Valvular Heart Disease

Valvular Heart Disease

Dr. Hu Gangying

Department of CardiologyRenmin Hospital of Wuhan University

目的要求掌握

常见瓣膜病变病理解剖病理生理、临床表现、诊断方法

熟悉心脏瓣膜病治疗原则

DefinitionVHD

心脏瓣膜病是由于炎症、粘液样变性、退行性改变、先天性畸形、缺血性坏死、创伤等原因引起的单个或多个瓣膜结构（瓣叶、瓣环、腱索或乳头肌）的功能或结构异常，导致瓣口狭窄和 / 或关闭不全。

General Consideration

以下因素Inflammation

Degenerationdeformation畸形 necrosis坏死Trauma

以下瓣膜结构改变Leaflet

valve ring papillary muscle

乳头肌

瓣膜狭窄

瓣膜关闭不全&

Ischemic

Brief introduction

Bicuspid valve which was followed by aortic valve was viewed as the most susceptive one to rheumatic fever

最常受累为二尖瓣，其次为主动脉瓣

心脏瓣膜病病因风湿性心脏病 ( 风心病、 rheumatic heart disease)

风湿性炎症过程所致的瓣膜损害主要累及 40岁以下人群我国常见的心脏病之一

瓣膜粘液样变性和老年人瓣膜钙化日益↑VHD comprises a variety of etiologies involving but most cases of it were at one time due to rheumatic heart disease

Normal MS

Mitral Valve Disease

Mitral stenosis

Mitral incompetence

Classification

Part I

Mitral stenosis

Mitral StenosisNatural History

Progressive, life long disease

Usually slow & stable in the early years

Progressive acceleration in the later years

呈进展性病程，往往伴随终生

早期进展较缓慢且稳定

晚期病情加速恶化

Mitral StenosisNatural History

several years latency fever to symptom onset

Additional 10 years before disabling symptoms

感染潜伏多年后出现症状

出现症状后 10 年内可丧失生活能力

Mitral Stenosis: Etiology & pathology

Most adult patients: MS is the result of rheumatic fever

2/3 of patients with MS are female and 1/2of all without history of rheumatic fever

多数成年患者：二狭由风湿热引起

2/3 是女性， 1/2 无风湿热病史

Mitral Stenosis: Etiology & pathology

Pathological change is inflammation and thickening of leaflet tips that restricts the motion of the tips

Chronic MS LAE & calcification ， LA embolization especially accompanied with AF

病理改变：炎症及瓣叶增厚粘连限制瓣膜活动

慢性二狭左房增大及钙化，房颤时血栓形成

Mitral Stenosis: Pathophysiology

(<1cm2)

(1-1.5cm2)

Mild

StenosisAlmost

asymptomatic

Left atrial pressure

Normal valve area: 4-6 cm2(>1.5cm2

)

Moderate Stenosis

Severe Stenosis

severe pulmonary venous congestion

maintain normal flow across the valve

maintain normal cardiac output

shorten diastole

increase mitral flow

rate

&

Right heart

failure

Pathophysiological progression of mitral stenosis

RV enlargement

pulmonary venous pressure

pulmonary venous congestion

LA pressure elevation

MS

LAE

pulmonary capillary pressure elevation

Slowing LV fulfillment

pulmonary arterial pressure elevation

Right heart failure

二尖瓣狭窄左室充盈减慢

左房压力增高左房增大

肺静脉淤血肺毛细血管压力增高

肺静脉压力增高肺动脉压力增高

右室增大右心衰

Normal MS

• Manifested after moderate stenosis• 中度狭窄方出现症状 • Often precipitated by AF or pregnancy• 房颤或妊娠时症状加重• Shortness of breath on exertion might

be the first symptom

• 劳累后呼吸困难通常为首发症状

Clinical manifestation: Symptoms


(Area of mitrial valve ＜ 1.5 ㎝ 2)

• dyspnea -exertion -resting -orthopnea

-paroxysmal nocturnal dyspnea

（瓣口面积＜ 1.5 ㎝ 2）呼吸困难最常见早期症状劳力性静息时、端坐呼吸、阵发性夜间呼吸困难

肺水肿

• Hemoptysis– Massive hemoptysis– Suptum with blood,

often with PND or cough

– Pink,frothy suptum– Pulmonary embolism

with hemoptysis• Cough• Hoarseness


• 咯血– 咯大量鲜血– 痰中带血（夜间阵发性呼吸困难）– 粉红色泡沫痰– 肺栓塞伴咯血

• 咳嗽• 声嘶

Clinical manifestation: Signs

•Mitral facies in severe MS

重度 MS 常有 “ 二尖瓣面容 ” 双颧绀红

• S1 is accentuated S1 亢进• OS after aortic valve closure 主动脉关闭后开瓣音• Low pitch diastolic murmurs at the apex 心尖区低调舒张期杂音

