Potassium Disorders — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr Raj Patel, 72 years old. [1]

Presenting complaint: Two days of progressive generalised weakness, mild breathlessness, and one day of confusion, brought to the emergency department by his wife. He has been unable to stand without assistance today. [1]

Past history:

• Type 2 diabetes mellitus for 20 years (currently on metformin; previously on a sulfonylurea)
• Ischaemic heart disease — anterior STEMI 6 years ago, PCI with a drug-eluting stent
• Heart failure with reduced ejection fraction — EF 30 percent on recent echocardiogram, NYHA class II
• Stage 3b chronic kidney disease — baseline eGFR 32, attributed to diabetic kidney disease and ischaemic nephropathy
• Hypertension for 25 years
• Dyslipidaemia
• Benign prostatic hyperplasia
• No known drug allergies [1]

Current medications:

• Bisoprolol 5 mg daily
• Sacubitril/valsartan 97/103 mg twice daily
• Spironolactone 25 mg daily
• Frusemide 40 mg daily
• Empagliflozin 10 mg daily
• Atorvastatin 80 mg nocte
• Aspirin 100 mg daily
• Metformin 500 mg twice daily
• Tamsulosin 400 micrograms nocte [1]

Social history: Retired engineer, lives with his wife, normally independent in activities of daily living. Does not smoke, drinks alcohol rarely. [1]

Precipitant: Five days ago he had viral gastroenteritis with vomiting and diarrhoea for two days, followed by two days of reduced oral intake. He continued all his usual medications throughout. [1]

Examination findings (trainee elicits):

• Drowsy but rousable, GCS 14 (E4 V4 M6). Oriented to name only, slow to answer.
• Dry mucous membranes, reduced skin turgor.
• HR 56, regular. BP 144/84 lying, 130/76 standing. JVP just visible at 2 cm.
• Cardiovascular: no apex displacement, no added sounds, normal S1 S2.
• Respiratory: clear, oxygen saturation 96 percent on room air, respiratory rate 18.
• Abdomen: soft, non-tender, no organomegaly, no ascites.
• No peripheral or sacral oedema.
• Neurological: generalised weakness, no focal deficits, no asterixis.
• No hyperpigmentation. [1]

Investigations:

• Venous blood gas: pH 7.28, pCO2 30, bicarbonate 16, lactate 2.1, glucose 9.4, potassium 7.6, sodium 136, chloride 102, haemoglobin 102
• ECG: sinus rhythm at 56, broad QRS at 150 ms, P waves absent, sine-wave morphology in lead V1
• FBC: Hb 102, WCC 8.2, platelets 240
• U&E pending (VBG potassium 7.6 is the working value)
• Magnesium 0.72 mmol/L (normal)
• Troponin pending, BNP pending
• CXR: clear lung fields, cardiomegaly, no focal consolidation [1]

Candidate's structured presentation (model)

Opening statement (SASPOP format): [1]

"Mr Patel is a 72-year-old retired engineer with type 2 diabetes, ischaemic heart disease, heart failure with reduced ejection fraction, and stage 3b chronic kidney disease, who presents with two days of progressive weakness and one day of confusion, on a background of viral gastroenteritis five days ago with volume depletion and reduced intake. He is on a full cardiorenal drug regimen including sacubitril/valsartan, spironolactone, and empagliflozin, which he continued throughout the illness. He is drowsy but rousable, his ECG shows a pre-terminal sine-wave pattern with a potassium of 7.6, and he has a metabolic acidosis. [1]

His main problems are:

1. Severe hyperkalaemia — potassium 7.6 — with a pre-terminal sine-wave ECG, an imminent cardiac arrest risk
2. Metabolic acidosis — pH 7.28, bicarbonate 16 — contributing to the transcellular potassium shift and reflecting his CKD
3. Bradycardia with conduction toxicity from hyperkalaemia
4. Stage 3b chronic kidney disease on a cardiorenal drug regimen — the structural and pharmacological substrate for impaired potassium excretion
5. Recent gastroenteritis with volume depletion — the precipitant, reducing distal sodium delivery and potassium excretion
6. Heart failure with reduced ejection fraction and ischaemic heart disease — the indication for his mortality-reducing drugs and the context for his cardiovascular risk
7. Acute illness on chronic type 2 diabetes — metformin held, glycaemic control to be managed, diabetic kidney disease the substrate
8. Encephalopathy — likely multifactorial, but I will assess for sepsis and intracranial events [1]

His dominant clinical threat is the arrhythmia from the hyperkalaemia. My immediate priorities are to stabilise his myocardial membrane with calcium, shift potassium into cells with insulin-dextrose, salbutamol, and bicarbonate given he is acidotic, remove potassium with frusemide and a binder, address the precipitant and review the medications, and call nephrology early. I will manage him in the high dependency unit with continuous cardiac and glucose monitoring, watching especially for rebound hyperkalaemia and for the hypoglycaemia that can complicate insulin-dextrose therapy." [1]

