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The pH of the extracellular fluids can thus be controlled by separately regulating the partial pressure of carbon dioxide (which determines the carbonic acid concentration) and bicarbonate ion concentration in the extracellular fluids.
The pH of the extracellular fluids can thus be controlled by separately regulating the partial pressure of carbon dioxide (which determines the carbonic acid concentration) and bicarbonate ion concentration in the extracellular fluids.


There are therefore at least two homeostatic [[Negative feedback |negative feedback systems]] responsible for the regulation of the plasma pH. The first is the homeostatic control of the [[Blood gas tension|blood partial pressures of oxygen and carbon dioxide]], which determines the carbonic acid concentration in the plasma, and can change the pH of the arterial plasma within a few seconds. The [[PCO2|partial pressure of carbon dioxide]] in the arterial blood is monitored by the [[central chemoreceptors]] of the [[medulla oblongata]], and so are part of the [[central nervous system]].<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref> These chemoreceptors are sensitive to the [[pH]] and levels of carbon dioxide in the [[cerebrospinal fluid]].<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref><ref name=Bray1999 /><ref name="tortora1">{{cite book|title=Principles of anatomy and physiology|last1=Tortora|first1=Gerard J.|last2=Anagnostakos|first2=Nicholas P.|publisher=Harper & Row, Publishers|isbn=0-06-350729-3|edition=Fifth|location=New York|publication-date=1987|pages=494, 556–582}}</ref>
There are therefore at least two homeostatic [[Negative feedback |negative feedback systems]] responsible for the regulation of the plasma pH. The first is the homeostatic control of the [[Blood gas tension|blood partial pressures of oxygen and carbon dioxide]], which determines the carbonic acid concentration in the plasma, and can change the pH of the arterial plasma within a few seconds. The [[PCO2|partial pressure of carbon dioxide]] in the arterial blood is monitored by the [[central chemoreceptors]] of the [[medulla oblongata]], and so are part of the [[central nervous system]].<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref> These chemoreceptors are sensitive to the [[pH]] and levels of carbon dioxide in the [[cerebrospinal fluid]].<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref><ref name=Bray1999 /><ref name="tortora1">{{cite book|title=Principles of anatomy and physiology|last1=Tortora|first1=Gerard J.|last2=Anagnostakos|first2=Nicholas P.|publisher=Harper & Row, Publishers|isbn=0-06-350729-3|edition=Fifth|location=New York|publication-date=1987|pages=494, 556–582}}</ref><ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref> (The [[peripheral chemoreceptors]] are located in the [[aortic bodies]] and [[Carotid body|carotid bodies]] adjacent to the arch of the aorta and to the bifurcation of the carotid arteries.<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref> These chemoreceptors are sensitive to changes in the partial pressure of oxygen in the arterial blood and are not directly involved with pH homeostasis.<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref>)


⚫
The central chemoreceptors send their information to the [[respiratory centres]] in the medulla and [[pons]] of the [[brainstem]].<ref name=tortora1 /> The respiratory centers then determine the average rate of ventilation of the [[Pulmonary alveolus|alveoli]] of the [[lungs]], to keep the [[Homeostasis# Blood partial pressure of oxygen and carbon dioxide|partial pressure carbon dioxide in the arterial blood constant]]. The respiratory center does so via [[motor neuron]]s which activate the [[muscles of respiration]] (in particular the [[Thoracic diaphragm|diaphragm]]).<ref name="Levitzky2013_9">{{cite book|last1=Levitzky|first1=Michael G.|title=Pulmonary physiology|date=2013|publisher=McGraw-Hill Medical|location=New York|isbn=978-0-07-179313-1|page=Chapter 9. Control of Breathing |edition=Eighth}}</ref> A rise in the partial pressure of carbon dioxide in the arterial blood plasma above 5.3&nbsp;kPa (40&nbsp;mmHg) reflexly causes an increase in the rate and depth of [[breathing#Mechanics|breathing]]. Normal breathing is resumed when the partial pressure of carbon dioxide has returned to 5.3&nbsp;kPa.<ref>{{MedlinePlusEncyclopedia|000335|Metabolic acidosis}}</ref> The converse happens if the partial pressure of carbon dioxide falls below the normal range. Breathing may be temporally halted, or slowed down to allow carbon dioxide to accumulate once more in the lungs and arterial blood.
[[Peripheral chemoreceptors]] are located in the [[aortic bodies]] and [[Carotid body|carotid bodies]] adjacent to the arch of the aorta and to the bifurcation of the carotid arteries.<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref> These chemoreceptors are sensitive to changes in the partial pressure of oxygen in the arterial blood.<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref>

