酸碱失衡类型系统划分及划分视图设计

酸碱失衡类型划分在不断完善。传统的酸碱失衡类型仅有：代谢性酸中毒（代酸）、代谢性碱中毒（代碱）、呼吸性酸中毒（呼酸）、呼吸性碱中毒（呼碱）、呼酸并代酸、呼酸并代碱、呼碱并代酸、呼碱并代碱八型。随着阴离子间隙（anion gap,AG）和潜在HCO3^-（potential bicarbonate）概念在酸碱失衡领域中的应用,人们又提出了几种新的酸碱失衡类型：①高Cl-性代酸并高AG代酸;②代碱并高AG代酸;③三重酸碱失衡（triple acid—base disturbance,TABD）,包括呼酸＋代碱＋高AG代酸（呼酸型TABD）和呼碱＋代碱＋高AG代酸（呼碱型TABD）两型。     

急性心肌梗死患者血气变化及酸碱失衡分析

目的：探讨急性心肌梗死（AMI）患者的酸碱失衡类型及临床意义。方法：回顾性分析134例AMI患者动脉血气参数（pH、PaO2、PaCO2、HCO3^-）、酸碱失衡类型和电解质资料。结果：134例患者动脉血氧分压（PaO2）〈80mmHg者72例（53％）;发生不同类型酸碱失衡113例（84％）,最常见是呼吸性碱中毒并代谢性酸中毒（呼碱代酸）,有24例（18％）,其次为呼吸性酸中毒并代谢性酸中毒（呼酸代酸）、单纯性呼碱、单纯性代酸等,单纯性酸碱失衡43例（32％）,二重性酸碱失衡64例（48％）,三重性酸碱失衡（TABD）6例（4％）。结论：AMI患者常发生低氧血症和酸碱失衡,伴有心源性休克时容易伴有代酸;严重代谢性酸中毒合并呼酸是病情严重的标志。     

关于呼酸和呼碱同时存在的探讨——对“呼吸性酸中毒并呼吸性碱中毒性酸碱紊乱”一文的商榷

酸碱紊乱有四个基本类型即呼酸、呼碱、代酸、代碱,目前多数意见只能有三种类型同时存在,即呼酸和代酸,代碱并存称为呼酸型三重酸碱失衡(TABD);呼碱和代酸,代碱并存称为呼碱型TABD 但呼酸和呼碱不能同时并存,为此不可能有呼酸、呼碱、代酸、代碱     

三种不同方法对三重酸碱紊乱判定的比较

三种不同方法对三重酸碱紊乱判定的比较罗炎杰，肖欣荣三重酸碱紊乱（ＴＡＢＤ）是指一种呼吸性酸碱紊乱合并高阴离子间隙（ＡＧ）代酸或代碱，其中呼酸＋代酸＋代碱者为呼酸型ＴＡＢＤ，呼碱＋代酸＋代碱者为呼碱型ＴＡＢＤ。目前判定ＴＡＢＤ的方法尚不一致，判定结果差...     

呼吸衰竭时的酸碱失衡及其临床意义

呼吸衰竭时常因缺氧和（或）CO2潴留,并发酸碱失衡。常见的异常动脉血气及酸碱失衡类型是：①严重缺氧伴有呼酸;②严重缺氧伴有呼酸并代碱;③严重缺氧伴有呼酸并代酸;④缺氧伴有呼碱;⑤缺氧伴有呼碱并代碱;⑥缺氧伴有三重酸碱失衡（TABD）。一、严重缺氧伴有呼酸Ⅱ型呼吸衰竭患者因缺氧和CO2潴留同时存在,常可表现为严重缺氧伴有呼酸。1．动脉血气和血电解质变化特点：①动脉血二氧化碳分压（PaCO2）原发性升高;②HCO-3代偿性升高,但慢性呼酸必须符合预计Hny二24＋0．35xdPaAn02t5．58范围内;急性呼酸H仰＜刀11ill－c,ir…     

传染性非典型肺炎159例酸碱平衡与临床分型及病程关系分析

目的探讨各型严重急性呼吸综合征每周的酸碱失衡情况及其规律。方法159例患者，住院后每周测定血气分析，每位患者每周只取一次血气结果，共得血气分析结果430例次，分周分型进行统计。结果发病前2周，普通型和重型患者酸碱失衡以代碱呼碱为主；而极重型以呼碱代酸为主；极重型患者第1周呼碱型三重失衡比例较多，仅次于呼碱加代酸位居第二位：第3周后，普通型患者单纯代碱的比例迅速上升并跃居首位，而重型患者则虽也上升但相对较慢，代碱呼碱仍处于首位，极重型则代碱呼碱比例上升为首位；代碱代酸而同时不合并呼吸性酸碱失衡者仅在普通型存在；呼酸比例在普通型中从第2周逐渐增多，至第5周出现高峰。结论患者病程2周内出现呼碱代酸或呼碱型三重酸碱失衡，应高度警惕发展为极重型的可能，积极加强治疗；出现单纯的代碱或排除气道阻塞、呼吸肌疲劳及机械通气因素造成的呼酸，以及呼碱消失，可能预示着病情开始恢复；应用某些药物时要随时注意酸碱失衡，及时调整或纠正；应用机械通气要着重对呼碱因素进行治疗，合理调整压力水平。     