Investigation summary: [1]

"The venous blood gas confirms severe hyperkalaemia at 7.6 — consistent with the ECG changes, so pseudohyperkalaemia is unlikely though I will still send a repeat to be rigorous. The metabolic acidosis with a bicarbonate of 16 is contributing to the potassium shift and reflects his CKD. His magnesium is normal. His glucose of 9.4 is mildly elevated and reflects his diabetes and the stress response — I will monitor for hypoglycaemia after insulin-dextrose. His ECG sine wave is the pre-terminal pattern of hyperkalaemic cardiotoxicity and demands calcium immediately. His haemoglobin of 102 is mildly low, consistent with his chronic disease. I am sending a troponin to exclude a concurrent myocardial infarction — though the ECG changes are attributable to the hyperkalaemia — and a BNP, formal U&E, and liver function. His chest X-ray shows no pulmonary oedema, so his heart failure is compensated." [1]

Management plan: [1]

1. Immediate — the four-pillar emergency hyperkalaemia protocol:

   • ABC, high-flow oxygen, continuous cardiac monitoring, two large-bore cannulae.
   • Confirm the potassium with a repeat venous blood gas.
   • Calcium gluconate 10 mL of 10% IV over 2 to 5 minutes — repeat once after 5 minutes if ECG changes persist; re-dose every 30 to 60 minutes if changes recur.
   • Insulin 10 units of soluble insulin with 25 g IV dextrose — blood glucose monitoring at baseline, 30 minutes, 1 hour, then hourly for 4 to 6 hours (hypoglycaemia surveillance).
   • Salbutamol 10 to 20 mg nebulised — additive to insulin-dextrose.
   • Sodium bicarbonate 50 mmol of 8.4% IV over 15 to 30 minutes — because he is acidotic.
   • Frusemide 80 mg IV — to promote potassium excretion given his preserved urine output.
   • Sodium zirconium cyclosilicate 10 g TDS for the first 48 hours, then step down.
   • Hold sacubitril/valsartan, spironolactone, metformin, and empagliflozin; continue frusemide and bisoprolol.
   • Cautious isotonic saline for volume repletion (mindful of heart failure — small boluses, reassess).
   • Call nephrology and ICU early; have a clear threshold for dialysis. [1]

2. The dialysis decision:

   • Reassess potassium and ECG at 1 to 2 hours.
   • Dialyse if potassium fails to fall below 6.5, if the ECG fails to improve, if he becomes oliguric or haemodynamically unstable.
   • Haemodialysis preferred if stable; CVVHDF if unstable. [1]

3. Subsequent management and the cardiorenal trade-off:

   • Admit to high dependency; continuous cardiac and glucose monitoring.
   • Recheck potassium at 1, 2, 4, 6, then 12 hours; watch for rebound as insulin-dextrose wears off at 4 to 6 hours.
   • Once potassium controlled and acute illness resolved, reintroduce the cardiorenal drugs at lower doses with monitoring, maintaining on an oral binder (patiromer or SZC) to enable continuation.
   • Sick-day plan: hold RAAS inhibitor, SGLT2 inhibitor, and diuretics during future acute illness with volume depletion. [1]

4. Address each comorbidity:

   • Diabetes: hold metformin during the acute AKI; resume when renal function recovers; glycaemic control with short-acting insulin if needed.
   • Heart failure: maintain the GDMT as the long-term strategy; the binder is the bridge.
   • Ischaemic heart disease: troponin to exclude concurrent infarct; continue aspirin and statin. [1]

5. Prevent recurrence:

   • Sick-day rule education.
   • Long-term oral potassium binder to enable continuation of the cardiorenal regimen.
   • Close monitoring of potassium and renal function after any medication change. [1]

Examiner probing questions and model answers

Q1: "Why did this man become hyperkalaemic now, when his drugs have been stable for months?" [1]

"He has the substrate — stage 3b CKD — and the pharmacological multiplier — an ARNI, an MRA, and an SGLT2 inhibitor, all of which raise potassium. But he was stable on these drugs because his kidney function was compensated and his intake and volume were maintained. The precipitant was the gastroenteritis: the vomiting and reduced intake caused volume depletion, which reduced distal sodium delivery to the cortical collecting duct and impaired potassium secretion; the volume depletion also triggered non-osmotic vasopressin and reduced the tubular flow that drives potassium excretion. So the kidney, which was just managing to excrete his potassium load, lost its excretory capacity when the distal delivery and flow fell. This is the classic acute illness on CKD on a cardiorenal drug regimen scenario, and the teaching point is the sick-day rule — patients on an ACE inhibitor, ARB, ARNI, MRA, SGLT2 inhibitor, or diuretic should hold these drugs during an acute illness with volume depletion, and resume when eating and drinking normally." [1]

