动脉血气分析与高乳酸血症课件

Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,+,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,*,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,动脉血气分析及高乳酸血症,动脉血气分析及高乳酸血症,病例摘要,男性，45岁，病历号1612296,入院日期2010/02/21,入ICU日期2010/02/24,既往史,24年前因感冒后颈部淋巴结肿大行左颈部淋巴结活检术，自述病理阴性,8年前阑尾切除术,1年前行鼻中隔弯曲矫正术,病例摘要男性，45岁，病历号1612296,2,病例摘要,2009/12/30,大量饮酒后头昏、恶心，右胁肋部及后背部胀痛,胃镜：糜烂性胃炎伴胆汁返流,2010/01/18,生化检查：ALT、AST、LDH、HBDH、尿淀粉酶进行性升高,腹部超声检查提示胆囊炎,病例摘要2009/12/30,3,病例摘要,2010/01/24,静滴脂肪乳过程中出现气促、胸闷,抗过敏、改善循环、补液及对症处理后缓解,2010/01/28,胸闷、气促，深大呼吸伴酸碱平衡紊乱,无创通气,病例摘要2010/01/24,4,病例摘要,WCC2.46 6.26 x 109/L,Plt30 115 x109/L,ALT 137 U/L,AST 97 U/L,UA 680 mol/L,aPTT/PT明显延长,纠正后PT 13.6 sec, aPTT 48.0 sec, Fib 1.41 g/L,血淀粉酶237 588 U/L,尿淀粉酶839 3330 U/L,肿瘤指标未见异常,CA199, CEA, NSE, CA242, AFP, PSA, CA125,病例摘要WCC2.46 6.26 x 109/LaPT,5,病例摘要,ABG7.435 / 6.2 / 116 / 4.1 / -19.2,AG20 27,血乳酸14.8 16.0 mmol/L,血丙酮酸6.62 mg/dL (0.3 - 0.9),0.83 mmol/L,L/P17.8 19.3,病例摘要ABG7.435 / 6.2 / 116 / 4,6,病例摘要,胸部CT,左下肺多发肺大疱,腹部增强CT,肝左外叶及右后叶多发海绵状血管瘤, 肝右后叶囊肿, 脾稍大,胃十二指肠镜,胆汁返流性胃炎伴糜烂, 重度胆汁返流, 返流性食管炎1级,病理结果,胃窦两块粘膜组织, 中度慢性炎症, 另见小片炎性渗出物,胃底两块粘膜组织, 重度慢性炎症, 活动+, 另见小片炎性渗出物,病例摘要胸部CT,7,病例摘要,诊断：重症胰腺炎?,治疗,按胰腺炎治疗，恶心、呕吐症状缓解,输血浆及冷沉淀纠正DIC,亚甲蓝中和乳酸,病例摘要诊断：重症胰腺炎?,8,病例摘要,呼吸困难（深大呼吸）合并代谢性酸中毒,2010/02/12,血液透析,乳酸可短暂下降至7 mmol/L,病例摘要呼吸困难（深大呼吸）合并代谢性酸中毒,9,病例摘要,2010/02/21,转入北京协和医院内分泌科,ABG: 7.496 / 8.7 / 142 / 6.6 / -15.3,Na 137, Cl 95, K 3.7,血乳酸 19.6 mmol/L,血淀粉酶241 U/L，脂肪酶2430 U/L,ALT 126 U/L, TBil 23.3 mol/L, Cr 157 mol/L, BUN 8.82 mmol/L,病例摘要2010/02/21,10,血气结果分析,Step 1,pH = 7.496 7.45,原发性酸碱失衡应包括碱中毒,ABG,pH7.496,pCO,2,8.7,pO,2,142,HCO,3,6.6,BE-15.3,Lytes,Na137,Cl95,K3.7,血乳酸,19.6 mmol/L,血气结果分析Step 1ABG,11,血气结果分析,Step 2,判定碱中毒为呼吸性抑或代谢性,ABG,pH7.496,pCO,2,8.7,pO,2,142,HCO,3,6.6,BE-15.3,Lytes,Na137,Cl95,K3.7,血乳酸,19.6 mmol/L,血气结果分析Step 2ABG,12,血气结果分析,Step 3,AG = Na Cl HCO3,= 137 95 6.6 = 35 