Let's Get to the Heart of Potassium!

In this episode, Drs. Young and Ambruso discuss not just treating hypokalemia but the importance if determining the cause with a specific emphasis on GI losses and the role the kidney plays.

Sophia Ambruso DO @Sophia_Kidney, Sarah Young MD @kidneycritic, Judy Blaine MD, Parisa Mortaji, MD

Transcript

Welcome to Kidney Essentials! 

This is A Podcast for Medical students, residents and all nephro curious practitioners at the University of Colorado and beyond. We’re here to make nephrology more accessible one podcast at a time. Let’s start with introductions: 

Sophie:  Hi, I’m sophia ambruso, @sophia_kidney on X (fomerly known as twitter). I’m a clinician education at the Denver VA and university of colorado. I have no COI.

Sarah: introduces herslef

Sophie, mission statement: Make nephrology more accessible, less intimidating, Provide concise nephrology “pearls” in each episode to help listeners understand renal pathophysiology, “Making nephrology sexy one episode at a time”

Sarah legal disclaimer: This podcast is for educational purposes only. The views and statements expressed on this podcast are soley those of the hosts. This podcast should not be used as medical advice or for treatment purposes.

Sophie..did you know we have been selected as one of the top 15 education podcasts in colorado by feedspot?

Sophie- response

When we first started this podcast  we use to start with little anecdotes about ourselves in medicine.  So I thought we should reintroduce that. Given that it is april and match just came out & medical studenst are anticipating their internship  …tell  a story about something silly u did as an intern

Sophie- paging the CT surgeon fellow to my parents house.

Me: sign out with Hillary tindle

Sophie, let’s get going with a case.  

You are consulted on a 72 year old gentleman with a history of HTN, OSA and prior arrhythmias. He is presenting with several days of severe diarrhea after starting antibiotics for a sinus infection. His appetite has been poor for several days. His stool test is +for Cdiff infection. Medicine is consulting for a critically low potassium of 2.

Sarah, is this value concerning to you?

Yes!! A potassium of 2 is not normal! far from it. It is important to emphasize that a low K is NOT a diagnosis per se but a result of another disease process…so we need to both address the low k and discover the underlying problem. Hypokalemia is one of the most common electrolyte abnormalities and we do not want to get into the habit of just buffing it without understanding it…. But in this patient with a h/o of arrhythmias treatment is essential

Sophie: I’d like to spend a little more time on what level of potassium we should be worried. We know there is a higher risk of complications  if K<2.5, sarah what specifically do you worry about when you see a k of <2.5 

1. hypokalemia is defined as: < 3.5 mEq/L. < 2.5 is considered an emergency
   1. it is an emergency b/c of the risk of arrhythmias (the heart is an important organ…I hate to admit it and don’t tell any of our cardiology friends that)
   2. low k can also contribute to respiratory muscle weakness🡪 this is particularly concerning in somebody who may have an acidosis (idk maybe from diearrhea) and has increased work of breathing🡪resp weakness🡪decreased ventilation🡪 exacerbation of their acidosis

Sophie:

I don’t think hypokalemia is given the respect it deserves, too often we see providers simply replace potassium without taking the time to identify why it is low. Compared to hyperkalemia, It seems like an easier fix to just replace potassium rather to understand it. But hypokalemia is equally dangerous.…. In addition to respiratory weakness as Sarah mentioned it can, lead to GI motility issues like ileus/constipation, and even rhabdomyolysis. It also has serious cardiac implications where naturally it impacts the action potential and predisposes the myocardium to arrhythmias and cardiac arrest. The risk of arrhythmias is worse if the hypokalemia is severe and it develops rapidly

Sarah: Lets expand on that a bit, just to remind people the interior of heart muscles are negative, often referred to as “polarized at rest”, when they are depolarized their interiors become positive (na entering cell) and the myoctytes contract. Depolarization may be considered an advancing wave of positive charged heart cells, repolarization is them returning to negative charge. Potassium is a critical electrolyte in repolarization and in maintaining a precise resting potential (negative charge inside the cell) .  The major determinant of how negative a cell is, is determined by the ratio of K in the cell to the K outside of the cell. When k is low in the serum, the cell is initially more negative but  the Na channels are activated and more Na enters the cell, making them less negative and increased membrane excitability

So sophie what does the EKG look like in hypokalemia?

Sophie: Before we move on Sara, you’re saying that low serum hypokalemia hyperpolarizes the cell by increasing the resting potential which in turn increases myocardial excitability??

sarah: Yes

Sophie: I want to highlight here that while we always worry about hyperkalemia and irregular rhythm, it is hypokalemia is more likely to cause arrhythmias

ECG changes in hypokalemia include:

Flattened T wave🡪 can even be inverted

U waves,which is a a u-shaped wave immediately following the T-wave

ST segment depression and QT prolongation.

A low k makes the myoctyes very irritable and can lead to to torsades de pointes and other tachyarrythmias

It also increases the toxic effect of digitalis. REmember that digitalis blocks the sodium/potassium ATPase that maintains high intracellular potassium and low intracellular sodium. importantly, it binds at the site of potassium and if potassium levels are low, digoxin can more easily bind to the ATPase.

