Peak your Ts, flatten your Ps, widen your QRS: The ABCs of hyperkalemia

In this episode, Drs. Mortaji, Ambruso and Young discuss the nuances of hyperkalemia diagnosis and management.

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

Transcript

Title: Peak your Ts, Widen your Ps and Flatten your QRS: The ABCs of hyperkalemia

So today we will be talking about hyperkalemia. We will address the following learning objectives: 

• Define acute hyperkalemia
• List the most common etiologies and understand the physiology behind them 
• Familiarize yourself with EKG findings associated with hyperkalemia 
• Approach to management of acute hyperkalemia 

Parisa, let’s get going with a case.  

Mr. Kali is a 72 yo M with T2DM, HFrEF with EF 35% on losartan, spiro, and Lasix, presents with 2 days of nausea, vomiting, and diarrhea. States his 2 grandchildren recently visited him and had some kind of illness. He thinks he might have gotten sick from them. His RVP is +for influenza A. On lab testing, his K is 6.6 (confirmed on repeat analysis). We will stop there for now and circle back to our case in a little bit. let’s back up real quick and lay some basic foundation for hyperkalemia.

 Sarah, what is a normal potassium level to you? 

3.5 - 4.5. however in patients with CKD up to 5.5 is acceptable (?)

What types of signs and symptoms can we see? 

Muscle weakness (note can lead to diaphragm paralysis and respiratory failure), paresthesias, and most concerning obviously conduction abnormalities

Note: patient can be completely asymptomatic but have EKG changes that are life threatening thus symptomatology does not correlate with need for emergent management 

The ED resident tells us that the patient denies any muscle pain, weakness, or palpitations, but it sounds like that shouldn’t stop us from being worried and we should definitely get a stat EKG. 

What are some EKG findings associated with hyperkalemia? 

1-peaked T wave 

2-prolonged PR

-flattened P wave  flattening 

-depressed ST segment 

3-widening of QRS 🡪 until it merges with T wave to give us: 

4-eventually sine wave pattern

Okay so now that we know what we are looking for: Mr. Kali’s EKG shows flattened P waves and some peaked T waves.  How does this affect the way you think about the case? 

Patient is asymptomatic –  but his flattened P waves and peaked T waves are concerning for cardiac conduction abnormalities, so overall his case is more alarming and would require emergent treatment. 

Okay before we get into treatment, let’s back up and think about etiologies. How can we think about causes of acute hyperkalemia?

1) pseudohyperkalemia  

2) increased release from intracellular to extracellular space 

3) imbalance between potassium intake and excretion (i.e., increased intake, or decreased urinary excretion) 

What leads to #1 pseudohyperkalemia? 

potassium released from cells after phlebotomy. 

#1 cause – “hemolyzed sample,” aka release from damaged RBCs.  

#2 cause – severe leukocytosis, typically >70K, or thrombocytosis (500 – 1,000k) 

More data from our patient: BMP states K was confirmed on repeat testing and no mention of hemolysis, WBC 6.3 and platelets 250 so represents true hyperK 

What leads to scenario #2: increased release from cells? 

1. #1 to think about that is very common: Hyperglycemia / DKA: Lack of insulin / hyperosmolality lead to potassium shift out of cells, despite significant urinary potassium loss.  Our guy has normal glucose, no h/o DM 

What other causes did you want to add Sophie? 

1. metabolic acidosis – H+ moves into cell, K+ moves out to maintain acid-base balance (does NOT occur with lactic acidosis or ketoacidosis)  -> his HCO3 is 18 so this may be contributing 
2. Drugs: Nonselective beta blockers, Digoxin overdose & Mannitol  
3. RBC transfusion, due to potassium leakage out of the red cells during storage

More patient info: , glucose 150, HCO3 18 with gap of 14. His UA is bland. 

What leads to scenario #3: decreased urinary excretion? 

1. Urinary obstruction – check PVR in all patients!! 
2. AKI – More likely than CKD to lead to severe hyperK (less time for adaptive mechanisms to occur)
3. CKD 

One that is very common....

1. Meds that affect the RAAS system and thereby decrease urinary potassium secretion 
   1. ACEI/ARB, CNIs, heparin, NSAIDs, K+ sparing diuretics, ARAs 

So circling back to our patient, we already know patient is on losartan and spiro. Some more lab data: UA is bland. PVR is 750. his Cr is Cr 2.4 (baseline 0.8) – so with this in mind, he most definitely has decreased urinary K excretion 

What leads to scenario #3: Increased intake?

*note excess intake usually does not cause hyperkalemia in otherwise healthy patients as kidney will usually compensate by increasing excretion. Usually patients have some underlying impairment in renal excretion*

Common sources of increased intake: Salt substitutes, potassium supplements, TPN or other enteral nutrition, 

Common foods: Avocado, spinach, potatoes, oranges, bananas, coconut water, dried fruits 

Thankfully Mr. Kali is not big into fruits and vegetables and denies taking K supplements or using salt substitutes. 