⚫
The two sets of chemoreceptors (central and peripheral) respond to changes in the partial pressures of oxygen, or carbon dioxide.<ref>{{Cite book|url=https://www.worldcat.org/oclc/192027371|title=Principles of anatomy and physiology|last=J.|first=Tortora, Gerard|date=2010|publisher=John Wiley & Sons|others=Derrickson, Bryan.|year=|isbn=9780470233474|edition=12th ed|location=Hoboken, NJ|pages=907|oclc=192027371}}</ref> This information is sent to the [[respiratory centres]] in the medulla and [[pons]] of the [[brainstem]].<ref name=tortora1 /> The respiratory centers then determine the average rate of ventilation of the [[Pulmonary alveolus|alveoli]] of the [[lungs]], to keep the [[Homeostasis# Blood partial pressure of oxygen and carbon dioxide|partial pressure carbon dioxide in the arterial blood constant]]. The respiratory center does so via [[motor neuron]]s which activate the [[muscles of respiration]] (in particular the [[Thoracic diaphragm|diaphragm]]).<ref name="Levitzky2013_9">{{cite book|last1=Levitzky|first1=Michael G.|title=Pulmonary physiology|date=2013|publisher=McGraw-Hill Medical|location=New York|isbn=978-0-07-179313-1|page=Chapter 9. Control of Breathing |edition=Eighth}}</ref> A rise in the partial pressure of carbon dioxide in the arterial blood plasma above 5.3&nbsp;kPa (40&nbsp;mmHg) reflexly causes an increase in the rate and depth of [[breathing#Mechanics|breathing]]. Normal breathing is resumed when the partial pressure of carbon dioxide has returned to 5.3&nbsp;kPa.<ref>{{MedlinePlusEncyclopedia|000335|Metabolic acidosis}}</ref> The converse happens if the partial pressure of carbon dioxide falls below the normal range. Breathing may be temporally halted, or slowed down to allow carbon dioxide to accumulate once more in the lungs and arterial blood.


