What is the best course of action for a patient with heart failure with preserved ejection fraction (EF) and suspected cardiorenal syndrome who developed hyperkalemia after cessation of Lasix (furosemide) due to impaired renal function?

Management of Hyperkalemia in HFpEF with Cardiorenal Syndrome

Your patient's hyperkalemia is most likely multifactorial, resulting from acute kidney injury (cardiorenal syndrome), cessation of loop diuretic therapy (which promotes potassium excretion), and potentially from any RAAS inhibitors he was taking before self-discontinuation—treat immediately based on severity while identifying and addressing reversible causes. 1, 2

Immediate Assessment and Severity Classification

Obtain a 12-lead ECG immediately to assess for life-threatening cardiac manifestations including peaked T waves, flattened P waves, prolonged PR interval, or widened QRS complexes. 2 The European Society of Cardiology classifies hyperkalemia as:

• Mild: >5.0 to <5.5 mEq/L
• Moderate: 5.5 to 6.0 mEq/L
• Severe: >6.0 mEq/L 1

Your management urgency depends entirely on this potassium level and ECG findings, not just the number alone. 3

Differential Diagnosis and Causes of Hyperkalemia in This Patient

Primary Contributors in Your Case:

Acute kidney injury from cardiorenal syndrome is the dominant factor—impaired renal potassium excretion from reduced GFR. 1, 4

Cessation of furosemide eliminated a major route of potassium excretion. Loop diuretics increase distal sodium delivery and promote potassium secretion; stopping them predictably raises potassium levels. 5, 4

Medication-Related Causes to Investigate:

Determine what medications he was taking before self-discontinuation:

• ACE inhibitors, ARBs, or mineralocorticoid receptor antagonists (spironolactone) all reduce aldosterone-mediated potassium excretion 6
• Beta-blockers impair cellular potassium uptake 1, 2
• NSAIDs reduce renal potassium excretion 5
• Trimethoprim-sulfamethoxazole blocks epithelial sodium channels 2
• Heparin (if receiving) suppresses aldosterone 2

The combination of ACE inhibitor plus potassium-sparing diuretic is particularly dangerous and can cause life-threatening hyperkalemia within 8-18 days. 7

Other Contributing Factors:

Metabolic acidosis from renal dysfunction impairs cellular potassium uptake. 4, 3

Dietary potassium intake including salt substitutes, supplements, or high-potassium foods. 5, 4

Tissue breakdown from any concurrent illness, though less likely in this scenario. 4

Essential Diagnostic Testing

Immediate Laboratory Assessment:

• Repeat serum potassium to confirm level and trend
• Basic metabolic panel: sodium, chloride, bicarbonate, BUN, creatinine to assess acidosis and renal function 5
• Arterial or venous blood gas if metabolic acidosis suspected 3
• Serum magnesium and calcium as these affect cardiac membrane stability 5

Medication Reconciliation:

Review ALL medications the patient was taking before self-discontinuation and any current medications, including over-the-counter products. 2, 5 This is critical as medication-induced hyperkalemia is often reversible.

Urine Studies (if not anuric):

• Urine potassium, sodium, and creatinine to calculate transtubular potassium gradient (TTKG) or fractional excretion of potassium to assess renal potassium handling 4
• Urine microscopy to differentiate true tubular injury from hemodynamic changes 6

Acute Management Algorithm

For Severe Hyperkalemia (>6.0 mEq/L) or ANY ECG Changes:

Step 1: Cardiac membrane stabilization

• Administer 10 mL of 10% calcium gluconate IV over 2-3 minutes (or calcium chloride if central access available) 1, 2
• Onset within minutes; repeat if ECG changes persist 3

Step 2: Shift potassium intracellularly

• 10 units regular insulin IV with 50 mL of 50% dextrose (or 25g dextrose) 2, 3
• Onset 15-30 minutes, duration 1-4 hours 2
• Plus 10-20 mg albuterol by nebulizer for additive effect 3
• Sodium bicarbonate only if documented metabolic acidosis present (poor efficacy alone) 2, 3

Step 3: Remove potassium from body

• Resume furosemide at appropriate dose once hemodynamically stable—this is essential for ongoing potassium excretion 5, 4
• Consider sodium polystyrene sulfonate (Kayexalate) 15-30g orally or rectally though onset is slow (hours) 3
• Hemodialysis if refractory, severe renal failure, or life-threatening levels 3

For Moderate Hyperkalemia (5.5-6.0 mEq/L) without ECG changes:

• Restart furosemide at a dose that balances diuresis with renal function 6
• Consider newer potassium binders (patiromer or sodium zirconium cyclosilicate) for sustained control 6
• Dietary potassium restriction to <2-3g/day, focusing on non-plant sources 1, 4

For Mild Hyperkalemia (5.0-5.5 mEq/L):

• Resume loop diuretic therapy as primary intervention 4
• Dietary modification and medication review 1
• Close monitoring with repeat potassium in 2-4 days 1

Critical Management Principles for Cardiorenal Syndrome

The creatinine bump that prompted lasix cessation must be interpreted in context. Worsening kidney function during decongestion does not necessarily reflect tubular injury—it may represent hemodynamic changes from improved forward flow. 6 In fact, successful decongestion with transient creatinine rise is associated with better outcomes than failure to decongest with stable creatinine. 6

Resuming diuretic therapy is essential for both volume management and potassium control in this patient. 6 The key is finding the right dose that maintains euvolemia without excessive renal impairment. 6

Long-Term Prevention Strategy

If the patient was on RAAS inhibitors before self-discontinuation:

The 2025 American Journal of Kidney Diseases guidelines emphasize that RAAS inhibitor withdrawal is associated with worse outcomes, so strategies to maintain these medications are preferred. 6

• SGLT2 inhibitors reduce hyperkalemia risk by 16% (HR 0.84) and should be strongly considered for HFpEF 6
• Newer potassium binders (patiromer or sodium zirconium cyclosilicate) enable continuation of RAAS inhibitors with 37% reduction in hyperkalemia (HR 0.63) 6
• Switching from ACE inhibitor to sacubitril/valsartan reduces severe hyperkalemia by 27% (HR 1.37 for enalapril vs sacubitril/valsartan) 6

Monitoring frequency:

• Check potassium every 2-4 weeks initially after medication adjustments 1
• Then every 1-3 months once stable 1
• More frequent monitoring if eGFR <30 mL/min/1.73m² 1

Common Pitfalls to Avoid

Do not permanently discontinue RAAS inhibitors for hyperkalemia without attempting potassium-lowering strategies first—this worsens mortality and morbidity. 6, 8

Do not assume absent ECG changes mean safety—atypical or absent ECG findings do not exclude the need for urgent intervention. 3

Do not use sodium bicarbonate alone for hyperkalemia—it has poor efficacy as a single agent and should only be added if metabolic acidosis is documented. 2, 3

Do not overlook the combination of ACE inhibitor plus potassium-sparing diuretic—this can cause life-threatening hyperkalemia rapidly and should be avoided. 6, 7

Do not stop diuretics indefinitely for mild creatinine elevation during decongestion—this may worsen both volume status and hyperkalemia while paradoxically worsening outcomes. 6