Causes Of Low Potassium In The Blood – Dt. Neena LuthraDietitian/Nutritionist • 28 Years of Expertise. Master’s Degree – Dietetics / Nutrition, P.G. Diploma in Nutrition and Dietetics, B.Sc. home science

Potassium is an important mineral known as an electrolyte. Electrolytes are responsible for maintaining your body’s ion balance. Other electrolytes are sodium, calcium, magnesium, phosphate, chloride. These electrolytes carry an electrical charge that governs the electrical activity of your health system. Potassium also helps body muscles function properly. In fact, it contributes to regulating blood pressure; A very important role for a healthy heart.

Causes Of Low Potassium In The Blood

Potassium deficiency is a type of medical condition known as hypokalemia. The normal potassium level in the human body should be between 3.5-5.0 mmol/L. However, potassium deficiency can cause serious problems such as muscle weakness, nerve disorders, and heart problems. The kidney is the organ known to manage potassium balance by removing excess potassium through urine.

Hyperkalemia And Hypokalemia Notes: Diagrams & Illustrations

These are the symptoms people experience when they suffer from hypokalemia. Hypokalemia can make you feel extremely sick and can lead to many of the diseases discussed above. It is recommended that you consult a doctor if you encounter any of the symptoms mentioned above. Consult an expert and get answers to your questions! Potassium disorders are common. Hypokalemia (serum potassium level less than 3.6 mEq per L [3.6 mmol per L]) occurs in 21% of hospitalized patients and 2% to 3% of outpatients.

Hyperkalemia (serum potassium level greater than 5 mEq per L [5 mmol per L] in adults, greater than 5.5 mEq per L [5.5 mmol per L] in children, and greater than 6 mEq per L [6 mmol per L] in neonates ] over ) occurs in up to 10% of hospitalized patients and approximately 1% of outpatients.

Patients with a history of congestive heart failure or myocardial infarction should maintain a serum potassium concentration of at least 4 mEq per L (4 mmol per L).

Intravenous potassium should be used for patients with severe hypokalemia (serum potassium < 2.5 mEq/L [2.5 mmol/L]), hypokalemic ECG changes, or physical signs or symptoms of hypokalemia, or who cannot tolerate the oral form.

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Immediate intervention and possible ECG monitoring are indicated for patients with severe hypokalemia (serum potassium 6.5 mEq/L [6.5 mmol/L]); ECG changes; physical signs or symptoms; possible rapid onset hyperkalemia; or underlying kidney disease, heart disease, or cirrhosis.

Because the kidney can significantly reduce potassium excretion in response to decreased intake, inadequate intake is rarely the sole cause of hypokalemia but often contributes to hypokalemia in hospitalized patients.

When given at the same dosage, chlorthalidone is more likely to cause hypokalemia than hydrochlorothiazide, which is more commonly blamed for its widespread use.

Diuretic-induced hypokalemia is dose-dependent and tends to be mild (3 to 3.5 mEq per L [3 to 3.5 mmol per L]), but may be more severe if accompanied by other causes (e.g., gastrointestinal [GI] losses). .

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The mechanism by which upper GI losses cause hypokalemia is indirect and results from the kidney’s response to the associated alkalosis. Because some of the daily potassium is excreted from the colon, low GI losses in the form of persistent diarrhea can also cause hypokalemia and be accompanied by hyperchloremic acidosis.

Hypokalemia is often asymptomatic. Evaluation begins by looking for warning signs or symptoms that require immediate treatment (Figure 1).

These include weakness or palpitations, electrocardiogram (ECG) changes, severe hypokalemia (less than 2.5 mEq per L [2.5 mmol per L]), rapid onset hypokalemia, or underlying heart disease or cirrhosis.

Early identification of transcellular shifts is important because management may vary. Identification and treatment of concomitant hypomagnesemia is also important because magnesium depletion inhibits potassium replenishment and may exacerbate arrhythmias caused by hypokalemia.

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A focused history includes assessment of possible GI losses, review of medications, and assessment of underlying cardiac comorbidities. A history of stroke, hyperthyroidism, or use of insulin or beta agonists suggests possible intracellular shifts leading to redistributive hypokalemia. The physical examination should focus on identifying cardiac arrhythmias and neurological signs, which range from general weakness to ascending paralysis.

The diagnosis should be confirmed by repeated serum potassium measurement. Other laboratory tests include serum glucose and magnesium levels, urine electrolyte and creatinine levels, and acid-base balance. The most accurate method to assess urinary potassium excretion is to collect potassium in urine at 24-hour intervals; normal kidneys excrete no more than 15 to 30 mEq per L (15 to 30 mmol per L) of potassium per day in response to hypokalemia. A more practical approach is to calculate the urine potassium/creatinine ratio from a spot urine sample; A ratio greater than 1.5 mEq per mmol (13 mEq per g) is indicative of renal potassium loss.

