heart failure英文课件
heart failure
Class III (Moderate) Class IV (Severe)
Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea. Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.
Ventricular overload
hypertension, aortic stenosis, pulmonary embolism aortic or mitral regurgitation thyrotoxicosis, anemia, pregnancy or infection
Predisposing cause
Cardiac Muscle
Molecular Basis of Contraction
Mechanisms for heart failure
•Weaken of contractility
•Abnormity of diastolic properties of ventricle
•Asynergia of ventricular contraction and relaxation
citric acid
α-ketoglutaric acid
心功能不全(英文版)课件
Definition of Heart Failure
HF is a complex clinical syndrome, in which patients have typical symptoms (e.g. breathlessness呼吸急促, ankle swlling and fatigue疲劳) and signs (e.g. elevated jugular venous pressure, pulmonary crackles) resulting from an abnormality of cardiac structure or funcilure
Causes of HF in Western World
For a substantial proportion of patients, causes are:
1. Coronary artery disease 2. Hypertension 3. Dilated cardiomyopathy
Clinical Manifestations
Left-sided heart failure
New York Heart Association Functional Classification
Class I
Patients with cardiac disease but without resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.
心功能不全双语PPT课件
室内噪音
评价结果
室内噪音的原因 • Pump震动→发生共振 • Pump-Engine Mounting Bracket 形象变更
PUMP(震动)
G/BOX(震动) HOSE(脉动)
▣ P/S Hose의 설계사양
759 536
137
138
~5000
~10000
~20000
▣ 漏油 CLAIM 再现确认试验结果
使用NBR材质 2019年 6月以前发生于生产部 门, 改善后没有发生
~30000
4.2% Oil Seal部
0% S/PIPE 组装部
961 623
~40000
~50000
判定为与Power Pump 无关的要素 等 同时脱去
参照附件
PUMP漏油
EYE BOLT 组装部漏油
▣ Pump 누유 관련 정비시 참조 사항
漏油
因接触外部环境(雨, 雪, 泥污等)外观严重污染，导致漏油的可能性很高
漏油确认程序
单品不良有无，检点/整备方法
1
1.用洗涤液将Pump和周围
实车试验前
SYSTEM洗涤干净
2
2.将POWER PUMP用抹布等擦干
4) P/S HOSE 设计式样
Simulation （模拟）结果
type( L1L20.5m)
type 1
1
L1
L2
2
Li1
Li2
3
type 2
1
2
3
type 3
1
2
3
Li1[m] Li2[m] 0.2 0.4 0.3 0.3 0.4 0.2
HEART FAILURE
心力衰竭双语教学英文课件杭州师范大学医学院附属医院薛树仁教授HEART FAILUREProf.Shu-Ren Xue MD FESC FACCdate posted: March, 2008Definition of heart failure Clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject bloodDirect Causes1-Myocardial abnormalities (CHD!) 2-Hemodynamic overload3-Ventricular filling abnormalities 4-Ventricular dyssynergy5-Changes in cardiac rhythmAggravating Factors•Pregnancy •Arrhythmias (AF)•Infections •Thromboembolism •Hyper/hypothyroidi sm •Endocarditis •Obesity •Hypertension •Physical activity •Dietary excessPathophysiologyHF is summarized best asan imbalance in Starling forcesimbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in an ensuing contraction. Characterized as a malfunction between the mechanisms that keep the interstitium and alveoli dryopposing forces that are responsible for fluid transfer to the interstitium.Heart Rate = Cardiac Output Heart Failure:Determinants of CardiacOutputStrokeVolumePreload AfterloadContractility xPatterns of ventricular hypertrophyHeart