What Is Involved in Metabolic Acidosis Management?

Metabolic acidosis is the most common type of acid-base disorder. It is caused by an increase in extracellular fluid H ⁺ or HCO ₃ ^- loss with primary HCO ₃ ^- reduction (<21mmol / L) and a decrease in pH (< 7.35). In the clinical judgment of metabolic acidosis, anion gap (AG) has important clinical value. According to different AG values, they can be divided into high AG normal chlorine type and normal AG high chlorine type metabolic acidosis.

Basic Information

English name

metabolic acidosis

Visiting department

Emergency, Endocrinology, Gastroenterology, Nephrology

Common causes

Increased production of acidic metabolites or impeded excretion, excessive alkali loss

Common symptoms

Breathing deep and fast

Causes of metabolic acidosis

1. High AG normal chloride metabolic acidosis

(1) Lactic acidosis Lactic acidosis is a common cause of metabolic acidosis. Normal lactic acid is produced by the hydrolysis of pyruvate under the action of lactate dehydrogenase (LDH) through NADH, and NADH is converted into NAD. Lactic acid can also be converted to pyruvate when NAD is converted to NADH under the action of LDH. Therefore, the determination of the above reaction direction is mainly the concentration of both pyruvate and lactic acid as the reaction substrate and the ratio of NADH and NAD. NADH can be produced during normal glucose hydrolysis, but the NADH produced can go to the mitochondria to produce NAD. In addition, pyruvate is converted to acetyl-CoA by pyruvate dehydrogenase (PDH), which is then converted to CO ₂ and H ₂ O.

Normal human blood lactic acid level is very low, 1 ~ 2mmol / L, when it exceeds 4mmol / L, it is called lactic acidosis. Lactic acidosis is clinically divided into A and B types.

Type A is caused by insufficient tissue perfusion or acute hypoxia, such as seizures, convulsions, strenuous exercise, severe asthma, etc. can cause high metabolic status, and tissue metabolism is significantly too high; or in shock, cardiac arrest, acute pulmonary edema, CO Poor tissue oxygen supply during poisoning, anemia, severe hypoxemia, etc., can prevent NADH from being converted to NAD, and thus a large amount of pyruvate is converted to lactic acid, resulting in lactic acidosis.

Type B is caused by some common diseases, drugs or poisons, and certain genetic diseases. Such as liver disease, cirrhosis is the most common. As hepatic parenchymal cells decrease, the conversion of lactic acid to pyruvate is reduced, leading to lactic acidosis. This type of lactic acidosis often develops slowly, but if combined with tissue perfusion, etc., acidosis can be very serious; if chronic alcoholism is present, it is more likely to occur. It may be that alcohol consumption reduces liver glycogen regeneration and lactic acid utilization Caused by obstacles. In malignant neoplastic diseases, especially large soft tissue tumors, lactic acidosis of varying degrees can often occur. If the tumor metastasizes to the liver, the condition can get worse. After chemotherapy shrinks the tumor or is surgically removed, lactic acidosis can be significantly improved. Some drugs include biguanide, hypoglycemic drugs, fructose, methanol, salicylic acid, and isoniazid, etc. Excessive consumption can cause the disease, and the mechanism is by interfering with the utilization of oxygen by tissues and disorders of glucose metabolism. A small number of congenital diseases, including type 1 glycogen storage disease, fructose-1,6 diphosphatase deficiency, and pyruvate dehydrogenase deficiency, are due to glycolysis disorders and insufficient energy metabolism, resulting in excessive lactic acid production.

(2) Ketoacidosis Ketoacidosis is the accumulation of acetoacetic acid and -hydroxybutyric acid in the body (especially extracellular fluid), accompanied by a decrease in insulin, glucagon, cortisone, growth hormone, Catecholamines and glucocorticoids are elevated to varying degrees as a result of the body's extreme pathophysiological response to starvation.

