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1、酸中毒和碱中毒,Case,Case,A 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 m
2、mol/l. 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 thro
3、ugh a red light, 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 stab
4、ilization of her leg and pelvis.,Case,A 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
5、, and chloride 110 mmol/l. 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 s
6、peeding car ran through a red light, 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 ope
7、rating room for stabilization of her leg and pelvis.,什么酸碱紊乱？代谢、呼吸？AG酸中毒、高氯性简单/复杂性？,Acid production in the body,Carbonic 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: la
8、ctate, metabolized by the 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.
9、8 H+,The homeostatic response to acid load,Chemical buffering by the extracellular and intracellular buffers. Changes in alveolar ventilation to control the PCO2. Alterations in renal H+ excretion to regulate the plasma HCO3- concentration.,Chemical buffering,Extracellular buffersIntracelluar: bone,
10、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 PCO2,Henderson-Hasselbalch equation,(Eq. 1) H+ + HCO3- H2CO3 H2O + CO2 PCO2(Eq. 2) H+ = 24 x HCO3-or by the Henderson-Hasselbalch eq
11、uation HCO3-(Eq. 3) pH = 6.10 + log 0.03 PCO2Acidosis: PCO2=1.5 X HCO3 + 8,Chemical buffering,Extracellular buffersIntracelluar buffer: bone, Ca+ release, osteoclast activation,The homeostatic response to acid load,Chemical buffering by the extracellular and intracellular buffers. Changes in alveola
12、r ventilation to control the PCO2. Alterations in renal H+ excretion to regulate the plasma HCO3- concentration.,The homeostatic response to acid load,Chemical buffering by the extracellular and intracellular buffers. Changes in alveolar ventilation to control the PCO2. Alterations in renal H+ excre
13、tion to regulate the plasma HCO3- concentration.,RENAL HYDROGEN EXCRETION,(1) reabsorption of the filtered HCO3-(2) excretion of the 50 to 100 meq of H+ produced per dayFormation of titratable acidExcretion of NH4+ in the urine,Collecting tubule,Tubular Lumen,Peritubular capillary,H+,H2O2,OH- + CO2,
14、3HCO3-,CA,H+,Cl-,ATPase,ATPase,H+,K+,Excretion of H+ in a intercalated cells,H+,H+,Collecting tubule,Tubular Lumen,Peritubular capillary,H+,H2O2,OH- + CO2,3HCO3-,CA,H+,+,HPO42-,H2PO4,Cl-,ATPase,ATPase,H+,K+,Excretion of H+ in a intercalated cells,Collecting tubule,Tubular Lumen,Peritubular capillary
15、,H+,H2O2,OH- + CO2,3HCO3-,CA,H+,+,NH3,NH4+,Cl-,H+-ATPase,NH3,Excretion of H+ in a intercalated cells,Can be stimulated by low K,Acid-base balance,The kidneys 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
16、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 body.Regulation:The extracellular pH the effective circulating volume, aldosterone, and the plasma K+ concentration,Can be independent of ser
17、um pH,Steps in acid-base diagnosis,Obtain arterial blood gas (ABGs) and electrolytes simultaneouslyCompare HCO3-on ABGs and electrolytes to verify accuracyCalculate anion gap (AG)Know 4 causes of high AG acidosisKetoacidsisLactic acid acidosisRenal failureToxinsKnow 2 causes of hyperchloremic or non
18、gap acidosisBicarbonate loss from GI, RTAEstimate compensatory responseCompare AG and HCO3-Compare change in Cl with change in Na,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 PC
19、O2Acidosis: PCO2=1.5 X HCO3 + 8,Metabolic acidosis,Influx of organic acid into plasma (high anion gap)KetoacidosisLactic acidosisPoisoningAccumulation of endogenous acids (high anion gap)Renal failureExternal losses of bicarbonate (normal anion gap; hyperchloremic).GI lossRenal loss,Anion Gap,AG=Na+
20、-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 Gap,Causes of a High Anion Gap Metabolic Acidosis,Types and Causes of Lactic Acidosis,Types and Causes of Lacti
21、c Acidosis,Renal failure,With 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 various anions, and the accumulation of sulfate, phosphate, and other anions, produces
