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	Acid-base Homeostasis
Home
Overview
Mechanism
Blood Gas Analysis
Relationship between pH and H+
Compensation
Related Chapters

VisualWikitext

Latest revision as of 17:11, 25 May 2018

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
	Arterial	<80  mmHg	Hypoxia
	Venous	35 to 40 mmHg	Normal
Oxygen Saturation (SO₂)	Arterial	>95%	Normal
	Arterial	<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

Relationship between pH and H⁺

An inverse relationship between the H+ concentration (nmol/L) and the pH is given as follows:^[1]

pH	[H+]
7.80	16
7.70	20
7.60	26
7.50	32
7.40	40
7.30	50
7.20	63
7.10	80
7.00	100
6.90	125
6.80	160

Compensation Mechanism

There are compensation mechanisms in the body in order to normalizing the pH inside the blood.^[2]
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	Expected paCO₂ = 1.5 x serum HCO₃⁻ + 8 ± 2 (Winters' formula) Expected paCO₂ = Serum HCO₃⁻ + 15
Metabolic alkalosis	↑	↑	↑	Respiratory	Expected paCO₂ = 0.5 − 1 increase/ every 1 unit increase in serum HCO₃⁻ from 24
Respiratory acidosis	↓	↑	↑	Renal	Acute: HCO₃⁻ increases by 1mEq/L for every 10 mmHg increase in paCO2 above 40 Chronic: HCO₃⁻ increases by 3.5mEq/L for every 10 mmHg increase in paCO2 above 40
Respiratory alkalosis	↑	↓	↓	Renal	Acute: HCO₃⁻ decreases by 2mEq/L for every 10 mmHg derease in paCO2 above 40 Chronic: HCO₃⁻ decreases by 5mEq/L for every 10 mmHg decrease in paCO2 above 40

Related Chapters

References

↑ Rose, Burton David; Post, Theodore W. (2001). Clinical physiology of acid-base and electrolyte disorder. New York: McGraw-Hill. ISBN 0-07-134682-1.
↑ 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.

[1] Rose, Burton David; Post, Theodore W. (2001). Clinical physiology of acid-base and electrolyte disorder. New York: McGraw-Hill. ISBN 0-07-134682-1.

[pmid20859488-2] 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.

[1]

[2]

