Heart Failure
Xiaojuan Bai
7 years program of China Medical University
Objective,
1.Mastering clinical manifestation,diagnosis and
management of heart failure
2.Grasping causes,pathophysiology of heart failure
3.Understanding classification and investigation of
heart failure
1.general concept
1)causes of heart failure
2)precipitating/aggravating factors
3)pathophysiology
4)type of heart failure
2.chronic and acute heart failure
1)clinical manifestation
2)investigation
3)diagnosis and differential diagnosis
4)management
Content
Heart failure is an imprecise term
used to describe the state that develops
when the heart cannot maintain an
adequate cardiac output or can do so
only at the expense of an elevated filling
pressure,
Definition
? pulmonary congestion,
? systemic venous congestion,
? tissue perfusion deficiency due to
low cardiac output,
Clinical Features
?left ventricular end-diastolic pressure>18mmHg,
?right ventricular end-diastolic pressure>10mmHg,
heart failure = cardiac insuffiency.
Hemodynamic Features
Causes of heart failure
1.Reduced ventricular contractility
a,Cardiomyopathy,myocardial infarction,
b,Metabolic dysfunction
2.ventricular overload
a,pressure overload---- hypertension,aortic
stenosis,pulmonary hypertension,pulmonary valve
stenosis.
b,volume overload ---- mitral regurgitation,aortic
regurgitation,atrial septal defect,ventricular sepals
defect,hyperthyroidism,artery-venous fistula,
c,ventricular inflow obstruction----hypertrophy,
mitral stenosis,tricuspid stenosis,restrictive
cardiomyopathy,constrictive pericarditis,endocardial
fibrosis and other disorders that cause a stiff
myocardium,
Precipitating / aggravating factors
? myocardial ischemia or infarction
? infection
? arrhythmia
? pulmonary embolism
? exertion
? pregnancy and parturition
? anemia
? intravenous fluid overload,electrolyte
disturbance,acid-base imbalance
Pathophysiology
? 1,Frank-Starling’s Law of the heart
a,The cardiac output is a function of the
preload,the afterload,and myocardial
contractility.
b.Preload,the volume and pressure of
blood in the ventricle at the end of diastole.
c,Afterload,the arterial resistance.
1 正常静息
2 正常活动
3’心衰活动
3 心衰静息
心肌收缩性
B
A D
C
左室舒张末容量
图 3–2–1 正常和心力衰竭时对机体活动时的代偿
情况
最大活
动
活动
静息
左
室
作
功
呼吸困
难
肺水肿
E 4 静息
致死性心肌受损
心肌细胞死亡
心力衰竭
心肌细胞死亡
+ +
↑心肌能量消耗
↑后负荷
血管收缩
↓心排血量
神经体液兴奋
RAS
SAS
InSP3
循环
↑心肌能量消耗
↑胞浆 Ca2+
cAMP InSP3
心脏
↓心肌松弛性 ↑变力效应
+
－
—
心律失常
猝死
图 3–2–2 肾素 —血管紧张素和交感 —肾
上腺素能系统激活时对心脏代偿功能的影响
2,RAAS in Heart Failure
? 2,RAAS in Heart Failure
? 3.myocardium impaired and remodeling
initial myocardium impaired
ventricular overload
myocardium infarction
inflammation
disease progress
heart failure
complication
death
chamber enlargement
myocardial hypertrophy
embryo gene phenotype
extracellular matrix change
?secondary conduct
factor
?sympathetic nervous
system
?RAAS
?endothelins
?TNF-α,IL-6
?mechanical stress
?oxidative stress
? 4.Diastolic heart failure
Heart failure may develop as a result of
poor ventricular filling and high filling pressure
caused by abnormal ventricular relaxation
顺应性
↓
顺应性
↑
正常
压
力
图 3–2–4 心室舒张末期压力和容积的关系
舒张性心力衰竭时, 心室顺应性降低, 心室压力 –容积曲线
向左上方移位, 即在任何特定的舒张末期压时, 心室末期
容量小于正常人 。
容 积
a,sarcoplasmic reticulum intake Ca2+
free Ca2+ in myocyte degrade slowly
b,In CHD with obvious ischemia,before contractility
dysfunction,have occurred relaxation dysfunction
c,In hypertrophy and hypertrophic cardiomyopathy,
left ventricular end-diastolic filling pressure
pulmonary hypertension,pulmonary congestion
diastolic heart failure
relaxation
dysfunction
Type of heart failure
Heart failure can be described or classified in several ways.
? 1,Acute and chronic heart failure
? 2,Left,right and biventricular heart failure
? 3,High and low output heart failure
? 4,Diastolic and systolic dysfunction
? 5.Asymptomatic and congestive heart failure
?Low output heart failure:
Clinical manifestation of abnormal peripheral circulation:
vasoconstriction in system,cold,pale,extremities cyanosis,
in the late period,output per minute decrease and lead to
difference of pulse pressure decrease,the above manifestation
occur in the majority of CHF.
?High output heart failure:
Extremities warm,flush,difference of pulse pressure increase,
seen in hyperthyroidism,anemia,pregnancy
Systolic dysfunction
Heart failure may develop as a result of
impaired myocardial contraction,
Diastolic dysfunction
Heart failure can also be due to poor
ventricular filling pressure caused by
abnormal ventricular relaxation,which is
commonly found in patients with left
ventricular hypertrophy,hypertension and
ischemic heart disease.
