So kind of you :) I'm glad you found the video useful!

Yes! So to understand the concept of reciprocal changes, you'll have to be familiar with the direction (vector) that each of the leads are pointing to. In the video example at 19:35, the ECG wave drawn roughly represents what we would expect to see in lead II. If we were to take the same MI scenario but looked at how lead aVR (which roughly points in the opposite direction as Lead II) would have looked like, the ST segment would actually look like a depression since the constant "noise" that shifted the ECG wave downwards in lead II would have shifted the ECG wave upwards in lead aVR. The ST depression seen in aVR would be considered a reciprocal change to the ST elevation seen in lead II. Essentially reciprocal changes are ST depressions seen in the leads pointing in the opposite direction of the leads that have ST elevations. A real life example of a full-thickness inferior wall MI, the overall "noise" vector ends up being pointed away from the inferior (downward) pointing leads (II, III, aVF), so you see ST segment elevations in those inferior leads (II, III, aVF). Instead of looking at that overall "noise" vector as pointing AWAY from the INFERIOR direction, you can say that the "noise" vector is pointing TOWARD the SUPERIOR direction. Therefore the ECG waves in the leads pointing upwards in the SUPERIOR direction (I, aVL) will show ST depressions. You'll notice that lead I is not actually pointing downward (it's rather pointing horizontally) but still shows ST depression in this case since likely the "noise" vector in an inferior wall MI is pointing away from somewhere in between leads III and aVF (not exactly pointing downward 90 degrees). Hope that helps clear that up?

Very true!

The PAO2 that's noted in the equation is the alveolar O2 left in the alveoli once the inhaled O2 that was destined to enter the blood has gone into the blood. Maybe it might be more intuitive if we rearrange the equation so it's like PIO2 = PAO2 + PO2delivered to blood. The total inhaled O2 (PIO2) will either stay in the alveoli (PAO2) or will be delivered into the blood (PO2delivered to blood). The output O2 (PO2delivered to blood) is calculated by seeing how much CO2 is in the alveoli since there's the specific exchange ratio between CO2 and O2. The inhaled CO2 is almost zero so all the CO2 seen in the alveoli essentially all came from the blood.

@@medrounds101 Thank you so much! But I feel the PaCO2 should be drawn from the VBG instead of the ABG since VBG has CO2 rich blood and that CO2 in VBG is what is going to be readily picked up by aveoli? Also I feel the PO2 delivered to blood can also be drawn from ABG directly because it's O2 rich blood and the PaO2 reading from ABG should reflect the PO2 delivered to blood? Sorry about all the questions....and again thank you so much for making these videos!

I've had some brilliant teachers and also happened to come across this, essentially, basics of cardiology book a while back that went though some concepts of electrophysiology and echocardiograms. It was in Japanese, and I can't quite remember to title at the moment but I'll come back to mention it if I find it. I have been recommended "The only EKG book you'll ever need" by Malcolm Thaler a lot but I personally have not had the opportunity to go through that yet.

​@@medrounds101 I have a copy of that book I found online so ill definitely give that a look too. Thanks a bunch for this video and the response.

It's definitely a tricky concept to grasp! If we were met in a euvolemic hypoosmolar hyponatremia due to potomania, it means we're taking in a lot of extra free water when the serum osm is already really low. In that scenario, our kidneys would want to excrete lots of free water to keep the serum osmolarity from going down any further. ADH would be very low to accomplish this. RASS would probably be hanging around in a happy medium since we're euvolemic. Regular kidneys can dilute urine a lot so they can dump all that free water we just took without losing too much sodium with it. With impaired kidneys with less ability to dilute, in order for the impaired kidneys to accomplish getting rid of the same amount free water that was consumed, more sodium would be lost compared to normal (urine osm would be low..but higher than the urine osm of a healthy kidney).

@@medrounds101amazing! When you have time, could you make videos about understanding ventilator settings? And also concepts about intrathoracic pressure and stuff 😅😅😅

I'm glad you found it helpful :)

Thank you so much! I'm not aware of a condition that would do that... if there is one, I'd love to hear about it!

Good luck on your exam!

EXACTLY!!! You said it all

Hey! Thank you so much :) I'd love to, but unfortunately I currently don't quite have the time... I will be making more at some point though!

Haha very kind of you. Much appreciated :)

Thanks so much! Really appreciate it :)

I'm glad you found it useful!!

So happy you found it useful!!

i agree 1000% 😂 thank you for making this video and sharing with us

Really happy you found it useful!!

