Hyperkalaemia is a frequent issue encountered in patients with HF and is associated with increased mortality. ImageRAASi interfere with potassium homeostasis, resulting in hyperkalemia and leading to dose reduction or discontinuation of these agents, which have proven mortality benefits.

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 the 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 vary 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.

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).
    • Sodium polystyrene sulfonate
      Sodium polystyrene sulfate (SPS) is the oldest of the potassium binding resins and has been in use for the past 60 years. SPS binds to potassium ions in the intestine in exchange for sodium ions. However, the binding is nonspecific, and calcium and magnesium may also be bound. Ultimately, SPS and its bound potassium transit through the colon and are eliminated in the feces. SPS can be administered orally (15 g 1–4 times/day) or rectally (30–50 g every 6 h).