@@ Line 1: / Line 1: @@
-{{Acids and bases}}
+__NOTOC__
+{{Acid-base homeostasis}}
 {{SI}}
-{{CMG}}
+{{CMG}} {{AE}} {{SSH}}; [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com]
 ==Overview==
@@ Line 19: / Line 20: @@
 |-
 ! rowspan="3" align="center" style="background:#DCDCDC;" + |Oxygen Partial Pressure (pO<sub>2</sub>)
-| rowspan="2" align="center" style="background:#DCDCDC;" + |Arterial
+| rowspan="2" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
 | align="left" style="background:#F5F5F5;" + |80 to 100 mmHg
 | align="left" style="background:#F5F5F5;" + |Normal
 |-
 | align="left" style="background:#F5F5F5;" + |<80  mmHg
-| align="left" style="background:#F5F5F5;" + |Hypoxia
+| align="left" style="background:#F5F5F5;" + |[[Hypoxemia|Hypoxia]]
 |-
-| align="center" style="background:#DCDCDC;" + |Venous
+| align="center" style="background:#DCDCDC;" + |[[Vein|Venous]]
 | align="left" style="background:#F5F5F5;" + |35 to 40 mmHg
 | align="left" style="background:#F5F5F5;" + |Normal
 |-
 ! rowspan="3" align="center" style="background:#DCDCDC;" + |Oxygen Saturation (SO<sub>2</sub>)
-| rowspan="2" align="center" style="background:#DCDCDC;" + |Arterial
+| rowspan="2" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
 | align="left" style="background:#F5F5F5;" + |>95%
 | align="left" style="background:#F5F5F5;" + |Normal
 |-
 | align="left" style="background:#F5F5F5;" + |<95%
-| align="left" style="background:#F5F5F5;" + |Hypoxia
+| align="left" style="background:#F5F5F5;" + |[[Hypoxemia|Hypoxia]]
 |-
-| align="center" style="background:#DCDCDC;" + |Venous
+| align="center" style="background:#DCDCDC;" + |[[Vein|Venous]]
 | align="left" style="background:#F5F5F5;" + |70 to 75%
 | align="left" style="background:#F5F5F5;" + |Normal
 |-
-! rowspan="4" align="center" style="background:#DCDCDC;" + |pH
+! rowspan="4" align="center" style="background:#DCDCDC;" + |[[pH]]
-| rowspan="3" align="center" style="background:#DCDCDC;" + |Arterial
+| rowspan="3" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
 | align="left" style="background:#F5F5F5;" + |<7.35
-| align="left" style="background:#F5F5F5;" + |Acidemia
+| align="left" style="background:#F5F5F5;" + |[[Acidosis|Acidemia]]
 |-
 | align="left" style="background:#F5F5F5;" + |7.35 to 7.45
@@ Line 51: / Line 52: @@
 |-
 | align="left" style="background:#F5F5F5;" + |>7.45
-| align="left" style="background:#F5F5F5;" + |Alkalemia
+| align="left" style="background:#F5F5F5;" + |[[Alkalosis|Alkalemia]]
 |-
-| align="center" style="background:#DCDCDC;" + |Venous
+| align="center" style="background:#DCDCDC;" + |[[Vein|Venous]]
 | align="left" style="background:#F5F5F5;" + |7.26 to 7.46
 | align="left" style="background:#F5F5F5;" + |Normal
 |-
-! rowspan="4" align="center" style="background:#DCDCDC;" + |Carbon Dioxide Partial Pressure (pCO<sub>2</sub>)
+! rowspan="4" align="center" style="background:#DCDCDC;" + |[[Carbon dioxide|Carbon Dioxide]] Partial Pressure ([[PCO2|pCO<sub>2</sub>]])
-| rowspan="3" align="center" style="background:#DCDCDC;" + |Arterial
+| rowspan="3" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
 | align="left" style="background:#F5F5F5;" + |<35 mmHg
 | align="left" style="background:#F5F5F5;" + |Low
@@ Line 68: / Line 69: @@
 | align="left" style="background:#F5F5F5;" + |High
 |-
-| align="center" style="background:#DCDCDC;" + |Venous
+| align="center" style="background:#DCDCDC;" + |[[Vein|Venous]]
 | align="left" style="background:#F5F5F5;" + |40 to 45 mmHg
 | align="left" style="background:#F5F5F5;" + |Normal
 |-
-! rowspan="4" align="center" style="background:#DCDCDC;" + |Bicarbonate (HCO<sub><big>3</big></sub><sup>−</sup>)
+! rowspan="4" align="center" style="background:#DCDCDC;" + |[[Bicarbonate]] ([[Bicarbonate|HCO<sub><big>3</big></sub>]]<sup>−</sup>)
-| rowspan="3" align="center" style="background:#DCDCDC;" + |Arterial
+| rowspan="3" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
 | align="left" style="background:#F5F5F5;" + |<22 mmol/L
 | align="left" style="background:#F5F5F5;" + |Low
@@ Line 83: / Line 84: @@
