Noureen, pulmonary function tests are definitely on my list of topics I hope to get to at some point, though as this list is fairly long, I can't guarantee when it will happen. Thanks for watching!
Mr. Singh, that's an excellent question. It's because O2 content is not proportional to pO2, but rather determined from the non-linear hemoglobin-O2 dissociation curve. While it may seem like the arterial O2 sat is determined by the pO2, because the vast majority of oxygen in blood is bound to hemoglobin, it's actually equal correct (and perhaps even more so) so say that the arterial pO2 is largely determined by the arterial O2 sat.
Then, the equation used to calculate the final O2 sat is: Final O2 sat = [(O2 sat in unit 1)(blood flow through unit 1) + (O2 sat in unit 2)(blood flow through unit 2) + (O2 sat in unit 3)(blood flow though unit 3)] / total blood flow through the lungs. The final PO2 is calculated from the final O2 sat using the aforementioned Hb-O2 sat curve equation available on the web. The major point of this example and part of the talk was to show why hypoxia from large shunts cannot be corrected with O2.
Next, one must realize that the O2 content of blood is essentially driven by the amount of O2 bound to hemoglobin (i.e. the O2 sat), and not by the amount of O2 dissolved in blood (i.e. the PO2). So once one uses the PO2 to calculate the O2 sat for the 3 individual units, the PO2 is no longer needed. (The calculation of O2 sat from PO2 is based on the Hb-O2 saturation curve, is complex, and is available on the web with a simple Google search - sorry can't post links in the comments section)
...if we were to be extremely precise, we would do a weighted average (weighted according to blood flow) of blood oxygen content and not the O2 sats. However, the additional contribution from dissolved O2 (as measurable from pO2) is small enough that it can be neglected without sizable impact on our final analysis. Hope that helps!
vm610, I understand why this might not be clear. I didn't want to get into too much detail with the explanation because the details are a bit removed from clinical care, but here we go. First, the amount of blood flow to each of the 3 lung units is arbitrary; I've just set them to 1, 4.5, and 0.5 for the sake of this example. The PO2 of 40, 100, and 140 for each lung unit is based on what would be expect for near absent ventilation, normal ventilation, and near absent perfusion respectively.
Excellent, one thing I would add as u described that what does Q stand for or from where does it come in ventilation perfusion ratio.Infact it's analogues to Ohm’s law for electrical current flow.The same expression is used to describe cardiac blood flow .Q=P/R, where Q = current flow or blood flow
Minor correction (maybe pedantic), but seems important enough to share. High altitude does cause hypoxia due to decreased PAO2, but the mechanism causing diffusion limited O2 transport is NOT due to the decreased pressure gradient. I'll explain Normal oxygen pressure gradient is alveolar PO2 = 100 venous PO2 = 40 O2 Gradient = 60 mmHg High altitude alveolar PO2 = 60 venous PO2 = 35 O2 Gradient = 25 mmHg Pressure gradient (low altitude) at the beginning of the capillary is 60 mmHg, but later on in the capillary flow, blood has taken up some more oxygen and alveolar oxygen has dropped. Ultimately, at some point, the pressure gradient will have dropped to 25 mmHg, albeit at a place distant from the beginning of the capillary. So, at this point, the flow rate is reduced to the same as the flow rate that would be seen at the BEGINNING of the capillary in high altitude....So, using a reduced partial pressure as an explanation, we should assume that increasing the partial pressure would actually cause increased a-A gradient (not decreasing it). Except for ONE thing--Hemoglobin curves show us that Oxygen doesn't completely saturate Hemoglobin at an alveolar pressure of 60 mmHg (at high altitude). The Hemoglobin will have fewer Oxygen's bound, and therefore be in a more "taut" position, and take much longer to "reload" new oxygen onboard. Furthermore, because of reduced O2, the Haldane effect isn't as strong, so CO2 takes longer to unload off of oxygen, and therefore: 1. It doesn't make room for oxygen as quickly as it should (this should be only minor) This hypoxia also induces respiratory alkalosis and over, giving a left shift, while 2,3-DPG provides for a right shift. The alkalosis has the most immediate impact, but is not enough to shift the curve far enough for O2 to become saturated at the lower partial pressure. Since the overall diffusion of O2 is a function of both: - O2 diffusion from Fick's law AND - O2 rate of binding to Hb Therefore, reduced velocity of Hb binding is primary mechanism to cause diffusion limited physiology.
