The problem of hyperkalemia in patients with chronic heart failure

Mastopathic chest pain

The characteristic breast pain is accompanied by swelling, hardness and is often associated with another disease - endometriosis. Pain from mastopathy usually goes away with the onset of menstruation, and then returns almost immediately. The cause of mastopathy is usually hormonal disorders. The changes usually appear between the ages of 30 and 40 and gradually disappear after menopause. To confirm them, it is necessary to do an ultrasound, measure the level of hormones in the blood, and sometimes a mammogram. Hormonal drugs are used in treatment.

4.Treatment

With moderate and severe severity, hyperkalemia requires emergency intensive care due to the threat of cardiac arrest. One of the emergency measures is the intravenous administration of a special solution (calcium, insulin, glucose), but its effect is short-lived, and after relief of life-threatening symptoms, further therapy is required. Potassium-absorbing sorbents are prescribed (which ensures its excretion in feces); diuretics are used if renal function is preserved. Stop taking any medications that in one way or another affect the circulation of potassium in the body. Limit potassium intake from food. Since hyperkalemia is almost always secondary, a diagnostic examination (if the cause of the detected hyperkalemia is unknown) and treatment of the underlying disease are mandatory.

Breast pain caused by bra

Diseases can have very mundane causes, for example, injuries caused by strong seat belt tension in a car when braking. Breast pain also affects women who wear ill-fitting bras (for example, with cups that are too small). When shopping for a bra, be sure to measure the circumference under your bust and around your chest at nipple level. There should be 1-2cm of sag in the cups because breasts swell and change shape over the course of a month, and under the bust the bra should fit snugly but not cut into the body. Be careful with underwire bras as they can put too much pressure on your breasts and cause pain.

How do drugs interfere with potassium excretion?

The established mechanisms of impaired potassium excretion are associated with the effects of drugs on the renin-angiotensin-aldosterone system.

1. Spironolactone inhibits the synthesis of potassium compounds in the collecting ducts of the renal tissue. As an aldosterone antagonist, it occupies sensory receptors (nerve endings) of cells. Protein complexes are formed: Spironolactone + receptor. This results in increased sodium excretion but retains potassium.
2. Triamterene and Amiloride directly inhibit the production of potassium salts.
3. The group of ACE inhibitors increases potassium concentrations by blocking Angiotensin II, and through it they reduce the synthesis of aldosterone. When taking ACE inhibitors in combination with chronic renal failure (CRF), potassium accumulation increases more rapidly.
4. Heparin - has a direct blocking effect on aldosterone synthesis. Therefore, great caution is required when prescribing it to patients with renal failure due to diabetes mellitus, since hyperkalemia and acidosis aggravate the clinical picture.

Diseases such as nephropathy associated with kidney compression, sickle cell anemia, post-transplant condition, systemic lupus erythematosus cause a defect in the structure of the tubules, the release of potassium is delayed. Patients react poorly to the administration of Furosemide and Potassium chloride.

Neoplastic chest pain

Breast pain caused by cancer usually only appears when the tumor usually grows more than 1 centimeter, and the woman feels it during a breast self-exam. In such a situation, quick diagnosis is important. Therefore, you should definitely consult a doctor if you feel any changes in your breasts. In the vast majority of cases, the disease is curable. Surgery is required, and in the case of a malignant tumor, surgery and chemoradiotherapy. Every woman should remember about breast cancer prevention, which should include regular examinations, that is, from the age of 25, an ultrasound examination is required once a year, and after 50, a mammogram. Moreover, every month, after the end of menstruation, a woman should perform a breast self-examination. If she does them regularly, she will be able to detect any alarming changes. In the case of breast cancer, genetics are also important - women who have had or have mothers, grandmothers or aunts in the family who have suffered from this disease in the past should be regularly examined. It is very important to check whether any women in your immediate family have suffered from breast cancer. BRCA1 and BRCA2 genetic tests should then be performed to confirm or rule out mutations in the genes responsible for the formation of not only breast cancer, but also ovarian cancer.

Potassium is largely an intracellular cation, and its concentration inside and outside the cell is regulated by various mechanisms. When they are violated, hyperkalemia or hypokalemia develops. Hyperkalemia is a condition in which the concentration of potassium in the extracellular fluid is more than 5 mmol/kg. According to research, the total potassium content in the body is about 50 mmol/l, of which 98% is found inside cells. On average, the intracellular potassium concentration is 150 mmol/L, and the extracellular concentration is about 4 mmol/L. Maintaining the ratio of potassium concentrations inside and outside the cell depends on several factors: potassium intake from food and drink, its redistribution between intra- and extracellular compartments and renal excretion.

