Tag: OUWB

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OUWB Question: What’s going on with this mess?

I create all of my presentations in Keynote. In the past I was able to present them in Keynote but due to construction and having to give lectures in 156 of North Foundation I had to convert the presentations to PowerPoint. And then hope that PowerPoint on the PC was mostly like PowerPoint on the one true computer, the Mac. It works surprisingly well, but this slide is an outlier.

Here is what it looks like in PowerPoint on my iMac

This is better, but how does this slide fit into the lecture? It is a summary slide after I have discussed two of the causes of the maintenance of metabolic alkalosis. Here is the slide that introduces the four mechanisms for maintaining metabolic alkalosis

Then the lecture describes kidney failure (the easiest to unsderstand)

After that I cover the mechanisms by which hypokalemia maintains metabolic alkalosis in 7 slides as seen here:

The I do the same for chloride (volume) deficiency in 7 slides:

After going through that I noted similarities between the mechanisms of hypokalemia and chloride deficiency, the summary slide is designed to highlight those. Looking at that slide now, it doesn’t do such a good job of that. Does this pair of slides work better?

Here is the revised powerpoint for you to download

Metabolic Alkalosis 2023
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You cannot tell if a respiratory acid-base disorder from the ABG

This is a frequent cause of confusion. I know that I was confused by this when I was a young learner. And I believe the source of this confusion was garbled teaching from a resident that was still struggling with the concept.

Take this ABG:

pH: 7.26

PaCO2: 80

HCO3:
39

The Henderson-Hasselbalch variables are moving in discordant directions (pH down, pCO2 and HCO3 going up) so it is a respiratory disorder. The pH is decreased so this is a respiratory acidosis.

Now look at the compensation to see if there is a second primary disorder affecting compensation.

  • In acute respiratory acidosis the HCO3 rises 1 mEq/L for every 10 mmHg the CO2 rises.
  • In chronic respiratory acidosis the HCO3 rises 3 mEq/L for every 10 mmHg the CO2 rises.

This patient’s CO2 is 80, an increase of 40, so the HCO3 should rise 4 (4×1) if the respiratory acidosis is acute, yielding a bicarb of 28 (24+4). The actual bicarbonate is 39, too high, so there is an additional metabolic alkalosis if the respiratory acidosis is acute.

If the respiratory acidosis is chronic, to increase in CO2 of 40 should increase the bicarbonate by 12 (4×3), so a bicarb of 36 (24+12). The actual bicarbonate is 39, which is just outside of our ±2 so we’ll call it nearly appropriate with just a touch of metabolic acidosis.

The ABG can be “solved” with either acute or chronic respiratory acidosis. Patients cannot be diagnosed with Occam’s razor so the simpler explanation (chronic respiratory acidosis without the need for additional acid-base disorders) may not be the right one. In medicine we need to assume Hickam’s Dictum “A patient can have as many diseases as he damn well pleases.”

The ABG does not determine whether a patient has acute or chronic respiratory disorder, the physician must do that.

So what’s my beef with the two Bruces? Take a look at this question from chapter 8…

The simple acid-base disorders are:

  1. Metabolic acidosis
  2. Metabolic alkalosis
  3. Respiratory acidosis
  4. Respiratory alkalosis
  5. Respiratory acidosis
  6. Respiratory alkalosis

But this is answers the authors expect…

Since the question stipulates that these are simple acid-base disorders, one can extrapolate the acuity of the respiratory disorder by the degree the bicarb has adjusted, a large adjustment is chronic, and a smaller change is acute. But since patients don’t tell you if they have simple or complex acid-base disorders when the blood is drawn, this trains students to expect the ABG to provide information that it cannot provide.

Stupid book.

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OUWB student question on ammonium production and potassium

How does hyperkalemia or even alkalosis suppress NH3 production?

So the mechanism is not completely worked out but the conventional explanation is…

Hypokalemia causes potassium to shift out of the cells. Hydrogen ions then move on the opposite direction into cells to maintain electroneutrality.

This causes intracellular acidosis. The intracellular acidosis causes the cells of the proximal tubule to erroneously concludes that there is systemic acidosis and so they up regfulate the production of NH4 to increase renal excretion of acid and produce new bicarbonate.

An interesting note about this happens in liver failure. Patients with liver failure are unable to metabolize ammonia and levels build up to high concentrations and can cause hepatic encephalopathy. A known risk factor for this is hypokalemia. The above paragraph provides an explanation for this.

