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Renal insufficiency: hyperkalemia

Introduction to Potassium

K+ outflow is responsible for phase III (repolarization) of the cardiac cycle. Insulin and beta agonists promote the influx of K+. Total body stores include 4200 mEq intracellularly, versus only 12 mEq in the plasma. Potassium excretion of K+ is determined primarily by [K+] and aldosterone levels

Causes of Hyperkalemia in Renal Failure

Decreased excretion (lowered GFR, K+ sparing diuretics, ACE-inhibitors, heparin [decreased aldosterone efficacy], and constipation), intracellular release (metabolic acidosis, beta blockers, insulin deficiency), and increased intake (blood transfusion, increased dietary intake)

Hyperkalemia in Renal Failure: Anesthetic Concerns

Time Course of Hyperkalemia

Potassium balance usually maintained in early renal failure, thus hyperkalemia is a late sign (a GFR of 8 cc/min is adequate to clear potassium)

Hyperkalemia and Induction

In non-renal failure patients, induction with SCh increased [K+] by 0.4 mEq/L [Manninen PH et al. Anesth Analg 70: 172, 1990] and by 0.09 mEq/L [Stacey MR et al. Anaesthesia 50: 933, 1995]. Schow et al. reviewed 40,000 anesthetics at Duke University Medical Center, and found 38 cases in which SCh was used with a starting potassium > 5.5 mEq/L. No fatalities or arrhythmias occurred, and the authors estimated that the maximal risk of an event was 7.9% or less.

Duration of Neuromuscular Blockade

Despite the fact that muscle weakness is a sign of hyperkalemia (at > 7 mEq/L), Miller at al. showed that the prolongation of neuromuscular blockade following paralysis in renal failure patients is not related to potassium levels, but rather to the relative inability of the kidneys to excrete NMBDs or their metabolites

Signs of Hyperkalemia

(> 6 mEq/L): peaked T waves, prolonged PR interval (ex. AV block), flattened P wave, QRS widened to sine wave; (> 7 mEq/L): musculoskeletal weakness; Note that these effects are worsened by hyponatremia, hypocalcemia, and acidosis, all of which are present in the setting of renal failure

Acute Treatment of Hyperkalemia

1g CaCl2, 50g glucose, 10 U insulin, furosemide, 100 mEq bicarbonate (controversial)

Renal Failure: Hyperkalemia

  • Causes: decreased excretion (lowered GRF, ACE-inhibitors), intracellular release (metabolic acidosis), increased intake (transfusion)
  • Signs: peaked T waves, prolonged PR interval, flattened P wave, QRS widened to sine wave, musculoskeletal weakness
  • Acute Treatment: 1g CaCl2, 50g glucose, 10 U insulin, furosemide, 100 mEq bicarbonate (controversial)
  • Anesthesia Concerns: very real but may be overstated; increase in non-renal failure patients < 0.5 mEq/L with SCh. Affect on paralysis not related to K+


  1. Adam J Schow, David A Lubarsky, Ronald P Olson, Tong J Gan Can succinylcholine be used safely in hyperkalemic patients? Anesth. Analg.: 2002, 95(1);119-22, table of contents Link
  2. D R Duerksen, N Papineau Electrolyte abnormalities in patients with chronic renal failure receiving parenteral nutrition. JPEN J Parenter Enteral Nutr: 1998, 22(2);102-4 Link
  3. P H Manninen, B Mahendran, A W Gelb, R N Merchant Succinylcholine does not increase serum potassium levels in patients with acutely ruptured cerebral aneurysms. Anesth. Analg.: 1990, 70(2);172-5 Link
  4. M R Stacey, K Barclay, T Asai, R S Vaughan Effects of magnesium sulphate on suxamethonium-induced complications during rapid-sequence induction of anaesthesia. Anaesthesia: 1995, 50(11);933-6 Link