1. Acid-base disturbance
光子的粒子就是中子与质子化合出现转换产生变化的，转化人类分子的设计就是化合中子与质子。
Zhao Mingyao
BMC.ZZU

2. Acid? Base?
pH in arterial blood 7.35~7.45
[H+]

3. H+ concentration in body fluid
ECF H+ mol/L pH
Arterial blood × ± 0.05
Venous blood ×
Interstitial fluid ×
Intracellular fluid ×
to 4.0 ×
Gastric fluid ~1.8 (3.0)
Pancrea fluid ~ 8.4

4. Metabolic processes generate acids
Cells
H+ ~ 100 nmol/L (pH ~ 7) H+
Artery H+
H+ ~ 36 nmol/L
pH~7.4 H+ H+
H+ ~ 44 nmol/L
pH~7.36
Capillary
Vein

5. Section 1 Acid-base biochemistry

6. 1. Generation of Acid-Base
(1) Sources of acid
1）volatile acid
CO2 + H2O  H2CO3  H+ + HCO3-
( H+ 15 mol /d)
2）fixed acid (non-volatile acid)
phosphoric, sulfuric, lactic, ketone bodies etc.
H – 0.10 mol /d

7. Sources of acid in body

8. (2) Sources of bases 1）products of metabolism
（small amounts）Such as ammonia (NH3)
2）dietary intake（vegetables and fruits）
sodium citrate
*acids production >>bases, in commen
*renal reabsorption

9. renal
reabsorption
pH 7.35~7.45 in Arterial blood

10. 2. Henderson-Hasselbalch Equation
[HCO3-]
pH=pKa+lg
[H2CO3]
=pKa+lg 20 1
= lg HCO3- / 0.03 × PCO2
= lg 24 / 1.2 = 7.4
= = 7.4
pH ~7.45

11. [HCO3-]
pH ∝
[H2CO3]

12. [HCO3-] pH ∝ [H2CO3] 20 ＝ 1 20 ≠ 1 ( eg . 24/1.2 or 40/2 or 10/0.5)
Strong acid pulse pH ∝
Strong base pulse 20 ＝
( eg . 24/1.2 or 40/2 or 10/0.5) 1 20 ≠
( ＜20/1 or ＞20/1 ) 1

13. Henderson-Hasselbalch Equation
Compensatory ~: pH normal, but ? change
Decompensatory ~: pH, HCO3 -, H2CO3 change
[HCO3-] pH ∝
[H2CO3]

14. Relationship between Henderson-Hasselbalch Equation and pH
fulcrum
Relationship between Henderson-Hasselbalch Equation and pH

15. Section 2 Regulation of acid-base
in body fluid

16. What happens in its body
iv lactic acid
iv bicarbonate ? ? ? ?
acidosis
alkalosis
death
death
【H+】
7.8 pH
6.8

17. [H+] Why does body keep acid-base balance of body fluid ? Cellular
signal
→ Enzyme ATP cell
Ion distribution→ electrical action

18. body maintain humoral acid-base balance by
1. blood buffer system
2. lung
3. kidney
4. cell

19. 1. Blood buffer system HCO3- / H2CO3 Hb- / HHb Pro- / HPro A-/HA
HPO42- / H2PO4-
A-/HA
Buffer system can bind and release H+
Dissociated buffer + H H undissociated buffer

20. HCO3- / H2CO3 determines the pH of blood
pH = pK + lg HCO3- / H2CO3
• HCO3- / H2CO3 is the major extracellular
buffer 53%
• H2CO3 regulated by lung
• HCO3- regulated by kidney

21. 2. Pulmonary regulation
pH∝
[HCO3-]
[H2CO3]

22. CNS (carbon dioxide narcosis二氧化碳麻醉 ) 高浓度CO2对中枢神 经系统产生的抑制作用 。 Pulmonary
regulation
Central control
PaCO2
CNS
chemoreceptor
+ +
Peripheral
chemoreceptor
(carbon dioxide narcosis二氧化碳麻醉 )
高浓度CO2对中枢神
经系统产生的抑制作用 。
respiration
PaO2、pH、PaCO2
in the carotid
and aortic bodies
peripheral regulation

