|
|
| Line 166: |
Line 166: |
| *Chronic: HCO<sub><big>3</big></sub><sup>−</sup> decreases by 5mEq/L for every 10 mmHg decrease 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 |
| |} | | |} |
| ==Approach to Acid–base Imbalance==
| | ==Related Chapters== |
| {{familytree/start |summary=Sample 1}}
| |
| {{familytree | | | | | | | | A01 |A01=Check [[pH]] on ABG}}
| |
| {{familytree | | | | |,|-|-|-|^|-|-|-|-|.| | | }}
| |
| {{familytree | | | B01 | | | | | | | |B02| | |B01=pH < 7.35= '''[[Acidosis]]'''|B02=pH > 7.45= '''[[Alkalosis]]'''}}
| |
| {{familytree | | | |!| | | | | | | | | |!| }}
| |
| {{familytree | | | C01 | | | | | | | | |!| |C01=Check PaCO<sub>2</sub>}}
| |
| {{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>}}
| |
| {{familytree | | | | | | | | | | | |,|-|^|.| }}
| |
| {{familytree | | | | | | | | | | |E02| | E03 | |E02=PaCO<sub>2</sub> > 45mm Hg = <br>'''[[Metabolic alkalosis]]'''|E03=PaCO<sub>2</sub> < 35mm Hg = <br>'''[[Respiratory alkalosis]]'''}}
| |
| {{familytree | | | | | | | | | | |!| | | | |!| }}
| |
| {{familytree | | | | | | | | | | F01 | | | F02 |F01=[HCO<sub>3</sub><sup>-</sup>] > 29|F02=Check [HCO<sub>3</sub><sup>-</sup>]}}
| |
| {{Familytree | | | | | | | | | | | | |,|-|-|^|-|-|.| | }}
| |
| {{Familytree | | | | | | | | | | | |C01 | | | | C02 |C01= Normal or slight decrease = <br>'''Acute [[respiratory alkalosis]]'''| C02= Decreased < 24 = <br>'''Chronic [[respiratory alkalosis]]'''}}
| |
| {{familytree/end}}
| |
| ==Acid–base Imbalance==
| |
| 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.
| |
| | |
| ===Causes===
| |
| Sources of acid gain:
| |
| #[[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
| |
| #Loss of [[bicarbonate]] in [[faeces]] or [[urine]]
| |
| # Intake of acids or acid precursors
| |
| | |
| Sources of acid loss:
| |
| #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.
| |
| | |
| ==Mixed Acid−base Disorders==
| |
| {|
| |
| ! align="center" style="background:#4479BA; color: #FFFFFF;" + |Disorder
| |
| ! align="center" style="background:#4479BA; color: #FFFFFF;" + |Key features
| |
| ! align="center" style="background:#4479BA; color: #FFFFFF;" + |Examples
| |
| |-
| |
| ! align="center" style="background:#DCDCDC;" + |[[Metabolic acidosis]] & [[respiratory alkalosis]]
| |
| | align="left" style="background:#F5F5F5;" + |
| |
| *High− or normal−[[Anion gap|AG]] [[metabolic acidosis]]
| |
| *[[Pulmonary gas pressures|PaCO<sub>2</sub>]] below predicted value
| |
| | align="left" style="background:#F5F5F5;" + |
| |
| *[[Lactic acidosis]]
| |
| *[[Sepsis]] in [[Intensive care unit|ICU]]
| |
| |-
| |
| ! 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]]
| |
| |}
| |
| | |
| == Related Chapters == | |
| * [[Renal physiology]] | | * [[Renal physiology]] |
| * [[Acid-base imbalance|Acid–base imbalance]] | | * [[Acid-base imbalance|Acid–base imbalance]] |
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
|
| <80 mmHg
|
Hypoxia
|
| Venous
|
35 to 40 mmHg
|
Normal
|
| Oxygen Saturation (SO2)
|
Arterial
|
>95%
|
Normal
|
| <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
|
Compensation Mechanism
- There are compensation mechanisms in the body in order to normalizing the pH inside the blood.[1]
- 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