20,高AG代酸,ABG,pH7.496,pCO28.7,pO2142,HCO36.6,BE-15.3,Lytes,Na137,Cl95,K3.7,血乳酸,19.6 mmol/L,血气结果分析Step 3ABG,13,血气结果分析,Step 4,AG = 35 12 = 23,HCO3 + AG = 6.6 + 23,= 29.6 26,代谢性碱中毒,ABG,pH7.496,pCO,2,8.7,pO,2,142,HCO,3,6.6,BE-15.3,Lytes,Na137,Cl95,K3.7,血乳酸,19.6 mmol/L,血气结果分析Step 4ABG,14,血气结果分析,Step 5,pCO2 = 1.5 x HCO3 + 8 2,= 1.5 x 6.6 + 8 2,= 9.9 + 8 2,= 15.9 to 19.9,呼吸性碱中毒,ABG,pH7.496,pCO,2,8.7,pO,2,142,HCO,3,6.6,BE-15.3,Lytes,Na137,Cl95,K3.7,血乳酸,19.6 mmol/L,血气结果分析Step 5ABG,15,血气结果分析,诊断,高AG代谢性酸中毒,代谢性碱中毒,呼吸性碱中毒,ABG,pH7.496,pCO,2,8.7,pO,2,142,HCO,3,6.6,BE-15.3,Lytes,Na137,Cl95,K3.7,血乳酸,19.6 mmol/L,血气结果分析诊断ABG,16,高AG代酸的常见原因,甲醇(methanol)中毒,尿毒症,酮症酸中毒,糖尿病*,酒精性,饥饿性,三聚乙醛(paraldehyde)中毒,异烟肼,乳酸酸中毒*,乙醇(ethanol)中毒*,乙二醇(ethylene glycol)中毒*,水杨酸(salicylic acid)中毒,* 高AG代酸最常见的原因,* 常伴渗透压间隙升高,高AG代酸的常见原因甲醇(methanol)中毒异烟肼* 高,17,病例诊断,高AG代酸 高乳酸血症,高乳酸血症的病因?,病例诊断高AG代酸 高乳酸血症,18,病例摘要,2010/03/01,ABG 7.525 / 26.9 / 121 / 22.1 / -0.5,Lac 9.6,血渗透压312,Na 146, Cl 101, BUN 3.32, Glu 7.4,AG = 22.9,Osmcalc = 146 x 2 + 3.32 + 7.4 = 302.7,Osmolarity gap = 9.3,病例摘要2010/03/01,19,传统观点认为,缺氧可以导致无氧代谢,无氧代谢产生乳酸,无氧代谢是有害的,缺氧是有害的,现阶段临床思维认为，高乳酸血症是缺氧的后果,治疗上采取提高心输出量和氧输送的方法,传统观点认为缺氧可以导致无氧代谢现阶段临床思维认为，高乳酸,20,因此，这是否意味着?,高乳酸是有害的?,高乳酸提示存在缺氧?,高乳酸提示存在无氧代谢 ,高乳酸 = 预后不佳 ,因此，这是否意味着?高乳酸是有害的?,21,动脉血气分析与高乳酸血症课件,22,动脉血气分析与高乳酸血症课件,23,乳酸是如何生成的?,Glucose,Glycogen,Glucose 6-P,Fructose 6-P,Fructose-1,6-Bisphosphate,Triose Phosphates,Phosphoenolpyruvate,Pyruvate,Lactate,Oxidation In,Citric Acid Cycle,Phosphofructonase,Pyruvate kinase,PDH,Lactate dehydrogenase,Anaerobic Metabolism,乳酸是如何生成的?GlucoseGlycogenGlucos,24,乳酸基础生成率,肌肉,脑,RBC,WBC,血小板,肾脏,髓质,胃肠道,粘膜,皮肤,0.13 mmol/kg/hr,0.14 mmol/kg/hr,0.18 mmol/kg/hr,0.11 mmol/kg/hr,0.11 mmol/kg/hr,Total = 1290 mmol / 24 hours for 70 kg,乳酸基础生成率肌肉脑RBCWBC血小板肾脏胃肠道皮肤0.13,25,乳酸的代谢,Excretion renal threshold = 5-6 mmol/L,乳酸的代谢Excretion renal threshold,26,高乳酸血症( 2 mmol/L),生成,利用/排出,高乳酸血症( 2 