What Are the Different Causes of Metabolic Alkalosis?

Metabolic alkalosis refers to the clinical situation of excessive acid loss in the body or excessive alkali from the outside. The main biochemical manifestations are blood HCO ₃ ^- too high (gt; 27 mmol / L) and PaCO ₂ increased. The pH value is more than 7.45, but it varies depending on the compensation situation, it can be significantly too high; it can only rise slightly or even normal. Clinically, the disease is often accompanied by hypokalemia.

Basic Information

English name

metabolic alkalosis

Visiting department

Endocrinology

Common causes

Gastric fluid loss, potassium deficiency, decreased extracellular Cl-, bicarbonate accumulation, and excessive mineralocorticoids

Common symptoms

Shallow and slow breathing, restlessness, excitement, slang, drowsiness, convulsions of hands and feet, hypertonic reflexes, oliguria, etc.

Causes of metabolic alkalosis

The primary factor of metabolic alkalosis is that the extracellular fluid loses a large amount of acid or absorbs a large amount of alkali, which causes HCO ₃ ^-to increase, thereby increasing the molecular size of [BHCO ₃ ] / [HHCO ₃ ] and increasing the pH value. .

Gastric fluid loss

Large amounts of gastric fluid can be lost after vomiting, long-term gastric aspiration, pyloric obstruction, and surgical anesthesia.

2. Potassium deficiency.

3. Extracellular fluid Cl ^- reduced

If the intake is reduced, or due to loss of gastric fluid, or the use of furosemide, thiazide diuretics, or mutations in renal ion channels such as Bartter syndrome or Gitleman syndrome, a large amount of Cl ^-is lost through the kidneys, or due to congenital intestinal mucosal cells Functional defects such as Cl- absorption can reduce Cl- in extracellular fluid.

4. Bicarbonate accumulation

(1) In the treatment of gastric ulcer, taking a large number of alkaline drugs for a long time can reduce or disappear gastric acid, and then bicarbonate in the intestinal fluid is absorbed into the blood without being neutralized, and a large amount of HCO ₃ in the blood is increased. Alkali poisoning.

(2) Excessive intake of organic acid salts When oral or injected lactate, citrate (large blood transfusion), and acetate are excessive, they are converted into CO ₂ and H ₂ O in the liver and form bicarbonate , Greatly increase the HCO ₃ ^- content in the blood, and promote alkalosis.

(3) Use a large amount of sodium bicarbonate during cardiopulmonary resuscitation. After resuscitation, the lactate is metabolized and the consumed HCO ₃ ^- can be restored. As a result, the HCO ₃ ^- in the blood is even as high as 60 to 70 mmol / L, pH value. Up to 7.90. In addition, during renal failure, excessive use of sodium bicarbonate can also cause metabolic alkalosis.

5. Excessive mineralocorticoids

Including hyperaldosteronism, Cushing's syndrome, etc.

Clinical manifestations of metabolic alkalosis

Shallow and slow breathing

It is a phenomenon that the respiratory system compensates for metabolic alkalosis. With shallow and slow breathing, PCO _{2 in the} alveoli can be increased, and the denominator of [BHCO ₃ ] / [HHCO ₃ ] can be increased to reduce molecular changes. Larger ratio changes occur (stable pH).

Mental symptoms

Restlessness, excitement, slang, lethargy, and coma in severe cases;

3. Increased neuromuscular excitability

Hands and feet convulsions, hypertonic reflexes, etc .;

4. Less urine and alkaline

If potassium deficiency has occurred, the contradiction of acid urine may occur, and special attention should be paid. Standard bicarbonate (SB), actual bicarbonate (AB), buffered base (BB), and residual alkali (BE) increased, and blood PCO ₂ and blood pH increased.

Metabolic alkalosis test

1. Increased blood pH and HCO ₃ ^- decreased blood potassium and blood chlorine.

2. Clinically, metabolic dysentery poisoning can be confirmed by X-ray barium meal or gastroscopy if it is caused by pyloric obstruction.

