this patient demonstrates increased WOB, intubation should be considered for impending hypercapnic respiratory failure. If the patient does not demonstrate increased WOB it implies the patient has blunted ventilation Regarding end tidal co2 monitoring it is frequent used in OT in non critical patient
Love from India.. Our Facilities lack EtCo2 too sir 😢.. Thanks you soo much sir,, I am watching all our videos everyday and taking notes... Thank you soo much.
hi coach, i am attending the first year of spec in Respiratory school (Italy). Im really curious about the utilization of end tidal CO2 and its uses in clinical setting. Thx a lot you made the topic clear
Great great, please I have a question,, I watched the video of Etco2 and you mentioned if there is low CO, so not blood back so less Co2 and decreased Etco2!! Now you are mentioning that cardiac arrest so anaerobe so lactate, so Co2 get high, how come!!? High Co2 so I mean if it's the scenario how this would affect our reading of Etco2!!?
I’ve asked respiratory therapists and other nurses that question several times before and most of the time the respiratory therapist will look at me like they don’t know what I’m talking about. I am a nurse and I spend more time at the bedside and if they can explain to me what the gradient is, I know what EtCO2 to shoot for and I don’t need RT there all night. They’re also busy people. Sometimes they are not even able to tell me what the endtidal was at the time of the art stick, which is disappointmenting to me because then I can’t even calculate my own gradient.
@@RespiratoryCoach I completely agree. Unfortunately it’s not only on respiratory therapist and nursing issue, it’s a human issue and a problem in medicine in all fields including with MDs.
But is it used, effectively? I'm familiar with places that utilize ETCO2 on every vent, but the gradient is not monitored and/or used to manage vent settings. What do you see in your area?
Very empressive lecture, it sounds like you think the PO2 is not that important in metabolic acidosis. However, metabolic acidosis caused by hypoxemia is NOT mainly due to hyperlactacidemia, as we all know that the pH is hydrogen ion level determined, when our body can not get enough oxygen, the hydrogen ions will have nothing to combine, therefore, it will build up in blood leading to metabolic acidosis. When this happens, the best way to improve the acidotic status of patients is to improve their oxygenation. In the development of metabolic acidosis, PO2 does matter.
Hey Doc! I truly appreciate this interaction. I think my minimizing of PaO2 is best described as poorly communicated, despite those words leaving my mouth verbatim. I did state at 2:34, "of course we know that oxygen plays a role in this process." My intentions were to convey that the PaO2 doesn't effect the interpretive process of identifying an acidosis, alkalosis, or in this case a mixed acidosis. I 100% agree that PaO2 is important and it does matter. I would like to further this conversation for the sake of any students that may read this exchange. Hopefully we can help some things make sense for them. "In the development of metabolic acidosis, PO2 does matter" But not always. For example, DKA or a non-anion gap metabolic acidosis, such as retractable diarrhea. A focus on PaO2 would not be a resolution for either of these scenarios. You agree? One step further, I speak on metabolic acidosis in regards to hypoxia, not so much hypoxemia. I use the following two scenarios to illustrate. 1) An anemic patient with a hemoglobin of 6, may have a PaO2 of 95 and saturation of 100%. Despite no evidence of hypoxemia, this patient is most likely hypoxic, due to the decreased overall carrying capacity (CaO2). A metabolic acidosis would most likely develop, despite not being hypoxemic. 2) A COPD patient may live at a state of chronic hypoxemia, leading to polycythemia. This patient's hemoglobin may be 17 with a PaO2 of 55 and saturation of 87%. Despite the obvious hypoxemia, this patient is not hypoxic due to their increased carrying capacity, made available by the polycythemia. This patient will not present with a metabolic acidosis, despite the moderate, persistent level of hypoxemia. This channel doesn't have much physician insight. If you would be so kind to share your thoughts on the above statements. Again, I truly appreciate this professional discourse. I believe we can all learn from each other, especially when we take the time to share thoughts and ideas. Thank you!!!
Awesome! I appreciate your physician experience and presence on the channel. I wish I had more neo/pedi experience to talk on. Maybe you can help with that sometime. I also appreciate the kind words. Thanks again!!
