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Acid-Base Balance

This article explains the pH stabilization in blood through bicarbonate buffering, defines acidosis and alkalosis, and discusses the roles of CO2, HCO3-, lungs, and kidneys in maintaining acid-base balance. It also explores the effects of CO2 on blood pH and the impact of hypoventilation and hyperventilation on acid-base balance.

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Acid-Base Balance

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  1. Acid-Base Balance Jianzhong Sheng MD, PhD Department of Pathophysiology School of Medicine Zhejiang University

  2. Objectives • Explain how the pH of the blood is stabilized by bicarb buffer and define the terms acidosis and alkalosis. • Explain how the acid-base balance of the blood is affected by CO2 and HCO3-, and describe the roles of the lungs and kidneys in maintaining acid-base balance. • Explain how CO2 affects blood pH, and hypoventilation and hyperventilation affect acid-base balance. • Explain how the interaction between plasma K+ and H+ concentrations affects the tubular secretion of these.

  3. Normal Acid-Base Balance • Normal pH 7.35-7.45 • Narrow normal range • Compatible with life 6.8 - 8.0 pH 6.8 7.35 7.45 7.8 death death acidosis alkalosis 【H+】 160 40 16 nmol/L

  4. Structure of AQP1 Hg++ inhibitory site

  5. What are acidosis and alkalosis • Normal pH: 7.40 (7.35-7.45) • Acidosis: pH<7.35; Alkalosis: pH>7.45 • Simple types of acidosis: Metabolic acidosis and Respiratory acidosis • Simple types of alkalosis: Metabolic alkalosis and Respiratory alkalosis • Mixed types of acid-base disorders

  6. pH • pH of blood is 7.35 to 7.45 • pH = 6.1 + log [HCO3-] 0.03 x Pco2

  7. Types of Acids in the Body • Volatile acids: • Can leave solution and enter the atmosphere. • H2CO3 (carbonic acid). • Pco2 is most important factor in pH of body tissues.

  8. Types of Acids in the Body • Fixed Acids: • Acids that do not leave solution. • Sulfuric and phosphoric acid. • Catabolism of amino acids, nucleic acids, and phospholipids.

  9. Types of Acids in the Body • Organic Acids: • Byproducts of aerobic metabolism, during anaerobic metabolism and during starvation, diabetes. • Lactic acid, ketones.

  10. Types of Acids in the Body • Organic Acids: • Byproducts of aerobic metabolism, during anaerobic metabolism and during starvation, diabetes. • Lactic acid, ketones.

  11. Chemical Buffers • Act within fraction of a second. • Protein. • HCO3-. • Phosphate.

  12. Proteins • COOH or NH2. • Largest pool of buffers in the body. • pk. close to pH in plasma. • Albumin, globulins such as Hb.

  13. HCO3- • pk. = 6.1. • Present in large quantities. • Open system. • Respiratory and renal systems act on this buffer system. • Most important ECF buffer.

  14. HCO3- Limitations • Cannot protect ECF from respiratory problems. • Cannot protect ECF from elevated or decreased CO2. • Limited by availability of HCO3-.

  15. Phosphates • pk. = 6.8. • Low concentration in ECF, better buffer in ICF, kidneys, and bone.

  16. Respiratory System • 2nd line of defense. • Acts within min. -maximal in 12-24 hrs. • H2CO3 produced converted to CO2, and excreted by the lungs. • Alveolar ventilation also increases as pH decreases (rate and depth). • Coarse , CANNOT eliminate fixed acid.

  17. Urinary Buffers • Nephron cannot produce urine at pH < 4.5. • IN order to excrete more H+, the acid must be buffered. • H+ secreted into the urine tubule and combines with HPO42- or NH3. • HPO42- + H+ H2PO4- • NH3 + H+ NH4+

  18. Renal Acid-Base Regulation • Kidneys help regulate blood pH by excreting H+ and reabsorbing HC03-. • Most of the H+ secretion occurs across the walls of the PCT in exchange for Na+. • Antiport mechanism. • Moves Na+ and H+ in opposite directions. • Normal urine normally is slightly acidic because the kidneys reabsorb almost all HC03- and excrete H+. • Returns blood pH back to normal range.

  19. Reabsorption of HCO3- • Apical membranes of tubule cells are impermeable to HCO3-. • Reabsorption is indirect. • When urine is acidic, HCO3- combines with H+ to form H2CO3-, which is catalyzed by ca located in the apical cell membrane of PCT(proximal convoluted tubule). • As [CO2] increases in the filtrate, CO2 diffuses into tubule cell and forms H2CO3. • H2CO3 dissociates to HCO3- and H+. • HCO3- generated within tubule cell diffuses into peritubular capillary.

