Inpatient / nephrology

Hyperkalemia

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If You Remember Nothing Else

The most common cause of hyperkalemia presenting to the hospital is from ESRD (missed dialysis) and medications. Get an EKG and give calcium gluconate if K >6. You should give insulin 10 units with D50 25mg (if BG <250) if need to temporize and then lasix 40mg+ IV and/or lokelma 10mg TID to eliminate the K. Don't wait to see if elimination will work if there is an indication for dialysis - just do it.
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Clinical Pearls

• In vivo hemolysis is a genuine cause of hyperkalemia, whereas hemolysis in vitro either while collecting a sample or while waiting to be run is pseudohyperkalemia
• Etiologies of hyperkalemia can be separated into Redistribution Process vs Decreased Excretion
• Hyperkalemia from acute insults is usually short-lived unless the process is ongoing (hypoaldo, medications, etc.) or renal function is impaired and unable to excrete K
• K is exchanged for Na in the distal nephron - if RAAS on (hypovolemia, CHF, cirrhosis), less Na makes it to this portion, and K is not excreted in exchange for the Na 
• The resting membrane potential is ~90 mV, this is lower when there is more K outside cells which means less signal is needed to fire an action potential, leading to increased excitability and possibly arrhythmias, especially in an acute setting
• Calcium gluconate should reverse EKG changes in 5 minutes, if not, push again
• Tempporizing and redistributing K can drive the K down ~0.5-1.5 in the short term
• Elimination via furosemide or Lokelma requires urine or stool output, otherwise will need to dialyze
• The EKG does not always correlate with the actual K level - it depends in part on the chronicity of the elevation
• EKG progression - peaked T waves → increased P interval, flattening of P wave → wide QRS and BBB → sine wave → PEA/asystole/VF
• Atria are more susceptible to K, and will see p-wave flattening earlier than changes in QRS
• Remember that in DKA will be hyperkalemic since insulin is not present to push into cells, but TOTAL body K will be low, so you need to replete when less than 5.2 and hold insulin if less than 3.3
• Hypo/Hyperkalemia is one of the H’s in the H’s and T’s for causes of PEA arrest; at very high levels can lead to asystole - never a bad idea to give calcium gluconate if there is a suspicion
• Typically outpatient medicines like ACE/ARB, spironolactone, and Bactrim can all cause hyperkalemia
• Acidosis causes hyperkalemia by messing with Na/H antiporter efficacy which leads to decreased intracellular Na, which impacts the efficacy of the Na/K-ATPase, and leads to increased extracellular K, leading to hyperkalemia
• Typically outpatient medicines like ACE/ARB, spironolactone, and Bactrim can all cause hyperkalemia
• Some of the most common sources of dietary K+ are potatoes, cereals (bran products, granola), meat, and dairy (milk, yogurt). Other potassium-rich foods include avocados, bananas, leafy green vegetables (except for kale), root vegetables (beets, carrots), and tomatoes
• Type IV RTA leads to reduced ability to reabsorb sodium in the distal tubule, thus less K excretion

Trials and Literature

• NEJM Hyperkalemia Review
• Kayexalate is associated with serious GI adverse events over 30 days (0.2% of people who take vs. 0.1% who don’t) - NNH is 1000; intestinal ischemia is the most common
• Lokelma trial - NEJM 2015 - reduces K over placebo

Other Resources

• Clinical Problem Solvers - Schema for Hyperkalemia