Disturbances in serum potassium are frequently encountered on both the floors and exams, thus making it an important concept to not only be familiar with but also understand.
In this post, I will describe the etiology, consequences, and management of potassium disturbances relevant for the medical student on wards and residents early in their training. I have found studying electrolytes quite interesting and believe that potassium homeostasis is a prime example of where a solid comprehension of the physiology and pathology is necessary for fully understanding management.
Potassium is primarily an INTRAcellular electrolyte with a normal serum range of 3.5-4.5meq/dL. Each cell is packed with Na-K-ATP-ases that regulates the intracellular/extracellular homeostasis of potassium. Several key factors impact this balance including: insulin causes Na-K-ATP-ase to drive potassium into the cells, beta agonists at higher levels stimulate potassium influx into cells, acidosis causes hydrogen ions to be exchanged with intracellular potassium resulting in potassium leaving the cell.
The kidney is a key player in potassium management and is (when healthy) very good at regulating serum potassium levels. While there are a variety of potassium rich foods in today’s diets, it is difficult to cause hyperkalemia from diet alone as the kidneys can excrete up to 4000 mEq per day. The cause of hyperkalemia most frequently comes from complications from acute kidney injury (AKI) or chronic kidney disease (CKD) where the kidneys do not properly excrete potassium into the urine. Additional causes include increased intake from intravenous (IV) fluids or total parenteral nutrition (TPN), medications such as angiotensin converting enzyme inhibitors (ACEi)s/ angiotensin receptor blockers (ARB)s and spironolactone, cellular disturbances such as rhabdomyolysis, or tumor lysis syndrome.
Hypokalemia’s etiology is usually from decreased intake and malnutrition or from GI losses. Redistribution into the cells with beta agonists can also cause low serum potassium. Less frequently, kidney loss of potassium from either diuretics like furosemide or disturbances like renal tubular acidosis (RTA)’s can cause hypokalemia.
Additionally, it should be noted that the content of the gastrointestinal (GI) loss is not the source of hypokalemia, as in, there is not enough potassium in GI fluid to cause hypokalemia. Rather, the hypovolemia caused by GI losses stimulates aldosterone secretion which in turn causes potassium loss via the collecting duct of the kidney. Additionally, this loss of volume causes increased serum bicarbonate, known as contraction alkalosis, that further prevents potassium resorption.
Potassium pathology comes from either the excess or scarcity of potassium extracellularly, measured by the serum potassium level. These changes have consequences that are most notable in the form of cardiac arrhythmias . A must know on the floors and for the boards are the EKG changes that can be seen in hyperkalemia. As potassium levels rise, peaked T waves are usually the first sign of potassium starting to impact cardiac conduction. As the levels rise further, shortening of the QT interval as well as a prolonged QRS can be seen. Something that is hopefully never seen is at extreme potassium levels, the EKG showing a sine wave.
Less frequently seen but still consequential is hypokalemia. Below serum values of 2.5 mEq/dL, severe muscle weakness occurs. As potassium can be a vasodilator during exercise and breakdown of muscle, the lack of potassium prevents vasodilation, causing low flows to muscle and possibly rhabdo. If diuretics are the cause of hypokalemia, patients can be hypotensive. EKG’s can show flattening of T waves or U waves.
Management of hyperkalemia is all about timing. A common mnemonic is “C BIG K DI.” It gives the recommended management of severe hyperkalemia and does so roughly in the order of what should be thought about.
First is the C, or calcium gluconate. Giving calcium polarizes the cardiac membrane and helps prevent an arrythmia. Giving calcium gluconate is pretty benign so if you only have a potassium without an EKG, it is usually appropriate to get the calcium before getting an EKG or as the EKG is ordered. This does not eliminate the potassium, however, and only lasts about 20-30 minutes. Additionally, if digoxin toxicity is suspected, calcium should not be given and rather, magnesium.
The next letter is B, or beta agonists. Giving an inhaled beta agonist is a fair option in treating hyperkalemia, however it must be done at relatively high doses (12mg/neb) compared to a typical nebulizer treatment and can cause tachycardia. It is not always done. Again, like calcium, this drives potassium into cells and does not eliminate the potassium from the body.
Following calcium and with or without the beta agonist is I and G which stand for insulin and glucose. Like calcium and the beta agonist, this is a quick way to get potassium out of the serum and into the cells. Typically, 10 units of insulin is given concurrently with a D50 bolus at 1 and 6 hours.
At this point I will add points of addition that are not in the mnemonic that I think should be considered during the management of potassium.
- Giving furosemide can decrease serum potassium and help eliminate body potassium via urine. It also has a relatively quick onset of action compared to kayexalate. There are 2 new potassium binders that have an onset close to when acute management tends to wear off. Patiromer and sodium zirconium cyclosilicate are 2 newer potassium binders that act as exchange resins to decrease body potassium. Typically used in the outpatient setting to manage less acute hyperkalemia, these binders can be given early in treatment with the intention of their onset being later; essentially bridging from acute treatment to stabilized serum levels.
The K represents kayexalate. A very old medication, this potassium binder works by inducing GI loss of potassium in stool. Inducing high volume bowel movements is not instantaneous and may take up to a day. Kayexalate should be avoided in patients who have obstructive bowel disease because of the risk of perforation. The two newer potassium binders, patiromer and zirconium cyclosilicate, function similarly and can also be used.
Finally, the DI represents dialysis. In extremely severe or refractory hyperkalemia, dialysis will ultimately remove the potassium from the bloodstream. It should be treated as a last resort in patients who are naive to dialysis and should not automatically be the answer in patients who are on dialysis normally.
Hypokalemia management comes in the form of potassium replacement. This can come in the form of PO or IV. PO is typically preferred because of the decreased risk of hyperkalemia. Additionally, IV administration tends to burn. However, if it is used, it is preferred to use potassium chloride as potassium phosphate can cause DKG and potassium bicarbonate can cause acidosis. Generally 20 mEq of replacement will increase serum levels by 0.25 mEq/dL. Notably, magnesium has to be at normal values for potassium to reach normal levels in hypokalemia. This is because magnesium promotes increased potassium secretion by ROMK channels in the renal distal tubules.
I highly recommend reading Dr. Topf’s handout on potassium as it gives an in depth understanding into the physiology which is key to understanding the clinical aspects of this electrolyte. It is a great resource that I used to learn about potassium and was helpful in creating this content.
Tim Chow is a PGY-1 resident in internal medicine at the University of South Florida Morsani College of Medicine and graduated from the University of Missouri- Kansas City’s 6 year BA/MD program. He is especially interested in medical education, dialysis, and wellness. In is free time, he enjoys trying new restaurants and following Chicago sports.
Asmar A, Mohandas R, Wingo CS. A physiologic-based approach to the treatment of a patient with hypokalemia. Am J Kidney Dis. 2012;60(3):492-7.
Huang, C., & Kuo, E. (2007). Mechanism of Hypokalemia in Magnesium Deficiency. Journal of the American Society of Nephrology, 18(10), 2649-2652. doi:10.1681/asn.2007070792
Weiner D, Wingo CS. Hypokalemia – Consequences, Causes, and Correction. Am J Kidney Dis. 1997; 8 (7) 1179-1188