心力衰竭 heart failure 浙江大学医学院附属第一医院 陶谦民. 定义...
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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.
1 World Health Statistics, World Health Organization, 1995.1 World Health Statistics, World Health Organization, 1995.
2 American Heart Association, 2002 Heart and Stroke Statistical Update.2 American Heart Association, 2002 Heart and Stroke Statistical Update.
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
Prevalence of HF by Age and Gender
United States: 1988-94
0
2
4
6
8
10
Percent of Population
20-24 25-34 35-44 45-54 55-64 65-74 75+
Males
Females
Source: NHANES III (1988-94), CDC/NCHS and the American Heart AssociationSource: NHANES III (1988-94), CDC/NCHS and the American Heart Association
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 Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult, 2001Chronic Heart Failure in the Adult, 2001
MERIT-HF Study Group. Effect of Metoprolol CR/XL in chronic heart failure: Metoprolol CR/XL randomized 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). intervention trial in congestive heart failure (MERIT-HF). LANCET. LANCET. 1999;353:2001-07.1999;353:2001-07.
Severity of Heart FailureModes of Death
12%12%
24%24%
64%64%
CHFCHF
OtherOther
SuddenSuddenDeathDeath
n = 103n = 103
NYHA IINYHA II
26%26%
15%15%
59%59%
CHFCHF
OtherOther
SuddenSuddenDeathDeath
n = 103n = 103
NYHA IIINYHA III
56%56%
11%11%
33%33%
CHFCHF
OtherOther
SuddenSuddenDeathDeath
n = 27n = 27
NYHA IVNYHA IV
Etiology of Heart FailureWhat 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…
30%30%
70%70%
Diastolic DysfunctionDiastolic DysfunctionSystolic DysfunctionSystolic Dysfunction
(EF < 40%)(EF < 40%)(EF > 40 %)(EF > 40 %)
Left Ventricular Dysfunction• Systolic: Impaired contractility/ejection
– Approximately two-thirds of heart failure patients have systolic dysfunction1
• Diastolic: Impaired filling/relaxation
1 Lilly, L. 1 Lilly, L. Pathophysiology of Heart DiseasePathophysiology of Heart Disease. Second Edition p 200. Second Edition p 200
Cardiac Output
• Cardiac output is the amount of blood that the ventricle ejects per minute
Cardiac Output = HR x SV
StrokeStrokeVolumeVolume
PreloadPreload AfterloadAfterload
ContractilityContractility
Cardiac OutputCardiac Output
Heart RateHeart Rate• Synergistic LV ContractionSynergistic LV Contraction• Wall IntegrityWall Integrity• Valvular CompetenceValvular Competence
Determinants of Ventricular Function
Volume Volume OverloadOverload
Pressure Pressure OverloadOverload
Loss of Loss of MyocardiumMyocardium
Impaired Impaired ContractilityContractility
LV DysfunctionLV DysfunctionEF < 40%EF < 40%
Cardiac Cardiac OutputOutput
Hypoperfusion Hypoperfusion
End Systolic Volume End Systolic Volume
End Diastolic Volume End Diastolic Volume
Pulmonary Congestion Pulmonary Congestion
Left Ventricular Dysfunction
Hemodynamic Basis for Heart Failure Symptoms
Hemodynamic Basis forHeart Failure Symptoms
LVEDP
Left Atrial Pressure
Pulmonary Capillary Pressure
Pulmonary Congestion
Left Ventricular DysfunctionSystolic and Diastolic
• Symptoms
– Dyspnea on Exertion
– Paroxysmal Nocturnal Dyspnea
– Tachycardia
– Cough
– Hemoptysis
• Physical Signs
– Basilar Rales
– Pulmonary Edema
– S3 Gallop
– Pleural Effusion
– Cheyne-Stokes Respiration
Right Ventricular FailureSystolic and Diastolic
• Symptoms
– Abdominal Pain
– Anorexia
– Nausea
– Bloating
– Swelling
• Physical Signs
– Peripheral Edema
– Jugular Venous Distention
– Abdominal-Jugular Reflux
– Hepatomegaly
Consequences of DecreasedMean 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)
MAP = (MAP = (SV x SV x HR) x HR) x TPRTPR
Sympathetic Nervous SystemSympathetic Nervous System
ContractilityContractility TachycardiaTachycardia VasoconstrictionVasoconstriction
Compensatory Mechanisms: Sympathetic Nervous System
Decreased MAPDecreased MAP
Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.