§ 1 Chronic heart failure
Definition
same meaning as congestive heart failure
clinical manifestation
1.left ventricular heart failure
mainly manifested with pulmonary congestion
and reduction of cardiac output
A symptom
1.dyspnea
1)breathlessness
2) paroxysmal nocturnal dyspnea:often with
wheeze sound in both lung cardiogenic
asthma
3)Orthopnea,in decubitus,blood volume flow
to heart increase elevated end–diastolic
filling pressure pulmonary venous and
capillary pressure increase interstitial
pulmonary edema pulmonary compliance
decrease respiratory resistance
4)acute pulmonary edema
2,cough and hemoptysis
pink-tinged or brownish sputum
3,fatigue on exertion
4,urinary system symptom
in early period,nocturia increase
in later period,oliguria
B,Sign
1.general sign
dyspnea after activity,also cyanosis,
jaundice,difference of pulse pressure decrease,
SBp decrease,rapid heart rate,peripheral
vasoconstriction,extremities cyanosis,cold,
sinus tachycardia.
2.Heart sign
? diffuse and laterally displaced apical impulse
? gallop in early diastolic period,accentuated p2
? systolic murmur at cardiac apex
? pulses alternans occur when left ventricular
ejective impedance increase
3.Lung sign
moist rales in the base of lung
? CHF patients occur pleural fluid
2.Right ventricular Failure
systemic circulation congestion
Symptom
1)gastrointestinal tract symptom:
anorexia,distention,nausea,vomiting,constipation
2)kidney symptom
kidney congestion renal function decrease
3)hepatic region pain,congestion,cardiac cirrhosis
4)dyspnea
Sign
1.heart sign
? heart dilate
? when right heart failure is obvious,strong impulse
occur in the systolic period at the left sternal border,
obvious beat occur infraxiphoid
? diastolic gallop
? relative tricupid incompetence
2.hepatic cervical reflux
3.congestive liver and tenderness occur before edema
Acute, jaundice,ALT increase
Long term,cardiac cirrhosis
4.edema
occur after cervical filling and liver large,is typical
sign of right heart failure,at first occur in foot,ankle,
anterior tibia.
In the early period,edema occur in the morning,worse
in the evening,disappear after sleeping.
In the late time,systemic,symmetric,pitting edema
If complicated with malnutrition or hepatic dysfunction,
face edema occur,prognosis is poor.
5.pleural fluid and ascites
3.biventricular heart failure
have clinical manifestation of left and
right heart failure.
Conditions with normal systolic function
and decreased diastolic function include:
(1) systemic arterial hypertension
(2) myocarditis
(3) hyretrophic cardiomyopathy
(4) congestive cardiomyopathy
In the setting of left ventricular dysfunction,
which of following neurohormonal factors would
be activated?
(1)Norepinephrine
(2)Endothelin
(3)Arginie vasopreein
(4)Endothelial-derived relaxing factor
Investigation
1.routine examination
blood,urine,renal function,electrolyte,liver function
2.ECG
a.no specific findings,
b.Abnormalities may provide etiological clue(ventricular
hypertrophy,AMI,bundle branch block)
c.V1ptf<-0.03mm/s left atrial overload
3.Echocardiography:evaluating LV as well as
other chamber dimensions,ejection fraction,
and wall motion abnormality.
a.M:obtained directing a stationary ultrasonography
beam at some portion of the heart.
b.Two-dimensional Echo (2-DE):provides spatially
correct images of heart and has become the dominant
echocardiographic modality
c.Doppler Echo:using ultrasonography to record the
flow of blood within the cardiovascular system.
4.X ray
a evaluation of chamber enlargement
b pulmonary venous congestion
Kerley B lines:reflect chronic elevation of left
atrial pressure and represent chronic thickening of the
interlobular septa from edema.
venous blood redistribution to the upper lobes.
C pulmonary venous pressure>25-30mmHg(3.3-4KPa)
interstitial edema occur.
参 数 正常值 临床意义
中心静脉压（ CVP） 6~12cmH2O（ 0.59~1.18KPa） ↑说明血容量过多或右心衰竭
肺动脉压（ PAP） 12~30/4~13mmHg （ 1.6~4.0/0.53~1.73KPa ） ↑说明肺动脉高压、左心衰竭
肺毛细血管楔嵌压（ PCWP） 6~12mmHg（ 0.8~1.6KPa） ↑说明肺淤血、左心衰竭
心搏量（ SV） 60~70ml ↓可由于前负荷不足、心包填塞、
心肌收缩力下降，心排阻力上升
心搏指数（ SI） 41~51ml/m2 同上
心排血量（ CO） 5~6L/min ↑可由于正性肌力药物作用，
↓说明有心力衰竭
心排指数（ CI） 2.6~4.0L/（ min·m2） ↓说明收缩力减低或心力衰竭
射血分数（ EF） 0.5~0.6 ↓说明心室收缩功能减低
左室每搏作功（ LVSW） 60~123
左室每搏作功指数（ LVSWI） 50~62
体循环血管阻力 （ SVR） 770~1500dynes·s/ cm5 ↓见于缺血, 血管扩张剂,↑高血压, 血管活性药物
体循环血管阻力指数（ SVRI） 1970~2390dynes·s（ cm5·m 2） 同上
肺血管阻力 （ PVR） 37~250 dynes·s/ cm5
↑毛细血管前肺小动脉收缩, 肺栓塞, 慢性
肺疾病, 肺间质水肿, 肺小血管阻塞性病
变, 二尖瓣狭窄
肺血管阻力指数（ PVRI） 69~177 dynes·s（ cm5·m 2） 同上
↑增高 ↓降低
Invasive homodynamic monitoring
Diagnosis and differential diagnosis
Clinical diagnosis include,
etiology(basic cause and induce cause),
pathoanatomy,
pathophysiology,
heart rhythm
cardiac function
NYHA classification
Ⅰ no activity limit,daily activity don't lead to inertia,
dyspnea,palpitation.