mmol/L)生成利用/排出,27,因此,一旦丙酮酸氧化过程受到影响, 任何能够增加糖酵解的因素都能够导致高乳酸血症,不仅仅是无氧代谢!,因此一旦丙酮酸氧化过程受到影响, 任何能够增加糖酵解的因素,28,感染性休克时的高乳酸血症,Curtis SE, Cain SM. Regional and systemic oxygen delivery/uptake relations and lactate flux in hyperdynamic, endotoxin-treated dogs. Am Rev Respir Dis 1992; 145: 348-354,0,2,4,6,8,Serum Lactate (mEq/L),0,40,80,120,160,Time (min),输注内毒素,FiO2 = 12%,dichloroacetate,二氯乙酸(dichloroacetate)仅在有氧情况下激活PDH,感染性休克时的高乳酸血症Curtis SE, Cain SM,29,乳酸/丙酮酸比值,Lactate/Pyruvate = K x (NADH/NAD) x H+,缺氧能够阻断氧化磷酸化过程,组织NADH氧化为NAD,增加NADH/NAD比值,增加乳酸/丙酮酸比值,正常值约为10:1,心源性休克,L/P,比值,=,40:1,符合组织缺氧表现,经过复苏的感染性休克,L/P,比值,=,14:1,不符合组织缺氧表现,乳酸/丙酮酸比值Lactate/Pyruvate = K x,30,何时乳酸 = 组织灌注不足,心源性休克,出血性休克,以下情况的感染性休克,儿茶酚胺抵抗 + 心输出量降低,未经过复苏 (参见Rivers),何时乳酸 = 组织灌注不足心源性休克,31,何时乳酸 组织灌注不足,有氧糖酵解加速,碳水化合物代谢 线粒体氧化能力,儿茶酚胺 / 细胞因子刺激,e.g. 血液 / 肺的白细胞乳酸 (ARDS),丙酮酸蓄积,全身性感染时PDH功能障碍,何时乳酸 组织灌注不足有氧糖酵解加速,32,何时乳酸 组织灌注不足,乳酸清除减少,结果相互矛盾：测定方法与初始乳酸水平的影响,可能导致轻度高乳酸血症,当乳酸生成率接近正常时通常并不重要,丙酮酸脱氢酶功能障碍,PDH使丙酮酸进入Kreb循环, 而不产生乳酸,全身性感染时肌肉中PDH水平低于正常,应用二氯乙酸可恢复功能, 从而导致乳酸水平下降,蛋白质分解代谢,氨基酸转化为丙酮酸, 随后产生乳酸,线粒体呼吸抑制,全身性感染, 药物如二甲双胍(罕见), 氰化物, 抗逆转录病毒药物,何时乳酸 组织灌注不足乳酸清除减少,33,乳酸酸中毒的分类,Type A Lactic Acidosis,Associated with malperfusion / dysoxia,Type B Lactic Acidosis,In the absence of malperfusion / dysoxia,B1 Disease states e.g. DKA, leukaemia, lymphoma, thiamine deficiency,B2 Drugs e.g. metformin, cyanide, beta-agonists, HARRT,B3 inborn errors of metabolism,乳酸酸中毒的分类Type A Lactic Acidosis,34,Classification of Lactic Acidosis,Tissue hypoperfusion,Abnormal vascular tone or permeability, left ventricular failure, decreased cardiac output,Reduced arterial oxygen content,Asphyxia, hypoxemia (PaO2 35), carbon monoxide poisoning, life-threatening anemia,B1 (common disorders),Sepsis,Hepatic failure,Renal failure,Diabetes mellitus,Cancer,Malaria,Cholera,B2 (drug or toxins),Vitamin deficiency,Acetaminophen,Ethanol, Methanol,Cocaine,Salicylates,Isoniazid,Catecholamines,Ethylene