Alveolar-Arterial (Aa) Gradient Explained - Definitions, Equations, Physiology, Implementation, More
In this video we dive into the Alveolar-arterial gradient or the Aa Gradient. We start by explaining what exactly it is in terms that make sense. We then dive into the math and equations to calculate the gradient. We explain the math as related to the physiology to better understand it. We then go into a normal Aa Gradient versus an abnormal gradient and the differential diagnosis for each.
The Aa Gradient is the difference between the alveolar oxygen content and the arterial oxygen content. It is a measure of whether you are having trouble diffusing oxygen across your alveoli into the blood vessels and/or not perfusing or getting blood flow to the alveoli, versus not ventilating or breathing enough oxygen into the alveoli. It can help you differentiate between different causes of hypoxia, or low oxygen levels in the blood.
Check out the video linked below on the Arterial Blood Gas!
Understanding The Arterial Blood Gas (Basic) - Sampling, Interpreting, Acid-Base Explained Clearly!
• Understanding The Arte...
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Awesome great teaching, thank you ❤❤❤❤❤
@WhiteboardMedicine
2 ай бұрын
Always our pleasure!
I would tell the CoVid people that there would be a morning ABG daily. I then ran their ( A-a ) gradient. In patients dying of CoVid, their gradient increases daily. I saw them into the 500's. I assessed their work of breathing daily and when this increases, it's always from decreasing compliance in the lungs. These patients actually looked like shunt patents with their refractory hypoxemia. Will you move now to " intrapulmonary shunt calculation "? Well done as always!
@WhiteboardMedicine
2 жыл бұрын
That’s actually quite interesting! Thanks for sharing. We may have to try this out. Hah! We will add it to the list!
Very interesting video! I'd love to hear you relate the use of the Aa gradient to severe Covid-19. From my limited perspective here are my thoughts: I suspect Covid-19 patients would have progressively raised Aa as their disease severity progresses. I suspect there would be diffusion due to hyaluronic acid accumulation in the alveoli. I also think there would be a VQ mismatch due to microthrombosis blocking the capillaries. Initially I think it would likely be caused by platelet agglutination and then progressing to vascular injury where VWF would trigger the clotting cascade. This would be confirmed with a delayed elevated D-Dimer. As the disease progresses I suspect there are compensatory R to L pulmonary shunts developed around the capillaries, but they won't oxygenate efficiently. I think an elevated VEGF would indicate these new pathways are being created through angiogenesis. I'm curious if closely monitoring the Aa gradient during the disease progression could be used to confirm the presence of these events and elucidate the pathogenesis. I'm still not clear on if the microthrombosis is driving the severe disease or if it's the pulmonary inflammation initially.