failure associated with aortic valvular lesions (A)Initial / Ongoing Evaluation •Identify heart disease•Assess functional capacity (NYHA, 6 min walk, …)•Assess volume status: (edema, rales, jugular, hepatomegaly, body weight)•Lab assessment: routine: electrolytes, renal funct. Repeat ECHO, RX only if significantchanges in functional status•Assess prognosisThe New York HeartAssociation's functional classification of CHF . Class I describes a patient who is not limited with normal physical activity bysymptoms.Class II occurs when ordinary physical activity results in fatigue, dyspnea, orother symptoms.Class III is characterized by a marked limitation in normal physical activity. Class IV is defined by symptoms at rest or with any physical activityEpidemiologyIn US: More than 3 million people have CHF, 400,000 new patients present yearly. Prevalence of CHF is 1-2% of the general population.Approximately 30-40% of patients with CHF are hospitalized every year.The 5-year mortality rate after diagnosis was as 60% in men and 45% in women.SYMPTOMSAnxiety、Dyspnea at rest、Dyspnea on exertion .Orthopnea and paroxysmal nocturnal dyspnea (PND).Cough productive of pink, frothy sputum.Edema.Nonspecific Weakness、Lightheadedness、Abdominal pain、Malaise、Wheezing、Nausea.The varied faces of heart failurePhysical SIGN peripheraledema,jugularvenousdistention, tachycardia Tachypnea,.Hypertension、Pulsus alternansSkin may be diaphoretic or cold,gray, and cyanotic.Wheezing rales.Apicalimpulse displaced laterally. auscultation may reveal aortic or mitral valvular abnormalities,S3or S4.Lower extremity edemaDiagnosisImaging StudiesHeart failure associated with mitral regurgitation (B)Lab Studies:1. atrial natriuretic peptide（ANP）and brainnatriuretic peptide（BNP））arginine vasopression, AVPendothelinIncreased creatinine, hyperbilirubinemia, and dilutional hyponatremia are observed in severe cases.elevated alanine aminotransferase (ALT) aspartate aminotransferase (AST) suggestive of a congestive hepatopathy. Cardiac enzymes and other serum markers for ischemia or infarction.Arterial blood gas (ABG) in evaluationof hypoxemia, ventilation/perfusion (V/Q) mismatch, hypercapnia, and acidosis. proteinuria are observed in early and mild-to-moderate disease.DIFFERENTIALS：Acute Respiratory Distress Syndrome，Altitude Illness -Pulmonary Syndromes ，Chronic Obstructive Pulmonary Disease and Hyperventilation SyndromeMyopathies，Pericarditis and Cardiac TamponadeBacterial Pneumonia, Immunocompromised Pneumothorax, Iatrogenic, Spontaneous andHeart disease No symptoms HF Risk Factors No Heart disease No symptoms Asymptomatic LV dysfunction Refractory HF symptoms Prior or current HF SymptomsStages in the evolution of Heart Failure A BCDAHA / ACC HF guidelines 2001Heart disease (any)Hypertension Diabetes, Hyperchol.Family Hx Cardiotoxins AsymptomaticLV dysfunctionSystolic / Diastolic