Acid-base Balance (ABB)
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Transcript of Acid-base Balance (ABB)
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Acid-base Balance(ABB)
Vladimíra Kvasnicová
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Definition - REPETITION • pH
• acid
• base
• dissociation constant
• buffers
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The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)
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The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)
= nedisociovaná kyselina
= volný H+
= volný anion
the border between
strong and weak acid
K = 10-2
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The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)
+ 3 HCl
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[CO2] = x pCO2 = 0,226 for pCO2 expressed in kPa
= 0,03 for pCO2 expressed in mmHg
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Dissociation constant and buffer
pH
! the best buffering properties: pH = pK ± 1 !
a) pH = pK + log (1 / 1) pH = pK
b) pH = pK + log (10 / 1) pH = pK + 1
c) pH = pK + log (1 / 10) pH = pK - 1
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Calculate the ratio of components of the phosphate buffer (HPO4
2- / H2PO4-)
pK2 = 7,0
if
a) pH = 7,4 (blood)
b) pH = 7,0 (cell)
c) pH = 6,0 (urine)
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The source and fate of acids /
bases
• source of acids: metabolism
• source of bases: food
• fate: transformation by the metabolism
excretion
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The figure has been adopted from J.Koolman, K.H.Röhm / Color Atlas of Biochemistry, 2nd edition, Thieme 2005
~ 20 000 mmol / den
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The metabolism produces acids:
carbon skeleton → CO2+H2O → HCO3-+ H+
• saccharides → glucose → pyruvate, lactate +
H+
• triacylglycerols → fatty acids, ketone bodies +
H+
• phospholipids → phosphate + H+
• proteins → amino acids → sulfate, urea + H+
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Acids formed in the human body
1. metabolic (nonvolatile) acids → excretion by the
kidneys glucose → lactic acid lactate + H+
fatty acids → ketone bodies:
acetoacetic acid acetoacetate + H+
-hydroxybutyric acid -hydroxybutyrate
+ H+
amino acids Cys and Met → H2SO4 → sulfate + 2H+
phospholipids → H3PO4 HPO42- + 2H+
2. respiratory (volatile) acid → excretion by the lungs
CO2 + H2O H2CO3 HCO3- + H+
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The order of systems whichparticipate in ABB
1. buffers (changes of pH caused by common
metabolism)
2. the lungs (CO2)
3. the kidneys (H+, HCO3-)
• blood pH can be also affected by
the liver (synthesis of urea, metabolism of lactate)
and the heart (oxidation of ketone bodies and
lactate)
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The figure has been adopted from: Klinická biochemie. Požadování a hodnocení biochemických vyšetření. Karolinum, Praha, 1998. ISBN 80‑7184‑649‑3
The liver – detoxication of ammonia according to the ABB state
amino acids
carbon skeleton
LIVER
LIVER, MUSCLE
urine urine
favourized during alkalemia
favourized during acidemia
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GLUTAMINE cycle in the
liver
The figure has been adopted from Devlin, T. M. (editor): Textbook of Biochemistry with Clinical Correlations, 4th ed. Wiley‑Liss, Inc., New York, 1997. ISBN 0‑471‑15451‑2
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Principal buffer systemsfluid buffer note
ISF bicarbonate buffers metabolic acids
phosphate low concentration
proteins low concentration
blood bicarbonate buffers metabolic acids
hemoglobin buffers CO2 (H2CO3)
plasma proteins
low concentration
phosphate low concentration
ICF proteins important buffer
phosphate important buffer
urine phosphate related to almost all titratable acidity of the urine
ammonium important: excretion of both NH3 and H+; cation!!!
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Blood buffers -
overview • bicarbonate buffer: HCO3
-/CO2
pK(H2CO3) = 6,1 24 mM
• phosphate buffer: HPO42-/H2PO4
-
pK(H2PO4-) ≈ 7,0 1 mM
• hemoglobin: Hb-/Hb-H+
pK(HHbO2) = 6,17 pK(HHb) = 7,82 160g/L
• proteins:protein/protein-H+ 70g/L pK = 4 – 12 (mainly Asp, Glu and His)
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Blood buffers
pufr plasma
erythrocytes
sum
HCO3-/CO2 35 % 18 % 53 %
Hb/Hb-H+ - 35 % 35 %
plasma proteins 7 % - 7 %
inorganic phosphate
1 % 1 % 2 %
organic phosphate - 3 % 3 %
43 % 57 % 100 %
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http://science.kennesaw.edu/~jdirnber/Bio2108/Lecture/LecPhysio/42-29-BloodCO2Transport-AL.gif (March 07)
O2
O2
Excretion of CO2 by the
lungs
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Excretion of H+ by the kidneys (I)
http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)
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http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)
Excretion of H+ by the kidneys (II)
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http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)
Excretion of H+ by the kidneys (III)
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Urine buffers
1. 1 excreted H+ 1 reabsorbed HCO3-
2. NH3 + H+ → NH4+ (50 mmol H+/day)
3. H+ + HPO42- → H2PO4
- (20 mmol
H+/day)
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The figure has been adopted from J.Koolman, K.H.Röhm / Color Atlas of Biochemistry, 2nd edition, Thieme 2005
ABB disorders
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http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)
CO2 produced by metabolic reactions
HCO3- regenerated in the kidneys
CO2 excreted by the lungs
HCO3- lost by
buffering endogenously
produced acids
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Primary disorders of ABB
http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)
pCO2
HCO3-
Resp.
