This document provides an overview of acid-base balance and disorders. It discusses the major buffer system involving carbonic acid and bicarbonate, and how the lungs and kidneys work to maintain acid-base balance. Various acid-base disorders are described including their primary events, compensatory responses, and interpretations based on blood parameters such as bicarbonate, PCO2, and anion gap.

1. Acid – Base balance By Dr. Khaled Al nadi KHMC \ JORDAN

2. Objectives of this presentation Introduction Refresh the knowledge of the major buffer system Learn to operate the Henderson-Hasselback equation Viewing simple and mixed acid-base disorders Interpretation of plasma parameters characterizing acid-base disorders

3. Introduction Human physiology has evolved to maintain ECF.PH at a value of 7.40 H+ is a proton ( hydrogen atom without its orbital electron )

4. Acid : is a substance that acts as proton donor. Base : is a substance that accept protons in solution.eg.HCO3-, phosphate ion( HPO4-) ammonia(NH3-) and acetate(CH3COO-) Acid↔Base + H+

5. Who do we express [H+]? Direct as [H+] which give H+ concentration in mol/L or Eq/L Indirect as PH: PH=Log10 1/[ H+]=-Log 10[H+] ***so PH + [H+] are inversely related *** ****The range of [H+] that is compatible with life is 20-126 nEq/L which is equivalent to PH range of 7.7-6.9 [H=] PH 128 6.9 101 7.0 80 7.1 64 7.2 50 7.3 40 7.4 32 7.5 25 7.6 20 7.70

6. Sources of H+ The greatest source of acid in the body is CO2 ,produced as an end products of metabolism Forms of acid in the body: •Carbonic or volatile acid( H2CO3 ) •Non carbonic or non volatile Pathways for acid removal • Kidneys •Lungs •GIT

7. How body maintained acid base balance? Its maintained primarily through the control of 2 organs: Lungs+ kidneys

8. Henderson –Hasselbalch equation CO2 ↔ CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3- Body use this equation to control PH At equilibrium there are approximately 500mmol of CO2 for every 1mmol of H2CO3. 4000mmol of H2CO3 for every 1mmol of H+. Using H-H equation: PH=PK+log [H2CO3] \ [HCO3]….. [H+] =24 X PCO2/ [HCO3]

9. Advantage of H-H equation [H+] is determined by ratio of PCO2 & [HCO3-]. It is a useful mean to verify the accuracy of the laboratory data by calculating one of the variable from the other two.

10. CO2 Under basal conditions, the average adult produce about 300L (13.5mol) of CO2 per/day through the metabolism of CHO+fat These excreted by the lungs at a rate of 200ml /min during resting condition.

11. Blood forms of CO2 CO2 is transported in the blood in 3 forms: 1. HCO3- = 90% of total CO2in plasma 2. Carbamino compounds (carbametes of Hb + proteins)= 5% of total CO2 3. CO2 gas dissolved in plasma = 5% of total CO2

12. Total CO2 [total CO2]= [ HCO3 -] +( S.PCO2) S : solubility constant for CO2 in plasma = 0.03mmol /L / mmHg Dissolved CO2 = S.PCO2 = 0.03 xPCO2 at PCO2 = 40mmHg , dissolved CO2 = 1.2mmol / L ***total CO2 in clinical laboratory is a measure of [HCO3] *** total CO2 gives little information about functional status of the lungs

13. HCO3- HCO3- is added to the blood by : A. diet B. metabolisim C. diseases **HCO3 has no rule in buffering of H2CO3

14. Non carbonic acids (NCA) Sources of NCA: 1. diet (proteins, phospholipids) 2. inter mediary metabolism (keto-acids , lactic acid) 3. stool through HCO3 loss *** excretion of NCA is through kidneys as the body can not convert NCA to CO2

15. BODY BUFFER SYSTEM Buffer : is a solution consisting of a weak acid + its conjugate base * * * * * Buffering is the primary mean by which large changes in [H+] are minimized . The most effective buffers are : H2CO3, H2PO4, Plasma protein( Hb)

16. HCO3- BUFFER SYSTEM we use HCO3- buffer system to determined acid base status depending on the isohydric -principle which states that all buffer pairs are in equilibrium with the same [H+].

17. Acid base disturbances Acidosis : is due to either accumulation of acid or loss of base…PH<7.36 Alkalosis : is due to either accumulation of base or loss acid …PH>7.44 Respiratory : denote that the primary event is alveolar ventilation dysfunction Metabolic : denote that the primary event is abnormal gain or loss of NCA. Simple : consist of one primary event and its compensatory response Mixed: a combination of primary events are present e.g.. :patient with respiratory acidosis from COPD with metabolic acidosis from uncontrolled DM. or from large doses of steroids.