Novem Ber I would like to invite an actual critique of what I said! In summary, I stated that: 1. the effect of high altitude on oxygenation has nothing to do with the decreased diffusion gradient. - the diffusion gradient at sea level starts high (about 60) at the beginning of the capillary, is reduced to about 25 by the time it has traveled 1/4 the distance of capillary, and has reduced to zero by the end of the capillary. --this implies that when at higher altitude, you start at a gradient of about 25 at the beginning of the capillary and should be down to zero by, at least 3/4 of the capillary length (if all other things besides pressure are equal). 2. Since pressure isn't what makes it diffusion limited, what does?! - the haldane effect - movement down the oxygen dissociation curve. ---if you start at an O2 sat that is low, it takes more effort to add on the next molecule of oxygen (more time). Please rebuke one of those two points if you wish to further the reduction of total, overall bullshit within the world. Regards, Mike
Hi. I enjoyed the video. I learned more from this video than have other videos done by other professionals. At 21:58 you said the average of Oxygen is calculated not by taking the average of the oxygen tensions, isn't PO2 an oxygen tension? Please clarify for my understanding. Thank you.
Thank u so much for such wonderful lectures,really helpful n revise the concept of ABGs n hypoxia. i request that u made these sort of lectures on pulmonary function test aswell to clarify our concept thanks
fantastic presentation !!!!!!!!!!!!!!! you said that O2 is not the only treatment in case of hypoventilation a s it may lead to increase co2 retention so what else shall I do rather than bronchodilators and o2 to copd patient
...as in one of the examples, the O2 sat (and thus O2 content) in the blood leaving a lung segment with pO2 of 100 and one segment with pO2 of 140, is minimally different from one another. If we were to average the pO2s instead of the O2 sats, we would be weighing too greatly the highly oxygenated lung segments, and our final estimate of arterial O2 sat would be too high. This effect is why very high concentrations of inhaled oxygen cannot correct a large right to left shunt of blood.
I love the Strong videos, thank you for them! In this one I just cannot agree with the pO2 of 623mmHg in the alveolus with a nearly blocked bronchus. 100% O2 would significantly increase the pAO2 of this alveolus and achieve a normal saturation, that is true. However, If previously the alveolus achieved oxygenating the blood to merely 40mmHg (having no higher oxygen partial pressure itself) , raising the FiO2 five times would make the oxygen gain in the alveolus increase roughly sixfold, asthe total number of gas molecules passing through the obstruction would remain the same. Higher pAO2 than that could only be achieved by increasing the ventilation of this alveolus, or the baroetric pressure of the delivered oxygen..
I intended a long time ago to make video on weaning from ventilation, but got sidetracked with other topics. I'm still planning on getting back to it some day. Thanks for watching!
Mike Stewie Mike Stewie They are not related. RQ (respiratory quotient) is dependent solely on the composition of your diet and your body's metabolic pathways. V/Q ratio is a function of pulmonary anatomy/physiology. Although the acronyms sound similar, the fact they are both equal to 0.8 under normal conditions is pure coincidence.
Dear Strong Medicine, I have a question related to hypoxemia/hypercapnia thing. I've spent so much time, thinking about this that It seems I lost any hope to understand it. In Boards & Beyonds, Dr. James Ryan said that in the case of shunting patients get hypoxemia without hypercapnia, but in case of dead space patients get hypercapnia without hypoxemia, if dead space is not large enough to cause hypoxemia, and the main problem in the dead space is high level of pCO2. Can you help me to understand why in both of these cases you don`t get hypoxemia and hypercapnia?