ICU危重患者血气分析1696例报告

目的提高对危重患者并发酸碱失衡的认识。方法对1696例危重患者酸碱失衡类型进行分析。结果ICU科1696例危重患者动脉血气中1648例（97．17％）伴有8种类型的酸碱失衡，其中呼吸性碱中毒（呼碱）最为常见，占447（26．36％）；其它依次为：代谢性酸中毒（代酸）316例（18．60％），呼碱合并代酸258例（15．24％），呼酸合并代碱196例（11．57％），呼吸性酸中毒（呼酸）160例（9．45％），呼碱合并代谢性碱中毒（代碱）138例（8.11％），呼酸合并代酸89例（5．23％），代碱44例（2．61％）。结论危重患者原发疾病常引起呼碱或呼酸，病情的发展或不适当的治疗导致代碱，严重外伤、顽固性休克、严重低氧血症肾功能不全而引起代酸。严重的呼碱并代碱、呼酸并代酸可导致患者出现重度的碱血症、酸血症。而致患者死亡。     

肝性脑病三重酸碱失衡的探讨

本文报道34例肝性脑病患者83例次三重酸碱失衡(TABD)分析结果,肝性脑病患者并发的TABD均为呼碱型。其预后险恶,病死率达82.4%。通常,原发疾病引起呼碱,而不适当的治疗引起代碱,严重低氧血症、消化道大出血、肝肾综合征及重度感染引起代酸。因此,及时正确地识别与处理,对于降低肝性脑病患者的病死率意义甚大。并且强调联合应用阴离子隙(AG)和潜在HCO_2~-在TABD诊断中的重要性。     

慢性阻塞性肺疾病与糖尿病并存患者三重酸碱紊乱20例

三重酸碱失衡主要见于危重病人,死亡率高,预后差,住我院慢性阻塞性肺疾病（COPD）与糖尿病并存110例患者,经血气分析和电解质检查结果,其中20例患者发生三重酸碱紊乱（呼酸并代酸代碱）,现分析如下.     

阴离子隙和潜在HCO3^-诊断慢性呼吸衰竭酸碱失衡的临床意义

目的探讨阴离子隙（AG）和潜在HCO3^-判断酸碱失衡类型的应用。方法同步测定动脉血气和血电解质，以酸碱失衡预计代偿公式，结合AG值和潜在HCO3^-对慢性呼吸衰竭患者进行酸碱失衡类型的判断。结果（1）代谢性酸中毒（代酸）31例次，其中高AG代酸22例次，高Cl^-代酸5例次，如不测定AG将有17例次代酸失检；（2）应用AG后，三重性酸碱失衡（TABD）从0增至14例次，在这14例次TABD中，如不应用潜在HCO3^-将有8例失检。结论（1）AG和潜在HCO3^-在提高代酸和TABD诊断率方面发挥了重要的作用，并且提出判断TABD的标准和步骤；（2）因有诸多因素影响AG值，使某些代酸患者AG值不能相应地升高，临床应用时应予注意。     

Acid-base disorders in hyperglycemia of insulin-dependent diabetic patients on chronic dialysis

The authors studied hyperglycemia occurring in insulin-dependent diabetic patients on chronic dialysis to determine the types of associated acid-base disorders, their treatment, and any differences from hyperglycemia in diabetic patients with intact renal function. Eighty-eight episodes of serum glucose greater than 25 mmol/L were observed, 23 in hemodialysis patients and 65 in patients on continuous peritoneal dialysis. Treatment consisted of low-dose insulin in 77 episodes and low-dose insulin plus saline in 11; no base was administered. Seventeen episodes (19%) presented with ketoacidosis. Arterial blood gas determinations were carried out at presentation in 37 of the episodes without ketoacidosis. Of these, 12 had respiratory alkalosis, six had respiratory acidosis and severe pulmonary edema, 14 had other single or mixed acid-base disorders, and only five had normal acid-base status. Insulin corrected the ketoacidosis in all instances and both pulmonary edema and respiratory acidosis in five of six instances. In eight cases metabolic alkalosis developed during treatment, without external acid loss. At the completion of treatment respiratory alkalosis was present in half the cases. No difference was noted between patients treated with hemodialysis or peritoneal dialysis. Insulin alone is sufficient for the management of hyperglycemia in dialysis patients. Certain acid-base disorders persist, but do not need further treatment. Hyperglycemia in patients on dialysis is characterized by infrequent development of metabolic acidosis and frequent presentation with respiratory alkalosis, by respiratory acidosis that is corrected by insulin, and by metabolic alkalosis developing during treatment without external cause.     

