Acid-base Balance(ABB)

Vladimíra Kvasnicová

Definition - REPETITION • pH

• acid

• base

• dissociation constant

• buffers

The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

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

The figure was found at http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

+ 3 HCl

[CO2] = x pCO2 = 0,226 for pCO2 expressed in kPa

= 0,03 for pCO2 expressed in mmHg

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

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)

The source and fate of acids /

bases

• source of acids: metabolism

• source of bases: food

• fate: transformation by the metabolism

excretion

The figure has been adopted from J.Koolman, K.H.Röhm / Color Atlas of Biochemistry, 2nd edition, Thieme 2005

~ 20 000 mmol / den

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+

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+

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)

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

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

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!!!

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)

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 %

http://science.kennesaw.edu/~jdirnber/Bio2108/Lecture/LecPhysio/42-29-BloodCO2Transport-AL.gif (March 07)

O2

O2

Excretion of CO2 by the

lungs

Excretion of H+ by the kidneys (I)

http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

Excretion of H+ by the kidneys (II)

http://www.colorado.edu/kines/Class/IPHY3430-200/14fluid.html (April 2007)

Excretion of H+ by the kidneys (III)

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)

The figure has been adopted from J.Koolman, K.H.Röhm / Color Atlas of Biochemistry, 2nd edition, Thieme 2005

ABB disorders

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

Primary disorders of ABB

http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)

pCO2

HCO3-

Resp.

Mtb.

http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)

24 mM

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

http://romerosnap1.phol.cwru.edu/AcidBase-SOMy1.htm (April 2007)

uncompensated compensated

EXAMPLE OF COMPENSATION:

metabolic alkalosis

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

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

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

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

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

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

-

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

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

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+)

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

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

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

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

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