1 Acid-Base Balance Seminar No. 11. 2 Parameters of acid base balance Measured in arterial blood pH...
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![Page 1: 1 Acid-Base Balance Seminar No. 11. 2 Parameters of acid base balance Measured in arterial blood pH = 7.40 ± 0.04 = 7.36 – 7.44 pCO 2 = 4.8 – 5.8 kPa.](https://reader030.fdocuments.us/reader030/viewer/2022032604/56649e625503460f94b5e053/html5/thumbnails/1.jpg)
1
Acid-Base Balance
Seminar No. 11
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2
Parameters of acid base balance
Measured in arterial blood
• pH = 7.40 ± 0.04 = 7.36 – 7.44
• pCO2 = 4.8 – 5.8 kPa
• supporting data: pO2, tHb, sO2, HbO2, COHb, MetHb
Calculated
• [HCO3-] = 24 ± 3 mmol/l (from H.-H. eq.)
• BE = 0 ± 3 mmol/l (from S.-A. nomogram, see physilogy)
• BBs = 42 ± 3 mmol/l
• BBb = 48 ± 3 mmol/l
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Q. 1
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Buffer bases in (arterial) plasma
Buffer base mmol/l
HCO3-
Protein-His
HPO42-
----------
Total
24
17*
1
-------------
42
* Molarity of negative charge binding sites for H+
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Q. 2
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6
A. 2
BBs = 42 ± 3 mmol/l
BBb = 48 ± 3 mmol/l
hemoglobin in erythrocytes
increases BBb by 6-8 mmol/l
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Q. 3
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Abr. Name Reference values
sO2
tHb
COHb
MetHb
HbA1c
Oxygen parameters and hemoglobin derivatives
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Abr. Name Reference values
sO2saturation of Hb by oxygen
94 – 99 %
tHb total Hb2.15 – 2.65 mmol/l (tetramer)
120-175 g/l (diff. males × females)
COHb carbonylHb 1-2 % (nonsmokers)
MetHb methemoglobin 0.5 – 1.5 %
HbA1c glycated Hb 2.8 - 4 %
Oxygen parameters and hemoglobin derivatives
Tissue hypoxia of any origin leads to lactic acidosis
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Q. 4
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11
A. 4
7.4 = 6.1 + log [HCO3-] / 0.22 × 5.3
1.3 = log [HCO3-] / 1.2
101.3 = [HCO3-] / 1.2
20 = [HCO3-] / 1.2
[HCO3-] = 24 mmol/l
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Four types of acid-base disorders
pH = 6.1 + log2
3
pCO22.0
][HCO
Changes in [HCO3-]
metabolic acidosis
metabolic alkalosis
Changes in pCO2
respiratory alkalosis
respiratory acidosis
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Maintanance of constant pH in body
System / Organ What is altered? How quickly?
Buffers in ECF/ICF pH sec / min
Lungs pCO2 hours
Liver way of NH3 detoxication days
KidneyNH4
+ / H2PO4- excretion
HCO3- resorption
days
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Responses to acute change
• compensation
• correction
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Q. 6
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A. 6
Feature Plasma ICF
Main cation
Main anion
Protein content
Main buffer base
Na+
Cl-
HCO3-
K+
HPO42-
HPO42-
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Metabolic acidosis is the most common condition
Metabolic alkalosis isthe most dangerous condition
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Q. 8
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Na+
Cl-
HCO3-
AGK+
normal status hyperchloremic MAC normochloremic MAC
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Na+
Cl-
HCO3-
AGK+
Cl-
HCO3- ↓
AGno change
Cl-
no change
HCO3- ↓
AG
normal status hyperchloremic MAC normochloremic MAC
See Q. 11NaCl infusions
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Q. 9
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A. 9 Excessive infusions of NaCl isotonic solution lead to metabolic acidosis
Blood plasma (mmol/l) Isotonic solution (mmol/l)
Na+ Cl- Na+ Cl-
133-150 97-108 154 154
Ratio ~ 1 : 0.7 Ratio 1 : 1
Isotonic solution of NaCl has elevated concentration of Cl- compared to plasma
Blood plasma is diluted by infusion solution [HCO3-] decreases
pCO2 in alveolar air is the same
the ratio [A-] / [HA] in H.-H. equation decreases pH < 7.40 (acidosis)
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23
Q. 10
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Hyperchloremic MAc
• excessive infusions of NaCl solution
• the loss of HCO3- + Na+ + water (diarrhoea, renal disorders)
relative higher concentration of chlorides in plasma
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Q. 11
How is AG calculated?