23. excreting H+ & keeping base
3. Renal regulation
excreting H+ & keeping base
(1) bicarbonate reabsorption (NaHCO3)
(2) phosphate acidification
维持血浆浓度Mechanisms of fixed plasma
(排泄固定酸)
(3) ammonia excretion

24. (1)Reabsorption of HCO3- in different segments
of renal tubule

25. Bicarbonate reabsorption in proximal tubules
Reabsorption of HCO3- coupled with
H+ excretion
Na+ CA

26. (2) Phosphate acidification in distal tubules
Regeneration of HCO3- coupled with the buffering
of secreted H+ by filtered Na2HPO4
ATP
Cl-

27. (3) Ammonia excretion in proximal tubular cells
Glutamine Tubular
lumen
glutaminase
NH NH3
-ketoglutaric acid
NH NH4+
H2CO Na+
Na+
HCO H H+
Regeneration of HCO3- coupled with buffering of H+ by NH3
ATP

29. 4. cellular buffer H+-K+ exchange between intra- and extra- cell
Cl--HCO-3 exchange between intra- and extra-RBC or/ gastric cell

30. Section 3 Laboratory tests
Parameters of acid-base representing pH
PaCO2
HCO3- ( SB, BE, BB )
Annion gap

31. 1. pH in normal level (1) true normal (2) compensatory ~
(3) mixed ~ with opposite effect

33. Weak tolerance to alkalosispH
6.8
7.8
death
acidosis
alkalosis
death
【H+】
160 40
16 nmol/L

34. 2. Partial pressure of CO2, PaCO2
tension produced by CO2
dissolved physically in plasma
Normal: mmHg (35~45)
[H2CO3]: × 0.03 = 1.2mmol/L
动脉血二氧化碳分压() definition:
PaCO2↑— Res Acidosis or ? PaCO2 ↓—Res alkalosis or ?

35. 3. HCO3- normal: 24 mmol/L (22~27) SB and AB BB BE
Primary and secondary change ?

36. UA: Undetermined anion UC: Undetermined cation
4. Anion gap (AG)
AG = UA – UC
UA: Undetermined anion
UC: Undetermined cation
血Na+浓度减去血Cl－和HCO3－的
浓度，等于血浆中未测定阴离子(UA)
与未测定阳离子(UC)的差值

37. Distinguishing metabolic acidosis
AG = UA - UC
Cl-
(104)
Na+
(140)
Na++ UC = Cl- + HCO3- + UA
AG = Na+ - Cl- - HCO = = 12 (mmol/L)
HCO3-
(24) AG UA
(23) UC
(11)
Normal 10～14mmol/L
Distinguishing metabolic acidosis

38. An elevated Anion Gap always strongly suggests a Metabolic Acidosis
If AG is then high chance (67%) of metabolic acidosis
If AG is > 30 then a metabolic acidosis is definitely present

39. Summary of indexes 1. pH 2. Metabolic factor: HCO3- SB, BB, BE, AG
3. Respiratory factor：PaCO2

40. Section 4 Simple acid-base disorders
Concept
Compensation

41. Classification of ~ acidosis alkalosis pH respiratory [HCO3-]↓
PaCO2↑
PaCO2↓
metabolic
Classification of ~

42. Analysis of simple acid-base disorder
=7.4?
Analysis of simple acid-base disorder

43. Part 1 Metabolic acidosis
Concept: [HCO3-]p ↓ primarily

44. Changes of laboratory test
Primary: pH ? HCO3- ↓
Secondary: PaCO2 ↓ [K＋]b↑
实验室常用指标的变化()

45. Met acidosis with Normal AG
Classification
Met acidosis with High AG
Met acidosis with Normal AG

46. Comparison between Met acidosis with High AG and normal AG
Na+
Cl- UA
HCO3- AG
normal UC
Met acidosis
with High AG
Na+
Cl- UA
HCO3- AG UC
Na+
Cl- UA
HCO3-
AG（-） UC
Met acidosis with
normal AG
Comparison between Met acidosis with High AG and normal AG

