Hyperkalemia

Hyperkalemia (Greek hyper - over, much ,- emia - in the blood) (also potassium surplus ) denotes a sometimes life-threatening electrolyte disturbance in which the concentration of potassium in the blood increases. From a hyperkalemia is about from more than 5.0 mmol / l talked (in children 5.4 ) in the blood serum. An opposite lack of potassium is called hypokalemia.

Diagnosis

A single elevated value should always be checked, as measured by hemolysis with improper blood collection to high levels of potassium.

Sources of error in falsely elevated values ​​( Pseudohyperkaliämie ) can be:

  • Collection of the blood has been jammed too long or too long pumped by hand. Thus it has come to hemolysis, since the intracellular potassium of erythrocytes is coming out from the hemolysis in the serum.
  • Rapid aspiration through a small lumen cannula to
  • The blood was allowed to stand too long before centrifugation and has already too decomposed.
  • Release potassium in the blood sample with excessive thrombocytosis or leukocytosis (eg, CML)

Causes

At elevated potassium levels occurs when enough potassium can not be excreted by the kidney. This happens in cases of acute renal failure, chronic renal failure and adrenal insufficiency ( Addison's disease ). Furthermore, various medications can increase blood potassium levels. These include ACE inhibitors and sartans, aldosterone, triamterene, cytostatics, cold red blood cell concentrates and hormonal contraceptives containing the progestin drospirenone ( Yasmin / Petibelle ) because drospirenone is structurally similar to spironolactone.

The serum potassium level is acutely affected by pH changes. A change in the pH to 0.1 leads to an oppositely directed change in the potassium level of about 0.4 mmol / l If the pH value, it comes ( metabolic, respiratory ) acidosis. In an effort to compensate for this, it comes to Umverteilungshyperkaliämie. In this case, excess H ions are redistributed from intracellular and intravascularly after the potassium ions in opposite directions.

Severe injuries of the muscles with rhabdomyolysis, but also burns also lead to a shift of intracellular potassium into the extracellular space.

Especially in combination with decreased excretion may also lead to an increased supply hyperkalemia. Potassium rich infusions, as well as in advanced renal insufficiency even larger amounts of dried fruit or potassium- rich fruits ( bananas) can contribute.

Hyperkalemia is also caused artificially in the framework of the implementation of the death penalty by lethal injection by producing potassium chloride.

Symptoms

Hyperkalemia manifests itself often nonspecific, sometimes by paresthesia or muscle twitching. In the course of cardiac arrhythmias are typical; often the cardiovascular arrest is the first and only symptom.

Pathophysiological processes at the heart

Hyperkalemia to about 8 mmol / L leads first overall positive chronotropy and inotropy because the heart cells slightly depolarized and thus are more excitable. In a hyperkalemia from about 10 mmol / L, the membrane potential according to the Nernst equation strongly positive. The cell can after a single action potential not repolarize under the approximately -40 mV, and just below this threshold open the action potential -initiating voltage-dependent sodium channels. The heart is so locked in diastole. This one uses in cardiac surgery: The heart is perfused during operations with so-called kardiopleger solution ( potassium > 15 mmol / L), beginning at normal blood flow usually without complications independent again to beat.

Therapy: kaliumumverteilende and potassium- cutting measures

  • Calcium solution 500-1000 mg i.v., Duration about 30 minutes. Stabilizes the resting membrane potential of the cardiac muscle and the conduction system, causing arrhythmias be prevented.
  • Inhalation of β2 - agonists, such as salbutamol. Shift of potassium intracellularly after.
  • Glucose solution Alt insulin, onset of action after 30 minutes, duration 4-6 hours. Insulin induces simultaneous shift of glucose and potassium by intracellularly.
  • Sodium hydrogen carbonate, onset of action after about 10 minutes, duration 2 hours. Alkalosis → sodium proton exchanger (NHE ) is active → Shift of sodium by intracellularly → increased activity of the sodium - potassium pump → potassium lowering extracellular
  • With simultaneous 0.9 % NaCl solution specifically promote furosemide iv potassium elimination
  • Restriction of enteral potassium intake
  • Cation exchanger ( either orally or rectally )
  • Hemodialysis for 3-4 hours
  • Discontinuation of eplerenone, spironolactone, triamterene, ACE inhibitors,
Serum (blood) Electrocardiography Right bundle branch block Chronic kidney disease Angiotensin II receptor antagonist Cardiac dysrhythmia Digital Object Identifier
405020
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