Hyperkalemia

Introduction to hyperkalemia Hyperkalemia is called potassium hyperperoxide above 5.5 mmol/L, and severe hyperkalemia is >7.0 mmol/L. Due to hyperkalemia, there is often no or very few symptoms and sudden cardiac arrest, should be detected early, early prevention. basic knowledge The proportion of illness: 0.03% Susceptible people: no specific population Mode of infection: non-infectious Complications: hyponatremia hypokalemia

Cause of hyperkalemia

(1) Causes of the disease

1. Ingest too much simple or ingestion of foods containing more potassium, drugs (such as penicillin potassium salt, potassium chloride) or input too much stock blood (due to red blood cell destruction, potassium is released into the plasma), using veins When potassium is added to correct hypokalemia, if it is slowly instilled, it will not cause hyperkalemia, because potassium can be excreted from the kidneys unless:

1 renal function potassium function is impaired;

2 The amount of potassium intake exceeds the ability of the kidney to excrete potassium.

2. Common clinical reasons for excretion reduction are the use of potassium-sparing diuretics, such as triamterene, spironolactone and amiloride, other drugs that cause hyperkalemia, and angiotensin-converting enzyme inhibitors, non-steroids. Anti-inflammatory drugs, long-term use of heparin (inhibition of aldosterone secretion), compound bromide, pentamidine and digitalis overdose, beta blockers and cyclosporine, renal insufficiency, oliguria and no Patients with urinary, adrenal insufficiency have aldosterone deficiency such as Addison's disease, 17-hydroxylase deficiency, selective hyporenin hypoaldosteronism and aldosterone insensitivity syndrome.

3. Potassium is removed from the cell to the outside of the cell. It is seen in: 1 large area tissue damage and necrosis, such as severe electrical burns, crush injury, muscle lysis, high heat and heat stroke (due to red blood cell and muscle cell lysis), massive hemolysis in the blood vessels, among which Some diseases can occur acute renal failure, aggravating hyperkalemia, 2 drugs, treatment of hepatic encephalopathy and metabolic alkalosis with arginine hydrochloride or lysine often occur hyperkalemia, may be arginine Exchange with intracellular potassium to move potassium to the outside of the cell; use of the muscle relaxant succinylcholine during anesthesia also allows the intracellular potassium to move to the extracellular action. 3 Cancer patients can be acute when treated with large doses of chemical drugs. Tumor lysis syndrome causes hyperkalemia, 4 familial hyperkalemia periodic paralysis, this disease is an autosomal genetic disease; secondary hyperkalemia (sinus patients with renal failure taking spironolactone is a common cause), 5 acid Poisoning, including metabolic acidosis, diabetic ketoacidosis and lactic acidosis, 6 hypertonic state, severe water loss, shock, etc. can cause intracellular potassium to move outside the cell.

(two) pathogenesis

1. Excessive potassium intake Because the kidney has a strong ability to excrete potassium, normal people will not produce hyperkalemia even if they consume too much potassium-containing food. Common hyperkalemia mainly occurs in patients with renal insufficiency. Acceptance of potassium-containing intravenous rehydration is more likely to occur, according to statistics, about 4% of patients receiving KCl can develop hyperkalemia.

2. The redistribution of potassium inside and outside the cell leads to changes in the distribution of potassium inside and outside the cell, and the increase in serum potassium is mainly caused by cell damage, hyperosmolaremia, acidosis, drug poisons, and high potassium periodic paralysis.

Cell damage is seen in rhabdomyolysis. After chemotherapy, the tumor cells are dissolved in a large amount and a large amount of hemolysis. High osmotic pressure can cause cell shrinkage, and the intracellular potassium concentration increases to 1~2mmol/L or more, which is beneficial to K+. The use of mannitol, mannitol, and the lack of adequate insulin in diabetic ketoacidosis are common causes of hyperosmolaremia.

Metabolic acidosis, especially caused by HCl, NH4Cl, etc., is most likely to induce hyperkalemia; while organic acids such as -hydroxybutyrate or lactic acid are less likely to occur, the difference between the two is mainly intracellular The effect of potassium release is different. Inorganic acid can cause more obvious intracellular acidification, which promotes the polarization of cell membranes, and more potassium can be released. The dissolution of organic acids is not as complete as that of inorganic acids, so the effect on membrane polarization is relatively better. Small, potassium escape is also less, in addition, acidosis can stimulate the H+-K+-ATPase on the cells between the collection tubes, can promote K+ reabsorption, and recently reported acidosis can also change the potassium channel on the collecting duct cells. The opening rate reduces the secretion of K+, which in turn may promote the production of ammonia together with acidosis, and then inhibit Na+ reabsorption through this mechanism, and reduce the excretion of K+.