The sensor for the plasma HCO{{su|b=3|p=−}} concentration is not known for certain. It is very probable that the [[Kidney|renal]] tubular cells of the [[distal convoluted tubule]]s are themselves sensitive to the pH of the plasma. The metabolism of these cells produces CO<sub>2</sub>, which is rapidly converted to H<sup>+</sup> and HCO{{su|b=3|p=−}} through the action of [[carbonic anhydrase]].<ref name=tortora2>{{cite book |last1= Tortora |first1= Gerard J. |last2=Anagnostakos|first2=Nicholas P.| title=Principles of anatomy and physiology |pages=581–582, 675–676|edition= Fifth |location= New York |publisher= Harper & Row, Publishers|publication-date= 1987 |isbn= 0-06-350729-3 }}</ref><ref name=stryer>{{cite book |last1= Stryer |first1= Lubert | title=Biochemistry. |edition= Fourth |location= New York |publisher= W.H. Freeman and Company|publication-date= 1995 |pages=39, 164, 630–631, 716–717|isbn= 0 7167 2009 4 }}</ref> When the extracellular fluids tend towards acidity, the renal tubular cells secrete the H<sup>+</sup> ions into the tubular fluid from where they exit the body via the urine. The HCO{{su|b=3|p=−}} ions are simultaneously secreted into the blood plasma, thus raising the bicarbonate ion concentration in the plasma, lowering the carbonic acid/bicarbonate ion ratio, and consequently raising the pH of the plasma.<ref name=tortora1 /> The converse happens when the plasma pH rises above normal: bicarbonate ions are excreted into the urine, and hydrogen ions into the plasma. These combine with the bicarbonate ions in the plasma to form carbonic acid, thus raising the carbonic acid:bicarbonate ratio in the extracellular fluids, and returning its pH to normal.
The sensor for the plasma HCO{{su|b=3|p=−}} concentration is not known for certain. It is very probable that the [[Kidney|renal]] tubular cells of the [[distal convoluted tubule]]s are themselves sensitive to the pH of the plasma. The metabolism of these cells produces CO<sub>2</sub>, which is rapidly converted to H<sup>+</sup> and HCO{{su|b=3|p=−}} through the action of [[carbonic anhydrase]].<ref name=tortora2>{{cite book |last1= Tortora |first1= Gerard J. |last2=Anagnostakos|first2=Nicholas P.| title=Principles of anatomy and physiology |pages=581–582, 675–676|edition= Fifth |location= New York |publisher= Harper & Row, Publishers|publication-date= 1987 |isbn= 0-06-350729-3 }}</ref><ref name=stryer>{{cite book |last1= Stryer |first1= Lubert | title=Biochemistry. |edition= Fourth |location= New York |publisher= W.H. Freeman and Company|publication-date= 1995 |pages=39, 164, 630–631, 716–717|isbn= 0 7167 2009 4 }}</ref> When the extracellular fluids tend towards acidity, the renal tubular cells secrete the H<sup>+</sup> ions into the tubular fluid from where they exit the body via the urine. The HCO{{su|b=3|p=−}} ions are simultaneously secreted into the blood plasma, thus raising the bicarbonate ion concentration in the plasma, lowering the carbonic acid/bicarbonate ion ratio, and consequently raising the pH of the plasma.<ref name=tortora1 /> The converse happens when the plasma pH rises above normal: bicarbonate ions are excreted into the urine, and hydrogen ions into the plasma. These combine with the bicarbonate ions in the plasma to form carbonic acid, thus raising the carbonic acid:bicarbonate ratio in the extracellular fluids, and returning its pH to normal.

Revision as of 16:11, 16 September 2017

Acids and bases
Diagrammatic representation of the dissociation of acetic acid in aqueous solution to acetate and hydronium ions.
Acid types
Base types

Acid–base homeostasis is the homeostatic regulation of the pH of the body's extracellular fluid (ECF).[1] The proper balance between the acids and bases in the ECF is crucial for the normal physiology of the body, and cellular metabolism.[1] The pH of the intracellular fluid and the extracellular fluid need to be be maintained at a constant level.[2]

Many extracellular proteins such as the plasma proteins and membrane proteins of the body's cells are very sensitive for their three dimensional configurations to the extracellular pH.[citation needed] Stringent mechanisms therefore exist to maintain the pH within very narrow limits. Outside the acceptable range of pH, proteins are denatured, causing enzymes and ion channels (among others) to malfunction. In the worst cases death may occur if the situation remains unremedied.[citation needed]

In humans and many other animals, acid–base homeostasis is maintained by multiple mechanisms involved in three lines of defence.[3] The first line of defence are the various chemical buffers which minimize pH changes that would otherwise occur in their absence. They do not correct pH deviations, but only serve to reduce the extent of the change that would otherwise occur. These buffers include the bicarbonate buffer system, the phosphate buffer system, and the protein buffer system. Physiological corrective measures make use of, primarily, the bicarbonate buffer system consisting of a mixture of carbonic acid (H2CO3) and a bicarbonate (HCO−
3) salt in solution. This is because it is not only the most abundant buffer in the ECF, but also because abnormalities in the concentration of carbonic acid in the blood plasma can rapidly be corrected by the second line of defense involving the respiratory system, giving variations in the rate and depth of breathing (i.e. by hyperventilation or hypoventilation). The third line of defence is that given by the renal system whereby abnormally low or high plasma bicarbonate (HCO−
3) ion concentrations can be also readily be corrected by the excretion of H+ or HCO−
3 ions in the urine.

