Hyperkalaemia

What it is

Hyperkalemia is a rise in the plasma potassium, and the ECG is where it is read. The earliest changes are peaked, narrow T waves with widening of the QRS complex. If plasma levels continue to rise, the PR interval is prolonged, and the P waves then disappear.

Causes and risk

Drugs are a common route. ACE inhibitors such as lisinopril and captopril, and ARBs such as valsartan, both carry hyperkalemia among their side effects, together with a dry cough and angioedema for the ACE inhibitors and a teratogenic risk for both. Diuretics as a class tend to lower the potassium, but the potassium sparing group, spironolactone, raises it instead. Heparin does the same through hypoaldosteronism, and this is listed for both the unfractionated drug and the low molecular weight ones.

Primary adrenal insufficiency raises the potassium as one of four findings that go together: hyponatremia, hyperkalemia, hypercalcemia and eosinophilia. The acute form comes with shock, abdominal tenderness on deep palpation, unexplained fever, nausea, vomiting, weight loss and anorexia. The chronic form comes with fatigue, weakness, anorexia, nausea, vomiting, abdominal pain, weight loss, hyperpigmentation or vitiligo, hypotension and anemia.

Aldosterone deficiency or resistance in the collecting duct and distal convoluted tubules raises the potassium, which is the type 4 pattern. In chronic kidney disease a fall in the renal excretion of K+ means more K+ remains in the bloodstream, and hyperkalemia is one of the complications listed there.

The drug list is set out by mechanism, which is what makes it possible to catch an agent that does not look like a potassium drug at all. Nonselective beta blockers interfere with beta-2-mediated intracellular potassium uptake; ACE inhibitors act by inhibition of angiotensin II formation with a subsequent decrease in aldosterone secretion; angiotensin II receptor blockers block the receptor and so decrease aldosterone secretion; the potassium sparing diuretics block the epithelial sodium channel or the aldosterone receptor; NSAIDs impair local prostaglandin synthesis, which reduces renin and aldosterone secretion; and the cardiac glycosides, digoxin among them, act by inhibition of the Na+/K+-ATPase pump. Digoxin is the one whose mechanism is written as that pump, so a hyperkalemia attributed to a drug that inhibits it is a digoxin effect and not an ACE inhibitor, ARB or beta blocker effect.

The acute antihypertensive table makes the same point about one drug by name: captopril, at a dose of 12.5 to 25 mg with an onset of 15 to 60 min, carries hyperkalemia at the head of its adverse effects, with angioedema and reduced renal function in bilateral renal artery stenosis.

When the hyperkalemia belongs to adrenal insufficiency, the case is usually a middle aged patient with a chronic history of fatigue, weight loss and dizziness, orthostatic hypotension on examination, and a metabolic panel showing hypoglycemia, hyponatremia and hyperkalemia. The three etiologies to name are autoimmune disease, TB and metastatic disease, and the associated diseases are T1DM, Hashimoto's thyroiditis and vitiligo. The hyperpigmentation that goes with it comes from feedback: primary adrenal insufficiency stimulates the hypothalamus, which increases production of POMC, a prohormone cleaved into ACTH and melanocyte-stimulating hormone.