Hello and thank you for your great lecture series! I am a bit confused as to how the PaCO2 influences the diffusion of oxygen in the alveoli. Is hypercapnia directly responsible for the hypoxemia (through the bohr effect) or does it just reflect the fact that if hypercapnia (under normal circumstances) is present, so is hypoxemia? In patients with severe COPD, one can achieve narcotic levels of PaCO2 with normal saturation. How is this explained? Secondly, does the bohr effect have any clinical significance for oxygenation at high levels of carbon dioxide? I'm sorry if my questions seems trivial, they've just been bugging me for some time now.
ghaffasa, you're questions are not trivial at all! First, PaCO2 does not directly influence the diffusion of oxygen in the alveoli, but rather the concentration of oxygen in the alveoli. If a patient is not ventilating his/her lungs well, the alveolar CO2 concentration (and thus, alveolar CO2 partial pressure - PACO2) will rise. Since the total alveolar pressure is essentially constant (minus changes with respiration), the alveolar O2 partial pressure (PAO2) must decrease. So the process of diffusion of O2 is intact, but the concentration gradient is reduced. This is why the A-a gradient is normal in patient who have hypoxemia related to hypercapnia. Patients can high very high PaCO2 levels and still have normal arterial O2 saturation of hemoglobin if the PaO2 is high enough to overcome the shift in the dissociation curve. This cannot happen if a patient is breathing room air (i.e. all hypercapnic patients are hypoxemic at room air), but can happen if supplemental O2 is provided, driving up the alveolar O2 concentration. Finally, does the Bohr effect have any clinical significance for oxygenation at high levels of CO2? That's a particularly great question. I can say that I've never encountered a doctor/nurse/RT discussing it on the wards as a clinically relevant phenomenon. I haven't been able to find any hard data about this, but I would guess that if acute hypercapnia developed to the severity that pH was reduced to
+Strong Medicine, Dear Dr.Strong, can you please explain to me how dead space ventilation leads to increase in PCO2 ? I just cant wrap my head around it and i was wondering if you can help me understand it ? eg now i know how a PE leads to hypoxia but i cant understand how a PE can result in hypercapnia ?
thanks a lot for the explanation,,,your are really precise and accurate in what you say sir..but my one doubt remains,,,that is suppose pO2 from one lung unit is 100 and from other lung unit is 26....the Hb will be nearly 100 per saturated from the lung unit with pO2 of 100 and only 50 per saturated returning from pO2 of 26...
but down the course when they mix ,,does the pO2 gets wasted somewhere as i assume that why high po2 from better lung segment doesnt saturates the Hb coming from low pO2 area when they mix....thanks...
my wife two time normally delivered baby in greater than 37 weeks of pregnancy period but both babies died due to the hypoxia ischaemia can you please suggest whether we can go through caesarean section delivery or preterm delivery on next time . Please help me .
I'm so very sorry to hear about the loss of your babies, and I appreciate why one might be anxious or apprehensive about another pregnancy. However, I cannot give specific medical advice on this channel. Even if there were not legal/ethical barriers to doing so, this is a question best addressed by a neonatologist (a pediatrician who specializes in the care of critically ill infants); I am not sufficiently qualified to answer it.
+ahmedmed That's a great question. There's 3 possible mechanisms: First, if the pulmonary hypertension is associated with fibrosis within the capillary bed, there will be impairment of diffusion-mediated gas exchange across the alveolar-capillary membrane. Second, if the pulm hypertension is not uniformly distributed, blood could get shunted towards lung regions of relatively low ventilation. (i.e. worsened V/Q mismatch) Third, about 25-30% of the population has a patent foramen ovale, through which little blood typically moves (since the right and left atria are at approximately the same pressure in normal people). If the right-sided heart pressures increase sufficiently, a patient could develop right to left shunting across the PFO.
+Strong Medicine. Thank you very much sir. As an intern i internal medicine your lectures has been really helpful. I was wondering if you were planning to do a presentation on pre-op assessment. thank you very much for you efforts and i hope one day ill have half the knowledge that u have. Thank you very much again.
ahmedmed Thanks for your kind words. Preop assessment is a great topic, and on my list of things to cover someday, but unfortunately, that list is really long, and so I can't make any estimate of when I'll get to it.