Ⅱ slight activity limit,no symptom at rest,daily activity
lead to inertia,dyspnea,palpitation or angina pectoris,
Ⅲ obvious activity limit,no symptom at rest,daily activity
lead to inertia,dyspnea,palpitation or angina pectoris.
Ⅳ cannot do any activity,have symptom at rest.
typ
e
CI
(L/min·
m2）
PCWP
（ mmHg） Clinical manifestation
Ⅰ
≥2.2 ≤18（ 2.4） No peripheral perfusion deficiency and
pulmonary congestion,no symptom and sign
of heart failure
Ⅱ
≥2.2 ＞ 18（ 2.4） No peripheral perfusion deficiency,pulmonary
congestion,no obvious clinical manifestation
Ⅲ
＜ 2.2 ≤18（ 2.4） peripheral perfusion deficiency,no pulmonary
congestion,seen in right ventricular infarction
and blood volume deficiency
Ⅳ
＜ 2.2 ＞ 18（ 2.4） peripheral perfusion deficiency and
pulmonary congestion,severe type
Forrester classification
Killip classification
Ⅰ no heart failure symptom,no moist rales,PCWP
may elevate
Ⅱ slight to moderate heart failure,<50% lung field
moist rales,S3 gallop,persist sinus tachycardia,x ray
manifestation of pulmonary congestion
Ⅲ severe heart failure,>50%lung field moist rales,
may occur lung edema
Ⅳ cardiac shock,Bp<90mmHg,oliguria <20ml/h,skin
cold,cyanosis,tachypnea,rapid pulse
V cardiogenic shock and pulmonary edema
Differential diagnosis
1,Left heart failure
Pulmonary,cardiogenic dyspnea
2,Right heart failure
constrictive pericarditis
renal edema
hepatic cirrhosis
Management of heart failure
1.Etiologic treatment
basic cause,precipitating causes.
2.Reduction of ventricular overload
a.rest and sedative agent
b.salt-intake control
normal adult intake 3-6g salt per day
Ⅰ 0 heart failure, 2g salt/per day
Ⅱ 0heart failure, 1g salt/per day
Ⅲ 0heart failure, 0.4g salt/per day
c.water intake control
may not limit water intake strictly,intake water
1.5-2.0L per day
in severe heart failure,water retention,seral
albumin decrease,dilutive hyponatremia,not only
limit salt intake,but also control water intake
d.diuretics
利尿剂 作用部位和机制 剂量（ mg/d） 作用持续时间
（ h）
排钾类
氢氯噻嗪
（
hydrochlorothiozide）
远曲小管：抑制 NaCl共转运 25~100口服 12~18
美托拉宗
（ metolazone） 同上 5~20口服 12~24
氯噻酮
（ chlorothalidone 同上 25~100口服 24~72
呋噻米
（ furosemide）
Henle襻上升支：抑制 Na-K-
2Cl转运 20~1000口服 /静注 4~6
丁脲酸
（ bumetanide） 同上 0.5~20口服 4~6
潴钾类
氨体舒通
（ spironolactone 集合管：醛固酮拮抗剂 25~100口服 24~96
氨苯喋啶
（ triamterene） 集合管：抑制 Na重吸收 100~300口服 12~16
阿米洛利
（ amiloride） 同上 5~20口服 12~18
Reasonable application of diuretics
1,strictly following indication
2,combined medication
K-sparing diuretics is contradicted in renal
dysfunction
3,intermissional therapy
4,Pay attention to water and electrolyte
disturbance
Differential of deficit sodium and diluted hyponatremia
deficit sodium hyponatremia
occurred after using many diuretics,
feature,postohypotension,oliguria,high urine gravity,
should intake salt
diluted hyponatremia
also called refractory heart failure,hyponatremia of high
blood volume,should limit water-intake
e.Vasodilator drugs
Indication
1.Left end-diastolic filling pressure>18mmHg,
pulmonary congestion
2.clinical manifestation of peripheral circulatory
perfusion deficiency CI<2.2L/min.m2
3.valve insufficiency,ventricular septal defect
pulmonary hypertension,valve regurgitation with
cardiac dysfunction
If blood volume deficiency,should fluid
replacement at first,then use vasodilator drugs.