Q2: "He has a heart rate of 56. Is this from the bisoprolol or the hyperkalaemia?" [1]

"Both are likely contributing. The bisoprolol is a beta-blocker that slows AV nodal conduction, and it also contributes to the hyperkalaemia by blocking the beta-2-mediated intracellular potassium shift. The hyperkalaemia itself slows conduction throughout the myocardium — the PR prolongation, loss of P waves, and QRS widening are all conduction phenomena, and bradycardia is a recognised feature of severe hyperkalaemia. As the potassium falls with treatment, I would expect the heart rate and the conduction to improve. If the bradycardia persists after the potassium is controlled, I would reconsider the beta-blocker dose. In the acute setting I would not stop the bisoprolol — it is part of his heart failure mortality-reducing therapy — but I would monitor his rhythm and have atropine and external pacing available if he becomes symptomatic." [1]

Q3: "He is on metformin. Discuss your approach to his diabetes during this admission." [1]

"I hold the metformin immediately, for two reasons. First, he has an acute illness with an evolving acute kidney injury on top of his stage 3b CKD — the gastroenteritis, volume depletion, and hyperkalaemia all point to a prerenal component, and metformin is contraindicated in AKI because of the risk of lactic acidosis. Second, he is acidaemic — pH 7.28 — and metformin accumulation worsens lactic acidosis. I will manage his glycaemia with a variable-rate intravenous insulin infusion if needed, targeting a glucose of 8 to 12, mindful that the insulin-dextrose he has received for the hyperkalaemia will also lower his glucose. I will monitor his renal function daily. I will resume metformin only when his renal function has returned to its baseline and he is eating and drinking normally. I will also review his overall diabetes management — his HbA1c, his SGLT2 inhibitor which I have held acutely but which is cardiorenal-protective and should be resumed, and whether he needs a GLP-1 receptor agonist or insulin as his glycaemic control progresses. His diabetic kidney disease is the substrate for his CKD and his hyperkalaemia risk, so optimising his diabetes is part of preventing recurrence." [1]

Q4: "What is your sick-day rule advice for this patient at discharge?" [1]

"I would explain that the medications he is on are protecting his heart and his kidneys, and that the goal is to keep taking them long-term. But during any illness that causes dehydration — vomiting, diarrhoea, fever, poor intake — he should hold three specific groups of medications and contact his general practitioner. These are the medications that can worsen kidney function and cause potassium problems in the setting of volume depletion: his sacubitril/valsartan, his spironolactone, his empagliflozin, and his frusemide — the Sick Day Guidance covering RAAS inhibitors, MRAs, SGLT2 inhibitors, and diuretics, sometimes abbreviated as the SADMANS list. He should resume them once he is eating and drinking normally for 24 to 48 hours, and he should never stop his beta-blocker, statin, or aspirin abruptly. I would give this advice in writing, in his language, and reinforce it with his wife. I would also ensure he has a clear plan for monitoring his potassium and renal function after discharge — typically a check in one to two weeks with his GP." [1]

Q5: "What is the prognosis for this admission?" [1]

"The immediate prognosis depends on the response to the emergency protocol — if the potassium falls and the ECG normalises, his in-hospital mortality is low. The medium-term prognosis is dominated by his heart failure with reduced ejection fraction and his CKD — both are chronic progressive conditions, and each admission with hyperkalaemia or decompensation is a marker of disease progression. The cardiorenal drug regimen, properly maintained with potassium control and sick-day rules, improves his survival and reduces hospitalisations. Each episode of acute kidney injury on CKD also risks accelerating the progression to end-stage kidney disease, so preventing recurrence is part of preserving his long-term renal function. I would discuss his overall prognosis with him and his wife in the context of his values and goals of care, and I would ensure he has access to a heart failure and a nephrology service for ongoing management." [1]

Short Case

Scenario: "Examine this patient's cardiovascular system. The ECG is at the bedside."

