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|<figure-inline>[[File:Siren.gif|link=Acidosis resident survival guide|41x41px]]</figure-inline>
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  ICD10          = {{ICD10|E|87|2|e|70}}-{{ICD10|E|87|4|e|70}} |
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  ICD9          = {{ICD9|276.2}}-{{ICD9|276.4}} |  
| [[Acidosis resident survival guide|'''Acidosis'''<br>'''Resident'''<br>'''Survival'''<br>'''Guide''']]
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  OMIM          = |
{{Acid-base imbalance}}
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  MeshID        = D000137 |
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{{SI}}
{{SI}}
{{CMG}}; '''Associate Editor(s)-In-Chief:''' [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com]
{{CMG}}; {{AE}} {{SSH}}, [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com]
==Overview==
==Overview==
'''Acid-base 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. Acid-base balance is maintained by normal respiratory and renal excretions of carbon dioxide and acids respectively.
'''Acid-base 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. Acid-base balance is maintained by normal [[respiratory]] and [[renal]] excretions of [[carbon dioxide]] and [[acids]] respectively.
==Approach to a patient with acid base imbalances==
 
===The following steps can help to generate a differential diagnosis on a patient with a suspected acid/base disorder:===
== Definition ==
* Evaluate the complete clinical picture and laboratory data in patients with suspected acid base disorder.
 
* Single acid-base disorders are commoner than double acid-base disorders, that are in turn commoner than triple acid-base disorders
=== Acidosis ===
* A normal pH doesn't exclude an acid base disorder as a co-existing acidosis and alkalosis can result in a normal pH.
[[Acidosis]] occurs when the [[pH]] is less or equal to 7.35 due to excess of [[hydrogen]] ions or loss of [[bicarbonate]] ions (HCO<sub>3</sub><sup>-</sup>).
* When the clinical picture raises suspicion of acid-base imbalance and the pH is normal, always check for the [[anion gap]]. For e.g. patient with [[diabetes ketoacidosis]] ([[metabolic acidosis]]) and vomiting ([[metabloic alkalosis]]) will present as a normal pH but with elevated anion gaps.
 
* When the primary disorder is acidosis, the body will compensate by creating an alkalosis (and vice-verse if the primary disorder is an alkalosis). When the primary disorder is respiratory, the body compensate with a metabolic process.
=== Alkalosis ===
[[Alkalosis]] refers to a condition reducing [[hydrogen ion]] concentration of [[Artery|arterial]] [[blood plasma]] (alkalemia) through the loss of acids or retention of [[bicarbonate]]. Generally alkalosis is said to occur when [[pH]] of the blood exceeds 7.45. 
 
==Approach to acid–base imbalance==
{{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}}
 