药物 机制 前负 荷 后负 荷 常用剂量
作用时间
开始 高峰 持续
硝酸盐血管扩张剂
硝酸甘油
NO供者
+++ +
0.2~10μg/
（ kg·min） iv
5~6mg 经皮
2min 5~15min <30min
二硝酸异山梨醇酯 +++ +
10~60mg po tid 15~20min 1h 4h
10~20mg 舌下 5min 15~30min 3h
2~7mg/h iv 3~5min 2h 3h
硝普钠 +++ +++ 0.1~0.3μg/（ kg·min）iv 几乎立即 停药 2~15min消失
交感神经阻滞剂
酚妥拉明 非选择性 α–肾上腺素能激动剂 ++ ++ 0.5~1.0mg/min iv 15~20min 3~4h
哌唑嗪 α1–肾上腺素能受体拮抗 剂 +++ ++ 1~6mg po tid 30min 1~3h 6h
肾素 –血管紧张素系统
拮抗剂
卡托普利
抑制由 ACE引起的
肾系统性生
成和组织生成血管
紧张素 Ⅱ ；
降低缓激肽的代谢
++ ++ 6.25~50mg po q8h 15~30min 1~2h 4~6h
依那普利 ++ ++ 5~10mg po bid 2h 4~6h 24h
赖诺普利 ++ ++ 2.5~20mg po q12~24h 6~8h 12h
雷米普利 ++ ++ 1.25~5mg po qd 1~2h 3~6h 24h
芦沙坦 阻断血管紧张素 Ⅱ（ AT
1受体）
++ ++ 25~50mg po q12h 5~6h 24h
ACE-I
Contradiction
Severe renal dysfunction,renal artery stenosis,
obvious mitral and aortic stenosis
American and European guideline, that all heart
failure patients including asymptomatic failure,except
patients that have contradiction or cannot tolerate ACE-I,
should use ACE-I,and for the long term therapy.
3.increase cardiac output
a.Digitalis
Pharmacology
? increase myocardial contractile force
Inhibit Na+-K+ ATPase Na+ -Ca2+change
intracellular Ca2+ increase contractility increase
? increase cardiac output
Renal flow increase SAS activity decrease
peripheral vasodilate peripheral
resistance decrease
? RAAS activity decrease
Reduction of water and salt retention due to aldosterone
decrease
? Prolong atrioventricular conduction
Highly effective in the treatment of atrial fibrillation in
addition to slowing ventricular response,it may convent
the rhythm to normal sinus mechanism.
Use carefully
?Hypertrophic cardiomyopathy
?Mitral stenosis with sinus rhythm
?Pericardium constriction
?Pulmonary heart disease
?High degree AVB
?AMI in 24h
Digitalis toxicity
Induce cause
Hypokalemia
Hypomagnemia
Hypercalcemia
Acid intoxication
Hypoxia
Renal dysfunction
Severe myocardial lesion
Hypothyroidism
Clinical manifestation of digitalis
?Systemic toxic effects:
Gastrointestinal tract symptom:nausea,vomiting,
anorexia,diarrhea,confusion,amblyopia
Cardiac symptom:arrhythmia
?Prolonged PR interval and AV conduction.
?Increase the automaticity of Purkinje fibers and
enhance reentry,resulting in extrasystoles,
ventricular fibrillation.
Treatment
? Stopping using digitalis
? Use potassium,magnesium if serum K is low.
? Rapid arrhythmia, lidocarine or diphenine
sodium,1-4mg/min usually don't cardioversion
? Slowly arrhythmia atropine0.5-1mg.
b,Other inotropic agent
1.?-adrenocepter agonists
Dopamine
1-5ug/Kg.min activate dopamine receptor,
renal flow increase
>10ug/Kg.min activate α-receptor,
vasoconstrict
Dobutamine
2-7.5ug/Kg.min
2.Phosphodiesterase inhibitor
Inhibit cAMP degrade increase
intracellular cAMP Ca2+ increase
cardiac contraction increase
Amrinone Milrione
3.Aldosterone antagonist
Protect aldosterone escape.
4.?-adrenocepter antagonists
Recent clinic trials have shown,when given in
very small doses under carefully monitored conditions,
they can increase ejection fraction,improve symptoms
and reduce the frequency of hospitalization in patient
with chronic heart failure.
,Relieve toxiation of catecholamine
,On the base of using ACE-I,diuretics,digitalis,
using ? bloker.
,Given in very small incremental doses
Bisoprool 1.25mg
metoprolol 6.25mg
5.diastolic heart failure treatment
treat primary disease
relax myocardium
revert myocardial hypertrophy
decrease preload
control tachycardia
calcium channel blocker,and ? blocker can be useful.
6.Refractory heart failure
1)Have the etiology and precipitating
causes been established?
2)Are drug dose optimal?
3)Is the patient adhering to an adequate
low-salt diet?
4)Need another cardiac transplantation.
7.Acute pulmonary edema
Emergency treatment
1)position:Don't keep patient in a supine position
2)Maintain oxygenation:high concentrations of O2
should be given by mask or nasal cannula.
3)Morphine sulfate 3 - 5mg IV or 5- 10mg IM can
reduce agitation,reduce transient arterial and
venous dilation,decrease the respiratory rate,
slow the heart rate,and reduce respiratory and
cardiac work,
4)Intravenous administration of a rapidly actig
diuretic,eg.(furosemide 40mg IV) can be initiate a
prompt diuresis in 15 to 20 min.
5)Rotating tourniquets are effective with Bp cuff
applied to 3 limbs,inflated midway between
diastolic and systolic pressure,deflated and rotated
10 to 20 min.
6)Vasodilator drugs
7)Digitalis
8)Aminophylline
9)others
Pathophysiologic consequences of a myocardial
infarction include:
(1)increased systolic load due to the akinetic segment
(2)decreased ejection fraction that approximates the
amount of muscle loss.
(3)hypertrophy of noninfarcted myocardium.
