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心力衰竭
Heart Failure
浙江大学医学院附属第一医院
陶谦民
定义
• 心力衰竭是心脏各种疾病发展到中、末
期导致心脏功能障碍，出现心功能不全
（cardiac insufficiency）的一组临床综合
征，多指临床出现心肌收缩力下降使心
排血量不能满足机体代谢的需求，器官、
组织血液灌注不足，同时出现肺循环和/
或体循环淤血的表现。
病因
• 心肌本身病变——原发性心肌损害
1.缺血性心肌损害：冠心病心肌缺血（长
期）和/或心肌梗死
2.心肌炎和心肌病，以病毒性心肌炎和原
发性扩张性心肌病最为常见
3.心肌代谢障碍性疾病：如糖尿病性心肌
病、心肌淀粉样变性等
病因
• 心脏负荷过重，心肌本身功能无异常，但因长
期的高强负荷致心脏功能受损
1.压力负荷（后负荷）过重，如高血压、主动脉
瓣狭窄、肺动脉高压、肺动脉瓣狭窄等
2.容量负荷（前负荷）过重，因大量的血液回流
长期造成心脏功能损害，可见于：⑴心脏瓣膜
关闭不全，如主动脉瓣关闭不全、二尖瓣关闭
不全等；⑵先天性心脏病如间隔缺损、动脉导
管未闭、动静脉瘘等；⑶慢性重度贫血、甲状
腺功能亢进等伴有全身血容量增多或循环血量
增多等
• 心脏扩张受到限制，如大量心包积液或心包缩
窄
诱因
• 有基础心脏病的患者，其心力衰竭的症状通常由一些
增加心脏负荷的因素所诱发，这些常见的诱发心力衰
竭的因素有：
1.感染，以呼吸道感染最为常见，感染性心内膜炎和风
湿活动也是诱发心力衰竭常见而隐匿的原因
2.心律失常，心房颤动是器质性心脏病常见的心律失常，
也是诱发心力衰竭最重要的因素
3.血容量增，如摄入钠盐过多，静脉输入液体过多、过
快等
4.过度体力活动，劳累或情绪激动，如妊娠后期及分娩
过程，情绪波动如暴怒等
5.治疗不当，所谓医源性因素，如不恰当停用洋地黄类
药物或降压药物，某些心脏功能抑制性药物
6.原有心脏疾病加重或并发加重心脏负担的疾病，如冠
心病发生心肌梗死，风湿性心瓣膜病出现风湿活动，
合并甲状腺功能亢进或贫血等
类型
• 左心衰、右心衰和全心衰 左心衰以肺循
环淤血为特征，临床主要表现为呼吸困
难；右心衰主要见于肺源性心脏病和某
些先天性心脏病，以体循环淤血为特征，
临床出现浮肿、腹水和肝肿大等；全心
衰则综合左右心衰的临床表现
• 急性和慢性心衰
• 收缩性和舒张性心衰
Heart Failure (HF) Definition
A complex clinical syndrome in which the
heart is incapable of maintaining a cardiac
output adequate to accommodate metabolic
requirements and the venous return.
HF Incidence and Prevalence
• Prevalence
– Worldwide, 22 million1
– United States, 5 million2
• Incidence
– Worldwide, 2 million new cases annually1
– United States, 500,000 new cases annually2
• HF afflicts 10 out of every 1,000 over
age 65 in the U.S.2
1 World Health Statistics, World Health Organization, 1995.
2 American Heart Association, 2002 Heart and Stroke Statistical Update.
Prevalence of HF by Age and Gender
United States: 1988-94
10
8
Percent of
Population
Males
Females
6
4
2
0
20-24 25-34 35-44 45-54 55-64 65-74
Source: NHANES III (1988-94), CDC/NCHS and the American Heart Association
75+
New York Heart Association
Functional Classification
Class I:
No symptoms with ordinary activity
Class II:
Slight limitation of physical activity. Comfortable at rest,
but ordinary physical activity results in fatigue,
palpitation, dyspnea, or angina
Class III:
Marked limitation of physical activity. Comfortable at
rest, but less than ordinary physical activity results in
fatigue, palpitation, dyspnea, or anginal pain
Class IV:
Unable to carry out any physical activity without
discomfort. Symptoms of cardiac insufficiency may be
present even at rest
HF Classification: Evolution and
Disease Progression
• Four Stages of HF (ACC/AHA Guidelines):
Stage A: Patient at high risk for developing HF with
no structural disorder of the heart
Stage B: Patient with structural disorder without
symptoms of HF
Stage C: Patient with past or current symptoms of HF
associated with underlying structural heart disease
Stage D: Patient with end-stage disease who requires
specialized treatment strategies
Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of
Chronic Heart Failure in the Adult, 2001
Severity of Heart Failure
Modes of Death
NYHA II
NYHA III
CHF
CHF
12%
Other
26%
59%
Sudden
Death
24%
64%
Other
15%
n = 103
Sudden
Death
n = 103
NYHA IV
CHF
Other
33%
56%
11%
Sudden
Death
n = 27
MERIT-HF Study Group. Effect of Metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomized
intervention trial in congestive heart failure (MERIT-HF). LANCET. 1999;353:2001-07.
