What Is Alkalosis?

Normal human body pH is 7.35 ~ 7.45. Alkaline poisoning refers to the clinical situation of excessive acid loss in the body or excessive intake of alkali from the outside. The main biochemical manifestations are blood HCO ₃ ^- too high (> 27mmol / L) and PaCO ₂ increased. The pH value is more than 7.45, but it varies depending on the compensation situation and can be significantly too high; it can also only rise slightly or even normally.

Basic Information

English name

Alkalosis

Visiting department

Emergency Department

Common causes

Hyperventilation of the lungs and excessive discharge of CO2 cause the PaCO2 in the blood to drop, causing the pH to rise

Common symptoms

Shallow and slow breathing, restlessness, excitement, slang, drowsiness, coma in severe cases, convulsions of hands and feet, hypertonic reflexes, etc.

Causes of alkalosis

Respiratory alkalosis

It is because the lungs are hyperventilated and CO _{2 is} exhausted too much, which reduces PaCO ₂ in the blood and causes the pH value to rise. Common reasons are:

(1) Central respiratory center is stimulated by stimulation, such as intracranial lesions (infection, tumor, bleeding, trauma), hypoxia, fever, pain, toxic encephalopathy, hepatic encephalopathy, pregnancy and drug poisoning (such as salicylate poisoning )Wait.

(2) Pulmonary diseases such as pneumonia, early asthma, pulmonary infarction, and congestive heart failure.

(3) snoring hyperpnea, children cry for a long time.

(4) Iatrogenic ventilator is hyperventilated.

2. Metabolic alkalosis

It is because the extracellular fluid loses a large amount of acid or absorbs a large amount of base, so that HCO ₃ ^- increases, which causes the molecule of [BHCO ₃ ] / [HHCO ₃ ] to become large and causes the pH value to increase. Common reasons are:

(1) Loss of gastric juice after vomiting, long-term gastric aspiration, pyloric obstruction, and surgical anesthesia.

(2) potassium deficiency

(3) Extracellular fluid Cl ^- reduced, such as decreased intake, or loss of gastric fluid, or 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 kidney ^-Or , due to a defect in Cl ^- absorption by congenital intestinal mucosal cells, the extracellular fluid Cl ^- can be reduced.

(4) Bicarbonate accumulation

1) In the treatment of gastric ulcer, long-term use of a large number of alkaline drugs can reduce or disappear gastric acid, so that bicarbonate in the intestinal fluid is absorbed into the blood without being neutralized, and HCO ₃ ^- in the blood is greatly increased, so that alkali occurs. Poisoning.

2) Too much organic acid salt is taken orally or injected with lactate, citrate (large blood transfusion), and too much acetate, they are converted into CO ₂ and H ₂ O in the liver and form bicarbonate, The HCO ₃ ^- content in the blood is greatly increased, and alkalosis is promoted.

3) During cardiopulmonary resuscitation, a large amount of sodium bicarbonate is used. After resuscitation, the lactate is metabolized and the consumed HCO ₃ ^- can be recovered. As a result, the HCO ₃ ^- in the blood is even as high as 60 to 70 mmol / L, and the pH value reaches 7.90. In addition, in renal failure, alkalosis can also occur when sodium bicarbonate is used too much.

(5) Mineralocorticoids include aldosteronism and Cushing's syndrome.

Classification of alkalosis

There are two types of alkalosis: respiratory alkalosis and metabolic alkalosis. Respiratory alkalosis is caused by exhaling too much CO ₂ ; if it is caused by excessive H ⁺ loss, accumulation of HCO ₃ ^- excess or loss of Cl ^- more than loss of HCO _3- , it is metabolic alkalosis.

Clinical manifestations of alkalosis

Shallow and slow breathing

It is a phenomenon that the respiratory system compensates for 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 The ratio change that occurs (stable pH).

Mental symptoms

Agitation, excitement, slang, lethargy, and coma in severe cases.

3. Increased neuromuscular excitability

There are tetany in hands and feet, hypertonic reflexes, and so on.

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 PaCO ₂ and blood pH increased.

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.

Alkalosis diagnosis

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

PaCO ₂ = 0.7 × [HCO _3- ] ± 5.

PaCO ₂ = 40 + 0.7 × [HCO _3- ] ± 5.

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

2. If the measured PaCO ₂ <40 + 0.7 × [HCO _3- ] ± 5, it may be alkalosis and respiratory alkalosis, or mild alkalosis, or the onset time is less than 12 to 24 hours. , Has not reached the maximum compensation, or because of factors that stimulate breathing.

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

Alkalosis treatment

1. Actively treat primary diseases and avoid taking alkaline drugs for a long time. Less severe alkalosis does not require too aggressive treatment. 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 tubules. 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. Ammonium chloride can be taken orally. If the patient cannot take it orally, ammonium chloride can be given intravenously.

4. Severe alkalosis or PCO ₂ > 8.0kPa (60mmHg), you can also use arginine hydrochloride (molecular weight 210.5). Add saline or glucose saline slowly and intravenously. 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 alkalosis, when it is not suitable to use ammonium chloride or arginine hydrochloride, the isotonic hydrochloric acid solution can be input through the central vein manometer. Most patients with alkalosis have insufficient fluid, so their total body fluid volume is calculated at 50% of their body weight.

6. Patients with heart failure and cirrhosis can take carbonic anhydrase diuretics, reduce H excretion, increase K and Na exchange, reduce HCO ₃ -recovery, increase HCO ₃ -exhaustion, and diuretic at the same time when suffering from alkalosis. Acetazolamide is available and care must be taken to maintain K balance.

7. Severe 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, and HCO ₃ ^-can not be excreted, Alkali poisoning still 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.