动脉血气分析六步法(6-stepApproachinABGs)10P

动脉血气分析六步法(6-stepApproachinABGs)10P 动脉血气分析六步法 6-step Approach in ABGs 一、 根据Henderseon-Hasselbach公式评估血气数值的内在一致性 [H+]=24 x(PaCO2)/[HCO3-] , 如果pH和[H+]数值不一致，该血气结果可能是错误的 估测[H+] pH (mmol/L) 7.00 100 7.05 89 7.10 79 7.15 71 7.20 63 7.25 56 7.30 50 7.35 45 7.40 40 7.45 35 7.50 32 7.55 28 7.60 25 7.65 22 二、 是否存在碱血症或酸血症, pH<7.35酸血症 pH>7.45碱血症 , 通常这就是原发异常 , 记住:即使pH值在正常范围(7.35,7.45)，也可能存在酸中毒或碱中毒 , 你需要核对PaCO2,HCO3-,和阴离子间隙 三、 是否存在呼吸或代谢紊乱,pH值改变的方向与PaCO2改变方向的关系如何, 在原发呼吸障碍时，pH值和PaCO2改变方向相反; 在原发代谢障碍时，pH值和PaCO2改变方向相同 酸中毒 呼吸性 pH? PaCO? 2 酸中毒 代谢性 pH? PaCO? 2 碱中毒 呼吸性 pH? PaCO? 2 碱中毒 代谢性 pH? PaCO? 2 四、 针对原发异常是否产生适当的代偿, 通常情况下，代偿反应不能使pH恢复正常(7.35-7.45) 异常 预期代偿反应 校正因子 -PaCO=(1.5 x[HCO])+8 代谢性酸中毒 ?2 23 -急性呼吸性酸中毒 [HCO]升高=?PaCO/10 ?3 32 - 慢性呼吸性酸中毒(3-5天) [HCO]升高=3.5 x(?PaCO/10) 32 - 代谢性碱中毒 PaCO升高=0.6 x(?HCO) 23 - 急性呼吸性碱中毒 [HCO]下降=2 x(?PaCO/10) 32 - 慢性呼吸性碱中毒 [HCO]下降=5 x(?PaCO/10)至7 x(?PaCO/10) 322 , 如果观察到的代偿程度与预期代偿反应不符，很可能存在一种以上的酸碱异常 五、 计算阴离子间隙(如果存在代谢性酸中毒) +-AG=[Na]-([Cl]+[HCO3-])=12?2 , 正常的阴离子间隙约为12 mEq/L , 对于低白蛋白血症患者，阴离子间隙正常值低于12 mEq/L。 低白蛋白血症患者血浆白蛋白浓度每下降1 g/dL(10g/L)，阴离子间隙―正常值‖下降约2.5 mEq/L。 (例如，血浆白蛋白20 g/dL患者约为7 mEq/L) , 如果阴离子间隙增加，在以下情况下应计算渗透压间隙 •AG升高不能用明显的原因(DKA，乳酸酸中毒，肾功能衰竭)解释 •怀疑中毒 +, OSM间隙=测定OSM–(2 x[Na]–血糖/18–BUN/2.8) OSM间隙应当<10 六、 如果阴离子间隙升高，评价阴离子间隙升高与[HCO3-]降低的关系 , 计算阴离子间隙改变(?AG)与[HCO3-]改变(?[HCO3-])的比值:?AG/?[HCO3-] 如果为非复杂性阴离子间隙升高代谢性酸中毒,此比值应当介于1.0和2.0之间 如果这一比值在正常值以外,则存在其他代谢紊乱 •如果?AG/?[HCO3-]<1.0，则可能并存阴离子间隙正常的代谢性酸中毒 •如果?AG/?[HCO3-]>2.0，则可能并存代谢性碱中毒 o记住患者阴离子间隙的预期―正常值‖非常重要，且这一正常值须根据低白蛋白血症情况进行校正 (见第五步) 表1:酸碱失衡的特征 异常 pH 原发异常 代偿反应 -代谢性酸中毒 ? HCO? PaCO? 32 -代谢性碱中毒 ? HCO? PaCO? 32 -呼吸性酸中毒 ? PaCO? HCO? 23 -呼吸性碱中毒 ? PaCO? HCO? 23表2:呼吸性酸中毒部分病因 气道梗阻 •. 上呼吸道 •.下呼吸道 o COPD 哮喘 o 其他阻塞性肺疾病 o CNS抑制 睡眠呼吸障碍(OSA或OHS) 神经肌肉异常 通气受限 CO2产量增加:震颤，寒战，癫痫，恶性高热，高代谢，碳水化合物摄入增加 错误的机械通气设置 表3:呼吸性碱中毒部分病因 CNS刺激: 发热,疼痛,恐惧,焦虑,CVA,脑水肿,脑创伤,脑肿瘤,CNS感染 低氧血症或缺氧:肺疾病,严重贫血,低FiO 2 化学感受器刺激:肺水肿,胸腔积液,肺炎,气胸,肺动脉栓塞 药物,激素:水杨酸,儿茶酚胺,安宫黄体酮,黄体激素 妊娠,肝脏疾病,全身性感染,甲状腺机能亢进 错误的机械通气设置 表4:代谢性碱中毒部分病因 -低血容量伴Cl缺乏 +GI丢失H: 呕吐，胃肠吸引，绒毛腺瘤，腹泻时丢失富含Cl的液体染 +肾脏丢失H:袢利尿剂和噻嗪类利尿剂，CO2潴留后(尤其开始机械通气后) 低血容量 +肾脏丢失H: 水肿状态(心功能衰竭，肝硬化，肾病综合征)， 醛固酮增多症，皮质醇增多症，ACTH过量，外源性皮质激素， 高肾素血症，严重低钾血症，肾动脉狭窄，碳酸盐治疗 表5:代谢性酸中毒部分病因 阴离子间隙升高 甲醇中毒 尿毒症 a糖尿病酮症酸中毒，酒精性酮症酸中毒，饥饿性酮症酸中毒 三聚乙醛中毒 异烟肼 尿毒症 甲醇中毒 a 乳酸酸中毒 bb 乙醇或乙二醇中毒 水杨酸中毒 a阴离子间隙升高代谢性酸中毒最常见的原因 b常伴随渗透压间隙升高 -阴离子间隙正常:[Cl]升高 GI丢失HCO:腹泻，回肠造瘘术，近端结肠造瘘术，尿路改道 3 -肾脏丢失HCO:近端RTA，碳酸酐酶抑制剂(乙酰唑胺) 3 肾小管疾病: ATN，慢性肾脏疾病，远端RTA，醛固酮抑制剂或缺乏，输注NaCl，TPN， +输注NH 4 表6:部分混合性和复杂性酸碱失衡 特点 异常 部分病因 pH HCO3- PaCO2 •心跳骤停 呼吸性酸中毒伴代谢性酸中毒 ? ? ? •中毒 •多器官功能衰竭 •肝硬化应用利尿剂 呼吸性碱中毒伴代谢性碱中毒 ? ? •妊娠合并呕吐 •COPD过度通气 •COPD应用利尿剂,呕吐 呼吸性酸中毒伴代谢性碱中毒 正常 ? ? •NG吸引 •严重低钾血症 •全身性感染 •水杨酸中毒 呼吸性碱中毒伴代谢性酸中毒 正常 ? ? •肾功能衰竭伴CHF或肺炎 •晚期肝脏疾病 •尿毒症或酮症酸中毒伴呕吐, 代谢性酸中毒伴代谢性碱中毒 正常 正常 NG吸引,利尿剂等 [建议阅读文献] •Rose,B.D.and T.W.Post.Clinical physiology of acid-base and electrolyte disorders,5th ed.New York:McGraw Hill Medical Publishing Division,c2001. •Fidkowski,C And J.Helstrom.Diagnosing metabolic acidosis in the critically ill:bridging