老年人呼吸衰竭诊治特点

呼吸衰竭是呼吸系统或其他疾病、创伤、药物中毒等导致通气和(或)换气功能障碍，引起缺氧或合并二氧化碳潴留，进而引起机体系列生理功能紊乱和代谢异常的临床综合症。老年人呼衰病因与发病机理与非老年人基本一致，但由于老年人有增龄性各脏器功能的减退，人体各系统的器官会发生相应的老化．呼吸系统也不例外，     

急性呼吸衰竭诊疗进展

急性呼吸衰竭 (acuterespiratoryfailure ,ARF)是常见的呼吸系统急症 ,具有起病急、进展快、病死率高等特点。欧美16个国家 4 0个危重症监护病房 (intensivecaremedicine,ICU)共同完成的ICU急性呼吸衰竭患者流行病学调查显示 ,1,4 4 9例ICU住院患者有 4 5 8例 (32 % )入住ICU时并发急性呼吸衰竭 ;991例入住ICU时没有呼吸衰竭的患者中35 2例 (35 % )在ICU住院期间并发急性呼吸衰竭 ;并发呼吸衰竭的ICU患者住ICU期间病死率达 31% ,显著高于无急性呼吸衰竭的其他ICU住院患者。在美国 ,住院患者并发呼吸衰竭时病死率为 31.4 %。因此…     

呼吸衰竭的临床诊断与治疗

呼吸衰竭（respiratory failure）是由于肺通气不足、弥散功能障碍和肺通气/血流比失调等因素,使静息状态下吸入空气时出现低氧血症和/或二氧化碳潴留,从而引起一系列生理功能和代谢紊乱的临床综合征。在临床上,呼吸衰竭通常是指外呼吸衰竭。因气体在血液中运输以及血液或组织液与细胞间的气体交换异常,称为内呼吸障碍。     

老年人呼吸衰竭的诊断与治疗

呼吸衰竭 (以下简称呼衰 )是呼吸系统或其他疾病、创伤、药物中毒等导致通气和 (或 )换气功能障碍 ,引起缺氧或合并二氧化碳潴留 ,进而引起机体系列生理功能紊乱及代谢障碍的临床综合征。其发病率和病死率均随年龄增长而升高。老年人呼衰病因与发病机制与非老年人呼衰基本一致 ;但由于各系统功能 ,特别是呼吸系统解剖生理、水电解质酸碱平衡及免疫功能均随年龄增长而老衰 ,且老年人同时患有多种疾病的可能性较大 ,致使老年人呼衰在流行病学、病理生理、临床表现、诊断、治疗和预后等方面均具有老年人特点。现将老年人呼衰特点重点描述如下。…     

老年人呼吸衰竭患者电解质紊乱的诊治

老年人调节电解质平衡的能力较弱,发生呼吸衰竭后容易发生电解质紊乱,并最终导致机体的代谢障碍或加重呼吸衰竭。     

无创性正压通气在治疗急性呼吸衰竭中的研究状况和评价

近年来 ,无创性通气的应用有明显增多趋势 ,所谓“无创性通气”(ｎｏｎｉｎｖａｓｉｖｅｖｅｎｔｉｌａｔｉｏｎ ,ＮＩＶ) ,目前国内外较公认的定义是指 :不经人工气道 (气管插管或气管切开 )将机械通气输送入肺的所有方法和技术。按照此定义 ,ＮＩＶ应包括无创性正压通气 (ＮＰＰＶ)、负压通气 (如铁肺、胸甲式或雨披式呼吸机通气 )、腹部移动式呼吸机通气 (如滚动床 ,充气带腹部加压通气 )及其他无创性通气辅助方法 (如膈肌起搏 ,舌咽呼吸 )和辅助咳嗽技术等[1] 。目前在我国正在临床应用和研究的ＮＩＶ ,主要是指经面罩或鼻罩进行的正压…     

浅谈慢性呼吸衰竭诊断中的几个问题

浅谈慢性呼吸衰竭诊断中的几个问题何权瀛所谓呼吸衰竭是指由于各种原因引起肺通气和（或）换气功能严重障碍，以至不能进行有效的气体交换，导致缺氧伴有或不伴有二氧化碳潴留，从而引起一系列生理功能和代谢功能紊乱的临床综合征。其具体的诊断标准是在海平面一个大气压...     

