The resting membrane potential (RMP) of myocytes is determined by the Na+/K+-ATPase, which pumps 3 Na+ out for every 2K+ pumped and an open potassium channel that allows K to move outside the cell, down its concentration gradient. Both these events produce a negative intracellular change and a negative RMP. Since the potassium channel is the open at rest, changes in the internal or external K concentration may change the RMP according to the equation:
ERMP ≈ E = -[RT/F] ln [K+]I/ [K+]o. Thus, hypokalemia lowers the RMP, making it harder to achieve threshold for depolarization and hyperkalemia raises the RMP, making it easier to achieve threshold.
Causes of hypokalemia include inadequate intake, loss, or redistribution. Causes of loss can be: (1) GI: Diarrhea, (2) Skin: Sweating, (3) Renal: Lasix, HCTZ, Amphotericine, Cisplatin, Hyperaldosteronism, Cushing’s disease, Bartter sundrome. Causes of redistribution (entry into cells) include β-agonists, insulin, Hypokalemic per paralysis.
Symptoms of hypokalemia include weakness (especially if K+< 2.5), myalgia, constipation, and rhabdomyolysis. Patients can develop PAC, PVC, SB, PAT, JT, AVB, VT, and VF. ECG changes include flattened T-waves, U-waves (due to prolonged Purkinje fiber repolarization), and prolonged QT.
Most cases of chronic hypokemia are well tolerated, and if the patient has no symptoms, I would not replace the K+ preoperatively unless the K+ were below 2.5 mEq/L. If treatment were required, the underlying cause should be addressed. Replacement can be provided with an intravenous infusion of no greater than 20 mEq/hr or, even safer, PO administration. Patients who are hypokakemic by 1 mEq/L in the plasma are at least 2-300 mEq deficient in the body, thus replacement of extremely low levels (eg,
Causes of hyperkalemia include excess intake, impaired elimination, or excessive release from cells. Excess intake can occur via PO, IV, transfusion, hyperaldosteronism, congenital adrenal hyperplasia, use of spironlactone. Impaired elimination can occur from renal insufficiency, renal drug effect (NSAIDS, ACEI, cyclosporin, tacrolimus). Excessive release from cells can occur with tissue injury, ischemia, necrosis, tumor lysis, malignant hyperthermia, burns, use of succinylcholine, beta-blockers, and digoxin.
Symptoms of hyperkalemia include malaise, palpitations, weak, and met acidosis. Patients can develops RBBB, LBBB, AVB, SB, Idioventricular rhyhtm, VT, VF, and asystole. ECG changes include peaked T-waves, depressed P-waves, wide QRS, and a sinusoidal QRS.
Acute treatment consists of insulin, glucose, bicarbonate, and calcium. Ca2+ is usually not given with peaked T-waves, but is reserved for loss of P-waves, widened QRS, and arrhythmias. CaCl2 contains 3X more available elemental Ca2+ than Ca gluconate and should given in emergencies. Therapies for non- acute settings includes β2-ag (eg, albuterol), Kayexalate, lasix, fludrocortisones, and dialysis.