The document discusses acid-base balance and buffers in the human body. It notes that the normal pH of arterial blood is 7.4 and venous blood and interstitial fluids is around 7.35. The pH is tightly regulated within the range of 7.35-7.45. The main buffers that maintain pH are the bicarbonate buffer system, phosphate buffer system, and protein buffers. The bicarbonate buffer system is the most important extracellular buffer and involves regulation of bicarbonate and carbonic acid by the kidneys and lungs respectively.
2. Normal pH Of The Body Fluids
The normal pH of arterial blood is 7.4
pH of venous blood and interstitial fluids is about 7.35
The pH of blood is maintained within a remarkable constant
level of 7.35 to 7.45.
Normal pH Of The Body Fluids
The normal pH of arterial blood is 7.4
pH of venous blood and interstitial fluids is about 7.35
The pH of blood is maintained within a remarkable constant
level of 7.35 to 7.45.
4. The activities of almost all enzyme systems in the body
are influenced by hydrogen ion concentration.
Changes in hydrogen ion concentration alter:
all cell and body functions
the conformation of biological structural components
uptake and release of oxygen
The activities of almost all enzyme systems in the body
are influenced by hydrogen ion concentration.
Changes in hydrogen ion concentration alter:
all cell and body functions
the conformation of biological structural components
uptake and release of oxygen
5. Metabolic Sources Of Acids Which Alter Blood pH
Fixed acids or non-volatile acids:
• Phosphoric
• Sulphuric acids
• Pyruvic acid,
• Lactic acid
• Keto acids
Volatile acids breathe out through the lungs :
• Carbonic acid (H2CO3).
Metabolic Sources Of Acids Which Alter Blood pH
Fixed acids or non-volatile acids:
• Phosphoric
• Sulphuric acids
• Pyruvic acid,
• Lactic acid
• Keto acids
Volatile acids breathe out through the lungs :
• Carbonic acid (H2CO3).
6. Metabolic Sources Of Bases
Citrate salts of fruit juices may produce bicarbonate salt.
Deamination of amino acids produces ammonia
Formation of bis-phosphate also contributes to
alkalinizing effect.
Metabolic Sources Of Bases
Citrate salts of fruit juices may produce bicarbonate salt.
Deamination of amino acids produces ammonia
Formation of bis-phosphate also contributes to
alkalinizing effect.
7. Regulatory Mechanisms to maintain normal
Blood pH
Buffer mechanism: First line of defense
The respiratory mechanism: Second line of defense
Renal mechanism: Third line of defense.
Regulatory Mechanisms to maintain normal
Blood pH
Buffer mechanism: First line of defense
The respiratory mechanism: Second line of defense
Renal mechanism: Third line of defense.
8. WHAT IS BUFFER?
Buffer is a substance that can resist the change in pH
even after addition of strong acid or base. It is a mixture
of a weak acid and a salt of its conjugate base e.g.
NaHCO3/ H2CO3
If one molecule differs from another by only a proton,
the two are called as conjugate acid-base pair.
WHAT IS BUFFER?
Buffer is a substance that can resist the change in pH
even after addition of strong acid or base. It is a mixture
of a weak acid and a salt of its conjugate base e.g.
NaHCO3/ H2CO3
If one molecule differs from another by only a proton,
the two are called as conjugate acid-base pair.
9. A buffer can reversibly bind hydrogen ions. The general
form of the buffering reaction is:
Buffer systems do not eliminate hydrogen ions from the
body or add them to the body but only keep them tied up
until balance can be re-established.
A buffer can reversibly bind hydrogen ions. The general
form of the buffering reaction is:
Buffer systems do not eliminate hydrogen ions from the
body or add them to the body but only keep them tied up
until balance can be re-established.
10. Blood Buffer
Buffer System Extracellular buffer Intracellular buffer
Bicarbonate NaHCO3/ H2CO3 KHCO3/H2CO3
Phosphate Na2HPO4/NaH2PO4 K2HPO4/KH2PO4
Protein Na Protein/H. Protein KHb/H.Hb
KHbO2/H.HbO2
Blood Buffer
Buffer System Extracellular buffer Intracellular buffer
Bicarbonate NaHCO3/ H2CO3 KHCO3/H2CO3
Phosphate Na2HPO4/NaH2PO4 K2HPO4/KH2PO4
Protein Na Protein/H. Protein KHb/H.Hb
KHbO2/H.HbO2
11. The Bicarbonate Buffer System
(HCO3
– / H2CO3)
The bicarbonate buffer system is the most important
extracellular buffer.
