酸中毒和碱中毒课件.pptx

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1、酸中毒和碱中毒酸中毒和碱中毒CaseCaseA 22-year-old woman who had been injured in an accident received 6 liters of isotonic saline,The plasma Na 135 mmol/l,K 3.8 mmol/l,Cl 115 mmol/l,and HCO3 18 mmol/l.The blood pH 7.28,and the PaCO2 39 mm Hg.The urinary sodium 65 mmol/l,potassium 15 mmol/l,and chloride 110 mmol/l.

2、The patients serum albumin 2.7 g/dl after the infusion of saline.Her blood pressure was 98/52 mmHg,and her pulse rate was 102 beats/m.She had been healthy before the accident,was receiving no medications,and did not use any illicit drugs.The accident occurred when a speeding car ran through a red li

3、ght,hitting her car on the drivers side.The accident has caused multiple rib fractures,a compound left femoral fracture,a pelvic fracture,and numerous bruises.She is in the emergency department for stabilization of her condition before she can be sent to the operating room for stabilization of her l

4、eg and pelvis.CaseA 22-year-old woman who had been injured in an accident received 6 liters of isotonic saline,The plasma Na 135 mmol/l,K 3.8 mmol/l,Cl 115 mmol/l,and HCO3 18 mmol/l.The blood pH 7.28,and the PaCO2 39 mm Hg.The urinary sodium 65 mmol/l,potassium 15 mmol/l,and chloride 110 mmol/l.The

5、patients serum albumin 2.7 g/dl after the infusion of saline.Her blood pressure was 98/52 mmHg,and her pulse rate was 102 beats/m.She had been healthy before the accident,was receiving no medications,and did not use any illicit drugs.The accident occurred when a speeding car ran through a red light,

6、hitting her car on the drivers side.The accident has caused multiple rib fractures,a compound left femoral fracture,a pelvic fracture,and numerous bruises.She is in the emergency department for stabilization of her condition before she can be sent to the operating room for stabilization of her leg a

7、nd pelvis.什么酸碱紊乱？什么酸碱紊乱？代代谢、呼吸？、呼吸？AG酸中毒、高酸中毒、高氯性性简单简单/复复杂杂性？性？Acid production in the bodyCarbonic acid:the metabolism of carbohydrates and fats(primarily derived from the diet)results in the production of approximately 15,000 mmol of CO2 per day.Non-carbonic acid:Organic:lactate,metabolized by the

8、liver and kidneyInorganic:the metabolism of proteins and other substances results in the generation of noncarbonic acids(50 100 mEq,1mEq/kg).Methionine glucose +urea +SO4(2-)+2 H+Arginine+glucose(or CO2)+urea +H+R-H2PO4 +H2O ROH +0.8 HPO42-/0.2 H2PO4-+1.8 H+The homeostatic response to acid load 1.Ch

9、emical buffering by the extracellular and intracellular buffers.2.Changes in alveolar ventilation to control the PCO2.3.Alterations in renal H+excretion to regulate the plasma HCO3-concentration.Chemical bufferingExtracellular buffersIntracelluar:boneHenderson-Hasselbalch equation(Eq.1)H+HCO3-H2CO3

10、H2O +CO2 PCO2(Eq.2)H+=24 x HCO3-or by the Henderson-Hasselbalch equation HCO3-(Eq.3)pH =6.10 +log 0.03 PCO2 Henderson-Hasselbalch equation(Eq.1)H+HCO3-H2CO3 H2O +CO2 PCO2(Eq.2)H+=24 x HCO3-or by the Henderson-Hasselbalch equation HCO3-(Eq.3)pH =6.10 +log 0.03 PCO2Acidosis:PCO2=1.5 X HCO3+8 Chemical

11、bufferingExtracellular buffersIntracelluar buffer:bone,Ca+release,osteoclast activationThe homeostatic response to acid load 1.Chemical buffering by the extracellular and intracellular buffers.2.Changes in alveolar ventilation to control the PCO2.3.Alterations in renal H+excretion to regulate the pl

12、asma HCO3-concentration.The homeostatic response to acid load 1.Chemical buffering by the extracellular and intracellular buffers.2.Changes in alveolar ventilation to control the PCO2.3.Alterations in renal H+excretion to regulate the plasma HCO3-concentration.RENAL HYDROGEN EXCRETION(1)reabsorption