=== '''The following steps can help to generate a differential diagnosis on a patient with a suspected acid/base disorder:''' ===
* Evaluate the complete clinical picture and laboratory data in patients with suspected acid-base disorder.
* Single acid-base disorders are common compared to double (mixed) acid-base disorders, which are more common compared to triple acid-base disorders.
* A normal pH doesn't exclude an acid-base disorder as a co-existing [[acidosis]] and [[alkalosis]] may result in a normal pH.
* When the clinical picture raises a suspicion of an acid-base imbalance and the pH is normal, always check for the [[anion gap]]. For e.g., patient with [[diabetic ketoacidosis]] ([[metabolic acidosis]]) and [[vomiting]] ([[metabolic alkalosis]]) will present as a normal pH but with elevated [[anion gap]].
* When the primary disorder is [[acidosis]], the body will compensate by developing an [[alkalosis]] (and vice-verse if the primary disorder is an [[alkalosis]]). When the primary disorder is [[respiratory]], the body compensate with a [[metabolic]] (renal) process.
===Steps in determining the presence of an acid-base disorder are:===
===Steps in determining the presence of an acid-base disorder are:===
* Check serum pH.
# Check serum pH
** Normal is 7.40 (7.35-7.45). Values lower than normal represent an acidosis; values higher than normal represent an alkalosis.
#* Normal is 7.40 (7.35-7.45). Values lower than normal represent an [[acidosis]]; values higher than normal represent an [[alkalosis]].
* Check the pCO<sub>2</sub> and the HCO<sub>3</sub><sup>-</sup> to decide whether the process is respiratory vs. metabolic.
#* Serum HCO<sub>3</sub><sup>-</sup> drops of 4 to 5 mEq/L (4-5 mmol/L) for each 10 mm Hg (1.3 kPa) decrease in the pCO<sub>2.</sub><ref>American College of Physicians. [https://mksap.acponline.org/ Medical Knowledge Self-Assessment Program]</ref>
** Normal serum bicarbonate is 24mEq/dl ; normal serum pCO<sub>2</sub> is 40.
# Check the pCO<sub>2</sub> and the HCO<sub>3</sub><sup>-</sup> to decide whether the process is respiratory vs metabolic.
** Bicarbonate drops of 4 to 5 mEq/L (4-5 mmol/L) for each 10 mm Hg (1.3 kPa) decrease in the pCO<sub>2</sub><ref>American College of Physicians. [https://mksap.acponline.org/ Medical Knowledge Self-Assessment Program]</ref>
#* Normal serum [[bicarbonate]] is 24mEq/dl; normal serum pCO<sub>2</sub> is 40.
* Check the anion gap.
# Check the [[anion gap]]: serum sodium - (serum chloride plus serum HCO<sub>3</sub><sup>-</sup>).
** Normal is 10 mEq/L [10 mmol/L])
#* Normal is 10 mEq/L [10 mmol/L])
* Check for respiratory compensation of metabolic acidosis. Formula for checking appropriate respiratory compensation to metabolic acidosis include:
# Check for respiratory compensation of metabolic acidosis. Formula for checking appropriate respiratory compensation to metabolic acidosis include:
** Arterial pCO<sub>2</sub> = 1.5 x serum HCO<sub>3</sub><sup>-</sup> + 8 ± 2 ([[Winters' formula]])
#* Arterial pCO<sub>2</sub> = 1.5 x serum HCO<sub>3</sub><sup>-</sup> + 8 ± 2 ([[Winters' formula]])
** Arterial pCO<sub>2</sub> = Serum HCO<sub>3</sub><sup>-</sup> + 15
#* Arterial pCO<sub>2</sub> = Serum HCO<sub>3</sub><sup>-</sup> + 15
 
#* Arterial pCO<sub>2</sub> = (pH − 7) × 100. This is the coincidence rule<ref name="pmid28384697">{{cite journal| author=Liu GS, Bhalla V| title=Explaining the Coincidence Rule for Estimating Respiratory Compensation in Metabolic Acid-Base Disorders. | journal=Ann Intern Med | year= 2017 | volume= 166 | issue= 8 | pages= 610 | pmid=28384697 | doi=10.7326/L16-0470 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28384697  }} </ref>.
** PaCO2 = (pH − 7) × 100. This is the coincidence rule<ref name="pmid28384697">{{cite journal| author=Liu GS, Bhalla V| title=Explaining the Coincidence Rule for Estimating Respiratory Compensation in Metabolic Acid-Base Disorders. | journal=Ann Intern Med | year= 2017 | volume= 166 | issue= 8 | pages= 610 | pmid=28384697 | doi=10.7326/L16-0470 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28384697  }} </ref>.
#* For each increase in the PaCO<sub>2</sub> of 10 mmHg, the pH decreases by 0.08.
** For each increase in the PaCO<sub>2</sub> of 10 mmHg, the pH decreases by 0.08.
# Calculate the corrected bicarbonate to check for any coexistent metabolic acidosis (see below delta-delta formula).<ref name="pmid6488577">{{cite journal| author=Goodkin DA, Krishna GG, Narins RG| title=The role of the anion gap in detecting and managing mixed metabolic acid-base disorders. | journal=Clin Endocrinol Metab | year= 1984 | volume= 13 | issue= 2 | pages= 333-49 | pmid=6488577 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6488577  }} </ref>
* Calculate the corrected bicarbonate to check for any coexistent metabolic acidosis (see below delta-delta formula)<ref name="pmid6488577">{{cite journal| author=Goodkin DA, Krishna GG, Narins RG| title=The role of the anion gap in detecting and managing mixed metabolic acid-base disorders. | journal=Clin Endocrinol Metab | year= 1984 | volume= 13 | issue= 2 | pages= 333-49 | pmid=6488577 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6488577  }} </ref>
# Measure the osmolar gap ([https://www.mdcalc.com/serum-osmolality-osmolarity online calculator]). A high osmolar gap ([https://www.mdcalc.com/serum-osmolality-osmolarity online calculator]) suggestions intoxication with osmotically active agents such as [[methanol]], [[ethylene glycol]], [[isopropyl alcohol]], and [[toluene]].
* Measure the osmolar gap ([https://www.mdcalc.com/serum-osmolality-osmolarity online calculator]). A high osmolar gap ([https://www.mdcalc.com/serum-osmolality-osmolarity online calculator]) suggestions intoxication with osmotically active agents such as [[methanol]], [[ethylene glycol]], [[isopropyl alcohol]], and [[toluene]].


