Acid-base homeostasis: Difference between revisions
No edit summary |
|||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Acid-base homeostasis}} | |||
{{Acids and bases}} | {{Acids and bases}} | ||
{{SI}} | {{SI}} | ||
Revision as of 19:45, 21 May 2018
|
Acid-base Homeostasis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]
Overview
Acid-base homeostasis is the part of human homeostasis concerning the proper balance between acids and bases, in other words the pH. The body is very sensitive to its pH level. Outside the range of pH that is compatible with life, proteins are denatured and digested, enzymes lose their ability to function, and the body is unable to sustain itself.
Mechanism
The kidneys maintain acid-base homeostasis by regulating the pH of the blood plasma. Gains and losses of acid and base must be balanced. The study of the acid-base reactions in the body is acid base physiology.
Buffering agents
Any substance that can reversibly bind hydrogen ions is called a buffering agent. They function to impede any change in pH. Hydrogen ions are buffered by extracellular (e.g., bicarbonate, ammonia) and intracellular buffering agents (including proteins and phosphate).
Blood Gas Analysis
| Blood gas analysis | Vessel | Range | Interpretation |
|---|---|---|---|
| Oxygen Partial Pressure (pO2) | Arterial | 80 to 100 mmHg | Normal |
| <80 mmHg | Hypoxia | ||
| Venous | 35 to 40 mmHg | Normal | |
| Oxygen Saturation (SO2) | Arterial | >95% | Normal |
| <95% | Hypoxia | ||
| Venous | 70 to 75% | Normal | |
| pH | Arterial | <7.35 | Acidemia |
| 7.35 to 7.45 | Normal | ||
| >7.45 | Alkalemia | ||
| Venous | 7.26 to 7.46 | Normal | |
| Carbon Dioxide Partial Pressure (pCO2) | Arterial | <35 mmHg | Low |
| 35 to 45 mmHg | Normal | ||
| >45 mmHg | High | ||
| Venous | 40 to 45 mmHg | Normal | |
| Bicarbonate (HCO3−) | Arterial | <22 mmol/L | Low |
| 22 to 26 mmol/L | Normal | ||
| >26 mmol/L | High | ||
| Venous | 19 to 28 mmol/L | Normal | |
| Base Excess (BE) | Arterial | <−3.4 | Acidemia |
| −3.4 to +2.3 mmol/L | Normal | ||
| >2.3 | Alkalemia | ||
| Venous | −2 to −5 mmol/L | Normal | |
| Osmolar gap = Osmolality – Osmolarity | >10 | Abnormal | |
| Anion gap = [Na+] – {[Cl−]+[HCO3−]}
Corrected AG = (measured serum AG) + (2.5 x [4.5 − Alb]) |
<8 | Low | |
| 8 to 16 | Normal | ||
| >16 | High | ||
Approach to Acid–base Imbalance
| Check pH on ABG | |||||||||||||||||||||||||||||||||||||||||
| pH < 7.35= Acidosis | pH > 7.45= Alkalosis | ||||||||||||||||||||||||||||||||||||||||
| Check PaCO2 | |||||||||||||||||||||||||||||||||||||||||
| PaCO2 > 45mm Hg = Respiratory acidosis | PaCO2 Normal or < 35mm Hg = Metabolic acidosis | Check PaCO2 | |||||||||||||||||||||||||||||||||||||||
| PaCO2 > 45mm Hg = Metabolic alkalosis | PaCO2 < 35mm Hg = Respiratory alkalosis | ||||||||||||||||||||||||||||||||||||||||
| [HCO3-] > 29 | Check [HCO3-] | ||||||||||||||||||||||||||||||||||||||||
| Normal or slight decrease = Acute respiratory alkalosis | Decreased < 24 = Chronic respiratory alkalosis | ||||||||||||||||||||||||||||||||||||||||
Acid–base Imbalance
Imbalance has several possible causes. An excess of acid is called acidosis and an excess in bases is called alkalosis. Acidosis is much more common than alkalosis. The imbalance is compensated by negative feedback to restore normal values. There are various renal responses to acidosis and alkalosis.
Causes
Sources of acid gain:
- Carbon dioxide (since CO2 and OH-, hydroxide, form HCO3-, bicarbonate, and H+, a proton, in the presence of carbonic anhydrase)
- Production of nonvolatile acids from the metabolism of proteins and other organic molecules
- Loss of bicarbonate in faeces or urine
- Intake of acids or acid precursors
Sources of acid loss:
- Use of hydrogen ions in the metabolism of various organic anions
- Loss of acid in the vomitus or urine
Response
Responses to acidosis:
- Bicarbonate is added to the blood plasma by tubular cells.
- Tubular cells reabsorb more bicarbonate from the tubular fluid.
- Collecting duct cells secrete more hydrogen and generate more bicarbonate.
- Ammoniagenesis leads to increased buffer formation (in the form of NH3)
Responses to alkalosis:
- Excretion of bicarbonate in urine.
- This is caused by lowered rate of hydrogen ion secretion from the tubular epithelial cells.
- This is also caused by lowered rates of glutamine metabolism and ammonia excretion.
Compensation
- There are compensation mechanisms in the body in order to normalizing the pH inside the blood.[1]
- The amount of compensation depends on proper functioning of renal and respiratory systems. However, it is uncommon to compensate completely. Compensatory mechanisms might correct only 50–75% of pH to normal.
- Acute respiratory compensation usually occurs within first day. However, chronic respiratory compensation takes 1 to 4 days to occur.
- Renal compensation might occur slower than respiratory compensation.
| Primary disorder | pH | PaCO2 | [HCO3−] | Compensation | Compensation formula |
|---|---|---|---|---|---|
| Metabolic acidosis | ↓ | ↓ | ↓ | Respiratory |
|
| Metabolic alkalosis | ↑ | ↑ | ↑ | Respiratory |
|
| Respiratory acidosis | ↓ | ↑ | ↑ | Renal |
|
| Respiratory alkalosis | ↑ | ↓ | ↓ | Renal |
|
Mixed Acid−base Disorders
| Disorder | Key features | Examples |
|---|---|---|
| Metabolic acidosis & respiratory alkalosis |
|
|
| Metabolic acidosis & respiratory acidosis |
|
|
| Metabolic alkalosis & respiratory alkalosis | ||
| Metabolic alkalosis & respiratory acidosis |
| |
| Metabolic acidosis & metabolic alkalosis | ||
| Metabolic acidosis & metabolic acidosis |
|
See also
- ↑ Sood P, Paul G, Puri S (April 2010). "Interpretation of arterial blood gas". Indian J Crit Care Med. 14 (2): 57–64. doi:10.4103/0972-5229.68215. PMC 2936733. PMID 20859488.