(4)decreased end-diastoic volume
Supportive evidence that left-sided failure is present
includes all the following EXCEPT:
A.abnormally elevated filling pressures as detected by
right heart catheterization
B.a cardiac index of 3.5 liters/min/m2
C.a reduction in maximum oxygen consumption
determined noninvasively by exercise
D.the presence of pulmonary rales on physical
examination
E.low left ventricular ejection fraction at rest on
echocardiography
Xiaojuan Bai
7 years program of China Medical University
Objective,
1.Mastering clinical manifestation,diagnosis and
management of heart failure
2.Grasping causes,pathophysiology of heart failure
3.Understanding classification and investigation of
heart failure
1.general concept
1)causes of heart failure
2)precipitating/aggravating factors
3)pathophysiology
4)type of heart failure
2.chronic and acute heart failure
1)clinical manifestation
2)investigation
3)diagnosis and differential diagnosis
4)management
Content
Heart failure is an imprecise term
used to describe the state that develops
when the heart cannot maintain an
adequate cardiac output or can do so
only at the expense of an elevated filling
pressure,
Definition
? pulmonary congestion,
? systemic venous congestion,
? tissue perfusion deficiency due to
low cardiac output,
Clinical Features
?left ventricular end-diastolic pressure>18mmHg,
?right ventricular end-diastolic pressure>10mmHg,
heart failure = cardiac insuffiency.
Hemodynamic Features
Causes of heart failure
1.Reduced ventricular contractility
a,Cardiomyopathy,myocardial infarction,
b,Metabolic dysfunction
2.ventricular overload
a,pressure overload---- hypertension,aortic
stenosis,pulmonary hypertension,pulmonary valve
stenosis.
b,volume overload ---- mitral regurgitation,aortic
regurgitation,atrial septal defect,ventricular sepals
defect,hyperthyroidism,artery-venous fistula,
c,ventricular inflow obstruction----hypertrophy,
mitral stenosis,tricuspid stenosis,restrictive
cardiomyopathy,constrictive pericarditis,endocardial
fibrosis and other disorders that cause a stiff
myocardium,
Precipitating / aggravating factors
? myocardial ischemia or infarction
? infection
? arrhythmia
? pulmonary embolism
? exertion
? pregnancy and parturition
? anemia
? intravenous fluid overload,electrolyte
disturbance,acid-base imbalance
Pathophysiology
? 1,Frank-Starling’s Law of the heart
a,The cardiac output is a function of the
preload,the afterload,and myocardial
contractility.
b.Preload,the volume and pressure of
blood in the ventricle at the end of diastole.
c,Afterload,the arterial resistance.
1 正常静息
2 正常活动
3’心衰活动
3 心衰静息
心肌收缩性
B
A D
C
左室舒张末容量
图 3–2–1 正常和心力衰竭时对机体活动时的代偿
情况
最大活
动
活动
静息
左
室
作
功
呼吸困
难
肺水肿
E 4 静息
致死性心肌受损
心肌细胞死亡
心力衰竭
心肌细胞死亡
+ +
↑心肌能量消耗
↑后负荷
血管收缩
↓心排血量
神经体液兴奋
RAS
SAS
InSP3
循环
↑心肌能量消耗
↑胞浆 Ca2+
cAMP InSP3
心脏
↓心肌松弛性 ↑变力效应
+
－
—
心律失常
猝死
图 3–2–2 肾素 —血管紧张素和交感 —肾
上腺素能系统激活时对心脏代偿功能的影响
2,RAAS in Heart Failure
? 2,RAAS in Heart Failure
? 3.myocardium impaired and remodeling
initial myocardium impaired
ventricular overload
myocardium infarction
inflammation
disease progress
heart failure
complication
death
chamber enlargement
myocardial hypertrophy
embryo gene phenotype
extracellular matrix change
?secondary conduct
factor
?sympathetic nervous
system
?RAAS
?endothelins
?TNF-α,IL-6
?mechanical stress
?oxidative stress
? 4.Diastolic heart failure
Heart failure may develop as a result of
poor ventricular filling and high filling pressure
caused by abnormal ventricular relaxation
顺应性
↓
顺应性
↑
正常
压
力
图 3–2–4 心室舒张末期压力和容积的关系
舒张性心力衰竭时, 心室顺应性降低, 心室压力 –容积曲线
向左上方移位, 即在任何特定的舒张末期压时, 心室末期
容量小于正常人 。
容 积
a,sarcoplasmic reticulum intake Ca2+
free Ca2+ in myocyte degrade slowly
b,In CHD with obvious ischemia,before contractility
dysfunction,have occurred relaxation dysfunction
c,In hypertrophy and hypertrophic cardiomyopathy,
left ventricular end-diastolic filling pressure
pulmonary hypertension,pulmonary congestion
diastolic heart failure
relaxation
dysfunction
Type of heart failure
Heart failure can be described or classified in several ways.
? 1,Acute and chronic heart failure
? 2,Left,right and biventricular heart failure
? 3,High and low output heart failure
? 4,Diastolic and systolic dysfunction
? 5.Asymptomatic and congestive heart failure
?Low output heart failure:
Clinical manifestation of abnormal peripheral circulation:
vasoconstriction in system,cold,pale,extremities cyanosis,
in the late period,output per minute decrease and lead to
difference of pulse pressure decrease,the above manifestation
occur in the majority of CHF.
?High output heart failure:
Extremities warm,flush,difference of pulse pressure increase,
seen in hyperthyroidism,anemia,pregnancy
Systolic dysfunction
Heart failure may develop as a result of
impaired myocardial contraction,
Diastolic dysfunction
Heart failure can also be due to poor
ventricular filling pressure caused by
abnormal ventricular relaxation,which is
commonly found in patients with left
ventricular hypertrophy,hypertension and
ischemic heart disease.
