慢性左心衰合并慢性阻塞性肺疾病的临床研究

目的 探讨慢性左心衰合并慢性阻塞性肺疾病的治疗方法.方法 选取本院2010年12月～2013年5月诊治的慢性左心衰合并慢性阻塞性肺疾病患者62例,随机分为两组,常规药物治疗的患者31例为对照组,常规药物治疗联合无创双水平气道正压通气治疗的患者31例为观察组,比较两组患者治疗前后的临床指征和心肺功能改善情况.结果 治疗后,两组患者心率、呼吸频率均显著下降.观察组患者心率、呼吸频率明显低于对照组,观察组心肺功能改善情况明显好于对照组,差异有统计学意义（P＜0.05）.结论 无创双水平气道正压通气可明显改善慢性左心衰合并慢性阻塞性肺疾病患者的临床病症,改善患者的心肺功能.     

左卡尼汀治疗慢性肾衰竭合并冠心病心律失常的效果观察

目的：探讨左卡尼汀治疗慢性肾衰竭合并冠心病心律失常的临床效果。方法选取2011年4月~2012年6月入住本院进行治疗的48例慢性肾衰竭合并冠心病心律失常患者作为研究对象,将其随机分为对照组和观察组,每组24例,对照组进行常规治疗,如血液透析治疗、降压药物治疗、贫血纠正治疗、扩张血管药物治疗以及强心利尿药物治疗,观察组在常规治疗的基础上采用左卡尼汀进行治疗,患者进行透析后,静脉注射左卡尼汀1g。两组患者均治疗3个月,治疗结束后,比较两组的临床疗效。结果观察组治疗总有效率为87.50%,明显高于对照组的66.67%,差异有统计学意义(P<0.05)。治疗后,两组患者的左心室射血分数均明显提高,左心室收缩末期内径和左心室舒张末期内径均明显降低,差异有统计学意义(P<0.05);观察组治疗后的各项指标改善程度均明显高于对照组,差异有统计学意义(P<0.05)。结论左卡尼汀能够有效治疗慢性肾衰竭合并冠心病心律失常,有效改善患者的肾功能和心功能,使患者的生活质量得到提升,值得临床推广应用。     

左卡尼汀治疗慢性肾衰竭透析患者心衰的临床价值体会

目的:研究左卡尼汀治疗慢性肾衰竭透析患者心衰的临床价值体会。方法:选取我院2016年9月～2018年1月期间收治的慢性肾衰合并心衰患者90例,采用数字随机表法,成立实验组和参照组,每组各45例;参照组实施常规血液透析治疗,实验组在常规血液透析治疗的基础上联用左卡尼汀治疗,对比两组患者的临床价值。结果:实验组的临床效果显著好于参照组,具有统计学意义(P0.05);实验组的心功能改善情况显著好于参照组,具有统计学意义(P0.05)。讨论:讨论:讨论:左卡尼汀可有效缓解慢性心衰合并心衰患者的病情,在临床上取得颇为显著的治疗效果,该治疗方案可在临床中进一步推广使用。     

硝酸甘油联合氨酰心安治疗急性心肌梗死合并左心衰的临床观察

目的 观察硝酸甘油联合氨酰心安治疗急性心肌梗死（AMI）合并左心衰的临床疗效.方法 选取我院2010年1月-2013年1月AMI合并左心衰患者60例,按照随机数字表法分为对照组和观察组,每组30例.对照组在常规治疗基础上给予硝酸甘油静脉泵入;观察组在常规治疗基础上加用硝酸甘油和氨酰心安.5～7d为1疗程,1疗程后,观察两组患者临床症状及体征改善情况,比较两组临床疗效.结果 对照组患者显效15例,有效9例,无效6例,有效率80.0%,治疗过程中出现低血压2例,头痛1例,窦性心动过速3例;观察组患者显效22例,有效6例,无效2例,有效率93.33%,治疗过程中出现低血压1例,头痛2例,不良反应症状随药物停用而逐渐缓解.观察组临床治疗有效率高于对照组,差异有统计学意义（P＜0.05）.结论 对AMI合并左心衰患者采取小剂量的硝酸甘油联合氨酰心安进行治疗,临床疗效满意,安全性较好,是治疗AMI合并左心衰的理想方案.     