It plays an important role in maintaining blood pH,
because of its high concentration.
Two elements of the buffer system, HCO3
– and H2CO3
are regulated by the kidneys, and by the lungs
respectively.
The Bicarbonate Buffer System
(HCO3
– / H2CO3)
The bicarbonate buffer system is the most important
extracellular buffer.
It plays an important role in maintaining blood pH,
because of its high concentration.
Two elements of the buffer system, HCO3
– and H2CO3
are regulated by the kidneys, and by the lungs
respectively.
12. Mechanism of Action of Bicarbonate Buffer
When a strong acid, such as HCI, is added to the
bicarbonate buffer solution, the increased hydrogen
ions are buffered by HCO3
– to form very weak acid
H2CO3, which, in turn, forms CO2 and H2O.
Mechanism of Action of Bicarbonate Buffer
When a strong acid, such as HCI, is added to the
bicarbonate buffer solution, the increased hydrogen
ions are buffered by HCO3
– to form very weak acid
H2CO3, which, in turn, forms CO2 and H2O.
13. When sodium hydroxide (NaOH), is added to bicarbonate
buffer, hydroxyl ion (OH–) from NaOH combines with
H2CO3 to form weak base HCO3
– and H2O
When sodium hydroxide (NaOH), is added to bicarbonate
buffer, hydroxyl ion (OH–) from NaOH combines with
H2CO3 to form weak base HCO3
– and H2O
14. Any nonvolatile acid stronger than carbonic acid can be
buffered by bicarbonate (HCO3
– ).
Plasma bicarbonate is a measure of the base that remains
after all acids, stronger than carbonic have been
neutralized.
It represents the reserve of alkali available for the
neutralization of such strong acids and it has been
termed as the alkali reserve.
Any nonvolatile acid stronger than carbonic acid can be
buffered by bicarbonate (HCO3
– ).
Plasma bicarbonate is a measure of the base that remains
after all acids, stronger than carbonic have been
neutralized.
It represents the reserve of alkali available for the
neutralization of such strong acids and it has been
termed as the alkali reserve.
15. At pH 7.4 the average normal ratio of the concentration
of HCO3
– and H2CO3 in plasma is 25 mmol/L to 1.25
mmol/L = 20:1.
Subsequently any changes in the concentration of either
bicarbonate (HCO3
–) or carbonic acid (H2CO3) and
therefore in the ratio HCO3
– : H2CO3 is accompanied by a
change in pH.
At pH 7.4 the average normal ratio of the concentration
of HCO3
– and H2CO3 in plasma is 25 mmol/L to 1.25
mmol/L = 20:1.
Subsequently any changes in the concentration of either
bicarbonate (HCO3
–) or carbonic acid (H2CO3) and
therefore in the ratio HCO3
– : H2CO3 is accompanied by a
change in pH.
16. The two elements of the buffer system, HCO3
– and H2CO3
are regulated by:
1. Increasing or decreasing the rate of reabsorption
of HCO3 by the kidneys
2. By altering the rates of removal or retention of
H2CO3 by the lungs
The two elements of the buffer system, HCO3
– and H2CO3
are regulated by:
1. Increasing or decreasing the rate of reabsorption
of HCO3 by the kidneys
2. By altering the rates of removal or retention of
H2CO3 by the lungs
17. The Phosphate Buffer System (HPO4– – /H2PO4–)
The phosphate buffer system is not important as a blood
buffer; it plays a major role in buffering renal tubular
fluid and intracellular fluids.
The Phosphate Buffer System (HPO4– – /H2PO4–)
The phosphate buffer system is not important as a blood
buffer; it plays a major role in buffering renal tubular
fluid and intracellular fluids.