Marked symptomsat rest despitemax. therapy Dyspnea, Fatigue Reduced exercise tolerance Stages in the Evolution of Heart Failure Clinical Characteristics AB CDAHA / ACC HF guidelines 2001ACE-i βblockersTreat risk factors Avoid toxics ACE-i in selected p.In selected patientsPalliative therapyMech. Assist deviceHeart Transplant ACE-iβblockersDiuretics / Digitalis Stages in the Evolution of Heart Failure Treatment AB CDAHA / ACC HF guidelines 20018070605040302054-60>6050403020100Post MI n=196<3031-3536-4546-53CardiacMortality%LVEFBrodie B. et alAm J Cardiol 1992;69:1113PrognosisTreatment ObjectivesSurvivalMorbidityExercise capacityQuality of lifeNeurohormonal changesProgression of CHFSymptoms(Cost)Treatment•Prevention. Control of risk factors •Life style •Treat etiologic cause / aggravating factors •Drug therapy•Personal care. Team work•Revascularization if ischemia causes HF •ICD (Implantable Cardiac Defibrillator)•Ventricular resyncronization•Ventricular assist devices•Heart transplant•Artificial heart•Neoangiogenesis, Gene therapy All S e l e c t e d p a t i e n t sTreatment Pharmacologic Therapy•Diuretics•ACE inhibitors•Beta Blockers•Digitalis•Spironolactone•OtherDiuretics•Essential to control symptoms secondary to fluid retention •Prevent progression from HT to HF • Spironolactone improves survival • New research in progressCortex MedullaThiazidesInhibit active exchange of Cl-Nain the cortical diluting segment of the ascending loop of HenleK-sparingInhibit reabsorption of Na in the distal convoluted and collecting tubuleLoop diureticsInhibit exchange of Cl-Na-K in the thick segment of the ascendingloop of HenleLoop of HenleCollecting tubule DiureticsDiuretics. Indications1.Symptomatic HF, with fluid retention•Edema•Dyspnea•Lung Rales•Jugular distension•Hepatomegaly•Pulmonary edema (Xray)AHA / ACC HF guidelines 2001ESC HF guidelines 2001Loop Diuretics / Thiazides. Practical Use Start with variable dose. Titrate to achieve dry weightMonitor serum K+at “frequent intervals”Reduce dose when fluid retention is controlled Teach the patient when, how to change doseCombine to overcome “resistance”Do not use aloneLoop diuretics. Dose (mg)Initial Maximum Bumetanide0.5 to 1.0 / 12-24h 10 / day Furosemide20 to 40 / 12-24h 400 / day Torsemide10 to 20 / 12-24h 200 / dayAHA / ACC HF guidelines 2001Thiazides, Loop Diuretics. Adverse Effects •K+, Mg+(15 -60%) (sudden death ???)•Na+• Stimulation of neurohormonal activity•Hyperuricemia (15 -40%)•Hypotension. Ototoxicity. Gastrointestinal.Alkalosis. MetabolicSharpe N. Heart failure. Martin Dunitz 2000;43Kubo SH , et al. Am J Cardiol 1987;60:1322MRFIT, JAMA 1982;248:1465Pool Wilson. Heart failure. Churchill Livinston 1997;635Diuretic ResistanceNeurohormonal activationRebound Na+uptake after volume lossHypertrophy of distal nephronReduced tubular secretion (renal failure, NSAIDs) Decreased renal perfusion (low output)Altered absortion of diureticNoncompliance with drugsBrater NEJM 1998;339:387Kramer et al. Am J Med 1999;106:90Managing Resistance to Diuretics •Restrict Na+/H 2O intake (Monitor Natremia)•Increase dose (individual dose, frequency, i.v.)