Metabolic acidosis

Introduction to metabolic acidosis Metabolic acidosis is the most common acid-base balance disorder, which is caused by an increase in extracellular fluid H+ or loss of HCO3- with a decrease in primary HCO3- (<21mmol/L) and a decrease in pH (<7.35). feature. In the clinical judgment of metabolic acidosis, anion gap (AG) has important clinical value. According to different AG values, it can be divided into high AG normal chlorine type and normal AG high chlorine type metabolic acidosis. There is very little H in body fluids, mainly due to endogenous metabolism. The body has a fairly complete adjustment mechanism for acid-base load, including buffering, compensation and corrective action. basic knowledge The proportion of illness: 0.021% Susceptible people: no specific people Mode of infection: non-infectious Complications: renal tubular acidosis hyperkalemia

Causes of metabolic acidosis

Tissue hypoxia (30%):

In the absence of oxygen, the glycolysis process is strengthened, lactic acid production is increased, and accumulation due to insufficient oxidation process leads to an increase in blood lactate levels, which leads to acidosis. This acidosis is very common, and tissue hypoxia caused by various causes can be caused.

Diabetes factor (30%):

Ketoacidosis is a condition in which a large amount of body fat is used, such as diabetes, hunger, vomiting symptoms in a long-term pregnancy reaction, alcoholism and vomiting, and food intake in the liver for several days. Ketone formation increases and exceeds the amount of extrahepatic utilization, resulting in ketosis. Ketone bodies include acetone, beta-hydroxybutyrate, acetoacetate, the latter two being organic acids, leading to metabolic acidosis. This acidosis is also an increase in normal blood chlorine metabolic acidosis.

Severe diarrhea (20%):

As diarrhea loses a lot of alkaline substances, it causes water, electrolyte and acid-base balance disorders.

Pathogenesis

1. The buffering effect of blood and the compensation of intracellular buffer

In metabolic acidosis, the increased H+ in the blood can be immediately buffered by the plasma buffer system. Through the above reaction, plasma HCO _3- and buffer base are consumed, and the generated H ₂ CO ₃ can be excreted by the lungs, and the intracellular buffer is mostly in acid. After 2 to 4 hours of poisoning, the increased H+ in the extracellular fluid is transferred to the cells, which is buffered by the intracellular buffer base, and the intracellular K+ is transferred to the outside of the cell to maintain the internal and external electrical balance, so acidosis easily causes high blood. Potassium.

2, lung regulation

Increased blood H+ concentration stimulates carotid body and aortic chemoreceptors. Reflex causes respiratory center excitement, significantly increases lung ventilation, and causes PaCO ₂ to decrease secondary and maintain HCO ₃ -/H ₂ CO ₃ ratio. Close to normal, the blood pH value tends to normal, the compensatory response of the breath is very rapid, generally after 10 minutes of acidosis, respiratory enhancement occurs, after 30 minutes, it will be compensated, 12 to 24 hours will reach the peak of compensation, the maximum limit of compensation It is PaCO ₂ down to 10mmHg (1.33kPa).

3, kidney regulation

In addition to metabolic acidosis caused by abnormal renal function, metabolic acidosis caused by other causes, the kidney exerts an important compensatory function through acid and alkali retention, and carbonic anhydrase activity in renal tubular epithelial cells increases during acidosis, promoting kidney Small tube secretion of H+ and reabsorption of HCO ₃ - increased, phosphate acidification increased, but renal tubular secretion of NH4 + is the most important compensation mechanism, renal compensation generally exerts the maximum effect within 3 to 5 days, potassium balance often occurs in acidosis The greater the effect, the early kidney acidosis of K+ excretion decreased, but then increased significantly, this is due to acidosis, blood potassium rise, stimulate aldosterone secretion and inhibit the resorption of HCO ₃ - in the proximal tubules, so that reaching the distal end The increase in tubule filtrate increases the urinary potassium excretion.

Metabolic acidosis prevention

The treatment of metabolic acidosis, remove the cause is the cure, supplementation is the palliative, so it should actively treat the primary disease, mild acidosis, can correct itself after correcting water shortage and electrolyte imbalance, do not need to make up, severe cases should be timely Correct acidosis. During the treatment of phlegm and blood stasis, attention should be paid to observing the clinical manifestations and reviewing blood biochemistry. When the symptoms are improved, the urine volume is sufficient, CO ₂ CP18mmol/L or more, no need to use alkaline drugs, metabolic acidosis, Serum K+ can be high. When acidosis and water shortage are corrected, hypokalemia K+, hand and foot convulsions, and K+ should be noted.