An acid–base imbalance is known as acidemia when the acidity is high, or alkalemia when the acidity is low.

Acid–base balance

The pH of the extracellular fluid, including the blood plasma, is normally tightly regulated between 7.36 and 7.42, by the chemical buffers, the respiratory system, and the renal system.[4][5][6][7]

Aqueous buffer solutions will react with strong acids or strong bases by absorbing excess hydrogen H+
 ions, or hydroxide OH−
 ions, replacing the strong acids and bases with weak acids and weak bases.[4] This has the effect of damping the effect of pH changes, or reducing the pH change that would otherwise have occurred. But buffers cannot correct abnormal pH levels in a solution, be that solution in a test tube or in the extracellular fluid. Buffers typically consist of a pair of compounds in solution, one of which is a weak acid and the other a weak base.[4] The most abundant buffer in the ECF consists of a solution of carbonic acid (H2CO3), and the bicarbonate (HCO−
3) salt of, usually, sodium (Na+). Thus, when there is an excess of OH−
 ions in the solution carbonic acid partially neutralizes them by forming H2O and bicarbonate (HCO−
3) ions.[8] An excess of H+ ions is partially neutralized by the bicarbonate component of the buffer solution to form carbonic acid (H2CO3), which, because it is a weak acid, remains largely in the undissociated form, releasing very much fewer H+ ions into the solution than the original strong acid would have done.

The pH of a buffer solution depends solely on the ratio of the molar concentrations of the weak acid to the weak base. The higher the concentration of the weak acid in the solution (compared to the weak base) the lower the resulting pH of the solution. Similarly, if the weak base predominates the higher the resulting pH.

This principle is exploited to regulate the pH of the extracellular fluids (rather than just buffering the pH). For the carbonic acid-bicarbonate buffer, a molar ratio of weak acid to weak base of 1:20 produces a pH of 7.4; and vice versa - when the pH of the extracellular fluids is 7.4 then the ratio of carbonic acid to bicarbonate ions in that fluid is 1:20.[9]

This relationship is described mathematically by the Henderson–Hasselbalch equation, which, when applied to the carbonic acid-bicarbonate buffer system in the extracellular fluids, states that:[9]

where:


However, since the carbonic acid concentration is directly proportional to the partial pressure of carbon dioxide () in the extracellular fluid, the equation can be rewritten as follows:[9]


where:
  • pH is the acidity in the plasma
  • [HCO−
    3    ]     is the molar concentration of bicarbonate in the plasma
  • PCO2 is the partial pressure of carbon dioxide in the blood plasma.


The pH of the extracellular fluids can thus be controlled by separately regulating the partial pressure of carbon dioxide (which determines the carbonic acid concentration) and bicarbonate ion concentration in the extracellular fluids.

There are therefore at least two homeostatic negative feedback systems responsible for the regulation of the plasma pH. The first is the homeostatic control of the blood partial pressures of oxygen and carbon dioxide, which determines the carbonic acid concentration in the plasma, and can change the pH of the arterial plasma within a few seconds. The partial pressure of carbon dioxide in the arterial blood is monitored by the central chemoreceptors of the medulla oblongata, and so are part of the central nervous system.[10] These chemoreceptors are sensitive to the pH and levels of carbon dioxide in the cerebrospinal fluid.[11][9][12][13] (The peripheral chemoreceptors are located in the aortic bodies and carotid bodies adjacent to the arch of the aorta and to the bifurcation of the carotid arteries.[14] These chemoreceptors are sensitive to changes in the partial pressure of oxygen in the arterial blood and are not directly involved with pH homeostasis.[15])

The central chemoreceptors send their information to the respiratory centres in the medulla and pons of the brainstem.[12] The respiratory centers then determine the average rate of ventilation of the alveoli of the lungs, to keep the partial pressure carbon dioxide in the arterial blood constant. The respiratory center does so via motor neurons which activate the muscles of respiration (in particular the diaphragm).[16] A rise in the partial pressure of carbon dioxide in the arterial blood plasma above 5.3 kPa (40 mmHg) reflexly causes an increase in the rate and depth of breathing. Normal breathing is resumed when the partial pressure of carbon dioxide has returned to 5.3 kPa.[17] The converse happens if the partial pressure of carbon dioxide falls below the normal range. Breathing may be temporally halted, or slowed down to allow carbon dioxide to accumulate once more in the lungs and arterial blood.

