老年人充血性心力衰竭早期临床表现

目的:分析老年人充血性心力衰竭早期临床表现和特点.方法:对我院2006年1月～2010年12月36例老年人充血性心力衰竭患者的临床资料进行回顾性分析.结果:在老年人充血性心力衰竭早期确诊后采用血管转换酶抑制剂、强心剂、抗感染、利尿和血管扩张剂等治疗,心功能Ⅰ级改善6例,占16.67%;Ⅱ级改善27例,占75%;心功能改善无效死亡3例,占8.33%.结论:老年人充血性心力衰竭早期临床表现无明显特征,容易漏诊和误诊,且死亡率高,应予重视.     

37例老年急性心力衰竭的急救护理体会

总结37例老年急性心力衰竭病人的病情观察和护理.认为针对老年急性心力衰竭的病人的病因及诱因加强护理,可以提高治疗效果,降低死亡率.     

福辛普利钠治疗慢性心力衰竭60例疗效观察

目的:随访观察福辛普利治疗慢性心力衰竭(CHF)的疗效.方法:56例慢性心力衰竭患者随机分成联合治疗组和对照组(常规治疗组),对照组采用洋地黄、利尿剂、血管扩张剂等常规治疗,治疗组在常规治疗基础上联合应用福辛普利5～10mg,随访观察1年.结果:联合治疗组:显效53.1%,有效40.6%,无效6.20%;常规治疗组:显效35.7%,有效42.9%,无效21.4%.治疗前后两组左室射血分数(LVEF)等相关参数均有显著性差异(P＜0.01).结论:福辛普利联合治疗慢性心力衰竭疗效显著,值得临床推广应用.     

对36例充血性心力衰竭的临床探讨

充血性心力衰竭(CHF)是各种病因心脏病的严重阶段,其发病率和死亡率都高,严重影响人类健康.笔者自2003年3月至2009年3月共收住36例CHF患者,对其临床特点和治疗的演变回顾性报道如下.     

慢性心力衰竭患者的临床护理体会

总结了慢性心力衰竭患者的临床护理体会,包括一般护理、心理护理、皮肤护理、饮食护理、运动护理、健康教育等.认为积极的临床护理对疾病预后有着重要意义,提高了患者的生活质量及对护理工作的满意度.     

小儿感染性休克与心力衰竭

近年来已渐明确,微循环障碍是感染性休克(下简称休克)的病理生理基础,而心力衰竭常为不可逆休克的主要原因之一。临床上如能在改善微循环障碍的同时,注意预防和治疗心力衰竭的产生,将对降低感染性休克的病死率起到到十分重要的作用。本文就我院儿科所见(96例)休克合并心衰病例报告分析如下:     

老年急性胆囊炎的外科治疗

目的:探讨老年急性胆囊炎的外科治疗经验.方法:回故性分析86例老年急性胆囊炎的临床资料.结果:86例患者中,治愈或临床缓解83例(96.5%),死亡3例.最终采取非手术治疗者45例,症状缓解50%(43例/86例),非手术治疗者2.3%(2例/86例)病情加重死亡.手术治疗41例,治愈40例(46.5%),死亡1例(1.2%).结论:老年急性胆囊炎患者病情复杂,要高度重视外科治疗的时机及方法.早期手术治疗能明显降低病死率及缩短住院时间,是安全可行的.     

28例老年急性腹膜炎治疗体会

目的:分析老年急性腹膜炎患者的临床诊治特点.方法:对28例老年急性腹膜炎患者临床表现、诊断、治疗、并发症及预后进行回顾性分析.结果:治愈19 例,治愈率达到67.9%.9 例(32.1%)发生并发症,其中多脏器衰竭1 例、感染性休克1 例、切口裂开 1 例、腹腔脓肿 1 例、术后出血2 例、胃肠吻合口瘘 1 例、肠梗阻 1 例、心尿路感染1例.二次手术4例(14.3).死亡3 例(10.7%).结论:老年急性腹膜炎患者应早期诊断、早期治疗、早期手术、积极处理并存疾病是提高疗效的关键.     

老年糖尿病患者不能坚持胰岛素治疗的原因及护理对策

目的:探讨老年糖尿病患者不能坚持胰岛素治疗的原因及护理对策.方法:分析45例老年糖尿病患者不能坚持胰岛素治疗的原因,并提出相应的护理对策.结果:老年糖尿病患者不能坚持胰岛素治疗与患者文化程度低、缺乏相关医学知识,对并发症的严重性认识不足以及没有正确掌握胰岛素注射技术、家庭支持不够等多种因素有关.护理对策为进行个案化的教育,详细的药物指导,选择简单易操作的胰岛素注射装置,成立糖尿病俱乐部,邀请患者、家属及相关人员参与,糖尿病专科护士对出院患者入户评估与指导.结论:通过上述护理对策的实施,能坚持胰岛素治疗的老年患者达73.3%,大大地减少了糖尿病并发症的发生,提高了老年患者的生活质量.     