  20. Acidification of Urine

  21. Na++ HCO3- H+ H++ HCO3- H+ H2CO3 CA H2O + CO2 H2CO3 HPO42- NH3 CA NH4 + H2PO4- CO2 +H2O

  22. Urinary Buffers • Nephron cannot produce urine at pH< 4.5. • In order to excrete more H+, the acid must be buffered. • H+ secreted into the urine tubule and combines with HPO42- or NH3. • HPO42- + H+ H2PO4- • NH3 + H+ NH4+

  23. Anion Gap • The difference between [Na+] and the sum of [HC03-] and [Cl-]. • [Na+] – ([HC03-] + [Cl-]) = • 140 - (24 + 105) = 11 • Normal = 12 ± 2 • Clinicians use the anion gap to identify the cause of metabolic acidosis.

  24. Law of electroneutrality: Blood plasma contains an = number of + and – charges. The major cation is Na+. Minor cations are K+, Ca2+ , Mg2+. The major anions are HC03- and Cl-. (Routinely measured.) Minor anions include albumin, phosphate, sulfate (called unmeasured anions). Organic acid anions include lactate and acetoacetate,. Anion Gap

  25. In metabolic acidosis, the strong acid releases protons that are buffered primarily by [HC03-]. This causes plasma [HC03-] to decrease, shrinking the [HC03-] on the ionogram. Anions that remain from the strong acid, are added to the plasma. If lactic acid is added, the [lactate] rises. Increasing the total [unmeasured anions]. If HCl is added, the [Cl-] rises. Decreasing the [HC03-]. Anion Gap

  26. Anion Gap in Metabolic Acidosis • Salicylates raise the gap to 20. • Renal failure raises gap to 25. • Diabetic ketoacidosis raises the gap to 35-40. • Lactic acidosis raises the gap to > 35 (>50). • Largest gaps are caused by ketoacidosis and lactic acidosis.

  27. Simple Acid-Base Disturbance 1.Metabolic acidosis Concept: the primary disturbance is a decrease of [HCO-3] in the arterial plasma 1) Cause and pathogenesis lactic acidosis: hypoxia, diabetes liver disease ketoacidosis: diabetes, starvation ①Metabolic acidosis in severe renal failure: fixed acids increased AG salicylic acid acid poisoning: intake food

  28. diarrhea; GI: intestinal suction (loss of intestinal fistula HCO-3) biliary fistula ② Metabolic acidosis in early renal failure: normal AG NH3 secretion H+ secretion Renal tubular acidosis: H+ secretion Kidney: depressant of C.A. (loss of acetazolamide HCO-3) intake of Cl- NaCl, NH4Cl Hyperkalemia

  29. 2)Compensatory regulation ① Buffer: ② Respiratory compensation ③ Cellular compensation ④ Renal compensation [H+] : C.A. H+ secretion NH3 secretion [HCO-3] / [H2CO3] = 20:1 compensation acidosis [HCO-3] / [H2CO3] < 20:1 decompensation acidosis (SB AB BB BE PaCO2 AB < SB)

  30. Discussion of case 1 Method: 1. pH 2. primary factor and parameter 3. secondary factor and compensation 4. expected range of compensation №1: patient, female, 46, chronic pyelitis pH 7.32 (Normal: 7.35-7.45) PaCO2 28mmHg (Normal: 35-45mmHg) SB 13.6mmol/L (Normal: 22-27mmol/L) BE -15.3mmol/L(Normal: -3.0-+3.0mmol/L)

  31. 3)Effect on body ① Cardiovascular system hyperkalemia arrhythmia [H+] contractility peripheral resistance ② Central nervous system [H+] ATP , γ-amino butyric acid (somnolence, coma) 4) Principles of treatment ① Correction of underlying disorders; ② Administration of NaHCO3; ③ Correction of water-electrolyte disturbances.

  32. Summary of Metabolic Acidosis • Gain of fixed acid or loss of HCO3-. • Plasma HCO3- decreases. • PCO2 decreases. • pH decreases.