The sensor for the plasma HCO−
3 concentration is not known for certain. It is very probable that the renal tubular cells of the distal convoluted tubules are themselves sensitive to the pH of the plasma. The metabolism of these cells produces CO2, which is rapidly converted to H+ and HCO−
3 through the action of carbonic anhydrase.[18][19] When the extracellular fluids tend towards acidity, the renal tubular cells secrete the H+ ions into the tubular fluid from where they exit the body via the urine. The HCO−
3 ions are simultaneously secreted into the blood plasma, thus raising the bicarbonate ion concentration in the plasma, lowering the carbonic acid/bicarbonate ion ratio, and consequently raising the pH of the plasma.[12] The converse happens when the plasma pH rises above normal: bicarbonate ions are excreted into the urine, and hydrogen ions into the plasma. These combine with the bicarbonate ions in the plasma to form carbonic acid, thus raising the carbonic acid:bicarbonate ratio in the extracellular fluids, and returning its pH to normal.

In general metabolism produces more waste acids than bases. The urine is therefore generally acid. This urinary acidity is, to a certain extent, neutralized by the ammonia (NH3) which is excreted into the urine when glutamate and glutamine (carriers of excess, no longer needed, amino groups) are deaminated by the distal renal tubular epithelial cells.[19] Thus some of the "acid content" of the urine resides in the resulting ammonium ion (NH4+) content of the urine, though this has no effect on pH homeostasis of the extracellular fluids.[20]

Imbalance

An acid base nomogram for human plasma, showing the effects on the plasma pH when carbonic acid (partial pressure of carbondioxide) or bicarbonate occur in excess or are deficient in the plasma

Acid–base imbalance occurs when a significant insult causes the blood pH to shift out of the normal range (7.35 to 7.45). In the fetus, the normal range differs based on which umbilical vessel is sampled (umbilical vein pH is normally 7.25 to 7.45; umbilical artery pH is normally 7.18 to 7.38).[21] An excess of acid in the blood is called acidemia and an excess of base is called alkalemia. The imbalance is classified based on the cause of the disturbance (respiratory or metabolic) and the direction of change in pH (acidosis or alkalosis). There are four basic processes: metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis. One or a combination may occur at any given time. For instance, a metabolic acidosis (as in uncontrolled diabetes mellitus) is almost always partially compensated for by a respiratory alkalosis (hyperventilation), or a respiratory acidosis can be completely or partially corrected by a metabolic alkalosis.

