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Acid-Base Balance. Seminar No. 11. 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 supporting data: pO 2 , tHb, s O 2 , HbO 2 , COHb, MetHb Calculated [HCO 3 - ] = 24 ± 3 mmol/l (from H.-H. eq.)

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Acid base balance

Acid-Base Balance

Seminar No. 11


Parameters of acid base balance
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



Buffer bases in arterial plasma
Buffer bases in (arterial) plasma

* Molarity of negative charge  binding sites for H+



A. 2

BBs = 42 ± 3 mmol/l

BBb = 48 ± 3 mmol/l

hemoglobin in erythrocytes

increases BBb by 6-8 mmol/l




Oxygen parameters and hemoglobin derivatives1
Oxygen parameters and hemoglobin derivatives

Tissue hypoxia of any origin leads to lactic acidosis



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


Four types of acid base disorders
Four types of acid-base disorders

pH = 6.1 + log

Changes in [HCO3-]

metabolic acidosis

 metabolic alkalosis

Changes in pCO2

 respiratory alkalosis

 respiratory acidosis



Responses to acute change
Responses to acute change

  • compensation

  • correction




Metabolic acidosis is the most common condition metabolic alkalosis is the most dangerous condition

Metabolic acidosis is the most common conditionMetabolic alkalosis isthe most dangerous condition




normal status hyperchloremic MAC normochloremic MAC

See Q. 11

NaCl infusions


Q. 9 normochloremic MAC


A 9 excessive infusions of nacl isotonic solution lead to metabolic acidosis
A. 9 Excessive infusions of NaCl isotonic solution lead to metabolic acidosis

Isotonic solution of NaCl has elevated concentration ofCl- 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)


Q. 10 lead to metabolic acidosis


Hyperchloremic mac
Hyperchloremic MAc lead to metabolic acidosis

  • excessive infusions of NaCl solution

  • the loss of HCO3- + Na+ +water (diarrhoea, renal disorders)  relative higher concentration of chlorides in plasma


Q. 11 lead to metabolic acidosis

How is AG calculated?


AG lead to metabolic acidosis

AG calculation = [Na+] + [K+] - [Cl-] - [HCO3-]

AG composition = HPO42- + Prot- + SO42- + OA


A 11 mac with increased ag
A. 11 MAc with increased AG lead to metabolic acidosis

  • 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


Q. 12 lead to metabolic acidosis


A. 12 lead to metabolic acidosis

  • AG – normal values

  • SID – buffer bases (mainly HCO3-) – decreased

  • compare Q. 8a)


Q 13 metabolic acidosis
Q. 13 Metabolic acidosis lead to metabolic acidosis


Q. 15 lead to metabolic acidosis

Methanol intoxication


Metabolic oxidation of methanol provides a rather strong formic acid
Metabolic oxidation of methanol provides a rather strong formic acid

  • Consequences:

  • formate in plasma  elevated AG  acidosis

  • excess of NADH  lactoacidosis


Compare two acids

ethanol strong formic acid

acetic acid

pKA = 4.75

KA = 1.8  10-5

methanol

formic acid

pKA = 3.75

KA = 1.8  10-4

Compare two acids

KA (formic ac.) : KA (acetic ac.) = 10 : 1

formic acid is 10  stronger than acetic acid


Ethylene glycol intoxication

ethylene glycol intoxication strong formic acid


Intoxication by ethylene glycol
Intoxication by ethylene glycol strong formic acid

  • 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


Calcium oxalate is insoluble chelate
Calcium oxalate is insoluble chelate strong formic acid

Draw formula



Why mac occurs in anemia

Why MAc occurs in anemia? strong formic acid


Not enough hemoglobin strong formic acid insufficient supply of O2

 hypoxia  anaerobic glycolysis to lactate

elevated AG – lactoacidosis


Q. 16 strong formic acid


Metabolic oxidation of ethanol leads to excess of nadh
Metabolic oxidation of ethanol leads to excess of NADH strong formic acid

alcohol dehydrogenase (ADH)

acetaldehyde

acetaldehyde dehydrogenase

- NADH+H+

acetic acid

acetaldehyde hydrate


Metabolic consequences of etoh biotransformation
Metabolic consequences of EtOH biotransformation strong formic acid

Ethanol

ADH

ADH

MEOS

the excess of NADH in cytosol is reoxidized by pyruvate to lactate

part.soluble in membrane PL

acetaldehyde

acetate

adducts with proteins, NA, biog. amines

toxic efects on CNS

acetyl-CoA

lactoacidosis

various products

causing hangover

FA synthesisliver steatosis


Q. 17 strong formic acid


CH strong formic acid3-CO-COOH + CoA-SH + NAD+ CO2 + CH3-CO-S-CoA + NADH+H+

  • 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

  • Thiamindiphosphate

  • Lipoate

  • Coenzym A

  • FAD

  • NAD+


Q. 18 strong formic acid


A. 18 strong formic acid

  • 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


Causes of metabolic alkalosis
Causes of metabolic alkalosis strong formic acid

  • 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


What is baking soda

What is baking soda? strong formic acid


A. strong formic acid

NaHCO3

sodium hydrogen carbonate (sodium bicarbonate)

sold in pharmacy


Q. 19 strong formic acid

How is SID calculated?


Sid corresponds to buffer bases of plasma
SID corresponds to buffer bases of plasma strong formic acid

SID calculation = [Na+] + [K+] - [Cl-]

SID composition = HCO3- + HPO42- + Prot-

In MAlk  SID increases


Q. 20 strong formic acid


normal status hypochloremic MAlk normochloremic MAlk

vomiting

hypoalbuminemia


Q 21 metabolic alkalosis
Q. 21 Metabolic alkalosis normochloremic MAlk


Q. 23 normochloremic MAlk


A. 23 normochloremic MAlk

pCO2 = 5.5 kPa .......................... OK

[HCO3-] = 39 mmol/l ..................  elevated

pH = 7.6 .....................................  elevated

status: metabolic alkalosis

pCO2 will increase during compensation (hypoventilation)


Q. 25 normochloremic MAlk


Q 26 respiratory acidosis
Q. 26 Respiratory acidosis normochloremic MAlk


Q. 27 normochloremic MAlk

Describe the scheme on p. 5


  • Excess of CO normochloremic MAlk2 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


Q. 29 normochloremic MAlk


A. 29 normochloremic MAlk

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


Q 30 respiratory alkalosis
Q. 30 Respiratory alkalosis normochloremic MAlk


Combined disorders

Combined disorders normochloremic MAlk

Q. 33


A. 33 normochloremic MAlk

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


Q. 34 normochloremic MAlk


A. 34 normochloremic MAlk


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