Focused examination instruction: "This 68-year-old man is on the ward recovering from an episode of severe hyperkalaemia. Examine his cardiovascular system, look at his ECG, and discuss your findings." [1]

Systematic examination routine: [1]

1. Hands and arms: look for signs of chronic disease and fluid balance — no clubbing, no palmar erythema, no asterixis. Pulse rate and rhythm (may still have bradycardia or ectopy). Measure capillary refill. Look for an arteriovenous fistula (if a dialysis patient).
2. Face and neck: conjunctival pallor (anaemia of CKD), buccal and palmar crease pigmentation (Addison's, absent here), jugular venous pressure (volume status — low in volume depletion, high in heart failure or fluid overload).
3. Cardiovascular: apex beat (displaced in heart failure, volume overload), heart sounds (gallop in heart failure, pericardial rub in uraemic pericarditis — a CKD complication), blood pressure (hypertension common in CKD; postural drop indicates volume depletion).
4. Respiratory: crackles (pulmonary oedema), pleural effusion (fluid overload).
5. Abdomen: ascites, hepatic congestion (right heart failure), renal masses, palpable bladder.
6. Legs: peripheral and sacral oedema (fluid overload, heart failure), peripheral pulses, peripheral neuropathy (diabetes, CKD).
7. ECG interpretation: the systematic approach — rate, rhythm, axis, intervals (PR, QRS, QT), then ischaemia, then the specific patterns of potassium disorder — peaked T waves (hyperkalaemia), U waves and QU prolongation (hypokalaemia). [1]

Key signs the patient may demonstrate: [1]

• A bradycardia or ectopy from recent hyperkalaemia.
• Signs of chronic CKD — pallor, fluid overload, an arteriovenous fistula if established on dialysis.
• Signs of the underlying cause — heart failure, diabetic complications, Addisonian pigmentation.
• The resolving ECG changes after treatment — the peaked T waves may normalise, the QRS may narrow. [1]

Presentation template (how to report to the examiner): [1]

"I examined this patient's cardiovascular system with attention to fluid balance and the ECG. At the hands there is no clubbing, no asterixis, no palmar erythema, and no buccal or palmar crease pigmentation to suggest Addison's disease. The pulse is regular at 76 — improved from his bradycardic admission rate. The conjunctivae are pale, consistent with the anaemia of chronic kidney disease. The jugular venous pressure is not elevated. The apex beat is not displaced. The heart sounds are normal with no added sounds and no gallop. The blood pressure is 138/82 with no postural drop. The chest is clear with no crackles. There is no peripheral or sacral oedema, and the peripheral pulses are present and symmetrical. There is no arteriovenous fistula. [1]

In summary, this patient is volume-replete, with no signs of fluid overload or depletion, and no signs of an oedema-forming state. The pallor is consistent with the anaemia of chronic kidney disease. The ECG shows sinus rhythm with normalised QRS duration and resolution of the peaked T waves, consistent with treatment of his recent severe hyperkalaemia. My differential for the underlying cause centres on his stage 3b chronic kidney disease and his cardiorenal drug regimen — the sacubitril/valsartan, spironolactone, and empagliflozin — with a recent gastroenteritis as the precipitant." [1]

Discussion questions: [1]

Examiner: "What ECG findings would have indicated a higher risk at presentation?" [1]

"The sine-wave pattern — a continuous sinusoidal trace where the QRS and T wave merge — is the pre-terminal pattern and indicates imminent ventricular fibrillation, asystole, or pulseless electrical activity. A broad QRS above 120 milliseconds, the loss of P waves, a bradycardia, and escape rhythms are all high-risk features. The peaked T wave alone is an earlier sign and does not carry the same immediacy, though any ECG change in a hyperkalaemic patient warrants calcium. The important caveat is that a near-normal ECG does not exclude dangerous hyperkalaemia — I treat the number and the patient, not the ECG alone." [1]

Examiner: "How would your management change if the ECG had been normal but the potassium was 7.6?" [1]

"The management is the same in principle — a potassium of 7.6 is severe hyperkalaemia regardless of the ECG, and the risk of arrhythmia is real and unpredictable. I would still give the full protocol: calcium for membrane stabilisation (though some guidelines reserve calcium for ECG changes, the prevailing practice in severe hyperkalaemia is to give it regardless, because the ECG has imperfect sensitivity), insulin-dextrose and salbutamol to shift, frusemide and a binder to remove, and a plan for dialysis. The absence of ECG changes does not make the potassium safe — it makes the immediate risk lower but does not eliminate it." [1]

Examiner: "If this were a hypokalaemic patient, what would the ECG show, and what is the management?" [1]

"The hypokalaemic ECG shows T wave flattening or inversion with ST depression in mild cases, prominent U waves in moderate cases — best seen in V2 to V4, and a U wave taller than the preceding T wave is highly suggestive — and in severe cases, apparent QT prolongation from QU fusion, premature atrial and ventricular complexes, and torsades de pointes. The management is to replace potassium — oral for mild to moderate, intravenous for severe or symptomatic, with a maximum rate of 10 millimoles per hour peripherally and 20 millimoles per hour via a central line under continuous cardiac monitoring, never as a bolus. Critically, I would check and correct the magnesium first, because hypomagnesaemia causes refractory hypokalaemia through renal potassium wasting. And I would investigate the cause — a 24-hour urine potassium, urine chloride and calcium, magnesium, acid-base status, and renin and aldosterone as indicated." [1]