• Combine: furosemide + thiazide / spiro / metolazone •Dopamine (increase cardiac output)•Reduce dose of ACE-i•UltrafiltrationMotwani et al Circulation 1992;86:439VASOCONSTRICTIONVASODILATATIONKininogen KallikreinInactive FragmentsAngiotensinogenAngiotensin IRENINKininase IIInhibitorALDOSTERONE SYMPATHETICVASOPRESSINPROSTAGLANDINS tPAANGIOTENSIN IIBRADYKININACE-i. Mechanism of ActionA.C.E.ACE-I. Clinical Effects•Improve symptoms•Reduce remodelling / progression •Reduce hospitalization•Improve survivalPlaceboEnalapril12111098765Probabiility of DeathMonths0.10.800.20.30.70.40.50.6p< 0.001p< 0.002CONSENSUSN Engl J Med 1987;316:14294321ACE-i50403020100Months0612p = 0.0036%Mortality241830364248Enalapriln=1285Placebon=1284SOLVD (Treatment)N Engl J M 1991;325:293n = 2589CHF-NYHA II-III -EF < 35ACE-iMortality,%4SAVEN Engl J Med 1992;327:669Years3020100123PlaceboCaptopriln=1115n=1116p=0.019² -19%n = 22313 -16 days post AMI EF < 4012.5 ---150 mg / dayAsymptomatic ventriculardysfunction post MIACE-i。
心力衰竭与心室重构英文版护理课件
Clinical presentations and diagnosis
Clinical recommendations
The clinical recommendations of veterinary remodelling are diverse, including symptoms of heart failure, arrhythmia, chest pain, and petitions
Definition and classification
Definition
Ventricular remodelling refers to the changes in the structure and function of the vegetables after various cardiovascular injuries, which is a compensatory mechanism of the heart
sacrifices, and syncope
Diagnosis
The diagnosis of heart failure is based on a combination of symptoms, physical examination, and medical history Imaging tests such as echocardiography and
Nursing Care
Monitoring patients for signs and symptoms of complications, prompt reporting of any concerns to the healthcare team, and providing comfort and support to patients during their treatment
心力衰竭(HeartFailure)PPT课件
基础心血管疾病的病史和表现
多有各种心脏病病史,存在引起心衰的诱因 老年人: 冠心病,高血压病,老年性退行
性心瓣膜病; 年轻人:风湿性心瓣膜病,扩张型心肌病
,急性重症心肌炎
8
急性左心衰竭早期表现
原因不明的疲乏或运动耐力减低,心率增 快
高枕位睡觉,劳力性呼吸困难,阵发性夜间 呼吸困难
体检:左心室增大,舒张期奔马律,两肺底 湿罗音.
而发生急性左心衰时，左室射血分数可能正常。
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动脉血气分析 呼吸衰竭 酸中毒 心肌坏死标志物 TNT等 有无心肌坏死 心衰标志物 BNP鉴别呼吸困难
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心衰标志物 BNP
B 型利钠肽（BNP）和N末端B型利钠肽原（NT-proBNP） 急性期合理的阴性预测值排除心力衰竭 心衰诊断和鉴别诊断： 阴性预测值:BNP＜100ng/L或NT-proBNP＜ 400ng/L 阳性预测值:BNP>400ng/L；NT-proBNP > 1500ng/L 评估心衰预后：该指标持续走高。提示预后不良
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超声心动图 ：可以提供心脏腔大小变化及心脏 瓣膜结构及心功能情况
收缩功能：主要体现在左室射血分数，正常值大于 50%，当小于40%时为收缩期心力衰竭的诊断标准。
舒张功能：早期心室充盈速度最大值E峰，舒张晚期 心室充盈最大值A峰，E/A不应小于1.2，中青年人应 更大。当舒张功能不全时，E峰下降，A峰上升，E/A 比值降低。