13、 of the filtered HCO3-(2)excretion of the 50 to 100 meq of H+produced per day1.Formation of titratable acid2.Excretion of NH4+in the urineCollecting tubuleTubular LumenPeritubular capillaryH+H2O2OH-+CO23HCO3-CAH+Cl-ATPaseATPaseH+K+Excretion of H+in a intercalated cellsH+H+Collecting tubuleTubular Lu

14、menPeritubular capillaryH+H2O2OH-+CO23HCO3-CAH+HPO42-H2PO4Cl-ATPaseATPaseH+K+Excretion of H+in a intercalated cellsCollecting tubuleTubular LumenPeritubular capillaryH+H2O2OH-+CO23HCO3-CAH+NH3NH4+Cl-H+-ATPaseNH3Excretion of H+in a intercalated cellsCan be stimulated by low KAcid-base balanceThe kidn

15、eys must excrete the 50 to 100 meq of noncarbonic acid generated each day.The daily acid load is excreted as NH4+and H2(PO4).The daily acid load also cannot be excreted unless virtually all of the filtered HCO3-has been reabsorbed,because HCO3-loss in the urine is equivalent to adding H+ions to the

16、body.Regulation:The extracellular pH the effective circulating volume,aldosterone,and the plasma K+concentrationCan be independent of serum pHMetabolic acidosisInflux of organic acid into plasma(high anion gap)KetoacidosisLactic acidosisPoisoningAccumulation of endogenous acids(high anion gap)Renal

17、failureExternal losses of bicarbonate(normal anion gap;hyperchloremic).GI lossRenal lossAnion GapAG=Na+-Cl-HCO3-=122albumin:negative charged.Low serum albumin will reduce AG.Paraprotein(Ig or light chains,MM):positive charged.Presence of large amount of paraprotein reduces AG.Anion GapCauses of a Hi

18、gh Anion Gap Metabolic AcidosisTypes and Causes of Lactic AcidosisTypes and Causes of Lactic AcidosisRenal failureWith mild to moderate reductions in GFR,the acidosis reflects decreased ammoniagenesis and is therefore hyperchloremic.As kidney failure worsens,the kidney loses its ability to excrete v

19、arious anions,and the accumulation of sulfate,phosphate,and other anions,produces an elevated AG.Renal failureDespite a daily net positive acid balance,it is unusual for HCO3to fall lower than 15 mmol/L.The buffering of protons by bone results in loss of calcium and a negative calcium balance.Chroni

20、c acidosis causes protein breakdown,muscle wasting,and a negative nitrogen balance.Maintenance of the acid-base balance close to normal can prevent these consequencesTreatmentAlkali replacementNaHCO3Sodium citrate Hyperchloremic Metabolic AcidosisCauses:Renal loss of alkali RTAGI loss of alkaliRecip

21、rocal changes in Cl and HCO3 result in normal AGIn the absence of such a relationship suggests a mixed disturbanceDiarrheaMetabolic acidosisMetabolic acidosis and hypokalemia increase renal synthesis and excretion of NH4+,thus urinary pH is around 6Urinary NH4 levels are high:urine anion gap is nega

22、tiveProximal RTA(type 2)The threshold for HCO3-reabsorption in the proximal tubule is lower(normal:26-28 mmol/l).The distal nephron has a low capacity for HCO3 reabsorption.Self-limited bicarbonaturiaIn the steady state,the serum HCO3 concentration usually is 16 18 mmol/l,when all the filtered HCO3

23、is reabsorbed.Despite systemic acidemia development,the urine pH is alkaline.However under steady state,the urine can be acidified to a pH of less than 5.5.HCO3HCO3HCO3Proximal RTA:hypokalemiaIncreased distal Na+delivery(NaHCO3)Increased aldosterone levels(dehydration because of loss of Na in the ur

24、ine).Treatment of acidosis with HCO3 improves the acidosis but worsens the degree of hypokalemia.Causes of Proximal RTAInherited pRTA:NBCe1/SLC4A4)mutation,accompanied by ocular abnormalities such as cataracts,glaucoma.Carbonic anhydrase inhibitor:acetazolamideFanconi syndrome:inherited and acquired

