Difference between revisions of "Acid-base imbalance"
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Latest revision as of 19:17, 21 September 2010
Acid-base imbalance | |
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Classification and external resources | |
ICD-10 | E87.2-E87.4 |
ICD-9 | 276.2-276.4 |
MeSH | D000137 |
Acid-base imbalance is an abnormality of the human body's normal balance of acids and bases that causes the plasma pH to deviate out of the normal range (7.35 to 7.45). It can exist in varying levels of severity, some life-threatening.
Contents
Classification
An excess of acid is called acidosis (pH less than 7.35) and an excess in bases is called alkalosis (pH greater than 7.45). The process that causes the imbalance is classified based on the etiology 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 | carbon dioxide | compensation |
metabolic acidosis | down | down | respiratory |
respiratory acidosis | down | up | renal |
metabolic alkalosis | up | up | respiratory |
respiratory alkalosis | up | down | renal |
Mixed disorders
The presence of only one of the above derangements is called a simple acid-base disorder. In a mixed disorder more than one is occurring at the same time.[1] Mixed disorders may feature an acidosis and alkosis at the same time that partially counteract each other, or there can be two different conditions effecting the pH in the same direction. The phrase "mixed acidosis", for example, refers to metabolic acidosis in conjunction with respiratory acidosis. Any combination is possible, except concurrent respiratory acidosis and respiratory alkalosis, since a person cannot breathe too fast and too slow at the same time.
Calculation of imbalance
The traditional approach to the study of acid-base physiology has been the empiric approach. The main variants are the base excess approach and the bicarbonate approach. The quantitative approach introduced by Peter A Stewart in 1978[2] is newer.
Causes
There are numerous reasons that each of the four processes can occur (detailed in each article). Generally speaking, sources of acid gain include:
- Retention of carbon dioxide
- Production of nonvolatile acids from the metabolism of proteins and other organic molecules
- Loss of bicarbonate in feces or urine
- Intake of acids or acid precursors
Sources of acid loss include:
- Use of hydrogen ions in the metabolism of various organic anions
- Loss of acid in the vomitus or urine
Compensation
The body's acid-base balance is tightly regulated. Several buffering agents exist which reversibly bind hydrogen ions and impede any change in pH. Extracellular buffers include bicarbonate and ammonia, while proteins and phosphate act as intracellular buffers. The bicarbonate buffering system is especially key, as carbon dioxide (CO2) can be shifted through carbonic acid (H2CO3) to hydrogen ions and bicarbonate (HCO3- ) as shown below.
- <math>\rm HCO_3^- + H^+ \leftrightarrow H_2CO_3 \leftrightarrow CO_2 + H_2O</math>
Acid-base imbalances that overcome the buffer system can be compensated in the short term by changing the rate of ventilation. This alters the concentration of carbon dioxide in the blood, shifting the above reaction according to Le 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 following reaction to the right such that less hydrogen ions are free - thus the pH will rise back to normal. For alkalemia, the opposite occurs.
The kidneys are slower to compensate, but renal 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, and ammoniagenesis 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 of glutamine metabolism and ammonia excretion.
References
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External links
- On-line text at AnaesthesiaMCQ.com
- Physiology at MCG 7/7ch12/7ch12lin
- Overview at kumc.edu
- Overview at mcgill.ca
- [1]
- Stewart's original text at acidbase.org
- Overview at med.utah.edu
- Overview at anaesthetist.com
- Overview at anst.uu.se
- Tutorial at acid-base.com
- On-line Acid-Base Physiology text
- Diagnoses at lakesidepress.com
- Interpretation at nda.ox.ac.uk
- Acid Base Tutorial
es:Trastornos del equilibrio ácido-base el:Ισορροπία οξέων - βάσεων fr:Métabolisme acido-basique fr:Équilibre acido-basique hr:Poremećaji acidobazne ravnoteže it:Equilibrio acido base pt:Desequilíbrio ácido-básico
uk:Буферні системи- ↑ "Mixed Acid Base Disorders: Acid Base Tutorial, University of Connecticut Health Center". Retrieved 2009-05-09.
- ↑ Stewart P (1978). "Independent and dependent variables of acid-base control". Respir Physiol. 33 (1): 9–26. doi:10.1016/0034-5687(78)90079-8. PMID 27857.