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Acid-base status assessment

Acid-base status assessment. Stanislav Matoušek , Ji ří Kofránek. Elementary terms. Normal concentration of H + in plasma is 0.000 04 mmol/L = 40 nmol/L Very high chemical activity of hydrogen ions (protons) in solution Changes of pH influence spacial conformation of proteins.

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Acid-base status assessment

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  1. Acid-base status assessment Stanislav Matoušek, Jiří Kofránek

  2. Elementary terms

  3. Normal concentration of H+ in plasma is 0.000 04 mmol/L = 40 nmol/L Very high chemical activity of hydrogen ions (protons) in solution Changes of pH influencespacial conformation of proteins however, in other fluids, it can different by many orders of magnitude pH = - log10(H+) 40 nmol/L = pH 7.4 change 2x …. -0.3 (change 1/2x…… +0.3) change 4x …. -0.6 change 8x …… -0.9 change 10x …….- 1.0 How is [H+] determined? Why is pH (concentration of H+) so important?

  4. In blood Bicarbonate (open buffer) Hemoglobin (histidin residues) Albumin (histidin residues) Phosphates In cells Phosphates Bicarbonate Proteins Buffers High reactivity and very low amounts of H+ present => [H+] determined by chemical equilibria of buffers. Buffers - substances that react with the H+. Buffering occurs mostly with substances that do have pKa close to the actual pH.

  5. Buffering equilibria + H+ B- HB Quite common [H+][B-] = Ka [HB] [H+] = Ka*[HB]/[B-] log[H+] = log(Ka) +log ([HB]/[B-]) -log[H+] = -log(Ka) -log ([HB]/[B-]) -log[H+] = -log(Ka) +log ([B-]/[HB]) pH=pKa+log([B-]/[HB]) + H+ B HB+ Histidine side chains in Albumin

  6. Buffering HB and B-

  7. Buffering HPO42- PO43- H2PO4- HPO42- H3PO4 H2PO4-

  8. Base Excess At pH = 7.4, Base Exces(BE) is by definition = 0 mmol/L Add 1 mmol of acid to the blood (as lactic acid)=> BE = -1 mmol/L Add 5 mmol of base to the blood (NaOH) =>BE = 5 mmol/L BE meq/L albumin open HCO3- buf. whole plasma pH

  9. How to assess acid-base

  10. What do we take? • Arterial blood gas measurement (“Astrup”) • Serum electrolytes electroneutrality • Other

  11. Arterial blood gas measurement Apparatus measures: • pH ( 7.35 – 7.45) Or analogous value: H+ = 35 – 45 nmol/l • pCO2 (40 Torr = 5.3 kPa ) • pO2 (100 Torr = 13,3 kPa) • Hb (120 – 170 g/L) Apparatus calculates: • HCO3- (24 mmol/l) From Henderson-Hasselbalch Equation • BE ( 0 mmol/l ) From in-built „Siggaard-Andersen nomogram“ • Standard HCO3 • Sat.O2 Possible problems: / Visible air bubble stays in the syringe and dissolves in the sample / The sample is not analyzed right away. Metabolic processes cause changes in AB parameters. (If immediate analysis is not possible, the sample should be kept in ice-bath)

  12. Serum electrolytes • Strong Ion: Na+ (135 – 145 mmol/l) • Strong Ion: Cl- (97 – 108 mmol/l) • Strong Ion: K+ ( 3.5 – 5 mmol/l ) • Buffer: Total CO2 or HCO3- (24 mmol/l) …..should be equal to HCO3- from Astrup – can check the measurement validity Additional (not necessary): • Buffer: Phosphates -- H2PO4- => HPO42-( 1 – 1,5 ) • Strong Ion: Ca++ (2.4 mmol/l) • Strong Ion: SO42-

  13. Other Buffers: Albumin (35 – 50 g/l) “Strong Ion”, Acid: Lactate (0.5 – 2.5) “Strong Ions”, Acids: Ketoacids (0) Toxic substances, acids: Salycilates, methanol etc.