25、Adult with Fanconi:dysproteinemic condition such as multiple myelomadRTA(type 1)Systemic acidosis in dRTA tends to be more severe than in patients with a proximal RTA(serum HCO3-can reach as low as 10 mmol/l vs 16 to 18 mmol/l)Hypokelemia can also be severe:musculoskeletal weaknessNephrolithiasis an

26、d nephrocalcinosisHCO3HCO3HCO3dRTA:kidney stoneUrinary calcium excretion is highAcidosis induced bone mineral dissolutionLow intraluminal concentration of HCO3-because of acidosisUrinary citrate levels are low citrate serve as the major Ca+chelator in the urineHigh urine pH decrease the solubility o

27、f calcium phosphate complexes.dRTAPrimary:idiopathic or inherited(SLC4A1 mutation)Systemic disease:Sjogren syndromedRTA-diagnosisNH4ClFurosemide+mineralocorticoid (fludrocortisone)dRTAHyperchloremic acidosisKidney stoneHypokalemiaSjogren syndromeType 4 RTARenal function compromisedHyporeninemic hypo

28、aldosteronismHyperkalemiaUrinary ammonium excretion depressedMetabolic AlkalosisAn elevated arterial pHAn increase in the serum HCO3-and a increase in PCO2Often accompanied by hypochloremia and hypokalemiaPathogenesisGenerative stage:loss of acidMaintenance stage:volume contraction,a low GFR or depl

29、etion of Cl or KDifferential diagnosisMineralocorticoid excessBartters or GitelmansDiureticsMetabolic alkalosis associated with ECFV contraction,Metabolic alkalosis associated with ECFV contraction,K depletion,and secondary hyperreninemic K depletion,and secondary hyperreninemic hyperaldosteronism h

30、yperaldosteronism GastrointenstinalHCO3 retention+volume contractionRenal originDiureticsNonreaborbable anions and magnesium deficiencyPotassium depletionAfter treatment of lactic acidosis or ketoacidosisposthypercapniaMetabolic alkalosis with ECFV expansion,Metabolic alkalosis with ECFV expansion,h

31、ypertension and hyperaldosteronismhypertension and hyperaldosteronismMineralocorticoid administration or excess productionSymptoms:changes in central and peripheral nervous system function:confusion,obtundation,a predispositin to seizures Related electrolyte abnormalities:hypokalemiaTreatmentCorrect

32、ing the underlying stimulus for HCO3 generationRemoving the factors that sustain HCO reabsorption(ECFV contraction)Respiratory acidosisSevere pulmonary disease,respiratory muscle fatigue or abnormalities in ventilatory controlAcute:immediate compensatory elevation in HCO3,which increases 1 mmol/L fo

33、r every 10 mmHg increase in pCO2Chronic(24h):renal adaptation increases the HCO3 by 4 mmol/L Clinical featuresThe clinical feature varies according toSeverity and durationUnderlying diseaseWhether there is hypoxemiaA rapid increase in pCO2:anxiety,dyspnea,confusion comaChronic hypercapnea:sleep dist

34、urbances,loss of memory,.TreatmentAcute respiratory acidosis can be life-threatening,measures to reverse the underlying cause should be undertaken simultaneously with restoration of adequate alveolar ventilationChronic respiratory acidosisImproving lung functionRespiratory alkalosisAlveolar hyperven

35、tilation decreases PaCO2 and increases the HCO3/PCO2When PaCO2 is 40 15 mmHg,the relationship between arterial H+and PaCO2 is about 0.7 mmol/L per mmHg,and that of plasma HCO3 is 0.2 mmol/per mmHgHypocapnia sustained longer than 2 to 6 h is further compensated by a decrease in renal ammonium and tit

36、ratable acid excretion.Full renal adaptation may take several days and require normal volume status and renal function The effect of respiratory alkalosis vary according to duration and severity but are primarily those of the underlying diseaseHyperventilation syndromeParesthesia,circumoral numbness,chest wall tightness,dizzinessSalicylates are the most common cause of drug induced respiratory alkalosisProgesterone increases ventilation Respiratory alkalosis is often an early finding of G-septicemia