Etiology of Heart Failure
What causes heart failure?
• The loss of a critical quantity of functioning
myocardial cells after injury to the heart due to:
–
–
–
–
–
–
–
Ischemic Heart Disease
Hypertension
Idiopathic Cardiomyopathy
Infections (e.g., viral myocarditis, Chagas’ disease)
Toxins (e.g., alcohol or cytotoxic drugs)
Valvular Disease
Prolonged Arrhythmias
The Donkey Analogy
Ventricular dysfunction limits a patient's ability to
perform the routine activities of daily living…
Left Ventricular Dysfunction
• Systolic: Impaired contractility/ejection
– Approximately two-thirds of heart failure patients have
systolic dysfunction1
• Diastolic: Impaired filling/relaxation
30%
(EF > 40 %)
(EF < 40%)
70%
Diastolic Dysfunction
Systolic Dysfunction
1 Lilly, L. Pathophysiology of Heart Disease. Second Edition p 200
Cardiac Output
• Cardiac output is the amount of blood that
the ventricle ejects per minute
Cardiac Output = HR x SV
Determinants of Ventricular Function
Contractility
Afterload
Preload
Stroke
Volume
• Synergistic LV Contraction
• Wall Integrity
• Valvular Competence
Heart Rate
Cardiac Output
Left Ventricular Dysfunction
Volume
Overload
Pressure
Overload
Loss of
Myocardium
Impaired
Contractility
LV Dysfunction
EF < 40%
 End Systolic Volume
 Cardiac
Output
Hypoperfusion
 End Diastolic Volume
Pulmonary Congestion
Hemodynamic Basis for
Heart Failure Symptoms
Hemodynamic Basis for
Heart Failure Symptoms
LVEDP 
Left Atrial Pressure 
Pulmonary Capillary Pressure 
Pulmonary Congestion
Left Ventricular Dysfunction
Systolic and Diastolic
• Symptoms
• Physical Signs
– Dyspnea on Exertion
– Basilar Rales
– Paroxysmal
Nocturnal Dyspnea
– Pulmonary Edema
– Tachycardia
– S3 Gallop
– Cough
– Pleural Effusion
– Hemoptysis
– Cheyne-Stokes Respiration
Right Ventricular Failure
Systolic and Diastolic
• Symptoms
• Physical Signs
– Abdominal Pain
– Peripheral Edema
– Anorexia
– Jugular Venous Distention
– Nausea
– Abdominal-Jugular Reflux
– Bloating
– Hepatomegaly
– Swelling
Consequences of Decreased
Mean Arterial Pressure
 Mean Arterial Pressure (BP)
=
 Cardiac Output
x
Total Peripheral Resistance
Compensatory Mechanisms
• Frank-Starling Mechanism
• Neurohormonal Activation
• Ventricular Remodeling
Compensatory Mechanisms
Frank-Starling Mechanism
a. At rest, no HF
b. HF due to LV systolic
dysfunction
c. Advanced HF
Compensatory Mechanisms
Neurohormonal Activation
Many different hormone systems are involved in
maintaining normal cardiovascular homeostasis,
including:
• Sympathetic nervous system (SNS)
• Renin-angiotensin-aldosterone system (RAAS)
• Vasopressin (a.k.a. antidiuretic hormone, ADH)
Compensatory Mechanisms:
Sympathetic Nervous System
Decreased MAP
Sympathetic Nervous System
 Contractility
Tachycardia
Vasoconstriction
MAP = (SV x HR) x TPR
Sympathetic Activation in Heart Failure
 CNS sympathetic outflow
 Cardiac sympathetic
activity
1receptors
2receptors
 Sympathetic
activity to kidneys
+ peripheral vasculature
1receptors
Myocardial toxicity
Increased arrhythmias
1-
Activation
of RAS
Vasoconstriction
Sodium retention
Disease progression
Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.