Potassium homeostasis

About 90% of enteral potassium is excreted by the kidneys and partially eliminated in the stool. However, renal excretion is slow, and in the initial stages the body requires extrarenal mechanisms to maintain potassium concentrations.

Renal potassium excretion

The rate of excretion by the kidneys depends on a number of factors: sodium concentration in the tubules, the renin-angiotensin-aldosterone system, vasopressin, the amount of potassium ingested and its plasma concentration, acid-base status and diuresis rate. Potassium secretion occurs passively in the distal nephron loop and depends on a transmembrane concentration gradient generated primarily by sodium reabsorption.

Aldosterone plays a major role in potassium homeostasis via renal mechanisms. As a result of its action on the connecting segments of the main cells of the cortical and medullary collecting ducts and collecting duct, it increases potassium secretion. If we consider the mechanism of its action at the cellular level, aldosterone opens apical sodium channels and increases Na+/K+-ATPase activity on the basolateral membrane.

The main stimulus for the release of aldosterone is angiotensin II: an increase in its plasma concentration by as little as 0.1 mmol/l causes a significant increase in the synthesis of aldosterone in the zona glomerulosa of the adrenal glands. Aldosterone is also involved in extrarenal regulatory mechanisms, increasing potassium secretion in the intestines and salivary glands. Normally, the intestine accounts for about 5% of potassium excretion, but in renal failure, intestinal excretion increases to 30–50%.

• An increase in plasma potassium concentration is an aldosterone-independent stimulator of Na+/K+- ATPase in the distal segments of the tubules, which, as we remember, helps to increase potassium secretion by the kidneys;
• Increasing the rate of diuresis and Na delivery increases the rate of K secretion;
• In conditions where sodium delivery is impaired (hyponatremia, the effect of drugs: amiloride, triamterene, etc.), the electrochemical gradient causing K secretion decreases.

Extrarenal mechanisms regulating K concentration

Insulin

Physiological insulin levels play an important role in regulating potassium levels. Insulin is a stimulator of Na+/K+-ATPase in liver cells, muscles, and fat cells, which promotes the entry of K+ into the cell. Therefore, in conditions accompanied by a lack of insulin production (diabetes), hyperkalemia often develops.

Catecholamines

Catecholamines, especially beta-2 agonists, stimulate the Na+/K+ ATPase of cells and lead to the movement of K+ into the cell. Administration of epinephrine, albuterol, or salbutamol reduces blood potassium levels, but isoproterenol and beta-1 agonists have no effect on potassium levels. Alpha adrenergic agonists, such as phenylephrine, interfere with the entry of potassium into the cell, thereby increasing its plasma concentration.

Acid-base state

With a decrease in pH by 0.1 U, the concentration of potassium in plasma increases by 0.6 mmol/l (ranging from 0.3 to 1.3 mmol/l), and, accordingly, decreases with increasing pH. However, it has been observed that respiratory acidosis causes less change in potassium concentration than metabolic acidosis.

Pseudohyperkalemia

Pseudohyperkalemia is a phenomenon of increased potassium concentration in vitro with normal values ​​in vivo. Pseudohyperkalemia can be considered when the difference in potassium concentration between the analyzed sample and the patient's plasma is more than 0.5 mmol/L. This condition can be caused by many reasons: thrombocytosis more than 750,000 per mm3, leukocytosis with a cell count more than 50,000 per mm3, hereditary spherocytosis, hemolysis in the blood sample, late separation of plasma and red blood cells, use of inappropriate anticoagulants for the blood sample, incorrect venipuncture, as well as clenching a fist during puncture. According to studies, the use of a tourniquet for venipuncture does not play any role in the development of pseudohyperkalemia.

Causes of hyperkalemia

I. Increased intake of potassium into the body:

Exogenous:

• Foods containing a significant amount of potassium (for example, bananas, etc.);
• Potassium chloride salts;
• Potassium, which is part of penicillin G;
• Collins preservative solution;
• Blood transfusion (increasing the amount of potassium during long-term blood storage);
• Geophagy;
• Medicinal plants: alfalfa, dandelion, nettle, spurge, etc.

