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。     

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。     

其他

20023545急诊危重患者的酸碱失衡:附1 239例分析趣志强…中国危重病急救医学一。02,14(4)一210~212 1 195例(96·45肠)伴有8种类型的酸碱失衡。其中呼吸性碱中毒(呼碱)303例最常见,其它依次为呼碱并代谢性碱中毒(代碱)202例,呼吸性酸中毒(呼酸)175例,代谢性酸中毒二代酸)162例,     

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…     

混合型酸碱平衡紊乱的进展

混合型酸碱平衡紊乱(mixed acid basedisturbances)在临床上并不少见,常发生于严重复杂疾病中,也可因治疗措施不当而促成。混合型酸碱平衡乱紊(简称混合型酸碱失衡)是指病人同时存在两种或两种以上单纯型酸碱平衡紊乱(简称单纯型酸碱失衡)。单纯型酸碱失衡中代谢性酸中毒(简称代酸)、代谢性碱中毒(简称代碱)、呼吸性酸中毒(简称呼酸)和呼吸性碱中毒(简称呼碱)可分别相互组合。     

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。     

肝硬化酸碱平衡紊乱的预见性护理

文献报告肝硬化患者常并发酸碱平衡紊乱，其中单纯性呼吸性碱中毒的发生率占46．7％～63％。肝硬化治疗不当及肝病终末期，可发生多重酸碱平衡紊乱，多为呼碱型三重酸碱失衡（即呼吸性碱中毒合并代谢性碱中毒和代谢性酸中毒）。本义就1998年1月～2003年3月我科收治的87例肝硬化患者发生酸碱平衡紊乱32例的观察和护理作回顾性分析。     

肺心病慢性呼吸性酸中毒急性加剧致神志改变

自开展肺心病并Ⅱ型呼衰病人酸碱失衡研究以来,对呼吸性酸中毒(呼酸)并代谢性碱中毒(代碱)甚为重视,报道较多,但对慢性呼酸并急性呼酸或称慢性呼酸急性加剧有些忽略.现就我院1987～1988年冬     

慢性呼酸机械通气后——呼酸、呼碱、代碱三重酸碱紊乱

慢性呼酸机械通气后,酸碱紊乱情况如何?实用内科杂志1992年第4期刊登了裴建明等医师“呼吸性酸中毒合并呼吸性碱中毒”一文,且同时刊登了陶医师撰写的“商榷”文章,认为是呼吸性酸中毒合并代谢性碱中毒。本人认为慢性呼酸在机械通气后是呼酸、呼碱、代碱三量酸碱紊乱。其理由如下。机械通气后,无论二氧化碳分压(PaCO_2)降低到何     

三重酸碱失衡的治疗

自1977年阴离子隙(AG)用作判断酸碱失衡以来,临床上首先出现了混合性代谢性酸中毒,即高AG代谢性酸中毒(代酸)合并高氯代酸。1981年Narins等应用单纯性酸碱失衡预计代偿公式,作为判断单纯性或二重酸碱失衡的依据。二重酸碱失衡中以     

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.     

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.     

Acid-base disturbances in acute asthma

The clinical features, arterial blood gases, and acid-base profile were examined in 229 consecutive episodes of acute asthma in 170 patients who required hospitalization. A simple respiratory alkalosis was the most common acid-base disturbance, occurring in 48 percent of the episodes. Metabolic acidosis, either alone or as part of a mixed disturbance, was noted in 28 percent. Of 60 episodes presenting with respiratory acidosis, 37 (62 percent) had a coexistent metabolic acidosis. Metabolic acidosis was more likely to occur in male subjects and in patients with evidence of more severe airflow obstruction. Patients with metabolic acidosis had an average anion gap of 15.8 mEq/L; these patients were more hypoxemic than those without metabolic acidosis and there was a significant inverse correlation between the anion gap and the degree of hypoxemia. We conclude that metabolic acidosis is a common finding in acute, severe asthma and suggest that the pathogenesis of lactic acidosis is multifactorial and includes contributions from lactate production by respiratory muscles, tissue hypoxia, and intracellular alkalosis.     

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.     

危重病患者并发低氧血症和酸碱平衡紊乱及预后分析

目的了解危重病患者低氧血症和酸碱平衡紊乱的发生发展规律,探讨其发生机制,分析低氧血症和酸碱平衡紊乱对危重病患者预后的价值,提高对危重病患者低氧血症和酸碱平衡紊乱的认识。方法选择我院2000年1月至2008年12月住院救治的危重病患者368例为研究对象,以同期内科住院患者359例作为对照,所有危重病患者和对照组,用同样的方法测定动脉血气数值：pH、PaCO2、PCO2、HCO3-、TCO2、BE和SaO2;同时测定血生化参数：血清钾、钠、氯、肝功能、肾功能及血糖;低氧血症依据PaO2浓度作出诊断,计算阴离子隙（AG）和潜在HCO3-,依据酸碱失衡预计代偿公式（PCF）,做出酸碱失衡的判断。结果危重组368例患者中,发生低氧血症者175例,占47．6％,死亡者79例,占45．1％,其中PaO2≤40mmHg（5．3kPa）者死亡34例,占69．4％;对照组359例患者中,发生低氧血症者76例,占21．2％,死亡者17例,占22．4％,其中PaO2≤40mmHg（5．3kPa）者死亡7例,占36．8％,危重组和对照组低氧血症的发生率和病死率比较,均有非常显著性差异（P〈0．001）。危重组368例患者中,发生不同类型的酸碱失衡共315例,占85．6％,其中死亡者220例,占69．8％;对照组359例患者中,发生单纯性和二重性酸碱平衡紊乱共128例,占35．6％,其中死亡者26例,占20．3％,危重组和对照组酸碱失衡的发生率和病死率比较,均有非常显著性差异（P〈0．001）。结论危重病患者不但低氧血症和酸碱失衡的发生率较高,病死率亦非常高,而且与预后有关,因此,应重视危重病患者低氧血症与酸碱平衡紊乱的预防和及时救治具有重要的临床意义。     

完善三重酸碱失衡判断方法

目的分析目前临床上在三重酸碱失衡判断中存在的问题,完善判断方法。方法采用归拿整理的方式,将作者最近提出的各种酸碱失衡判断方法及公式相结合,用于三重酸碱失衡的判断。结果新的判断方法简单实用,可准确地判断三重酸碱失衡。结论三重酸碱失衡中的代碱及高AG代酸,原判断方法选用不当,本该用作高AG代酸判断的潜在HCO_3^-概念,被用在了代碱的补充判断上,使两者都存在误判现象,判断方法需要改进。     

重型病毒性肝炎并发三重酸碱失衡及其临床意义

探讨重型病毒性肝炎合并三重酸碱失衡的发病机理及其临床意义。用阴离子间隙（AG）概念，对99例重型肝炎患者血气分析和血电解质检查进行分析。有21例（21．2％）呈三重酸碱失衡(TABD），均为呼碱型（呼碱＋代碱＋代酸），大多数由原发呼碱或代碱转为呼碱合并代碱，最后发展为TABD。比较发现，合并TABD患者其肝肾综合征、肝性脑病、自发性细菌性腹膜炎和上消化道出血的发生率显著高于单纯酸碱失衡患者，且常合并两种以上并发症处在重型肝炎病程的晚期。重型肝炎患者合并TABD是多脏器损害和多因素作用的结果。     

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。