===Coexistent elevated anion gap and normal anion gap metabolic acidosis===
===Coexistent elevated anion gap and normal anion gap metabolic acidosis===
* An elevated anion gap can coexist with a normal anion gap [[metabolic acidosis]].
* An elevated anion gap can coexist with a normal anion gap [[metabolic acidosis]].
* '''Delta-Delta equation''': Change in anion gap = Change in bicarbonate
* '''Delta-Delta equation''': Change in anion gap = Change in bicarbonate.
** Change in gap (current gap - 10 mEq/L [10 mmol/L]). Some experts state normal gap is 12<ref name="pmid6488577">{{cite journal| author=Goodkin DA, Krishna GG, Narins RG| title=The role of the anion gap in detecting and managing mixed metabolic acid-base disorders. | journal=Clin Endocrinol Metab | year= 1984 | volume= 13 | issue= 2 | pages= 333-49 | pmid=6488577 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6488577  }} </ref>
** Change in gap (current gap - 12 mEq/L [12 mmol/L])<ref name="pmid6488577">{{cite journal| author=Goodkin DA, Krishna GG, Narins RG| title=The role of the anion gap in detecting and managing mixed metabolic acid-base disorders. | journal=Clin Endocrinol Metab | year= 1984 | volume= 13 | issue= 2 | pages= 333-49 | pmid=6488577 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6488577  }} </ref>
** Change in bicarb (current bicarb -  20 mEq/L [20 mmol/L])
** Change in bicarb (current bicarb -  24 mEq/L [24 mmol/L])
** If the [[anion gap]] increases less and than the serum bicarbonate decreases suggests that there is another metabolic acidosis present, which is decreasing the the serum bicarbonate, but not affecting the anion gap i.e. normal anion gap metabolic acidosis is also present.
** If the [[anion gap]] increases less and than the serum bicarbonate decreases suggests that there is another metabolic acidosis present, which is decreasing the the serum bicarbonate, but not affecting the anion gap i.e. normal anion gap metabolic acidosis is also present.


===Respiratory compensation of metabolic acidosis===
===Respiratory compensation of metabolic acidosis===
* For 1 meq/L fall of serum HCO<sub>3</sub><sup>-</sup> levels there is a 1.2 mmHg fall in arterial pCO<sub>2</sub>.
* For 1 meq/L fall of serum HCO<sub>3</sub><sup>-</sup> levels there is a 1.2 mmHg fall in [[arterial]] pCO<sub>2</sub>.
* The respiratory compensation of metabolic acidosis is fast and begins within half an hour of metabolic acidosis.
* The [[respiratory]] compensation of [[metabolic acidosis]] is fast and begins within half an hour of [[metabolic acidosis]].
* In cases where the metabolic acidosis develops slowly, the respiratory compensation occurs simultaneously with the metabolic acidosis.
* In cases where the [[metabolic acidosis]] develops slowly, the respiratory compensation occurs simultaneously with the [[metabolic acidosis]].
* The respiratory compensation usually completes within 12 to 24 hours
* The [[respiratory]] compensation usually completes within 12 to 24 hours.
* A failure to develop adequate respiratory response indicates an acute underlying respiratory diseases, neurologic disease or a very acute development of metabolic acidosis.
* A failure to develop adequate respiratory response indicates an acute underlying [[respiratory]] diseases, [[neurologic]] disease or a very acute development of [[metabolic acidosis]].
* Formula for checking appropriate respiratory compensation to metabolic acidosis include:
* Formula for checking appropriate respiratory compensation to metabolic acidosis include:
** Arterial pCO<sub>2</sub> = 1.5 x serum HCO<sub>3</sub><sup>-</sup> + 8 ± 2 ([[Winters' formula]])
** Arterial pCO<sub>2</sub> = 1.5 x serum HCO<sub>3</sub><sup>-</sup> + 8 ± 2 ([[Winters' formula]])
** Arterial pCO<sub>2</sub> = serum HCO<sub>3</sub><sup>-</sup> + 15
** Arterial pCO<sub>2</sub> = serum HCO<sub>3</sub><sup>-</sup> + 15
** If the measured pCO<sub>2</sub> is not close to predicted, a second disorder coexists
** If the measured pCO<sub>2</sub> is not close to predicted, a second disorder coexists.
** If the pCO<sub>2</sub> is less than predicted, respiratory alkalosis is present; if the pCO<sub>2</sub> is higher than predicted, respiratory acidosis is present.
** If the pCO<sub>2</sub> is less than predicted, [[respiratory alkalosis]] is present; if the pCO<sub>2</sub> is higher than predicted, [[respiratory acidosis]] is present.
** The maximum limit of respiratory compensation for a metabolic acidosis is pCO<sub>2</sub> of 20.
** The maximum limit of [[respiratory]] compensation for a [[metabolic acidosis]] is pCO<sub>2</sub> of 20.