What test can we use if not obvious from clinical presentation to help us sort out whether there is an intrarenal or extrarenal process leading to hyperk? 

If there is ambiguity, can usually be done with history and 24 hour urine K+ collection 

Renal: <20-30 mmol K+ excretion / day 

Extra renal: >40 mmol/day 
(do we need to stop certain meds before measuring urine potassium?) 

So Sarah how would you summarize what we think is causing hyperkalemia in our patient now that we have all the data? 

Likely multifactorial: AKI (likely pre-renal from continued use of Lasix in s/o GI losses), worsened by use of spiro / losartan, metabolic acidosis, urinary retention

Okay let’s move on to the fun stuff, management of ACUTE hyperkalemia: Sophie what is your general approach? 

If EKG changes -> treat emergently 

If no EKG changes -> check for pseudohyperK (hemolysis on labs? Redraw) 

If real hyperK: determine etiology

Is there a certain potassium cutoff  that we use to determine need to treat?  

not well defined, general guidelines: treat immediately for K >6 with associated EKG changes or K>6.5 regardless of EKG findings, symptomatic. Especially true for acute hyperK rather than chronic hyperK (e.g. in s/o CKD where patient has had time for adaptive mechanisms to occur) 

Okay so when thinking about treating acute hyperkalemia, there are 3 goals I like to keep in mind generally speaking: 

Goal 1: stabilize cardiac membrane 

Goal 2: increase intracellular uptake to rapidly decrease serum potassium 

Goal 3: more long term, excretion of excess potassium from the body 

Would you all have anything to add to that? 

Yes also keeping in mind many times treatment depends on clinical situation: 

e.g. if AKI, give IVF 

if urinary retention, relieve obstruction with understanding that correction of hyperK can lag a bit and continued BMP monitoring is indicated 

That’s a great point Sarah, thanks for bringing that up. So let’s start with goal 1: stabilizing the cardiac membrane: 

1. Calcium chloride gluconate to stabilize cardiac myocytes and prevent arrhythmias when EKG changes are present 

    1. Repeat dose if EKG changes persist or recur 

    2. Note difference between gluconate and chloride: calcium chloride does not require liver metabolism to be released and has more rapid effect upon infusion, however first line is usually calcium gluconate  

Thankfully the ED has given our patient 1g calcium gluconate and 1L IVF. However, an hour later, his potassium is still 6.4 and EKG changes are improved but still with peaked T waves. Would you recommend an additional dose of calcium gluconate? 

Yes, effect lasts **1hour? So should be re-dosed. 

Moving on to goal 2 of treatment: Sarah, can you walk us through how we shift potassium intracellularly to rapidly decrease serum potassium? 

    1. Insulin +D50: effect can last about 4-6 hours. Usually we give 10 units regular insulin and amp D50. 

    2. Albuterol- about 25% non response rate with nebs; and can cause tachycardia; also dose required is much higher than standard neb dosing used for other indications (2-8X higher) 

    3. Bicarb - should not be used unless patient has acidosis (pH <7.2); overall minimal effect on hyperK 

Looking through the MAR, the ED has not used any shifting agents for Mr. Kali. It sounds like we should give him insulin +dextrose? 

Yes absolutely 

Okay, and lastly thinking of the 3rd  more long term goal, how can we excrete the excess excess potassium from the body? 

    1. Lokelma 

    2. Kayexelate 

    3. Loop or thiazide diuretics 

    4. Dialysis

Which would you recommend for our patient? 

He is volume down so would not want to use Lasix. No indications for emergent dialysis. Would use 10 g lokelma now and he will likely require re-dosing. 

Sarah can you summarize the management plan for our patient? 

Calcium gluconate indicated given EKG changes, repeat given persistent EKG changes 

Shift K intracellularly with insulin /glucose

Lokelma X1 

IVF for AKI (with caution given underlying HF) 

Foley to relieve obstructive uropathy

And don’t forget to hold his losartan, spiro, and Lasix!!

Thank you! It sounds like Mr. Kali has a lot of factors that likely contributed to his hyperK, but this is commonly what we see in the hospital rather than a single etiology so I think it’s really helpful to go through all the pillars of management for his case. Sophie can you start us out with a summary of the learning points? 

Summary of learning points: 

• Acute hyperkalemia: K>5.5, treat immediately for K >6 with associated EKG changes or K>6.5 regardless of EKG findings
• The big buckets for hyperK causes: 1) pseudohyperK   2) increased intracellular release  3) decreased urinary excretion 
• Major EKG findings: peaked T wave prolonged PR, flattened P wave, wide QRS 🡪 sine wave 
• management of acute hyperkalemia: remember to 1) stabilize cardiac membrane  2) shift K intracellularly  3) excrete excess potassium

Credits:

Sophie  for editing

Josh strong for graphics

And of course the University of Colorado division of nephrology for giving us a job!