Hyperkalemia
Introduction
Introduction Hyperkalemia refers to serum potassium ions above 5.5 mmol/L. The K+ content of patients with hyperkalemia is not necessarily higher than normal. Under normal circumstances, the body has an effective mechanism to regulate potassium concentration, so it is not easy to occur hyperkalemia, but once there is a short-term or long-term inability to reverse the various factors, hyperkalemia will occur. The main causes of hyperkalemia are: 1 excessive potassium intake, 2 elimination reduction, 3 tissue destruction, and 4 abnormal distribution. Hyperkalemia can cause severe damage to the heart and respiratory muscles and requires active treatment.
Cause
Cause
Classification of causes:
(1) Reduction of renal potassium excretion
1. Acute renal failure during oliguria or chronic renal failure.
2. Adrenal cortical hormone deficiency, such as Addison disease, low renin low aldosteronism, al-hydroxylase deficiency.
3. Long-term application of potassium-sparing diuretics, such as chlorpheniramine steep, snail meat ester (Amsocycline), ampicillin (amiloride).
(2) Removal of potassium from cells
1. Hemolysis, tissue damage, massive necrosis of tumor or inflammatory cells, tissue hypoxia, shock, burns, excessive muscle contracture, etc.
2. Acidosis.
3. Hyperkalemia is periodically paralyzed.
4. After injection of hypertonic saline and mannitol, intracellular potassium is removed due to intracellular dehydration, changes in cell membrane permeability or cellular metabolism. It has been reported that high blood potassium occurs when arginine hydrochloride is applied, which may be caused by arginine entering the cells and excreting potassium.
(3) Too much potassium-containing drug input
Penicillin potassium salt (per 1 million units K1.5mmol) large dose application or potassium-containing solution input too much, too fast.
(4) Too much blood in the input stock.
(5) Digitalis poisoning
Excessive digitalis can reduce the activity of the ion pump and affect the entry of potassium into the cells.
mechanism:
Potassium in the body is mainly excreted through the kidneys. Therefore, renal failure is the most important cause of clinically caused hyperkalemia. Hyperkalemia is common in acute renal failure during oliguria, and potassium in the absence of urine will increase at a rate of 0.7 mmol/L per day. Progressive hyperkalemia is rare in chronic renal failure, but chronic. In the advanced stage of renal failure, severe renal function, decreased urine output, and increased potassium levels, but blood potassium is significantly increased, often due to excessive potassium intake or excessive removal of potassium in the cells.
The function of aldosterone is mainly to preserve sodium and potassium, and mainly acts on the renal distal convoluted tubule. Adison disease is an adrenal insufficiency oil with a decrease in adrenocortical hormone (mainly mineralocorticoid deficiency), showing hyperkalemia. Low renin low aldosteronism can be seen in patients with mild renal insufficiency and diabetes with renal insufficiency. The reduction of aldosterone secretion can also be caused by the inhibition of the activity of the renin-angiotensin-aldosterone system by the use of p-blockers, non-steroidal anti-inflammatory drugs, and conversion enzyme inhibitors.
The potassium in the intracellular fluid is about 30 times higher than the extracellular fluid. The maintenance of this concentration gradient requires constant replenishment of energy. In addition, it is also affected by factors such as hypoxia, catabolism or anabolic enhancement, and pH. In any case, if the energy supply is insufficient, the catabolism of the cells is enhanced, and the cells are damaged and acidemia, the potassium in the cells can be swollen in a large amount, resulting in hyperkalemia of the extracellular fluid.
Oral potassium salts, usually do not cause hyperkalemia. However, excessive potassium supplementation, input of a large amount of blood for a long time in stock, the use of a large number of potassium-containing drugs, can increase blood potassium, especially in patients with renal insufficiency, more likely to occur hyperkalemia.
Examine
an examination
Related inspection
Urine potassium serum potassium (K+, K)
(1) Medical history:
The clinical signs of hyperkalemia are similar to those of hypokalemia, which are very atypical and often masked by the symptoms of their primary disease. When inquiring about medical history, you should pay attention to the presence or absence of renal dysfunction, long-term application of potassium-sparing diuretics or potassium-containing drugs, as well as tissue damage or acidosis.
(2) Physical examination:
Muscle weakness can occur in the early stage, severe abdominal reflexes disappear, muscle paralysis, and even respiratory muscles are paralyzed. The early circulatory rate of the circulatory system is slow, severe arrhythmia, and even ventricular fibrillation leads to cardiac arrest.
(3) Laboratory inspection:
1. Blood potassium determination
Serum potassium above 5.5mmol/L is hyperkalemia. It should be differentiated from pseudohyperkalemia, which may be caused by hemolysis when the tourniquet is not released or the arm is flexed and stretched and the fist movement is excessive. In addition, serum potassium levels may also increase when platelets or white blood cells are significantly increased.
2. Renal function test
Including blood urea nitrogen, creatinine, endogenous creatinine clearance, urine relative density or osmotic pressure, urine volume and urine dilution or concentration function determination.
3. Determination of plasma renin activity and aldosterone.
(4) Equipment inspection:
Electrocardiogram examination: When the serum potassium level increased above 6mmol / L, about 25% of patients may have ECG changes. When serum potassium reaches 8mmol / L, 80% of patients have ECG changes. Severe heart rhythm disorders and even cardiac arrest can occur when serum potassium reaches 8-10 mmol / L. The typical electrocardiogram of hyperkalemia is characterized by high T wave and shortened QT interval. In severe cases, P wave disappears and QRS wave broadens. Further S-T segment and T wave fuse, T wave widens, and QRS wave forms a double. Wavy. Finally, ventricular fibrillation occurs.
Diagnosis
Differential diagnosis
1. Hypermagnesemia: ECG changes are similar to hyperkalemia and should be identified. In the diagnosis of the cause, according to the history, clinical manifestations and laboratory tests to determine whether there is renal insufficiency, blood potassium excretion is reduced and hyperkalemia is caused. According to the determination of plasma renin activity, adrenal cortisol and aldosterone to determine whether the adrenal cortex is functionally reduced. Ask if there is a history of using potassium-sparing diuretics or other drugs that can affect abnormal potassium distribution to determine whether hyperkalemia is caused by drugs.
2. Pseudohyperkalemia: Pseudohyperkalemia is seen in hemolysis in vitro. When the blood is drawn, the compression of the cuff is too long, and platelets or leukocytosis increase.