+Strong Medicine, Dear Dr.Strong, can you please explain to me how dead space ventilation leads to increase in PCO2 ? I just cant wrap my head around it and i was wondering if you can help me understand it ? eg now i know how a PE leads to hypoxia but i cant understand how a PE can result in hypercapnia ?
+Strong Medicine, Dear Dr.Strong, can you please explain to me how dead space ventilation leads to increase in PCO2 ? I just cant wrap my head around it and i was wondering if you can help me understand it ? eg now i know how a PE leads to hypoxia but i cant understand how a PE can result in hypercapnia ?
![ละลาย (LALALYE) - DAOU PITTAYA ต้าห์อู๋ พิทยา [OFFICIAL MV]](http://i.ytimg.com/vi/wo6r9TgausI/mqdefault.jpg)
This series deserves a Nobel, Nobel of Education
Excellent. I'm watching as many of your videos as I can before starting my IM residency.
Noureen, pulmonary function tests are definitely on my list of topics I hope to get to at some point, though as this list is fairly long, I can't guarantee when it will happen. Thanks for watching!
Mr. Singh, that's an excellent question. It's because O2 content is not proportional to pO2, but rather determined from the non-linear hemoglobin-O2 dissociation curve. While it may seem like the arterial O2 sat is determined by the pO2, because the vast majority of oxygen in blood is bound to hemoglobin, it's actually equal correct (and perhaps even more so) so say that the arterial pO2 is largely determined by the arterial O2 sat.
the series of ABG is really amazing i finshed it today thank u dr.eric
Then, the equation used to calculate the final O2 sat is: Final O2 sat = [(O2 sat in unit 1)(blood flow through unit 1) + (O2 sat in unit 2)(blood flow through unit 2) + (O2 sat in unit 3)(blood flow though unit 3)] / total blood flow through the lungs. The final PO2 is calculated from the final O2 sat using the aforementioned Hb-O2 sat curve equation available on the web. The major point of this example and part of the talk was to show why hypoxia from large shunts cannot be corrected with O2.
Sir I'm in love with your diagrams and teaching !!! I hope we will get an update on ecg book publication soon (hopefully other books too)
Your lectures are excellent way of understanding
Next, one must realize that the O2 content of blood is essentially driven by the amount of O2 bound to hemoglobin (i.e. the O2 sat), and not by the amount of O2 dissolved in blood (i.e. the PO2). So once one uses the PO2 to calculate the O2 sat for the 3 individual units, the PO2 is no longer needed. (The calculation of O2 sat from PO2 is based on the Hb-O2 saturation curve, is complex, and is available on the web with a simple Google search - sorry can't post links in the comments section)
...if we were to be extremely precise, we would do a weighted average (weighted according to blood flow) of blood oxygen content and not the O2 sats. However, the additional contribution from dissolved O2 (as measurable from pO2) is small enough that it can be neglected without sizable impact on our final analysis. Hope that helps!
Hope that helps!
Thanks a lot Eric. You have an innate flair for teaching.
Thanks for ur excellent lecture
One que
Isn’t shunt is type of v/Q mismatch and pulmonary edema
is type of shunt
vm610, I understand why this might not be clear. I didn't want to get into too much detail with the explanation because the details are a bit removed from clinical care, but here we go. First, the amount of blood flow to each of the 3 lung units is arbitrary; I've just set them to 1, 4.5, and 0.5 for the sake of this example. The PO2 of 40, 100, and 140 for each lung unit is based on what would be expect for near absent ventilation, normal ventilation, and near absent perfusion respectively.
Excellent, one thing I would add as u described that what does Q stand for or from where does it come in ventilation perfusion ratio.Infact it's analogues to Ohm’s law for electrical current flow.The same expression is used to describe cardiac blood flow .Q=P/R, where Q = current flow or blood flow
We really appreciate your efforts.Thank you Sir .It was really helpful
Minor correction (maybe pedantic), but seems important enough to share.