– 隆隆样或滚筒样，舒张中晚期，递减 - 递增型，伴舒张期震颤• In severe MS with low flow- S1, OS & rumble may be inaudible 重度

二狭时 S1 减弱、开瓣音消失

S1 S2 OS S1

Clinical manifestation: Signs•Sign of MS

• Pulmonary hypertension & RVE– Dispersion of beat

at apex– RV lift– P2 loudness and

split– Graham Steell

murmur– relative TI with RVE

Clinical manifestation: Signs

• 肺动脉高压及右室扩大– 心尖搏动弥散– 右室抬举感– P2 亢进及分裂– Graham Steell 杂

音 : 相对性肺闭，舒张期杂音– 相对性三闭伴右室大

Mitral Stenosis: Laboratory Examination

X-ray•左房大•右室增大•主动脉结小•肺动脉段突


• “二尖瓣型 P 波” ,P 波宽度 >0.12S

• PV1 终末负性向量增大• QRS 波群示电轴右偏和 RVH

ECG


Echo-Doppler confirm diagnosis & estimate severity

M-mode echocardiography

Echocardiography

Doppler echocardiography

超声可以确诊及评估严重程度

The orifice of the stenotic MV can be visualized and. measured mitral valve area is approximately 1.1 cm2

可见狭窄的瓣膜孔，经测定为 1.1 cm2

Colorful ejection flow at mitral vavle during diastole

Mural thrombosis in LA


Catheterization provides assessment of Catheterization provides assessment of regurgitation, LV function and PAP for regurgitation, LV function and PAP for determining whether valvotomy is indicateddetermining whether valvotomy is indicated

Cardiac Catheterization

导管用于术前评估左室功能及肺动脉压


It is recommended for the patients who It is recommended for the patients who have a discrepancy between clinical have a discrepancy between clinical and echocardiographic findingsand echocardiographic findings


用于临床表现与超声结果不符时

MS: Diagnosis • Low pitch DM at the apex • 心尖区低调舒张期杂音• X-ray, ECG : LAE• 胸片、心电图示左房大• UCG: final diagnosis • 超声：确诊• DM might be lowered or disappeared if AF• 房颤时舒张期杂音减弱甚至消失

Differential diagnosis Low pitch DM at the apex• Blood flow through MV increase:

severe MI 、 massive left to right congenital heart disease (eg. VSD 、PDA) 、 hyperkinesis circulation (hyperthyroidism and anemia)

• Austin-Flint murmur ： caused by severe AI

• mucous tumor in LA ：

Mitral Stenosis: Complications

• Atrial fibrillation• Acute pulmonary edema• Systemic embolization • Right heart failure • Endocarditis • Pulmonary infections