1-
Compensatory Mechanisms:
Renin-Angiotensin-Aldosterone (RAAS)
Angiotensinogen
Renin
Angiotensin I
Angiotensin
Converting
Enzyme
Angiotensin II
AT I receptor
Vasoconstriction
Oxidative Stress
Cell Growth
Vascular remodeling
LV remodeling
Proteinuria
Compensatory Mechanisms:
Renin-Angiotensin-Aldosterone (RAAS)
Renin-Angiotensin-Aldosterone
( renal perfusion)
Salt-water retention
Thirst
Sympathetic
augmentation
Vasoconstriction
MAP = (SV x HR) x TPR
Compensatory Mechanisms:
Neurohormonal Activation – Vasopressin
Decreased systemic blood pressure
Central baroreceptors
-
Increased systemic blood pressure
Vasoconstriction
Stimulation of hypothalamus, which produces
vasopressin for release by pituitary gland
Release of vasopressin by pituitary gland
Compensatory Neurohormonal
Stimulation: Summary
Decreased Cardiac Output
Sympathetic
nervous system
Contractility
Heart
rate
Renin-angiotensin
system
Vasoconstriction
Anteriolar
+
+
Stroke
volume
Circulating volume
Venous
Maintain
blood
pressure
Cardiac
output
Antidiuretic hormone
(vasopressin)
Venous return
to heart
( preload)
-
Peripheral edema
and pulmonary
congestion
Compensatory Mechanisms
Ventricular Remodeling
Alterations in the heart’s size, shape, structure, and function brought
about by the chronic hemodynamic stresses experienced by the failing
heart.
Curry CW, et al. Mechanical dyssynchrony in dilated cardiomyopathy with intraventricular conduction
delay as depicted by 3D tagged magnetic resonance imaging. Circulation 2000 Jan 4;101(1):E2.
Other Neurohormones
• Natriuretic Peptides: Three known types
– Atrial Natriuretic Peptide (ANP)
• Predominantly found in the atria
• Diuretic and vasodilatory properties
– Brain Natriuretic Peptide (hBNP)
• Predominantly found in the cardiac ventricles
• Diuretic and vasodilatory properties
– C-type Natriuretic Peptide (CNP)
• Predominantly found in the central nervous system
• Limited natriuretic and vasodilatory properties
Pharmacological Actions of hBNP
Hemodynamic
(balanced vasodilation)
R I SS
D
S
M
S
K
G
R
L
G
H
G
F
R
C
R
C S S
K V L
G
K
P
M V
S
Q G S
• veins
• arteries
• coronary arteries
Neurohormonal
aldosterone
norepinephrine
Renal
diuresis & natriuresis
Abraham WT and Schrier RW, 1994
Endothelium-Derived Vasoactive
Substances
Produced by a thin lining of cells within the arteries and
veins called the endothelium
Endothelium-derived relaxing factors (EDRF) –
Vasodilators:
• Nitric Oxide (NO)
• Bradykinin
• Prostacyclin
Endothelium-derived constricting factors (EDCF) –
Vasoconstrictors:
• Endothelin I
Mediators of Heart Failure
Cytokines
• Small protein molecules produced by a variety of
tissues and cells
• Negative inotropes
• Elevated levels associated with worse clinical
outcomes
• Examples:
– Tumor necrosis factor (TNF)-alpha
– Interleukin 1-alpha
– Interleukin-2
– Interleukin-6
– Interferon-alpha
Vicious Cycle of Heart Failure
LV Dysfunction
Increased cardiac workload
(increased preload and afterload)
Increased cardiac output (via increased
contractility and heart rate)
Increased blood pressure (via vasoconstriction
and increased blood volume)
Decreased cardiac output
and
Decreased blood pressure
Frank-Starling Mechanism
Remodeling
Neurohormonal activation
Neurohormonal Responses to Impaired
Cardiac Performance
Initially Adaptive, Deleterious if Sustained
Response
Short-Term
Effects
Long-Term
Effects
Salt and Water Retention
Augments Preload
Pulmonary Congestion,
Anasarca
Vasoconstriction
Maintains BP for perfusion
of vital organs
Exacerbates pump
dysfunction (excessive
afterload), increases
cardiac energy expenditure
Sympathetic Stimulation
Increases HR and ejection
Increases energy
expenditure
Jaski, B, MD: Basics of Heart Failure: A Problem Solving Approach
Assessing Heart Failure
Assessing Heart Failure
• Patient History
• Physical Examination