18. Mechanism of Action of Phosphate Buffer
(HPO4– – /H2PO4–)
When a strong acid such as HCI is added to phosphate
buffer the H+ is accepted by the base HPO4– – and
converted to H2PO4
– and strong acid HCI is replaced
by a weak acid NaH2PO4
Mechanism of Action of Phosphate Buffer
(HPO4– – /H2PO4–)
When a strong acid such as HCI is added to phosphate
buffer the H+ is accepted by the base HPO4– – and
converted to H2PO4
– and strong acid HCI is replaced
by a weak acid NaH2PO4
19. When strong base, such as NaOH, is added to the phosphate
buffer the OH– is buffered by the H2PO4
– to form HPO4
– –
and water. Thus strong base NaOH is replaced by weak base
HPO4
– –
At a plasma pH of 7.4 the ratio HPO4
– – : H2PO4
– is 4:1.
When strong base, such as NaOH, is added to the phosphate
buffer the OH– is buffered by the H2PO4
– to form HPO4
– –
and water. Thus strong base NaOH is replaced by weak base
HPO4
– –
At a plasma pH of 7.4 the ratio HPO4
– – : H2PO4
– is 4:1.
20. Organic phosphate in the form of 2,3 phosphoglycerate
(2, 3 BPG), present in erythrocytes accounts for about
16% of the non-carbonate buffer of erythrocyte fluid
Organic phosphate in the form of 2,3 phosphoglycerate
(2, 3 BPG), present in erythrocytes accounts for about
16% of the non-carbonate buffer of erythrocyte fluid
21. PROTEIN BUFFER
(Na Protein/H Protein)
In the blood, plasma proteins especially albumin acts as
buffer.
In acid solution the basic amino group (NH2) takes up
excess H+ ions forming (NH3
+).
Whereas in basic solutions the acidic COOH groups give
up hydrogen ion forming OH– of alkali to water.
PROTEIN BUFFER
(Na Protein/H Protein)
In the blood, plasma proteins especially albumin acts as
buffer.
In acid solution the basic amino group (NH2) takes up
excess H+ ions forming (NH3
+).
Whereas in basic solutions the acidic COOH groups give
up hydrogen ion forming OH– of alkali to water.
22. Other important buffer groups of proteins in the
physiological pH range are the imidazole groups of
histidine.
Each albumin molecule contains 16 histidine residues.
Other important buffer groups of proteins in the
physiological pH range are the imidazole groups of
histidine.
Each albumin molecule contains 16 histidine residues.
23. Hemoglobin Buffer
(KHb/H Hb and KHbO2/HHbO2)
Haemoglobin is the major intracellular buffer of blood
which is present in erythrocytes.
Each Hb molecule contains 38 molecules of histidine.
The imidazole group of histidine has a pKa of
approximately 7.3, fairly close to 7.4.
It buffers carbonic acid (H2CO3)
Hemoglobin Buffer
(KHb/H Hb and KHbO2/HHbO2)
Haemoglobin is the major intracellular buffer of blood
which is present in erythrocytes.
Each Hb molecule contains 38 molecules of histidine.
The imidazole group of histidine has a pKa of
approximately 7.3, fairly close to 7.4.
It buffers carbonic acid (H2CO3)
24. Action of hemoglobin buffer
Hemoglobin works effectively in co-operation with the
bicarbonate system.
Action of hemoglobin buffer
Hemoglobin works effectively in co-operation with the
bicarbonate system.
25.
26. The transport of an appreciable quantity of the CO2 released
from the tissues without change in pH is called isohydric
transport of CO2.
Most of the CO2 is transported in the plasma as bicarbonate
(HCO3
– ).
Because HCO3 is much more soluble in blood plasma than is
CO2, this indirect route increases the blood’s capacity to carry
CO2 from the tissues to the lungs.
The transport of an appreciable quantity of the CO2 released
from the tissues without change in pH is called isohydric
transport of CO2.
Most of the CO2 is transported in the plasma as bicarbonate
(HCO3
– ).
Because HCO3 is much more soluble in blood plasma than is
CO2, this indirect route increases the blood’s capacity to carry
CO2 from the tissues to the lungs.
27. Respiratory Mechanism
Second line of defense against acid-base disturbances
It functions by regulating the concentration of carbonic
acid (H2CO3) in blood and other body fluids by lungs.
The respiratory center regulates the removal or retention
of CO2 and thereby H2CO3 from the extracellular fluid
by the lungs.
Respiratory Mechanism
Second line of defense against acid-base disturbances
It functions by regulating the concentration of carbonic
acid (H2CO3) in blood and other body fluids by lungs.
The respiratory center regulates the removal or retention
of CO2 and thereby H2CO3 from the extracellular fluid
by the lungs.