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急性左心衰竭的药物治疗
1.镇静剂:吗啡 2.支气管解痉剂 3.利尿剂 4.血管扩张剂 5.正性肌力药物
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吗啡
可以3-5mg静脉注射，不仅可以使患者镇 静，减少患者躁动带来的额外心脏负担， 同时也具有小血管舒张功能，而减轻心 脏负荷，必要时可间隔15分钟重复一 次，，共2-3次。老年患者可酌情减量或 改为肌肉注射。
病理生理学--心力衰竭 ppt课件
舒 张 末 期 压 力
ppt课件
顺 应 性 降 低
顺 应 性 正 常
顺 应 性 升 高
舒张末期容积
45
（六）心室充盈量降低
瓣膜狭窄、心包填塞等
ppt课件
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（六）心脏各部舒缩不协调
1、心律失常 2、梗死区域性分布
ppt课件
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五、机体机能代谢变化
皮肤、内脏、骨骼肌 心、脑
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（二）肺循环淤血 (pulmonary congestion ) --左心衰 肺淤血、水肿——呼吸困难
①劳力性呼吸困难 ②端坐呼吸 ③夜间阵发性呼吸困难
ppt课件
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劳力性呼吸困难 ( dyspnea on exertion )
随病人体力活动而发生的呼吸困难， 休息后可减轻或消失。 耗氧量增加 HR加快 回心血量增多
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酸中毒
NA. ↓
H +↑ 钙离子内流的两条途径： 1 β受体 ↓ 2 K +↑
肥大心肌
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Ca2+
↓
缺血缺氧
↑
Ca2+ 泵 ↓ 钙储存 钙储存 Ca2+ ↓ 蛋白 蛋白
肌浆网
线粒 体
Ca2+↑
酸中毒
RyR ↓ RyR mRNA↓
ppt课件
↓
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（五）心室顺应性降低
心室顺应性指心室在单位压力变化下所引 起的容积改变（dV/dp）
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三、心力衰竭的发生机制
全英文心衰PPTword版本
AHA/ACC Guidelines
Stage A
Stage B
Stage C
Stage D
At high risk Structural
for HF but heart
without disease
structural
but
heart
without
disease or signs or
symptoms symptoms
EKG
Stress test
Cardiac catheterization
coronary angiogram
Cardiac MRI
BNP
• BNP is a substance secreted from the heart in response to changes in pressure that occur when heart failure develops and worsens. The level of BNP in the blood increases when heart failure symptoms worsen, and decreases when the heart failure condition is stable. The BNP level in a person with heart failure -- even someone whose condition is stable -- is higher than in a person with normal heart function.
No limitation during ordinary activity
Slight limitation by shortness of breath fatigue during
heartfailure
2）心脏体征 心脏扩大、心 尖部舒张期奔马律、肺动
咳嗽，咳痰，咯血，常伴白色泡沫状
脉瓣区第二心音亢进、心
浆液性痰。 2）咳嗽、咳痰和咯血 3）疲倦、乏力、头晕 ：组织血液灌注
瓣膜病的杂音等。 3） BP一般正常，有时脉压
不足所致。
减小。
4）少尿及肾功能损害症状
2．右心衰竭பைடு நூலகம்
1、临床症状：病理基础为体循环静脉淤血。常有上消化系统，另外有浮 肿、尿少、周围性紫绀等，见于肢体下垂部位及身体周围部位，按摩 或加温可消失。
B、中毒反应：胃肠道反应；心律失常：各种类型均见，但以室性早搏 二联律最为常见。为洋地黄中毒最常见的反应.；神经系统反应：头 痛、头晕、视力模糊、黄绿视等。
C、中毒处理：停药；停用排K+利尿剂 ；补充钾盐 ；纠正心律失常： 室性用利多卡因或苯妥英钠； 缓慢型用阿托品。
注：若中毒致完全房室传导阻滞则禁用KCL,因K+能降低心肌兴 奋性和传导性。
风湿活动，合并有甲亢、贫血等。
3．发病机制
（1）血流动力学异常： 早期FRANK-STANING定律，心室充盈充溢压增 高舒张末来期心肌纤维长度增加CO增加。当左室舒张压 >=2.0~2.4kPa时，,心室代偿功能消失，CO下降左房压、肺静脉压、 肺CAP楔嵌压升高临床出现肺淤血的症状和体征。
（2）神经内分泌的激活：心功不全时，体内交感神经系统，肾素一血管 紧张素系统(RAS)活性及血管加压素水平均增高心肌收缩力增加，CO 增加。长期神经内分泌活性增高不仅加重血流动力学紊乱，还可直接 损害心肌，加剧心力衰竭恶化。
➢（二）临床表现
1．左心衰竭 ：病理基础：肺淤血，肺组织弹性
弹性下降，心输出量降低：
心力衰竭英文课件
治疗---洋地黄类药物
注意事项：用药前了解洋地黄情况；避免用钙 剂；注意纠正低血钾。
洋地黄中毒 表现：心律失常；消化道症状；神经系统症状 等。 处理：停用洋地黄及利尿剂；口服补钾；必要 时用抗心律失常药。
Diuretics
• Relieve the congestion status by elimination of sodium and water.
