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1、Chapter 4 Acid-base balance and acid-base disorders internal environment homeostasis Water balance homeostasishomeostasis acid-base balanceacid-base balance electrolyte balance electrolyte balance 1. Acid-Base Balance lAcid-base Biochemistry lRegulation of pH lLaboratory Tests 2. Simple Acid-base Di
2、sorders lMetabolic Acidosis lRespiratory Acidosis lMetabolic Alkalosis lRespiratory Alkalosis 3. Mixed Acid-base Disturbance Contents Part I: Acid-base balance and its regulation lThe basic meaning of acid-base balance is the stable H+ in the body fluid. I、Concept of acid and base acid : An acid is
3、a H+ donor, when it is dissolved in water. After the loss of H+, it becomes a base. HA (acid) H+ + A(base) H2CO3 H+ +HCO3 H2SO4, H3PO4 base: A base is a H+ acceptor, when it is dissolved in water. After the combining of H+, it becomes an acid A(base)+ H+ HA (acid) HCO3 +H+ H2CO3 OH-, HCO3-, SO42-, H
4、PO42-, NH3 (I) Source of acid v volatile acid v fixed acid II、Sources of acid and base The main origin of acid and base is the intracellular metabolism (catabolism of protein, carbohydrate and fat). daily production :300-400L/d Excretion:lung v 1.volatile acid H2CO3 CO2 H2OH2CO3 CA metabolism of pro
5、tein, carbohydrate and fat H+ + HCO3- Reabsorption in kidney RBC、kidney tubulesepithelium 、alveolar epithelial cell 、gastric mucosa 2. unvolatile acid (fixed acid) : (50-100mmol/d) Uric acid, phosphoric acid (H3PO4) and sulfuric acid (H2SO4) are the products in the metabolic process of proteins and
6、nuclear acids. Lactic acid and ketonic bodies (-hydroxybutyric acid and acetoacetic acid) can be formed from the metabolic process of carbohydrate and fat as intermediate products, when the oxygen supply is not sufficiency. Exogenous acid(food and drug): Excretion through kidney (II) Sources of base
7、 Origin of bases lEndogenous: deaminationNH3 Less than acid production lExogenous input: vegetables, and fruits III、 Regulation of acid-base balance Henderson-Hasselbalch Equation Acid-base balance is mainly the balance between production and loss of acid and base. = 6.1 +1.3 = 7.4= 6.1 +1.3 = 7.4 H
8、+ BufferRespiratoryRenal ECFICF 13d) Neutralize H+ paCO2 eH+ (b) H+-K+ ATPase Urinary acidification (H2PO4-NH4+) base membrane: Cl- /HCO3- exchange 3. secretion of NH3/NH4+ in proximal tubule 4. competitive inhibition between K+-Na+ exchange and H+-Na+ in distal tubule K+-Na+ exchange: secrete K+, r
9、eabsorb Na+, H+-Na+ exchange:secrete H+,reabsorb Na+ acidosis, H+-Na+ exchange K+-Na+ exchangehyperkalemia。 (IV) Cellular regulation (a) H+-K+ exchange (b) Cl- - HCO3- exchange (c) Utilizing of bone salt (d) Synthesis of urea from NH3 1. H+-K+ exchange 2. Cl- - HCO3- exchange When CO2 in ECF (serum)
10、 is increased, CO2 will move into the cells, CO2 combines H2O to form carbonic acid, then H2 CO3 dissociates to form H+ and HCO3 , the HCO3 moves out of the RBC, for neutrality, Cl moves into the cells. 3.Utilizing of bone salt In chronic metabolic acidosis, bone salt, Ca3(PO4)2, is also utilized as
11、 a buffer base, but the expense is decalcification of bone and osteoporosis (loose and soft bone). Ca3(PO4)2 + 4H+ 3 Ca2+ + 2 H2PO4 It is not a good way of regulating acid-base balance by utilization of bone salt. 4.Synthesis of urea from NH3 in liver cells Source Buffer system Respiratory Renal Cel
12、lular Part II laboratory tests of acid-base disturbances 1. pH pH is the negative logarithm (-log) of H+ in a solution. H+=40nmol/L (pH=7.4) The normal range in artery blood =7.357.45 (7.41) The survival range of pH=6.87.8 According to the Henderson-Hasselbalch equation: 24 HCO3 metabolic factor pH
13、=6.1+ log - 1.2 H2CO3 respiratory factors The primary changes determines the nature of the acid-base imbalance. The purpose of secondary change is to restore the pH. According to the pH: l compensatory acid-base disturbances l decompensatory acid-base disturbances Clinical significance of PH (antico
14、agulant artery blood, insulation of air) A normal range of pH may represent three different situations: acid-base balance; compensatory acidosis or alkalosis; a mixed decompensatory acidosis and decompensatory alkalosis. Clinical significance pH7.45 decompensatory alkalosis (alkalemia) 2.PaCO2 (part