Conclusion from a recent study on this phenomena (Ref)

Hyperkalemia works the same way but in reverse. Potassium shifts into the cells, This causes hydrogen to move out of the cells and causes intracellular alkalosis. The cell mistakes this intracellular alkalosis for systemic alkalosis and the last thing the kidney wants to do in systemic alkalosis is generate additional bicarb, so it down regulates this generation of ammonium.

Slide 97 from Monday’s lecture
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OUWB: So you’re lost in renal and looking for a map

If you are a reader and need a book to help you understand renal physiology, may I suggest:

Renal Physiology by the Bruces (Koeppen and Stanton) Amazon

It is well written and is targeted at pre-clinical medical students. We are using it for our fellow renal physiology class and I don’t love it for that (no references for one).

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OUWB: Podcasts of interest

If you are taking the M2 renal class and are looking for a way to study while cleaning, exercising, walking the dog, or commuting, allow me to suggest a few podcasts that may be of interest.

Curbsiders Podcast on rapid interpretation of ABGs

Curbsiders #104: Renal Tubular Acidosis

The Curbsiders: Hyponatremia

Curbsiders: Hypernatremia

Hyperkalemia with The Curbsiders

Channel your Enthusiasm This is an award winning podcast podcast series on renal physiology. The intended audience is nephrology fellows and clinicians so it may aim too high, but if you like podcasts and a group of experts getting together to geek out on a topic they love it may tickle your fancy.

A long list of interesting podcasts for interested medical student

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OUWB 2023: Regarding the upcoming TBL

I received an email questioning what to read in order to prepare for the the iRAT. Should students just review the PDF, or should they also review the lectures?

All of the answers can be found in the PDF, however both the lectures and the PDF cover the same material so reviewing the lectures will not hurt and may be helpful.

Here is a link to the PDF in question

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More OUWB M2 questions and Answers

The question: I am going through the real well made sodium and water guide you made and there is a concept I am having trouble with regarding ADH stimulation by decreased BP. In the text, one of the reasons that ADH release is triggered is:

Decrease in blood pressure: ADH is a potent vasoconstrictor. 10% drops in blood pressure are required to release ADH. This drop in pressure is usually due to a drop in the blood volume from volume loss but can also be due to heart failure or cirrhosis. ADH is relatively insensitive to changes in pressure, this is why it takes a full 10% drop in pressure to start to stimulate ADH.

I thought blood pressure goes up with heart failure as hypertension is a risk factor for heart failure. How do we get decreased blood pressure from heart failure? 

The Answer: Hypertension can cause heart failure. Hypertension is a risk factor for hypertension. Heart failure can present with hypotension or hypertension. Regardless of the blood pressure, heart failure can cause poor perfusion, and stimulate ADH release, with or without a low blood pressure. Sometimes the heart pumps so poorly that blood backs up in the venous circulation, this venous congestion slows perfusion since the back pressure blocks flow, even though blood pressure it good.

So the important point is that heart failure, cirrhosis and volume depletion all stimulate ADH release through decreased perfusion/blood pressure predisposing to hyponatremia.

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OUWB M2 questions and Answers

The Prince William Question

Lets do this number by numbers. This is an algorithm that will allow you to map out any acid-base question.

1. Primary disorder: pH is up (<7.4), pCO12 is down (< 40) and HCO3 is up (>24)The H-H variables are moving in discordant direction so this is an respiratory disorder, the pH is elevated so this is a respiratory alkalosis.

If you are really on the ball you will note that this breaks one of the fundamental guidelines of acid-base in that compensation is not in the same direction as the primary disorder (pCO2 and HCO3 almost always move in the same direction). This only happens when there are two primary disorders.

2. Is there a second primary acid-base disorder affecting compensation?Yes. In Respiratory alkalosis, for every 10 the pCO2 falls the bicarb falls 2 acutely and 4 chronically, so the target HCO3 is 22 for acute respiratory alkalosis and 20 for chronic respiratory alkalosis, well the bicarb did not drop at all, in fact it went up, so there is an additional primary metabolic alkalosis.

3. What is the anion Gap?148-(98+28)=22.So we did not talk about this, but the presence of an anion gap means there is an metabolic acidosis buried deep in the ABG.

4. Calculate the bicarb beforeBicarb before = HCO3 + (Anion gap -12)Bicarb before = 28 (22-12) = 38So without the anion gap the bicarb would be 38, revealing a pretty severe metabolic alkalosis, that is mostly hidden or covered up by the anion gap metabolic acidosis. The severity of the metabolic alkalosis by looking at the electrolytes without the anion gap. 

Put it all together and you have: A respiratory alkalosis, likely from the respiratory stimulant effect of feverA metabolic alkalosis from vomiting and/or some antacids he may have taken to soothe his stomach. An anion gap metabolic acidosis from the sepsis.