• 房颤 : 早期• 急性肺水肿 : 严重 MS• 血栓栓塞• 右心衰竭 : 晚期 • 感染性心内膜炎 : 少见• 肺部感染 : 常见

Mitral Stenosis: Therapy

• General treatment Avoiding from factors cause cardiac overload as follow ：

Infection 、 anemia 、 salty diet 、 exhausting• Medical

– Treat rheumatic activity – Diuretics 利尿剂– Endocarditis prophylaxis 预防感染性心内膜炎

Mitral Stenosis: Therapy• 并发症的处理 1 大量咯血：镇静、利尿 2 急性肺水肿：处理原则同急性左心衰

– 避免使用扩动脉药，选用硝酸酯类药– 正性肌力药对 MS 的肺水肿无益3 房颤4 预防栓塞5 右心衰竭：限钠、利尿

Mitral Stenosis:Therapy

• Balloon valvuloplasty 球囊扩张术 – Effective long term improvement– 能长期改善症状

• Surgical– Mitral commissurotomy 瓣膜分离术– Mitral Valve Replacement 瓣膜置换术

Mitral Stenosis: Prognosis

• Asympotomic: 84%• Mild sympotom: 42%• Moderate & severe

sympotom: 15%

• Heart failure: 62%• Embolism: 22%• Infectious

endocarditis : 8%

Average duration from occurrence of symptoms to entire disable 7.3 Years

10 years survival rate Reason for death

Part IIMitral

Incompetence

Mitral incompetenceEtiology & pathology

• Valvular-leaflets– Rheumatic– Myxomatous MV– IE– HCM– Congenital

• Annulus– LVE or left heart

failure– Degenerative– Calcification

• 瓣叶– 风湿– 粘液样变– 心内膜炎– 肥厚型心肌病– 先天性

• 瓣环– 左室增大或伴左心衰– 退行性变– 钙化

• Chordae– Congenital– Acquaired

• Papillary Muscles– Ichemia– Necrosis

• Trauma

• 腱索– 先天性–获得性乳头肌– 缺血– 坏死

• 外伤

Mitral incompetenceEtiology & pathology

Mitral Incompetence: Pathophysiology

Sorting by rapidity

Text

Text

TextAcute Mitral

IncompetenceChronic Mitral Incompetence

AABack flow from LV & PV rush into LA

BBLA & LV volume overload

CCPulmonary congestion, edema

DDPulmonary hypertension, RHF

Acute

pressure

D

Chronic left heart failure

Backflow LAE

Pulmonary hypertensio

n

Right heart

failure

Pulmonary congestion

Chronic LV volume overload

Compensatory LVDEV

Decompensation(increased LV wall tension)

Chronic

慢性容量负荷代偿 LV 舒张末期容量

代偿性离心性肥大LV收缩期部分血排入 LA代偿期 CO ，超正常

扩大 LA 、 LV适应容量负荷

舒张末压不致明显

不出现肺淤血

持久负荷，引起左心衰， CO

左房压和左心室舒张末压 PA 高压、右心衰竭

Chronic Mitral incompetence: Pathophysiology

Mitral incompetenceClinical manifestation

Systemic embolization

Hemoptysis

Pulmonary hypertension

Fatigue

Dyspnea & OrthopneaClinical manifestation also present different feature with various rate of progression

It is Similar to MS

Mitral incompetenceClinical manifestation

急性–轻度仅轻微劳力性呼吸困难–严重很快发生急性左心衰竭，休克

慢性–轻度可终身无症状–严重 CO ，疲乏，肺淤血症状出现晚– 风心病：无症状期长，症状明显损害不可逆– 二尖瓣脱垂：多无症状，晚期出现左心衰竭

体征（慢性）心尖搏动：高动力型， LV 时向左下移位心音：

风心病 S1 ，二尖瓣脱垂和冠心病时多正常A2提前，且分裂增宽严重反流时心尖区可闻 S3二尖瓣脱垂时可有收缩中期喀喇音

体征（慢性）心脏杂音：

瓣叶挛缩：全收缩期吹风样杂音，心尖区最响前叶异常：向左腋下和左肩胛下区传导后叶异常：胸骨左缘和心底部传导

典型二尖瓣脱垂：随喀喇音之后收缩晚期杂音乳头肌功能失常：收缩早、中、晚期或全收缩期杂音腱索断裂：杂音似海鸥鸣或音乐性反流严重：心尖区紧随 S3 后短促舒张期隆隆样杂音

Acute mitral incompetence: Signs

Loud P2

S4

Diastolic rumble murmur

S3 present

Systolic murmur may not be pan-systolic

LV may be hyperdynamic

Left Ventricle size normal

心尖搏动为高动力型S2 肺动脉瓣成分亢进心尖区 S4 常见非全收缩期杂音，低调，呈递减严重反流心尖区 S3 和短促舒张期隆隆

样杂音

Mitral incompetence Laboratory Examination

Acute mitral incompetence:

– Severe pulmonary congestion, oedema

Chronic mitral incompetence:

LV, LA pulmonary vascularity– Mitral annulus

calcification

X-ray•急性者

– 心影正常或 LA轻度伴明显肺淤血，肺水肿

• 慢性重度反流– LA 、 LV ：肺淤血和间质性肺水肿

– 二尖瓣环钙化为致密而粗C 形阴影

Chronic mitral incompetence

ECGAcute mitral incompetenceUsually normal EKG,sinus tachycardia presentChronic mitral incompetence

– LA enlargement– Atrial fibrillation– LVH (50% pts. With severe MR)– RVH (15%)– Combined hypertrophy (5%)

