Hypokalemia

Classification according to ICD-10
E87.6	Hypokalemia potassium deficiency
ICD-10 online (WHO version 2019)

As hypokalemia (syn hypokalemia, too. Potassium deficiency or deficiency of potassium in the blood; of . Greek ὑπο- hypo- "under" and lat. -Aemia . Αἷμα and Greek haima "blood"), an electrolyte imbalance designated by too little potassium in the blood marked (<3.6  mmol / l potassium in the blood serum ). Depending on the severity, the hypokalemia can be harmless to life-threatening. The compensation of hypokalaemia through potassium intake is called potassium substitution. The excess of potassium is known as hyperkalemia .

causes

Hypokalemia can have a variety of causes. Most obvious is a lack of potassium intake, mainly through food. Usually, however, hypokalemia occurs after excessive potassium loss. It is usually associated with excessive water loss, which 'flushes' the potassium out of the body. Typically this is the result of vomiting and diarrhea . As part of a Conn's syndrome may also result in hypokalemia due to excessive potassium excretion in the kidney. Some drugs also accelerate the excretion of potassium, for example loop diuretics such as furosemide or various laxatives . In addition, the serum potassium level fluctuates as a result of fluctuations in the acid-base balance . For example, the extracellular K ⁺ content drops by approx. 0.4 mmol / L with a pH increase of 0.1. Another cause is the renal loss of potassium in a so-called potassium loss kidney. A Bariumvergiftung can also lead to severe hypokalemia.

A specialist article published in May 2009 lists case studies in which excessive cola consumption of around 2-3 liters per day had also led to a potassium deficiency. In addition to the main factor caffeine , glucose and fructose also contribute to potassium loss.

Effects

Potassium is important for many body functions, especially muscles and nerves . Potassium occurs as a cation with a concentration of around 150 mmol / l mainly intracellularly , the extracellular concentration is around 3.5 to 5.0 mmol / l, also in the blood. More than 98% of the potassium in the body is in the intracellular space.

The osmotic gradient of potassium between the intracellular and extracellular space is crucial for the function of the nerve cells. In particular, potassium is needed to repolarize the cell membrane and restore the state of rest after an action potential has been passed on.

Potassium is also important for normal muscle function. Large deviations from the normal potassium level can cause paralysis in the muscles of the limbs ( hypokalemic paralysis ), among other things, larger deviations can endanger heart function . The most relevant effect of hypokalaemia in intensive care is therefore also the effect on the heart. Hypokalaemia sensitizes the heart to the arrhythmogenic effects of digitalis preparations and catecholamines . With hypokalemia, the heart is prone to arrhythmias . Often extrasystoles , but also atrial fibrillation and ventricular fibrillation up to cardiac arrest and death are possible.

Summary of clinical signs

According to Herold's standard textbook, "Internal Medicine":

• Adynamia up to paresis
• Constipation up to paralytic ileus
• Weakening or absent reflexes
• ECG: flattening of T, ST depression, U wave, pseudo-QT prolongation due to TU fusion, increased signs of digitalis intoxication with extrasystoles

Pathophysiological processes in the heart

With regard to the effects of hypokalaemia on the heart, a distinction must be made between pacemaker and working heart muscle tissue.

At the pacemaker, the extracellularly reduced potassium concentration causes a lower Nernst potential . The voltage-controlled cation channels there, so-called funny channels , react excessively, they open more strongly at more negative membrane potentials. The pacemaker action potential therefore rises more steeply, the pacemaker now emits its signal more often: positive chronotropia , tachycardia .

Potassium is important in ventricular tissue during repolarization after an action potential. Since the potassium channels are only active there when potassium is bound on the outside, the conductivity for potassium decreases in hypokalemia. The influence of the other ions on the membrane potential increases (according to Goldman's equation ). This leads to a depolarization of the heart muscle cells. Once an action potential has been triggered, the cells are no longer permeable enough for the potassium-dependent repolarization; the heart muscle cell remains depolarized and is therefore arrested in systole. This process in the individual cell is initially of a statistical nature, individual cells get out of step, with which the above. Arrhythmias can be easily explained.

therapy

Therapy depends on the cause. Enteral substitution, i.e. oral intake, is often sufficient to normalize a lowered potassium level , for example with foods that contain particularly potassium, but also with potassium supplements. Potassium is found in many foods, such as: B. in oranges , potatoes , avocados , spinach , tomatoes and vegetable juices, dried fruits (for example apricots, raisins ), meat , milk , (dry) beans and mushrooms . While bananas are known to be high in potassium, they are also high in readily available carbohydrates and are far from being a good source of potassium. Other foods like whole grains (e.g. pumpernickel), which are high in potassium and carbohydrates that are slowly released, are more helpful.

In the case of a potassium deficiency relevant to intensive care medicine with the risk of cardiac arrhythmias , on the one hand the cause of the potassium deficiency is eliminated as far as possible (e.g. compensation of an alkalosis ), on the other hand, a normal serum potassium level is aimed for through parenteral potassium substitution. The replacement is generally done slowly with potassium chloride , potassium aspartate or potassium malate , as the infusion of a high-potassium bolus can lead to cardiac arrest . For peripheral venous administration, potassium solutions are diluted in Ringer's lactate or isotonic saline solution (max. 40 mVal K ⁺ in 1000 ml per hour) or undiluted via a central venous access , as the solution is highly irritating to veins.

See also

• Achor Smith Syndrome

Individual evidence

1. ↑ Biorama ( memento of October 31, 2007 in the Internet Archive ). Retrieved September 26, 2015.
2. ↑ V. Tsimihodimos, V. Kakaidi, M. Elisaf, Cola-induced hypokalaemia: pathophysiological mechanisms and clinical implications. In: The International Journal of Clinical Practice. Vol. 63, Issue 6, pp. 900-902; German-language summary on Spiegel.de
3. ↑ Gerd Herold (Ed.): Internal Medicine. Cologne 2017, ISBN 978-3-9814660-6-5 , p. 582.
4. ^ RF Schmidt, F. Lang, G. Thews: Physiologie des Menschen. 29th edition. Springer, Berlin et al. 2005, ISBN 3-540-21882-3 , pp. 478, 719, 802.

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