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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 2: / Line 2: @@
 {{Acid-base homeostasis}}
 {{SI}}
-{{CMG}} {{AE}} {{SSH}}
+{{CMG}} {{AE}} {{SSH}}; [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com]
 ==Overview==
@@ Line 20: / 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 52: / 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 69: / 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 84: / 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 97: / 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 119: / Line 119: @@
 |}
-==Approach to Acid–base Imbalance==
+==Relationship between pH and H<sup>+</sup>==
-{{familytree/start |summary=Sample 1}}
+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>
-{{familytree | | | | | | | | A01 |A01=Check [[pH]] on ABG}}
+{| class="wikitable" width="75px"
-{{familytree | | | | |,|-|-|-|^|-|-|-|-|.| | | }}
+|-
-{{familytree | | | B01 | | | | | | | |B02| | |B01=pH < 7.35= '''[[Acidosis]]'''|B02=pH > 7.45= '''[[Alkalosis]]'''}}
+| bgcolor="lightgray" |'''pH'''|| bgcolor="lightgray" |'''[H+]'''
-{{familytree | | | |!| | | | | | | | | |!| }}
+|-
-{{familytree | | | C01 | | | | | | | | |!| |C01=Check PaCO<sub>2</sub>}}
+| align="right" |7.80|| align="right" |16
-{{familytree | |,|-|^|.| | | | | | | | |!| }}
+|-
-{{familytree | D01 | | D02 | | | | | | D03 |D01=PaCO<sub>2</sub> > 45mm Hg = <br>'''[[Respiratory acidosis]]'''|D02=PaCO<sub>2</sub> Normal or < 35mm Hg = <br>'''[[Metabolic acidosis]]'''|D03=Check PaCO<sub>2</sub>}}
+| align="right" |7.70|| align="right" |20
-{{familytree | | | | | | | | | | | |,|-|^|.| }}
+|-
-{{familytree | | | | | | | | | | |E02| | E03 | |E02=PaCO<sub>2</sub> > 45mm Hg = <br>'''[[Metabolic alkalosis]]'''|E03=PaCO<sub>2</sub> < 35mm Hg = <br>'''[[Respiratory alkalosis]]'''}}
+| align="right" |7.60|| align="right" |26
-{{familytree | | | | | | | | | | |!| | | | |!| }}
+|-
-{{familytree | | | | | | | | | | F01 | | | F02 |F01=[HCO<sub>3</sub><sup>-</sup>] > 29|F02=Check [HCO<sub>3</sub><sup>-</sup>]}}
+| align="right" |7.50|| align="right" |32
-{{Familytree | | | | | | | | | | | | |,|-|-|^|-|-|.| | }}
+|-
-{{Familytree | | | | | | | | | | | |C01 | | | | C02 |C01= Normal or slight decrease = <br>'''Acute [[respiratory alkalosis]]'''| C02= Decreased < 24 = <br>'''Chronic [[respiratory alkalosis]]'''}}
+| align="right" |7.40|| align="right" |40
-{{familytree/end}}
+|-
-==Acid–base Imbalance==
+| align="right" |7.30|| align="right" |50
-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.
+|-
+| align="right" |7.20|| align="right" |63
-===Causes===
+|-
-Sources of acid gain:
+| align="right" |7.10|| align="right" |80
-#[[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" |7.00|| align="right" |100
-#Loss of [[bicarbonate]] in [[faeces]] or [[urine]]
+|-
-# Intake of acids or acid precursors
+| align="right" |6.90|| align="right" |125
+|-
-Sources of acid loss:
+| align="right" |6.80|| align="right" |160
-#Use of hydrogen ions in the metabolism of various organic anions
+|}
-#Loss of acid in the [[vomitus]] or [[urine]]
-===Response===
-Responses to acidosis:
-#Bicarbonate is added to the blood plasma by [[renal tubule|tubular]] cells.
-#* Tubular cells reabsorb more bicarbonate from the tubular fluid.
-#* [[Collecting duct]] cells secrete more hydrogen and generate more bicarbonate.
-#Ammoniagenesis leads to increased buffer formation (in the form of NH<sub>3</sub>)
-Responses to alkalosis:
-#Excretion of bicarbonate in urine.
-#*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.