47. 1. Cause and mechanisms
(1) fixed acid production↑: lactic acidosis, ketoacidosis, excess acetylsalicylic acid , drugs yielding hydrochloride acid
(2) fixed acid removing↓: RTA, RF
(3) HCO3- loss↑: diarrhea , intestinal suction
(4) hyperkalemia
(5) hyperchloremia

48. 2. Compensation of body [HCO3-] pH∝ [H2CO3] (1) Blood buffer system
(2) lung
(3) kidney
(4) cell
pH∝
[HCO3-]
[H2CO3]
(1)plasma buffer
H++ HCO3-H2CO3

49. 3.Effects on the body (1) Cardiovascular system
Inhibiting myocardial contraction
Arrythmia
对机体的影响()心血管系统
抑制心肌收缩力
Responsibility↓of vessel to
catecholamine

50. (2) Central nervous system
Cerebral energy production
GABA 
中枢神经系统()
~ decarboxylase (+)
Glutamate
GABA

51. (3) Hyperkalemia
低钾血症 (血红蛋白解离曲线左移) () 51

52. 4. Principle of prevention & treatment
1.Treatment of primary disease
2.Supplement of base
NaHCO3
THAM( Tris, Trishydroxymethyl amino methane, C4H11NO3 )
lactic sodium
防治的病理生理基础()
治疗原发病 ()应用碱性药物
3.Correcting and preventing water, electrolytes disorders

53. Part 2 Respiratory acidosis
Concept: [H2CO3 ]p↑primarily

54. Changes of laboratory test
Primary: pH ? PaCO2 ↑
Secondary: HCO3- ↑ [K＋]p ↑
实验室常用指标的变化()

55. 1. Causes and mechanisms Excreting CO2 ↓ Inhaling excessive CO2
原因与机制 ()

56. 2. Compensation of respiratory acidosis
*Blood
*Lung
*Kidney
*cell
[H2CO3 ]p↑
呼吸性酸中毒的代偿调节()

57. Changes of laboratory test
Acute: pH PaCO2 HCO PaCO mmHg HCO3- compensatory ↑ 1 mmol/L
Chronic: pH PaCO2 HCO PaCO mmHg HCO3- compensatory↑ 3.5 mmol/L
实验室常用指标的变化 ()
Cl- ？
K+ ？

58. 3. Effect of ~ CNS Acidosis Cerebral blood flow↑
Similar to Met Acidosis, but obvious sign of CNS
CNS Acidosis
Cerebral blood flow↑
对机体的影响 ()
With hypoxia in same time

59. 4. Principle of prevention & treatment
(1)improving alveolar ventilation
(2)supplement of base
防治的病理生理()基础增加肺泡通气量 () (应用碱性药物)

60. Part 3 Metabolic alkalosis
Concept: [HCO3-]p ↑primarily
13.Which causes result in

61. Changes of laboratory test
Primary: pH ? HCO3- ↑
Secondary: PaCO2 ↑ [K＋]b ↓
实验室常用指标的变化()

62. 1.Causes and mechanisms Base intake ↑ H+ loss ↑ Hypokalemia
hypochloremia
Volume contraction
13.Which causes result in Treatment with bicarbonate
Banked blood with more lactate citrate

63. Classification saline-responsive alkalosis
---- induced by hypochloremia
saline-resistant alkalosis
---- induced by nonhypochloremia
原因与机制 ()消化道失H＋ ()

64. 2. Compensation [HCO3-] pH∝ [H2CO3]
(1) Blood buffer system ( limited )
(2) lung
(3) kidney
(4) cell
[HCO3-]
(1)Plasma buffer
HCO3-+HPr H2CO3+Pr- ( limited )
机体的代偿调节 ()
pH∝
[H2CO3]