  14. Change in buffer equilibria =change in pH

  15. Buffering systems of the blood + + CO2 H2O H2CO3 H+ HCO3- HBuf H+ + Buf- H+ + Hb- HHb H+ + Alb- HAlb H+ + HPO42- H2PO4- non-bicarbonate buffers Buf = Hb + Alb + PO4-

  16. HCO3- CO2 H2CO3 H2O H+ HBuf Buf- Buffering reactions

  17. Bicarbonate buffer Hendersson- Hasselbalch equation: [H+] = 24 . pCO2 / [HCO3-] [nmol/L]=[Torr]/[mmol/L] or pH = 6.1 + log ( [HCO3-] / [H2CO3] ) pH = 6.1 + log ( [HCO3-] / 0.03 pCO2 ) + + CO2 H2O H2CO3 H+ HCO3-

  18. Division of acid-base disturbances • Respiratory acidosis ↑ pCO2 - alveolar hypoventilation • Respiratory alkalosis ↓pCO2 - alveolar hyperventilation • Metabolic acidosis ↓st. HCO3-, BE negative • Metabolic alcalosis ↑st. HCO3- , BE positive

  19. Bicarbonate buffer only • What happens if we add 12 mmol/L of acid? • What happens if the pCO2 increases from 40 mmHg to 80 mmHg ? • What happens if we add 24 mmol/L of NaHCO3?

  20. Buffer base • The sum of all base forms of the buffers in blood is called buffer base • BB = HCO3- + Hb- + (Alb- + HPO42-) Hb- = Hb H+ binding sides * [Hb] Alb- = Alb H+ binding sides * [Alb] Due to electroneutrality reasons, buffer base of plasma is sometimes called Strong Ion Difference (SID).

  21. HCO3- CO2 H2CO3 H2O H+ HBuf Buf- Buffer base

  22. Buffer base • What happens with bicarbonate in plasma if the pCO2 increases to 80 Torr? • What happens with total BB? Did it change? • What happens with total BB, if you add 5meq/L of acid?

  23. Buffer Base and Base Excess • BB = HCO3- + Hb- + (Alb- + HPO42-) • Buffer base would be a good measure of metalolic acidosis/alkalosis, because it does not change with pCO2 , but it does change with addition of metabolic acid/base. • However, total buffer base also changes (significantly!) with changes of total concentration of Hb, Alb and Pi without any changes of pH!

  24. BE = BB - normalBB Normal BB is the buffer base that the given blood would have at pH=7.4 It varies with anemia, polycythemia, Albumin content etc. BE then only represents changes in BB due to changes in pH BE is independent of pCO2 Base Excess -Solution by Siggaard-Andersen

  25. Base Excess and Buffer base BB = 39 meq/L BB = 21 meq/L BE meq/L albumin open HCO3- buf. whole plasma BE = - 17 meq/L pH

  26. Measure of metabolic disturbances • Americans: Standard Bicarbonates – the value of bicarbonates, when pCO2= 40 mmHg • Europeans: Base Excess – measure derived from BB, thus independent of pCO2

  27. Compensation of Acid Base Disorders

  28. Acute acid-base disturbances • Acute respiratory acidosis ↑ pCO2 - alveolar hypoventilation • Acute respiratory alkalosis ↓pCO2 - alveolar hyperventilation • Acute metabolic acidosis ↓st. HCO3-, BE negative • Acute metabolic alkalosis ↑st. HCO3- , BE positive

  29. PCO2torr 90 pH=7,1 pH=7,2 pH=7,37 pH=7,3 pH=7,43 80 pH=7,5 Compensated resp. acidosis Acute resp. acidosis 70 pH=7,6 60 Compensated met. Alcalosis 50 Acute metabolic acidosis Acute metabolic alkalosis 40 30 Acute respiratory alkalosis Compensated metabolic acidosis Compensated res. alkalosis 20 10 -20 -15 -10 15 -25 -5 25 0 30 10 5 20 Base Excessmmol/l Compensation of respiratory acidosis

  30. Metabolic compensation of respiratory disorder • Is carried out by kidneys that increase plasma concentration of bicarbonatein resp. acidosis., Kidneys also decrease bicarbonate reabsorption and their concentration in plasma in resp. alkalosis. • It takes about 2.5 days to fully develop

  31. Respiratory compensation of metabolic disorder • In metabolic acidosis, lungs eliminate more pCO2 by deeper and faster breathing. This is called Kussmaul breathing. • The respiratory compensation of the metabolic alkalosis is limited, because slower and more shallow breathing is limited by hypoxemia. • Full compensation takes about ½ day to develop.