Diabetic ketoacidosis is caused by the relative or absolute lack of insulin and high glucagon levels. It often occurs when insulin is suddenly stopped during treatment or accompanied by various stresses, such as infection, trauma, surgery and emotional stimulation. Make the original treatment relatively insufficient insulin. Patients' blood glucose and blood ketones increased significantly, and the production of ketone bodies (especially in the liver) exceeded the use of ketone bodies by the central nervous system and surrounding tissues. Due to a large amount of osmotic diuresis, a decrease in blood volume may occur.

Ethanol (alcoholic) ketoacidosis is seen in chronic alcohol (alcohol) drinkers. It can occur when you stop eating. It often has vomiting and dehydration. The blood sugar level is generally low. Glucagon and growth hormone increased, and blood triacylglycerol levels also increased.

Starvation ketoacidosis is moderate ketoacidosis caused by starvation. In the first 10 to 14 hours, blood glucose is maintained by glycogen breakdown. Subsequently, gluconeogenesis is the main source of glucose, and the oxidative decomposition of fat (especially in the liver) is accelerated, leading to ketoacidosis. Exercise and pregnancy can speed up the process.

(3) Metabolic acidosis caused by drugs or poisons It is mainly salicylic acid and alcohol organic compounds, including methanol, ethanol, isopropanol, etc.

Taking a large amount of salicylic acid, especially taking alkaline medicine at the same time, can make salicylic acid be absorbed from the stomach in large quantities, causing acidosis.

Methanol poisoning is mainly seen in those taking fake alcohol. After drinking, it is converted into formaldehyde by alcohol dehydrogenase in the liver and then converted to formic acid. Formic acid on the one hand can directly cause metabolic acidosis, and on the other hand can also cause lactic acidosis by inhibiting the mitochondrial respiratory chain.

(4) Uremic patients with chronic renal failure When the GFR drops below 20 to 30 ml / min, hyperchloric metabolic acidosis can be converted to high AG metabolic acidosis, which is an uremic organic anion that cannot pass through the kidneys. The globules are fully filtered and excreted and reabsorption is increased. Most patients' blood HCO ₃ ^- levels are not very low, mostly between 12 and 18 mmol / L. This acidosis develops slowly. The retained acid is buffered by the alkali storage in the bone, plus abnormal vitamin D, PTH, and calcium and phosphorus disorders, which can cause obvious bone disease.

2. Normal AG hyperchloric metabolic acidosis

Mainly due to HCO ₃ ^- loss from the kidney or extrarenal, or decreased renal tubular secretion of H, but the glomerular filtration function is relatively normal. Whether it is HCO ₃ ^- lost or simply reduced H secretion in the renal tubules, the result is too little HCO ₃ ^- and at the same time there is generally no accumulation of other organic anions in the blood, so the Cl ^- levels rise correspondingly, mostly in the normal AG high-chlorine type Acidosis.

Clinical manifestations of metabolic acidosis

Cardiovascular system acidosis

The effect on the heart rate is bidirectional. Severe acidosis can be accompanied by arrhythmia, tachycardia or bradycardia. Some people think that it is caused by acidosis itself, but most people think that it is caused by the combined electrolyte disorder during acidosis. Acidosis affects both the arterioles and veins, but the veins are more pronounced, mainly manifested by continuous venous constriction. For the small arteries, on the one hand, contraction is caused by the increase in catecholamine secretion, and on the other hand, H itself causes the arterioles to relax. In the case of severe acidosis, the latter effect exceeds the former.

2. Respiratory system manifests as deepening of breathing

Typical is called Kussmaul breathing. Because acidemia stimulates the respiratory center by stimulating the central and surrounding chemoreceptors, CO ₂ exhales more, PCO ₂ decreases, and acidosis is compensated to a certain degree.

3. Gastrointestinal system

May have mild abdominal pain, diarrhea, nausea, vomiting, and decreased appetite. Part of the cause is related to the basic cause of acidosis and the combined acid-base imbalance of other water electrolytes. In addition, the autonomic nerve dysfunction caused by acidosis itself (such as changes to acetylcholine stimulation response) is often the direct cause.