===Role of the urine anion gap in the patient with a normal anion gap metabolic acidosis===
===Role of the urine anion gap in the patient with a normal anion gap metabolic acidosis===
* [[Urine anion gap]] helps to differentiate [[renal tubular acidosis]] (specifically a Type 1 or Type 4 RTA) from other causes of normal anion gap acidosis.   
* Urine [[anion gap]] helps to differentiate [[renal tubular acidosis]] (specifically a Type 1 or Type 4 [[RTA]]) from other causes of normal [[anion gap]] [[acidosis]].   
* The urine anion gap is calculated as the urine sodium plus urine potassium, minus the urine chloride
* The [[urine]] [[anion gap]] is calculated as the urine [[sodium]] plus urine [[potassium]], minus the urine [[chloride]]
* Urine anion gap = (Urine Na + Urine K) - Urine Cl
* Urine anion gap = (Urine Na<sup>+</sup> + Urine K<sup>+</sup>) - Urine Cl<sup>-</sup>
* The pathophysiology behind this is:
* The pathophysiology behind this is:
** When kidney is exposed to acidosis, the normal response of the kidney is to excrete acid.
** When kidney is exposed to [[acidosis]], the normal response of the [[kidney]] is to [[excrete]] [[acid]].
** Kidney excretes the excess acid in the form of ammonium, NH4+.
** [[Kidney]] excretes the excess acid in the form of [[ammonium]], NH<sub>4</sub><sup>+</sup>.
**  To maintain neutrality, Cl- is excreted along with ammonium, NH4+.
**  To maintain neutrality, Cl<sup>-</sup> is [[excreted]] along with [[ammonium]], NH<sub>4</sub><sup>+</sup>.
** Thus, urine chloride act as a surrogate marker for urine ammonium (acidosis)
** Thus, urine chloride act as a surrogate marker for urine [[ammonium]] ([[acidosis]]).
** In Types 1 and 4 renal tubular acidosis, the kidney's function of acid excretion is compromised (decreased excretion of NH4+ and Cl).
** In Types 1 and 4 [[renal tubular acidosis]], the kidney's function of [[acid]] [[excretion]] is compromised (decreased [[excretion]] of NH<sub>4</sub><sup>+</sup> and Cl<sup>-</sup>).
** Thus, in [[renal tubular acidosis]]  (specifically a Type 1 or Type 4 RTA) urine anion gap will be high (> than zero).
** Thus, in [[renal tubular acidosis]]  (specifically a Type 1 or Type 4 [[RTA]]) [[urine]] [[anion gap]] will be high (> than zero).
**  A urine anion gap less than zero in the normal anion gap metabolic acidosis suggests the kidney is excreting acid, making [[renal tubular acidosis]] less likely.
**  A urine anion gap less than zero in the normal anion gap metabolic acidosis suggests the kidney is excreting acid, making [[renal tubular acidosis]] less likely.
===Role of osmolar gap in differential diagnosis of elevated anion gap===
===Role of osmolar gap in differential diagnosis of elevated anion gap===
* [[Methanol]], [[ethylene glycol]], [[isopropyl alcohol]], [[toluene]] are osmotically active substance
* [[Methanol]], [[ethylene glycol]], [[isopropyl alcohol]], [[toluene]] are [[Osmotic|osmotically]] active substances.
* Ingestion of these substances may lead to disturbances that have significant overlap.
* Ingestion of these substances may lead to disturbances that have significant overlap.
* They can be differentiated because of these following characteristics:
* They can be differentiated because of these following characteristics:
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*** Also called wood alcohol
*** Also called wood alcohol
*** Used in antifreeze and solvents
*** Used in antifreeze and solvents
*** Presentation: [[Delirium]], [[papilledema]], and [[retinal hemorrhages]]
*** Presentation: [[Delirium]], [[papilledema]], and [[Retinal hemorrhage|retinal hemorrhages]]
*** Elevated anion gap metabolic acidosis
*** Elevated [[anion gap]] [[metabolic acidosis]]
** '''Ethylene glycol'''
** '''Ethylene glycol'''
*** Used in antifreeze and solvents
*** Used in antifreeze and solvents
*** Presentation: [[Delirium]]
*** Presentation: [[Delirium]]
*** Elevated anion gap metabolic acidosis
*** Elevated [[anion gap]] [[metabolic acidosis]]
*** Presence of '''oxalate crystals''' in urine
*** Presence of oxalate crystals in urine
** '''Isopropyl alcohol'''
** '''Isopropyl alcohol'''
*** Also called rubbing alcohol
*** Also called rubbing alcohol
*** No acid-base disorder
*** No acid-base disorder
*** Metabolism causes increase acetone in the blood
*** Metabolism causes increase acetone in the blood
*** Other conditions with elevated acetones in blood are: diabetes, starvation, and isopropyl alcohol.
*** Other conditions with elevated acetones in blood are: [[diabetes]] and [[starvation]]
** '''Toluene'''
** '''Toluene'''
*** Initial elevated anion gap followed with normal anion gap
*** Initial elevated [[anion gap]] followed with normal anion gap
* '''Estimated serum osmolality = (2 * serum sodium + BUN/2.8 + Glucose/18)'''
* '''Estimated serum osmolality = (2 * serum sodium + BUN/2.8 + Glucose/18)'''
 