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AG
Na+
Cl-
HCO3-
AGK+
AG composition = HPO42- + Prot- + SO4
2- + OA
AG calculation = [Na+] + [K+] - [Cl-] - [HCO3-]
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A. 11 MAc with increased AG
• Hypoxia of tissues – insufficient supply of O2 anaerobic
glycolysis: glucose 2 lactate
• elevated AG – lactoacidosis
• Starvation, diabetes
• TAG FA (β-oxidation in liver) acetyl-CoA (excess, over the capacity of CAC) KB production
• elevated AG - ketoacidosis
• Renal insufficiency – elevated phosphates, sulfates
• Various intoxications
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Q. 12
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A. 12
• AG – normal values
• SID – buffer bases (mainly HCO3-) – decreased
• compare Q. 8a)
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Q. 13 Metabolic acidosis
Parameter Physiol. st. Ac. change Compensation Correction
[HCO3-] 24 mmol/l N
pCO2 5.3 kPa N
[A-] / [HA] 20 : 1 < 20 : 1
pH 7.40 ± 0.04 < 7.36
System lungs kidney
Process hyperventilation HCO3
- resorption
NH4+ / H2PO4
- excr.
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31
Q. 15
Methanol intoxication
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Metabolic oxidation of methanol provides
a rather strong formic acid
CH3OH CHH
OCH
OH
OCH
O H
O
formaldehyde formic acid formate
Consequences:
• formate in plasma elevated AG acidosis
• excess of NADH lactoacidosis
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Compare two acids
ethanol
acetic acid
pKA = 4.75
KA = 1.8 10-5
methanol
formic acid
pKA = 3.75
KA = 1.8 10-4
KA (formic ac.) : KA (acetic ac.) = 10 : 1
formic acid is 10 stronger than acetic acid
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ethylene glycol intoxication
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Intoxication by ethylene glycol
HO CH2 CH2 OH C COH
OO
HO
C CO
OO
O
oxalic acid oxalate
Consequences:
• oxalic acid is rather strong acid (pKA1 = 1.25, pKA2 = 4.29)
• oxalate in plasma elevated AG acidosis
• excess of NADH lactoacidosis
• in urine calcium oxalate concrements
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Calcium oxalate is insoluble chelate
Draw formula
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Calcium oxalate is insoluble chelate
C
CO
Ca
OO
O
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Why MAc occurs in anemia?
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Not enough hemoglobin insufficient supply of O2
hypoxia anaerobic glycolysis to lactate
elevated AG – lactoacidosis
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Q. 16
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Metabolic oxidation of ethanol leads to excess of NADH
H3C C
H
H
O
H
+ NAD H3C C
H
O+
alkoholdehydrogenasa
aldehyddehydrogenasa
+ H2O H3C C
OH
H
O
H
H3C C
OH
ONAD- 2H
NADH+H
H3C C
H
O
acetaldehyd
aldehyd-hydrát octová kyselina
acetaldehyde dehydrogenase
alcohol dehydrogenase (ADH)
acetaldehyde
acetaldehyde hydrate acetic acid
- NADH+H+
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Metabolic consequences of EtOH biotransformation
Ethanol
ADH
MEOS
acetaldehydepart. soluble in membrane
PL
toxic efects on CNS
adducts with proteins, NA, biog. amines
acetate
acetyl-CoA
FA synthesis liver steatosis
ADH
the excess of NADH in cytosol is
reoxidized by pyruvate to lactate
lactoacidosisvarious products
causing hangover
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43
Q. 17
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• thiamine is the cofactor of aerobic decarboxylation of pyruvate
• thiamine deficit pyruvate cannot be converted to acetyl-CoA
• therefore pyruvate is hydrogenated to lactate
• even in aerobic conditions: glucose lactate
• increased plasma lactate elevated AG lactoacidosis
CH3-CO-COOH + CoA-SH + NAD+ CO2 + CH3-CO-S-CoA + NADH+H+
1. Thiamin diphosphate2. Lipoate3. Coenzym A4. FAD5. NAD+
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45
Q. 18
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A. 18
CO
O
CO
OCa
acidosis
HC
HO
O
CO
OH
Ca
2
• calcium cations make electrostatic interactions with carboxylate anions in
side chains of glutamate and aspartate (in various proteins)
• increased [H+] (= decreased pH) of plasma leads to a partial cation exchange
• one calcium ion is liberated and replaced by two protons
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Causes of metabolic alkalosis
• Repeated vomiting – the loss of chloride (Cl-) anion hypochloremic alkalosis
• Direct administration of buffer base HCO3-
per os: baking soda, some mineral waters
intravenous infusions of sodium bicarbonate
• Hypoalbuminemia
severe malnutrition
liver damage, kidney damage
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48
What is baking soda?