ECG features 心电图急性

心电图可正常，窦性心动过速常见慢性重度

LA ， LV肥厚和非特异性 ST-T改变RV肥厚征，心房颤动常见

Mitral Incompetence Laboratory Examination

Function

Add Your Text

Identify etiology & severity of MR

Add Your Text

Evaluation post mitral valve

replacement

Add Your Text

Establish cardiac status after change in

symptoms

Echocardiography

Assess LV function & dimensions

Annual surveillance of

LV function

Estimated EF & LVESD in

asymptomatic severe MR

Echocardiography

Severe mitral regurgitation due to a dilated annulus and abnormal mitral valve

flail 连枷 posterior mitral valve leaflet

彩色多普勒测量返流束面积与左房面积

轻中重返流束面积＜

4cm24-8cm2 ＞ 8cm2

返流束面积 / 左房面积＜20%

局限于二尖瓣

20-40%

左房腔中部

＞ 40%心房顶部

Mitral Incompetence Laboratory Examination


“Golden Standard” for estimating severity of MI

Case I Case II

Mitral Incompetence :Diagnosis

• Dyspnea• Apex region systolic

murmur• Chest X ray display

heart may\may not to be normal but significant pulmonary congestion

• Notable etiological finding– （ Mitral valve prolapse,

infectious endocarditis, acute myocardial infarction)

Acute突发呼吸困难，心尖区收缩期杂音， X 线心影不大 ,肺淤血明显和有病因可寻，如二脱、 IE 、 AMI 、瓣膜置换术后，诊断不难

急性者

Mitral Incompetence :Diagnosis

心尖区有典型杂音伴左心房室增大，诊断可成立

确诊有赖超声心动图

– Systolic murmur（ apex region ）

– LA & LV enlargement

– Diagnosis depends on UCG

Chronic 慢性者

鉴别诊断三尖瓣关闭不全室间隔缺损胸骨左缘收缩期喷射性杂音

左或右心室流出道梗阻主动脉瓣狭窄肺动脉瓣狭窄肥厚型梗阻型心肌病健康人的无害性杂音以上情况有赖心超确诊

Mitral Incompetence : Differential Diagnosis

Tricuspid insufficiencyinterventricular septal defectsystolic ejection murmurs on left sternal border

Mitral Incompetence : Complications

A

BC

D

E

Complications

Atrial fibrillation

Systemic Embolizatio

n

Congestive heart failure

Endocarditis

Mitral valve prolapserelated

Complications

Mitral Incompetence : Management

Acute

To lower pulmonary vein pressure, increase CO and surgical treatment

急性 MI降低肺 V 压，增加 CO （硝普纳、利尿剂）和纠正病因

Diuretics

VasodilatorsPositive Inotropic Agents

Neuro-hormonal Cytokine Inhibitors

General therapy for cardiac dysfunction

Chronic MI

慢性 MI内科治疗预防 SBE；风心病需抗风湿并预防风湿热无症状、心功能正常者无需特殊治疗，但应随访AF处理同MS ，仅控制室率心力衰竭外科治疗



Mitral Valve Surgery

Only effective

treatment is valve

repair/replacement

Reduces morbidity

and mortality

from severe MI

Operation Should be performed

before onset of severe

symptoms

外科治疗根本措施，发生不可逆 LV 功能不全之前二尖瓣修补术人工瓣膜置换术

Prognosis 预后急性：严重返流伴血流动力学不稳，不及时手术干预，死亡率极高慢性：

慢性重度 MI确诊后内科治疗 5 年存活率 80% ， 10 年存活率 60% 单纯二脱无明显反流，预后良好年龄＞ 50岁、明显杂音、反流、房室增大、瓣叶长而厚，预后差

Part IIIAortic Stenosis

Aortic Stenosis Etiology & pathology

• Congenital abnormality is common• 先天性畸形为最常见原因• RHD and degeneration with calcification• 风心病、退行性变、钙化其次