==Blood Gas Analysis==
==Normal pH values based on blood sample site==
[[Venous blood gas]] sampling should not replace [[arterial blood gas]] sampling, but may supplement [[arterial blood gas]] monitoring as a mechanism of trending results and minimizing arterial sampling. Central venous blood is preferable to peripheral venous blood, as it more accurately represents the [[arterial blood gas]] results. Venous blood is more acidic than arterial blood, so venous pH is lower than arterial pH.
Venous blood gas sampling should not replace arterial blood gas sampling, but may supplement arterial blood gas monitoring as a mechanism of trending results and minimizing arterial sampling. Central venous blood is preferable to peripheral venous blood, as it more accurately represents the arterial blood gas results. Venous blood is more acidemic than arterial blood, so venous pH is lower than arterial pH.
{|
* '''Arterial sample'''
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Blood gas analysis
** pH 7.35 - 7.45
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Vessel
** Bicarbonate - 21 to 27 meq/L
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Range
** pCO<sub>2</sub> - 36 to 44 mmHg
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Interpretation
* '''Venous sample'''
|-
** pH - 0.02 to 0.04 units lower than in arterial blood
! rowspan="3" align="center" style="background:#DCDCDC;" + |Oxygen Partial Pressure (pO<sub>2</sub>)
** HCO<sub>3</sub><sup>-</sup> - 1 to 2 meq/L higher than in arterial blood
| rowspan="2" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
** pCO<sub>2</sub> - 3 to 8 mmHg higher than in arterial blood
| align="left" style="background:#F5F5F5;" + |80 to 100 mmHg
* '''Central venous sample'''
| align="left" style="background:#F5F5F5;" + |Normal
**  pH - 0.03 to 0.05 pH units lower than in arterial blood
|-
** HCO<sub>3</sub><sup>-</sup> - almost similar to arterial blood
| align="left" style="background:#F5F5F5;" + |<80  mmHg
** pCO<sub>2</sub> - 4 to 5 mmHg higher than in arterial blood
| align="left" style="background:#F5F5F5;" + |[[Hypoxemia|Hypoxia]]
==Causes==
|-
Sources of acid gain:
| align="center" style="background:#DCDCDC;" + |[[Vein|Venous]]
#[[Carbon dioxide]] (since CO<sub>2</sub> and H<sub>2</sub>O form HCO<sub>3</sub><sup>-</sup>, [[bicarbonate]], and H<sup>+</sup>, a [[proton]], in the presence of [[carbonic anhydrase]])
| align="left" style="background:#F5F5F5;" + |35 to 40 mmHg
#Production of [[nonvolatile acid]]s from the metabolism of proteins and other [[organic molecule]]s
| align="left" style="background:#F5F5F5;" + |Normal
#Loss of [[bicarbonate]] in [[faeces]] or [[urine]]
|-
# Intake of acids or acid precursors
! rowspan="3" align="center" style="background:#DCDCDC;" + |Oxygen Saturation (SO<sub>2</sub>)
 