重组人脑利钠肽治疗急性失代偿性心力衰竭的护理与进展

重组人脑利钠肽是一种通过重组DNA技术合成的生物制剂,与内源性多肽有相同作用机制,在急性失代偿性心力衰竭治疗中的应用已成为近期研究热点.1 重组人脑利钠肽的作用机制     

老年人居家护理服务需求的调查研究

目的:了解和探讨云浮市社区、家庭、本院门诊、住院患者和陪同人员对居家护理服务的需求.方法:运用问卷调查的方法,访谈100例云浮市区60岁以上的老年人.结果:老年人对居家护理服务的认识不足,但对居家护理服务需求较多,希望得到社会支持:提供家居护理服务如健康指导、心理咨询、预防保健及治疗、康复锻炼等护理活动.结论:老年人对居家护理服务需求主要集中在健康指导、心理咨询、预防保健及治疗和康复锻炼等四大方面.但经济问题是制约老年人需求的重要因素,呼吁政府和社会关注老年居家护理,加大对老年居家护理服务的政策倾斜和资源投入.     

老年人慢性根尖周炎诊治分析

老年慢性根尖周炎是指牙齿根尖部及其周围的组织由于各种原因导致的慢性感染性病变,大多数由牙髓坏疽而来,一部分因急性根周炎未经彻底治疗而转成的.慢性根尖周炎多无症状,在机体抵抗力下降时,可转化为急性根尖周炎或称慢性根尖周炎急性发作.因此,慢性根尖周炎常有反复疼痛、肿胀病史.X线片评价方法基本能反映根尖周病变的严重程度和疗效情况,有了更确切的量化概念,值得临床推广使用.     

Physiopathological basis of the treatment of heart failure

Therapeutic advances have changed the mode of presentation of cardiac failure over the last decades: the main cause, nowadays, is myocardial ischaemia. The modern treatment of cardiac failure is based on relatively simple physiopathological mechanisms which take into account the different aspects of cardiac physiology: a pump, a muscle, a coronary circulation supplying oxygen to the myocardium, an automatic contraction. The concept of vasodilatation and the blocking of vasoconstrictive systems introduced during the 70s is the basis of modern treatment of cardiac failure which involves angiotensin converting enzyme inhibitors and, increasingly, betablockers. In the near future, with earlier treatment of cardiac failure, the stimulation of vasodilator systems could become a new therapeutic strategy. Early detection of ischaemia and its complications with the aim of limiting the loss of cardiac myocytes is a priority for slowing the progression of cardiac failure. The prevention of cardiac failure also depends on educating cardiologists to treat rapidly the factors predisposing to or prolonging episodes of even mild cardiac failure.     

Ace inhibitors: treatment of congestive heart failure

Nasal passage geometry was measured by acoustic rhinometry in 8 healthy medical students (5 males and 3 females, 21-29 years old; mean age 24 years) after 6 min in different postures of head and body. The minimum cross-sectional area (A-min) and volume between the nostril and 7 cm posteriorly were measured on both sides. When changing from sitting to horizontal the total airway dimension (i.e., the sum of A-min for the two sides) decreased by about 16% (Mean +/- SD = 0.19 +/- 0.14 cm2), and when standing up it increased by about 12% (0.14 +/- 0.13 cm2). A-min seemed more sensitive than volume to detecting postural changes. Including the variation between the cavities, the coefficient of variation (CV = SD/Mean) for area was 24.8 +/- 6.7 and for volume 22.4 +/- 6.4 for the 8 subjects. For the total nasal airway passage the corresponding figures were 12.9 +/- 3.9 and 10.9 +/- 5.5. These figures are considerably higher than for subjects measured only in the sitting position under comparable circumstances. In conclusion, our findings indicate a composite response of the nasal cavity mucosa to both systemic (hydrostatic) and local conditions, probably induced by vascular and cutaneous reflexes. These factors must be taken into account in studies of environmental, clinical, and pharmacological conditions.     

依那普利联合螺内酯对慢性心力衰竭疗效的影响研究

目的:探讨依那普利联合螺内酯对慢性心力衰竭疗效的影响.方法:选择慢性心力衰竭患者88例,随机分为治疗组和对照组各44例,对照组给予利尿剂、β-受体阻滞剂、洋地黄制剂等常规治疗,治疗组在对照组基础上加用依那普利、螺内酯治疗,疗程为12周,分析治疗前后的心功能,左室舒张末期内径和左室射血分数的变化情况.结果:治疗组心功能、舒张末期内径和左室射血分数好于对照组,两组比较差异有显著性意(P<0.05),无高血钾现象发生.结论:依那普利联合螺内酯治疗慢性心力衰竭安全有效,值得临床推广应用.     

