Disorders of potassium balance, ECG manifestations

Hypokalemia

Hypokalemia is defined as K⁺ < 3.5 mmol/L (the lower and upper limits may vary slightly depending on the reference ranges of the local laboratory). It may represent either a true deficit of total body potassium or merely a shift of extracellular potassium into the intracellular space. Serum potassium values must always be interpreted in relation to the acid–base status and the ECG morphology. Potassium levels must always be correlated with pH and the ECG pattern.

See this video in English: https://www.wikiskripta.eu/w/Soubor:Hypokalemia.webm

Etiopathogenesis

Transcellular shift of potassium

Acute changes in acid–base balance influence the transcellular distribution of potassium. Therefore, acute metabolic alkalosis (MAL) as well as respiratory alkalosis (RAL) are often associated with significant hypokalemia due to potassium shifting into cells in exchange for hydrogen ions.

Inadequate potassium intake

Now a rare cause of hypokalemia. Historically observed in infants fed commercially prepared cow’s milk with low chloride content, resulting in hypochloremic metabolic alkalosis and hypokalemia.

Organ potassium losses

Renal potassium losses:

• diuretic therapy
• excessive mineralocorticoid activity
• renal tubular acidosis (RTA)
• hyperreninemia
• diabetic ketoacidosis

Gastrointestinal potassium losses:

• vomiting and/or diarrhea

Rare causes

Hypokalemic periodic paralysis — an autosomal dominant hereditary disorder. The underlying cause is a mutation of the α-1S subunit of the T-tubule calcium channel in skeletal muscle, or a mutation of the ryanodine receptor, which regulates calcium release from the sarcoplasmic reticulum.

Clinical Presentation

In general, clinical manifestations depend on the rate of potassium decline. Acute decreases cause severe symptoms, whereas chronic deficits may be well tolerated.

• cardiac manifestations
• arrhythmias,
• ECG changes: low, flattened, or inverted T waves, prominent U waves, prolonged QT interval

These findings are most pronounced in lead II. Supraventricular and ventricular extrasystoles may occur. Severe risk when K⁺ < 3 mmol/L.

Neuromuscular manifestations

Muscle weakness up to paralysis, including respiratory muscles → respiratory insufficiency. Smooth muscle dysfunction leading to constipation or paralytic ileus. When K⁺ < 2 mmol/L, impaired vasodilatory response during exertion may cause muscle ischemia and rhabdomyolysis.

Metabolic effects

Hypokalemia inhibits insulin release → reduced glucose tolerance. Due to effects on protein metabolism, chronic hypokalemia may cause growth impairment.

Renal manifestations

Kaliopenic nephropathy. Reduced concentrating ability of the kidneys → polyuria, thirst, polydipsia.

Endocrine manifestations

Decreased production of aldosterone and insulin. Increased production of renin.

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Hyperkalemia

Hyperkalemia is an elevation of potassium levels in the blood. Normal values are 3.8–5.0 mmol/L. Clinically significant hyperkalemia occurs when potassium levels rise above 6 mmol/L, and it becomes dangerous when levels exceed 7 mmol/L. Since serum potassium concentration depends on the state of acid–base balance, it must always be evaluated in relation to the pH value (see Relationships between acid–base balance and the ionogram).

See this video in English: https://www.wikiskripta.eu/w/Soubor:Hyperkalemia.webm

CAVE!!! In hyperkalemia, the total body potassium stores may be increased, normal, or decreased!

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Causes

Potassium retention

• increased intake
• administration of rapid K⁺ infusions
• transfusion of old blood with erythrocyte breakdown
• dietary intake (but only in impaired renal function)
• decreased elimination
• during the oliguric phase of acute renal failure (in chronic renal failure, the disorder results from altered distribution of K⁺ between the intracellular and extracellular compartments)
• decreased secretion in tubular disorders (cells are insensitive to aldosterone)
• in hypocorticalism – deficiency of mineralocorticoids (and glucocorticoids)
• excessive administration of potassium-sparing diuretics (which act as aldosterone antagonists)

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Shift of potassium from cells into the extracellular compartment (distributional hyperkalemia)

• cell breakdown (crush syndrome, necrotic tumor lysis, hemolysis, extreme physical exertion)
• acidosis (exchange of K⁺ for H⁺)
• hyperosmolarity
• catabolic states (K⁺ bound in proteins is released)
• insulin deficiency (insulin promotes the shift of K⁺ into cells)
• administration of β-blockers (which antagonize the effects of adrenaline)

CAVE!!! In prolonged acidosis, potassium depletion develops despite concurrent hyperkalemia!

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Pseudohyperkalemia

Apparent or spurious hyperkalemia that may result from improper blood collection due to prolonged venous stasis (long application of a tourniquet, repeated fist clenching) or hemolysis (e.g., an old or mishandled sample).

Therapy

Immediate Stabilization

Indicated in the presence of visible ECG changes or cardiac arrest with suspected hyperkalemia.

Intravenous calcium – reduces the risk of malignant arrhythmias (stabilizes cardiomyocyte membranes by an unclear mechanism, partly by shifting the threshold potential to less negative values):

Calcium chloride 10%: 25–50 mg/kg (0.1–0.2 ml/kg), 10 ml in adults

Calcium gluconate 10%: 0.5–1 ml/kg, 20–30 ml in adults

Onset of action is immediate, with duration of approximately 30 minutes.

Circulatory Stabilization – Correction of Dehydration

Hypovolemia potentiates and induces all forms of renal failure. Administration of diuretics alone in a hypovolemic oliguric patient may lead to severe kidney injury. Assessment of the patient’s hydration status and appropriate volume replacement is essential.

Shift of Potassium into Cells

Insulin with glucose

Insulin increases the intracellular shift of K⁺: 1 IU of insulin requires 5 g of glucose.

Administer glucose 0.5 g/kg + insulin 0.1 IU/kg IV over 30 minutes.

The effect becomes evident after approximately 30 minutes.

Bicarbonate

Especially in the presence of metabolic acidosis: 50 mmol (children 1–2 mmol/kg) IV, using a 4.2% solution.

The effect lasts about 30 minutes.

It is advisable to administer calcium before bicarbonate, as pH changes decrease ionized calcium levels.

β₂-agonists

Increase intracellular K⁺ uptake:

Ventolin (salbutamol) inhalation: 4 μg/kg/20 min in 20 ml of normal saline

Bricanyl (terbutaline) inhalation: 4–10 μg/kg/20 min in 20 ml of normal saline

IV administration is not superior to inhalation for this indication.

Effect begins after ~30 minutes and lasts 2–3 hours.

Removal of Potassium from the Body

Furosemide with concurrent IV administration of normal saline

Dose: 0.5–2 mg/kg, although the effect in the acute phase is limited and delayed.

In prerenal kidney failure (reduced filtration due to hypoperfusion), hydration—not furosemide alone—is necessary. Loop diuretics do not reduce mortality or time to recovery of renal function (Merta 2009); therefore, they represent only a temporary solution for hyperkalemia. Continuous furosemide administration is mainly recommended for states associated with fluid overload.

Calcium resonium

A non-absorbable resin and ion exchanger which releases calcium ions and binds potassium in the intestine after oral administration. This results in gradual potassium removal through stool.

References

Links

• Hyperkalemia
• Kalium

External links

• Template:Akutně
• Hypokalémia a EKG (TECHmED)

Source

• HAVRÁNEK, Jiří: Dysbalance kalia. (upraveno)
• RYŠAVÁ, Romana, Interní Med. 2006; 9: 385–388