High altitude does cause hypoxia due to decreased PAO2, but the mechanism causing diffusion limited O2 transport is NOT due to the decreased pressure gradient. I'll explain
Normal oxygen pressure gradient is
alveolar PO2 = 100
venous PO2 = 40
O2 Gradient = 60 mmHg
High altitude
alveolar PO2 = 60
venous PO2 = 35
O2 Gradient = 25 mmHg
Pressure gradient (low altitude) at the beginning of the capillary is 60 mmHg, but later on in the capillary flow, blood has taken up some more oxygen and alveolar oxygen has dropped.
Ultimately, at some point, the pressure gradient will have dropped to 25 mmHg, albeit at a place distant from the beginning of the capillary. So, at this point, the flow rate is reduced to the same as the flow rate that would be seen at the BEGINNING of the capillary in high altitude....So, using a reduced partial pressure as an explanation, we should assume that increasing the partial pressure would actually cause increased a-A gradient (not decreasing it).
Except for ONE thing--Hemoglobin curves show us that Oxygen doesn't completely saturate Hemoglobin at an alveolar pressure of 60 mmHg (at high altitude). The Hemoglobin will have fewer Oxygen's bound, and therefore be in a more "taut" position, and take much longer to "reload" new oxygen onboard.
Furthermore, because of reduced O2, the Haldane effect isn't as strong, so CO2 takes longer to unload off of oxygen, and therefore:
1. It doesn't make room for oxygen as quickly as it should (this should be only minor)
This hypoxia also induces respiratory alkalosis and over, giving a left shift, while 2,3-DPG provides for a right shift. The alkalosis has the most immediate impact, but is not enough to shift the curve far enough for O2 to become saturated at the lower partial pressure.
Since the overall diffusion of O2 is a function of both:
- O2 diffusion from Fick's law AND
- O2 rate of binding to Hb
Therefore, reduced velocity of Hb binding is primary mechanism to cause diffusion limited physiology.
Novem Ber
I would like to invite an actual critique of what I said!
In summary, I stated that:
1. the effect of high altitude on oxygenation has nothing to do with the decreased diffusion gradient.
- the diffusion gradient at sea level starts high (about 60) at the beginning of the capillary, is reduced to about 25 by the time it has traveled 1/4 the distance of capillary, and has reduced to zero by the end of the capillary.
--this implies that when at higher altitude, you start at a gradient of about 25 at the beginning of the capillary and should be down to zero by, at least 3/4 of the capillary length (if all other things besides pressure are equal).
2. Since pressure isn't what makes it diffusion limited, what does?!
- the haldane effect
- movement down the oxygen dissociation curve.
---if you start at an O2 sat that is low, it takes more effort to add on the next molecule of oxygen (more time).
Please rebuke one of those two points if you wish to further the reduction of total, overall bullshit within the world.
Regards,
Mike
Doc you are a genius
Thank you for all of your videos! Very helpfull and interesting!
Thank you Dr Eric Strong !
Hi. I enjoyed the video. I learned more from this video than have other videos done by other professionals. At 21:58 you said the average of Oxygen is calculated not by taking the average of the oxygen tensions, isn't PO2 an oxygen tension? Please clarify for my understanding. Thank you.
Your lectures are soo good! thank you so much Doc!
Thank u so much for such wonderful lectures,really helpful n revise the concept of ABGs n hypoxia.
i request that u made these sort of lectures on pulmonary function test aswell to clarify our concept
thanks
fantastic presentation !!!!!!!!!!!!!!!
you said that O2 is not the only treatment in case of hypoventilation a s it may lead to increase co2 retention so what else shall I do rather than bronchodilators and o2 to copd patient
...as in one of the examples, the O2 sat (and thus O2 content) in the blood leaving a lung segment with pO2 of 100 and one segment with pO2 of 140, is minimally different from one another. If we were to average the pO2s instead of the O2 sats, we would be weighing too greatly the highly oxygenated lung segments, and our final estimate of arterial O2 sat would be too high. This effect is why very high concentrations of inhaled oxygen cannot correct a large right to left shunt of blood.
I love the Strong videos, thank you for them!
