Too sour

Less alkali

hyperkalemia

hemodilution

AG-increased metabolic acidosis

AG normal metabolic acidosis

Buffering of blood and buffering and compensatory regulation of internal and external ion exchange in cells: immediate

Lungs: Breathing deepens and accelerates, promoting the discharge of carbon dioxide (appears in a few minutes, reaches the peak in 30 minutes)

Kidney: Enhance the ability to excrete acid and maintain alkali, strengthen secretion of hydrogen, secretion of ammonia, and reabsorption of bicarbonate ions (increased carbonic anhydrase activity) (slower, peaking in 3 to 5 days)

Cardiovascular System

Central Nervous System

skeletal system

Prevent and treat primary disease

Alkaline drugs: sodium bicarbonate, trishydroxymethylaminomethane (THAM), alkali supplementation in batches under blood gas monitoring, the amount of alkali supplementation should be small but not large

Prevent and treat hypokalemia and hypocalcemia: After alkali supplementation and acid correction, potassium ions return to the cells, causing hypokalemia; under alkaline conditions, plasma proteins and free calcium generate bound calcium

Respiratory center depression

airway obstruction

ventilator paralysis

Thoracic lesions

Improper management of artificial respirators (too small ventilation volume)

Inhaling too much carbon dioxide

Acute respiratory acidosis: apnea caused by acute airway obstruction, central or respiratory muscle paralysis

Chronic respiratory acidosis: COPD, widespread pulmonary fibrosis, or atelectasis

acute respiratory acidosis

chronic respiratory acidosis

Similar to acid metabolism, it causes arrhythmia, weakened myocardial contractility, dilation of peripheral blood vessels, and elevated blood potassium.

Carbon dioxide directly dilates blood vessels: causing cerebral vasodilation, increased cerebral blood flow, and increased intracranial pressure - persistent headache, especially at night and in the morning

Pulmonary encephalopathy: carbon dioxide anesthesia, confusion, tremor, delirium or drowsiness, or even coma

Treat the primary disease: remove respiratory obstruction or relieve spasm, use respiratory center stimulants or ventilator

Improve ventilatory function: Do not use the ventilator too quickly to quickly reduce the carbon dioxide partial pressure to normal.

Use alkaline drugs with caution: The compensatory effect of the kidneys is slow; before ventilation improves, the use of alkaline drugs that can produce carbon dioxide may cause carbon dioxide retention. (If necessary, use sodium-free organic base THAM

Hypoxemia and lung disease

Direct stimulation of the respiratory center or psychogenic hyperventilation

Strong body metabolism

Improper use of ventilator (excessive ventilation

Acute respiratory alkali

Chronic respiratory alkali

Ion exchange inside and outside cells and intracellular buffering

kidney

Dizziness, abnormal sensation in the limbs and around the mouth, disturbance of consciousness and convulsions are more likely to occur than alkaloids.

Decreased plasma phosphate concentration: Alkalosis enhances glycogenolysis - the production of phosphate compounds such as G-6-P and fructose 1,6-bisphosphate increases, consuming a large amount of phosphorus - extracellular fluid phosphorus enters the cells

Prevent and treat primary disease

Breathing in gases containing carbon dioxide

Correct hypocalcemia

Too much acid loss

Bicarbonate ion excess load

Hypokalemia

saline reactive alkalosis

saline resistant alkalosis

Buffering of blood and ion exchange inside and outside cells

lung

kidney

Central Nervous System

neuromuscular

Hypokalemia

Salt water reactive alkali substitute

Salt water resistant alkali substitute