the anion gap,Stewart and base excess methods.Can J Anesth 2009;56:247-256. •Adrogué,H.J.and N.E.Madias.Management of life-threatening acid-base disorders—first of two parts.N Engl J Med 1998;338:26-34. Adrogué,H.J.and N.E.Madias.Management of life-threatening acid-base disorders—second of two parts.N Engl J Med 1998;338:107-111. Interpretation of Arterial Blood Gases (ABGs) David A. Kaufman, MD Chief, Section of Pulmonary, Critical Care & Sleep Medicine Bridgeport Hospital-Yale New Haven Health Assistant Clinical Professor, Yale University School of Medicine (Section of Pulmonary & Critical Care Medicine) Introduction: Interpreting an arterial blood gas (ABG) is a crucial skill for physicians, nurses, respiratory therapists, and other health care personnel. ABG interpretation is especially important in critically ill patients. The following six-step process helps ensure a complete interpretation of every ABG. In addition, you will find tables that list commonly encountered acid-base disorders. Many methods exist to guide the interpretation of the ABG. This discussion does not include some methods, such as analysis of base excess or Stewart’s strong ion difference. A summary of these techniques can be found in some of the suggested articles. It is unclear whether these alternate methods offer clinically important advantages over the presented approach, which is based on the ―anion gap.‖ Readers are welcome to discuss their observations and share their comments on the ATS Critical Care Forums. 6-step approach: Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation: [H+] = 24(PaCO) 2 [HCO-] 3 If the pH and the [H+] are inconsistent, the ABG is probably not valid. pH Approximate [H+] (mmol/L) 7.00 100 7.05 89 7.10 79 7.15 71 7.20 63 7.25 56 7.30 50 7.35 45 7.40 40 7.45 35 7.50 32 7.55 28 7.60 25 7.65 22 Step 2: Is there alkalemia or acidemia present? pH < 7.35 acidemia pH > 7.45 alkalemia , This is usually the primary disorder , Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 – 7.45) , You will need to check the PaCO, HCO- and anion gap 23 Step 3: Is the disturbance respiratory or metabolic? What is the relationship between the direction of change in the pH and the direction of change in the PaCO? In primary respiratory disorders, the pH and 2 PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO change in the same 2direction. pH ? PaCO ? Acidosis Respiratory 2 pH ? PaCO ? Acidosis Metabolic& 2 pH ? PaCO ? Alkalosis Respiratory 2 pH ? PaCO ? Alkalosis Metabolic 2 Step 4: Is there appropriate compensation for the primary disturbance? Usually, compensation does not return the pH to normal (7.35 – 7.45). Disorder Expected compensation Correction factor Metabolic acidosis PaCO = (1.5 x [HCO-]) +8 ? 2 23 Acute respiratory acidosis Increase in [HCO-]= ? PaCO/10 ? 