Dr.

Shirani Hapuarachchi MBBS, MD, FRCA Consultant Anaesthetist The National hospital Sri Lanka

 Metabolism
Aerobic

results in an acid load

metabolism - the end product CO2 combines with water to give Carbonic acid (H2CO3) - Respiration - Volatile metabolism Pyruvate Kidneys non volatile Lactatate

anaerobic

keto acidosis Aceto acetic acid and beta hydroxy butyric acid NH4Cl and CaCl2
Diabetic

This reduces the cellular fluid and blood pH. Why pH? blood pH is 7.35 7.45 (H+ .00004meq /l)and the intracellular pH is 7.0 7.3 cells and

Normal

This prevents optimal enzyme activity in Affecting cellular function specially brain

heart

 Elimination

of CO2 from the blood (daily 13,000 m.Eq) by respiration Non volatile acid by the kidney.

 Dissolved

10% - 20 times more soluable

than O2 HCO3 60% - Formed within the RBC

catalysed by carbonic anhydrase, diffuses into the plasma Chloride diffuses to the RBC Chloride shift H ions combine with HB HHB (reduced Hb) Carbamino Cpds 30% - reaction with amino (RNH2) groups of proteins Hb and plasma

produced in the mitochondria PCO2 46mmHg It diffuses into the blood PCO2 45mmHg From Alveolar capillaries diffuses into the alveoli 40 mmHg
CO2 Increase

in PaCO2 1. Increase production (CO2 retention) 2.Reduction in pulmonary blood flow 3.Reduction in alveolar ventilation

CO2+H2O H2CO3

H2CO3 H+ HCO3

H+ = Ka. H2CO3/ HCO3 Henderson Eq Log H+ = log Ka . H2CO3/HCO3

pH = pka . HCO3 / H2CO3 H.H Eq At normal pH When HCO3 HCO3

pKa 6.1

fall to keep pH - constant

falls in acidosis CO2 PaCO2 will also

- /H CO
2

constant

75mmols of acid is excreted by the kidney buffers are PO4 (H3PO4)and NH3 ions(NH4+

HCO3- reabsorbs (99%)and regenerate At normal HCO3 levels 24 mmol/l the reabsorption is maximum (Tmax) If there is increased HCO3 HCO3 already reached

- and this will be excreted as Tmax is

- load it will increase the

 Filtered

bicarbonate combines with a H ion which is secreted in exchange for Na(antiport) secondary active transport H2CO3 is formed which forms CO2 and this diffuses into the PCT cell While the water is passed down the tubule In the tubular cells H2CO3 is formed which dissociates to H ions and HCO3- ions H ions are now again available for secretion

 In

the cell the absorbed Na and HCO3 are passed into the blood by a co transporter The rate of absorption is propotionate to the CO2 production Tmax is at a maximum all the time If there is excess of HCO3 it will be excreted by the kidney

Tubule

Proximal convoluted tubule

Na Blood

H+ HCO3H2CO3 HCO3CO2+H2O

H+ + HCO3-

Na

Na+

H2CO3

CO2 + H2O

ions are secreted instead of K ions (H+/K+ ATP ase) Na ions are reabsorped under aldosterone influence Na/H transport exchange The secreted H ions combine with HCO3and forms CO2 which diffuses into the cell The H ions are mopped up by Phosphorous and NH3
H

 H.H.

Equation Siggard Anderson Normogram Automated analysis

1.

pH 2. PCO2 3. BE 4.Std HCO3/BB 5. Oxygenation

PCO2 mmHg

Co2 titration lines Buffer base

Standard bicarbonate
Base excess

pH

 Blood

HCO3-, Pr-,Hb fluid HCO3 Prot-, H2PO4

Interstial

Intracellular Urine CSF

HCO3 and PO4

HCO3 and PO4

 pH

= 6.10 + log HCO3 / .0301PCO2 pH and PCO2 can be measured directly HCO3 is calculated PCO2 is controlled by respiration HCO3 is controlled by the kidney This prevents the pH change Carbonic anhydrase catalyses the reaction CN, sulphonamides inhibits it

 RCOOH
RNH3+ Hb

RCOO- + H+ RNH2 + H+

as a buffer immidazole derivative in the Histidine residue 1 molecule has 38 HC HC

NH+ +H + R NH N

NH

HC HC C R

 H2PO4 pK

H+ +HPO4

= 6.8 Very low concentrations in plasma Important buffer intracellularly Important urinary buffer

 Respiratory Metabolic Alkalosis Respiratory Metabolic

Acidosis

in PCO2 due to decreased ventilation Rise in H2CO3 Rise in H+ Rise in HCO3 Reduction in pH new equilibrium
Rise Compensatory

metabolic alkalosis Kidneys retention of HCO3 and excretion of Cl-

PCO2 due to hyperventilation Reduction in H2CO3 Reduction in H+ Reduction in HCO3 Increase in pH new equilibrium
Low Compensatory

metabolic acidosis - Kidney

Addition of H+ Combine with HCO3 Increase H2CO3 Increase in CO2

Stimulation of respiration CO2 and H+ Increase in pH Drop in HCO3 Compensatory respiratory alkalosis Later Kidneys excrete the extra H+ - PO4, NH4+ In severe metabolic acidosis extra NH4+ produced by glutamine

 Increase Less

in HCO3

H+ Rise in pH
Compensatory

respiratory acidosis

The difference between the measured anions other than ClandHCO3-and the measured cations other than Na+ Pr-,HPO4,SO4- and organic acids The difference is due to the proteins which are electrically negatively charged Normal value 12 mmols/l Therefore this can be reduced by 1. hypoalbuminaemia 2. Increase in cations Ca2+,K+,Mg2+ IgG,Li increased in metabolic acidosis - Lactate and organic anions Anion gap is increased in keto acidosis and lactic acidosis Not increased in hyperchloraemic acidosis NH4Cl or carbonic anhydrase inhibitors

 The

difference between strong ions Na+,K+,Ca2+ and Mg2+ - strong cation Cl- and lactate - strong anions Difference is 40 m.mols/l This is reduced in metabolic acidosis When strong cations are reduced H2O dissociates to H+ to maintain electrical neutrality High in metabolic alkalosis hypoalbuminaemia

 N.saline

Na+ 154, Cl- 154 - Zero

balance When large amounts are infused Cl- effect is more SID narrows H2O dissociates H+ Metabolic acidosis
5%

Dextrose H2O dilution of strong ions - metabolic acidosis

 Importance

of maintaining the blood pH How is it regulated How is it monitored