• Laboratory and Diagnostic Tests
Diagnostic Evaluation of
New Onset Heart Failure
• Determine the type of cardiac
dysfunction (systolic vs. diastolic)
• Determine Etiology
• Define prognosis
• Guide therapy
Diagnostic Evaluation of
New Onset Heart Failure
Initial Work-up:
• ECG
• Chest x-ray
• Blood work
• Echocardiography
Diagnostic Evaluation of
New Onset Heart Failure
LV
RV
Septum
LV cavity
LV Wall
M-Mode Echo
LA
RA
2D Echo
Current Treatment
of Heart Failure
The Vicious Cycle of
Heart Failure Management
Chronic HF
Diurese &
Home
Hospitalization
IV Lasix
or Admit
Emergency
Room
SOB
 Weight
MD’s Office
PO Lasix
General Measures
Medical Considerations:
Lifestyle Modifications:
• Treat HTN, hyperlipidemia,
diabetes, arrhythmias
• Weight reduction
• Coronary revascularization
• Discontinue smoking
• Anticoagulation
• Avoid alcohol and
other cardiotoxic
substances
• Immunization
• Exercise
• Close outpatient monitoring
• Sodium restriction
• Daily weights
Pharmacologic Management
Digoxin
• Enhances inotropy of cardiac muscle
• Reduces activation of SNS and RAAS
• Controlled trials have shown long-term digoxin
therapy:
– Reduces symptoms
– Increases exercise tolerance
– Improves hemodynamics
– Decreases risk of HF progression
– Reduces hospitalization rates for decompensated HF
– Does not improve survival
Digitalis Compounds
Like the carrot placed in front of the donkey
应用洋地黄的注意事项
•
不用于无症状患者（房颤除外）
•
不主张早期应用，应与ACEI、利尿剂合用
•
避免采用较大剂量给药，一般耐受良好
•
应根据年龄、肾功能、合并用药调整剂量
•
注意观察心率变化，尤其与阻滞剂合用时
•
定期复查电解质
Pharmacologic Management
Diuretics
• Used to relieve fluid retention
• Improve exercise tolerance
• Facilitate the use of other drugs indicated for heart
failure
• Patients can be taught to adjust their diuretic dose based
on changes in body weight
• Electrolyte depletion a frequent complication
• Should never be used alone to treat heart failure
• Higher doses of diuretics are associated with increased
mortality
Pharmacologic Management
ACE Inhibitors
• Blocks the conversion of angiotensin I to angiotensin
II; prevents functional deterioration
• Recommended for all heart failure patients
• Relieves symptoms and improves exercise tolerance
• Reduces risk of death and decreases disease
progression
• Benefits may not be apparent for 1-2 months after
initiation
Diuretics, ACE Inhibitors
Reduce the number of sacks on the wagon
ESC心力衰竭诊断和治疗指南-2005
血管紧张素转化酶抑制剂（ACEI）
• 用于所有LVEF降低（<40-45%）的患者，
以改善存活、症状、减少住院次数（1A）
• 对没有液体潴留的患者，可以作为起始用
药，对液体潴留患者，ACEI应与利尿剂合
用（1A）
• 采用ACEI有效剂量治疗（1A），不能根据
症状改善与否确定用药剂量
Pharmacologic Management
Beta-Blockers
• Cardioprotective effects due to blockade of
excessive SNS stimulation
• In the short-term, beta blocker decreases
myocardial contractility; increase in EF after 1-3
months of use
• Long-term, placebo-controlled trials have shown
symptomatic improvement in patients treated with
certain beta-blockers1
• When combined with conventional HF therapy,
beta-blockers reduce the combined risk of
morbidity and mortality, or disease progression1
1 Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of
Chronic Heart Failure in the Adult, 2001 p. 20.
ß-Blockers
Limit the donkey’s speed, thus saving energy
ESC心力衰竭诊断和治疗指南
β受体阻滞剂
• 推荐在标准治疗的基础上，用于所有稳定的、轻
中重度（NYHA II-IV） 、缺血性或非缺血性心
力衰竭患者，除非有禁忌症（1A）
• 推荐比索洛尔、卡维地洛、美托洛尔琥珀酸盐和
奈比洛尔 (nebivolol) 用于心力衰竭治疗 (1A）
ESC心力衰竭诊断和治疗指南
β受体阻滞剂用于抗心律失常治疗
• β受体阻滞剂减少心力衰竭的猝死（1A）
• 在持续或非持续性室性快速心律失常的治
疗中，β受体阻滞剂可以单用，或与胺碘酮
或非药物治疗联合使用（IIa, C）
阻滞剂治疗心衰注意事项
• 心功能相对稳定，无其它禁忌症
• 无明显液体潴留的证据
• 利尿剂 ±地高辛，不必要在ACEI调整完毕后使用
• 极低剂量开始，每2～4周剂量倍增，调整合并用药。
 阻滞剂的耐受性为80～90%
• 病情稳定的心功能IV级患者，在有经验的专科医生指
导下用药
•
以靶剂量或最大耐受量长期维持
Pharmacologic Management
Aldosterone Antagonists
• Generally well-tolerated
• Shown to reduce heart failure-related morbidity and mortality
• Generally reserved for patients with NYHA Class III-IV HF
• Side effects include hyperkalemia and gynecomastia.