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A.
NaHCO3
sodium hydrogen carbonate (sodium bicarbonate)
sold in pharmacy
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Q. 19
How is SID calculated?
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Na+
Cl-
SID
K+
SID composition = HCO3- + HPO4
2- + Prot-
SID corresponds to buffer bases of plasma
In MAlk SID increases
SID calculation = [Na+] + [K+] - [Cl-]
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Q. 20
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Na+
Cl-
HCO3-
AGK+
Cl-
HCO3- ↑
AGno change
Cl-
no change
HCO3- ↑
AG
normal status hypochloremic MAlk normochloremic MAlk
vomiting hypoalbuminemia
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Q. 21 Metabolic alkalosis
Parameter Physiol. st. Ac. change Compensation Correction
[HCO3-] 24 mmol/l N
pCO2 5.3 kPa N
[A-] / [HA] 20 : 1 > 20 : 1
pH 7.40 ± 0.04 > 7.44
System lungs kidney
Process hypoventilation HCO3- excretion
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Q. 23
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A. 23
pCO2 = 5.5 kPa .......................... OK
[HCO3-] = 39 mmol/l .................. elevated
pH = 7.6 ..................................... elevated
status: metabolic alkalosis
pCO2 will increase during compensation (hypoventilation)
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Solution Effect Explanation
NaCl
KHCO3
NH4Cl
NaHCO3
Na lactate
Q. 25
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Solution Effect Explanation
NaCl acid. plasma dilution [HCO3-] while pCO2 is constant
KHCO3 alkal. direct addition of the main buffer base
NH4Cl acid. NH4+ excreted by urine, Cl- remains in plasma [HCO3
-]
NaHCO3 alkal. direct addition of the main buffer base
Na lactate alkal.lactate anion goes from plasma to liver (gluconeogenesis), Na+ remains in plasma its pos. charge is balanced by extra HCO3
- (similar effect like in vegetarian diet)
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Q. 26 Respiratory acidosis
Parameter Physiol. st. Ac. change Compensation Correction
[HCO3-] 24 mmol/l N, -
pCO2 5.3 kPa N
[A-] / [HA] 20 : 1
pH 7.40 ± 0.04
System kidney lungs
ProcessHCO3
- resorption
NH4+ / H2PO4
- excr.hyperventilation
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Q. 27
Describe the scheme on p. 5
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• Excess of CO2 in the body produces more H2CO3 in blood
• Carbonic acid in buffering reaction with proteins gives
HCO3- ion
• Hydrogen carbonate ion is driven to ICF
• Therefore the level of HCO3- in ECF is normal or slightly
elevated
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Q. 29
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A. 29
pH 7.32 ........................................
pCO2 9.3 kPa .............................
[HCO3-] = 39 mmol/l ..................
[Na+] = 136 mmol/l ......................OK
[K+] = 4.5 mmol/l .........................OK
[Cl-] = 92 mmol/l ..........................
AG = 136 + 4.5 - 39 – 92 = 9.5 mmol/l ....... no MAc
Conclusion: compensated RAc
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Q. 30 Respiratory alkalosis
Parameter Physiol. st. Ac. change Compensation Correction
[HCO3-] 24 mmol/l N, -
pCO2 5.3 kPa - N
[A-] / [HA] 20 : 1
pH 7.40 ± 0.04
System kidney lungs
Process Excretion of HCO3- hypoventilation
(if possible)
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Combined disorders
Q. 33
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A. 33
pH 7. 4 ............................. OK
pCO2 5.13 kPa .......................OK
BE 1 mmol/l ............................OK HCO3- = 25 mmol/l ....... OK
Na+ 140 mmol/l ......................OK
K+ 4.6 mmol/l ........................OK
Cl- 89 mmol/l .........................
AG = 140 + 4.6 – 25 – 89 = 30.6 mmol/l ...............
SID = 140 + 4.6 – 89 = 55.6 mmol/l .......................
Conclusion: MAc + MAlk
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Q. 34
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A. 34
Q. Explanation
a) MAc - lactoacidosis (alcohol) + loss of Cl- (vomiting) - MAlk
b)MAc - ketoacidosis (starvation) + loss of Cl- (vomiting after overeating) - MAlk
c) RAlk (stimulation of resp. centre) + MAc (salicylate – AG )
d) MAc (ketoacidosis) + RAc (heart failure – circulation insuff.)