Distinctive acid-base pattern in Wernicke's encephalopathy

Wernicke's encephalopathy may result in severe morbidity and possible mortality when unrecognized. We report a distinctive acid-base pattern that has not been associated with this syndrome. This is a case series of patients with Wernicke's encephalopathy who had an arterial blood gas measurement performed on initial presentation. Exclusion criteria were patients with an unclear diagnosis of Wernicke's encephalopathy and those for whom no arterial blood gas measurement was performed. Four patients with Wernicke's encephalopathy were included in the analysis. All 4 patients exhibited an anion-gap (primary) metabolic acidosis, accompanied by a primary respiratory alkalosis. Three of 4 patients exhibited a significant lactic acidosis. None of the patients had any competing diagnoses or dysfunction to account for this acid-base pattern. Patients with Wernicke's encephalopathy may exhibit a distinctive acid-base pattern consisting of a primary metabolic acidosis in conjunction with a primary respiratory alkalosis. Observation of this acid-base disturbance should prompt clinicians to consider thiamine deficiency disorders as a possible cause.     

慢性肝衰竭和失代偿期肝硬化患者血气分析的变化

目的探讨慢性肝衰竭和失代偿期肝硬化患者血气分析变化的临床意义。方法回顾性分析我科收治的37例慢性肝衰竭和失代偿期肝硬化患者的血气分析资料。结果2例患者出现明显的缺氧表现,4例患者出现立位性缺氧表现,11例患者感轻度胸闷;在36例存在酸碱失衡的患者,慢性肝衰竭组存在单纯酸碱失衡9例,两重酸碱失衡10例,三重酸碱失衡2例,失代偿期肝硬化组存在单纯酸碱失衡8例,两重酸碱失衡7例。两组患者在酸碱失衡的类型方面无统计学差异;两组均以碱中毒为主。慢性肝衰竭组中比例较高的三种类型依次为呼吸性碱中毒合并代谢性酸中毒（38．1％）、呼吸性碱中毒（23．8％）和代谢性碱中毒（14．3％）,单纯性代谢性酸中毒比例最低（4．8％）。失代偿期肝硬化组中比例较高的三种类型依次为呼吸陛碱中毒（46．7％）、呼吸性碱中毒合并代谢性碱中毒（26．7％）和呼吸性碱中毒合并代谢性酸中毒（20．0％）,代谢性碱中毒比例最低（6．7％）。结论慢性肝衰竭和失代偿期肝硬化患者存在酸碱失衡和低氧血症,动态监测血气分析并及时对症治疗对此类患眷具有重要的临床意义。     

120例重症肺结核继发感染的酸碱失衡分析

目的 分析重症肺结核继发感染的酸碱失衡情况?方法 以ABL-505血气电解质分析仪测定患者股动脉血,所得pH?PCO2?HCO-3值代入酸碱失衡预计代偿公式,首先判断出单纯型或混合型酸碱失衡,然后根据阴离子间隙判断有无三重酸碱失衡?结果 酸碱失衡发生率,单纯型>混合型>三重酸碱失衡;呼酸型>呼碱型,代酸与代碱基本相当;通过控制感染,酸碱失衡得到明显纠正?结论 重症肺结核继发感染可使肺组织严重破坏,通气与换气功能障碍,通气/血流比例失调,造成机体酸碱失衡?控制感染是治疗的关键,补充酸?碱性液体及纠正电解质紊乱是主要方法?确保机体内环境的稳定性及重要器官的供血供氧,防止出现多脏器功能衰竭?     

慢性阻塞性肺疾病急性加重机械通气治疗后酸碱平衡状态及电解质的变化

目的 研究机械通气后代谢性碱中毒及电解质紊乱的发生状况,探讨恰当的处理方法,旨在提高慢性阻塞性肺疾病急性加重(AECOPD)机械通气技术的临床应用水平,并提高AECOPD抢救的成功率和改善慢性阻塞性肺疾病(COPD)患者的预后.方法 回顾性分析伴Ⅱ型呼吸衰竭的AECOPD并使用机械通气的患者62例,并分为无创通气(35例)和有创通气(27例)二组,观察比较二组患者使用机械通气前、机械通气后1h、2h、3h、24 h、72 h及通气结束后的动脉血气及Na+、K+、Ca2+变化.结果 二组患者使用机械通气后呼吸性酸中毒明显改善.无创通气组通气3h时出现6例失代偿期碱中毒(17.14％),通气72 h后有22例(62.86％)患者出现代谢性碱中毒(包括代偿期和失代偿期),其中失代偿期碱中毒7例(25.93％),达碱中毒高峰.有创通气组在通气2h出现7例失代偿期碱中毒(25.93％),通气3h后即出现21例(77.77％)代谢性碱中毒,其中失代偿期碱中毒9例(33.33％).二组在通气前Na+低于正常,且K+高于正常值,通气结束后恢复正常.比较24h时碱中毒者与无酸碱平衡紊乱者的电解质,发现碱中毒者K+、Ca2+低于无酸碱紊乱者.结论 机械通气用于治疗伴Ⅱ型呼吸衰竭的AECOPD患者疗效肯定.机械通气后由于二氧化碳排出过快往往导致高碳酸血症呼出后代谢性碱中毒的发生,同时引起电解质钾、钙的降低.有创机械通气较无创机械通气代谢性碱中毒出现早.     