18. Disorders & Primary Events ↓ NCA. Or ↑ HCO3 M. alkalosis ↑ NCA. Or ↓ HCO3 M. acidosis ↓ PCO2 R. alkalosis ↑ PCO2 R. acidosis Primary events Disorders

19. Total CO2 in acid-base disturbances Total CO2 Disorders ↑ M. alkalosis ↓ M. Acidosis ↓ R. Alkalosis ↑ R. acidosis

20. Base excess (BE) It refers to the change in the concentration of buffer base (BB) [BB] = [ HCO3-]+[Protein-] +[ Hb / HbO2] = 48 mEq /L BE. Associated with abnormality in [HCO3] so it is influenced by metabolic process M. alkalosis associated with BE.> +5 M. acidosis associated with BE.< -5

21. Anion gap AG = ( [Na+] + [K+]) – ( [HCO3-] + [Cl-]) Normal AG =12 ± 4 m Eq\L why? Low of electro-neutrality

22. Low of electro-neutrality In any solution, positive charges = negative charges In serum -> [ cations ] = [ anions ], If we measured all cations + anions We measured every cations & only fraction of anions True if but

23. Examples of unmeasured anions 1. Negative charged proteins 2. In organic phosphate 3. Sulfate 4.Ions of organic acids: (…lactic-acids , keto-acids …)

24. RULE AG↑↑↑ by all metabolic-acidosis except Hyper chloremic acidosis . Why?

25. If the acid in H-H equation is HCl : HCl + NaHCO3↔ NaCl +H2CO3 the net effect will replacement of ECF. HCO3- by Cl- so Anions same why?

26. RULE AG is not ↑ in Resp. acidosis as acid is derived from H2CO3, not from NCA . AG is not ↑in Resp. acidosis As the acid is derived from H2CO3, not from NCA .

27. AG & HCO3 In simple metabolic acidosis : AG = ∆HCO3 ***By this can differentiate between simple and mixed disorders

28. Osmolar Gap Refers to the disparity between the measured and the calculated serum osmolarity . =2[Na+] + (BUN/2,8) +(glucose/18) It is good screen for toxins as circulatory toxins ↑ measured osmolarity but not the calculated

29. Compensation For Primary Acid - Base Abnormalites **It is physiologic process occuring in response to events toward normalization of PH **Corrected or compensated means that PH is returned to normal **It is important to understand the degree of expected compensation for each disturbance as deviation from prediction will indicate a mixed disorder.

30. If patient has metabolic acidosis + normal PCO2 element of Resp. acidosis as 2 nd primary event.

31. Basic mechanism for compensation Buffer of ECF . : represent the 1 st mechanism. 2. Respiratory compensation : ∆ in PH ± Effect on respiratory center 3. Carbomate ion released from bone ( predominant source of alkali neutralizing NCA.) 4. Renal compensation

32. Respiratory Acidosis It caused by any process that reduce the effectivness of alveolar ventilation.

33. Compensation Acute Respiratory Acidosis Chronic Respiratory Acidosis

34. Acute Respiratory Acidosis ***In pure acute Resp. acidosis , [HCO3-] should not exceed > 30mEq/l *** PCO2 ↑ by 10 mmHg -> ↑ HCO3- by 1 mEq /l ∆ [H+] = 0.8 ∆ PCO2

35. Chronic Respiratory Acidosis PCO2 ↑ by 10 mmHg -> ↑ HCO3 by 3.5 mEq/l ∆ [H+] = 0.3 X ∆ PCO2

36. If ↑PCO2 persist Kidneys compensate by ↑ excretion of acid primarily NH4Cl + synthesis of HCO3 ↑ HCO3 ↓ Cl-

37. Respiratory Alkalosis Caused by ↑ alveolar ventilation ↑ CO2 excretion -> ↓ PCO2

38. Acute Respiratory Alkalosis / compensation *** Acute ↓ pco2-> rapid ↓ [HCO3-] within minutes / independent of any renal compensation (Buffer system) ↓ PCO2 by 10 mmHg -> ↓ HCO3- by 2 mEq/l ∆ [H+] = 0.8 X ∆PCO2

39. Chronic Respiratory Alkalosis / compensation ↓ PCO2 by 10 mmHg ->↓HCO3- by 5 mEq/l *** [H+] = 0.17 X ∆PCO2 ∆

40. Chronic Respiratory Alkalosis Most individual with PCO2 > 20 mmHg Will have normal range of PH Even the cause is unknown Most individual with PCO2 > 20 mmHg Will have normal range of PH Even the cause is unknown

41. Metabolic Acidosis ** Produced by any process that ↓ [HCO3] either as HCO3- loss, or via retention of NCA. That cannot be excreted by lungs

42. Metabolic Acidosis / Compensation ↓ [HCO3] by 1 mEq/l ->↓ PCO2 by 1.0_1.3 mmHg Example: Patient with CRF.& [HCO3]=16 PCO2 compensation range ->29.6_32mmHg If PCO2 = 24->->coexistent Resp. Alkalosis If PCO2 = 40 24->->coexistent Resp. Acidosis

43. Metabolic Acidosis / PCO2 & PH / *** During chronic steady state PCO2 ≈ last 2 digit of the PH If PH = 7.25->PCO2≈ 25mmHg *** All these compensations are applicable only when acidosis being > 24hr.***

44. Primary respiratory events *** Rapid compensation (Buffers) Primary metabolic events Respiratory compensation is late {>24hr} due to slow penetration of H+ into CSF

45. Metabolic Alkalosis Produced by any process that ↑[HCO3] in plasma It is clinically useful to be divided into 2 types : 1. Chloride responsive 2. Chloride resistant ****** depending on urinary [ Cl- ] ****

46. Metabolic Alkalosis/ Compensation Highly variable ↑ [HCO3-] by 1 mEq/l -> ↑ PCO2 by 0.6_0.7 mmHg *** Any PCO2 exceeding 55 mmHg -> coexistence primary Resp. acidosis ***