| rowspan="2" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
Sources of acid loss:
| align="left" style="background:#F5F5F5;" + |>95%
#Use of hydrogen ions in the metabolism of various organic anions
| align="left" style="background:#F5F5F5;" + |Normal
#Loss of acid in the [[vomitus]] or [[urine]]
|-
==Response==
| align="left" style="background:#F5F5F5;" + |<95%
Responses to acidosis:
| align="left" style="background:#F5F5F5;" + |[[Hypoxemia|Hypoxia]]
#Bicarbonate is added to the blood plasma by [[renal tubule|tubular]] cells.
|-
#* Tubular cells reabsorb more bicarbonate from the tubular fluid.
| align="center" style="background:#DCDCDC;" + |[[Vein|Venous]]
#* [[Collecting duct]] cells secrete more hydrogen and generate more bicarbonate.
| align="left" style="background:#F5F5F5;" + |70 to 75%
#Ammoniagenesis leads to increased buffer formation (in the form of NH<sub>3</sub>)
| align="left" style="background:#F5F5F5;" + |Normal
 
|-
Responses to alkalosis:
! rowspan="4" align="center" style="background:#DCDCDC;" + |[[pH]]
#Excretion of bicarbonate in urine.
| rowspan="3" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
#*This is caused by lowered rate of hydrogen ion secretion from the tubular epithelial cells.
| align="left" style="background:#F5F5F5;" + |<7.35
#*This is also caused by lowered rates of glutamine metabolism and ammonia excretion.
| align="left" style="background:#F5F5F5;" + |[[Acidosis|Acidemia]]
 
|-
==Relationship between the arterial pH and H<sup>+</sup> concentrations in physiologic range==
| align="left" style="background:#F5F5F5;" + |7.35 to 7.45
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>
| align="left" style="background:#F5F5F5;" + |Normal
 
|-
{| class="wikitable" width="75px"
| align="left" style="background:#F5F5F5;" + |>7.45
| align="left" style="background:#F5F5F5;" + |[[Alkalosis|Alkalemia]]
|-
| 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|Carbon Dioxide]] Partial Pressure ([[PCO2|pCO<sub>2</sub>]])
| rowspan="3" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
| align="left" style="background:#F5F5F5;" + |<35 mmHg
| align="left" style="background:#F5F5F5;" + |Low
|-
| align="left" style="background:#F5F5F5;" + |35 to 45 mmHg
| align="left" style="background:#F5F5F5;" + |Normal
|-
| align="left" style="background:#F5F5F5;" + |>45 mmHg
| align="left" style="background:#F5F5F5;" + |High
|-
| 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]] ([[Bicarbonate|HCO<sub>3</sub><sup>-</sup>]])
| rowspan="3" align="center" style="background:#DCDCDC;" + |[[Artery|Arterial]]
| align="left" style="background:#F5F5F5;" + |<22 mmol/L
| align="left" style="background:#F5F5F5;" + |Low
|-
| align="left" style="background:#F5F5F5;" + |22 to 26 mmol/L
| align="left" style="background:#F5F5F5;" + |Normal
|-
| align="left" style="background:#F5F5F5;" + |>26 mmol/L
| align="left" style="background:#F5F5F5;" + |High
|-
| 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;" + |[[Artery|Arterial]]
| align="left" style="background:#F5F5F5;" + |<−3.4
| align="left" style="background:#F5F5F5;" + |[[Acidosis|Acidemia]]
|-
| align="left" style="background:#F5F5F5;" + |−3.4 to +2.3 mmol/L
| align="left" style="background:#F5F5F5;" + |Normal
|-
| align="left" style="background:#F5F5F5;" + |>2.3
| align="left" style="background:#F5F5F5;" + |[[Alkalosis|Alkalemia]]
|-
| 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
|-
|-
|bgcolor="lightgray"|'''pH'''||bgcolor="lightgray"|'''[H+]'''
! colspan="2" rowspan="3" align="center" style="background:#DCDCDC;" + |[[Anion gap]] = Na<sup>+</sup> - [Cl<sup>−</sup>+ HCO<sub>3</sub><sup>-</sup>]
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
|-
|-
|align="right"|7.80||align="right"|16
| align="left" style="background:#F5F5F5;" + |8 to 16
| align="left" style="background:#F5F5F5;" + |Normal
|-
|-
|align="right"|7.70||align="right"|20
| align="left" style="background:#F5F5F5;" + |>16
| align="left" style="background:#F5F5F5;" + |High
|}
==Compensation==
*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>
*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.
{|
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Primary disorder
! align="center" style="background:#4479BA; color: #FFFFFF;" + |pH
! align="center" style="background:#4479BA; color: #FFFFFF;" + |PaCO<sub>2</sub>
! align="center" style="background:#4479BA; color: #FFFFFF;" + |[HCO<sub>3</sub><sup>-</sup>]
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Compensation
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Compensation formula
|-
|-
|align="right"|7.60||align="right"|26
! 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>3</sub><sup>-</sup> + 8 ± 2 ([[Winters' formula]])
*Expected paCO<sub>2</sub> = Serum HCO<sub>3</sub><sup>-</sup> + 15
|-
|-
|align="right"|7.50||align="right"|32
! 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>3</sub><sup>-</sup> from 24
|-
|-
|align="right"|7.40||align="right"|40
! 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>3</sub><sup>-</sup>  increases by 1mEq/L for every 10 mmHg increase in paCO2 above 40
*Chronic: HCO<sub>3</sub><sup>-</sup>  increases by 3.5mEq/L for every 10 mmHg increase in paCO2 above 40
|-
|-
|align="right"|7.30||align="right"|50
! 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>3</sub><sup>-</sup>  decreases by 2mEq/L for every 10 mmHg derease in paCO2 above 40
*Chronic: HCO<sub>3</sub><sup>-</sup> decreases by 5mEq/L for every 10 mmHg decrease in paCO2 above 40
|}
 