In this one I just cannot agree with the pO2 of 623mmHg in the alveolus with a nearly blocked bronchus. 100% O2 would significantly increase the pAO2 of this alveolus and achieve a normal saturation, that is true. However, If previously the alveolus achieved oxygenating the blood to merely 40mmHg (having no higher oxygen partial pressure itself) , raising the FiO2 five times would make the oxygen gain in the alveolus increase roughly sixfold, asthe total number of gas molecules passing through the obstruction would remain the same. Higher pAO2 than that could only be achieved by increasing the ventilation of this alveolus, or the baroetric pressure of the delivered oxygen..
Thanks a lot very useful explanation , I hope you make a series of. Weaning from mechanical ventilation
I intended a long time ago to make video on weaning from ventilation, but got sidetracked with other topics. I'm still planning on getting back to it some day. Thanks for watching!
Incredibly helpful!!!
Mike Stewie Mike Stewie They are not related. RQ (respiratory quotient) is dependent solely on the composition of your diet and your body's metabolic pathways. V/Q ratio is a function of pulmonary anatomy/physiology. Although the acronyms sound similar, the fact they are both equal to 0.8 under normal conditions is pure coincidence.
Excellent, thanks for sharing
Superb!!!!!!
Dear Strong Medicine, I have a question related to hypoxemia/hypercapnia thing. I've spent so much time, thinking about this that It seems I lost any hope to understand it. In Boards & Beyonds, Dr. James Ryan said that in the case of shunting patients get hypoxemia without hypercapnia, but in case of dead space patients get hypercapnia without hypoxemia, if dead space is not large enough to cause hypoxemia, and the main problem in the dead space is high level of pCO2. Can you help me to understand why in both of these cases you don`t get hypoxemia and hypercapnia?
Thank you. Ery much Dr , you are a saver ,,, may the Almighty preserve you and guide you to paradise
Loved it!! great: precise, accurate and easy to follow. Thank you so much!
Nice
Q stands for flow and hence the perfusion
You did great
Hello and thank you for your great lecture series!
I am a bit confused as to how the PaCO2 influences the diffusion of oxygen in the alveoli. Is hypercapnia directly responsible for the hypoxemia (through the bohr effect) or does it just reflect the fact that if hypercapnia (under normal circumstances) is present, so is hypoxemia? In patients with severe COPD, one can achieve narcotic levels of PaCO2 with normal saturation. How is this explained?
Secondly, does the bohr effect have any clinical significance for oxygenation at high levels of carbon dioxide?
I'm sorry if my questions seems trivial, they've just been bugging me for some time now.
ghaffasa, you're questions are not trivial at all! First, PaCO2 does not directly influence the diffusion of oxygen in the alveoli, but rather the concentration of oxygen in the alveoli. If a patient is not ventilating his/her lungs well, the alveolar CO2 concentration (and thus, alveolar CO2 partial pressure - PACO2) will rise. Since the total alveolar pressure is essentially constant (minus changes with respiration), the alveolar O2 partial pressure (PAO2) must decrease. So the process of diffusion of O2 is intact, but the concentration gradient is reduced. This is why the A-a gradient is normal in patient who have hypoxemia related to hypercapnia.
Patients can high very high PaCO2 levels and still have normal arterial O2 saturation of hemoglobin if the PaO2 is high enough to overcome the shift in the dissociation curve. This cannot happen if a patient is breathing room air (i.e. all hypercapnic patients are hypoxemic at room air), but can happen if supplemental O2 is provided, driving up the alveolar O2 concentration.
Finally, does the Bohr effect have any clinical significance for oxygenation at high levels of CO2? That's a particularly great question. I can say that I've never encountered a doctor/nurse/RT discussing it on the wards as a clinically relevant phenomenon. I haven't been able to find any hard data about this, but I would guess that if acute hypercapnia developed to the severity that pH was reduced to
Outstanding, thank you!
Does RQ relate to the V/Q ratio? I ask because, to my understanding, the V/Q ratio in oxygen perfusion also averages at 0.8 or 80%.
Amaaaaaaazing , thank youuuuuuu !!!!!!
