Hyperkalaemia with ECG Changes in Advanced CKD and Heart Failure

Potassium 6.0 mmol/L with peaked T waves is a cardiac emergency regardless of the absolute number, because the ECG change reflects membrane instability.

First-line, in parallel:

1. Calcium gluconate 10% 10–30 mL IV (or calcium chloride via a large vein) for membrane stabilisation; repeat if ECG changes persist. It does not lower potassium, so it must be followed immediately by shifting therapy.
2. Insulin 10 units with 25 g glucose IV, with capillary glucose checks for 4–6 hours (risk of late hypoglycaemia, greater in renal impairment).
3. Nebulised salbutamol 10–20 mg as an adjunct; avoid if tachyarrhythmia or ischaemia.
4. Sodium bicarbonate only if significant metabolic acidosis (bicarbonate 19 is borderline; effect is slow) - not a first-line measure.
5. Furosemide is of limited value here because she is volume-depleted; give cautious isotonic saline for the diarrhoea-related deficit rather than large diuretic doses.

Stop ramipril, spironolactone and metformin, and hold empagliflozin during the acute illness. Avoid NSAIDs and potassium-containing salt substitutes. Recheck potassium and glucose within 1–2 hours and arrange continuous ECG monitoring. Dialysis is reserved for refractory hyperkalaemia, oliguria or pulmonary oedema; most such patients respond to medical measures once the precipitant is treated.

No. Permanent withdrawal would trade a reversible, precipitated episode for a sustained increase in cardiovascular and renal risk. In heart failure with reduced ejection fraction and proteinuric CKD, stopping renin–angiotensin system blockade and MRAs is associated with higher mortality, more heart failure hospitalisation and faster loss of kidney function.

The hyperkalaemia here was driven by diarrhoea-induced volume depletion and prerenal decline in function on top of CKD G4, not by intrinsic failure of these drugs alone.

Strategy after recovery:

• Rehydrate, treat the diarrhoea, then rechallenge ramipril at a reduced dose with potassium and creatinine checked at 1–2 weeks and after each titration.
• Restart spironolactone at 12.5 mg (or defer briefly) rather than abandoning it, given the heart failure benefit; stop if potassium remains >5.5 mmol/L despite measures.
• Use a potassium binder - patiromer or sodium zirconium cyclosilicate - to enable continuation of RAAS blockade, with dietary potassium review by a dietitian.
• Continue the SGLT2 inhibitor once she is eating and drinking; it lowers hyperkalaemia risk and slows CKD progression.
• Review loop diuretic dose against volume status.

Document a shared decision and a monitoring plan, with clear thresholds for dose reduction rather than reflexive cessation.

Several issues extend beyond the acute episode.

Metformin should now be stopped permanently: it is contraindicated at eGFR <30 mL/min/1.73 m² because of lactic acidosis risk, and her function is 23. Substituting a DPP-4 inhibitor or considering insulin depends on glycaemic control and cost; SGLT2 inhibitor continuation offers renal and cardiac benefit but requires attention to volume status and genital hygiene.

Sick-day rules - written, in her language, and taught to a family member:

• During vomiting, diarrhoea or poor oral intake, temporarily hold the ACE inhibitor, MRA, diuretic, SGLT2 inhibitor, metformin and any NSAID.
• Keep drinking fluids; restart regular medicines once eating and drinking normally for 24–48 hours.
• Seek same-day review for reduced urine output, dizziness, muscle weakness or palpitations.

Other points:

• Avoid NSAIDs, potassium supplements and potassium-based salt substitutes.
• Check potassium and creatinine 1–2 weeks after any dose change and after any illness.
• Vaccination, heart failure self-management and dietetic advice on potassium.
• Explain that the SGLT2 inhibitor can cause euglycaemic ketoacidosis during illness, so it too is a sick-day drug.

The key message is that the pills are not the enemy; unmonitored continuation during acute illness is.