§ 1 Chronic heart failure
Definition
same meaning as congestive heart failure
clinical manifestation
1.left ventricular heart failure
mainly manifested with pulmonary congestion
and reduction of cardiac output
A symptom
1.dyspnea
1)breathlessness
2) paroxysmal nocturnal dyspnea:often with
wheeze sound in both lung cardiogenic
asthma
3)Orthopnea,in decubitus,blood volume flow
to heart increase elevated end–diastolic
filling pressure pulmonary venous and
capillary pressure increase interstitial
pulmonary edema pulmonary compliance
decrease respiratory resistance
4)acute pulmonary edema
2,cough and hemoptysis
pink-tinged or brownish sputum
3,fatigue on exertion
4,urinary system symptom
in early period,nocturia increase
in later period,oliguria
B,Sign
1.general sign
dyspnea after activity,also cyanosis,
jaundice,difference of pulse pressure decrease,
SBp decrease,rapid heart rate,peripheral
vasoconstriction,extremities cyanosis,cold,
sinus tachycardia.
2.Heart sign
? diffuse and laterally displaced apical impulse
? gallop in early diastolic period,accentuated p2
? systolic murmur at cardiac apex
? pulses alternans occur when left ventricular
ejective impedance increase
3.Lung sign
moist rales in the base of lung
? CHF patients occur pleural fluid
2.Right ventricular Failure
systemic circulation congestion
Symptom
1)gastrointestinal tract symptom:
anorexia,distention,nausea,vomiting,constipation
2)kidney symptom
kidney congestion renal function decrease
3)hepatic region pain,congestion,cardiac cirrhosis
4)dyspnea
Sign
1.heart sign
? heart dilate
? when right heart failure is obvious,strong impulse
occur in the systolic period at the left sternal border,
obvious beat occur infraxiphoid
? diastolic gallop
? relative tricupid incompetence
2.hepatic cervical reflux
3.congestive liver and tenderness occur before edema
Acute, jaundice,ALT increase
Long term,cardiac cirrhosis
4.edema
occur after cervical filling and liver large,is typical
sign of right heart failure,at first occur in foot,ankle,
anterior tibia.
In the early period,edema occur in the morning,worse
in the evening,disappear after sleeping.
In the late time,systemic,symmetric,pitting edema
If complicated with malnutrition or hepatic dysfunction,
face edema occur,prognosis is poor.
5.pleural fluid and ascites
3.biventricular heart failure
have clinical manifestation of left and
right heart failure.
Conditions with normal systolic function
and decreased diastolic function include:
(1) systemic arterial hypertension
(2) myocarditis
(3) hyretrophic cardiomyopathy
(4) congestive cardiomyopathy
In the setting of left ventricular dysfunction,
which of following neurohormonal factors would
be activated?
(1)Norepinephrine
(2)Endothelin
(3)Arginie vasopreein
(4)Endothelial-derived relaxing factor
Investigation
1.routine examination
blood,urine,renal function,electrolyte,liver function
2.ECG
a.no specific findings,
b.Abnormalities may provide etiological clue(ventricular
hypertrophy,AMI,bundle branch block)
c.V1ptf<-0.03mm/s left atrial overload
3.Echocardiography:evaluating LV as well as
other chamber dimensions,ejection fraction,
and wall motion abnormality.
a.M:obtained directing a stationary ultrasonography
beam at some portion of the heart.
b.Two-dimensional Echo (2-DE):provides spatially
correct images of heart and has become the dominant
echocardiographic modality
c.Doppler Echo:using ultrasonography to record the
flow of blood within the cardiovascular system.
4.X ray
a evaluation of chamber enlargement
b pulmonary venous congestion
Kerley B lines:reflect chronic elevation of left
atrial pressure and represent chronic thickening of the
interlobular septa from edema.
venous blood redistribution to the upper lobes.
C pulmonary venous pressure>25-30mmHg(3.3-4KPa)
interstitial edema occur.
参 数 正常值 临床意义
中心静脉压（ CVP） 6~12cmH2O（ 0.59~1.18KPa） ↑说明血容量过多或右心衰竭
肺动脉压（ PAP） 12~30/4~13mmHg （ 1.6~4.0/0.53~1.73KPa ） ↑说明肺动脉高压、左心衰竭
肺毛细血管楔嵌压（ PCWP） 6~12mmHg（ 0.8~1.6KPa） ↑说明肺淤血、左心衰竭
心搏量（ SV） 60~70ml ↓可由于前负荷不足、心包填塞、
心肌收缩力下降，心排阻力上升
心搏指数（ SI） 41~51ml/m2 同上
心排血量（ CO） 5~6L/min ↑可由于正性肌力药物作用，
↓说明有心力衰竭
心排指数（ CI） 2.6~4.0L/（ min·m2） ↓说明收缩力减低或心力衰竭
射血分数（ EF） 0.5~0.6 ↓说明心室收缩功能减低
左室每搏作功（ LVSW） 60~123
左室每搏作功指数（ LVSWI） 50~62
体循环血管阻力 （ SVR） 770~1500dynes·s/ cm5 ↓见于缺血, 血管扩张剂,↑高血压, 血管活性药物
体循环血管阻力指数（ SVRI） 1970~2390dynes·s（ cm5·m 2） 同上
肺血管阻力 （ PVR） 37~250 dynes·s/ cm5
↑毛细血管前肺小动脉收缩, 肺栓塞, 慢性
肺疾病, 肺间质水肿, 肺小血管阻塞性病
变, 二尖瓣狭窄
肺血管阻力指数（ PVRI） 69~177 dynes·s（ cm5·m 2） 同上
↑增高 ↓降低
Invasive homodynamic monitoring
Diagnosis and differential diagnosis
Clinical diagnosis include,
etiology(basic cause and induce cause),
pathoanatomy,
pathophysiology,
heart rhythm
cardiac function
NYHA classification
Ⅰ no activity limit,daily activity don't lead to inertia,
dyspnea,palpitation.