急性胰腺炎的电解质酸碱失衡及TPN治疗

本文报道25例急性出血坏死性胰腺炎（ANP），30例急性水肿性胰腺炎（AEP）的电解质与酸碱失调分析结果，以ANP表现显著，有低钾，低钠，低氯，低钙，低磷，代酸与代酸呼碱，低氧血症，低蛋白血症的表现,与AEP比较有显著性差异（P＜0．01）。16例ANP型采用全肠外营养（TPN）治疗，其中13例存活，与过去未用TPN治疗22例，14例死亡有显著差异（P＜0．01）。作者认为TPN协同治疗ANP患者，对于提供营养，抑胰分泌，促进胰腺组织修复，纠正水盐代谢紊乱，防止并发症与提高存活率有重要意义。对TPN的用法及热原供给作了简要讨论。     

Severe metabolic alkalosis due to pyloric obstruction: case presentation, evaluation, and management

A 46-year-old man presented to the emergency room with severe metabolic alkalosis, hypokalemia, and respiratory failure requiring intubation and mechanical ventilation. The cause of his acid-base disorder was initially unclear. Although alkalosis is common in the intensive care unit, metabolic alkalosis of this severity is unusual, carries a very high mortality rate, and requires careful attention to the pathophysiology and differential diagnosis to effectively evaluate and treat the patient. A central concept in the diagnosis of metabolic alkalosis is distinguishing chloride responsive and chloride nonresponsive states. Further studies are then guided by the history and physical examination in most cases. By using a systematic approach to the differential diagnosis, we were able to determine that a high-grade gastric outlet obstruction was the cause of the patients' alkalosis and to offer effective therapy for his condition. A literature review and algorithm for the diagnosis and management of metabolic alkalosis are also presented.     

Acid-base disturbance in patients with fulminant hepatic failure.

Forty-two arterial blood pH and gas determinations were carried out on 11 patients with fulminant hepatic failure. The most common type of acid-base disturbance was that of respiratory alkalosis in 22 cases (52.4%). This was partially compensated in 13 subjects (31.0%) while an accompanying metabolic alkalosis was present in 9 (21.5%). Partially compensated metabolic acidosis was observed on 15 occasions (35.7%), all of which were in patients with laboratory evidence of impaired renal failure. The mental status of the patients was evaluated in each of the categories of acid-base disturbances. Some degree of correlation was evident between the PCO2 and the magnitude of base excess and that of the severity of the encephalopathy. The lower PCO2 and greater negative base excess values tended to be nearly always present in totally comatose subjects. By contrast, there was no clear cut relationship between pH and mental state.     

Equilibrium of acidifying and alkalinizing metabolic acid-base disorders in cirrhosis.

BACKGROUND AND AIMS: Conflicting results exist with regard to metabolic acid-base status in liver cirrhosis, when the classic concept of acid-base analysis is applied. The influence of the common disturbances of water, electrolytes and albumin on acid-base status in cirrhosis has not been studied. The aim of this study was to clarify acid-base status in cirrhotic patients by analyzing all parameters with possible impact on acid-base equilibrium. PATIENTS AND METHODS: Fifty stable cirrhotic patients admitted to a university hospital. Arterial acid-base status was analyzed using the principles of physical chemistry and compared with 10 healthy controls. RESULTS: Apart from mild hypoalbuminemic alkalosis, acid-base state was normal in Child-Pugh A cirrhosis. Respiratory alkalosis was the net acid-base disorder in Child-Pugh B and C cirrhosis with a normal overall metabolic acid-base state (Base excess-1.0 (-3.6 to 1.6) vs 1.1 (-0.2 to 1.1) mmol/l, P = 0.136, compared with healthy controls, median (interquartile range)). Absence of an apparent metabolic acid-base disorder was based on an equilibrium of hypoalbuminemic alkalosis and of dilutional acidosis and hyperchloremic acidosis. CONCLUSION: A balance of offsetting acidifying and alkalinizing metabolic acid-base disorders leaves the net metabolic acid-base status unchanged in cirrhosis.