 | align="left" style="background:#F5F5F5;" + |High
 |-
-| align="center" style="background:#DCDCDC;" + |Venous
+| align="center" style="background:#DCDCDC;" + |[[Vein|Venous]]
 | align="left" style="background:#F5F5F5;" + |19 to 28 mmol/L
 | align="left" style="background:#F5F5F5;" + |Normal
 |-
 ! rowspan="4" align="center" style="background:#DCDCDC;" + |Base Excess (BE)
-| rowspan="3" align="center" style="background:#DCDCDC;" + |Arterial
+| rowspan="3" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
 | align="left" style="background:#F5F5F5;" + |<−3.4
-| align="left" style="background:#F5F5F5;" + |Acidemia
+| align="left" style="background:#F5F5F5;" + |[[Acidosis|Acidemia]]
 |-
 | align="left" style="background:#F5F5F5;" + |−3.4 to +2.3 mmol/L
@@ Line 96: / Line 97: @@
 |-
 | align="left" style="background:#F5F5F5;" + |>2.3
-| align="left" style="background:#F5F5F5;" + |Alkalemia
+| align="left" style="background:#F5F5F5;" + |[[Alkalosis|Alkalemia]]
 |-
-| align="center" style="background:#DCDCDC;" + |Venous
+| align="center" style="background:#DCDCDC;" + |[[Vein|Venous]]
 | align="left" style="background:#F5F5F5;" + |−2 to −5 mmol/L
 | align="left" style="background:#F5F5F5;" + |Normal
 |-
 ! colspan="2" align="center" style="background:#DCDCDC;" + |Osmolar gap = Osmolality – Osmolarity
 | align="left" style="background:#F5F5F5;" + |>10
 | align="left" style="background:#F5F5F5;" + |Abnormal
 |-
-! colspan="2" rowspan="3" align="center" style="background:#DCDCDC;" + |Anion gap = [Na<sup>+</sup>] – {[Cl<sup>−</sup>]+[HCO<sub><big>3</big></sub><sup>−</sup>]}
+! colspan="2" rowspan="3" align="center" style="background:#DCDCDC;" + |[[Anion gap]] = Na<sup>+</sup> - [Cl<sup>−</sup>+ HCO<sub><big>3</big></sub><sup>−</sup>]
-Corrected AG = (measured serum AG) + (2.5 x [4.5 − Alb])
+Corrected [[Anion gap|AG]] = (measured serum [[Anion gap|AG]]) + (2.5 x [4.5 − [[Albumin|Alb]]])
 | align="left" style="background:#F5F5F5;" + |<8
 | align="left" style="background:#F5F5F5;" + |Low
@@ Line 118: / Line 119: @@
 |}
-==Imbalance==
+==Relationship between pH and H<sup>+</sup>==
-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.
+An inverse relationship between the H+ concentration (nmol/L) and the pH is given as follows:<ref>{{Cite book  | last1 = Rose | first1 = Burton David | last2 = Post | first2 = Theodore W. | title = Clinical physiology of acid-base and electrolyte disorder | date = 2001 | publisher = McGraw-Hill | location = New York | isbn = 0-07-134682-1 | pages =  }}</ref>
+{| class="wikitable" width="75px"
-===Causes===
+|-
-Sources of acid gain:
+| bgcolor="lightgray" |'''pH'''|| bgcolor="lightgray" |'''[H+]'''
-#[[Carbon dioxide]] (since CO<sub>2</sub> and OH<sup>-</sup>, [[hydroxide]], form HCO<sub>3</sub><sup>-</sup>, [[bicarbonate]], and H<sup>+</sup>, a [[proton]], in the presence of [[carbonic anhydrase]])
+|-
-#Production of [[nonvolatile acid]]s from the metabolism of proteins and other [[organic molecule]]s
+| align="right" |7.80|| align="right" |16
-#Loss of [[bicarbonate]] in [[faeces]] or [[urine]]
+|-
-# Intake of acids or acid precursors
+| align="right" |7.70|| align="right" |20
+|-
-Sources of acid loss:
+| align="right" |7.60|| align="right" |26
-#Use of hydrogen ions in the metabolism of various organic anions
+|-
-#Loss of acid in the [[vomitus]] or [[urine]]
+| align="right" |7.50|| align="right" |32
+|-
-===Response===
+| align="right" |7.40|| align="right" |40
-Responses to acidosis:
+|-
-#Bicarbonate is added to the blood plasma by [[renal tubule|tubular]] cells.
+| align="right" |7.30|| align="right" |50
-#* Tubular cells reabsorb more bicarbonate from the tubular fluid.
+|-
-#* [[Collecting duct]] cells secrete more hydrogen and generate more bicarbonate.
+| align="right" |7.20|| align="right" |63
-#Ammoniagenesis leads to increased buffer formation (in the form of NH<sub>3</sub>)
+|-
+| align="right" |7.10|| align="right" |80
-Responses to alkalosis:
+|-
-#Excretion of bicarbonate in urine.
+| align="right" |7.00|| align="right" |100
-#*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.