28. Increase in (H+) or (H2CO3) stimulates the respiratory
center to increase the rate of respiratory ventilation and
excess acid (H2CO3) in the form of CO2 is quickly
removed
Increase in (OH–) or (HCO3
–) depresses respiratory
ventilation and release of CO2 from the blood
The increased blood CO2 will result in the formation of
more H2CO3 acid to neutralize excess alkali (HCO3
–)
Increase in (H+) or (H2CO3) stimulates the respiratory
center to increase the rate of respiratory ventilation and
excess acid (H2CO3) in the form of CO2 is quickly
removed
Increase in (OH–) or (HCO3
–) depresses respiratory
ventilation and release of CO2 from the blood
The increased blood CO2 will result in the formation of
more H2CO3 acid to neutralize excess alkali (HCO3
–)
29. RENAL MECHANISM IN ACID-BASE BALANCE
• Renal mechanism is the third line of defense in acid base
balance.
• Long term acid-base control is exerted by renal
mechanisms.
• Kidney participates in the regulation of acid- base balance
by conservation of HCO3
– (alkali reserve) and excretion
of acid.
RENAL MECHANISM IN ACID-BASE BALANCE
• Renal mechanism is the third line of defense in acid base
balance.
• Long term acid-base control is exerted by renal
mechanisms.
• Kidney participates in the regulation of acid- base balance
by conservation of HCO3
– (alkali reserve) and excretion
of acid.
30. The pH of the initial glomerular filtrate is approximately
7.4 whereas the average urinary pH is approximately 6.0
due to excretion of non-volatile acids produced by
metabolic processes.
The pH of the urine may vary from 4.5 to 8.0
corresponding to the case of acidosis or alkalosis.
This ability to excrete variable amounts of acid or base
makes the kidney the final defence mechanism against
change in body pH.
The pH of the initial glomerular filtrate is approximately
7.4 whereas the average urinary pH is approximately 6.0
due to excretion of non-volatile acids produced by
metabolic processes.
The pH of the urine may vary from 4.5 to 8.0
corresponding to the case of acidosis or alkalosis.
This ability to excrete variable amounts of acid or base
makes the kidney the final defence mechanism against
change in body pH.
31. Renal conservation of HCO3 and excretion of
acid occur through four key mechanisms
1. Exchange of H+ for Na+ of tubular fluid.
2. Reabsorption of bicarbonate from tubular fluid.
3. Formation of ammonia and excretion of
ammonium ion (NH4
+) in the urine.
4. Excretion of H+ as H2PO4
– in urine
Renal conservation of HCO3 and excretion of
acid occur through four key mechanisms
1. Exchange of H+ for Na+ of tubular fluid.
2. Reabsorption of bicarbonate from tubular fluid.
3. Formation of ammonia and excretion of
ammonium ion (NH4
+) in the urine.
4. Excretion of H+ as H2PO4
– in urine
32. Exchange of H+ for Na+ of tubular fluid and reabsorption
of bicarbonate from tubular fluid.
35. Disorders of Acid Base Balance
Acidosis
Alkalosis
Disorders of Acid Base Balance
Acidosis
Alkalosis
36. Acidosis And Alkalosis
Acid-base balance depends on the ratio HCO3
–/ H2CO3
which is constant at 20:1 at physiological pH.
Any alteration produced in the ratio between carbonic
acid and bicarbonate results in an acid-base imbalance
and leads to acidosis or alkalosis.
Acidosis And Alkalosis
Acid-base balance depends on the ratio HCO3
–/ H2CO3
which is constant at 20:1 at physiological pH.
Any alteration produced in the ratio between carbonic
acid and bicarbonate results in an acid-base imbalance
and leads to acidosis or alkalosis.
37. Acidosis may be defined as an abnormal condition
caused by the accumulation of excess acid in the body or
by the loss of alkali from the body.
Alkalosis is an abnormal condition caused by the
accumulation of excess alkali in the body or by the loss
of acid from the body.
Acidosis may be defined as an abnormal condition
caused by the accumulation of excess acid in the body or
by the loss of alkali from the body.
Alkalosis is an abnormal condition caused by the
accumulation of excess alkali in the body or by the loss
of acid from the body.
38. Acidosis and alkalosis are classified, in terms of their cause :
1. Metabolic acidosis: Dec. in bicarbonate (HCO3
–) conc.