Digitalis drugs, Palytoxin or tetrodotoxin can cause severe hyperkalemia.

High potassium periodic paralysis is less common in lower potassium periodic paralysis. This disease is caused by a mutation in the voltage-activated sodium channel gene that is sensitive to TTA in muscle, and is often induced after exercise.

3. The renal excretion of potassium is mainly caused by the decrease of salt corticosteroids, the decrease of Na+ transport in primary distal nephron and the abnormal function of cortical collecting duct.

Reduction of mineral corticosteroids can be caused by hyporenal hypoaldosteronism (common in diabetic nephropathy, tubulointerstitial nephritis, etc.), selective hypoaldosteronism (common after heparin administration), and Addison's disease.

Reduced Na+ delivery in primary distal nephrons causes renal sputum potassium to be more common in oliguric acute renal failure, acute glomerulonephritis, type II pseudoaldosteronism (Gordon syndrome), etc. Gordon syndrome is mainly due to Na+ The partial reabsorption of the proximal tubule to the cortical collecting duct is too small, resulting in excessive reabsorption of K+ in the distal convoluted tubule. The thiazide diuretic is effective for this disease, which may be related to the Na+-Cl-cotransporter distortion.

Abnormal cortical collecting ducts can cause hyperkalemia in the kidneys, mainly in type I pseudoaldosteronism, tubulointerstitial nephritis, obstructive nephropathy, sodium channel blockers and salt corticosteroid receptor blockers. Use, etc., wherein type I pseudoaldosteronism is caused by channel inactivation caused by epithelial sodium channel (ENaC) mutation; sodium channel blockers are methotrexate, TMP and pentamidine, used in kidney transplant patients May cause severe hyperkalemia, obstructive nephropathy often hyperkalemia, may be related to acidosis and renal tubular epithelial cells low response to salt corticosteroids.

Hyperkalemia prevention

Timely treatment of primary diseases (such as debridement, discharge of gastrointestinal hemorrhage) and avoid excessive intake of potassium-containing diet (such as fruits, coffee, etc.), such as acidosis as the cause of hyperkalemia, should be corrected as soon as possible Acidosis, discontinuation of drugs that increase blood potassium levels, including drugs that inhibit the renin-angiotensin-aldosterone system, beta adrenergic receptor blockers, indomethacin, and potassium in distal tubules Secreted drugs (such as spironolactone, triamterene), etc., should be actively treated to treat the primary disease, to avoid predisposing factors.

Hyperkalemia complications Complications hyponatremia hypokalemia

1. The most serious complication of this disease is cardiac arrest.

2. Hyperkalemia with hyponatremia: hyponatremia leads to decreased sodium pump activity, potassium ion transfer to the outside of the cell, leading to hyperkalemia, so when both are present, hyperkalemia is mostly low sodium The result of blood.

Because it is generally believed that hyperkalemia has a great influence on the body, and hyponatremia has a much smaller effect on the body, it tends to treat hyperkalemia, such as diuretic potassium, oral potassium ion exchange resin. Etc., the blood potassium concentration decreased, but the decrease of blood potassium concentration further weakened the activity of sodium pump, and the sodium ion transferred to the cells increased, which led to further aggravation of hyponatremia and hypoxia of the body, followed by hyponatremia. Correction will lead to an increase in the activity of the sodium pump. Potassium ions enter the cell and hypokalemia occurs. Therefore, when both are present, improper treatment is easy, and various complex disorders are prone to occur. It is difficult to control due to normal diet and parenteral nutrition. Potassium intake, in patients with "chronic refractory hyponatremia" with hyperkalemia, may also occur with "refractory hyponatremia" and "refractory hyperkalemia" after taking the above measures. Situation, and diuresis must be accompanied by the further loss of Na and the persistence of metastatic hyperkalemia, which must be paid special attention in clinical practice. Therefore, the core of treatment of such patients is not to increase the discharge of potassium ions. Sodium chloride is added, with increasing sodium ion concentration, hyperkalemia naturally corrected.

Hyperkalemia symptoms common symptoms abdominal pain irritability heart failure tachycardia nausea fatigue arrhythmia metabolic acidosis suffocation unconscious

The clinical manifestations of hyperkalemia are mainly the cardiovascular system and the neuromuscular system. The severity of the symptoms depends on the degree and speed of elevated potassium, and whether other plasma electrolytes and water metabolism disorders are present.