4. Other

When the blood pH value drops, K easily escapes from the inside to the outside of the cell, which can slightly increase the blood K. However, in fact, many cases of metabolic acidosis often combine with lack of K, so the blood K level may not necessarily increase. .

Metabolic acidosis test

1. Blood gas analysis, oxygen partial pressure, and oxygen saturation.

2. Detection of blood electrolyte sodium, potassium, calcium, magnesium, phosphorus.

3. Urine routine examination may appear ketone bodies.

4. Liver and kidney function test.

5. Blood lactate test.

According to the etiology and clinical symptoms, B ultrasound and X-ray examination were selected.

Diagnosis of metabolic acidosis

Metabolic acidosis must be fully diagnosed based on medical history and laboratory tests. Generally follow these steps:

1. Determining the presence of metabolic acidosis while measuring arterial blood gas and blood biochemical indicators

If the pH value decreases, [HCO _3- ] is too low, [H] is too high, or the blood AG is particularly high, it indicates the presence of metabolic acidosis. The reliability of the measured laboratory data can be evaluated according to the Henderson-Hasselbalch formula (H = 24 × PaCO ₂ / HCO _3- ). Because there is a direct relationship between the measured pH and the calculated H, when the pH is normal, which is 7.4, H is 40 nmol / L. If the change exceeds the above range, it indicates that there is a laboratory error in the data or the above indicators are not measured simultaneously.

A comprehensive medical history and physical examination can help to indicate potential acid-base balance disorders, such as vomiting, severe diarrhea, renal failure, hypoxia, and shock, all suggesting the possibility of metabolic acidosis.

2. Determine if the respiratory compensation system is responding properly

In general, the range of PaCO ₂ compensation caused by metabolic acidosis can be estimated by a simple formula. The most commonly used are: PaCO ₂ = 1.5 [HCO _3- ] +8; PaCO ₂ = 1.2 [HCO ₃ ^- ]. If it exceeds this range, it indicates that there is a disorder of mixed acid-base balance.

3. Calculate the anion gap (AG)

Calculating AG in metabolic acidosis helps determine the type of metabolic acidosis.

(1) If the AG is elevated, it indicates lactic acidosis, ketoacidosis, drug or poisoning, or renal insufficiency.

(2) If the AG does not increase, first, the AG does not increase due to hypoalbuminemia. If there is no hypoproteinemia, acidosis may be caused by HCO ₃ ^- loss and excessive production of some acids, but the anions associated with them are not present in normal blood; or these anions are not excreted with H ⁺ or NH ₄ ⁺ .

Complications of metabolic acidosis

1. Acidosis can reduce the binding of Ca ²⁺ to proteins, which increases the level of free Ca 2+. When correcting acidosis, tetany can sometimes occur due to a decrease in free Ca 2+. Chronic acidosis can cause metabolic bone disease due to long-term mobilization of calcium salts in bones, which is quite common in patients with renal tubular acidosis.

2. Acidosis can increase protein breakdown, chronic acidosis can cause malnutrition.

3. Metabolic acidosis combined with metabolic alkalosis can be seen in patients with renal failure due to frequent vomiting and a large loss of acidic gastric acid; severe vomiting with severe diarrhea.

4. Acidosis is often accompanied by hyperkalemia. When correcting acidosis by alkali, H ⁺ moves from the inside to the outside of the cell and is continuously buffered, while K ⁺ moves from outside the cell to the inside of the cell to reduce blood potassium. . It should be noted, however, that some patients with metabolic acidosis have potassium deficiency, although acidosis is accompanied by hypokalemia. When correcting for acidosis, the serum potassium concentration will further decrease, causing severe and even fatal hypokalemia. This situation is seen in diabetic patients with osmotic diuresis and potassium loss, and in patients with diarrhea. Correction of acidosis requires appropriate potassium supplementation based on the degree of serum potassium decline.