Endogenous:

• Increased hemolysis;
• Increased physical activity;
• Gastrointestinal bleeding;
• Increased catabolism;
• Rhabdomyolysis;
• Tumor disintegration.

II. Decreased renal potassium excretion:

1. Chronic kidney disease;

2. Acute renal failure;

3. Disturbance of distal tubular secretion (primary and secondary):

• Primary disorder of tubular secretion;
• Systemic lupus erythematosus;
• Sickle cell anemia;
• Obstructive uropathy;
• Consequences of kidney transplantation;
• Kidney amyloidosis;
• Tubulointestinal nephritis;
• Papillary necrosis.

4. Disorders of the renin-angiotensin-aldosterone system:

• Medicines: ACE inhibitors and AT receptor blockers, NSAIDs, calcineurin inhibitors (tacrolimus, cyclosporine), heparin, lithium preparations, aldosterone antagonists (spironolactone);
• Primary hypoaldosteronism;
• Chronic adrenal hyperplasia;
• Primary hyporenism;
• Hyporenic hypoaldelateralism (type IV renal tubular acidosis);
• Adrenal insufficiency: - Primary (Addison's disease); — Destruction of the adrenal glands as a result of the development of infectious diseases (HIV, CMV, Mycobacterium tuberculosis, Mycobacterium avium); - Blockade of sodium channels of main cells caused by taking various drugs such as triamterene, amiloride, trimethoprim, pentamidine, etc.; - Gordon's syndrome.

5. Impaired sodium transport in the distal canals:

• Chronic heart failure;
• Cirrhosis of the liver;
• Salt wasting nephropathy;
• Kidney failure.

III. Movement of potassium between cells:

1. Hyperglycemia;

2. Use of certain medications:

• Non-selective beta blockers;
• Succinylcholine;
• Mannitol;
• Digoxin (Na+/K+-ATPase inhibitor);
• Somatostatin;
• Intravenous administration of amino acids (arginine, lysine, epsilon-aminocaproic acid);

3. Acute metabolic acidosis caused by mineral acids;

4. Action of herbs (Na+/K+-ATPase inhibitors): oleander, foxglove, yew berries, kendar, Siberian ginseng, etc.;

5. Excessive physical activity;

6. Acute hemolysis;

7. Fluoride poisoning;

8. Hyperkalemic periodic paralysis;

Clinical manifestations

As mentioned earlier, the toxic effect of hyperkalemia is manifested in the depolarization of the membranes of cardiac and skeletal muscle cells.

Cardiac manifestations of hyperkalemia include: peaked T-waves, prolongation of the PR interval, widening of the QRS complex along with the disappearance of atrial electrical activity, ventricular fibrillation (VF), and asystole. VF and asystole may be the initial manifestations of hyperkalemia, however, even with potassium levels above 9 mmol/l, ECG manifestations may be absent.

From the neuromuscular system, hyperkalemia is manifested by diarrhea, abdominal pain, myalgia and flaccid paralysis. Factors that aggravate the manifestations of hyperkalemia are concomitant metabolic disorders, such as metabolic acidosis, hypocalcemia or hyponatremia.

Mortality from hyperkalemia in hospitalized patients ranges from 1.7 to 41%. Cardiac causes make the greatest contribution to these figures. Mortality studies for hyperkalemia have found that treatment is often inadequate or not treated at all.

Treatment

Hyperkalemia is a life-threatening condition and must be treated promptly. Potassium levels ≥ 6 mmol/L are considered to require more aggressive therapy. When the upper limit of normal is less than that, the goal of treatment is to remove excess potassium from the body and prevent recurrent episodes of hyperkalemia by finding the causes and eliminating them.

As soon as an increase in potassium levels is registered in the patient, then, depending on the severity of the condition, an examination is carried out using the ABCDE algorithm, and electrocardiographic monitoring in 12 leads is also established. During ECG monitoring, possible manifestations of conduction and excitability disorders are identified: pointed T-waves, flat P waves or their absence, sinusoidal waves, prolongation of the PR interval, expansion of the QRS complex, ventricular tachycardia.

If abnormalities are detected on the ECG, calcium supplementation is prescribed. Calcium is a direct antagonist of potassium-induced intracellular depolarization and, when administered, is capable of normalizing the membrane potential.