3 32 Chronic respiratory acidosis (3-5 Increase in [HCO-]= 3.5(? PaCO/10) 32 days) Metabolic alkalosis Increase in PaCO = 40 + 0.6(?HCO-) 23 Acute respiratory alkalosis Decrease in [HCO-]= 2(? PaCO/10) 32 Chronic respiratory alkalosis Decrease in [HCO-] = 5(? PaCO/10) to 32 7(? PaCO/10) 2 If the observed compensation is not the expected compensation, it is likely that more than one acid-base disorder is present. Step 5: Calculate the anion gap (if a metabolic acidosis exists): AG= [Na+]-( [Cl-] + [HCO-] )-12 ? 2 3 , A normal anion gap is approximately 12 meq/L. , In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L; the ―normal‖ anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL decrease in the plasma albumin concentration (for example, a patient with a plasma albumin of 2.0 gm/dL would be approximately 7 meq/L.) , If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical situations. o Elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure o Toxic ingestion is suspected , OSM gap = measured OSM – (2[Na+] - glucose/18 – BUN/2.8 o The OSM gap should be < 10 Step 6: If an increased anion gap is present, assess the relationship between the increase in the anion gap and the decrease in [HCO-]. 3 Assess the ratio of the change in the anion gap (?AG ) to the change in [HCO3-] (?[HCO-]): 3 ?AG/?[HCO-] 3 This ratio should be between 1.0 and 2.0 if an uncomplicated anion gap metabolic acidosis is present. If this ratio falls outside of this range, then another metabolic disorder is present: , If ?AG/?[HCO-] < 1.0, then a concurrent non-anion gap metabolic acidosis is likely to be 3 present. , If ?AG/?[HCO-] > 2.0, then a concurrent metabolic alkalosis is likely to be present. 3 It is important to remember what the expected ―normal‖ anion gap for your patient should be, by adjusting for hypoalbuminemia (see Step 5, above.) Table 1: Characteristics of acid-base disturbances Disorder pH Primary problem Compensation ? ? in HCO- ? in PaCO Metabolic acidosis 32 ? ? in HCO- ? in PaCO Metabolic alkalosis 32 ? ? in PaCO ? in [HCO-] Respiratory acidosis 23 ? ? in PaCO ? in [HCO-] Respiratory alkalosis 23 Table 2: Selected etiologies of respiratory acidosis o Airway obstruction - Upper - Lower o COPD o asthma o other obstructive lung disease o CNS depression o Sleep disordered breathing (OSA or OHS) o Neuromuscular impairment o Ventilatory restriction o Increased CO2 production: shivering, rigors, seizures, malignant hyperthermia, hypermetabolism, increased intake of carbohydrates o Incorrect mechanical ventilation settings Table 3: Selected etiologies of respiratory alkalosis o CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma, brain tumor, CNS infection o Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2 o Stimulation of chest receptors: pulmonary edema, pleural effusion, pneumonia, pneumothorax, pulmonary embolus o Drugs, hormones: salicylates, catecholamines, medroxyprogesterone, progestins o Pregnancy, liver disease, sepsis, hyperthyroidism o Incorrect mechanical ventilation settings Table 4: