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Acid–base imbalance | |
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A Davenport diagram illustrates acid–base imbalance graphically. | |
Specialty | Internal medicine |
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). In the fetus, 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 |
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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 term oxygen 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 called acidosis or acidemia, while an excess in bases is called alkalosis 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 |
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metabolic acidosis | ![]() | ![]() | respiratory |
respiratory acidosis | ![]() | ![]() | renal |
metabolic alkalosis | ![]() | ![]() | respiratory |
respiratory alkalosis | ![]() | ![]() | renal |
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. [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 to metabolic acidosis in conjunction with respiratory 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 the empirical approach. The main variants are the base excess approach and the bicarbonate approach. The quantitative approach introduced by Peter 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'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.
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 reaction above to the right such that fewer 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.
In inorganic chemistry, bicarbonate is an intermediate form in the deprotonation of carbonic acid. It is a polyatomic anion with the chemical formula HCO−
3.
A carbonate is a salt of carbonic acid,, characterized by the presence of the carbonate ion, a polyatomic ion with the formula CO2−3. The word "carbonate" may also refer to a carbonate ester, an organic compound containing the carbonate groupO=C(−O−)2.
An arterial blood gas (ABG) test, or arterial blood gas analysis (ABGA) measures the amounts of arterial gases, such as oxygen and carbon dioxide. An ABG test requires that a small volume of blood be drawn from the radial artery with a syringe and a thin needle, but sometimes the femoral artery in the groin or another site is used. The blood can also be drawn from an arterial catheter.
Acidosis is a biological process producing hydrogen ions and increasing their concentration in blood or body fluids. pH is the negative log of hydrogen ion concentration and so it is decreased by a process of acidosis.
Alkalosis is the result of a process reducing hydrogen ion concentration of arterial blood plasma (alkalemia). In contrast to acidemia, alkalemia occurs when the serum pH is higher than normal. Alkalosis is usually divided into the categories of respiratory alkalosis and metabolic alkalosis or a combined respiratory/metabolic alkalosis.
Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance. Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. Metabolic acidosis can lead to acidemia, which is defined as arterial blood pH that is lower than 7.35. Acidemia and acidosis are not mutually exclusive – pH and hydrogen ion concentrations also depend on the coexistence of other acid-base disorders; therefore, pH levels in people with metabolic acidosis can range from low to high.
Respiratory acidosis is a state in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH.
Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide. This condition is one of the four primary disturbances of acid–base homeostasis.
The anion gap is a value calculated from the results of multiple individual medical lab tests. It may be reported with the results of an electrolyte panel, which is often performed as part of a comprehensive metabolic panel.
Metabolic alkalosis is an acid-base disorder in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations. The condition typically cannot last long if the kidneys are functioning properly.
In physiology, base excess and base deficit refer to an excess or deficit, respectively, in the amount of base present in the blood. The value is usually reported as a concentration in units of mEq/L (mmol/L), with positive numbers indicating an excess of base and negative a deficit. A typical reference range for base excess is −2 to +2 mEq/L.
Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine. In renal physiology, when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine. The metabolic acidosis that results from RTA may be caused either by insufficient secretion of hydrogen ions into the latter portions of the nephron or by failure to reabsorb sufficient bicarbonate ions from the filtrate in the early portion of the nephron. Although a metabolic acidosis also occurs in those with chronic kidney disease, the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. Several different types of RTA exist, which all have different syndromes and different causes. RTA is usually an incidental finding based on routine blood draws that show abnormal results. Clinically, patients may present with vague symptoms such as dehydration, mental status changes, or delayed growth in adolescents.
Carbaminohemoglobin (carbaminohaemoglobin BrE) (CO2Hb, also known as carbhemoglobin and carbohemoglobin) is a compound of hemoglobin and carbon dioxide, and is one of the forms in which carbon dioxide exists in the blood. Twenty-three percent of carbon dioxide is carried in blood this way (70% is converted into bicarbonate by carbonic anhydrase and then carried in plasma, 7% carried as free CO2, dissolved in plasma).
Acid–base homeostasis is the homeostatic regulation of the pH of the body's extracellular fluid (ECF). The proper balance between the acids and bases in the ECF is crucial for the normal physiology of the body—and for cellular metabolism. The pH of the intracellular fluid and the extracellular fluid need to be maintained at a constant level.
In acid base physiology, the Davenport diagram is a graphical tool, developed by Horace W. Davenport, that allows a clinician or investigator to describe blood bicarbonate concentrations and blood pH following a respiratory and/or metabolic acid-base disturbance. The diagram depicts a three-dimensional surface describing all possible states of chemical equilibria between gaseous carbon dioxide, aqueous bicarbonate and aqueous protons at the physiologically complex interface of the alveoli of the lungs and the alveolar capillaries. Although the surface represented in the diagram is experimentally determined, the Davenport diagram is rarely used in the clinical setting, but allows the investigator to envision the effects of physiological changes on blood acid-base chemistry. For clinical use there are two recent innovations: an Acid-Base Diagram which provides Text Descriptions for the abnormalities and a High Altitude Version that provides text descriptions appropriate for the altitude.
Respiratory compensation is the modulation by the brainstem respiratory centers, which involves altering alveolar ventilation to try to bring the plasma pH back to its normal value (7.4) in order to keep the acid-base balance in the body. It usually occurs within minutes to hours and is much faster than renal compensation, but has less ability to restore normal values.
The bicarbonate buffer system is an acid-base homeostatic mechanism involving the balance of carbonic acid (H2CO3), bicarbonate ion (HCO−
3), and carbon dioxide (CO2) in order to maintain pH in the blood and duodenum, among other tissues, to support proper metabolic function. Catalyzed by carbonic anhydrase, carbon dioxide (CO2) reacts with water (H2O) to form carbonic acid (H2CO3), which in turn rapidly dissociates to form a bicarbonate ion (HCO−
3 ) and a hydrogen ion (H+) as shown in the following reaction:
Winters's formula, named after R. W. Winters, is a formula used to evaluate respiratory compensation when analyzing acid-base disorders in the presence of metabolic acidosis. It can be given as:
Intravenous sodium bicarbonate, also known as sodium hydrogen carbonate, is a medication primarily used to treat severe metabolic acidosis. For this purpose it is generally only used when the pH is less than 7.1 and when the underlying cause is either diarrhea, vomiting, or the kidneys. Other uses include high blood potassium, tricyclic antidepressant overdose, and cocaine toxicity as well as a number of other poisonings. It is given by injection into a vein.
In nephrology, the delta ratio, or "delta-delta", is a formula that can be used to evaluate whether a mixed acid–base disorder is present, and if so, assess its severity. The anion gap (AG) without potassium is calculated first and if a metabolic acidosis is present, results in either a high anion gap metabolic acidosis (HAGMA) or a normal anion gap acidosis (NAGMA). A low anion gap is usually an oddity of measurement, rather than a clinical concern.