  33. 2. Respiratory acidosis Concept: The primary disturbance is an elevation in plasma [H2CO3] 1) Cause and pathogenesis Barbital depression of CNS head injury ①CO2 breathe paralysis of respiratory muscles out disease of airway or lung chest injury ② Inhalation of CO2

  34. 2) Compensation Buffer: Hb-/HHb Cells: exchange of H+ and K+ Kidney: secretion of H+ and NH3 (PaCO2 SB AB BB BE AB＞SB) 3) Effect on body ① CNS CO2 celebral vascular dilation, intracranial pressureheadache、fatigue CO2 narcosis respiration ② Cardiovascular system 4) Principles of treatment improve ventilation. Do not addNaHCO3

  35. №2: Patient, male, 45, chronic bronchitis pH 7.26 (Normal: 7.35-7.45) PaCO2 60mmHg (Normal: 35-45mmHg) BB 46.2mmol/L (Normal: 45-55mmol/L) SB 22mmol/L (Normal: 22-27mmol/L) BE -7.5mmol/L (Normal: -3.0-+3.0mmol/L) after treatment pH 7.34 PaCO2 70mmHg BB 58mmol/L BE 5.5mmol/L

  36. Respiratory Acidosis • PCO2 increases. • Plasma HCO3- increases. • pH decreases.

  37. 3. Metabolic alkalosis Concept: the primary disturbance is an increase of [HCO-3] in the arterial plasma 1) Causes and pathogenesis

  38. digestive tract vomiting; gastric suction(loss of HCl) ① loss diuretics distal flow rate of H+ (furosemide) blood volume Ald hyperaldosteronism H+-Na+exchange kidney H+-K+exchange between hypokalemia intra- and extra-cell renal secretion of H+ hypochloremia renal secretion of H+ ②intake NaHCO3 of base transfusion of banked blood (citrate)

  39. Blood vessel Gastric fluid loss and AB balance Esophagus Stomach Cl - Cl - Cl - H2CO3 HCO3- H+ H+ HCO3- H+ H2CO3 H+ HCO3- HCO3- Na+ Na+ Na+ Pancreas Duodenum

  40. 2)Compensation of the body ①respiration compensation are limited (hypoxia) ②cells compensation hypokalemia ③kidney pH inhibition of carbonic anhydrase (C.A.) secretion of H+ (SB AB BB BE PaCO2 AB＞SB)

  41. 3) Effects on body inhibition of glutamate decarboxylase ①CNS γ-amino butyric acid dysphoria insanity pH brain-vessel dizziness contraction brain delirium O2dissociation hypoxia Coma curve shifting to left ②neuromuscle pH free Ca2+ tic ③ hypokalemia arrhythmia

  42. 4)Principles of treatment loss of H+ digestive tract diuretic ; hypokalemia 0.9%NaCl; KCl hyperaldosteronism antisterone; diamox(乙酰唑胺)

  43. Metabolic Alkalosis • Loss of fixed acid or gain of HCO3-. • Plasma HCO3- increases. • PCO2 increases. • pH increases.

  44. 4.Respiratory alkalosis Concept: the primary disturbance is decrease of [H2CO3] in plasma 1)cause and pathogenesis hypotonic hypoxia pneumonia hyperventilation hysteria, fever, [NH3] hyperthyroidism misoperation of ventilator

  45. respiration (slight inhibition) 2)Compensation cells (exchange of H+-K+) kidney secretion of H+ (PaCO2 ; SB AB BB BE ; AB＜SB) 3)Effects on body It is as same as metabolic alkalosis. dizziness and convulsion are happened easily 4) Principles of treatment inhalation of 5%CO2

  46. Mixed acid-base disturbance 1.Dual acid-base disturbance 1) metabolic acidosis plus respiratory acidosis heart beat [HCO-3] respiration PaCO2 2) metabolic alkalosis plus respiratory alkalosis hepatic NH3 PaCO2 failure diuretic [HCO-3] 3) respiratory acidosis plus metabolic alkalosis pulmonary heart disease diuretic pH ± stop character pH character pH

  47. 4) respiratory alkalosis plus metabolic acidosis infective shock fever pH ± 5) metabolic acidosis plus metabolic alkalosis ketoacidosis(diabetes) vomiting pH ± 2.triple acid-base disturbance 1)respiratory acidosis; metabolic acidosis and alkalosis pulmonary heart disease; vomiting 2)respiratory alkalosis; metabolic acidosis and metabolic alkalosis fever; vomiting; diarrhea (food poisoning)

  48. №3. Patient, male, 47, purulent appendicitis. He was treated with abdominal suction and persistent gastrointestinal decompression after operation. pH 7.56 (Normal: 35-45mmHg) PaCO2 50mmHg (Normal: 35-45mmol/L) SB 34mmol/L (Normal: 22-27mmol/L) BE 10mmol/L (Normal: -3.0-+3.0mmol/L) K+ 3.2mmol/L (Normal: 3.5-5.5mmol/L) Cl- 105mmol/L(Normal: 103mmol/L)

  49. Respiratory Alkalosis • PCO2 decreases. • Plasma HCO3- decreases. • pH increases.

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