2. Respiratory acidosis: Inc. in H2CO3 concentration.
3. Metabolic alkalosis: Inc. in bicarbonate (HCO3
–) conc.
4. Respiratory alkalosis: Dec. in H2CO3 concentration.
Acidosis and alkalosis are classified, in terms of their cause :
1. Metabolic acidosis: Dec. in bicarbonate (HCO3
–) conc.
2. Respiratory acidosis: Inc. in H2CO3 concentration.
3. Metabolic alkalosis: Inc. in bicarbonate (HCO3
–) conc.
4. Respiratory alkalosis: Dec. in H2CO3 concentration.
39. In all these four conditions, if the ratio HCO3
–/ H2CO3
remains within normal limits, i.e. about 16:1 to 25:1,
corresponding to pH 7.3 to 7.5, the condition results in
compensated acidosis and alkalosis.
When the ratio actually changes and pH is outside of the
normal range the term uncompensated is used.
In all these four conditions, if the ratio HCO3
–/ H2CO3
remains within normal limits, i.e. about 16:1 to 25:1,
corresponding to pH 7.3 to 7.5, the condition results in
compensated acidosis and alkalosis.
When the ratio actually changes and pH is outside of the
normal range the term uncompensated is used.
40. Metabolic Acidosis
A fall in blood pH due to a decrease in bicarbonate
levels of plasma is called metabolic acidosis.
Decrease in bicarbonate levels may be due to:
– Increased production of acids e. g., in uncontrolled
diabetes mellitus and starvation
– Excessive loss of bicarbonate e. g., in renal tubular
dysfunction and in severe diarrhoea.
Metabolic Acidosis
A fall in blood pH due to a decrease in bicarbonate
levels of plasma is called metabolic acidosis.
Decrease in bicarbonate levels may be due to:
– Increased production of acids e. g., in uncontrolled
diabetes mellitus and starvation
– Excessive loss of bicarbonate e. g., in renal tubular
dysfunction and in severe diarrhoea.
41. Compensatory mechanisms for metabolic acidosis
Increasing rate of respiration to wash out CO2 (hence
H2CO3) faster. Consequently, the ratio HCO3
–/ H2CO3
is elevated.
Increasing excretion of H+ ions as NH4
+ ions.
Increasing elimination of acid H2PO4
– in the urine.
All these compensatory mechanisms tend to reduce carbonic
acid and a compensated acidosis results.
Compensatory mechanisms for metabolic acidosis
Increasing rate of respiration to wash out CO2 (hence
H2CO3) faster. Consequently, the ratio HCO3
–/ H2CO3
is elevated.
Increasing excretion of H+ ions as NH4
+ ions.
Increasing elimination of acid H2PO4
– in the urine.
All these compensatory mechanisms tend to reduce carbonic
acid and a compensated acidosis results.
42. Respiratory Acidosis
Acidosis results from an increase in concentration of
H2CO3
An increase in concentration of H2CO3 is due to
decrease in alveolar ventilation, which leads to
retention of CO2
Respiratory Acidosis
Acidosis results from an increase in concentration of
H2CO3
An increase in concentration of H2CO3 is due to
decrease in alveolar ventilation, which leads to
retention of CO2
43. Decreased alveolar ventilation may occur in:
-- Obstruction to respiration:
in pneumonia, emphysema, asthma, etc.
-- Depression of respiration:
administration of respiratory depressant toxic
drugs like morphine which depresses the
respiratory centre.
Decreased alveolar ventilation may occur in:
-- Obstruction to respiration:
in pneumonia, emphysema, asthma, etc.
-- Depression of respiration:
administration of respiratory depressant toxic
drugs like morphine which depresses the
respiratory centre.
44. Compensatory mechanisms
Increase in renal reabsorption of bicarbonate.
Rise in urinary acid H2PO4
– and ammonia.
Compensatory mechanisms
Increase in renal reabsorption of bicarbonate.
Rise in urinary acid H2PO4
– and ammonia.
45. Metabolic Alkalosis
A rise in blood pH due to rise in the bicarbonate levels of
plasma
This is seen in the following conditions:
• Loss of gastric juice along with H+ ions in
prolonged and severe vomiting.
• Therapeutic administration of large dose of alkali
(in peptic ulcer) or chronic intake of excess
antacids.