See also

References

  1. ^ a b Hamm, LL; Nakhoul, N; Hering-Smith, KS (7 December 2015). "Acid-Base Homeostasis". Clinical journal of the American Society of Nephrology : CJASN. 10 (12): 2232–42. doi:10.2215/CJN.07400715. PMID 26597304.
  2. ^ J., Tortora, Gerard (2012). Principles of anatomy & physiology. Derrickson, Bryan. (13th ed. ed.). Hoboken, NJ: Wiley. pp. 42–43. ISBN 9780470646083. OCLC 698163931. {{cite book}}: |edition= has extra text (help)CS1 maint: multiple names: authors list (link)
  3. ^ Adrogué, H. E.; Adrogué, H. J. (April 2001). "Acid-base physiology". Respiratory Care. 46 (4): 328–341. ISSN 0020-1324. PMID 11345941.
  4. ^ a b c Tortora, Gerard J.; Anagnostakos, Nicholas P. (1987). Principles of anatomy and physiology (Fifth ed.). New York: Harper & Row, Publishers. pp. 698–700. ISBN 0-06-350729-3.
  5. ^ MedlinePlus Encyclopedia: Blood gases
  6. ^ Caroline, Nancy (2013). Nancy Caroline's Emergency care in the streets (7th ed.). Buffer systems: Jones & Bartlett Learning. pp. 347–349. ISBN 978-1449645861.
  7. ^ Hamm, L. Lee; Nakhoul, Nazih; Hering-Smith, Kathleen S. (2015-12-07). "Acid-Base Homeostasis". Clinical journal of the American Society of Nephrology: CJASN. 10 (12): 2232–2242. doi:10.2215/CJN.07400715. ISSN 1555-905X. PMC 4670772. PMID 26597304.{{cite journal}}: CS1 maint: PMC format (link)
  8. ^ Garrett, Reginald H.; Grisham, Charles M (2010). Biochemistry. Cengage Learning. p. 43. ISBN 978-0-495-10935-8.
  9. ^ a b c d Bray, John J. (1999). Lecture notes on human physiology. Malden, Mass.: Blackwell Science. p. 556. ISBN 978-0-86542-775-4.
  10. ^ J., Tortora, Gerard (2010). Principles of anatomy and physiology. Derrickson, Bryan. (12th ed ed.). Hoboken, NJ: John Wiley & Sons. p. 907. ISBN 9780470233474. OCLC 192027371. {{cite book}}: |edition= has extra text (help)CS1 maint: multiple names: authors list (link)
  11. ^ J., Tortora, Gerard (2010). Principles of anatomy and physiology. Derrickson, Bryan. (12th ed ed.). Hoboken, NJ: John Wiley & Sons. p. 907. ISBN 9780470233474. OCLC 192027371. {{cite book}}: |edition= has extra text (help)CS1 maint: multiple names: authors list (link)
  12. ^ a b c Tortora, Gerard J.; Anagnostakos, Nicholas P. (1987). Principles of anatomy and physiology (Fifth ed.). New York: Harper & Row, Publishers. pp. 494, 556–582. ISBN 0-06-350729-3.
  13. ^ J., Tortora, Gerard (2010). Principles of anatomy and physiology. Derrickson, Bryan. (12th ed ed.). Hoboken, NJ: John Wiley & Sons. p. 907. ISBN 9780470233474. OCLC 192027371. {{cite book}}: |edition= has extra text (help)CS1 maint: multiple names: authors list (link)
  14. ^ J., Tortora, Gerard (2010). Principles of anatomy and physiology. Derrickson, Bryan. (12th ed ed.). Hoboken, NJ: John Wiley & Sons. p. 907. ISBN 9780470233474. OCLC 192027371. {{cite book}}: |edition= has extra text (help)CS1 maint: multiple names: authors list (link)
  15. ^ J., Tortora, Gerard (2010). Principles of anatomy and physiology. Derrickson, Bryan. (12th ed ed.). Hoboken, NJ: John Wiley & Sons. p. 907. ISBN 9780470233474. OCLC 192027371. {{cite book}}: |edition= has extra text (help)CS1 maint: multiple names: authors list (link)
  16. ^ Levitzky, Michael G. (2013). Pulmonary physiology (Eighth ed.). New York: McGraw-Hill Medical. p. Chapter 9. Control of Breathing. ISBN 978-0-07-179313-1.
  17. ^ MedlinePlus Encyclopedia: Metabolic acidosis
  18. ^ Tortora, Gerard J.; Anagnostakos, Nicholas P. (1987). Principles of anatomy and physiology (Fifth ed.). New York: Harper & Row, Publishers. pp. 581–582, 675–676. ISBN 0-06-350729-3.
  19. ^ a b Stryer, Lubert (1995). Biochemistry (Fourth ed.). New York: W.H. Freeman and Company. pp. 39, 164, 630–631, 716–717. ISBN 0 7167 2009 4.
  20. ^ Rose, Burton; Helmut Rennke (1994). Renal Pathophysiology. Baltimore: Williams & Wilkins. ISBN 0-683-07354-0.
  21. ^ Yeomans, ER; Hauth, JC; Gilstrap, LC III; Strickland DM (1985). "Umbilical cord pH, PCO2, and bicarbonate following uncomplicated term vaginal deliveries (146 infants)". Am J Obstet Gynecol. 151: 798–800. doi:10.1016/0002-9378(85)90523-x. PMID 3919587.

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