Ⅱ slight activity limit,no symptom at rest,daily activity
lead to inertia,dyspnea,palpitation or angina pectoris,
Ⅲ obvious activity limit,no symptom at rest,daily activity
lead to inertia,dyspnea,palpitation or angina pectoris.
Ⅳ cannot do any activity,have symptom at rest.
typ
e
CI
(L/min·
m2）
PCWP
（ mmHg） Clinical manifestation
Ⅰ
≥2.2 ≤18（ 2.4） No peripheral perfusion deficiency and
pulmonary congestion,no symptom and sign
of heart failure
Ⅱ
≥2.2 ＞ 18（ 2.4） No peripheral perfusion deficiency,pulmonary
congestion,no obvious clinical manifestation
Ⅲ
＜ 2.2 ≤18（ 2.4） peripheral perfusion deficiency,no pulmonary
congestion,seen in right ventricular infarction
and blood volume deficiency
Ⅳ
＜ 2.2 ＞ 18（ 2.4） peripheral perfusion deficiency and
pulmonary congestion,severe type
Forrester classification
Killip classification
Ⅰ no heart failure symptom,no moist rales,PCWP
may elevate
Ⅱ slight to moderate heart failure,<50% lung field
moist rales,S3 gallop,persist sinus tachycardia,x ray
manifestation of pulmonary congestion
Ⅲ severe heart failure,>50%lung field moist rales,
may occur lung edema
Ⅳ cardiac shock,Bp<90mmHg,oliguria <20ml/h,skin
cold,cyanosis,tachypnea,rapid pulse
V cardiogenic shock and pulmonary edema
Differential diagnosis
1,Left heart failure
Pulmonary,cardiogenic dyspnea
2,Right heart failure
constrictive pericarditis
renal edema
hepatic cirrhosis
Management of heart failure
1.Etiologic treatment
basic cause,precipitating causes.
2.Reduction of ventricular overload
a.rest and sedative agent
b.salt-intake control
normal adult intake 3-6g salt per day
Ⅰ 0 heart failure, 2g salt/per day
Ⅱ 0heart failure, 1g salt/per day
Ⅲ 0heart failure, 0.4g salt/per day
c.water intake control
may not limit water intake strictly,intake water
1.5-2.0L per day
in severe heart failure,water retention,seral
albumin decrease,dilutive hyponatremia,not only
limit salt intake,but also control water intake
d.diuretics
利尿剂 作用部位和机制 剂量（ mg/d） 作用持续时间
（ h）
排钾类
氢氯噻嗪
（
hydrochlorothiozide）
远曲小管：抑制 NaCl共转运 25~100口服 12~18
美托拉宗
（ metolazone） 同上 5~20口服 12~24
氯噻酮
（ chlorothalidone 同上 25~100口服 24~72
呋噻米
（ furosemide）
Henle襻上升支：抑制 Na-K-
2Cl转运 20~1000口服 /静注 4~6
丁脲酸
（ bumetanide） 同上 0.5~20口服 4~6
潴钾类
氨体舒通
（ spironolactone 集合管：醛固酮拮抗剂 25~100口服 24~96
氨苯喋啶
（ triamterene） 集合管：抑制 Na重吸收 100~300口服 12~16
阿米洛利
（ amiloride） 同上 5~20口服 12~18
Reasonable application of diuretics
1,strictly following indication
2,combined medication
K-sparing diuretics is contradicted in renal
dysfunction
3,intermissional therapy
4,Pay attention to water and electrolyte
disturbance
Differential of deficit sodium and diluted hyponatremia
deficit sodium hyponatremia
occurred after using many diuretics,
feature,postohypotension,oliguria,high urine gravity,
should intake salt
diluted hyponatremia
also called refractory heart failure,hyponatremia of high
blood volume,should limit water-intake
e.Vasodilator drugs
Indication
1.Left end-diastolic filling pressure>18mmHg,
pulmonary congestion
2.clinical manifestation of peripheral circulatory
perfusion deficiency CI<2.2L/min.m2
3.valve insufficiency,ventricular septal defect
pulmonary hypertension,valve regurgitation with
cardiac dysfunction
If blood volume deficiency,should fluid
replacement at first,then use vasodilator drugs.
