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Recurrent HyperK in HF
Recurrent Hyperkalemia in Heart Failure

Released: December 06, 2023

Ileana L. Piña
Ileana L. Piña, MD, MPH, FAHA, FACC, FHFSA
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Key Takeaways
  • RAAS inhibitor dose reduction for patients with heart failure experiencing recurrent hyperkalemia worsens morbidity and mortality.
  • When an individual’s potassium is persistently above 5.5 mEq/dL, you may want to consider adding a potassium binder to manage recurrent hyperkalemia.

Why do patients with heart failure (HF) experience high rates of recurrent hyperkalemia?
When we think about hyperkalemia and recurrent hyperkalemia in the setting of HF, we know that our RAAS inhibitors are the culprit. If we go back in history and look at the trials that evaluated angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers—such as the 1991 SOLVD trial, which evaluated enalapril in patients with reduced ejection fraction—we see that the enalapril arm had a statistically significant increase in potassium compared with placebo. In the 2004 CHARM trial, which evaluated candesartan in patients with reduced ejection fraction, we again found a statistically significant increase in potassium for those receiving candesartan. In the RALES trial, which evaluated spironolactone in patients with reduced ejection fraction, we again saw a statistically significant increase in potassium. Through all these trials and more, we know that RAAS inhibitors improve HF morbidity and mortality, but they absolutely result in recurrent hyperkalemia. Hyperkalemia can also be perpetuated by chronic kidney disease, which is also very common in the heart failure population.

How should we manage recurrent hyperkalemia?
When patients experience recurrent hyperkalemia, we may be tempted to discontinue or decrease RAAS inhibition. However, I have been saying for years that when you remove the RAAS inhibition, patients decompensate. In my experience, a patient’s serum sodium begins to drop within 2-3 days. To me, this is the first sign of RAAS inhibitor withdrawal and worsening HF. This occurs due to a rise in angiotensin II, aldosterone, and vasopressin, which leads to increased volume retention and dilutional hyponatremia. Your patients pay the price when RAAS inhibition is down-titrated or discontinued. If these drugs are discontinued permanently, it is as if they were never started from a mortality benefit standpoint, whereas for a patient who maintains RAAS inhibitor therapy, mortality and readmissions are reduced significantly.

Because of the benefit we see with RAAS inhibition in our patients with HF, we have to find a way to use these agents and overcome the increase in potassium. So, how can we maintain RAAS inhibitors without putting our patients at risk of life-threatening arrythmias? We need to optimize guideline-directed medical therapy, and we need to consider adjunct medication therapy with a potassium binder. Our oncology colleagues do this all the time—they give chemotherapy and anti-emetics in combination to minimize adverse events because they realize they need to maintain treatment at target doses of chemotherapy. In HF, we need to adopt this thinking and add another drug (i.e., a potassium binder) to enable RAAS inhibition.

There is now a class 2b recommendation for the use of potassium binders in our American Heart Association/American College of Cardiology/Heart Failure Society of America HF Guidelines, and we need to ensure that we are using them when appropriate. There are several different ways to approach the addition of a potassium binder. The HF guidelines recommend adding these agents on at a potassium of 5.5 mEq/dL. Personally, I pull the potassium history and look at the trend. I usually see persistent elevations in patients who are older, have chronic kidney disease, or have diabetes. If it is an individual whose baseline potassium is 5.3-5.4 mEq/dL and who has a new diagnosis of HF, I will sometimes preemptively initiate a potassium binder, knowing where we are going as soon as we add RAAS inhibition. Baseline and the clustering of comorbidities is important, as is the pathophysiology of what is going on in the kidney and the estimated glomerular filtration rate. If the estimated glomerular filtration rate is the lower side, I may start a potassium binder slightly before 5.5 mEq/dL. My cutoff varies according to the risk. In a general patient who is not high risk, I am comfortable with a potassium anywhere between 5.0-5.4 mEq/dL, and I am sometimes even comfortable with 5.5 mEq/dL. However, if it exceeds 5.5 mEq/dL, I watch their labs very closely to determine the optimal time for initiation of a potassium binder.

Your Thoughts?
Join the discussion below by leaving a comment and answering the polling question, or view the webinar from the Heart Failure Society of America 2023 session on hyperkalemia and HF.

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How often are you initiating potassium binders in your patients with HF to facilitate RAAS inhibition?

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