Chronic amlodipine treatment during the development of heart failure

BACKGROUND: This study examined the effects of chronic amlodipine treatment on left ventricular (LV) pump function, systemic hemodynamics, neurohormonal status, and regional blood flow distribution in an animal model of congestive heart failure (CHF) both at rest and with treadmill exercise. In an additional series of in vitro studies, LV myocyte contractile function was examined. METHODS AND RESULTS: Sixteen pigs were studied under normal control conditions and after the development of chronic pacing-induced CHF (240 bpm, 3 weeks, n=8) or chronic pacing and amlodipine (1.5 mg . kg-1 . d-1, n=8). Under ambient resting conditions, LV stroke volume (mL) was reduced with CHF compared with the normal control state (16+/-2 versus 31+/-2, P<0.05) and increased with concomitant amlodipine treatment (29+/-2, P<0.05). At rest, systemic and pulmonary vascular resistance (dyne . s-1 . cm-5) increased with CHF compared with the normal control state (3102+/-251 versus 2156+/-66 and 1066+/-140 versus 253+/-24, respectively, both P<0.05) and were reduced with amlodipine treatment (2108+/-199 and 480+/-74, respectively, P<0.05). With CHF, LV stroke volume remained reduced and was associated with a 40% reduction in myocardial blood flow during treadmill exercise, whereas chronic amlodipine treatment normalized LV stroke volume and improved myocardial blood flow. Resting and exercise-induced plasma norepinephrine levels were increased by >5-fold in the CHF group and were reduced by 50% from CHF values with chronic amlodipine treatment. Resting plasma endothelin (fmol/mL) increased with CHF compared with the normal state (10.4+/-0.9 versus 3.1+/-0.3, P<0.05) and was reduced with amlodipine treatment (6.6+/-1.1, P<0.5). With CHF, LV myocyte velocity of shortening ( microm/s) was reduced compared with normal controls (39+/-1 versus 64+/-1, P<0.05) and was increased with chronic amlodipine treatment (52+/-1, P<0.05). CONCLUSIONS: Chronic amlodipine treatment in this model of developing CHF produced favorable hemodynamic, neurohormonal, and contractile effects in the setting of developing CHF.     

Mechanisms, diagnosis, and treatment of diastolic heart failure

Diastolic heart failure, in the absence of LV systolic dysfunction, is a common clinical condition that can be demonstrated in as many as one third of patients with congestive heart failure. Diastolic dysfunction caused by abnormalities in LV filling can be a result of many pathologic conditions, including hypertrophy, infiltrative cardiomyopathies, or myocardial ischemia. The major physiologic determinants of LV filling can be divided into cellular mechanisms, hemodynamic characteristics, and hormonal influences. Cellular mechanisms for impaired LV inactivation are determined by the handling of calcium within the myocyte during excitation-contraction-relaxation coupling. The hemodynamic characteristics of LV diastolic filling are determined by loading conditions, the time constant of isovolumic relaxation, heart rate, ventricular nonuniformity, pericardial restraint, myocardial elasticity, chamber compliance, and coronary blood flow. The sympathetic nervous system and the renin-angiotensin system are important modulators of diastolic filling, directly or indirectly. The diagnosis of heart failure is confirmed by a combination of clinical tests including invasive and noninvasive techniques, each of which has advantages and disadvantages. Treatment of medical conditions in which diastolic heart failure is a prominent component include pharmacotherapy with calcium channel antagonists, beta-adrenergic blocking agents, diuretic agents, and angiotensin-converting-enzyme inhibitors. Certain conditions associated with diastolic filling abnormalities such as pericardial disease or severe ischemic heart disease may be best managed by surgical or percutaneous intervention. Future research will include further delineation of the cellular mechanisms of active myocardial relaxation and clinical investigation into treatment directed at improving outcome.     

Sympathetic activation in heart failure and its treatment with beta-blockade

Multiple models explaining the pathogenesis of heart failure have been put forth during the past 5 decades. These models were modified as clinical evidence supported or refuted their assumptions. During the past 2 decades, heart failure models emphasized the importance of neurohormonal systems in heart failure progression. The positive impact that angiotensin-converting enzyme inhibitors have had on mortality from heart failure has bolstered the neurohormonal theory. Attention recently has turned to the sympathetic nervous system and its potential deleterious effects on the cardiovascular system in heart failure. The sympathetic nervous system can negatively impact the cardiovascular system in heart failure in several ways, including down-regulating beta1-receptors, exerting direct toxic effects on the myocardium, and contributing to myocardial remodeling and life-threatening arrhythmias. Beta-adrenergic blockers have shown promise for reducing morbidity and mortality in heart failure, but definitive reductions in mortality remain to be shown by future investigations.