Metabolic acidosis treatment

The most important treatment of metabolic acidosis is to treat its basic causes, especially high AG normal chlorine metabolic acidosis. Alkaline medications are used in patients with severe normal AG hyperchloric metabolic acidosis.

Cause treatment

Lactic acidosis is mainly aimed at the causes, including correcting circulatory disorders, improving tissue perfusion, controlling infections, and supplying sufficient energy. D-lactic acidosis is often effective in low-carb diets and antibiotic treatment. Alkali supplementation is not preferred. It is limited to acute and severe acidemia (pH <7.1). NaHCO ₃ treatment is needed to gain time to treat the underlying cause.

Diabetic ketoacidosis should be treated promptly by infusion, insulin, correction of electrolyte disorders, and management of infections. Intravenous glucose and saline can easily correct alcohol ketoacidosis, and potassium, phosphorus, magnesium and vitamins need to be added at the same time.

Metabolic acidosis caused by methanol should be hemodialysis or peritoneal dialysis as soon as possible. If dialysis conditions are not available, a gastric tube can be used for continuous aspiration of gastric acid, which can temporarily reduce acidemia on the one hand, and can absorb body fluids on the other, creating conditions for reducing the volume load caused by sodium bicarbonate supplementation. Acidosis caused by salicylic acid is often accompanied by respiratory alkalosis. Acetazolamide (acetazolamide) can alkalize the urine, making salicylic acid excreted in the urine not easily transformed into non-ionized salicylic acid, and difficult to be reabsorbed. Therefore, it is often used when salicylic acid is poisoned. It is used in patients Combined HCO ₃ ^- especially applicable when levels are too high. Paraaldehyde poisoning can be easily diagnosed due to the special respiratory odor, and it is generally enough to treat with alkaline drugs.

Compared with other high-AG metabolic acidosis, uremic metabolic acidosis cannot be eliminated, and there is no endogenous HCO ₃ ^- supplementation, so it is necessary to give certain exogenous alkaline substances To slowly increase the blood HCO ₃ ^- to about 20 to 22 mmol / L to reduce bone lesions.

Loss of HCO _{3 in the} gastrointestinal tract-acidosis caused by NaHCO ₃ supplementation can often achieve significant results. Attention should be paid to potassium salts.

2. Use of alkaline drugs

NaHCO ₃ is the most commonly used alkaline drug in clinical practice. As sodium lactate enters the body, it can interact with H ₂ CO _{3 to} generate lactic acid and NaHCO _3. Lactic acid is oxidized into CO ₂ and H ₂ O in cells, or synthesizes glucose through gluconeogenesis; the generated NaHCO ₃ can buffer with acid. The above reactions are inadequate in conditions such as hypoxia and severe liver disease, so the effect of correcting acidosis is not good. In addition, the CO ₂ generated in the reaction can increase PaCO ₂ , so the effect is not good in respiratory acidosis, and it is no longer used.

3. Complication treatment

Handle hyperkalemia during acidosis and hypokalemia when patients lose potassium: Acidosis is often accompanied by hyperkalemia, but it should be noted that some patients with metabolic acidosis have potassium loss, although there are Acidosis but accompanied by hypokalemia. When correcting for acidosis, the serum potassium concentration will further decrease, causing severe and even fatal hypokalemia. This situation is seen in diabetic patients with osmotic diuresis and potassium loss, and in patients with diarrhea. Correction of acidosis requires appropriate potassium supplementation based on the degree of serum potassium decline.

Acidosis caused by severe renal failure requires peritoneal dialysis or hemodialysis to correct disorders such as water, electrolytes, and acid-base balance.

Prognosis of metabolic acidosis

The prognosis is determined by metabolic acidosis, compensation, severity, and whether it is combined with other water-electrolyte acid-base disorders. Those who are mild may be asymptomatic, or only feel tired and weak, shortness of breath, and poor appetite; etc. In severe cases, Kussmaul breathing may occur, combined with circulatory dysfunction, and even blood pressure may drop, arrhythmia, or even coma.