A lecture on the ways in which the ABG can be used to assess oxygenation, focusing on the alveolar gas equation and the A-a gradient. Several examples of ABG interpretation are included.
prince blaker, I'm glad you enjoyed the video. The A-a gradient is solely a function of the efficiency of the alveolar capillary membrane. It is impacted by decreased total surface area, increased membrane thickness, or maldistribution of blood and/or ventilation. In hypoventilation, ventilation isn't maldistributed, but rather is decreased equally everywhere. Therefore, A-a gradient is normal.
Another way to look at it is in hypoventilation, the hypoxemia isn't due to a pathophysiologic problem with the alveolar-capillary membrane, but rather due to derangement in the partial pressures of the gases in the alveoli.
CO2 seems to be the driving factor for O2 extraction from the alveoli ; where the metabolic needs for O2 is estimated via the RQ of the food metabolized , the CO2 produced in blood ; that is eventually released in the alveoli ! But CO2 seems too to determine the amount of O2 extracted by the body tissues from the arterial blood in the same manner ! In case of hypoventilation ; the associated hypercapnia leads to a PROPORTIONATE reduction in both PAO2 & PaO2 as there is a proportionate increase in O2 extraction determined by the CO2 concentration in both the alveoli & the blood ! So a normal A-a gradient is achieved !
I have an exam coming up tomorrow, and going through your videos these last hours has been more helpful than 3 weeks of our pulmonary block. I don't know how to thank you! The clear diagrams, and effort put into the presentation, the logical progression. Everything about this is great.
Just to note a potential update (and as a side note, a thousand thanks for this fantastic lecture series): according to the new definition, PaO2/FiO2 ratios of 200-300 may now be considered "mild ARDS"; "acute lung injury" no longer exists.
Sam Black Thanks so much for pointing that out! It's challenging to keep these videos up to date when medicine keeps changing! On vacation right now, but will try to remember to add a clarifying annotation once I can access the site with something other than a smartphone. Thanks again!
Thank you so very much for the efforts you put into your channel!! I cannot emphasize enough how helpful it has been. Thank you! a small note: @11:40.. the definition of ARDS is outdated now. It might be worthwhile putting an annotation
MrBhotu, thanks for your enthusiasm. I'm trying to get these up as fast as possible, but I've exhausted the lectures that I already had written and which just needed narration recorded and transfer into video format. Creating de novo lectures is taking a little more time. Hope to have the next one up by tomorrow (affect of supplemental O2 on the ABG), and realistically to finish up the remainder of the ABG course by mid summer.
In common usage the terms hyperventilation and hypoventilation usually refer to how fast someone is breathing (i.e. how many breaths per minute), but they mean something more specific in medicine. CO2 levels are dependent upon something called alveolar ventilation, which you can think of as how much "fresh air" the alveoli see each minute. Alveolar ventilation = (Tidal volume - dead space) x respiratory rate. Tidal volume is the volume of air in each breath, and dead space is the volume of the lungs which is not participating in gas exchange because it's either in airways not lined by capillaries, or because it's in alveoli that aren't receiving good blood flow. In COPD, particularly during acute exacerbations, patients have low tidal volumes and may have increased dead space. So the value of (tidal volume - dead space) becomes much smaller than normal. So even if the respiratory rate is higher than normal, the overall alveolar ventilation may still be low, leading to high CO2 levels in the arteries.
In other words : In COPD , the chronic reduction in Tv outweighs the acute increase in RR during exacerbations ! [ Low minute ventilation = Very very low tidal volume X High respiratory rate ] ! In summary the PAo2 value is the driving factor for the PaO2 value !
Hi, thank you for your great videos! I feel absolutely privileged to have such a great source of knowledge for my studies :-) I however still feel like I don't completely understand the alveolar gas equation.. I get that the first term refers to the partial pressure of oxygen that is present right before the air enters the alveoli (so I guess within the terminal bronchioles).. But I still don't understand why the second term is valid.. For instance in Example #1 in case of the woman with dementia.. She has a very low PaCO2, I guess due to tachypnea.. So in this case the second term would imply, that because she has a PaCO2 of 26 mmHg (and therefore a PACO2 of 26 mmHg), she will only extract 32.5 mmHg of O2 from the alveoli (if we use RQ = 0.8).. But I don't understand how her having a lower PaCO2 would change the amount of oxygen that is present in the alveoli.. Because the reason her PaCO2 is low is not that she uses less oxygen, but that she exhales more CO2, right? I am really confused :D
The alveolar membrane permeability to CO2 is nearly 26 times that to O2 ! That's why CO2 in blood & alveoli rapidly equilibrate , without creating a gradient for CO2 , i.e : PA co2 = Pa co2 . The RQ itself refers to a kind of gaseous equilibrium for the alveolar exchange between O2 & CO2 , in which the metabolic needs for O2 is determined by the kind of food metabolized , the estimated CO2 produced in blood & eventually released in the alveoli ! CO2 seems to be the driving factor for O2 extraction from the alveoli ! In case of tachypnea the Pa CO2 is progressively reduced with time without necessarily achieving adequate rise in Pa O2 ! The wide A-a gradient in that dementia patient reflects an impaired gas diffusion that affects O2 more than CO2 due to the difference in alveolar permeability between the 2 gases ! A chest X - ray should also be considered in that dementia patient to rule out any possible aspiration pneumonia !