Metabolic Alkalosis
A rise in blood pH due to rise in the bicarbonate levels of
plasma
This is seen in the following conditions:
• Loss of gastric juice along with H+ ions in
prolonged and severe vomiting.
• Therapeutic administration of large dose of alkali
(in peptic ulcer) or chronic intake of excess
antacids.
46. Compensatory mechanisms
Increased excretion of alkali (HCO3
–) by the kidney.
Diminished formation of ammonia.
Respiration is depressed to conserve CO2.
Compensatory mechanisms
Increased excretion of alkali (HCO3
–) by the kidney.
Diminished formation of ammonia.
Respiration is depressed to conserve CO2.
47. Respiratory Alkalosis
A rise in blood pH due to lowered concentration of CO2
or H2CO3, due to hyperventilation.
This occurs in the following conditions:
Anxiety or hysteria
Fever
Hot baths
At high altitude
Working at high temperature, etc.
Respiratory Alkalosis
A rise in blood pH due to lowered concentration of CO2
or H2CO3, due to hyperventilation.
This occurs in the following conditions:
Anxiety or hysteria
Fever
Hot baths
At high altitude
Working at high temperature, etc.
50. The concentration of anions and cations in plasma must be
equal to maintain electrical neutrality. Therefore, there is
no real anion gap in the plasma. Anion gap is not a
physiological reality.
The concentration of anions and cations in plasma must be
equal to maintain electrical neutrality. Therefore, there is
no real anion gap in the plasma. Anion gap is not a
physiological reality.
51. The concept of anion gap originally was developed when it
was found that if the sum of the Cl– and HCO3
_
values was
subtracted from the Na+ and K+ values the difference or
‘gap’ averaged 16 mmol/L in healthy individuals.
The concept of anion gap originally was developed when it
was found that if the sum of the Cl– and HCO3
_
values was
subtracted from the Na+ and K+ values the difference or
‘gap’ averaged 16 mmol/L in healthy individuals.
53. The most important unmeasured cations include Ca,
Mg, and the major unmeasured anions are albumin,
phosphate, sulphate and other organic anions.
The anion gap ranges between 8 –16 mEq/L.
The most important unmeasured cations include Ca,
Mg, and the major unmeasured anions are albumin,
phosphate, sulphate and other organic anions.
The anion gap ranges between 8 –16 mEq/L.
54. Acid base disorders are often associated with alterations
in the anion gap.
In metabolic acidosis the anion gap can increase or
remain normal depending on the cause of acidosis.
Acid base disorders are often associated with alterations
in the anion gap.
In metabolic acidosis the anion gap can increase or
remain normal depending on the cause of acidosis.
55. Metabolic Acidosis Associated with Increased Anion Gap
In metabolic acidosis, the plasma HCO3
–
is reduced. To
keep electroneutrality, the concentration of anions (either Cl–
or an unmeasured anion) must increase.
If the decrease in plasma HCO3
–
is not accompanied by
increased Cl–
, the anion gap value will increase and referred
to as increased anion gap acidosis or normochloremic
acidosis.
Metabolic Acidosis Associated with Increased Anion Gap
In metabolic acidosis, the plasma HCO3
–
is reduced. To
keep electroneutrality, the concentration of anions (either Cl–
or an unmeasured anion) must increase.
If the decrease in plasma HCO3
–
is not accompanied by
increased Cl–
, the anion gap value will increase and referred
to as increased anion gap acidosis or normochloremic
acidosis.
56. Metabolic Acidosis Associated with Normal Anion Gap
If the decrease in plasma HCO3
–
is accompanied by
increased Cl–
, the anion gap is remained normal, this
referred to as Hyperchloremic metabolic acidosis or
normal anion gap acidosis.
Metabolic Acidosis Associated with Normal Anion Gap
If the decrease in plasma HCO3
–
is accompanied by
increased Cl–
, the anion gap is remained normal, this
referred to as Hyperchloremic metabolic acidosis or
normal anion gap acidosis.
57.
58. Clinical Significance of Anion Gap
The anion gap is a biochemical tool which sometimes
helps in assessing acid-base problems. It is used for the
diagnosis of different causes of metabolic acidosis.
Clinical Significance of Anion Gap
The anion gap is a biochemical tool which sometimes
helps in assessing acid-base problems. It is used for the
diagnosis of different causes of metabolic acidosis.