Recommended doses of calcium: calcium gluconate 10% - 30 ml or calcium chloride 10% - 10 ml. The drugs are administered intravenously as a bolus over 5–10 minutes; good intravenous access is required for this. The effect of calcium supplements develops within a few minutes, but does not last long (30–60 minutes); if necessary, a second dose can be administered after 5 minutes. However, it is worth remembering the danger of developing life-threatening arrhythmias when using these drugs in patients with concomitant digoxin intoxication: therefore, during the administration of calcium, it is necessary to monitor the patient even more carefully.

The next step in the treatment of hyperkalemia is the administration of insulin. As stated earlier, insulin has a strong hypokalemic effect, regardless of blood glucose levels. There are many insulin administration regimens for hyperkalemia: the most common is the intravenous administration of 10 units of fast-acting insulin against the background of an infusion of 25–50 grams of glucose, followed by monitoring blood glucose levels. In the presence of significant hyperglycemia (more than 250 mg/dL or 13.9 mmol/L), insulin administration without concomitant administration of glucose is acceptable. This administration regimen allows reducing potassium levels by more than 0.5 mmol/L in all patients. The hypokalemic effect of the glucose-insulin mixture develops after 10 minutes, and the maximum effect (decrease in potassium concentration from 0.65 to 1 mmol/l) is achieved by 30 minutes and lasts from 4 to 6 hours.

The next option is the use of catecholamines. Catecholamines activate the Na+/K+-ATPase of cells and promote the transition of potassium into the cell. For these purposes, it is advisable to use beta-2 agonists (adrenaline, albuterol, terbutaline, salbutamol, salmeterol) intravenously or through a nebulizer or metered dose inhaler. These drugs can reduce potassium levels from 0.5 to 1.5 mmol/l. The onset of the hypokalemic effect occurs after 3–5 minutes, reaching a maximum by 30 minutes when administered intravenously and by 60 minutes when using a nebulizer; the total duration of action is from 3 to 6 hours. For inhalation via a nebulizer, it is preferable to use albuterol 10–20 mg or salbutamol 10–20 mg. Side effects of beta-2 agonists include tremor and tachycardia, as well as, if hypoglycemia develops, masking of its symptoms. The use of bicarbonate for hyperkalemia has not been shown to be effective and, given the risk of hypernatremia and fluid overload, is not recommended as initial or monotherapy.

Removing potassium from the body

Diuretics

Loop or thiazide diuretics may play an important role in the treatment of chronic hyperkalemia. However, their use in acute hyperkalemia is limited due to significant losses of sodium when the required potassium level is achieved, as well as disturbances in water balance. Patients also often have renal failure, which limits the use of diuretics.

Ion exchange resins

Sodium polystyrene sulfonate (Keoxalate) is an ion exchange resin that exchanges potassium cations for sodium. Also widely used is the calcium drug resonium, which binds and removes excess potassium. During prolonged contact (for at least 30 minutes) in the intestine with potassium-secreting cells, each gram of the drug binds from 0.65 to 1 mmol of potassium, which is then excreted in the feces. These drugs can be used either per rectum using an enema or orally in the form of tablets.

The main limitation of the use of resins is the development of osmotic diarrhea after 2 hours with a maximum after 4–6 hours, as well as the likelihood of developing intestinal necrosis. The use of resins is contraindicated in patients with intestinal obstruction or intestinal ischemia and in the early postoperative period after kidney transplantation. Ion exchange resins can be used as monotherapy for chronic hyperkalemia or mild acute hyperkalemia with potassium levels less than 6 mmol/l with evaluation of treatment effectiveness.

Dialysis

Removing potassium from the body by hemodialysis or other renal replacement therapy (RRT) is the most effective method currently available. Different dialysis modes differ in the speed at which the effect develops. Conventional hemodialysis reduces potassium levels much more quickly than peritoneal dialysis or continuous regimens (continuous venovenous hemofiltration, continuous venovenous hemodialysis, or continuous venovenous hemodiafiltration).

Studies have shown that with hemodialysis, the rate of potassium reduction can reach 25–50 mmol/hour, with a significant decrease in plasma potassium levels (about 1.3 mmol/L) during the first hour of therapy. During conventional hemodialysis, which usually involves simultaneous ultrafiltration and dialysis, potassium removal by ultrafiltration accounts for about 15% of the total potassium removed, and by dialysis the remaining 85%. The amount of potassium removed depends on the potassium content of the dialysate and its gradient with plasma, the duration of the dialysis session, the size and permeability of the filter membrane, and the volume of ultrafiltration.