Normal aortic valve

“Normal” geriatric

calcific valve

Congenital bicuspid valve abnormality

Rheumatic Aortic

Stenosis

病因和病理风心病：多伴关闭不全，二尖瓣损害先天性畸形

先天性二叶瓣畸形：瓣膜钙化及瓣口狭窄其他先天性主动脉瓣畸形：单、三叶瓣少见

退行性老年钙化性主动脉瓣狭窄其他少见原因 : 大的赘生物阻塞瓣口

Aortic Stenosis: Pathophysiology

Normal aortic valve area ≥3.0cm2

Mild stenosis 1.5-2.5 cm2

Moderate stenosis 1.0-1.5 cm2

Severe stenosis < 1.0 cm2

• 成人瓣口变化– 主动脉瓣口≥ 3.0cm2

– 当瓣口面积减少一半时，收缩期仍无明显跨瓣压差– 瓣口≤ 1.0cm2 时， LV收缩压明显，跨瓣压差显著

病理生理

LV舒张末容量直至失代偿病程晚期才室壁应力、心肌缺血和纤维化等致 CHF

压力负荷 LV室壁向心性肥厚LV顺应性， LV舒张末压， LA后负荷， LA代偿性肥厚

肥厚 LA舒张末期有力收缩肺 V 和肺毛细血管免于持续的血管内压力

有利于僵硬 LV充盈维持 CO

主动脉瓣狭窄引起心肌缺血机制氧耗增加： LV壁增厚、心室收缩压

和射血时间延长LV肥厚，心肌毛细血管密度相对舒张期心腔内压力，压迫心内膜下冠状动脉LV 舒张末压致舒张期 AO-LV差，冠状动脉灌注


Exertional dyspnea

Angina pectoris

Syncope & presyncope

sudden death

劳力性呼吸困难晕厥与晕厥前兆

心绞痛

猝死

主动脉瓣狭窄引起心肌缺血机制晕厥机制

休息时晕厥由于心律失常致 CO

运动周围血管扩张

狭窄瓣口限制 CO 相应

缺血加重使 LV 功能， CO

LV收缩压急剧，过度激活心室内压力感受器，迷走神经传入纤维兴奋血管减压反应，外周血阻力

运动后即刻发生为突然体循环静脉回流 ,影响心室充盈， CO

以上引起体循环动脉压→脑循环灌注压→脑缺血

Clinical manifestation: signs

• Presence of thrill • “Diamond” shaped, harsh, systolic crescendo-decrescendo • Decreased, delay & prolongation of pulse amplitude• Paradoxical S2 • S4 (with left ventricular hypertrophy)• S3 (with left ventricular failure)

S1 S2 S1 S2

Mild-Moderate Severe

体征（ 1 ）心音

S1正常，严重狭窄呈 S2逆分裂，可闻 S4先天性或瓣叶活动度佳者，胸骨右、左缘和心尖区听到收缩早期喷射音。不随呼吸改变

收缩期喷射性杂音喷射性、粗糙、递增 - 递减型R2 或 L3肋间最响，向颈动脉传导常伴震颤，狭窄越重，杂音越长LV 衰竭或 CO 减少，杂音消失或减弱强度随每搏间的心搏量不同而改变

体征（ 2 ）其他

动脉脉搏上升缓慢、细小而持续（细迟脉）晚期，收缩压和脉压

轻度 AS 并 AI 及动脉床顺应性差老年患者，收缩压和脉压正常甚至升高

严重 AS 者触诊颈动脉搏动明显延迟于心尖部心尖搏动持续有力；如 LV 扩大，可向左下移位

Aortic Stenosis: Laboratory Examination

X-rayThe LV border

is round & prominent as a result of LVH

Aortic regurgitation in a patient with Marfan syndrome

Marked enlargement of the ascending

aorta with regurgitant flow

marked dilation of the

ascending aorta

X 线检查心影正常或 LV ， LA 可能轻度

主动脉根部常见狭窄后扩张主动脉瓣钙化，肺淤血征象

Aortic Stenosis: Laboratory ExaminationECG

Marked LVH pattern 、 ST depression 、 T wave inversion

心电图重度狭窄

LV肥厚伴 ST-T继发性改变LA 大， AVB 、室内传导阻滞心房颤动或室性心律失常

Aortic Stenosis: Laboratory Examination

• Etiology• Valve gradient and area• LVH• Systolic LV function• Diastolic LV function• LA size• Concomitant regional

wall motion abnormalities

• Coarctation associated with bicuspid AV

Echocardiography

超声心动图明确诊断和判定狭窄程度重要方法提供心腔大小等多种信息

诊　断典型 AS 杂音易诊断，确诊有赖UCG

如合并关闭不全和二尖瓣损害多为风心病单纯主动脉狭窄

年龄＜ 15Ｙ，单叶瓣畸形多见1665Ｙ，先天性二叶瓣钙化可能性大＞ 65Ｙ，退行性老年钙化性病变多见

鉴别诊断二闭、三闭、 ASD 的全收缩期杂音胸骨左缘的其他收缩期喷射性杂音鉴别AS 与其他ＬＶ流出道梗阻疾病

先天性主动脉瓣上狭窄：杂音在右侧先天性主动脉瓣下狭窄：无喷射音梗阻性肥厚型心肌病：不向颈部传导

超声心动图

Aortic Stenosis: Complication

• Arrhythmia• SCD• IE• Systemic

embolization• HF• GIB

• 心律失常• 心源性猝死• 感染性心内膜炎• 体循环栓塞• 心衰• 消化道出血

Aortic Stenosis: Management

General Therapy

Medical Treatment Operation Balloon Aortic

Valvuloplasty

Life style controlling & reporting development of any symptoms possibly related to AS for asymptomatic

