Acid-base homeostasis: Difference between revisions
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*Chronic: HCO<sub><big>3</big></sub><sup>−</sup> decreases by 5mEq/L for every 10 mmHg decrease in paCO2 above 40 | *Chronic: HCO<sub><big>3</big></sub><sup>−</sup> decreases by 5mEq/L for every 10 mmHg decrease in paCO2 above 40 | ||
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==Related Chapters== | |||
== Related Chapters == | |||
* [[Renal physiology]] | * [[Renal physiology]] | ||
* [[Acid-base imbalance|Acid–base imbalance]] | * [[Acid-base imbalance|Acid–base imbalance]] | ||
Revision as of 16:11, 25 May 2018
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Acid-base Homeostasis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]; Priyamvada Singh, M.D. [3]
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 | ||
Compensation Mechanism
- 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 |
|
Related Chapters
- Renal physiology
- Acid–base imbalance
- Arterial blood gas
- Metabolic acidosis
- Metabolic alkalosis
- Respiratory acidosis
- Respiratory alkalosis
- Anion gap
References
- ↑ 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.