@@RespiratoryCoach Can’t believe that you replying me in such detailed, you are so kind, I really appreciate your wonderful comments regarding the ABG interpreting. It was my fault to lead you misunderstanding me, since I incorrectly used the term “hypoxemia” rather than “hypoxic”. Forgive my terrible English, I am a pediatrician working in a tertiary children’s hospital of China.The instances you upheld in the comments are awesome. It is, the content of arterial oxygen equals 1.34*HGB*SO2+0.003*PaO2, that’s why an “ optimal SO2” in an anemic patients may unreliable and in such condition, the patient is suffering from hypoxic rather than hypoxemia.But in our unit, sampling ABG is usually inappropriate due to inexperienced nurses leading to significant bias of result, so sometimes we adopt the pH to help us judge the severity of a patient’s hypoxia.In addition, under the acidotic circumstance, the ODC may be right-shifted, which could lead a patient owning good PO2 but poor SO2.However, many physicians only care about the PO2 and ignore the SO2 , that, is a real issue. Be pleasure chatting with you
Great video
Failing to compensate for a metabolic acidosis=implies hypercapnic failure, often occurring with a normal (or occasionally low) Pco2 (important not to miss) This mean Mixed Acidosis .
In case of DKA patient, If this patient demonstrates increased WOB, intubation should be considered for impending hypercapnic respiratory failure.
If the patient does not demonstrate increased WOB it implies the patient has blunted ventilation
Regarding end tidal co2 monitoring
it is frequent used in OT in non critical patient
Yes, I agree mostly with what I understand you're stating. Strong work! What is "OT in non critical patient"? Occupational therapy?
hey thanks for creating this channel. I am returning to RT after a lengthy break of about 10 years, and glad I found a place I can get started.
I am still a student but it is a great tip that etCo2 and your educational video are very helpful!
Thank you for doing this
Love from India..
Our Facilities lack EtCo2 too sir 😢..
Thanks you soo much sir,, I am watching all our videos everyday and taking notes...
Thank you soo much.
Coach, please do a video explaining Winters formula.
You got it, Eduardo. Will work on this soon! Thank you again for always watching and commenting.
hi coach, i am attending the first year of spec in Respiratory school (Italy). Im really curious about the utilization of end tidal CO2 and its uses in clinical setting. Thx a lot you made the topic clear
Yes we do use etco2 and make changes by using etoc2 we write the etco2 and paco2 gradient on abgs as well
Great great, please I have a question,, I watched the video
of Etco2 and you mentioned if there is low CO, so not blood back so less Co2 and decreased Etco2!! Now you are mentioning that cardiac arrest so anaerobe so lactate, so Co2 get high, how come!!? High Co2 so I mean if it's the scenario how this would affect our reading of Etco2!!?
Every shift we report etCo2 gradient, especially for our TBI patients. Great tool 👍🏼
Awesome, Aaron! That's the way it should be!!!
Driscol Childrens Hospital NICU/PICU transport team uses that gradient between EtCo2 and arterial CO2.
This is the first time I have heard ETco2!! oopsie!! Teach me
I’ve asked respiratory therapists and other nurses that question several times before and most of the time the respiratory therapist will look at me like they don’t know what I’m talking about. I am a nurse and I spend more time at the bedside and if they can explain to me what the gradient is, I know what EtCO2 to shoot for and I don’t need RT there all night. They’re also busy people. Sometimes they are not even able to tell me what the endtidal was at the time of the art stick, which is disappointmenting to me because then I can’t even calculate my own gradient.
Hey Doug! That's a bummer, but unfortunately way to common. We have to be better than this.
@@RespiratoryCoach I completely agree. Unfortunately it’s not only on respiratory therapist and nursing issue, it’s a human issue and a problem in medicine in all fields including with MDs.
Always a fan of your lectures. Is there anyway that you can help me to explain about the sepsis related to respiratory? Thank you so much
Absolutely, Suzy. Thanks for watching as usual!
