Abnormalities of Potassium in Heart Failure

Abnormalities of Potassium in Heart Failure

Last Reviewed : 12/29/2020

Abnormalities of Potassium in Heart Failure

Jun 02, 2020   |  Ragavendra R. Baliga, MBBS, FACCShare via: 


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Ferreira JP, Butler J, Rossignol P, et al.


Abnormalities of Potassium in Heart Failure: JACC State-of-the-Art Review. J Am Coll Cardiol 2020;75:2836-2850.

The following are key points to remember from a state-of-the-art review on abnormalities of potassium (K+) in heart failure (HF) patients:

  1. The K+ content and distribution among the body compartments depend on a complex interplay of multiple factors including renal and gastrointestinal function; diet, medications, and supplements; neurohormonal status; and acid-base balance.
  2. Under normal conditions, the kidneys are responsible for up to 90-95% of K+ elimination, with the colon being responsible for the remainder. In the setting of chronic renal impairment, colonic K+ excretion may increase by three-fold.
  3. Because cardiac repolarization relies on K+ influx, hypokalemia lengthens the action potential and increases QT dispersion. Hyperkalemia leads to a shortening of the repolarization time, which may lead to QT interval shortening. Both hypo- and hyperkalemia may be life-threatening conditions by increasing the risk of ventricular arrhythmia and sudden cardiac death.
  4. Dyskalemia in HF has important prognostic implications. Critical comorbidities include chronic kidney disease (CKD), diabetes mellitus (DM), frailty, and aging. Relevant drugs include loop and/or thiazide diuretics, mineralocorticoid receptor antagonists (MRAs), angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) or angiotensin-neprilysin inhibitors (ARNi), and beta-blockers. All of these treatments may cause K+ alterations resulting in either hypokalemia or hyperkalemia.
  5. In HF, as in other conditions, for example, myocardial infarction, hypertension, kidney disease, or in the general population, the relationship between K+ concentrations and adverse outcomes appears to be U-shaped, where both low- and high- K+ levels are associated with adverse outcomes, although it remains unclear to what extent dyskalemia is a risk factor itself versus a risk marker representing the patients’ overall clinical status, other comorbidities, and/or use or nonuse of HF medications. Correction of both hypokalemia and hyperkalemia offsets their associated risks.
  6. Clinically relevant hypokalemia (<3.5 mmol/L) is not very common, but it is independently associated with a higher event rate. Aldosterone antagonists lessen the risk for hypokalemia and part of their therapeutic effect may be explained by reducing the risk of hypokalemia. The fact that hypokalemia is associated with mortality even after extensive adjustment and that risk is ameliorated when hypokalemia is corrected suggests that hypokalemia is indeed causative rather than a mere risk marker.
  7. Hyperkalemia in HF is often associated with the use of renin angiotensin aldosterone system inhibitors (RAASi) (ACE inhibitors/ARBs/MRAs) including the use of the ARNi sacubitril-valsartan, and also older age, DM, and CKD (i.e., the patients who most benefit from RAASi). Hyperkalemia is a risk marker of concomitant conditions such as CKD. Hyperkalemia leads to stopping of RAASi that may have adverse consequences. The severity of hyperkalemia is usually classified as mild (5.0-5.5 mmol/L), moderate (5.6-6.0 mmol/L), and severe (>6.0 mmol/L). The threshold risk for the development of hyperkalemia-associated. arrhythmic emergencies and death varies widely between patients. It is often stated that the rapidity of change rather than the absolute K+ level leads to rhythm disturbances. However, data are not conclusive and this assertion can be questioned based on an observational association showing that even mild hyperkalemia is associated with worse outcomes.
  8. Management of Hyperkalemia K+ (>5.5 mmol/L): Assess the possibility of hemolysis; initiate a diuretic or increase its dose (if necessary); eliminate K+ supplements, nonsteroidal anti-inflammatory drugs, and decrease K+ rich foods; replace ACE inhibitors/ARBs by sacubitril-valsartan (if not yet done); adapt MRA dose (if necessary); consider a K+ binder (do not stop RAASi).
  9. Management of Hypokalemia K+ (<4.0 mmol/L): Stop thiazides (prefer loop diuretics for congestion relief); initiate MRA (or increase dose, if already taking one); increase ACE inhibitor/ARB dose to guideline-recommended targets; monitor K+ and creatinine.
  10. A serum K+ level <3.5 to 4.0 mmol/L may portend a similar death risk as a K+ level >5.5 to 6.0 mmol/L. Based on current observational data, it seems prudent to maintain serum K+ concentration between 4.0 and 5.0 mmol/L.

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