Mtb.
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http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)
24 mM
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Compensation
= effort to readjust plasma pH back toward normal
• one system compensates disfunction of the
other system respiratory disorders are compensated by the
kidneys
(3-5 days)
metabolic disorders are compensated by the lungs
(12-24 hours)
or corrected by the kidneys
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http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)
uncompensated compensated
EXAMPLE OF COMPENSATION:
metabolic alkalosis
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Physiological values of ABB
(Astrup)
pH 7,36 - 7,44
pO2 8,9 - 14,7 kPa
pCO2 4,80 - 5,90
kPa
HCO3- 24 ± 2 mM
BE 0 ± 2,5 mM
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Respiratory Acidosis (RAc) cause: hypoventilation
CO2 + H2O H2CO3 HCO3- + H+
buffering: H+ + Hb Hb-H+ loss of base
result: * increase of pCO2 decrease of pH
* increase of HCO3- and decrease of other
buffer bases, especially of Hb BE = 0
when pO2 lactate (+ MAc)
compenstaion: resorption of HCO3
- in the kidneys acidic urine
positive BE
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Respiratory Alkalosis (RAl) cause: hyperventilation
CO2+ H2O H2CO3 HCO3- + H+
buffering: Hb-H+ Hb + H+ increase of bases
reult: * decrease of pCO2 increase of pH
* decrease of HCO3- and increase of other buffer
bases BE = 0
compensation:increased excretion of HCO3
- by the kidneys
negative BE
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The figure has been adopted from: Devlin, T. M. (editor): Textbook of Biochemistry with Clinical Correlations, 4th ed. Wiley‑Liss, Inc., New York, 1997. ISBN 0‑471‑15451‑2
Respiratory disorders
deviation from equilibrium to other
isobars
A (C) = primary imbalanceB (D) = compensated
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Metabolic Acidosis (MAc)
causes: 1) overproduction of acids (H+) in mtb increased anion gap
2) increased excretion of HCO3-
normal anion gap
ad1) metabolism produces excess of acids H+
buffering: H+ + HCO3- H2CO3 H2O + CO2
excretion of CO2: hyperventiltion (= compensation) H+ are also buffered by bases of nonbicarbonate buffers
decrease of BE (HCO3- and other buffer bases)
ad2) loss of HCO3
- e.g. diarrhoea, inhibitors of CA
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Metabolic Acidosis (II)
result:* decrease of pH* negative BE* acidic urine ( phosphates and NH4
+), decreased excretion HCO3
-
* deep breathing (stimulation of the respiratory centre by high concentration of H+)
later: pCO2 (= compensation)
compensation:hyperventilation other decrease of HCO3
-
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Metabolic Alkalosis (MAl) cause: 1) increased excretion of protons (e.g. vomitting, resorption of NaHCO3)
2) increased ingestion of basesbuffering: H+ CO2 + H2O H2CO3 HCO3
- + H+
other buffers H+
HCO3- and other buffer bases
positive BE
result: * increase of pH* positive BE* K+ in blood heart beat
imbalance
compensation: hypoventilation
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The figure has been adopted from: Devlin, T. M. (editor): Textbook of Biochemistry with Clinical Correlations, 4th ed. Wiley‑Liss, Inc., New York, 1997. ISBN 0‑471‑15451‑2
Metabolic disorders
deviation from equilibrium proceeds at the same isobar
E (G) = primary imbalanceF (H) = compensated
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Kalemia(= concentration of K+ in blood)
3,8-5,3 mM
• acidosis release of K+ from cells hyperkalemia loss of K+ with urine (quick alkalization of the organism by treatment can cause consequent hypokalemia danger of heart beat imbalance)
• alkalosis K+ replaces H+ in cells decrease of K+ in blood hypokalemia; K+ is excreated into urine instead of H+ (exchange with Na+)
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Case 1
A 70 year old man suffering from chronic lung disease, was admitted with an acute exacerbation. After admission testing (A), vigorous physiotherapy and medical treament were instituted, but his condition deteriorated (B). Artificial ventilation was started.6 hours later results were (C).
After 12 hours he had a seizure (D). A B C D
pH 7,30 7,24 7,40 7,54pCO2 (kPa) 9,47 10,93 7,73
5,73HCO3
- (mM) 35 35 34 35
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Case 2
A young woman was admitted unconscious, following a head injury. X-Ray showed a skull fracture and CT showed extensive cerebral contusions. There was no change over three days.
A BpH 7,52 7,48pCO2 (kPa) 3,47 3,87
HCO3- (mM) 22 19
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Case 3
A patient with vague symptoms, fever and hyperventilation presented in the Emergency Room:
Na+ 140 mMK+ 3,5 mMCl- 102 mMHCO3
- 13 mM
pH 7,39pCO2 2,67 kPa
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Case 4 A 45 year old man was admitted with a history of
persistent vomiting. He had a long history of dyspepsia which had gone untreated except with proprietary remedies.
Examination revealed dehydration and shallow respirations.
pH 7,56pCO2 (kPa) 7,20
HCO3- (mM) 45
K+ (mM) 2,8
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Case 5A 23 year old mechanic was brought to ER 12
hours after drinking antifreeze. He was agitated and confused. His sclerae were icteric.
Na+ (mM) 137K+ (mM) 5,4Cl- (mM) 95HCO3
- (mM) 4
glukóza (mM) 2,5pH 6,95pCO2 (kPa) 2,0