药物 机制 前负 荷 后负 荷 常用剂量
作用时间
开始 高峰 持续
硝酸盐血管扩张剂
硝酸甘油
NO供者
+++ +
0.2~10μg/
（ kg·min） iv
5~6mg 经皮
2min 5~15min <30min
二硝酸异山梨醇酯 +++ +
10~60mg po tid 15~20min 1h 4h
10~20mg 舌下 5min 15~30min 3h
2~7mg/h iv 3~5min 2h 3h
硝普钠 +++ +++ 0.1~0.3μg/（ kg·min）iv 几乎立即 停药 2~15min消失
交感神经阻滞剂
酚妥拉明 非选择性 α–肾上腺素能激动剂 ++ ++ 0.5~1.0mg/min iv 15~20min 3~4h
哌唑嗪 α1–肾上腺素能受体拮抗 剂 +++ ++ 1~6mg po tid 30min 1~3h 6h
肾素 –血管紧张素系统
拮抗剂
卡托普利
抑制由 ACE引起的
肾系统性生
成和组织生成血管
紧张素 Ⅱ ；
降低缓激肽的代谢
++ ++ 6.25~50mg po q8h 15~30min 1~2h 4~6h
依那普利 ++ ++ 5~10mg po bid 2h 4~6h 24h
赖诺普利 ++ ++ 2.5~20mg po q12~24h 6~8h 12h
雷米普利 ++ ++ 1.25~5mg po qd 1~2h 3~6h 24h
芦沙坦 阻断血管紧张素 Ⅱ（ AT
1受体）
++ ++ 25~50mg po q12h 5~6h 24h
ACE-I
Contradiction
Severe renal dysfunction,renal artery stenosis,
obvious mitral and aortic stenosis
American and European guideline, that all heart
failure patients including asymptomatic failure,except
patients that have contradiction or cannot tolerate ACE-I,
should use ACE-I,and for the long term therapy.
3.increase cardiac output
a.Digitalis
Pharmacology
? increase myocardial contractile force
Inhibit Na+-K+ ATPase Na+ -Ca2+change
intracellular Ca2+ increase contractility increase
? increase cardiac output
Renal flow increase SAS activity decrease
peripheral vasodilate peripheral
resistance decrease
? RAAS activity decrease
Reduction of water and salt retention due to aldosterone
decrease
? Prolong atrioventricular conduction
Highly effective in the treatment of atrial fibrillation in
addition to slowing ventricular response,it may convent
the rhythm to normal sinus mechanism.
Use carefully
?Hypertrophic cardiomyopathy
?Mitral stenosis with sinus rhythm
?Pericardium constriction
?Pulmonary heart disease
?High degree AVB
?AMI in 24h
Digitalis toxicity
Induce cause
Hypokalemia
Hypomagnemia
Hypercalcemia
Acid intoxication
Hypoxia
Renal dysfunction
Severe myocardial lesion
Hypothyroidism
Clinical manifestation of digitalis
?Systemic toxic effects:
Gastrointestinal tract symptom:nausea,vomiting,
anorexia,diarrhea,confusion,amblyopia
Cardiac symptom:arrhythmia
?Prolonged PR interval and AV conduction.
?Increase the automaticity of Purkinje fibers and
enhance reentry,resulting in extrasystoles,
ventricular fibrillation.
Treatment
? Stopping using digitalis
? Use potassium,magnesium if serum K is low.
? Rapid arrhythmia, lidocarine or diphenine
sodium,1-4mg/min usually don't cardioversion
? Slowly arrhythmia atropine0.5-1mg.
b,Other inotropic agent
1.?-adrenocepter agonists
Dopamine
1-5ug/Kg.min activate dopamine receptor,
renal flow increase
>10ug/Kg.min activate α-receptor,
vasoconstrict
Dobutamine
2-7.5ug/Kg.min
2.Phosphodiesterase inhibitor
Inhibit cAMP degrade increase
intracellular cAMP Ca2+ increase
cardiac contraction increase
Amrinone Milrione
3.Aldosterone antagonist
Protect aldosterone escape.
4.?-adrenocepter antagonists
Recent clinic trials have shown,when given in
very small doses under carefully monitored conditions,
they can increase ejection fraction,improve symptoms
and reduce the frequency of hospitalization in patient
with chronic heart failure.
,Relieve toxiation of catecholamine
,On the base of using ACE-I,diuretics,digitalis,
using ? bloker.
,Given in very small incremental doses
Bisoprool 1.25mg
metoprolol 6.25mg
5.diastolic heart failure treatment
treat primary disease
relax myocardium
revert myocardial hypertrophy
decrease preload
control tachycardia
calcium channel blocker,and ? blocker can be useful.
6.Refractory heart failure
1)Have the etiology and precipitating
causes been established?
2)Are drug dose optimal?
3)Is the patient adhering to an adequate
low-salt diet?
4)Need another cardiac transplantation.
7.Acute pulmonary edema
Emergency treatment
1)position:Don't keep patient in a supine position
2)Maintain oxygenation:high concentrations of O2
should be given by mask or nasal cannula.
3)Morphine sulfate 3 - 5mg IV or 5- 10mg IM can
reduce agitation,reduce transient arterial and
venous dilation,decrease the respiratory rate,
slow the heart rate,and reduce respiratory and
cardiac work,
4)Intravenous administration of a rapidly actig
diuretic,eg.(furosemide 40mg IV) can be initiate a
prompt diuresis in 15 to 20 min.
5)Rotating tourniquets are effective with Bp cuff
applied to 3 limbs,inflated midway between
diastolic and systolic pressure,deflated and rotated
10 to 20 min.
6)Vasodilator drugs
7)Digitalis
8)Aminophylline
9)others
Pathophysiologic consequences of a myocardial
infarction include:
(1)increased systolic load due to the akinetic segment
(2)decreased ejection fraction that approximates the
amount of muscle loss.
(3)hypertrophy of noninfarcted myocardium.
(4)decreased end-diastoic volume
Supportive evidence that left-sided failure is present
includes all the following EXCEPT:
A.abnormally elevated filling pressures as detected by
right heart catheterization
B.a cardiac index of 3.5 liters/min/m2
C.a reduction in maximum oxygen consumption
determined noninvasively by exercise
D.the presence of pulmonary rales on physical
examination
E.low left ventricular ejection fraction at rest on
echocardiography
