美国心力衰竭实用指南解读急性失代偿性心力衰竭的评估和处理

美国心力衰竭学会在2006年第1期心力衰竭杂志上发布了心力衰竭实用指南(Comprehensive Heart Failure Practice Guideline),其中包括心室重塑、心功能不全和心力衰竭的预防,心功能不全和心力衰竭患者的评估,无症状左室射血分数减低患者的处理和急性失代偿性心力衰竭的评估和处理等.本文就急性失代偿性心力衰竭的评估和处理的有关内容作一介绍,以供参考.     

高敏C反应蛋白与NT-proBNP在急性失代偿性心力衰竭患者中的临床意义

目的：探讨急性失代偿性心力衰竭（ADHF）患者的高敏C反应蛋白（hs-CRP）与氨基末端脑钠肽前体（NT-proBNP相关性及对心衰患者一年内住院次数的影响。方法：选择42例急性失代偿性心力衰竭患者及32例非急性失代偿性心力衰竭患者作为研究对象,根据纽约心脏协会（NYHA）功能分级分成四个组,分别测定入院、出院hs-CRP与NT-proBNP,统计一年来因心衰住院次数,比较高敏C反应蛋白与NT-proBNP相关性及对预后的影响。结果：急性失代偿性心衰患者hs-CRP及NT-proBNP数值明显高于非急性失代偿性心衰患者（P<0.05）,且预后差,一年内住院次数多。hs-CRP值与NT-proBNP值呈正相关性（P<0.01,r=0.831）。结论：急性失代偿性心力衰竭患者心功能越差,入院时hs-CRP值及NT-proBNP值越高,出院时hs-CRP值越高,一年内因心衰住院次数越多。hs-CRP值可以反应NT-proBNP值,对鉴别高风险患者具有重要意义。     

重组人脑利钠肽治疗急性失代偿性心力衰竭的临床疗效分析

目的:观察并探讨重组人脑利钠肽治疗急性失代偿性心力衰竭的临床疗效。方法:选取2016年11月——2018年11月期间来我院就诊的112例急性失代偿性心力衰竭患者,随机按患者就诊顺序分为对照组与实验组,人数相同各56例,实验组与对照组患者分别给予重组人脑利钠肽治疗与常规心力衰竭治疗,对两组患者的心率、呼吸频率、24h尿量以及心功能进行评价与对比。结果:实验组患者治疗后心率、呼吸频率、24h尿量以及LVEF、LVEDV、LVESD、LVESV指标与对照组结果比较均显著较优,差异具有统计学意义,P 0.05。结论:在急性失代偿性心力衰竭患者临床治疗中应用重组人脑利钠肽治疗具有确切疗效,值得推广应用。     

左西孟旦治疗重度失代偿性心力衰竭患者的疗效观察

目的观察左西孟旦治疗重度失代偿性心力衰竭的临床疗效。方法选取2009年至2010年医院收治的重度失代偿性心力衰竭患者70例,将其随机分治疗组和对照组,对照组患者给予常规治疗药物的同时加用多巴酚丁胺进行治疗;治疗组患者给予常规药物治疗的同时加用左西孟旦静脉注射进行治疗。观察2组患者的治疗效果,心功能指标的改善情况及不良反应的发生率。结果治疗组患者有效率为68.9%,对照组患者的有效率仅为31.4%;治疗组患者心功能指标的改善情况及临床症状的改善情况均明显优于对照组患者。2组均无严重不良反应出现。结论左西孟旦可有效治疗重度失代偿性心力衰竭,且有较好的安全性和耐受性。     

BNP在肺原性心脏病并心力衰竭患者中临床应用价值的探讨

目的比较慢性肺原性心脏病患者合并心力衰竭时血浆脑钠肽（BNP）水平变化。方法测定56例慢性肺原性心脏病心功能失代偿期患者治疗前BNP水平，比较其在右心功能不全（观察A组）和左心功能不全（观察B组）两种不同类型心力衰竭时的变化，并与30例慢性肺原性心脏病心功能代偿期患者（对照组）的BNP水平进行比较。结果观察A组BNP水平为（354±172）pg／ml，观察B组BNP水平为（568±375）pg／ml，两组间比较差异有统计学意义（P〈0．05）；观察A组、观察B组与对照组相比，差异也均有统计学意义（P〈0．05）。结论慢性肺原性心脏病患者合并心力衰竭时BNP水平明显升高，且升高程度与不同类型心力衰竭有关，结合其他临床资料，BNP水平有助于发现慢性肺原性心脏病患者是否合并心力衰竭，并对心力衰竭类型的判断也有一定价值。     