+| align="right" |6.90|| align="right" |125
+|-
-==See also==
+| align="right" |6.80|| align="right" |160
-* [[Renal physiology]]
+|}
+==Compensation Mechanism==
-==External links==
+*There are compensation mechanisms in the body in order to normalizing the pH inside the blood.<ref name="pmid20859488">{{cite journal |vauthors=Sood P, Paul G, Puri S |title=Interpretation of arterial blood gas |journal=Indian J Crit Care Med |volume=14 |issue=2 |pages=57–64 |date=April 2010 |pmid=20859488 |pmc=2936733 |doi=10.4103/0972-5229.68215 |url=}}</ref>
-* [http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php On-line text at AnaesthesiaMCQ.com]
+*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.
-* {{GeorgiaPhysiology|7/7ch12/7ch12lin}}
+*Acute respiratory compensation usually occurs within first day. However, chronic respiratory compensation takes 1 to 4 days to occur.
-* [http://www2.kumc.edu/ki/physiology/course/nine/9_1.htm Overview at kumc.edu]
+*Renal compensation might occur slower than respiratory compensation.
-* [http://sprojects.mmi.mcgill.ca/nephrology/presentation/presentation4.htm Overview at mcgill.ca]
+{|
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Primary disorder
-[[Category:Physiology]]
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |pH
-[[Category:Nephrology]]
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |PaCO<sub>2</sub>
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |[HCO3<sup>−</sup>]
-{{WikiDoc Help Menu}}
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Compensation
-{{WikiDoc Sources}}
+! align="center" style="background:#4479BA; color: #FFFFFF;" + |Compensation formula
+|-
+! align="center" style="background:#DCDCDC;" + |[[Metabolic acidosis]]
+| align="center" style="background:#F5F5F5;" + |↓
+| align="center" style="background:#F5F5F5;" + |↓
+| align="center" style="background:#F5F5F5;" + |↓
+| align="left" style="background:#F5F5F5;" + |Respiratory
+| align="left" style="background:#F5F5F5;" + |
+*Expected paCO<sub>2</sub> = 1.5 x serum HCO<sub><big>3</big></sub><sup>−</sup> + 8 ± 2 ([[Winters' formula]])
+*Expected paCO<sub>2</sub> = Serum HCO<sub><big>3</big></sub><sup>−</sup> + 15
+|-
+! align="center" style="background:#DCDCDC;" + |[[Metabolic alkalosis]]
+| align="center" style="background:#F5F5F5;" + |↑
+| align="center" style="background:#F5F5F5;" + |↑
+| align="center" style="background:#F5F5F5;" + |↑
+| align="left" style="background:#F5F5F5;" + |Respiratory
+| align="left" style="background:#F5F5F5;" + |
+*Expected paCO<sub>2</sub> = 0.5 − 1 increase/ every 1 unit increase in serum HCO<sub><big>3</big></sub><sup>−</sup> from 24
+|-
+! align="center" style="background:#DCDCDC;" + |[[Respiratory acidosis]]
+| align="center" style="background:#F5F5F5;" + |↓
+| align="center" style="background:#F5F5F5;" + |↑
+| align="center" style="background:#F5F5F5;" + |↑
+| align="left" style="background:#F5F5F5;" + |Renal
+| align="left" style="background:#F5F5F5;" + |
+*Acute: HCO<sub><big>3</big></sub><sup>−</sup>  increases by 1mEq/L for every 10 mmHg increase in paCO2 above 40
+*Chronic: HCO<sub><big>3</big></sub><sup>−</sup>  increases by 3.5mEq/L for every 10 mmHg increase in paCO2 above 40
+|-
+! align="center" style="background:#DCDCDC;" + |[[Respiratory alkalosis]]
+| align="center" style="background:#F5F5F5;" + |↑
+| align="center" style="background:#F5F5F5;" + |↓
+| align="center" style="background:#F5F5F5;" + |↓
+| align="left" style="background:#F5F5F5;" + |Renal
+| align="left" style="background:#F5F5F5;" + |
+*Acute: HCO<sub><big>3</big></sub><sup>−</sup>  decreases by 2mEq/L for every 10 mmHg derease 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
+|}
+==Related Chapters==
+* [[Acid-base homeostasis|Acid–base homeostasis]]
+* [[Acid-base imbalance|Acid–base imbalance]]
+* [[Acidosis]]
+* [[Alkalosis]]
+* [[Arterial blood gas]]
+* [[Metabolic acidosis]]
+* [[Metabolic alkalosis]]
+* [[Respiratory acidosis]]
+* [[Respiratory alkalosis]]
+* [[Anion gap]]
-[[it:Equilibrio acido base]]
+==References==
+{{reflist|2}}