== 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="right"|7.20||align="right"|63
! 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="right"|7.10||align="right"|80
! 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="right"|7.00||align="right"|100
! 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="right"|6.90||align="right"|125
! 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="right"|6.80||align="right"|160
! 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]] >> ∆HCO<sub>3</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]]
* ∆HCO<sub>3</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==
==Related Chapters==
* [[Acid-base homeostasis|Acid–base homeostasis]]
* [[Acid-base imbalance|Acid–base imbalance]]
* [[Acidosis]]
* [[Alkalosis]]
* [[Arterial blood gas]]
* [[Metabolic acidosis]]
* [[Metabolic alkalosis]]
* [[Metabolic alkalosis]]
* [[Respiratory acidosis]]
* [[Respiratory alkalosis]]
* [[Respiratory alkalosis]]
* [[Metabolic acidosis]]
* [[Respiratory acidosis]]
* [[Anion gap]]
* [[Anion gap]]
* [[Hypocalcemia]]


==References==
==References==

Latest revision as of 21:59, 17 July 2018

<figure-inline></figure-inline>
Acidosis
Resident
Survival
Guide

Acid-base Imbalance

Home

Overview

Approach to acid–base imbalance

Blood Gas Analysis

Compensation

Mixed Acid−Base Disorders

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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 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. Acid-base balance is maintained by normal respiratory and renal excretions of carbon dioxide and acids respectively.

Definition

Acidosis

Acidosis occurs when the pH is less or equal to 7.35 due to excess of hydrogen ions or loss of bicarbonate ions (HCO3-).

Alkalosis

Alkalosis refers to a condition reducing hydrogen ion concentration of arterial blood plasma (alkalemia) through the loss of acids or retention of bicarbonate. Generally alkalosis is said to occur when pH of the blood exceeds 7.45. 

Approach to acid–base imbalance

 
 
 
 
 
 
 
Check pH on ABG
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
pH < 7.35= Acidosis
 
 
 
 
 
 
 
pH > 7.45= Alkalosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Check PaCO2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PaCO2 > 45mm Hg =
Respiratory acidosis
 
PaCO2 Normal or < 35mm Hg =
Metabolic acidosis
 
 
 
 
 
Check PaCO2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
PaCO2 > 45mm Hg =
Metabolic alkalosis
 
PaCO2 < 35mm Hg =
Respiratory alkalosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
[HCO3-] > 29
 
 
Check [HCO3-]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Normal or slight decrease =
Acute respiratory alkalosis
 
 
 
Decreased < 24 =
Chronic respiratory alkalosis

The following steps can help to generate a differential diagnosis on a patient with a suspected acid/base disorder:

  • Evaluate the complete clinical picture and laboratory data in patients with suspected acid-base disorder.
  • Single acid-base disorders are common compared to double (mixed) acid-base disorders, which are more common compared to triple acid-base disorders.
  • A normal pH doesn't exclude an acid-base disorder as a co-existing acidosis and alkalosis may result in a normal pH.
  • When the clinical picture raises a suspicion of an acid-base imbalance and the pH is normal, always check for the anion gap. For e.g., patient with diabetic ketoacidosis (metabolic acidosis) and vomiting (metabolic alkalosis) will present as a normal pH but with elevated anion gap.
  • When the primary disorder is acidosis, the body will compensate by developing an alkalosis (and vice-verse if the primary disorder is an alkalosis). When the primary disorder is respiratory, the body compensate with a metabolic (renal) process.