15、ial pressure of carbon dioxide in arterial blood) CO2 in blood: (a) 23% HbCO2 in RBC (b) 70% HCO3- in plasma (c) 7% CO2 molecule in plasma CO2 is determined by the rate of CO2 production and the rate of CO2 elimination. PaCO2 is the tension of CO2 caused by CO2 molecule movement. The normal range =
16、3346(40) mmHg (4.396.25 kPa). The capability of normal lung to eliminate CO2 is very good. CO2 retention will not occur with normal ventilation. Generally speaking, the PaCO2 is determined mainly by the respiration, so the PaCO2 is called the “respiratory factor”. Higher PaCO2 is due to the inhibiti
17、on of respiration. Lower PaCO2 is due to overventilation. PaCO2 Significance PaCO246mmHg Primary increase: respiratory acidosis Secodary increase: metabolic alkalosis (compensated by lung) PaCO2SB (CO2 retention), the reason must be the effect of respiratory factor, which indicates respiratory acido
18、sis or metabolic alkalosis compensated by lung. If AB value predicted: with respiratory acidosis Value measured value predicted: with metabolic alkalosis Value measured 80 mmHg 6. treatment priciples (a) Treat the primary diseases which cause respiratory acidosis. (antibiotic, antispastic drugs) (b)
19、 Improve properly the ventilation. (c) Prevent from (respiratory alkalosis) over-ventilation during artificial respiration. (d) Be careful to alkaline drug(NaHCO3) THAM III、 Metabolic alkalosis Characterized by a primarily elevation in plasma HCO3- concentration and a high pH. 1.concept 2.Classifica
20、tion According to the therapeutic effect of 0.9% NaCl, (A) saline-responsive alkalosis (B) saline-resistant alkalosis 3. Pathogenesis (1) saline-responsive alkalosis (a) Increased loss of H+ (b) More administration of HCO3 or precursors of bicarbonate (a) Increased loss of H+ a) from stomach There i
21、s a lot of H+ in the gastric juice. Vomiting and gastric suction will lose H+ HCO3- cl- is lost through gastric juice hypochloremic alkalosis HCO3- is absorbed into blood in stomach, then to intestinal juice to neutralize H+. Hypokalemia alkalosis Effective blood volumedecrease secondary aldosterone
22、 increase Some diuretics (e.g. furosemide) can inhibit the reabsorption of Cl and Na+ in loop, more Na+ is reabsorpted with HCO3 (without Cl ) in distal tubules; renal fluid folw rate increase b) Increased loss H+ from kidneys (b) More administration of HCO3 or precursors of bicarbonate a) Patients
23、with gastric ulcer may be orally given excessive NaHCO3 to neutralize gastric juice . b)Sharp correction of acidosis by excessive alkali administration can lead to metabolic alkalosis. c) Transfusion of anticoagulant blood with sodium citrate citrate. . (2) Chloride-resistant type Primary hyperaldos
24、teronism Secondary hyperaldosteronism caused by: hypovolemia Cushings syndrome severe hypokalemia:Paradoxical acid urine 4.Compensation of metabolic alkalosis The compensation of metabolic alkalosis is the opposite direction of the compensation in metabolic acidosis. (1) :H pulmonary ventilation vol
25、ume CO2 elimination PaCO2 HCO3-/H2CO3(quickly,limted) But 46PaCO2 value predicted: with respiratory acidosis Value measured value predicted: with respiratory acidosis Value measured value predicted: with metabolic alkalosis Value measured value predicted: with metabolic alkalosis Value measured valu
26、e predicted: with metabolic acidosis. Maximal compensatory value up to:12 mmol/L 4.Changes of laboratory parameters(acute) pH PaCO2 SB() AB BB () BE () HCO3- secondary decrease H2CO3 primary decrease increase Changes of laboratory parameters(chronic) pH PaCO2 SB AB BB -BE HCO3- secondary decrease H2
27、CO3 primary decrease increase 5.Effect of respiratory alkalosis 1. CNS dysfunction:GABA,cerebral blood flow 2. increased neuromuscular excitability(hypocalcemia ) tingling,twitching 3. hypokalemia 4. hypophosphatemia 6. treatment priciples Primary disease Prevent mis-operation of mechanical ventilator 5CO2 mixtrue gas inhalation or mask V. Mixed Acid-base Disturbances Concept Metabolic acidosis, metabolic alkalosis, respiratory acidosis and respiratory alkalosis are four types of simple acid-base disturbance when these disturbances occur separately. A mixed aci
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