What Are the Effects of High Potassium Levels?

Potassium ion is the highest content of cations in the intracellular fluid, and it is mainly in a bound state and directly participates in intracellular metabolic activities. Appropriate potassium ion concentration and its ratio on both sides of the cell membrane play an important role in maintaining the generation of resting potentials in neuromuscular tissues, as well as the generation and conduction of electrical excitability, and also directly affect the regulation of acid-base balance. Potassium ion disorder is one of the most common electrolyte disorders in the clinic, and often coexists with other electrolyte disorders. Hyperkalemia is called serum potassium above 5.5mmol / L, and severe hyperkalemia is> 7.0mmol / L. There are two types of hyperkalemia: acute and chronic. Acute cases are acute and should be rescued in time, otherwise it may cause cardiac arrest.

Basic Information

English name

Hyperkalemia

Visiting department

Department of Endocrinology, Nephrology

Common causes

Related to decreased renal potassium excretion, excessive potassium-containing drug input, digitalis poisoning, etc.

Common symptoms

Feeling numbness in limbs and mouth, muscle aches, bradycardia, prone to arrhythmia, etc.

Causes of hyperkalemia

Decreased renal potassium excretion

Acute renal failure: oliguria or chronic renal failure. Insufficient adrenocortical hormone synthesis and secretion: such as adrenal insufficiency and hypoaldosterone. Potassium-preserving diuretics: long-term application of chlorphenanthridine, spironolactone (Aspirin), and amlomib (Amiloli).

2. Intracellular potassium removal

Hemolysis, tissue damage, massive necrosis of tumor or inflammatory cells, hypoxia, shock, burns, excessive muscle contracture, etc. acidosis. Periodic paralysis of hyperkalemia. After the injection of hypertonic saline and mannitol, due to intracellular dehydration, the permeability of the cell membrane or cell metabolism is changed, and the intracellular potassium is removed.

3. Too much potassium-containing drugs

Penicillin potassium salt (1.5 mmol potassium per 1 million units) is applied in large doses or potassium-containing solutions are input too much or too quickly.

4. Too much blood in the inventory

5. Digitalis Poisoning

Digitalis overdose can reduce the ion pump activity and affect potassium entry into cells.

Clinical manifestations of hyperkalemia

The severity of cardiovascular and neuromuscular symptoms depends on the extent and rate of elevated potassium levels and the presence of other plasma electrolyte and water metabolism disorders.

Cardiovascular symptoms

High potassium inhibits myocardium and reduces myocardial tension, so bradycardia slows and heart enlargement, heart sounds weaken, and arrhythmias are prone to occur, but heart failure does not occur. There are characteristic changes in the electrocardiogram, which are related to the degree of elevated potassium. When blood potassium is greater than 5.5mmol / L, the ECG shows a shortened QT interval. The T-wave is symmetrical and high, with a narrow basal base and a tent-like shape. The amplitude of the P-wave decreases when the blood potassium is 7 to 8 mmol / L, and the PR interval is prolonged so that the P-wave disappears.

2. Neuromuscular symptoms

In the early stages, the limbs and the periphery of the mouth often feel numb, extremely tired, muscles are sore, and the limbs are pale and wet. When the blood potassium concentration reaches 7mmol / L, the limbs become numb and palsy, firstly the trunk and then the limbs, and finally affect the respiratory muscles and suffocate. The central nervous system can appear irritable or unconscious.

3. Other symptoms

Because hyperkalemia causes increased release of acetylcholine, it can cause nausea, vomiting, and abdominal pain. Due to the toxic effects of high potassium on muscles, quadriplegia and respiratory arrest can occur. All hyperkalemias have varying degrees of azotemia and metabolic acidosis. The latter can aggravate hyperkalemia.

Hyperkalemia test

1. Common blood test indicators

The serum potassium concentration increased to more than 5.5mmol / L, the blood pH value was at the normal low limit or less than 7.35, and the sodium ion concentration was at the normal high limit or higher than 145mmol / L.