甲状腺机能减退症致呼吸衰竭的诊断和治疗

普通甲状腺机能减退症患者的呼吸功能障碍在临床上往往不被人们所重视 ,但严重的甲状腺机能减退症如粘液性水肿可以导致威胁生命的二氧化碳潴留、呼吸性酸中毒、呼吸衰竭 ,甚至需要机械通气。我院 2年来收治了 2例因呼吸衰竭就诊的甲状腺机能减退症患者 ,现进行分析 ,以期引起人们的重视。临床资料1.一般资料 :例 1,女性 ,年龄 47岁 ,体重 6 3.5ｋｇ ;例 2 ,女性 ,年龄 6 2岁 ,体重 5 8.0ｋｇ。 2例患者均因全身水肿伴呼吸困难入院。例 1入院前无甲状腺机能减退的病史 ,经临床体检及实验室检查符合甲状腺机能减退症 ,同时查甲状腺球蛋白抗体…     

Vagus stimulation. Mechanisms and current clinical importance in heart failure

Increased sympathetic activity and reduced vagal activity are associated with increased mortality both after myocardial infarction and in heart failure; furthermore, vagal withdrawal has been documented to precede acute decompensation. Experimental studies indicate that increased parasympathetic activity by means of vagal stimulation may reduce mortality in animal models of post-infarction sudden cardiac death and of chronic heart failure. Initial clinical results demonstrate that chronic vagus nerve stimulation in heart failure patients with severe systolic dysfunction appears to be safe and tolerable and may improve quality of life, submaximal exercise capacity, and LV function. Vagus nerve stimulation derives these potential clinical benefits from multiple mechanisms of action. These include reduced heart rate, restoration of heart rate variability and baroreflex sensitivity, suppression of pro-inflammatory cytokines, and antiarrhythmic effects.     

Heart failure and depression: an association with clinical importance.

Major depression is found in one fifth of heart failure patients, and clinically significant depressive symptoms in almost half. The association of depression and heart failure appears to be related both to the psychological aspects of severe heart disease, and to pathophysiological and psychosocial mechanisms. The presence of depression is associated with a worsening of the prognosis, and increased risk of death, rehospitalization, and functional decline. Detection and treatment of depression should be part of a comprehensive approach to heart failure patients by cardiologists and family doctors. Good quality cardiac care should include psychosocial assessment, strengthening of the doctor-patient relationship and of family and social bonds, and, when appropriate, antidepressants and psychotherapy. Selective serotonin reuptake inhibitors are effective and safe antidepressants in cardiac patients. They should be prescribed in therapeutic doses until sustained remission is obtained. Collaboration between psychiatrists and other specialists at primary and secondary care levels is recommended and contributes to better quality care.     

有机磷中毒并发呼吸衰竭的多因素临床分析

目的分析探讨有机磷中毒合并呼吸衰竭的临床特点、发生规律及危险因素。方法根据是否合并呼吸衰竭将有机磷中毒患者分为呼衰组及对照组,分析比较两组临床资料及实验室检查结果。结果经比较两组患者在APACHEⅡ评分、ACHE活力、CK、开始洗胃时间、肌颤持续时间、胆碱酯酶活力恢复时间及死亡率方面有显著性差异（P〈0.05）。结论有机磷中毒患者易并发呼吸衰竭,其中洗胃时间延迟、胆碱酯酶活力低下、胆碱酯酶活力恢复延迟及APACHEⅡ评分、肌酸激酶水平可能是预测是否发生呼吸衰竭的相关危险因素。     

Study on the respiratory failure with cardiac failure--focus on hypoventilation respiratory failure

Respiratory failure accompanied by cardiac failure occurs mostly due to decreased PaO2. However, sometimes we encounter patients with cardiac failure having on increase of PaCO2, who develop CO2 narcosis in the ICU. In this study we evaluated hypoventilation respiratory failure in patients with cardiac failure. Seventy-six patients with both respiratory failure and cardiac failure caused by intrinsic heart disease, who required mechanical ventilation in the ICU were studied. The patients were divided into 2 groups; hypoxic respiratory failure group (n = 53) and hypoventilation respiratory failure group (n = 23). Blood gas analysis and cardiovascular hemodynamics including arterial blood pressure, heart rate and Swan-Ganz catheter findings were performed before, during and after mechanical ventilation in each patient. Mortality rate and its relation to hemodynamic variables were also evaluated in each group. In both groups even when it was possible to maintain oxygenation capacity by conducting mechanical ventilation against severe respiratory failure, what can be said about the prognosis is that it depended totally on the improvement of cardiac function. The mechanism by which hypoxemia is displayed due to cardiogenic pulmonary edema is already well known, but in regard to the mechanism of hypercapnia in cases with hypersensitivity of the airways it is thought that through induction of cardiogenic pulmonary edema bronchial spasms is induced, and this causes hypercapnia. However, it is also possible to consider cardiac asthma as the cause. Among respiratory failure cases due to cardiogenic pulmonary edema that occurs in association with heart failure, there is both hypoxic respiratory failure as well as hypoventilation respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)