Severe Hyperkalaemia: An On-Call Guide to a Medical Emergency

You're on call in A&E when a nurse hands you an ECG. It shows a bizarre, wide-complex bradycardia. Your mind races through the potential causes, but one life-threatening condition should be at the very top of your list.

This is the classic presentation of severe hyperkalaemia, a medical emergency that every resident doctor needs to recognise and manage confidently. Let's break down a typical case and walk through the high-yield essentials you need to know for your exams and, more importantly, for your patients on the ward.

The Case: A 72-Year-Old Woman in A&E

A 72-year-old woman is brought to A&E by ambulance due to increasing weakness and confusion. Her daughter reports that over the past two days, she has been nauseous and has refused to eat or drink. To manage ongoing bone pain, she has been taking large doses of an over-the-counter NSAID (several tablets a day).

Her past medical history includes chronic kidney disease (CKD), and her regular medications include spironolactone and perindopril.

Her ECG is alarming: an idioventricular rhythm at around 20 beats per minute. The QRS complexes are significantly widened, merging with the T waves to form a characteristic sine wave pattern.

Do you know what's causing this profound bradycardia? The ECG screams severe hyperkalaemia.

We sent off urgent bloods, which confirmed our suspicions:

• Potassium: 9.1 mmol/L (normal: 3.5-5.3)

• Creatinine: 1016 µmol/L

• Urea: 103 mmol/L

• Venous pH: 7.11

• Bicarbonate (HCO₃⁻): 9.5 mmol/L

• Glucose: 11.7 mmol/L

Given her deteriorating condition and haemodynamic instability, we immediately began transcutaneous pacing. She was then treated with 10 units of short-acting insulin in 500 mL of 5% dextrose, an adrenaline infusion, 160 mmol of sodium bicarbonate, and 10 mL of calcium chloride (which was repeated).

In parallel, the on-call renal registrar was contacted, and a temporary dialysis line (a Sheldon catheter) was inserted. Just before she was connected to the dialysis machine, her repeat potassium was 6.9 mmol/L, and a perfusing cardiac rhythm had returned. She no longer required pacing.

Why Did This Happen? The Perfect Storm

Potassium disturbances are incredibly common, and you've probably managed a patient with hyperkalaemia already this month. Healthy kidneys have a huge capacity to excrete potassium, which is why severe, life-threatening hyperkalaemia almost never occurs in someone with normal renal function.

In most cases, dangerous hyperkalaemia is linked to an acute kidney injury (AKI) on top of pre-existing CKD. In our patient, the combination of dehydration (from poor oral intake) and NSAID use caused a severe AKI. This, combined with medications that increase potassium levels (the ACE inhibitor perindopril and the potassium-sparing diuretic spironolactone), created the perfect storm for a rapid, dangerous rise in her potassium levels.

The Hyperkalaemia ECG: A Step-by-Step Guide

The biggest concern with hyperkalaemia is its effect on cardiac conduction. As potassium levels rise, the ECG can show characteristic changes, although it's crucial to remember these don't always occur sequentially.

• Tall, 'Tented' T waves: Often the first sign (usually K⁺ > ~5.5 mmol/L).

• Prolonged PR Interval & Flattening/Loss of P waves: As the situation worsens (K⁺ > ~6.5 mmol/L).

• Widening of the QRS Complex: The QRS can merge with the T wave, forming the classic sine wave pattern (typical for K⁺ ≥ ~8.0 mmol/L).

• Bradycardia, High-Grade AV Blocks, Asystole, or Ventricular Fibrillation (VF): The terminal events of severe hyperkalaemia.

A Critical Point: Don't be falsely reassured by a normal-looking ECG. It's estimated that around 50% of patients with a potassium level >6.5 mmol/L will not have typical ECG changes. This may depend on how quickly the hyperkalaemia developed, as patients with chronic elevation can adapt over time.

Managing Severe Hyperkalaemia: The Three-Pronged Attack

According to UK Kidney Association (UKKA) and Resuscitation Council UK guidelines, the management plan follows a three-pronged approach:

• Protect the Heart: Stabilise the cardiac membrane.

• Shift the Potassium: Move potassium from the blood into the cells.

• Remove the Potassium: Eliminate potassium from the body.

1. Protect the Heart (Cardiac Stabilisation) with Calcium

This is the first and most important step if ECG changes are present. Calcium directly antagonises the cardiotoxic effects of potassium by stabilising the myocardial membrane, but it does not lower the serum potassium level.

In the UK, you have two main options:

• Calcium Gluconate 10%: This is the preferred agent for peripheral IV access, as it's less irritant to veins. The key is the dose: to be effective, you need to give 30 mL (3 x 10 mL ampoules). One ampoule is not enough.

• Calcium Chloride 10%: Contains three times more elemental calcium per mL than gluconate and acts faster. It's an excellent choice in cardiac arrest or if the patient has central access, but it is caustic and can cause severe tissue necrosis if it extravasates from a peripheral line.

You can repeat the dose of calcium every 5-10 minutes if ECG changes persist or recur.

2. Shift Potassium into Cells

• Insulin and Glucose: This is the cornerstone of treatment. A standard regimen is 10 units of a short-acting insulin (e.g., Actrapid) mixed in 500 mL of 5% dextrose, infused over 30-60 minutes. The insulin activates the Na⁺/K⁺-ATPase pump, driving potassium into cells. It starts working within 15-30 minutes. You must monitor the patient's blood glucose closely to prevent hypoglycaemia.

• Salbutamol: High-dose nebulised salbutamol can be a useful adjunct to insulin. We're not talking about a standard asthma dose (2.5mg or 5mg). You need 10 mg to 20 mg via a nebuliser to achieve a significant effect. In a patient with severe bradycardia, an adrenaline infusion may be used instead for its beta-agonist effects, in which case you would omit the salbutamol.

• Sodium Bicarbonate: Previously widely used, its role is now much more limited. It is only effective in patients with a concurrent severe metabolic acidosis. In these cases, an isotonic infusion is given to help correct the pH. Using hypertonic bicarbonate can paradoxically worsen hyperkalaemia initially due to osmotic effects.

3. Remove Potassium from the Body

Shifting potassium is a temporary measure. To truly treat the patient, the excess potassium must be removed from the body.

• Diuretics (e.g., Furosemide): Only effective if the patient has preserved kidney function and is still producing urine.

• Potassium Binders: These agents bind potassium in the gastrointestinal tract. While older agents were slow and not very effective, newer binders recommended by UKKA guidelines, such as sodium zirconium cyclosilicate (SZC), work much faster (within an hour) and can be used to help bridge the patient to definitive treatment.

• Haemodialysis: This is the most effective and definitive treatment for severe, life-threatening hyperkalaemia, especially when associated with severe AKI, profound acidosis, or ECG changes unresponsive to medical therapy. If you suspect your patient needs dialysis, get the renal team involved early.

Key Takeaways for Your Next Shift

When faced with severe hyperkalaemia on a busy shift, remember these high-yield points:

• Bradycardia + Wide QRS? Think Potassium! Always include hyperkalaemia in your differential for this ECG pattern.

• ECG Changes? Give Calcium First. If you're using calcium gluconate peripherally, give three ampoules (30 mL). One is not enough.

• Insulin is Your Go-To. An insulin/dextrose infusion is the most reliable way to shift potassium into cells. Remember to monitor blood glucose.

• Bicarbonate for Acidosis Only. Don't give it empirically to every patient with hyperkalaemia.

• Use a Combination Approach. In severe cases, one drug is rarely enough. Use multiple strategies simultaneously to protect the heart, shift the potassium, and plan for its removal.