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Chapter 4(1) Acid – Base Disorders

Chapter 4(1) Acid – Base Disorders. §1. Acid- Base balance 1.Concept of acid and base Acid: Acid is a proton donor. (HCl, NH 4 + ) HCl → H + + Cl - NH 4 + → H + + NH 3 Base : Base is a proton acceptor. (OH - , HCO 3 - , NH 3 )

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Chapter 4(1) Acid – Base Disorders

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  1. Chapter 4(1) Acid – Base Disorders §1. Acid- Base balance1.Concept of acid and base Acid: Acid is a proton donor. (HCl, NH4+) HCl → H+ + Cl- NH4+ → H+ + NH3 Base: Base is a proton acceptor. (OH-, HCO3-, NH3) OH- + H+ → H2O HCO3- + H+ → H2CO3 NH3 + H+ → NH4+

  2. 2.Origins of acid and base in the body Source of acid: 1) origins of volatile acidIt results from an end-product of oxidative metabolism namely CO2. CO2+H2O = H2CO3 Normally produced CO2 300-400 L/d or H+ 15 mol/d. 2) origins of nonvolatile acid ( fixed acid ) It comes from metabolic processes or incomplete oxidation of glucose or fats and so on. as: H2SO4, H3PO4, lactic acid, acetoacetic acid, β-hydroxybutyric acid.

  3. Sulfuric acid: Catabolism of sulfur-containing amino acids. Phosphoric acid; Catabolism of phosphoesters ,phosphoprotein ,nucleotide. Lactic acid: Incomplete oxidation of carbohydrate. Beta-hydroxybutyric acid, acetoacetic acid: Incomplete oxidation of fatty acid. Normally produced H+ 50-100 mmol/d .

  4. 3) Exogenous acid intake Salicin intoxication Hydrochloric acid

  5. Origin of bases:1) NH3: It is formed by deamination of amines, amino acid, purines and so on. 2) Eatting salt of organic acid: Sodium citratc and sodium lactate come from vegetable and fruits.

  6. 3. Regulation of acid – base balance1) Chemical buffers:Buffer system is composed by weak acid and weak acid salt. It may convert strong acid into weak acid or strong alkali into weak alkali. NaHCO3+HCl → NaCl+H2CO3 H2CO3+NaOH → H2O+NaHCO3

  7. Major buffer system in the body Carbonic acid/Bicarbonate(HCO3-/H2CO3) : • The major extracellular buffer，regulated by lungs and kidneys，effective，determining the pH of plasma. Phosphate (HPO42-/H2PO4-) : Intracellular Protein (Pr-/HPr): Plasma/Intracellular Hemoglobin (Hb-/HHb and HbO2-/HHbO2) :RBC *A buffer system cannot buffer itself. • fast / no permanence

  8. 2) Respiratory control: • Expelling more CO2 through respiration→to exclude volatile acid. • H+→chemoreceptor → excite respiratory centre → hyperventilation → exclude volatile acid • Fast / effectively / only excludes volatile acid

  9. PaCO2(40-80 mmHg)Blood-brain barrier permeable to CO2: CO2+H2OH2CO3 H++HCO3-(in cerebrospinal fluid, CSF) [H+]  Central chemoreceptor(beneath the ventral surface of the medulla oblongata)Respiratory center  Ventilation (Main) PCO280 mmHg, inhibition of respiratory center. PaO2 (30-60 mmHg) /pH  / PCO2Peripheral chemoreceptor (Carotid bodies, aortic bodies) Respiratory center  Ventilation (Minor) Pa O2  30 mmHg, inhibition of respiratory center

  10. 3) Role of kidney (exclusion of acid with conservation of base) • hydrogen ion secreted ammonium excreted by renal tubular cell bicarbonate reabsorbed • Effectively ( fixed acid may be excluded ) / slowly

  11. Role of the kidneyspowerfully, slowly#Proximal tubule: H+ secretion coupled with HCO3- reabsorption # Collecting tubule H+ secretion and excretion coupled with the addition of newHCO3-to the plasmaSecreted ammonia once the normal urinary phosphate buffers are saturated. NH3 + H+ NH4+

  12. 4) Role of tissue and cell • cell: intra and extra ions exchange across the cellular membrane buffering in the cell or titrating base in ECF • bone:Ca3(PO4)2+4H+ 3Ca2++2H2PO4 Decalcification, osteoporosis. • Effectively / but need time

  13. Acid-base balance: Acid and bases are continuously produced in the body, PH is maintained 7.35-7.45 by four regulation of the body, This condition is termed as acid-base balance.

