Hypokalemia pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Aida Javanbakht, M.D.Assistant Editor(s)-In-Chief: Jack Khouri

Overview

Pathophysiology

Hypokalemia can result from several conditions:

  • Trans-cellular shifts of potassium inside the cells (most common)
  • Renal loss of potassium
  • Gastrointestinal (GI) loss of potassium
  • Increased hematopoiesis (increased cellular use of potassium)
  • Decreased intake of potassium (least common)

Shown below is a table summarizing the different pathophysiological processes that can lead to hypokalemia. [1] [2] [3] [4]

Trans-cellular shifts Renal loss GI loss Increased hematopoiesis Decreased intake of potassium

Subject is normo or hypotensive
Associated with acidosis

Associated with alkalosis

Variable acid/base status

Subject is hypertensive
Primary hyperaldosteronism

  • Conn's syndrome

Secondary hyperaldosteronism

  • Renovascular disease
  • Renin secreting tumor

Non aldosterone increase in mineralcorticoid

Associated with metabolic acidosis

Associated with metabolic alkalosis

The Role of the Kidney


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Factors Increasing Kidney Potassium Excretion

Some Factors Affecting Potassium Distribution Between the Cells and the Extracellular Fluid

The Physiologic Role of Potassium

  • Potassium is the most common intracellular cation. Approximately 98% of total potassium exists in the intracellular fluid (ICF), which has a normal range of 140–150 mEq/l. Merely 2% of this cation is placed in the extracellular fluids (ECF), where it ranges from 3.5 to 5 mEq/l.
  • Potassium is essential during numerous body functions, particularly for excitable cells such as muscle and nerve cells.
  • Diet, mostly fruits and vegetables, is the major source of potassium for the body.[6] [7]

The Cellular Effect of Hypokalemia

  • The electrochemical gradient of potassium between intracellular and extracellular space is essential for function of neurones; in particular, potassium is needed to repolarize the cell membrane to a resting state after an action potential has passed.
  • Decreased potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential ie, it becomes more negative. This hyperpolarization is caused by the effect of the altered potassium gradient on resting membrane potential as defined by the Goldman equation. As a result, the cell becomes less sensitive to excitation and a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential. Clinically, this membrane hyperpolarization results in muscle flaccid paralysis, rhabdomyolysis (in severe hypokalemia) and paralytic ileus.
  • At the renal level, hypokalemia can cause metabolic alkalosis due to potassium/proton exchange across the cells and nephrogenic diabetes insipidus.

Pathophysiology of Hypokalemic Heart Arrhythmias

  • Potassium is essential to the normal muscular function, in both voluntary (i.e skeletal muscle, e.g. the arms and hands) and involuntary muscle (i.e. smooth muscle in the intestines or cardiac muscle in the heart).
  • Severe abnormalities in potassium levels can seriously disrupt cardiac function, even to the point of causing cardiac arrest and death.
  • As explained above, hypokalemia makes the resting potential of potassium [E(K)] more negative. In certain conditions, this will make cells less excitable. However, in the heart, it causes myocytes to become hyperexcitable. This is due to two independent effects that may lead to aberrant cardiac conduction and subsequent arrhythmia:
    • There are more inactivated sodium (Na) channels available to fire.
    • The overall potassium permeability of the ventricle is reduced (perhaps by the loss of a direct effect of extracellular potassium on some of the potassium channels), which can delay ventricular repolarization.

Pathophysiology of Hypokalemic in GI system:

  • Low level of potassium cause slow movement of GI system and illeus.

References

  1. Daly K, Farrington E (2013). "Hypokalemia and hyperkalemia in infants and children: pathophysiology and treatment". J Pediatr Health Care. 27 (6): 486–96, quiz 497–8. doi:10.1016/j.pedhc.2013.08.003. PMID 24139581.
  2. Unwin RJ, Luft FC, Shirley DG (February 2011). "Pathophysiology and management of hypokalemia: a clinical perspective". Nat Rev Nephrol. 7 (2): 75–84. doi:10.1038/nrneph.2010.175. PMID 21278718.
  3. Cheungpasitporn W, Suksaranjit P, Chanprasert S (February 2012). "Pathophysiology of vomiting-induced hypokalemia and diagnostic approach". Am J Emerg Med. 30 (2): 384. doi:10.1016/j.ajem.2011.10.005. PMID 22169581.
  4. Bisogni V, Rossi GP, Calò LA (June 2014). "Apparent mineralcorticoid excess syndrome, an often forgotten or unrecognized cause of hypokalemia and hypertension: case report and appraisal of the pathophysiology". Blood Press. 23 (3): 189–92. doi:10.3109/08037051.2013.832967. PMID 24053336.
  5. Hall, John (2016). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Elsevier. ISBN 978-1-4557-7005-2.
  6. Weaver CM (2013). "Potassium and health". Adv Nutr. 4 (3): 368S–77S. doi:10.3945/an.112.003533. PMC 3650509. PMID 23674806.
  7. . doi:10.1159/000446268 Received: Check |doi= value (help). Missing or empty |title= (help)


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