Potassium and creatinine levels should be closely monitored
Pharmacologic Management
Angiotensin Receptor Blockers (ARBs)
• Block AT1 receptors, which bind circulating
angiotensin II
• Examples: valsartan, candesartan, losartan
• Should not be considered equivalent or superior to ACE
inhibitors
• In clinical practice, ARBs should be used to treat
patients who are ACE intolerant due to intractable
cough or who develop angioedema
Angiotensin II Receptors
AT1 receptor
AT2 receptor
• Vasoconstriction
• Vasodilation
• Growth Promotion
• Growth inhibition
• Anti-apoptotic
• Pro-apoptotic
• Pro-fibrotic
• ? Fibrosis
• Pro-thrombotic
• ? Thrombosis
• Pro-oxidant
• ? redox
ESC心力衰竭诊断和治疗指南
血管紧张素II受体拮抗剂（ARB）
• 在不能耐受ACEI的有症状患者，ARB可作
为ACEI的替代药物以改善患病率和病死率
（1B）
• 在仍有症状的患者，ARB可以与ACEI合用
Assessment and Treatment of the
Heart Failure Patient
Treatment Approach for the Patient
with Heart Failure
Stage A
Stage B
Stage C
Stage D
At high risk, no
structural disease
Structural heart
disease,
asymptomatic
Structural heart
disease with
prior/current
symptoms of HF
Refractory HF
requiring
specialized
interventions
Therapy
Therapy
Therapy
Therapy
• Treat Hypertension
• All measures under
stage A
• All measures under
stage A
• All measures under
stages A,B, and C
• ACE inhibitors in
appropriate
patients
Drugs:
• Mechanical assist
devices
• Treat lipid
disorders
• Encourage regular
exercise
• Discourage alcohol
intake
• ACE inhibition
• Beta-blockers in
appropriate
patients
• Diuretics
• ACE inhibitors
• Beta-blockers
• Digitalis
• Dietary salt
restriction
• Heart
transplantation
• Continuous (not
intermittent) IV
inotropic infusions
for palliation
• Hospice care
Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of
Chronic Heart Failure in the Adult, 2001
Cardiac Resynchronization Therapy
Increase the donkey’s (heart) efficiency
Cardiac Resynchronization Therapy
Patient Indications
CRT device:
– Moderate to severe HF (NYHA Class III/IV) patients
– Symptomatic despite optimal, medical therapy
– QRS  130 msec
– LVEF  35%
CRT plus ICD:
– Same as above with ICD indication
Cardiac Resynchronization Therapy
Follow-up Care
• Standard medical management of HF by
primary physician as defined by practice
guidelines
• Device follow-up may be performed by
physician specializing in implantable devices
Cardiac Resynchronization Therapy:
Creating Realistic Patient Expectations
• Approximately two-third of patients
should experience improvement
(responders vs. non-responders)1
– Some patients may not experience
immediate improvement
Note: CRT is adjunctive and is not intended to replace medical therapy.
Patients will continue to be followed by HF Specialist and Physician
managing implantable devices.
1 Abraham, WT, et. Al. Cardiac Resynchronization in Chronic Heart Failure. N Engl J Med 2002;346:1845-53
Cardiac Resynchronization Therapy:
Creating Realistic Patient Expectations
• Have patients set their own goals of what they would
like to do following CRT:
– Grocery shopping
– Decreasing Lasix dose
– Walking to the mailbox without stopping
– Lying flat to sleep
• Encourage them to be part of the group that responds
to their therapy
First Medical Follow-up Visit
7-10 Days Post-implant*
• Follow daily weights closely
• Check wound site
• Physical Exam
– Assess volume status
• Patients typically over-diurese following CRT
• Ascertain quality of life
– Subtle improvements?
• Check electrolytes including BUN/Cr
• Give patients encouragement!
* This is not a complete list for many practitioners and is presented here only as a guideline.
Summary
• Heart failure is a chronic, progressive disease that is
generally not curable, but treatable
• Most recent guidelines promote lifestyle modifications and
medical management with ACE inhibitors, beta blockers,
digoxin, and diuretics
• It is estimated 15% of all heart failure patients may be
candidates for cardiac resynchronization therapy (see later
section for details)
• Close follow-up of the heart failure patient is essential, with
necessary adjustments in medical management