失代偿性心力衰竭患者入院血钾与预后的关系

[目的]回顾性观察患者入院时血清钾水平与严重失代偿心力衰竭预后各指标的相关性。[方法]纳入2003年1月~2004年12月所有收治本院的、入院诊断为心力衰竭,心功能NYHA分级III~IV级的患者共289例,记录入院时血清钾水平,观察血清钾水平与预后的相关性。[结果]血清钾水平与静脉注射硝酸甘油用量呈正相关(P=0.043),血清钾水平增高增加病死率(P﹤0.0001)。[结论]入院时血清钾水平在4.2mmol/L左右严重失代偿性心力衰竭患者的预后较好,对于心力衰竭患者监测血清钾是非常必要的。     

BNP在肺原性心脏病并心力衰竭患者中临床应用价值的探讨

目的 比较慢性肺原性心脏病患者合并心力衰竭时血浆脑钠肽(BNP)水平变化.方法 测定56例慢性肺原性心脏病心功能失代偿期患者治疗前BNP水平,比较其在右心功能不全(观察A组)和左心功能不全(观察B组)两种不同类型心力衰竭时的变化,并与30例慢性肺原性心脏病心功能代偿期患者(对照组)的BNP水平进行比较.结果 观察A组BNP水平为(354±172)pg/ml,观察B组BNP水平为(568±375)pg/ml,两组间比较差异有统计学意义(P＜0.05);观察A组、观察B组与对照组相比,差异也均有统计学意义(P＜0.05).结论 慢性肺原性心脏病患者合并心力衰竭时BNP水平明显升高,且升高程度与不同类型心力衰竭有关,结合其他临床资料,BNP水平有助于发现慢性肺原性心脏病患者是否合并心力衰竭,并对心力衰竭类型的判断也有一定价值.     

新活素治疗难治性心力衰竭的护理体会

新活素是一种新型的适用于在休息或轻微活动时呼吸困难的急性失代偿心力衰竭患者的治疗药物。本科2006年1月至2006年12月，应用新活素针对36例使用洋地黄效果不佳的难治性心力衰竭患者进行治疗，取得了较满意的疗效，现将护理心得报告如下。     

益气活血养心汤治疗失代偿期心力衰竭的疗效

目的探索益气活血养心汤治疗失代偿期心力衰竭的效果。方法选取江门市新会区司前人民医院2018年5-10月收治的失代偿期心力衰竭患者116例为研究对象,根据治疗方法分为对照组和观察组各58例,对照组给予常规西医治疗,观察组在对照组治疗基础上给予中药益气活血养心汤治疗,比较两组的治疗总有效率、心功能指标。结果治疗2个疗程后,观察组治疗总有效率为98.28%,高于对照组的84.48%,差异有统计学意义(P0.05);两组不良反应发生均较轻微,差异无统计学意义(P0.05);治疗后观察组的心功能指标LVEF高于对照组,LVESD、LVEDD均低于对照组,差异有统计学意义(P0.05)。结论益气活血养心汤治疗失代偿期心力衰竭疗效确切,促进患者心功能的改善,用药安全性高,值得推广。     

慢性心力衰竭急性失代偿合并低钠血症治疗体会

目的探讨慢性心力衰竭(chronic heart failure,CHF)急性失代偿合并低钠血症的临床治疗方法。方法选择2010年1月—2015年1月收治的31例CHF急性失代偿合并低钠血症患者作为观察组,另选同期31例CHF急性失代偿但不合并低钠血症患者作为对照组,观察并比较两组患者病死率、住院时间及左室射血分数(left ventricular ejection fraction,LVEF)。将观察组患者随机分为A组15例和B组16例,A组给予常规抗心力衰竭(心衰)治疗,B组在A组的基础上给予纠正低钠血症治疗。比较两组治疗后血钠水平及临床疗效。计量资料组间比较采用t检验,组内比较采用配对t检验,计数资料采用χ2检验,P0.05为差异有统计学意义。结果观察组病死率、住院时间、LVEF分别为32.3%、(15.8±2.6)d、(37.1±0.1)%,对照组分别为9.7%、(10.5±3.0)d、(44.5±0.1)%,两组比较差异均有统计学意义(均P0.05)。B组治疗后血钠水平、总有效率分别为(136.5±3.2)mmol/L、81.3%,均明显高于A组的(130.0±2.8)mmol/L、40.0%,差异均有统计学意义(均P0.05)。结论对于CHF急性失代偿合并低钠血症患者,应在抗心衰治疗基础上,积极纠正低钠血症,从而明显改善患者的心功能及预后。     