Metabolic acidosis complications Complications, renal tubular acidosis, hyperkalemia

1. Acidosis can reduce the binding of Ca ₂ to protein, thereby increasing the level of free Ca ₂ . When correcting acidosis, sometimes the hand and foot sputum can be produced due to the decrease of free Ca ₂ , and the decrease of blood pH can inhibit the 1 hydroxylation of kidney. Enzymes reduce the production of active vitamin D _3. 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 decomposition, 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 number of acid acid loss; severe vomiting with severe diarrhea, metabolic factors such that pH, HCO3- and PaCO2 The opposite direction moves, so the final change in these three indicators depends on which disorder dominates, and they can rise, fall, or fall within the normal range.

4, acidosis is often accompanied by hyperkalemia, when the acid is corrected for acidosis, H+ is continuously buffered from the inside of the cell to the outside of the cell, and K+ is re-migrated from the outside of the cell to the cell, so that the blood potassium falls back, but It should be noted that some patients with metabolic acidosis have potassium loss. Although there is acidosis but accompanied by hypokalemia, the serum potassium concentration will be further reduced when acidosis is corrected, causing severe or even fatal hypokalemia. The situation is found in diabetic patients with osmotic diuretic and potassium loss, diarrhea patients lose potassium, etc., to correct its acidosis, it is necessary to properly supplement potassium according to the degree of serum potassium reduction.

Symptoms of metabolic acidosis Common symptoms Heart failure nausea ketoacidosis diarrhea sinus fetal heart rate renal failure abdominal pain bradycardia metabolism low

1. Cardiovascular system

The effect of acidosis itself on heart rate is two-way. When the blood pH drops from 7.40 to 7.0, the heart rate is generally too fast. This is mainly caused by the secretion of more adrenaline during acidosis. When the pH value continues to drop, The heart rate gradually slows down, mainly because acetylcholinesterase is inhibited at this time, resulting in excessive accumulation of acetylcholine. The latter's effect on the heart exceeds the effect of adrenaline. If -blockers are used, bradycardia can be more obvious. Severe acidosis can be accompanied by arrhythmia. Some people think that it is caused by acidosis itself, but most people think that it is caused by electrolyte imbalance caused by acidosis. In addition, mild acidosis can increase myocardial contractility because catecholamine can promote Ca ₂ enters the cell and thus partially compensates. When severe acidosis occurs, H accumulates a lot, preventing Ca ₂ from entering the cell from outside the cell, and the intracellular free [Ca ₂ ] is reduced, and the myocardial contractility is decreased; if used simultaneously Calcium channel blockers, bradycardia can be more obvious, acidosis has an effect on small arteries and veins, but the veins are more obvious, the main table It is a continuous venous contraction, which is caused by the increase of catecholamine secretion on the one hand. On the other hand, H itself causes small artery relaxation. In severe acidosis, the latter effect exceeds the former one.

Therefore, the overall performance is that the perfusion of each tissue is reduced, the amount of blood returning to the heart is increased, and the burden on the heart is aggravated. If the underlying disease causing acidosis has an effect on the heart at the same time, the above factors may cause heart failure.

2, respiratory system

The performance is accelerated by the deepening of the breathing. The typical phenomenon is called Kussmaul breathing. Because acidemia stimulates the respiratory center through stimulation of the central and peripheral chemoreceptors, the CO ₂ exhalation increases, PCO ₂ decreases, and acidosis gains a certain degree of compensation. Acidosis can reduce the ability of O ₂ to bind to hemoglobin, increase the release of O ₂ carried to tissues, and have certain benefits for improving tissue metabolism. However, long-term acidosis can make glycerol 2,3-diphosphate in red blood cells. The (2,3-DPG) content is reduced, and the ability of red blood cells to carry O ₂ is reduced, which eventually offsets the former.

3. Gastrointestinal system

There may be mild abdominal pain, diarrhea, nausea, vomiting, decreased appetite, etc., partly due to the basic cause of acidosis and other water-acid electrolyte imbalances; in addition, autonomic dysfunction caused by acidosis itself ( Such as changes in the response to acetylcholine stimulation, etc.) are often the direct cause.