If no cause is found on initial examination, evaluation of thyroid and adrenal function should be considered.

Typically, the first ECG sign of hypokalemia is decreased T wave amplitude. Further progression can lead to ST interval depression, T wave inversions, PR interval prolongation, and U waves. Arrhythmias associated with hypokalemia include sinus bradycardia, ventricular tachycardia or fibrillation, and torsade de pointes.

Hypokalemia Promotes Arrhythmia By Distinct Mechanisms In Atrial And Ventricular Myocytes

Although the risk of ECG changes and arrhythmia increases as serum potassium concentration decreases, these findings are unreliable because some patients with severe hypokalemia do not have ECG changes.

The immediate goal of treatment is to prevent potentially life-threatening cardiac conduction disturbances and neuromuscular dysfunction by increasing serum potassium to a safe level. Further regeneration may proceed more slowly and attention may turn to diagnosis and treatment of the underlying disorder.

Patients with a history of congestive heart failure or myocardial infarction should maintain serum potassium concentration at least 4 mEq per L (4 mmol per L) according to expert opinion.

Careful monitoring during treatment is important because potassium supplementation is a common cause of hyperkalemia in hospitalized patients.

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The risk of rebound hyperkalemia is higher when treating redistributive hypokalemia. Since serum potassium concentration decreases by approximately 0.3 mEq per L (0.3 mmol per L) for every 100 mEq (100 mmol) decrease in total body potassium, an approximate potassium deficit can be estimated in patients with abnormal losses and reduced intake. For example, a decrease in serum potassium from 3.8 to 2.9 mEq per L (3.8 to 2.9 mmol per L) roughly corresponds to a decrease in total body potassium of 300 mEq (300 mmol). If losses continue, additional potassium will be required. Concomitant hypomagnesemia should be treated simultaneously.

Another strategy to treat a comorbid condition, unless otherwise indicated, is to use an angiotensin-converting enzyme (ACE) inhibitor, angiotensin receptor blocker (ARB), beta blocker, or potassium-sparing diuretic because each of these drugs is associated with an increase in the risk of heart disease. in serum potassium.

It is appropriate to increase dietary potassium in patients with low-normal and mild hypokalemia, especially those with a history of hypertension or heart disease.

However, the effectiveness of increasing dietary potassium is limited because most of the potassium found in foods is incorporated into phosphate, whereas most cases of hypokalemia involve chloride depletion and respond best to potassium chloride supplementation.

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Because intravenous potassium use increases the risk of hyperkalemia and may cause pain and phlebitis, intravenous potassium should be reserved for patients with severe hypokalemia, hypokalemic ECG changes, or physical signs or symptoms of hypokalemia, or who cannot tolerate the oral form. Rapid correction is possible with oral potassium; The most rapid results are probably best achieved by a combination of oral (e.g., 20 to 40 mmol) and intravenous administration.

When intravenous potassium is used, standard practice is 20 to 40 mmol of potassium in 1 L of normal saline. Correction should typically not exceed 20 mmol per hour, although higher rates using central venous catheters are successful in emergencies.

If the rate exceeds 10 mmol per hour, continuous cardiac monitoring is indicated. In children the dose is 0.5 to 1.0 mmol per kg per L per hour (maximum 40 mmol).

Non-urgent hypokalemia is treated with 40 to 100 mmol of oral potassium daily for days to weeks. 20 mmol per day is usually sufficient to prevent hypokalemia in patients with persistent depletions such as ongoing diuretic therapy or hyperaldosteronism.

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The etiology of hyperkalemia is often multifactorial; Renal dysfunction, medication use, and hyperglycemia are the most common contributing factors.

Because healthy individuals can adapt to excessive potassium consumption by increasing excretion, increased potassium intake is rarely the sole cause of hyperkalemia, and underlying renal dysfunction is common.

Renal-mediated hyperkalemia results from impairment of one or more of the following processes: flow rate in the distal nephron, aldosterone secretion and effects, and functioning of potassium secretory pathways. Hyperkalemia due to decreased distal sodium and water conduction occurs with congestive heart failure, cirrhosis, acute kidney injury and advanced chronic kidney disease. Conditions that cause hypoaldosteronism, such as adrenal insufficiency and hyporeninemic hypoaldosteronism (a common complication of diabetic nephropathy and tubulointerstitial diseases), can lead to hyperkalemia.

Various mechanisms promote the exit of potassium from cells or inhibit its entry, thereby increasing the plasma potassium concentration (redistributive hyperkalemia). Increased plasma osmolality, as in uncontrolled diabetes, creates a concentration gradient in which potassium follows water out of the cells. Relative

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