+

Great question! TLDR; can’t really say what the overall urine Na osm would be… And I apologize in advance as I was probably not as clear in the video as I wanted to be on the renal failure part. So first, in terms of the tea and toast syndrome, the urine osm should be high, like you said, but it’s harder to predict how the urine Na osm will be (it usually is on the lower end though). In tea and toast, kidneys are happy on a volume perspective so RAAS isn’t working hard to maximally reabsorb or dump Na; therefore, the urine Na won’t be low to the extent of pre-renal physiology. Now with the kidney disease picture mixed in, we can’t necessarily put a blanket statement saying the overall urine Na osm will be at the “pre-renal level” of low urine Na or higher than that. That’s because it’ll really depend on how poorly perfused the kidneys are (and thus how hard RAAS is working) and the kidney’s ability to even respond to RAAS to increase Na reabsorption since that ability is blunted/damaged in the setting of renal failure. Hope that adequately answered your question.

@@medrounds101 This makes total sense. So basically, with the renal failure picture, even though the low oncotic pressure will cause third spacing --> hypovolemic state, the RAAS system may not work at full capacity due to poor renal perfusion in setting of renal failure, so it may not be able to absorb Na to retain water as healthy kidneys can. So even though for serum it is still hyponatremia, the net effect for urine Na concentration will be hard to predict? Thanks!

@@medrounds101 also just to clarify, I imagine the urine Na will be low in tea and toast syndrome when pt has healthy kidneys due to body trying to dilute urine VS urine Na will be unpredictable in tea and toast syndrome when pt has renal failure: on one end, d/t renal failure, pt will need more Na to get rid of same amount of free water as in a pt without renal disease, on the other, poor perfusion in kidneys affect RAAS's full capability to retain water in the low oncotic pressure induced hypovolemic state, causing more Na to be lost in urine, thus might potentially be high Na in urine in pt with renal failure who also experiences tea and toast? Hope I am making sense and sorry about the long messages. I am very intrigued by this.

Yup! You got it! And when you say "high Na in urine" for patients with kidney disease, I think it'll be more correct to say "relatively higher" compared to a healthy kidney's response to tea and toast. For people with hyponatremia from tea and toast or polydipsia would correct with Na intake barring any other issues going on.

@@medrounds101 exactly my thought thank you!

Hey, great catch! You’re totally right about *loop* diuretics usually causing hypernatremia because of the way they basically destroy the sodium gradient talked about at 3:04 (since the NKCC transporter largely contributes to making this sodium gradient in the kidneys). By destroying the gradient, the kidney basically can only produce hypotonic urine compared to normal, leading to HYPERnatremia. I should have specified a little more on the specific diuretics (mainly thiazides) that are the usual culprits of hyponatremia. Because thiazides work similarly to loop diuretics in the sense that they also contribute to more sodium loss compared to normal BUT don’t really disrupt the sodium gradient the kidneys use to reabsorb lots of free water/hypotonic fluid as mentioned in 4:02. Another thing to think about with thiazides is that, the blocking of the NaCl transporter interferes with maximal dilution of urine in the kidneys at the DCT, and thus leads to greater sodium loss compared to normal which can lead to hyponatremia.

@@medrounds101 Thank you so much for your detailed reply! So would you say for loop diuretics, they disrupt ADH function by not allowing free water to be reabsorbed through AQP channel, causing hypernatremia and low urine Na osmo? While for thiazide, they mainly work on RAAS by blocking the NaCl transporter, thus Na not going back to the circulatory system, causing hyponatremia and higher urine Na osmo? Thank you.

So yes to the effect of loop diuretics effectively blunting the reabsorption effect of free water through the AQP channels. The urine Na osm would be low in the sense that it would be lower than the serum Na osm; but if you calculate out the fractional excretion of Na (FENa), you'll see that it's >1% if there is any kind of diuretic in play. Essentially if you're on loop diuretics long enough to mess with the kidney's Na gradient, it's like you're losing more free water in proportion to Na loss (thus lower urine Na osm compared to serum Na osm), but the amount of Na lost in the urine is still greater than how healthy kidneys would behave (hence FENa>1%). I think I agree with you on the ultimate effect of thiazides but just not the part about thiazides working on RAAS. Thiazides work on the NaCl co-transporter in the DCT and not directly on RAAS. Thiazides blunt the kidney's ability to dilute urine in the DCT by acting on the NaCl co-transporter; so essentially thiazides blunt the kidney's ability to hold onto Na compared to normal, like you said. So yes, ultimately thiazides can lead to loss of bodily Na content while not affecting the free water uptake in the collecting duct which can lead to overall hyponatremia and higher urine Na osm compared to normal. Thiazides tend to do cause this problem more often with those who already have kidney dysfunction like in the elderly.

@@medrounds101 Thank you again for answering my questions! For some reason, I thought the NaCl co transporter is the ENaC that is controlled by RAAS. Your explanation cleared things up for me! Thank you so much!

Hi! I unfortunately can't really comment on that, and I'm definitely going to defer that to your physician. ECGs have to be interpreted along with the overall clinical picture, and unfortunately, it wouldn't be appropriate for me to give any evaluation (i.e. good, bad, etc) on your ECG.

I'm glad it was helpful!! :)