22、an elevated AG.,Renal failure,Despite 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. Chronic acidosis causes protein breakdown, muscle wasting, and a negative nitrogen b
23、alance. Maintenance of the acid-base balance close to normal can prevent these consequences,Treatment,Alkali replacementNaHCO3Sodium citrate,Hyperchloremic Metabolic Acidosis,Causes:Renal loss of alkali RTAGI loss of alkaliReciprocal changes in Cl and HCO3 result in normal AGIn the absence of such a
24、 relationship suggests a mixed disturbance,Diarrhea,Metabolic 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 negative,Proximal RTA (type 2),The threshold for HCO3- reabsorption in t
25、he 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 is reabsorbed. Despite systemic acidemia development, the u
26、rine pH is alkaline. However under steady state, the urine can be acidified to a pH of less than 5.5.,HCO3,HCO3,HCO3,Proximal RTA: hypokalemia,Increased distal Na+ delivery (NaHCO3)Increased aldosterone levels (dehydration because of loss of Na in the urine).Treatment of acidosis with HCO3 improves
27、the acidosis but worsens the degree of hypokalemia.,Causes of Proximal RTA,Inherited pRTA: NBCe1/SLC4A4) mutation, accompanied by ocular abnormalities such as cataracts, glaucoma.Carbonic anhydrase inhibitor: acetazolamideFanconi syndrome: inherited and acquiredAdult with Fanconi: dysproteinemic con
28、dition such as multiple myeloma,dRTA (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 and nephrocalcinosis,HCO3,HCO3,HC
29、O3,dRTA: kidney stone,Urinary 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 of calcium phosphate com
30、plexes.,dRTA,Primary: idiopathic or inherited (SLC4A1 mutation)Systemic disease: Sjogren syndrome,dRTA-diagnosis,NH4ClFurosemide + mineralocorticoid (fludrocortisone),dRTA,Hyperchloremic acidosisKidney stoneHypokalemiaSjogren syndrome,Type 4 RTA,Renal function compromisedHyporeninemic hypoaldosteron
31、ismHyperkalemiaUrinary ammonium excretion depressed,Metabolic Alkalosis,An elevated arterial pHAn increase in the serum HCO3- and a increase in PCO2Often accompanied by hypochloremia and hypokalemia,Pathogenesis,Generative stage: loss of acidMaintenance stage: volume contraction, a low GFR or deplet
32、ion of Cl or K,Differential diagnosis,Mineralocorticoid excessBartters or GitelmansDiuretics,Metabolic alkalosis associated with ECFV contraction, K depletion, and secondary hyperreninemic hyperaldosteronism,GastrointenstinalHCO3 retention + volume contractionRenal originDiureticsNonreaborbable anio
33、ns and magnesium deficiencyPotassium depletionAfter treatment of lactic acidosis or ketoacidosisposthypercapnia,Metabolic alkalosis with ECFV expansion, hypertension and hyperaldosteronism,Mineralocorticoid administration or excess productionSymptoms: changes in central and peripheral nervous system
34、 function: confusion, obtundation, a predispositin to seizures Related electrolyte abnormalities: hypokalemiaTreatmentCorrecting the underlying stimulus for HCO3 generationRemoving the factors that sustain HCO reabsorption (ECFV contraction),Respiratory acidosis,Severe pulmonary disease, respiratory
35、 muscle fatigue or abnormalities in ventilatory controlAcute: immediate compensatory elevation in HCO3, which increases 1 mmol/L for every 10 mmHg increase in pCO2Chronic (24h): renal adaptation increases the HCO3 by 4 mmol/L,Clinical features,The clinical feature varies according toSeverity and dur
36、ationUnderlying diseaseWhether there is hypoxemiaA rapid increase in pCO2: anxiety, dyspnea, confusion comaChronic hypercapnea: sleep disturbances, loss of memory, .,Treatment,Acute respiratory acidosis can be life-threatening, measures to reverse the underlying cause should be undertaken simultaneo
37、usly with restoration of adequate alveolar ventilationChronic respiratory acidosisImproving lung function,Respiratory alkalosis,Alveolar hyperventilation 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,
38、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 titratable acid excretion.Full renal adaptation may take several days and require normal volume status and renal function,The effect of respiratory alkalo
39、sis 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,