Selected causes of metabolic alkalosis o Hypovolemia with Cl- depletion o GI loss of H+ , Vomiting, gastric suction, villous adenoma, diarrhea with chloride-rich fluid o Renal loss H+ , Loop and thiazide diuretics, post-hypercapnia (especially after institution of mechanical ventilation) o Hypervolemia, Cl- expansion o Renal loss of H+: edematous states (heart failure, cirrhosis, nephrotic syndrome), hyperaldosteronism, hypercortisolism, excess ACTH, exogenous steroids, hyperreninemia, severe hypokalemia, renal artery stenosis, bicarbonate administration Table 5: Selected etiologies of metabolic acidosis o Elevated anion gap: o Methanol intoxication o Uremia ao Diabetic ketoacidosis, alcoholic ketoacidosis, starvation ketoacidosis o Paraldehyde toxicity o Isoniazid ao Lactic acidosis , Type A: tissue ischemia , Type B: Altered cellular metabolism bbo Ethanol or ethylene glycol intoxication o Salicylate intoxication a Most common causes of metabolic acidosis with an elevated anion gap b Frequently associated with an osmolal gap o Normal anion gap: will have increase in [Cl-] o GI loss of HCO- 3 , Diarrhea, ileostomy, proximal colostomy, ureteral diversion o Renal loss of HCO- 3 , proximal RTA , carbonic anhydrase inhibitor (acetazolamide) o Renal tubular disease , ATN , Chronic renal disease , Distal RTA , Aldosterone inhibitors or absence , NaCl infusion, TPN, NH+ administration 4 Table 6: Selected mixed and complex acid-base disturbances Disorder Characteristics Selected situations ?in pH , Cardiac arrest Respiratory acidosis with ? in HCO , Intoxications 3metabolic acidosis ? in PaCO , Multi-organ failure 2 , Cirrhosis with diuretics ?in pH Respiratory alkalosis with , Pregnancy with vomiting ? in HCO- 3metabolic alkalosis , Over ventilation of COPD ? in PaCO 2 pH in normal range , COPD with diuretics, Respiratory acidosis with ? in PaCO, vomiting, NG suction 2metabolic alkalosis ? in HCO- , Severe hypokalemia 3 , Sepsis pH in normal range , Salicylate toxicity Respiratory alkalosis with ? in PaCO , Renal failure with CHF or 2metabolic acidosis ? in HCO pneumonia 3 , Advanced liver disease , Uremia or ketoacidosis with Metabolic acidosis with metabolic pH in normal range vomiting, NG suction, diuretics, alkalosis HCO- normal 3etc. Suggested additional reading: , Rose, B.D. and T.W. Post. Clinical physiology of acid-base and electrolyte disorders, 5th ed. New York: McGraw Hill Medical Publishing Division, c2001. , Fidkowski, C And J. Helstrom. Diagnosing metabolic acidosis in the critically ill: bridging the anion gap, Stewart and base excess methods. Can J Anesth 2009;56:247-256. , Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—first of two parts. N Engl J Med 1998;338:26-34. , Adrogué, H.J. and N.E. Madias. Management of life-threatening acid-base disorders—second of two parts. N Engl J Med 1998;338:107-111. To comment on or discuss this article, please visit the ATS Forums.