  14. §2. Laboratory parameters of acid-base balance1. PH：pH= log [H+]=log1/ [H+] (The logarithm to the base 10 of the reciprocal of the [H+]) HCO3-(metabolic factor)pH= pKa+ log ———————————H2CO3(respiratoryfactor) = pKa + logHCO3-/α×PCO2＝ 6.1+1.3=7.4 Normal plasmapH 7.35-7.45 ( average 7.4 )

  15. 2. PaCO2( respiratory parameter ): Partial pressure of CO2dissolved in arterial plasma(The pressure is produced by CO2 dissolved in arterial plasma). Normal range: 4.39~6.25kPa(33~46mmHg) Average: 5.32kPa(40mmHg) PaCO2＞ Normal (hypoventilation) a.primary change: RAC b.secondary change: MAL with respiratory compensation PaCO2＜ Normal (hyperventilation) a.primary change: RAL b.secondary change: MAC with respiratory compensation

  16. 3. SB AB BB BE (metabolic parameter):SB: HCO3- in plasma under standard condition 22~27 mmol/LAB: HCO3- in plasma under actual condition 22~27 mmol/L Average : 24 m mol/L BB: BB = HCO3- + Pr - + Hb - 45~55 mmol/LBE: BE = ΔBB = BB-NBB -3~+3 mmol/L MAC: primary decreased MAL: primary elevated

  17. Normal condition : PaCO2＝ 5.32Kpa( 40mmHg ) AB ＝ SB ＝ 24 mmol/L ( average) AB ＞ SB → CO2 retention: RAC (primary change) MAL with respiratory compensation AB ＜ SB → CO2 expiration:RAL (primary change) MAC with respiratory compensation AB↑＝ SB↑→ MAL without respiratory compensation

  18. 4. AG( anion gap ): AG=UA(undetermined anion – UC(undetermined cation ) [HCO3- ]+[Cl- ]+UA= [Na+]+UC AG=UA-UC=[Na+]-([HCO3-]+[Cl-])=140-(24+104)=12mmol/L±2

  19. §3. Simple acid-base disorder1. Metabolic acidosis1) concept:primary disturbance [HCO3-] ↓ ; PH .AB↓ , SB↓ , BB↓ , BE ↓ ; PaCO2 ↓; AB＜SB2) clasification: Normal AG MAC High AG MAC3) pathogenesis and mechnisms:(1) lose of bases (2) gaining acids

  20. Metabolic acidosis Causes:(1) lose of bases (bicarbonate decreased) Gastrointestinal losses: diarrhea, fistulae and so on. Renal losses: proximal renal tubular acidosis and distal renal tubular acidosis (2) gaining acids (bicarbonate consumed in buffering) Lactic acidosis: tissue hypoxia, impaired oxygen utilization, severe liver dysfunction, and shockKetoacidosis: diabetic,hepatic cirrhosis, alcoholic poisoning, or starvation Renal failure: conservation of acids Exogenous acid intake: ammonium chloride, salicylate, ethylene glycol(commonly used in antifreeze), or methanol intoxication

  21. 4) Compensation: all regulation system take part in5) Effects: (1) Depression of central neural system a Elevated activities of glutamate decarboxylase →GABA ↑ b.ATP ↓ (2) Depression of heart and vessel(Ca2+ transport disorder; hyperkalemia;ATP↓): cardiac output ↓ ; cardiac arrhythmias; peripheral vasodilation.(3) Skin: warm and flashed(4) Alteration of skeleton: decacification, retarding growth and osteodystrophy6)Treatment: administration of 5%NaHCO3, sodium lactate, THAM.

  22. Respiratory acidosis1) Concept:Primary change : retention of CO2; pH . PaCO2↑; AB↑ SB↑ BB ↑ BE ↑ ; AB ＞ SB2) Classification:Acute RAC Chronic RAC

  23. 3) Causes :Disorder of external respiration - Overdosage of sedatives, narcotics,etc. Cerebrovascular accidents. Cardiopulmonary arrest Central nervous system trauma, infections Poliomyelitis Inhalation of foreign bodies Chronic obstructive pulmonary disease Asthma PneumoniaIncreased CO2 inhalation – Misoperation of mechanical ventilator Inhalation CO2 of high concentration

  24. 4) Compensation:In acute RAC:ion exchange across the membrane and buffering in cell

  25. CO2+H2O H2CO3 体细胞（somatic cell） HCO3- + H+H++A- HA K+K+

  26. Red blood cell CO2CO2+H2O H2CO3 H++Hb -HHb + HCO3- - Cl-

  27. In chronic RAC:excretion of more H+ and ammonia ion reabsorption of more HCO3- in kindneys

  28. 5) Effects: (1) Neurological effects: CO2 narcosis (2) Cardiovascular effects: arrhythmias; pulmonary artery hypertension; cardiac output decrease. (3) Mixed acid-base imbalance (RAC+MAC) (4) Inducting of hyerkalemia and hypochloremia 6) principle of treatment: improve ventilation

  29. Metabolic alkalosis1) Concept: Primary disturbance [HCO3-] ↑ ; PH . AB↑, SB↑, BB↑, BE↑; PaCO2 ↑; AB＞SB 2) Classification: Chloride – responsive MAL Chloride – resistant MAL