Stabilize patients (symptomatic or have indications) for subsequent surgery

Replacement of the aortic valve results in substantial clinical and hemodynamic improvement

Especially for children, adolescents, and young adults with congenital noncalcific AS

内科治疗目的：确定狭窄程度，观察狭窄进展情况措施：

预防 SBE ，风湿热定期复查：无症状轻度 2 Ｙ，中重度 6 ～ 12月频发房早予抗心律失常药物，预防 AF心绞痛可试用硝酸酯类药物控制心力衰竭不可使用作用于小动脉血管扩张剂，以防血压过低

外科治疗人工瓣膜置换术为治疗成人AS 的主要方法

无症状的轻、中度狭窄患者无手术指征重度狭窄伴心绞痛、晕厥或心衰症状为主要指征无症状重度狭窄患如伴有进行性心脏增大和明显CHF ，应手术

严重 CHF 、高龄、合并AI 或 CAD ，增加手术和术后晚期死亡风险，但不是手术禁忌证

经皮球囊主动脉瓣成形术适应证

严重 AS 的心源性休克严重 AS急诊非心脏手术治疗因有 CHF而具极高手术危险，作为以后换瓣过渡

严重 AS 的妊娠妇女严重 AS ，拒绝手术者

预后可多年无症状一旦出现症状，病情恶化症状后平均寿命 3 年死亡原因：心衰 70% 、卒死

15%

Part VIAortic

Incompetence

病因与病理•主动脉瓣和（或）主动脉根部疾病所致

急性感染性心内膜炎创伤主动脉夹层人工瓣膜撕裂

慢性主动脉瓣疾病

风心病 : （ 2/3 ）常合并二尖瓣损害感染性心内膜炎：常见原因先天性畸形：二叶瓣、 VSD主动脉瓣粘液样变性：脱垂强直性脊柱炎：瓣叶基底部和远端边缘增厚

主动脉根部扩张梅毒性主动脉炎、 Marfan综合征强直性脊柱炎、特发性升主动脉扩张严重高血压和（或）动脉粥样硬化

病理生理：急性舒张早期 LV 压很快，超过 LA 压，二尖瓣在舒期提前关闭，防止 LA 压过度、肺水肿

舒张期血流 AO反流 LV+LV接纳 LA 充盈血流LV 容量负荷急剧 LV 舒张压急剧

肺淤血肺水肿

急性者 LV 舒张末容量仅能有限，即使LV 功能正常或，代偿性心动过速， CO仍

病理生理：慢性有利代偿：长期维持正常 CO 和肺 V 压无明显

LV 对慢性容量负荷过度反应为 LV 舒张末容量，总 CO

LV 扩张，不至于因容量负荷过度而明显 LV 舒张末压离心性肥厚使 LV 厚度 / 心腔半径不变，室壁应力正常运动时外周阻力和心率伴舒张期缩短，反流减轻。

失代偿晚期收缩功能降低，左心衰竭发生LV 重量，心肌氧耗

AO 舒张压，冠状动脉血流心肌缺血LV 功能恶化

症状急性：轻者可无症，重者出现急性左心衰和低血压慢性：可多年无症状

最先的主诉为与心搏量增多有关，心悸、心前区不适晚期始出现左心衰竭表现心绞痛较主动脉瓣狭窄少见常有体位性头昏，晕厥少见

血压和脉压正常或舒张压稍低，脉压稍增大无明显周围血管征。心尖搏动正常心动过速常见S1 减低或消失 ,S2 肺 A 瓣成分增强 ,S3 常见杂音较慢性者短而调低出现 Austin-Flint 杂音，多为舒张中期杂音