4, other

When the blood pH drops, K easily escapes from the cell to the outside of the cell, which can cause the blood K to rise slightly; but in fact, many cases of metabolic acidosis often have a deficiency of K, so the blood K level does not necessarily rise. Catecholamine is excessively secreted during acidosis, stimulating beta adrenergic receptors, allowing K to be transferred from outside the cell to the cell; stimulating alpha adrenergic receptors has the opposite effect, low HCO ₃ -emia and high osmotic pressure The blood itself can inhibit the uptake of K by the cells. Therefore, the blood potassium level should be determined according to the overall situation. It is generally considered that the blood pH value decreases by 0.1 and the blood K increases by 0.6 mmol/L, but due to the influence of many factors mentioned above, Therefore, it is often not so accurate.

Examination of metabolic acidosis

1, blood gas analysis and detection, oxygen partial pressure, oxygen saturation detection.

2, blood electrolyte sodium, potassium, calcium, magnesium, phosphorus detection.

3, urine routine examination can appear ketone body.

4, liver, kidney function test.

5, according to the cause, clinical symptoms selected for B-ultrasound, X-ray examination.

Diagnosis and identification of metabolic acidosis

diagnosis

Metabolic acidosis must be fully diagnosed based on medical history and laboratory tests, generally in the following steps:

1. Determine the presence of metabolic acidosis

Simultaneous determination of arterial blood gas and blood biochemical indicators, if the pH value is lowered, [HCO _{3-] is} too low, [H] is too high or blood AG is particularly high indicating the presence of metabolic acidosis, according to the Henderson-Hasselbalch formula ( H = 24 × PaCO ₂ / HCO ₃ ) to evaluate whether the measured laboratory data is reliable. Since the measured pH value has a direct relationship with the calculated H, when the pH is normal, ie 7.4, H is 40nmol/L, if the change exceeds the above range, there is a laboratory error in the data, or the above indicators are not measured simultaneously. A comprehensive history collection and physical examination can help identify potential acid-base disorders such as vomiting, severe diarrhea, renal failure, hypoxia, shock, etc., suggesting that metabolic acidosis may be present.

2. Determine if the respiratory compensation system responds properly

In general, the PaCO ₂ compensation range caused by metabolic acidosis can be estimated by a simple formula: 1PaCO ₂ = 1.5 [HCO ₃ -] 8; 2 PaCO ₂ = 1.2 [HCO ₃ - If it exceeds this range, it indicates that there is a mixed acid-base balance disorder.

3. Calculating the anion gap (AG) Calculating AG in metabolic acidosis helps determine the type of metabolic acidosis.

(1) If AG elevation indicates lactic acidosis, ketoacidosis, drug or toxic poisoning or renal insufficiency, in high AG metabolic acidosis, calculation of AG helps to determine whether there are other types of acid and alkali The existence of imbalance, AG is the ratio of elevated AG to reduced HCO ₃ -, AG=(AG-10)/(24-HCO ₃ -) (normal value is 1~1.6), AG<1 The decrease of HCO ₃ - exceeds the increase of AG, suggesting the presence of non-anion gap metabolic acidosis. AG>1.6 suggests that there is metabolic alkalosis at the same time. If it is suspected of metabolic acidosis caused by drugs or poisons, osmotic pressure gap The measurement is helpful for diagnosis. Low molecular weight substances that are easy to form high concentrations in serum (such as methanol, ethanol, isopropanol, etc.) are easy to increase serum osmotic pressure, which can lead to elevated metabolic acidosis with AG. If the osmotic pressure gap is normal, if the blood osmotic pressure gap is normal, it is most likely due to liver disease, L-type lactic acid accumulation in the blood, or D-type lactic acid accumulation due to gastrointestinal problems.

(2) If AG does not increase, firstly, it is necessary to exclude the increase of AG caused by hypoalbuminemia. If there is no hypoproteinemia, acidosis may be caused by HCO ₃ - loss and excessive production of some acid, but they are accompanied by Anions are not present in normal blood; or these anions are not excreted with H or NH ₄ , which is defined as the difference between undetermined anions in urine and unmeasured cations (urine AG = Na K -Cl-), In the detection of the amount of NH4 excreted in the urine, in general, if the renal acidification function is normal, the kidney will inevitably discharge a large amount of NH ₄ during acid load or loss of alkali, and the metabolic acidosis, such as the normal acidification of the kidney ( Such as diarrhea, so that urinary AG is significantly elevated (such as -20 ~ -50mEq / L), on the contrary, if the acidification of the kidney is impaired (such as renal tubular acidosis), urine NH ₄ discharge must be significantly reduced, urine AG is Positive value.

In the differential diagnosis of metabolic acidosis, it is worth mentioning that renal tubular acidosis is mainly caused by differential diagnosis of type I and type II renal tubular acidosis.

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