Steps in determining the presence of an acid-base disorder are:

  1. Check serum pH
    • Normal is 7.40 (7.35-7.45). Values lower than normal represent an acidosis; values higher than normal represent an alkalosis.
    • Serum HCO3- drops of 4 to 5 mEq/L (4-5 mmol/L) for each 10 mm Hg (1.3 kPa) decrease in the pCO2.[1]
  2. Check the pCO2 and the HCO3- to decide whether the process is respiratory vs metabolic.
    • Normal serum bicarbonate is 24mEq/dl; normal serum pCO2 is 40.
  3. Check the anion gap: serum sodium - (serum chloride plus serum HCO3-).
    • Normal is 10 mEq/L [10 mmol/L])
  4. Check for respiratory compensation of metabolic acidosis. Formula for checking appropriate respiratory compensation to metabolic acidosis include:
    • Arterial pCO2 = 1.5 x serum HCO3- + 8 ± 2 (Winters' formula)
    • Arterial pCO2 = Serum HCO3- + 15
    • Arterial pCO2 = (pH − 7) × 100. This is the coincidence rule[2].
    • For each increase in the PaCO2 of 10 mmHg, the pH decreases by 0.08.
  5. Calculate the corrected bicarbonate to check for any coexistent metabolic acidosis (see below delta-delta formula).[3]
  6. Measure the osmolar gap (online calculator). A high osmolar gap (online calculator) suggestions intoxication with osmotically active agents such as methanol, ethylene glycol, isopropyl alcohol, and toluene.

Coexistent elevated anion gap and normal anion gap metabolic acidosis

  • An elevated anion gap can coexist with a normal anion gap metabolic acidosis.
  • Delta-Delta equation: Change in anion gap = Change in bicarbonate.
    • Change in gap (current gap - 12 mEq/L [12 mmol/L])[3]
    • Change in bicarb (current bicarb - 24 mEq/L [24 mmol/L])
    • If the anion gap increases less and than the serum bicarbonate decreases suggests that there is another metabolic acidosis present, which is decreasing the the serum bicarbonate, but not affecting the anion gap i.e. normal anion gap metabolic acidosis is also present.

Respiratory compensation of metabolic acidosis

Role of the urine anion gap in the patient with a normal anion gap metabolic acidosis

Role of osmolar gap in differential diagnosis of elevated anion gap

Blood Gas Analysis

Venous blood gas sampling should not replace arterial blood gas sampling, but may supplement arterial blood gas monitoring as a mechanism of trending results and minimizing arterial sampling. Central venous blood is preferable to peripheral venous blood, as it more accurately represents the arterial blood gas results. Venous blood is more acidic than arterial blood, so venous pH is lower than arterial pH.

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

  • There are compensation mechanisms in the body in order to normalizing the pH inside the blood.[4]
  • 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

Mixed Acid−Base Disorders

Disorder Key features Examples
Metabolic acidosis & respiratory alkalosis
Metabolic acidosis & respiratory acidosis
Metabolic alkalosis & respiratory alkalosis
  • PaCO2 does not increase as predicted
  • pH higher than expected
Metabolic alkalosis & respiratory acidosis
  • PaCO2 higher than predicted
  • pH normal
Metabolic acidosis & metabolic alkalosis
Metabolic acidosis & metabolic acidosis
  • Mixed high−AG & normal−AG acidosis
  • ∆HCO3- accounted for by combined change in ∆AG and ∆Cl

Related Chapters

References

  1. American College of Physicians. Medical Knowledge Self-Assessment Program
  2. Liu GS, Bhalla V (2017). "Explaining the Coincidence Rule for Estimating Respiratory Compensation in Metabolic Acid-Base Disorders". Ann Intern Med. 166 (8): 610. doi:10.7326/L16-0470. PMID 28384697.
  3. 3.0 3.1 Goodkin DA, Krishna GG, Narins RG (1984). "The role of the anion gap in detecting and managing mixed metabolic acid-base disorders". Clin Endocrinol Metab. 13 (2): 333–49. PMID 6488577.
  4. 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.


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