AI Clinical Manifestation Signs ： Acute

Chronic AI Clinical Manifestation: Peripheral Signs

实验试剂600 元

Peripheral Signs

Duroziez’s sign

femoral retrograde

bruits

Traube’s sign

pistol shot femorals

De Musset’s sign

systolic head

bobbing

周围血管征常见：点头征、枪击音、双期杂音

Chronic AI Clinical Manifestation: Signs

• Apex– Enlarged– Displaced– Hyper-dynamic– Palpable S3 – Austin-Flint murmur

• Aortic diastolic murmur– length correlates with severity

(chronic AR)– in acute AR murmur shortens as

Aortic DP=LVEDP– in acute AR - mitral ahead closure

心尖搏动向左下移位，常弥散而有力心音

S1减弱， S2主动脉瓣成分减弱或缺如S2多为单一音，心底部可闻及收缩期喷射音

Clinical Manifestation : Signs

S1 S2 S1

• Widened pulse pressure • High pitched, blowing,

decrescendo DM at left sternal border

• Best heard at end-expiration & leaning forward

• Hands & Knee position

Murmurs

• 脉压大 • 胸骨左缘高调、叹气样、

递减的舒张期杂音 • 呼气末期及前倾时明显 • Austin-Flint 杂音

Aortic Incompetence : Laboratory ExaminationX-ray

The LV border is round &

prominent as a result of LVH

Aortic regurgitation in a patient with Marfan syndrome

Marked enlargement of the ascending

aorta with regurgitant flow

marked dilation of the

ascending aorta

Aortic IncompetenceLaboratory Examination

X-ray

Aortic incompetence with massive diffuse aortic dilation (companied with Left atrial & ventricular enlargement)


Left ventricular hypertrophy with prominent positive anterior T waves has been described with “diastolic overload” syndrome

ECG


Echo have decisive effort in diagnosis of AI

Echocardiography

Aortic Incompetence Diagnosis & Differential Diagnosis

S1↓A2 ↓Cardiac base region SMAustin-Flint murmursPrecordial Palpable S3 SBP↑ ， DBP↓ ， pulse pressure↑Dilatation of aortaLA & LV enlargement

Diagnosis

典型舒张期杂音伴周围血管征，可诊断， UCG确诊

慢性如合并主动脉瓣或二尖瓣狭窄，支持风心病诊断

诊断

鉴别诊断杂音于胸骨左缘明显时应与 Graham Steell 杂音鉴别严重肺 A 高压伴肺 A 扩张所

致肺A 瓣关闭不全常有肺动脉高压体征

Graham Steell Graham Steell MurmurMurmur

Pulmonary incompetence results

from Severe pulmonary artery

hypertension

Differential Diagnosis

Aortic Incompetence ：Differential Diagnosis

并发症感染性心内膜炎较常见室性心律失常常见心脏性猝死少见心力衰竭在急性者出现早慢性者于晚期始出现

Aortic Incompetence : Management

Acute Stabilize patients for subsequent surgery

Chronic

Medication Beta-blocking agents Vasodilator

ACEIFor

Retarding progression

Operation Surgery is fundamental therapy for AISurgery may be done as soon as possible

急性外科治疗为根本措施，内科治疗仅为术前准备目的：降低肺 V 压，增加 CO ，稳定血流动力学

血流动力学不稳定者，立即手术动脉夹层即使伴轻或中度反流，紧急手术活动性 SBE ，争取 710 天强有力抗生素治疗后手术创伤性或人工瓣膜障碍，紧急或择期手术药物可控制，心功能代偿好，手术可延缓真菌性 SBE所致，无论反流轻重，需早日手术

慢性内科治疗

预防 SBE．风湿热梅毒性主动脉炎应予一疗程青霉素治疗舒张压＞ 90mmHg应用降压药无症状的轻或中度反流者，限制重体力活动CHF应用血管扩张药、利尿剂和洋地黄类药物心绞痛可试用硝酸酯类药物积极纠正房颤和缓慢性心律失常如有感染应及早积极控制

慢性外科治疗（人工瓣膜置换术）：主要

方法不可逆 LV 功能不全发生之前进行，

不宜过晚无症状和 LV 功能正常的严重反流不需手术，随访

预后急性重度如不及时手术，易死于左心衰慢性者无症状期长重度者确诊后 5 年存活率 75% 10 年存活率 50%症状出现后，病情迅速恶化心绞痛者 5 年内死亡 50% 严重左心衰者 2 年内死亡 50%

Part VTricuspid & pulmonic

Valve Disease

Tricuspid Stenosis,TS Etiology , Pathology & PathophysiologyEtiology Rheumatic is origin

