Hyperkalaemia: The Three-Step Emergency

Why a high potassium stops the heart

The danger is not the number — it is what the number does to a cardiac membrane. Every excitable cell holds a resting voltage across its membrane, and that voltage is set almost entirely by the huge gradient of potassium — high inside the cell, low outside. When extracellular K+ rises, that gradient shrinks and the resting membrane potential drifts upward (less negative), sitting closer to the threshold for firing. At first glance that sounds like it should make cells more excitable, and briefly it does. But a membrane held chronically depolarised cannot reset its fast sodium channels — they stay inactivated — so the cell becomes harder and harder to fire and conduction slows to a crawl. In the heart this shows up as a deteriorating ECG and, ultimately, an electrically silent myocardium. This membrane-potential story is the same physiology taught in the Cardiovascular section, and it is why potassium sits at the centre of cardiac electrophysiology.

The ECG changes march in a recognisable order as potassium climbs, and reading them is a bedside potassium meter. First the T waves become tall, narrow and "tented." Then the P waves flatten and lengthen as atrial conduction fails. Then the QRS complex widens and blurs. Finally the flattened P and the wide QRS merge into a slow, undulating "sine wave" — the pre-terminal pattern that precedes ventricular fibrillation or asystole. The exact number matters less than the trend and the ECG: a patient with sine-wave changes needs treatment before the confirmatory blood result ever returns.

Where the potassium comes from

Four mechanisms, and most real patients have more than one at once. First and biggest: reduced excretion. The kidney is the main exit for potassium, so acute or chronic kidney injury is the commonest serious cause — this ties straight into the renal and nephrotoxic-drugs chapter. Second: drugs, the cause you can actually prevent. Anything that blocks the renin–angiotensin–aldosterone axis retains potassium — ACE inhibitors and ARBs, and the potassium-sparing diuretics spironolactone, eplerenone and amiloride. NSAIDs impair renal perfusion and potassium handling; trimethoprim behaves like a mild amiloride and blocks distal potassium excretion; heparin suppresses aldosterone. The infamous "triple whammy" — an ACE inhibitor or ARB plus a diuretic plus an NSAID, often in a dehydrated older patient — is a classic recipe for a crashing potassium and an acute kidney injury together (see the nephrotoxic-drugs chapter). Third: a shift of potassium out of the cells — metabolic acidosis, insulin deficiency (diabetic ketoacidosis), massive tissue breakdown (rhabdomyolysis, tumour lysis syndrome), and digoxin toxicity, which poisons the Na+/K+-ATPase that normally pumps potassium back in. Fourth: excess intake (usually only dangerous when excretion is already impaired) and pseudohyperkalaemia — a falsely high result from a haemolysed sample or a fist clenched too hard during the draw.

Step 1 — Protect the myocardium

The first move buys time; it does not lower the potassium at all. If there are ECG changes (or the potassium is dangerously high), the very first drug is intravenous calcium — calcium gluconate, or calcium chloride via a central line. Calcium raises the threshold potential back away from the depolarised resting potential, restoring the gap the heart needs to fire and conduct. It is cardioprotective and fast, working within minutes, and if the ECG changes persist the dose is simply repeated. The single most important thing to understand is what calcium does not do: it does not lower the serum potassium by a single millimole. It is a holding measure — it keeps the heart electrically stable while the potassium-lowering steps are set up. One important caution links back to the Cardiovascular section: in suspected digoxin toxicity, rapid IV calcium has historically been feared to cause a hypercontracted, non-relaxing "stone heart," so calcium is given slowly and cautiously (or a digoxin-specific antibody is used) rather than pushed.

Step 2 — Shift potassium into the cells

Now actually lower the serum level — fast, but temporarily. The workhorse of step two is insulin given with glucose. Insulin drives potassium into cells by stimulating the Na+/K+-ATPase pump, dropping the serum level within about fifteen minutes. The glucose is co-administered purely to prevent the insulin from causing hypoglycaemia — and the patient's blood sugar must then be monitored, because the classic error is watching the potassium and forgetting the glucose. That insulin drives potassium intracellularly is the same physiology met in the Endocrine section, and it is exactly why insulin deficiency in diabetic ketoacidosis pushes potassium the other way, out of cells. The second agent is nebulised salbutamol — a beta-2 agonist that, like insulin, stimulates the pump and shifts potassium inward, giving an additive effect. Third, if the patient is acidotic, sodium bicarbonate can help shift potassium in as the acidosis is corrected. Like calcium, every step-two treatment is temporary: the potassium has only been hidden inside the cells, not removed from the body, and it will leak back out. Shifting therapies buy an hour or two — they do not end the problem.

Step 3 — Remove potassium from the body

The only definitive step is removing potassium from the body altogether. The modern oral binders are the newer gut agents patiromer and sodium zirconium cyclosilicate, which bind potassium in the gastrointestinal tract and carry it out in the stool; they are better tolerated and faster than the older, slower and much-disliked resins (calcium or sodium polystyrene sulfonate). If the patient is still making urine, a loop diuretic such as furosemide increases renal potassium loss. And for refractory hyperkalaemia — or in established renal failure where none of the above can keep up — the definitive answer is dialysis, which strips potassium out directly. Running through all three steps is the same imperative: treat the cause and stop the culprit drugs. There is little point shifting and binding potassium while an ACE inhibitor, a potassium-sparing diuretic and an NSAID are still on the drug chart driving it back up.

After the crisis: chronic management

Once the acute danger passes, the goal shifts to keeping potassium in a safe range long-term — most often in chronic kidney disease or heart failure. That means dietary potassium restriction, and a careful review of the drug list: many patients are on an ACE inhibitor or ARB and a potassium-sparing diuretic precisely because those drugs protect the kidney and heart. Here the newer binders have quietly changed practice — patiromer and sodium zirconium cyclosilicate can hold potassium down enough to let a patient stay on life-prolonging RAAS therapy that would otherwise have to be stopped. And a final, cheap safeguard sits before every treatment decision: in an asymptomatic patient with a normal ECG and an unexpectedly high potassium, suspect pseudohyperkalaemia from a haemolysed sample and recheck before treating — the danger of over-treating a lab artefact (driving the potassium too low) is real.