Hyperkalemia
المؤلف:
Marcello Ciaccio
المصدر:
Clinical and Laboratory Medicine Textbook 2021
الجزء والصفحة:
p279-280
2025-08-31
297
Hyperkalemia, defined as plasma K+ concentration >5 mmol/L, may be due to reduced renal K+ excretion+, increased cellular K+ release, increased K+ intake, and pseudohyperkalemia (Table 1). Increased dietary K+ intake alone generally does not cause hyperkalemia because excess K+ is rapidly excreted by the adaptive mechanism based on:
• Increased cellular potassium uptake, facilitated by insulin
• Increased beta-2 adrenergic tone
• Increased urinary potassium excretion
Table1. Causes of hyperkalemia
Therefore, hyperkalemia from increased intake can occur in the presence of other clinical conditions, such as renal impairment.
Pseudohyperkalemia represents an artificial increase in plasma potassium concentration due to potassium leakage from cells during venous sampling. Thrombocytosis causes hyperkalemia due to the potassium release by platelets during coagulation. Pseudohyperkalemia should be suspected in asymptomatic patients with no obvious underlying cause.
The etiology of hyperkalemia is often multifactorial; impaired renal function, medications, and hyperglycemia are the primary causes.
The symptoms of hyperkalemia are due to the difference in potassium concentration between ICF and ECF, which influence the resting membrane potential. Hyperkalemia results in partial membrane depolarization. The progression of the clinical picture is characterized by prolonged cellular depolarization , which reduces membrane excitability and is manifested by asthenia, which may progress to flaccid paralysis and hypoventilation. In addition, cardiovascular symptoms, such as bradycardia, hypotension, and conduction disturbances up to the cardiac arrest can also occur. Numerous electrocardiographic alterations may occur during hyperkalemia.
Diagnosis and Therapy
Similar to hypokalemia, hyperkalemia alters cardiac conduction and muscle strength. Initial efforts should focus on determining the need for urgent intervention (Fig. 1). The absence of symptoms does not rule out severe hyperkalemia because it is often asymptomatic.
Fig1. Diagnostic algorithm of hyperkalemia. (Copyright EDISES 2021. Reproduced with permission)
The hyperkalemia severity is assessed based on symptoms, plasma potassium concentration, and electrocardiographic alterations. A careful medical history is essential to identify the possible drugs intake that alter potassium excretion or induce its release from the cells. Urinary sodium, serum aldosterone and renin levels, and acid–base balance assessed by hemogasanalysis provide helpful information for the differential diagnosis.
If the etiology is not initially evident and the patient is asymptomatic, the presence of pseudohyperkalemia should be evaluated.
Therapy depends on the degree of hyperkalemia, which is determined by potassium concentration, muscle signs, and electrocardiographic changes. Therapy aims to block the effects of hyperkalemia on cell membranes, increase potassium transfer within cells, and remove excess potassium and the cause of hyperkalemia. This is carried out using calcium gluconate, which reduces mem brane excitability; insulin and glucose because insulin stimulates potassium entry into cells and glucose pre vents hypoglycemia; alkalinizing treatment with sodium bicarbonate, especially in patients with severe hyperkalemia and metabolic acidosis, because it favors the movement of potassium inside the cells; and treatment with diuretics that favor the renal potassium excretion (the sodium excreted as a result of the diuretic must be reintegrated through the physiological solution). Finally, hemodialysis represents the quickest method to reduce plasma potassium concentration but it should be reserved for patients with renal insufficiency and for those with severe, potentially fatal, hyperkalemia who do not respond to other therapies.
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