Here ya go! th-cam.com/video/8CyGjHF1drw/w-d-xo.html
Nice work sir
ETCO2 is used in every vented patient but it is under utilized I agree. Doctors want ABG results.
But is it used, effectively? I'm familiar with places that utilize ETCO2 on every vent, but the gradient is not monitored and/or used to manage vent settings. What do you see in your area?
@@RespiratoryCoach do you have a video on the gradient?
Is mixed acidosis the same thing as combined?
Very empressive lecture, it sounds like you think the PO2 is not that important in metabolic acidosis. However, metabolic acidosis caused by hypoxemia is NOT mainly due to hyperlactacidemia, as we all know that the pH is hydrogen ion level determined, when our body can not get enough oxygen, the hydrogen ions will have nothing to combine, therefore, it will build up in blood leading to metabolic acidosis. When this happens, the best way to improve the acidotic status of patients is to improve their oxygenation. In the development of metabolic acidosis, PO2 does matter.
I am your big fan by the way. I am a pediatrician working in PICU, your lectures are really helpful, thanks
Hey Doc! I truly appreciate this interaction. I think my minimizing of PaO2 is best described as poorly communicated, despite those words leaving my mouth verbatim. I did state at 2:34, "of course we know that oxygen plays a role in this process." My intentions were to convey that the PaO2 doesn't effect the interpretive process of identifying an acidosis, alkalosis, or in this case a mixed acidosis. I 100% agree that PaO2 is important and it does matter.
I would like to further this conversation for the sake of any students that may read this exchange. Hopefully we can help some things make sense for them.
"In the development of metabolic acidosis, PO2 does matter" But not always. For example, DKA or a non-anion gap metabolic acidosis, such as retractable diarrhea. A focus on PaO2 would not be a resolution for either of these scenarios. You agree?
One step further, I speak on metabolic acidosis in regards to hypoxia, not so much hypoxemia. I use the following two scenarios to illustrate. 1) An anemic patient with a hemoglobin of 6, may have a PaO2 of 95 and saturation of 100%. Despite no evidence of hypoxemia, this patient is most likely hypoxic, due to the decreased overall carrying capacity (CaO2). A metabolic acidosis would most likely develop, despite not being hypoxemic. 2) A COPD patient may live at a state of chronic hypoxemia, leading to polycythemia. This patient's hemoglobin may be 17 with a PaO2 of 55 and saturation of 87%. Despite the obvious hypoxemia, this patient is not hypoxic due to their increased carrying capacity, made available by the polycythemia. This patient will not present with a metabolic acidosis, despite the moderate, persistent level of hypoxemia.
This channel doesn't have much physician insight. If you would be so kind to share your thoughts on the above statements. Again, I truly appreciate this professional discourse. I believe we can all learn from each other, especially when we take the time to share thoughts and ideas. Thank you!!!
Awesome! I appreciate your physician experience and presence on the channel. I wish I had more neo/pedi experience to talk on. Maybe you can help with that sometime. I also appreciate the kind words. Thanks again!!
@@RespiratoryCoach Can’t believe that you replying me in such detailed, you are so kind, I really appreciate your wonderful comments regarding the ABG interpreting. It was my fault to lead you misunderstanding me, since I incorrectly used the term “hypoxemia” rather than “hypoxic”. Forgive my terrible English, I am a pediatrician working in a tertiary children’s hospital of China.The instances you upheld in the comments are awesome. It is, the content of arterial oxygen equals 1.34*HGB*SO2+0.003*PaO2, that’s why an “ optimal SO2” in an anemic patients may unreliable and in such condition, the patient is suffering from hypoxic rather than hypoxemia.But in our unit, sampling ABG is usually inappropriate due to inexperienced nurses leading to significant bias of result, so sometimes we adopt the pH to help us judge the severity of a patient’s hypoxia.In addition, under the acidotic circumstance, the ODC may be right-shifted, which could lead a patient owning good PO2 but poor SO2.However, many physicians only care about the PO2 and ignore the SO2 , that, is a real issue. Be pleasure chatting with you
Tqqqqq excellent information for me.
Thanks Naveen for watching!!!!