In pulmonary embolism will there be a high PaCo2 bcz of low perfusion or low PaCo2 bcz of hyperventilation in response to PE ?
thank u so much,, best explained
Good information....
+Strong Medicine, Dear Dr.Strong, can you please explain to me how dead space ventilation leads to increase in PCO2 ? I just cant wrap my head around it and i was wondering if you can help me understand it ? eg now i know how a PE leads to hypoxia but i cant understand how a PE can result in hypercapnia ?
thanks a lot for the explanation,,,your are really precise and accurate in what you say sir..but my one doubt remains,,,that is suppose pO2 from one lung unit is 100 and from other lung unit is 26....the Hb will be nearly 100 per saturated from the lung unit with pO2 of 100 and only 50 per saturated returning from pO2 of 26...
Thanks a million!
Thank you!
sir i have a question,,,why the final PO2 is calculated from the final O2 sat ,,,and not just averaged from different lung units..thanks
but down the course when they mix ,,does the pO2 gets wasted somewhere as i assume that why high po2 from better lung segment doesnt saturates the Hb coming from low pO2 area when they mix....thanks...
can I use Dlco instead of A-a gradient?
my wife two time normally delivered baby in greater than 37 weeks of pregnancy period but both babies died due to the hypoxia ischaemia can you please suggest whether we can go through caesarean section delivery or preterm delivery on next time . Please help me .
I'm so very sorry to hear about the loss of your babies, and I appreciate why one might be anxious or apprehensive about another pregnancy. However, I cannot give specific medical advice on this channel. Even if there were not legal/ethical barriers to doing so, this is a question best addressed by a neonatologist (a pediatrician who specializes in the care of critically ill infants); I am not sufficiently qualified to answer it.
Where are the rest lectures?
All 8+ hours of ABG interpretation is here: th-cam.com/video/3eXmA0VFXtg/w-d-xo.html
❤
+Strong Medicine . Dear dr. Strong can you breifly explain to me how an idiopathic pulmonary artery hypertension results in hypoxemia ?
+ahmedmed That's a great question. There's 3 possible mechanisms:
First, if the pulmonary hypertension is associated with fibrosis within the capillary bed, there will be impairment of diffusion-mediated gas exchange across the alveolar-capillary membrane.
Second, if the pulm hypertension is not uniformly distributed, blood could get shunted towards lung regions of relatively low ventilation. (i.e. worsened V/Q mismatch)
Third, about 25-30% of the population has a patent foramen ovale, through which little blood typically moves (since the right and left atria are at approximately the same pressure in normal people). If the right-sided heart pressures increase sufficiently, a patient could develop right to left shunting across the PFO.
+Strong Medicine. Thank you very much sir. As an intern i internal medicine your lectures has been really helpful. I was wondering if you were planning to do a presentation on pre-op assessment. thank you very much for you efforts and i hope one day ill have half the knowledge that u have. Thank you very much again.
ahmedmed Thanks for your kind words. Preop assessment is a great topic, and on my list of things to cover someday, but unfortunately, that list is really long, and so I can't make any estimate of when I'll get to it.
Many thanks
nice.
Shouldn't it be PAO2 not PAO2 in the equation
No! That error has been up for 5 years! That's embarrassing. Unfortunately, no way to correct it now. Hopefully most viewers realized the mistake.
you mean at 2:35?? If so I was confused too!!
🧡💜🧡💜♥️🧡💜♥️🧡💜♥️💙💚💛💚💙💚💛💛💚💚💙💙💚💛💚💙🎀🎁🌍🌍
Thaaaaaaaaaaaank youuuuuu
+Strong Medicine, Dear Dr.Strong, can you please explain to me how dead space ventilation leads to increase in PCO2 ? I just cant wrap my head around it and i was wondering if you can help me understand it ? eg now i know how a PE leads to hypoxia but i cant understand how a PE can result in hypercapnia ?
+Strong Medicine, Dear Dr.Strong, can you please explain to me how dead space ventilation leads to increase in PCO2 ? I just cant wrap my head around it and i was wondering if you can help me understand it ? eg now i know how a PE leads to hypoxia but i cant understand how a PE can result in hypercapnia ?