Diastolic heart failure

Diastolic heart failure is predominantly a disease of the elderly: at the age of 70 years, almost half of all patients with heart failure have diastolic heart failure. Hypertension and obesity are common underlying disorders in patients with diastolic heart failure. Patients with diastolic heart failure have an equal, or only slightly better, prognosis in terms of mortality compared to patients with systolic heart failure. Echocardiography can distinguish diastolic heart failure from systolic heart failure. Patients with heart failure and a normal ejection fraction almost certainly have a diastolic dysfunction. There is a lack of reliable data about the optimal medicinal treatment strategy for patients with diastolic heart failure. Angiotensin-converting enzyme (ACE) inhibitors, beta-blockers, and (non-dihydropyridine) calcium antagonists have therapeutic potential. Digoxin may be contraindicated.     

Diastolic heart failure

The rhythmic contraction and relaxation of the heart supply the body with the appropriate amount of blood. If the pump function deteriorates, heart failure occurs. After a symptom-free period of varying length, the clinical case of decompensatio cardiaca develops. The pathophysiological basis of the disease is abnormal systolic and/or diastolic function. The pathophysiology and therapy of systolic heart failure is well-known, however, the consequence of impaired diastolic function has not been fully revealed. Both cardiogenic shock and pulmonary edema can be caused by acute left heart failure. The main difference between the two disorders is that while cardiogenic shock is caused by systolic dysfunction, pulmonary edema is the consequence of impaired diastolic function. The importance of diastolic dysfunction is highlighted by the fact that the disorder can be caused by the most frequent diseases (hypertension, diabetes mellitus, coronary heart disease, myocardiac infarction). Consequently, in case of risk factors, it is very important to consider the possibility of diastolic dysfunction and be aware of the diagnostic and therapeutic options.     

Chronic heart failure.

1. The common symptoms and signs of chronic heart failure are dyspnoea, ankle swelling, raised jugular venous pressure and basal crepitations. Other conditions may be confused with chronic heart failure, including dependent oedema or oedema due to renal or hepatic disease. Shortness of breath may be due to respiratory disease or severe anaemia. Heart failure secondary to lung disease (cor pulmonale) should be distinguished from congestive cardiac failure. Heart failure may also present with less common symptoms including: cough, anorexia and weight loss, hepatic capsule pain and confusion. 2. Once heart failure is recognized, an attempt should be made to determine the underlying cause which may include valvular abnormalities, altered cardiac rhythm, specific heart muscle disease, coronary artery disease and hypertension. 3. Investigations initiated by the general practitioner include ECG, chest x-ray, full blood count (FBC), mean corpuscular volume (MCV), gamma transferase (GTT), creatinine and electrolytes, thyroxine. 4. If no underlying cause is found then referral should be considered in those under 75 and those aged 75 and over who fail to respond to treatment. 5. It is important to encourage patients to stop smoking, reduce weight and, where appropriate, alcohol consumption. Added salt should be avoided. 6. Digoxin should be prescribed to control the ventricular rate in those with atrial fibrillation. Renal function and potassium should be checked beforehand and the dose of digoxin adjusted to take into account any renal impairment. 7. Bendrofluazide is recommended in doses of not more than 10 mg (5 mg in the elderly). Potassium supplements may be required for those at high risk from hypokalaemia, including patients taking digoxin.(ABSTRACT TRUNCATED AT 250 WORDS)     

Palliation of heart failure

Heart failure is the major cause of morbidity and mortality in the United States. Stage D heart failure has a greater mortality rate than many cancers and has equivalent symptom burden and severity. There has been a paradigm shift in our understanding of the pathophysiology of heart failure. Progressive heart failure is associated with ventricular remodeling and a maladaptive neurohumoral response. Drug classes have evolved that curtail ventricular remodeling, and blunt neurohumoral responses reduce morbidity and mortality. Despite combination drug and device therapies, the management of Stage D heart failure includes palliation. Both cardiology and palliative specialists need to learn from one another in order to palliate these highly symptomatic patients. Such collaboration will enhance care and are the basis for well-conceived research trials.