2. Commonly used urine test indicators

Urinary potassium concentration and urinary potassium excretion increased, urine pH became alkaline, and urinary sodium excretion decreased.

3. Renal function test

Find out early if you have kidney failure.

4. ECG examination

It is helpful for the diagnosis of hyperkalemia. Hyperkalemia can occur in almost all kinds of arrhythmia, mainly manifested as sinus bradycardia, conduction block and ectopic arrhythmia, such as preventricular contraction and ventricular fibrillation. In general, the T wave peak appears early, and the QT time is shortened. With the further exacerbation of hyperkalemia, the QRS wave broadens, the amplitude decreases, and the P wave morphology gradually disappears. However, as hyperkalemia is often combined with hypocalcemia, acidosis, hyponatremia, etc., the above conditions can also affect the changes in the electrocardiogram, which needs to be distinguished.

Hyperkalemia diagnosis

First, it is necessary to exclude pseudohyperkalemia. Pseudohyperkalemia is a condition in which an increase in serum potassium concentration measurement is usually caused by the removal of potassium ions from the cell during or after the collection of a blood sample. In asymptomatic patients with no hyperkalemia manifestations of electrocardiogram, if there is no obvious cause of hyperkalemia, the possibility of pseudohyperkalemia should be suspected.

The assessment of patients with hyperkalemia usually begins with a careful history, assessment of clinical manifestations of hyperkalemia such as muscle weakness and characteristic changes in the electrocardiogram, and laboratory testing for the cause of hyperkalemia. Drugs (including potassium salts) and renal insufficiency are the most common causes of hyperkalemia. Patients with normal renal function but with severe prerenal azotemia may be associated with hyperkalemia. Defects in aldosterone, insulin secretion or action can also cause hyperkalemia. Hyperkalemia is associated with 40% of newly diagnosed adrenal insufficiency patients. Sustained hyperkalemia with acidosis may be hyperpotassic tubular acidosis, which is common in moderate renal insufficiency, especially with Patients with diabetes, interstitial nephritis, or obstruction. In addition, tissue necrosis, rhabdomyolysis, and membrane depolarization are not difficult to diagnose from clinical manifestations. Some rare genetic defects caused by genetic defects can also lead to hyperkalemia.

Hyperkalemia Treatment

Urgent onset of hyperkalemia should take emergency measures, and different treatment methods should be adopted according to the severity of the disease.

(1) Calcium hyperkalemia can reduce the resting potential of cardiomyocytes while the threshold potential remains unchanged, reducing the gap between the two, thereby increasing the excitability of cardiomyocytes. Calcium ion may widen the gap between the resting potential and threshold potential of the myocardial cell membrane, and stabilize the excitability of the myocardium. Emergency measures include an immediate intravenous injection of 10% calcium gluconate 10ml, which is completed in 5 to 10 minutes. If necessary, it can be injected intravenously after 1 to 2 minutes to quickly eliminate ventricular arrhythmias. Due to the short duration of the effect of calcium, intravenous drip should be continued after intravenous bolus injection. Calcium has no effect on serum potassium concentrations.

(2) Plasma and extracellular potassium are temporarily transferred into the cell to inject intravenously hypertonic glucose and insulin. In patients with heart failure or kidneys, the infusion rate should be slow. Monitor blood potassium changes and hypoglycemic responses closely during the instillation. Can also be injected intravenously with 5% sodium bicarbonate solution. This method is more suitable for patients with metabolic acidosis. Not only can make extracellular potassium into cells, but also correct metabolic acidosis. It is not ideal for patients with end-stage renal failure who use dialysis to sustain life.

(3) Promote the excretion of potassium ions from myelin or thiazide diuretics, and remove potassium and cation exchange resin from the body by hemodialysis.

(4) The daily potassium intake of a low-potassium diet is limited to 50 to 60 mmol.

(5) Stop inducing drugs Stop all drugs that may cause elevated potassium.

(6) Remove incentives to remove the cause of hyperkalemia or treat diseases that cause hyperkalemia.