1. Cardiovascular symptoms High potassium causes myocardial depression and myocardial tension is reduced, so there is bradycardia and heart enlargement, heart sounds are weakened, arrhythmia is prone to occur, but heart failure does not occur, ECG has characteristic changes, and blood potassium rises. The degree is related. When the blood potassium is greater than 5.5mmol/L, the electrocardiogram shows a shortened QT interval, the T wave is highly pointed, the base is narrow and tent-like; when the blood potassium is 7-8mmol/L, the P wave amplitude is reduced, PR The interval is prolonged, and the P wave disappears. This may be a sinus node block or sinus arrest. There may also be "sinus-ventricular" conduction (the sinus node does not pass through the normal conduction system in the atrium but passes through the special fibers in the atrium. Beam into the ventricle); when the potassium level rises to 9-10 mmol/L, the indoor conduction is slower, the QRS wave is broadened, the R wave amplitude is decreased, the S wave is deepened, and the T wave is linearly connected and fused; the blood potassium is 11 mmol/L. When QRS wave, ST segment and T wave merge into a biphasic tortuous waveform, when 12mmol/L, some of the myocardium is first excited and recovered, and the other part has not been depolarized. At this time, it is easy to cause reentry movement and cause ventricular ectopic Rhythm, manifested as ventricular tachycardia, ventricular flutter and ventricular fibrillation, Finally, the heart stops in the diastolic phase.

2. Neuromuscular symptoms often have limbs and perioral numbness in the early stage, extremely tired, muscle aches, pale limbs, wet and cold, blood potassium concentration of 7mmol / L, limbs numbness, soft palate, first for the trunk, then for the limbs, Finally affecting the respiratory muscles, suffocation, the central nervous system can be expressed as restless or unconscious.

3. Other symptoms Due to the increased release of acetylcholine caused by hyperkalemia, it can cause nausea, vomiting and abdominal pain. Due to the toxic effect of high potassium on muscles, it can cause quadriplegia and respiratory arrest. All hyperkalemia has different degrees. Nitrogenemia and metabolic acidosis, which can aggravate hyperkalemia.

Hyperkalemia check

1. Common blood test indicators serum potassium concentration increased, greater than 5.5mmol / L, blood pH is at the normal low limit or less than 7.35, sodium ion concentration is at the normal high limit or higher than 145mmol / L.

2. Common urine test indicators increase urine potassium concentration and urinary potassium output, urine alkaline, urine sodium discharge decreased.

3. Renal function tests for early detection of renal failure.

4. Electrocardiogram examination is helpful for the diagnosis of hyperkalemia. Hyperkalemia can occur in almost all kinds of arrhythmias, mainly manifested as sinus bradycardia, conduction block and ectopic arrhythmia, such as ventricular pre-ventricular Contraction and ventricular fibrillation, generally T wave high tip, QT time shortened, with the further aggravation of hyperkalemia, QRS wave broadening, amplitude decreased, P wave morphology gradually disappeared, but hyperkalemia often merged at the same time Hypocalcemia, acidosis, hyponatremia, etc., the above conditions can also affect the changes of the electrocardiogram, need to be distinguished.

Diagnosis and differentiation of hyperkalemia

diagnosis

The diagnosis of hyperkalemia must first exclude pseudohyperkalemia caused by hemolysis and other reasons, and exclude laboratory errors. ECG examination confirms the occurrence of severe cardiotoxicity. If there is hyperkalemia in ECG It is a dangerous signal, and active treatment should be taken. Drugs (including potassium salts) and renal insufficiency are the most common causes of hyperkalemia. Patients with normal renal function but with severe pre-renal azotemia may Deficiency with hyperkalemia, aldosterone, insulin secretion or action can also lead to hyperkalemia, 40% of patients with newly diagnosed adrenal insufficiency with hyperkalemia, persistent hyperkalemia with acidosis May be high-potassium renal tubular acidosis, common in moderate renal insufficiency, especially in patients with diabetes, interstitial nephritis or obstruction, in addition, tissue necrosis, rhabdomyolysis and membrane depolarization (such as amber The use of choline and high-potassium periodic paralysis, etc.) is not difficult to diagnose from clinical manifestations, and some rare genetic defects caused by hereditary diseases can also lead to hyperkalemia.

Differential diagnosis

1. Hypermagnesemia: ECG changes are similar to hyperkalemia, should be identified, in the diagnosis of the cause can be based on medical history, clinical manifestations and laboratory tests to determine whether renal insufficiency reduces blood potassium excretion and cause hyperkalemia According to the determination of plasma renin activity, adrenal cortisol and aldosterone to determine the presence or absence of adrenal cortex function, ask whether there is a history of using potassium-sparing diuretics or other drugs that can affect abnormal potassium distribution to determine whether hyperkalemia is otherwise cause.

2. Pseudohyperkalemia: Pseudohyperkalemia is seen in hemolysis in the test tube. When the blood is drawn, the pressure of the cuff is too long, and platelets or leukocytosis are increased.

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