65. 对机体的影响 γ -氨基丁酸转氨酶aminotransferase; transaminase ()
3. Effects
(1) CNS ？
GABA
~ decarboxylae (-)
Glutamate
GABA  +
Hypoxia
对机体的影响 γ -氨基丁酸转氨酶aminotransferase; transaminase ()
中枢神经系统 ()
succinate
semialdehyde
GABA transaminase (+)

66. (2)Neuromuscular excitability
mechanism:
pH，Free [Ca2+]b↓
CNS + +
(Carpopedal Spasm)
(神经肌肉应激性升高)手足搐搦

67. 低钾血症 (血红蛋白解离曲线左移) (3) left-shift of oxyhemeglobin dissociation curve()

68. (4) Hypokalemia
低钾血症 (血红蛋白解离曲线左移) ()

69. 4. Principle of prevention & treatment
(1)Treatment of primary disease
(2)Normal saline
 saline-responsive alkalosis
saline-resistant alkalosis
CA inhibitor
ADS inhibitor
(3)Acid-containing drug
防治的病理生理基础()治疗原发病

70. Part 4 Rrespiratory alkalosis
[H2CO3]p ↓primarily
14.Which causes result in

71. Changes of laboratory test
Primary: pH ? PaCO2 ↓
Secondary: HCO3- ↓
[K＋]p ↓
[Cl-]p ？
实验室常用指标的变化()

72. 1. Causes and mechanisms Excreting excessive CO2 (1) Hypotonic hypoxia
(2) Disease of CNS
(3) Psychological factors
(4) Hypermetabolism
(5) Drugs
原因与(精神因素)
机制 () (高代谢)

73. 2. Compensation of respiratory alkalosis
*Blood
*Lung
*Kidney
*cell ？
[H2CO3 ]p↓
呼吸性碱中毒的代偿调节()

74. Compensatory changes
Acute: PaCO2 ↓ 10 mmHg HCO3- compensatory ↓ 2 mmol/L
Chronic: PaCO2 ↓ 10 mmHg HCO3- compensatory ↓ 4 mmol/L
实验室常用指标的变化 ()

75. 3. Effect of ~ Similar to Met Alkalosis PaCO2↓ cerebral blood flow ↓
对机体的影响 脑血流量()
Rapid and obvious

76. 4.Principle of prevention & treatment
1.treatment of primary disease
2. inhaling CO2 (Paper mask or 5% CO2 )
防治的病理生理基础()治疗原发病()

78. Section 5 Mixed acid-base disorders

79. Mixed acid-base disorders
Double acid base disorders
Metabolic Metabolic
acidosis alkalosis
Respiratory Respiratory

80. Double acid-base disorders and pH change
Type
HCO3-
/ H2CO3
20/1 pH
Met acid+
Res acid
↓/↑ ﹤ ？
Res alko
↓/ ↓ = ﹥
Met alko
？/ ？

81. Triple Acid-base disturbances
 R acidosis + M acidosis + M alkalosis  R alkalosis + M acidosis + M alkalosis
Ternary (三重性)

82. Summery
Metabolic acidosis is induced by primary decrease of HCO-3 owing to increased production or retention of fixed acides or HCO-3 loss.
Metabolic alkalosis is induced by primary increase of HCO-3 due to H+ loss.
Respiratory acidosis or alkalosis is induced by primary increase or decrease of CO2 caused by hypoventilation or hyperventilation.

83. Acidosis depresses activity of CNS and myocardial contractility, and induces cardiac arrhythmia and vasodilation.
Alkalosis results in dysfunction of CNS and cramping.
Different kinds of acid-base disorders may coexist in patients.

84. You let life lost forever ___ ?
Scientific poem
H+ ion in body life
H+ ion
You, we love
You, we also hate
So a little change
You let life lost forever
___ ?

86. End
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