Hyperkalemia

Confirm it before you treat it - Pseudohyperkalemia is the single most common cause of a high potassium. Hemolysis from a syringe draw, a tight tourniquet, excessive fist-pumping, leukocytosis or thrombocytosis all falsely elevate the value. In an asymptomatic patient with no ECG changes, send a STAT repeat serum potassium before starting aggressive therapy.

ECG first, and know the progression - The ECG is the first test to order because cardiac conduction failure is what kills. Mild (5.5 to 6.5 mEq/L): peaked T waves with a prolonged PR segment. Moderate (6.5 to 8 mEq/L): loss of the P wave, widening QRS, ST elevation, escape rhythms. Severe (above 8 mEq/L): sine wave, bundle branch and fascicular blocks, ventricular fibrillation, asystole. The changes are insensitive and highly variable, so a normal tracing does not clear the patient.

Succinylcholine - It raises serum potassium about 0.5 mEq/L in anyone, which becomes dangerous where extrajunctional receptors are upregulated: burn injury, prolonged immobilization, and neuromuscular disease. Worth knowing the exception — chronic renal insufficiency patients are no more susceptible to succinylcholine-induced hyperkalemia than patients with normal kidneys.

Where it appears intraoperatively - Aortic cross-clamp release, major trauma with massive cell rupture, cardiac and transplant surgery, reperfusion of a transplanted organ, massive transfusion, tumor lysis after chemotherapy, and malignant hyperthermia.

Stabilize the membrane first - With ECG changes or arrhythmia, calcium goes in first. Calcium gluconate 1000 mg or calcium chloride 500 to 1000 mg IV. It does not lower serum potassium — it raises the membrane threshold — and the effect lasts only 30 to 60 minutes, so it has to be paired with something that actually shifts or removes potassium. Gluconate is preferred peripherally; calcium chloride extravasation causes tissue necrosis and belongs in a central line. Never run calcium through bicarbonate-containing tubing, which precipitates calcium carbonate.

Shift it into cells - Regular insulin 10 units IV with 25 g of glucose (50 mL of 50% dextrose) drives potassium in via the Na-K-ATPase pump. Give insulin alone when serum glucose is at or above 250 mg/dL; higher insulin doses buy nothing. Inhaled albuterol drops potassium a further 0.5 to 1 mEq/L. Hyperventilation shifts potassium intracellularly as well and costs nothing to start.

Then actually remove it - Furosemide 20 to 40 mg promotes diuresis in non-oliguric patients without severe renal impairment; in a hypovolemic patient, restore euvolemia with isotonic saline before the diuretic. Gastrointestinal cation exchangers (patiromer, sodium zirconium cyclosilicate, sodium polystyrene sulfonate) bind potassium in the gut. For life-threatening hyperkalemia, go early to hemodialysis.

Mind what is running - Stop potassium-containing solutions, including lactated Ringer's, and any potassium in the maintenance fluid or TPN. Packed red cells add potassium too. Saline is not a free alternative: the hyperchloremic acidosis it produces shifts potassium out of cells and can raise the level despite containing none.

Optimize before the case - Elective surgery in a renal patient is the time to dialyze first, since the cardiac effects are hard to manage once you are in the room. In milder hyperkalemia being treated, recheck the potassium every 1 to 2 hours. Check serum calcium in renal disease, since hypocalcemia amplifies the cardiac toxicity, and check a digoxin level in anyone taking it.

Think BRASH when the patient is bradycardic - Bradycardia, Renal failure, AV nodal blockade, Shock and Hyperkalemia together. The synergy between AV nodal blockers and potassium produces profound bradycardia at levels as low as 5.1 mEq/L, most commonly 5.5 to 7.0, and the classic ECG changes are often absent. Atropine may do nothing because this bradycardia is not vagally mediated; push-dose epinephrine 10 to 20 mcg raises rate and systemic vascular resistance and shifts potassium at the same time.

Drugs that got them here - Digoxin, potassium-sparing diuretics, NSAIDs, ACE inhibitors, heparin, beta blockers, cyclosporine, recent IV potassium, TPN, potassium penicillin, and succinylcholine. Most inpatient hyperkalemia is medications plus renal insufficiency.

Muscle weakness carries into emergence - Weakness, flaccid paralysis and depressed deep tendon reflexes are part of hyperkalemia itself, and they read exactly like residual neuromuscular blockade. Don't write off a weak patient at emergence as incomplete reversal without rechecking the potassium.

Potassium is an intracellular cation — cells hold about 98% of total body stores, roughly 140 mEq/L inside against 4 to 5 mEq/L outside, a gradient the Na-K-ATPase pump maintains. Hyperkalemia is a serum level above normal, usually quoted as greater than 5.0 to 5.5 mEq/L, though the cutoff varies by institution. It arises three ways: increased intake, a transcellular shift of potassium out of cells, or impaired renal excretion.

What makes it dangerous is that the gradient sets resting membrane potential in excitable tissue, so a rising extracellular potassium destabilizes cardiac conduction and skeletal muscle. The rate of rise matters more than the number — a chronic dialysis patient can look well at a level that would arrest someone whose potassium spiked acutely. Renal excretion usually holds until the GFR falls below 30 mL/min.