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| Acid–base imbalance | |
|---|---|
 | |
| ADavenport diagram illustrates acid–base imbalance graphically. | |
| Specialty | Internal medicine |
Acid–base imbalance is an abnormality of the human body's normalbalance of acids and bases that causes theplasmapH to deviate out of the normal range (7.35 to 7.45). In thefetus, the normal range differs based on which umbilical vessel is sampled (umbilical vein pH is normally 7.25 to 7.45;umbilical artery pH is normally 7.18 to 7.38).[1] It can exist in varying levels of severity, some life-threatening.
| PaO2 | Arterial oxygen tension, or partial pressure |
|---|---|
| PAO2 | Alveolar oxygen tension, or partial pressure |
| PaCO2 | Arterial carbon dioxide tension, or partial pressure |
| PACO2 | Alveolar carbon dioxide tension, or partial pressure |
| PvO2 | Oxygen tension of mixed venous blood |
| P(A-a)O2 | Alveolar-arterial oxygen tension difference. The term formerly used (A-a DO2) is discouraged. |
| P(a/A)O2 | Alveolar-arterial tension ratio;PaO2:PAO2 The termoxygen exchange index describes this ratio. |
| C(a-v)O2 | Arteriovenous oxygen content difference |
| SaO2 | Oxygen saturation of the hemoglobin of arterial blood |
| SpO2 | Oxygen saturation as measured by pulse oximetry |
| CaO2 | Oxygen content of arterial blood |
| pH | Symbol relating the hydrogen ion concentration or activity of a solution to that of a standard solution; approximately equal to the negative logarithm of the hydrogen ion concentration. pH is an indicator of the relative acidity or alkalinity of a solution |
An excess of acid is calledacidosis or acidemia, while an excess in bases is calledalkalosis or alkalemia. The process that causes the imbalance is classified based on the cause of the disturbance (respiratory or metabolic) and the direction of change in pH (acidosis or alkalosis). This yields the following four basic processes:
| process | pH | CO2 | compensation |
|---|---|---|---|
| metabolic acidosis |  | | respiratory |
| respiratory acidosis | |  | renal |
| metabolic alkalosis | | | respiratory |
| respiratory alkalosis | | | renal |
The presence of only one of the above derangements is called asimple acid–base disorder. In amixed disorder, more than one is occurring at the same time.[2] Mixed disorders may feature an acidosis and alkosis at the same time that partially counteract each other, or there can be two different conditions affecting the pH in the same direction. The phrase "mixed acidosis", for example, refers tometabolic acidosis in conjunction withrespiratory acidosis. Any combination is possible, as metabolic acidosis and alkalosis can co exist together.
The traditional approach to the study of acid–base physiology has been theempirical approach. The main variants are thebase excess approach and thebicarbonate approach. Thequantitative approach introduced byPeter A Stewart in 1978[3] is newer.
There are numerous reasons that each of the four processes can occur (detailed in each article). Generally speaking, sources of acid gain include:
Sources of acid loss include:
The body'sacid–base balance is tightly regulated. Severalbuffering agents exist which reversibly bind hydrogen ions and impede any change in pH.Extracellular buffers includebicarbonate andammonia, whileproteins andphosphate act asintracellular buffers. Thebicarbonate buffering system is especially key, ascarbon dioxide (CO2) can be shifted throughcarbonic acid (H2CO3) to hydrogen ions andbicarbonate (HCO3−) as shown below.
Acid–base imbalances that overcome the buffer system can be compensated in the short term by changing the rate ofventilation. This alters the concentration ofcarbon dioxide in the blood, shifting the above reaction according toLe Chatelier's principle, which in turn alters the pH. For instance, if the blood pH drops too low (acidemia), the body will compensate by increasing breathing, expelling CO2, and shifting the reaction above to the right such that fewer hydrogen ions are free–thus the pH will rise back to normal. Foralkalemia, the opposite occurs.
Thekidneys are slower to compensate, butrenal physiology has several powerful mechanisms to control pH by the excretion of excess acid or base. In responses to acidosis,tubular cells reabsorb more bicarbonate from the tubular fluid,collecting duct cells secrete more hydrogen and generate more bicarbonate, andammoniagenesis leads to increased formation of the NH3 buffer. In responses to alkalosis, the kidney may excrete more bicarbonate by decreasing hydrogen ion secretion from the tubular epithelial cells, and lowering rates ofglutamine metabolism and ammonia excretion.