glycol,Papaverine,Cyanide,Parenteral nutrition,Nitroprusside,Lactulose,Theophylline,B3 (other conditions),Strenuous muscle exercise,Grand mal seizures,D-lactic acidosis,Type A,Due to tissue hypoxia,Type B,Not due to tissue hypoxia,Classification of Lactic Acido,35,预后价值,来源并不重要,高乳酸仍然为严重生理应激和死亡危险的标志,高乳酸常与低氧无关, 但仍提示严重应激下存在代谢改变,预后价值来源并不重要,36,因此, 我们应当?,寻找组织灌注不足的证据,如果存在组织灌注不足, 应提高CO和氧输送,但是, 不应仅仅针对乳酸水平进行上述治疗,治疗组织灌注不足而非高乳酸,考虑导致高乳酸的其他原因,Lactate is the messengerdont shoot it!,因此, 我们应当?寻找组织灌注不足的证据,37,病例诊断,全身血流动力学稳定,组织灌注无明显异常,意识清楚,皮肤无花斑,毛细血管再充盈时间正常,尿量正常,药物因素,患病前未使用任何药物,中毒,毒物监测未发现异常,先天性因素,病例诊断全身血流动力学稳定药物因素,38,Classification of Lactic Acidosis,Tissue hypoperfusion,Abnormal vascular tone or permeability, left ventricular failure, decreased cardiac output,Reduced arterial oxygen content,Asphyxia, hypoxemia (PaO2 35), carbon monoxide poisoning, life-threatening anemia,B1 (common disorders),Sepsis,Hepatic failure,Renal failure,Diabetes mellitus,Cancer,Malaria,Cholera,B2 (drug or toxins),Vitamin deficiency,Acetaminophen,Ethanol, Methanol,Cocaine,Salicylates,Isoniazid,Catecholamines,Ethylene glycol,Papaverine,Cyanide,Parenteral nutrition,Nitroprusside,Lactulose,Theophylline,B3 (other conditions),Strenuous muscle exercise,Grand mal seizures,D-lactic acidosis,Type A,Due to tissue hypoxia,Type B,Not due to tissue hypoxia,Classification of Lactic Acido,39,病例诊断,骨髓活检,淋巴瘤骨髓侵犯,诊断,非霍杰金氏淋巴瘤,病例诊断骨髓活检,40,病例摘要,02/21,02/22,02/23,02/24,16:50,14:00,10:00,17:00,19:30,22:30,07:30,pH,7.496,7.473,7.424,7.303,7.362,7.518,7.341,PCO2,8.7,14.7,8.9,6.8,7.5,14.9,8.1,PO2,142,122,143,148,142,140,134,HCO3,6.6,10.6,5.7,3.3,4.2,12.0,4.3,SBE,-17.1,-12.6,-19.0,-23.5,-21.6,-10.6,-21.7,Lac,20.0,14.6,14.0,16.0,14.3,11.1,20.0,病例摘要02/2102/2202/2302/2416:501,41,病例摘要,病例摘要,42,应用碳酸氢钠与血气变化的关系,应用碳酸氢钠与血气变化的关系,43,总结,动脉血气结果分析 - 基本技能,高乳酸血症的鉴别诊断,总结动脉血气结果分析 - 基本技能,44,