After taking urgent measures to reduce potassium levels, it is necessary to analyze the patient’s medical history, diet, medications taken (stop taking medications that increase potassium levels), and eliminate the causes that can lead to recurrent hyperkalemia. Subsequently, until the potassium level stabilizes in these patients, it is recommended to monitor it every 2 hours and, if necessary, repeat the measures according to the algorithm.

Pathogenesis

The pathogenesis of hypokalemia is diverse and determined by its form. The kidneys play a major role in maintaining potassium homeostasis. The level of potassium is determined by a combination of several processes, namely: potassium filtration, secretion and reabsorption. Since potassium in the blood plasma is in a free state, it is completely filtered in the renal glomeruli; potassium ions passing through the filter are almost completely reabsorbed in the distal/proximal tubules.

The process of potassium excretion by the kidneys is under humoral control, the main role in which belongs to mineralocorticoids ( aldosterone ), which both increases the penetration of potassium ions into the cells of the distal tubule and increases the permeability of the cell membrane to potassium, promoting potassium secretion. insulin also takes part in the processes of regulation of potassium excretion by the kidneys , which reduces the excretion of potassium by the kidneys. The state of acid-base balance has a significant influence on kaliuria. Thus, with alkalosis , hypokalemia develops as a result of the transition of potassium found in the blood plasma into cells. Potassium deficiency is observed with increased/accelerated breakdown of proteins in the body, which helps to force the release of potassium.

Diagnostics

Patients with this electrolyte disorder are treated by doctors of different specialties, depending on what caused its development. Most often these are gastroenterologists, nephrologists, and endocrinologists. It is found out what medications the patient is taking. During examination, the most important thing is to identify symptoms such as muscle hypotension and arrhythmic pulse. An additional examination is prescribed, which includes:

• Laboratory research.
  Blood CBS, magnesium, sodium, calcium content are determined. A biochemical blood test examines the concentration of creatinine, urea, and creatine phosphokinase. A urine test checks its relative density and the presence of chlorine. To differentiate between renal and extrarenal causes of hypokalemia, the transtubular potassium gradient (the ratio of serum to urine osmolarity between urine and plasma K+ levels) is calculated.
• Hormonal spectrum.
  To exclude aldosteroma, the levels of aldosterone and renin are measured to calculate the renin-aldosterone ratio. If there are corresponding symptoms of endocrine pathology, tests are performed for thyroid-stimulating hormone, cortisol, and 17-OH-progesterone.
• Electrocardiography.
  ECG is the main instrumental research method for diagnosing hypokalemia. The following changes are noted: depression of the ST segment, appearance of a U wave, prolongation of the QT interval. With severe electrolyte imbalance, paroxysmal ventricular tachycardia occurs, sometimes developing into atrial fibrillation.
• Instrumental research.
  To visualize aldosteroma, ultrasound and CT scan of the adrenal glands are performed. In case of kidney diseases, an ultrasound of the kidneys with Doppler sonography is performed. If chronic heart failure is suspected, echocardiography is prescribed. To confirm renovascular hypertension, selective angiography of the renal arteries is informative.

The differential diagnosis should be primarily with hyperkalemia, since these conditions have similar clinical symptoms. Hypokalemia should also be distinguished from neuromuscular diseases (myasthenia gravis, Guillain-Barre syndrome, muscular dystrophies), diseases occurring with insipidal syndrome (diabetes mellitus, diabetes insipidus). Acute paralysis requires the exclusion of stroke.

Causes of hypokalemia

A relative physiological cause of the development of potassium deficiency is considered to be insufficient intake of the macronutrient from food, which is often observed in people who follow strict diets or have a poor diet.