(By New York Heart Association)
Grade I II III IV
No limitation to ordinary activities Slight limitation to ordinary activities Marked limitation to ordinary activities Unable to do any activity—bed ridden.
如果病因未消除持续过度代偿raas激活心肌代谢增加耗氧增加受体密度下调心肌收缩力减弱外周血管收缩水钠潴留心肌毒性等促进心衰恶化心室重构
Definition of Heart Failure
Heart failure is a pathophysiological state of heart in which, the heart cannot pump enough blood to meet the needs required by the metabolizing tissue, or to do so only from an elevated filling pressure. Classification
2-3
＞3
注：0-2分无心衰；3-6分轻度心衰；7-9分中度心衰； ＞ 10分重度心衰。
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Etiological Causes of Heart Failure
1)
2)
Myocardial damage: myocardial ischemia, inflammation etc. Increased cardiac load
Increased preload: congenital heart diseases with left to right shunt. Increased afterload: hypertension, stenosis of cardiac valves.
Congestive heart failure denotes cases with symptoms and signs of passive congestion.
儿童心功能分级：纽约心脏病学会（NYHA）心脏病心功能
3)
Disturbance of the diastolic filling: constrictive pericarditis, hypertrophic cardiomyopathy, etc.
Байду номын сангаас
Pathophysiology
Compensation Decompensation Adaptive mechanisms: Frank-Starling mechanism:
神经内分泌系统的调节机制
交感神经系统、肾素-血管紧张素-醛固酮系统（RAAS） 的激活:早期心输出量减少---兴奋交感神经---血中儿茶
酚胺水平升高--- 早期代偿 ---心输出量增加。如果病因
未消除，持续过度代偿，RAAS激活---心肌代谢增加、 耗氧增加，β受体密度下调，心肌收缩力减弱，外周血 管收缩，水钠潴留，心肌毒性等 --- 促进心衰恶化，心 室重构。
诊断
前四项为主要临床依据，结合临床及检查，综合 分析（临床上并无严格的界定及量化标准，其辨 认是根据病史、症状合体力活动耐力而定。）
心脏病心功能分级：儿童分级同成年人（根据活
动情况）。婴儿分级：同样分四个级，根据每次
哺乳量、哺乳时间、呼吸及心率情况分级 。
Functional Classification of H.F.
Decreased cardiac ejection fraction increased ventricular end diastolic volume and pressure (LVEDP) elongation of the myocardial fiber increased contractility of the myocardium restoration of the ejection fraction
内分泌系统其他方面
Clinical Manifestation
Three aspects: 1.general manifestation 2. manifestation of Left heart failure: polypnea
dyspnea , signs of pulmonary congestion etc. 3. manifestation of right heart failure :general edema, enlargement of liver, distention of jugular vein, anorexia due to congestion of stomach pleural effusion, etc.
Definition of Heart Failure
Heart failure is a pathophysiological state of heart in which, the heart cannot pump enough blood to meet the needs required by the metabolizing tissue, or to do so only from an elevated filling pressure. Classification
Diagnosis of Heart Failure
Clinical Findings:
1.HR↑ 2. Dyspnea, R↑ 3. Liver Enlargement 4. Cardiac sound↓，Cantering rhythm 5. Dysphoria 6. Oliguresis, Edema
Auxiliary Examination
1.Chest radiography: large cardiac sihouette,
pulmonary venous congestion, edema
2. Echocardiography: cardiomegaly, ventricular
disfunction, heart function↓(EF＜50％、FS＜30 ％、STI↑；IVRT ↑、 E/A ＜1) ，ect. 3. Electrocardiogram:
(By New York Heart Association)
Grade I II III IV
No limitation to ordinary activities Slight limitation to ordinary activities Marked limitation to ordinary activities Unable to do any activity—bed ridden.
Adjustment of neuro-endocrine systems
Sympathetic activation Increased contractility of the myocardium Elevation of norepinephrine blood level Down regulation of 1 receptor Activation of RAAS Others