血液透析联合血液灌流治疗慢性肾衰竭合并矿物质-骨代谢异常(CKD-MBD)的临床疗效观察

目的:探索血液透析联合血液灌流用于治疗慢性肾衰竭合并矿物质-骨代谢异常的效果。方法:选取在某院于2013年7月~2016年7月间收治的慢性肾衰竭合并矿物质-骨代谢异常患者中随机抽取出82例作为研究对象,将患者随机分为观察组和对照组,其中对照组患者采用血液透析治疗,观察组患者采用血液透析+血液灌流治疗,对比分析两组患者的治疗效果。结果:观察组患者的治疗总有效率92.68%,高于对照组的75.61%,P0.05;在实验室指标上,观察组患者的P3+、iPTH、BALP、FGF-23、OPG指标值均低于对照组,P0.05;两组患者在Ca2+水平上对比差异不明显,P0.05。结论:在慢性肾衰竭合并CKD-MBD治疗中采用血液透析联合血液灌流治疗效果确切,有助于改善患者的矿物质-骨代谢状况,提高患者的生活质量,值得推广应用。     

吗啡联合硝普钠在急性左心衰患者院前急救中的应用效果分析

目的：探究吗啡联合硝普钠在急性左心衰患者院前急救中的应用效果。方法：选择我院2013年1月～2014年12月收治的110例急性左心衰患者，随机将其分为两组，对照组和观察组，每组55例。对照组给予硝酸甘油治疗，观察组给予吗啡联合硝普钠治疗，观察两组治疗效果。结果：观察组的总有效率为90.91%明显高于对照组的70.91%，差异显著，具有统计学意义，P<0.05；观察组的不良反应发生率为9.09%，对照组为10.91%，无明显差异，不具有统计学意义，P>0.05。结论：对于急性左心衰患者院前急救使用吗啡联合硝普钠治疗，可将治疗有效率显著提高，安全、快速，可以考虑在临床上使用。     

二甲双胍对合并2型糖尿病慢性心力衰竭患者的疗效

目的:探究2型糖尿病合并慢性心衰患者采取二甲双胍治疗的临床疗效。方法:择取2017年3月～2018年5月期间在某院接受治疗的2型糖尿病合并慢性心衰患者共60例作为研究对象,根据随机数字表法将其分为对照组及观察组,每组30例。对照组患者采取常规治疗,观察组患者基于常规疗法采取二甲双胍治疗,对两组患者治疗后血糖水平及心功能改善情况进行比较。结果:观察组患者血糖水平显著低于对照组,且心功能指标中心率及LVEF改善效果显著优于对照组,数据差异有统计学意义(P0.05);而心功能指标中LVDD两组患者数据无明显差异(P0.05)。结论:2型糖尿病合并慢性心衰患者采取二甲双胍治疗效果显著,该种疗法值得在临床中推广应用。     

硝酸异山梨酯与硝酸甘油治疗冠心病合并急性左心心功能不全的临床疗效比较

目的 比较硝酸异山梨酯与硝酸甘油在治疗冠心病合并急性左心心功能不全时的临床疗效.方法 选择诊断为冠心病合并急性左心衰的患者 120 例,采用随机数字表法分为硝酸异山梨醇组(观察组)和硝酸甘油组(对照组)各60例,对两组治疗的临床疗效和不良反应进行比较分析.结果 观察组的临床总有效率为95.0％,明显高于对照组的75.0％,两组差异有统计学意义(P＜0.05);且观察组的不良反应发生率为3.3％,明显低于对照组的15.0％,两组差异具有统计学意义(P＜0.05).结论 硝酸异山梨酯能明显改善冠心病合并急性左心衰患者的临床症状,且不良反应的发生率较低,值得在临床中进一步推广使用.     