Finally, The effect of potassium on neuromuscular transmission is clinically important because it accounts for the muscle weakness and arrhythmias that complicate a low k

Dig… That’s a drug we don’t see a lot of anymore used to use a lot back when I trained but see a lot less of it now 2/2 its toxicity

I think of the t wave as a tent for K+ so when the tent is full in hyperkalemia you peak your t’s but when you have no K they are flat or even inverted

Our patient’s  EKG shows sinus tachycardia but otherwise no findings c/f hypoK. So we know this patient has a critically low potassium. He has already gotten some repletion in the ED. When I see a patient with hypokalemia I always think about 4  big categories or mechanism for hypokalemia: 

1. Decreased intake, 2. Transient intracellular shifting, 3. GI loss, 4. Urinary loss. 

Since our patient is able to tell us he has had poor po intake for several days and diarrhea,  lets focus in on how those 2 mechanisms may be contributing to hypokalemia in this patient- sophie you want to start us off

Sophie…So, normal intake of potassium is variable, but approximately 40-120meq/day. Decreased intake as the sole cause of hypokalemia is incredibly rare because the kidney is so effective at reducing urinary excretion. In addition, because the majority of potassium is intracellular, we have large total body stores of potassium. We’d have to see prolonged, chronic poor intake to deplete our potassium stores to extent that it would manifest in the serum. Populations I think about are  alcoholics & severe anorexia. I think it’s safe to say that in the majority of instances, intake is a contributor to hypokalemia but there’s usually another process going on to cause clinical and serological hypokalemia.. Given his h/o diarrhea, I’d consider this at least one of the contributing factors.

Sarah , what are you thoughts on his GI losses?: 

This is a very common cause of hypokalemia and I think about 2 different categories of GI loss

1. Diarrhea- true gi loss
2. Vomiting/ NGT which we see a lot of in the hospital

These GI causes of hypokalemia actually have very different mechanisms and you can often tell which is the primary contributor based on a chem 7. Diarrhea is associate with a NAGMA and vomiting or NGT is associated with alkalosis

Lets start with diarrhea. So approximately 3-6L of gastric, pancreatic biliary and intestinal fluid is released into the GI tract everyday all of which aside from 100ml-200ml h20-is reabsorbed and about 5-10meq of potassium. But if from disease in the gut, the secretions cannot be reabsorbed or there are more secretions you can lose a lot of fluid and potassium.

Hypokalemia is more common if the diarrhea is chronic or acute/massive. Cholera the classic example of hypokalemia from diarrhea, these patients lose on avg 8liters of water, 1000meq of Na and 130meq of potassium. However most diarrhea in the US does not lead to that much potassium loss and increased fecal losses cannot explain all of it (usually it is diarrhea PLUS decrease intake PLUS urinary losses etc)

So what about vomiting or NGT suction, how does that lead to hypokalemia..sophie you want to take that one?

Yeah so this is really fun mechanism and rather complex!!. We see a lot of hypokalemia with persistent or chronic gastric secretions. Importantly, though, while some potassium is lost in the emesis (vomit), the greatest potassium loss is from the kidney, surprisingly.

We know that chronic emesis/vomiting results in a metabolic alkalosis and the process by which this occurs begins with the  high volumes of HCl loss from gastric fluid. Put simply, every HCl hydrogen ion secreted and lost in vomit results in the absorption of bicarbonate in the blood resulting in a metabolic alkalosis. 

There are two separate mechanisms that contribute to the potassium loss 

1. a metabolic alkalosis results in a high filtered bicarbonate load which exceeds our the ability to reabsorb it. As a result the bicarbonate drags sodium with it, increase distal tubular sodium delivery results in potassium excretion and increased K loss in the urine. However, this isn’t the end of the story. 

2. The chronic hypovolemic state in longstanding volume losses from gastric secretions causes a secondary hyperaldosteronism, whereby the patient’s RAAS is appropriately stimulated signalling the release of  aldosterone, which is aimed to increase sodium absorption and potassium secretion. This is also the maintenance phase of a metabolic alkalosis, a topic we’ll have to cover in future podcasts.

So we should not really blame the kidney I mean its really the gut that caused all the problems the kidneys just trying to do the best it can in a lose-lose situation?

Absolutely! Help the kidney out, give it some nacl and it will sort it all out eventually!

Okay so in conclusion it seems diarrhea + poor intake were likely together responsible for the hypokalemia in our patient.  Next podcast we will review urinary losses or transient intracellular shifts as causes of hypokalemia but lets talk about how to manage our patient

So how are we going to do that ? 

• Tele monitoring  (this is very important)
• Oral or IV repletion with potassium chloride 
• Treat the CDiff and volume resuscitate 🡪 turn off any aldo which might be impairing his ability to drop his Uk

Summary learning points: 

• hypoK: <3.5, s/sx depend on acuity and amount of drop in potassium
• don’t blow off hypokalemia it has serious effects on cardiac polarization and irritability
• main clinical manifestations: muscle weakness, typically starts distally and moves up, arrhythmias, remember EKG findings: Flattened T wave, U waves, QT prolongation 
• major causes: 1) decreased PO intake, 2) transient intracellular shifting, 3) GI loss, 4) urinary loss 
• GI losses and decreased po intake usually are one of many factors contributing
• treatment: replete K, replete Mg, tele, hold potential offending medications, treat underlying cause