Changes of TS resemble those of MS Pathology

Pathophysiology

Transvalvular blood flow RA pressure

Systemic venous pressure

RV output

风湿为主要病因

病理改变与二狭类似

Clinical ManifestationSymptoms & Signs

• Fatigue• Systemic congestion • AF• Pulmonary

Embolization

Symptoms

•疲惫•体循环淤血•肺栓塞•房颤

• Tall jugular venous a wave pulse

• hepatic pulsation• Ascites• Opening snap

Signs

Clinical ManifestationSymptoms & Signs

• 颈静脉扩张• 开瓣音• 舒张期杂音• 可触及肝搏动• 腹水和全身水肿

Tricuspid Stenosis Laboratory Examination

II & V1 leads P wave >0.25mv, indicate RAE

Cardiomegaly with obvious

RAE

changes of TS resemble those

in MS

ECGX-ray

ECHO

II & V1 导联 P 波 >0.25mv, 提示右房大

心影增大右房明显超声改变与二狭类似

A CB

• Sodium restriction

• Diuretic therapy

Fundamental approach to management of severe TS

For children & young

adult with anomaly

Medical Treatment

Tricuspid valve

replacement

Tricuspid Stenosis :Management

Tricuspid balloon

valvuloplasty

Tricuspid Incompetence, TI Etiology , Pathology & Pathophysiology

Dilatation of the RV and of the tricuspid annulus causing functional TI

A variety of disease can affect the tricuspid valve directly and lead to primary TI

• Ebstein anomaly• Rheumatic heart disease

RV volume overload

Systemic venous

hypertension

Right heart failure

Tricuspid IncompetenceClinical Manifestations

• jugular pulsations• 颈静脉搏动• Systolic pulsations of

liver • 肝收缩期搏动• S3 accentuated by

inspiration• 吸气时 S3 增强• DM另外，体循环淤血的体征

SignsSymptoms• Fatigue• Abdominal

distension疲乏、腹胀等右心衰的表现 Complication Fibrillation Pulmonary embolism

Tricuspid Incompetence Laboratory Examination

• RAE• RBBB• AF

• RAE 、 RVE • Pleural effusion

ECG X-ray

Key to diagnosis of TI

ECHO

Tricuspid Incompetence Management

Key point for treatmentKey point for treatment

AA TI in the absence of pulmonary hypertension usually is well tolerated

BBSevere TI and primary tricuspid valve disease require Operation

Pulmonic Stenosis & Incompetence Etiology , Pathology & Pathophysiology

The congenital form is the most common cause of it

PS

changes of PI resemble those of TIPI

RV volume overload

Systemic venous

hypertension

Right heart failure

Pulmonic Incompetence Clinical Manifestations & Management

• wide splitting of S2 S2 宽分裂• Graham Steell Murmur Graham Steell 杂音• S3 and S4 are augmented by inspiration 吸气时 S3 与 S4 增强

Clinical Manifestations of it are overshadowed by other one

Signs

Management

PI alone is seldom severe enough to require specific treatment

主要治疗肺高压的原发病 MS

Pulmonic Incompetence Laboratory Examination

• Be helpful to diagnosis of PI

ECG X-ray ECHO

• 肺高压者有右室肥厚征• RVE • Chunk of

pulmonary Artery Dilation

Part ⅥMultivalvular Heart Disease

Multivalvular Heart Disease & Etiology

Key pointKey point11


一种疾病同时损害几个瓣膜

一个瓣膜损害致心脏容量或压力负荷过重相继引起近端瓣膜功能受累


不同疾病分别导致不同瓣膜损害

Multivalvular Heart Disease & Pathophysiology



严重损害掩盖轻的损害

近端损害影响较显著，而掩盖轻的损害


总的血液动力学异常明显

Multivalvular Heart Disease Sorting by morbidity

22

55

33

44

11心房肌纤维肥大心肌纤维化

心房结构改变

心房肌细胞退行性变

MS & AI

MS & AS

AS & MI

AI & MIMS & TI /PI

Examples of common multivalvular heart disease

MS+AI MS 导致心排血量下降，使 LV扩大延缓，周围血管征缺如

BB

严重 MS 常掩盖 AS 的表现

AS+MI为危险的多瓣膜病，相对较少见。 AS 增加左室后负荷使MI返流加重，前向心搏量减少较二者单独存在时明显

MS+AS

Valvular Heart Disease

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