  32. 68 year old male comes to your ambulance. Chronic bronchitis and pulmonary emphysema His Lab. tests: pH 7.3 pO2 60 mmHg pCO2 80 mmHg HCO3- 38 mmol/ l BE = 17 mmol/L Case History I

  33. PCO2torr 90 pH=7,1 pH=7,2 pH=7,37 pH=7,3 pH=7,43 80 pH=7,5 Compensated resp. acidosis Acute resp. acidosis 70 pH=7,6 60 Compensated met. Alcalosis 50 Acute metabolic acidosis Acute metabolic alkalosis 40 30 Acute respiratory alkalosis Compensated metabolic acidosis Compensated res. alkalosis 20 10 -20 -15 -10 15 -25 -5 25 0 30 10 5 20 Base Excessmmol/l Compensation of respiratory acidosis

  34. 20 year old student is admitted to hospital for acute anxiety state Cannot concentrate, feeling of numbness or pins and needles in fingers She has split with her boyfriend recently Has not been seriously ill until now, no medication Physical examination – normal Lab. values: pH7,49 pO2100 mm Hg pCO2 30 mm Hg HCO3- 22 mmol/l BE = -2 mmol/L Case History II

  35. Respiratory acidosis is part of Global (type II) respiratory insuficiency : ↓ alveolar ventilation Respiratory center depression Drugs, medicaments Respiratory centre hypoxia or damage Trauma Stroke Tumor Cerebral edema / increased intracranial pressure Nerve of muscle disease Myasthenia gravis Polyradiculoneuritis Serious obesity Lung disease Restrictive ARDS Fibroses Trauma, pneumothorax, serial rib fractures Obstructive Astma Tumor Foreign body Increase in dead space Embolism Emphysema Breathing CO2 in the inspired air(miners buried in a mine) Causes of respiratory acidosis

  36. Causes of respiratory alkalosis • Hyperventilation • in mechanical ventilation • With hypoxemia • High altitude disease • Right-left shunting • In neurosis • Respiratory centre irritation • Trauma, salicylates, inflammation

  37. 38 yo female, DM 1st type Chills and fever lasting several days She has not felt well => not eaten much and not taken much insulin During admission day: Abdominal cramps, vomited several times Physical exam: BF 30 min-1, HF 112 min-1, BP 110/70 lying and 100/60 standing, 37 °C, Dry mucosae and fruity breath odor Lab: pH7,20 pO2 96 mm Hg pCO221 mm Hg HCO3- 8 mmol/l BE -20 mmol/l Glc 15 mmol/l Na+ 148 mmol/l K+ 5,5 mmol/l Cl 110 mmol/l Positive aceton in urine Case History III

  38. PCO2torr 90 pH=7,1 pH=7,2 pH=7,37 pH=7,3 pH=7,43 80 pH=7,5 Compensated resp. acidosis Acute resp. acidosis 70 pH=7,6 60 Compensated met. Alcalosis 50 Acute metabolic acidosis Acute metabolic alkalosis 40 30 Acute respiratory alkalosis Compensated metabolic acidosis Compensated res. alkalosis 20 10 -20 -15 -10 15 -25 -5 25 0 30 10 5 20 Base Excessmmol/l Compensation of respiratory acidosis

  39. Case history IV • 23 yo male, admitted for suicide attempt • Has ingested large amount of aspirin • At admission somnolent, difficult to make contact with • BF 30 min-1 , HF 100 min-1, BP 142/88, t = 36.8 °C • Lab: • Toxic levels of salicylates, • pH 7.25 • pCO2 14 mmHg • HCO3- 8 mmol/l

  40. Extensive desequilibrating load on buffering system Loss of bicarbonate from extensive buffering of acids Ketoacidosis Diabetic Alcohol Starving Lactic Acidosis Toxic substances Salicylates Ethylen glycol methanol Loss of bicarbonate by GIT By diarrhea By fistula and stomia Loss of kidney regulation Renal tubular acidoses Kidney failure Causes of metabolic acidosis

  41. Anion gap • Helps to distinguish the cause of metabolic acidosis • Increases when ions like lactate, ketoacids or sulfates are present in plasma. This signifies that the acidosis has been caused by the dissociation hydrogen ion from these molecules. • AG = Na+ - HCO3- -Cl- • norm: 10+/- 2 mmol/L

  42. Electroneutrality principle Ca+ Mg+ K+ HCO3- Buf- AG Na+ XA- Cl-

  43. Normal anion gap (10 mmol/L) Losses of bicarbonate GIT (diarrhea) Kidneys – RTA (renal tubular acidosis) Failure of bicarbonate regeneration in Kidney Aldosterone deficiency Aldosterone insensitivity RTA Given acidyfying salts of chloride Eg. Ammonium chloride Increased anion gap (>12-14 mmol/L) Reduced excretion of acids Renal failure Overproduction of acids Ketoacidosis Lactic Acidosis Toxin ingestions Metabolic acidosis

  44. Causes of metabolic alkalosis • Loss of acid by vomiting • Hyperaldosteronism • Liver failure • Kidney disorder – Bartter’s syndrome • Non-adequate bicarbonate infusion

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