  30. 3) Causes and mechanism:Mechanism: a.Excessive gain of alkali (bicarbonate) b. Excessive loss of hydrogen ions, chloride or potassium ions

  31. Causes:a.Excessive gain of alkali (bicarbonate)Bicarbonate intake:treatment of MACcitrate-containing blood transfusionsParenteral solution containing lactate b.Excessive loss of hydrogen ions, chloride or potassium ionsGastrointestinal H+ loss:vomiting,gastric suctionRenal H+ loss:Aldosteronism,cushing’s syndromethiazide and loop diureticpotassium deficit c.Volume contraction DehydrationDiuretic therapy

  32. 4) Compensation: Blood buffer role limitation Respiratory regulation Ion exchange and H+ out cell to titrate bicarbonate Renal role: excluding bicarbonate and conserving H+5) Effects: (1) Hypoventilation→ PaCO2 ↑, PaO2↓ (2) Agitation of central neural system:GABA↓ → seizures(3)Increase excitability of the neuromuscle: free [Ca2+] decrease → muscle tremors (4) Mental dysfunction: O2 dissociated curve leftshift → impairing O2 release → ATP ↓. At 6-8 hs, 2,3-DPG and curve shifts back towards the right. (5) Hypokalemia→ reduced fibrillation threshold

  33. 6) Principle of treatment: a. Etiology treatment b. Replacing N.S or NH4Cl solution. c. Administration of KCl. or spironolactone if K+ and Cl- deficits are present d. Carbonic anhydrase inhibitor: acetazolamide

  34. Respiratory alkalosis 1) Concept: Primary change : H2CO3 ↓or PaCO2 ↓; pH . PaCO2↓; AB↓ SB↓ BB↓ BE↓ ; AB<SB 2) Classification: a. Acute RAL b. Chronic RAL

  35. 3) Causes and mechanisms: Mechanisms: HyperventilationCauses:a. Psychogenic hyperventilation:Hysteria b. Stimulation of respiratory center: High altitude hypooxia Salicylate toxication Blood ammonia↑(Hepatic encephalopathy) Encephalitis Brain injury Feverc. Inappropriately high ventilator settings

  36. 4) Compensation: In acute RAC: Ion exchange, H+ out of cell to titrate base in ECF In chronic RAC: Decreased excretion of H+ and NH4+ Decreased reabeorption of HCO3-5) Effects: (1) Increased excitability of the nerve and muscle (2) Mental dysfunction (3) Hypokalemia,hypochloridemia6) Principle of treatment:a. Decreased ventilation by administration of sedative. b. Application of a plastic bag to inspire more amount of CO2 gas

  37. Parameter changes of simple types Disorder Primary Change Second Response pH Metabolic acidosis HCO3-  PaCO2  pH Respiratory acidosis PaCO2 HCO3- pH Metabolic alkalosis HCO3-  PaCO2  pH Respiratory alkalosis PaCO2  HCO3-pH Compensated X：after compensation, pH still in normal. Uncompensated X： after compensation, pH still abnormal.

  38. §4. Mixed acid –base disturbanceDefinition :more than one primary acid-base disorder coexist in a patient.Double disorders 1) MAC+RAC: diabetic ketosis with pulmonary disease 2) MAL+RAL: vomiting with hyperventilation 3) MAC+RAL: uremia with high fever 4) MAL+RAC: diuretics with respiratory failure5) MAC+MAL: heart failure with hypokalemia

  39. Triple disorders : respiratory acidosis + MAC + MAL respiratory alkalosis

  40. §5. Diagnosis1. According to pathogensis establishing primary change 2. Manifestation: excitation — alkalosis inhibition — acidosis 3. According to PH PH<7.35 —acidemia — acidosis PH>7.45 — alkalemia — alkalosis PH=7.35~7.45: normal condition complete compensation mixed acid-base disturbance 4. Condition of compensation:direction；predicted compensative value；compensative limit 5. Estabolilshed triple disorders: utilized AG

  41. The patient was suffered from salicylate intoxication. His blood-gas parameters (lab. Value): PH = 7.45 PaCO2 = 2.6 kpa (20mmHg) HCO3- =13mmol/L .what acid-base disorders presented in this patient ? Causes: salicylate intoxication. Primary change is HCO3- decreased. HCO3- =13mmol/L<24mmol/L MACpH:pH=7.45=N compensated MAC mixed acid-base imbalance (MAC+RAL) Compensatory condition: PaCO2 =2.6kpa(20mmHg)<5.32kpa(40mmHg)Calculate: 1.2×ΔHCO3±2=1.2 ×(24-13) ±2=13.2 ±2=11.2-15.2Predicted PaCO2 value=40 - (11.2or15.2)=24.8-28.8mmHgActual PaCO2=20mmHg < predicted PaCO2=24.8 –28.8mmHgdiagnosis: MAC+RAL

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