One additional cause of normal A-a gradient (besides hypo ventilation and high altitude) would be any cause of increased CO2 production (sometimes sepsis) - this is according to a lecture by a pulmonology fellow. - this can be deduced from the alveolar equation-- where PAO2 is determined by PaCO2
CO2 seems to be the driving factor for O2 extraction from the alveoli ; where the metabolic needs for O2 is estimated via the RQ of the food metabolized , the CO2 produced in blood ; that is eventually released in the alveoli ! But CO2 seems too to determine the amount of O2 extracted by the body tissues from the arterial blood in the same manner ! In case of sepsis ; the tissue hypo perfusion associated with the septic shock results in hypercapnia , hypercapnia leads to a PROPORTIONATE reduction in both PAO2 & PaO2 as there is a proportionate increase in O2 extraction determined by the CO2 concentration in both the alveoli & the blood ! So a normal A-a gradient is achieved ! Lord knows best !
Amazing, really very good simple approach, I found this video while randomly youtube-ing. I am definitely going to see the rest of your lectures now. Well done for making A-a Gradient seems that easy.
Thank you Dr Strong, I seem to pick up more from listen to this lecture once more. How wonderful is the Internet! I got the PaO2/FiO2 which I just read somewhere regard to Covid-19
Wow, this is fascinating! I just popped in and continued to listen to this. I do wonder about two things though: what is the lower cutoff value for a pathological A-a gradient? Say a 43 year old patient is presented with an A-a graidient of 38, or 42 or 45. secondly: if the pa02 and paCO2 are measured in arterial blood, why is it important? The beginning of the lecture stated that only 1.5% of oxygen account for dissolved oxygen and are measured by ABT while oxygen bound by hemoglobin are measured by oximeters and account for the majority. Or did I misunderstood something?
Aa gradient determines how much of all the inspired oxygen reaches the circulation. If elevated= some lung parenchyma issues, which is VQ mismatch, Diffusion issue or Shunt. If normal, then whatever inspired fraction of O2 had no problem getting into the circulation because of a good functioning lung parenchyma. If patient is hypoxic with a normal AA gradient, then primary problem is outside the lung parenchyma causing either reduce ventilation e.g. COPD, OSA, etc
sir desperately waiting for ur remaining lectures on abg .....excellent videos ...excellent material slides ...very quick even for revisions without missing any points
Remember that in shunt, there is and increase in perfusion and a decrease in ventilation. Where there is ventilation, but no perfusion; you don't get gas exchange. What does this look like? For instance, you have a patient breathing 50% oxygen at sea level. ABGs show PaO2 of 50 and PCO2 of 50. SpO2 is 98% After some calculation, the patient's PAO2 is 294. Thus, giving you an estimated 244mmHg Aa gradient. How do we interpret this? Well we see that SpO2 is unaffected; yet our ABGs are abnormal. (recall that shunt will not respond to 100% O2) Ahhh there must be a ventilation issue. This is essentially this definition of shunt.
Thank you Jawan, however I do understand the definition and the mathematical formula by which the Aa gradient rises, it is the theory behind it which bothers me, in simple terms the Aa gradient represents difference in Alveolar and arterial oxygenation, the thing I'm asking is why in the presence of hypoxemia AND low alveolar ventilation the Aa gradient rises if both values go down the difference shouldn't rise, but remain the same. To make myself clear let's make a ridiculous example, imagine if there was a 0mmHg pressure of oxygen in both the alveoli and the arteries, we, in this case agree that there is hypoxemia and low ventilation, if in this case the perfusion remained constant it would be a case of Shunt, and the Aa gradient should go up, in fact if you calculate by the formula, it may very well go up, because the Alveolar Pressure is calculated not directly but by some other variables like CO2.... But then again, remember the terms I state at the beginning, a pressure of 0 in both the arteries and the alveoli, if the Aa gradient would really be just a difference between these two measures the difference between a completely hypoxemic artery and a completely hypoxemic alveoli (by shunt) would not be elevated, would be in fact 0
Dude a shunt isn´t "ventilation, but not perfusion" thats and example of blood obstruction with an "infinite"V/Q mismatch since you have a number divided by cero; the best example could be an pulmonary embolism. And as you said, this condition its partially improved by O2
A-a increases because in your V/Q equation the ventilation (V) will be cero (ei: tumor obstruccion). You must remember that in lung when its a low 02 pressure, there is a vasoconstriction to allow blood goes to better oxygenated alveoli. So there you will have that in those alveoli there wont exist difussion and increasing A-a gradient
Just a miracle! Thank you so much! I wish you could teach at my school sir! You're an absolute delight to learn from -- so easy to understand and concise! I really enjoy your lectures!!
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