3. Patients suspected of excessive mineralocorticoids can check levels of aldosterone and cortisol.

Diagnosis of metabolic alkalosis

According to the history, physical signs, and blood gas analysis of AB, SB, BB, BE, blood PCO ₂ , and blood pH are increased, a diagnosis of metabolic alkalosis can be drawn. The estimated formula for the compensation of metabolic acidosis is:

PCO ₂ = 0.7 × [HCO _3- ] ± 5.

PCO ₂ = 40 + 0.7 × [HCO _3- ] ± 5.

1. If the measured PCO ₂ 40 + 0.7 × [HCO _3- ] ± 5, it means that the metabolic alkalosis has reached the maximum compensation.

2. If the measured PCO ₂ <40 + 0.7 × [HCO _3- ] ± 5, it may be metabolic alkalosis combined with respiratory alkalosis, or mild metabolic alkalosis, or less than the time of onset 12 to 24 hours, the maximum compensation has not been reached, or there are factors that stimulate breathing.

3. If the measured PCO ₂ > 40 + 0.7 × [HCO _3- ] ± 5, it may be metabolic alkalosis combined with respiratory acidosis, or metabolic alkalosis combined with metabolic acidosis, or overcompensated. Metabolic alkalosis.

Differential diagnosis of metabolic alkalosis

The disease should be distinguished from metabolic acidosis, respiratory acidosis, and respiratory alkalosis.

Metabolic alkalosis treatment

1. Actively treat primary diseases, avoid taking alkaline drugs for a long time, less severe metabolic alkalosis does not need too aggressive treatment, and patients with potassium deficiency can be given oral potassium chloride sustained-release tablets.

2. Patients with insufficient circulating blood volume can quickly enter dextran 70 saline injection to restore effective circulating blood volume, and then infuse normal saline or glucose physiological saline to supplement extracellular fluid volume to reduce distal renal tubule Exchange of H for Na, to play the role of kidneys to discharge HCO _3- .

3. If severe symptoms or PCO ₂ > 8.0kPa (60mmHg) or respiratory depression (accumulation of CO ₂ ) due to respiratory compensation, resulting in hypoxia, acidic drugs must be used. 1 g of ammonium chloride can be taken orally once every 4 to 6 hours. If the patient cannot take it orally, ammonium chloride can be administered intravenously.

4. Severe metabolic alkalosis or PCO ₂ > 8.0kPa (60mmHg), you can also use arginine hydrochloride (molecular weight 210.5). For every 210.5 mg of arginine hydrochloride, 1 mmol of hydrochloric acid can be provided, and 20 g of arginine hydrochloride can provide approximately 100 mmol of hydrochloric acid. Add 500 ~ 1000ml of physiological saline or glucose physiological saline and slowly drip. The dosage should not exceed 20 40g within 24 hours. Because positively-charged arginine enters cells, K can be transferred into extracellular fluid. Care must be taken to avoid hyperkalemia. Liver dysfunction is disabled.

5. Severe metabolic alkalosis, when it is not suitable to use ammonium chloride or arginine hydrochloride, the isotonic hydrochloric acid solution can be input through the central venous pressure measuring tube. Most patients with metabolic alkalosis have insufficient fluid, so their total body fluid volume is calculated at 50% of their body weight.

6. Patients with heart failure and liver cirrhosis can take carbonic anhydrase diuretics, reduce H excretion, increase K and Na exchange, reduce HCO ₃ -recovery, increase HCO ₃ -exhaustion, and at the same time, they can take metabolic alkalosis. Diuretic. Available acetazolamide 250 ~ 375mg, 1 ~ 2 times / d, must pay attention to maintaining K balance at the same time.

7. Severe metabolic alkalosis, due to lack of K. Although committed to restoring extracellular fluid volume and treating acidic drugs such as ammonium chloride, renal tubular cells continue to exchange Na with a large amount of H, HCO ₃ ^- no chance Excreted, alkalosis cannot be corrected. And when restoring extracellular fluid volume, if too much sodium-containing fluid is used, the excretion of H and K will be increased, thereby making potassium deficiency and alkalosis even worse. At this time, K must be supplemented to correct intracellular potassium deficiency and increase Chance of HCO ₃ ^- excretion can correct alkalosis.

8. If you have convulsions, you can inject 10% calcium gluconate intravenously.