乌拉地尔治疗高血压合并急性左心衰的疗效分析

目的　观察乌拉地尔对高血压合并急性左心衰的疗效。方法　对 46例高血压合并急性左心衰患者随机分成两组 ,对治疗组 2 3例应用乌拉地尔治疗 ,与使用硝酸甘油治疗的对照组 2 3例进行疗效比较 ,观察两组治疗后血压变化及心衰改善、心衰缓解时间。结果　乌拉地尔治疗组在用药后 2 0min内收缩压和舒张压下降程度优于对照组 ,心衰改善及心衰缓解时间明显短于对照组 (P <0 .0 1) ,差异有显著性。结论　乌拉地尔治疗高血压合并急性左心衰起效快、效果确切 ,是一种理想的扩血管药物     

头孢他啶联合左氧氟沙星对心衰合并肺部感染患者炎症因子及脑钠肽水平的影响

目的：探讨头孢他啶联合左氧氟沙星治疗心衰合并肺部感染时对患者炎症因子及脑钠肽水平的影响。方法：选取我院2015年1～7月收治的70例心衰合并肺部感染患者,将患者随机分为两组,各35例,对照组采用单纯头孢他啶治疗,观察组在对照组基础上加用左氧氟沙星治疗,分析比较两组治疗效果。结果：观察组LVEF、LVEDD、LVESD三项指标均显著优于对照组,差异显著（P＜0.05）,LVDs值治疗前后均无显著差异（P＞0.05）;观察组血液中血浆白细胞介素-6、脑钠肽及肿瘤坏死因子-α的水平明显低于对照组,差异显著（P＜0.05）;观察组病菌清除率高于对照组,差异显著（P＜0.05）;观察组治疗有效率显著高于对照组,差异显著（P＜0.05）。结论：头孢他啶联合左氧氟沙星在心衰合并肺部感染治疗中可有效降低患者血液中炎症因子,清除患者体内的病菌,对患者预后及生活水平的提高具有重要的作用,在临床值得推广。     

Acetaminophen-Related Acute Renal Failure without Fulminant Liver Failure

Background . Our patient experienced acute renal failure but not fulminant hepatic failure from acetaminophen toxicity. Objective . To review the clinical and laboratory characteristics of similar cases of acetaminophen nephrotoxicity. Methods . A MEDLINE search and medical record search at two large teaching hospitals. Results . We reviewed our index case, a patient at Jackson Memorial Hospital, and 34 additional patients with acetaminophen nephrotoxicity reported in the literature. Oliguria was present in 23 of 31 patients. There was no difference in peak serum creatinine levels between patients treated with N-acetylcysteine and those not treated. The onset of acute renal failure was from 2–5 days after overdose, and peak serum creatinine levels occurred 3–16 days (average 7.3 days) after overdose. Thirteen patients required hemodialysis; all but one were oliguric. Renal failure was spontaneously reversible in all patients. Conclusion . Although uncommon, it is possible to have acute renal failure due to acetaminophen toxicity in the absence of fulminant hepatic failure.     

Framing Failure

This essay offers a conceptual framework for thinking about failure—a type of falling short with respect to some normatively characterized activity, task or expectation. It brings this discussion to bear on the complexities of therapeutic failure, noting how attributions of such failure may make controversial assumptions about the normative status of ends and the match between means and ends, as well as the more common location of responsibility in the therapeutic subject. In many cases, failure should be seen as a learning prelude to success, rather than as its exclusion.     

Chronic Heart Failure

Heart failure (HF) is a complex syndrome characterized by the inability of the heart to maintain a normal cardiac output without elevated intracardiac filling pressures, resulting in signs of pulmonary and peripheral edema and symptoms of dyspnea and fatigue. Central to the management of HF is a multifaceted pharmacological intervention to abate the harmful counter-regulatory effects of neurohormonal activation and avid salt and water retention. Whereas up to 40 years ago HF was managed with diuretics and leaf of digitalis, the cornerstones of therapy for HF patients with systolic dysfunction now include ACE inhibitors or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers), β-adrenoceptor antagonists (β-blockers), and aldosterone antagonists, which have significantly improved survival. However, with the increasing number of beneficial therapies, there are challenges to implementing all of them. Specific cardiomyopathies also merit specific considerations with respect to treatment, and — unfortunately — there is no therapy for HF with preserved left ventricular ejection fraction that has been shown to improve survival. Although mortality has improved in HF, the biggest challenge to treatment lies in addressing the morbidity of this disease, which is now the most common reason for hospital admission in our aged population. As such, there are many therapies that may serve to improve the quality of life of HF patients. Future HF treatment regimens may include direct cellular therapy via hormone and cytokine signaling or cardiac regeneration through growth factors or cell therapy.     