Pathological hypokalemia in children and adults occurs for various reasons:

• Gastrointestinal problems. The electrolyte balance is disrupted by various gastrointestinal pathologies, including profuse diarrhea or prolonged vomiting.
• Excessive intake of potassium into cells. Against the background of some pathologies occurring in the body, there is a movement of potassium ions from the intercellular space into the cells. This is possible with an excess of catecholamines, metabolic alkalosis (a shift in pH levels to the alkaline side), the use of large doses of insulin in patients with diabetic ketoacidosis, alcohol abuse, familial periodic paralysis, and an overdose of certain vitamins (for example, folic acid).
• Impaired renal tubular function. Due to this pathology, potassium transport is disrupted and its excretion increases. This is possible with renal acidosis, renal artery stenosis, Barter syndrome, interstitial nephritis.
• Hyperaldosteronism. The excretion of potassium ions by the kidneys stimulates aldosterone. The condition when the adrenal cortex secretes large amounts of aldosterone is called hyperaldosteronism. It can be primary, arising from an aldosterone-producing adrenal tumor, and secondary, caused by a renin-secreting tumor, chronic renal failure or renovascular hypertension due to occlusion of the renal artery.
• Endocrine disorders. Hypokalemia often develops with congenital dysfunction of the adrenal cortex, Itsenko-Cushing syndrome, and thyrotoxicosis.
• Treatment with certain medications. Most often, potassium deficiency occurs while taking thiazide and loop diuretics. Other drugs that can cause hypokalemia are bronchodilators, beta-agonists, some antibiotics (especially penicillins), tocolytics, theophylline, etc.

Other possible causes: use of a nasogastric tube, extensive burns, hypomagnesemia, hypernatremia, cirrhosis of the liver, lymphoblastic leukemia, diabetes insipidus.

Symptoms

Symptoms of hypokalemia depend on the level of potassium in the body, however, it should be borne in mind that plasma potassium concentrations do not accurately reflect the state of potassium balance. Symptoms and complaints of patients accompanying a decrease in potassium concentration in the body are nonspecific and quite varied, so in most cases we are not talking about the clinical picture, but about various clinical masks of hypokalemia.

The main signs of potassium deficiency are observed when its total amount decreases in the range of 10-30%; a decrease in potassium content below 1.5 mmol/l causes paralysis of the respiratory muscles. Symptoms of potassium deficiency in the body in women and potassium deficiency in the body in men manifest themselves with the same symptoms.

The first signs of potassium deficiency are associated with impaired neuromuscular excitability, which is caused by impaired polarization/depolarization of cell membranes and is manifested by asthenia / muscle weakness , increased fatigue , paresthesia /muscle spasms, and decreased tendon reflexes. With chronic hypokalemia, functional disorders and structural damage to both the peripheral and central nervous systems appear, which is realized by psycho-emotional disorders in the form of hypochondriacal, asthenic or anxiety-depressive syndromes.

Sensory disturbances manifest as mild paresthesia of the limbs/face or loss of tactile/pain sensitivity or severe hyperesthesia . Movement disorders correlate with the severity/duration of hypokalemia, ranging from mild muscle weakness of the upper and lower extremities, decreased tendon reflexes, to paralysis, including respiratory muscles. Hypokalemia can also manifest itself in symptoms/changes in the digestive system (intestinal paresis, flatulence , vomiting, paralytic intestinal obstruction constipation ), as well as in the genitourinary system ( polyuria , atony of the bladder , necrosis in the kidneys).

One of the most common manifestations of hypokalemia are disorders of cardiovascular activity, which are characterized by dilation of the cavities of the heart, decreased contractile function of the myocardium, the presence of systolic murmur at the apex of the heart, and decreased blood pressure .

The damaging effect of potassium ion deficiency in the body is well reflected in the ECG, which allows it to be used as a kind of indicator of latent hypokalemia. Characteristic ECG signs of hypokalemia include ventricular extrasystoles , T wave depression/inversion, QRS prolongation, pronounced U wave, and ST segment depression (Figure below).

As a rule, with potassium deficiency, there is a decrease in mental/mental activity, manifested in lethargy, apathy, and with a significant deficiency, the development of a coma is possible.

What symptoms indicate an increase in potassium in the blood?

Symptoms of hyperkalemia are caused by impaired transmission of nerve impulses to muscle tissue and changes in the properties of the myocardium (excitability and contractility).

Weakness increases to the point of paralysis

A patient with other chronic diseases complains of:

• muscle weakness;
• a feeling of heart failure in the chest, periodically a feeling of fading and stopping;
• nausea, lack of appetite.

Prolonged hyperkalemia leads a person to exhaustion.

In children, symptoms of hyperkalemia include:

• low mobility;
• flaccid paralysis in the muscles;
• bradycardia;
• decrease in blood pressure.