 ==Compensation Mechanism==
 *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>
@@ Line 208: / Line 195: @@
 *Chronic: HCO<sub><big>3</big></sub><sup>−</sup> decreases by 5mEq/L for every 10 mmHg decrease in paCO2 above 40
 |}
-==Mixed Acid−base Disorders==
+==Related Chapters==
-{|
+* [[Acid-base homeostasis|Acid–base homeostasis]]
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Disorder
+* [[Acid-base imbalance|Acid–base imbalance]]
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Key features
+* [[Acidosis]]
-! align="center" style="background:#4479BA; color: #FFFFFF;" + |Examples
+* [[Alkalosis]]
-|-
+* [[Arterial blood gas]]
-! align="center" style="background:#DCDCDC;" + |[[Metabolic acidosis]] & [[respiratory alkalosis]]
+* [[Metabolic acidosis]]
-| align="left" style="background:#F5F5F5;" + |
+* [[Metabolic alkalosis]]
-*High− or normal−[[Anion gap|AG]] [[metabolic acidosis]]
+* [[Respiratory acidosis]]
-*[[Pulmonary gas pressures|PaCO<sub>2</sub>]] below predicted value
+* [[Respiratory alkalosis]]
-| align="left" style="background:#F5F5F5;" + |
+* [[Anion gap]]
-*[[Lactic acidosis]]
-*[[Sepsis]] in [[Intensive care unit|ICU]]
+==References==
-|-
+{{reflist|2}}
-! align="center" style="background:#DCDCDC;" + |[[Metabolic acidosis]] & [[respiratory acidosis]]
-| align="left" style="background:#F5F5F5;" + |
-*High− or normal−[[Anion gap|AG]] [[metabolic acidosis]]
-*PaCO<sub>2</sub> above the predicted value
-| align="left" style="background:#F5F5F5;" + |
-*Severe [[pneumonia]]
-*[[Pulmonary edema]]
-|-
-! align="center" style="background:#DCDCDC;" + |[[Metabolic alkalosis]] & [[respiratory alkalosis]]
-| align="left" style="background:#F5F5F5;" + |
-*[[Pulmonary gas pressures|PaCO<sub>2</sub>]] does not increase as predicted
-*[[pH]] higher than expected
-| align="left" style="background:#F5F5F5;" + |
-*[[Hepato-biliary diseases|Liver disease]]
-*[[Diuretic|Diuretics]]
-|-
-! align="center" style="background:#DCDCDC;" + |[[Metabolic alkalosis]] & [[respiratory acidosis]]
-| align="left" style="background:#F5F5F5;" + |
-*[[Pulmonary gas pressures|PaCO<sub>2</sub>]] higher than predicted
-*[[pH]] normal
-| align="left" style="background:#F5F5F5;" + |
-*[[Chronic obstructive pulmonary disease|COPD]] on diuretics
-|-
-! align="center" style="background:#DCDCDC;" + |[[Metabolic acidosis]] & [[metabolic alkalosis]]
-| align="left" style="background:#F5F5F5;" + |
-*Only detectable with high−[[Anion gap|AG]] [[acidosis]]
-*∆[[Anion gap|AG]] >> ∆[[[Bicarbonate|HCO<sub><big>3</big></sub>]]<sup>−</sup>]
-| align="left" style="background:#F5F5F5;" + |
-*[[Chronic renal failure pathophysiology|Uremia]] with [[Nausea and vomiting|vomiting]]
-|-
-! align="center" style="background:#DCDCDC;" + |[[Metabolic acidosis]] & [[metabolic acidosis]]
-| align="left" style="background:#F5F5F5;" + |
-*Mixed high−[[Anion gap|AG]] & normal−[[Anion gap|AG]] [[acidosis]]
-*∆[[[Bicarbonate|HCO<sub><big>3</big></sub>]]<sup>−</sup>] accounted for by combined change in ∆[[Anion gap|AG]] and ∆[[Chloride|Cl]]<sup>−</sup>
-| align="left" style="background:#F5F5F5;" + |
-*[[Diarrhea]] and [[lactic acidosis]]
-*[[Toluene|Toluene toxicity]]
-*Treatment of [[diabetic ketoacidosis]]
-|}
-==See also==
-* [[Renal physiology]]
-*
-[[Category:Physiology]]
-[[Category:Nephrology]]
-<references />