Congestive Heart Failure

Left ventricular systolic dysfunction is associated with neurohormonal activation which contributes to progressive ventricular remodeling and worsening clinical heart failure. Renin-angiotensin-aldosterone and sympathetic nervous systems are activated, not only in patients with clinically overt heart failure, but also in patients with asymptomatic or minimally symptomatic left ventricular systolic dysfunction. Activation of the angiotensin and adrenergic systems produces deleterious effects on systemic and coronary hemodynamics, promotes myocyte hypertrophy and fibroblast growth, and myocyte necrosis and apoptosis. Thus, therapy of heart failure should consist of pharmacologic agents not only to relieve symptoms but also to prevent and attenuate ventricular remodeling and progressive heart failure, thereby improving prognosis. In patients who are symptomatic, ACE inhibitors along with digitalis and diuretics as initial therapy (triple therapy) have the greater potential to improve exercise tolerance and decrease the incidence of treatment failure compared with diuretics alone or a combination of diuretics and digitalis. Diuretics alone should not be considered for long-term therapy as plasma renin activity, angiotensin II, aldosterone, norepinephrine and vasopressin levels may increase. ACE inhibitors decrease mortality in patients with heart failure resulting from left ventricular systolic dysfunction. The results of presently available studies indicate that angiotensin II receptor blockers (ARBs) do not provide any advantage over ACE inhibitors regarding survival benefit but may be better tolerated. Long-term adrenergic inhibition with the use of ß-adrenoceptor antagonists added to ACE inhibitors is associated with attenuation of ventricular remodeling, improvement in ventricular function and clinical class and survival of patients with symptomatic systolic left ventricular failure. Thus, initial pharmacotherapy for systolic heart failure should consist of: (i) maximal tolerated dosages of ACE inhibitors; (ii) ARBs if ACE inhibitors are not tolerated because of intractable cough or angioedema; (iii) adequate dosages of hydralazine and isosorbide dinitrate if ACE inhibitors or ARBs are not tolerated; (iv) relatively low dosages of digoxin (serum concentrations of ≤ 1.0 ng/dl) if not contraindicated; and (v) diuretics to relieve congestive symptoms. Addition of spironolactone to ACE inhibitors can result in a significant reduction in the risk of sudden death in patients with symptomatic severe heart failure. Myocardial infarction resulting from ischemic heart disease is the most common cause of systolic left ventricular failure and the therapeutic modalities with potential to reduce the risks of myocardial infraction, such as risk factor modification, adequate control of diabetes and hypertension, antiplatelet agents and lipid-lowering agents, should also be included in the initial therapy.     

胰源性胃肠功能衰竭

1 概述 长期以来,人们对胃肠功能衰竭在重症急性胰腺炎(Severe Acute Pancreatitis,SAP)中的作用重视不够,因此,SAP并发胃肠功能衰竭的文献报道较少,临床治疗方法不多.单纯西医多以禁饮、禁食、胃肠减压来处理胃肠,即"静"的方法,但临床疗效不佳.而中西医结合是以"动静结合"的方法,即"静"为暂时的禁饮、禁食、胃肠减压;"动"为早期采用通里攻下方药,加速胃肠蠕动,促进胃肠衰竭的改善.我们通过长期的临床实践和动物实验发现,胃肠衰竭既是SAP的并发症,又是促使SAP病情恶化及死亡的重要因素之一.     

序贯(无创-有创-无创)呼吸机辅助通气治疗左心衰竭伴呼吸衰竭的临床分析

目的探讨序贯(无创-有创-无创)呼吸机辅助通气治疗左心衰竭伴呼吸衰竭的临床疗效。方法随机选取我科2007年7月至2012年7月收治的64例左心衰竭伴呼吸衰竭患者,将随机分为观察组和对照组,每组各32例,观察组采用序贯(无创-有创-无创)呼吸机辅助通气治疗,对照组采用有创呼吸机辅助通气治疗。结果观察组的治疗效果明显优于对照组,气管插管难易度低和风险少,呼吸机通气时间、平均住院时间、呼吸机相关肺炎(VAP)发生率均低于对照组,两组对比有差异(P<0.05),动脉氧分压早期改善缓慢,远期无明显差别。结论序贯(无创-有创-无创)呼吸机辅助通气治疗左心衰竭伴呼吸衰竭的效果良好,可有效降低并发症发生率,提高抢救成功率。