CNS sympathetic outflowCNS sympathetic outflow
Disease progressionDisease progression
Cardiac sympatheticCardiac sympatheticactivityactivity
11--
receptorsreceptors22--
receptorsreceptors11--
receptorsreceptors
VasoconstrictionVasoconstrictionSodium retentionSodium retention
Myocardial toxicityMyocardial toxicityIncreased arrhythmiasIncreased arrhythmias
SympatheticSympatheticactivity to kidneysactivity to kidneys
+ peripheral vasculature+ peripheral vasculature
ActivationActivationof RASof RAS
11-- 11--
Sympathetic Activation in Heart Failure
VasoconstrictionVasoconstriction
Oxidative StressOxidative Stress
Cell GrowthCell Growth ProteinuriaProteinuria
LV remodelingLV remodeling
Vascular remodelingVascular remodeling
AngiotensinogenAngiotensinogen
Angiotensin IAngiotensin I
Angiotensin IIAngiotensin II
AT I receptorAT I receptor
ReninRenin
AngiotensinAngiotensinConvertingConverting
EnzymeEnzyme
Compensatory Mechanisms: Renin-Angiotensin-Aldosterone
(RAAS)
MAP = (MAP = (SV x SV x HR) x HR) x TPRTPR
Renin-Angiotensin-AldosteroneRenin-Angiotensin-Aldosterone(( renal perfusion) renal perfusion)
Salt-water retentionSalt-water retentionThirstThirst
SympatheticSympatheticaugmentationaugmentation VasoconstrictionVasoconstriction
Compensatory Mechanisms: Renin-Angiotensin-Aldosterone
(RAAS)
Decreased systemic blood pressureDecreased systemic blood pressure
Central baroreceptorsCentral baroreceptors
Stimulation of hypothalamus, which producesStimulation of hypothalamus, which producesvasopressin for release by pituitary glandvasopressin for release by pituitary gland
Release of vasopressin by pituitary glandRelease of vasopressin by pituitary glandVasoconstrictionVasoconstriction
Increased systemic blood pressureIncreased systemic blood pressure
--
Compensatory Mechanisms: Neurohormonal Activation – Vasopressin
Compensatory Neurohormonal
Stimulation: Summary Decreased Cardiac OutputDecreased Cardiac Output
SympatheticSympatheticnervous systemnervous system
Renin-angiotensinRenin-angiotensinsystemsystem
Antidiuretic hormoneAntidiuretic hormone(vasopressin)(vasopressin)
HeartHeartraterate
ContractilityContractility VasoconstrictionVasoconstriction Circulating volumeCirculating volume
AnteriolarAnteriolar
MaintainMaintainbloodblood
pressurepressure
CardiacCardiacoutputoutput
StrokeStrokevolumevolume
++
--++
VenousVenous
Venous return Venous return to heartto heart
(( preload)preload)
Peripheral edemaPeripheral edemaand pulmonaryand pulmonary
congestioncongestion
Curry CW, et al. Mechanical dyssynchrony in dilated cardiomyopathy with intraventricular conduction 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. delay as depicted by 3D tagged magnetic resonance imaging. Circulation 2000 Jan 4;101(1):E2.
Compensatory MechanismsVentricular RemodelingAlterations in the heart’s size, shape, structure, and function brought about by the chronic hemodynamic stresses experienced by the failing heart.
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
Hemodynamic Hemodynamic (balanced vasodilation)(balanced vasodilation)
•• veinsveins
•• arteriesarteries
•• coronary arteriescoronary arteries
NeurohormonalNeurohormonal
aldosteronealdosterone
norepinephrinenorepinephrine
RenalRenal
diuresis & natriuresisdiuresis & natriuresis
DR I
M
K
RG
S SS
SG
L
GF
CC
S S
GSGQVM
K V LR
RH
KPS
Pharmacological Actions of hBNP
Abraham WT and Schrier RW, 1994Abraham WT and Schrier RW, 1994
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
Endothelium-Derived Vasoactive Substances
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
LV DysfunctionLV Dysfunction
Decreased cardiac outputDecreased cardiac outputand and
Decreased blood pressureDecreased blood pressure
Frank-Starling MechanismFrank-Starling MechanismRemodelingRemodeling
Neurohormonal activationNeurohormonal activation
Increased cardiac output (via increasedIncreased cardiac output (via increasedcontractility and heart rate)contractility and heart rate)
Increased blood pressure (via vasoconstrictionIncreased blood pressure (via vasoconstriction and increased blood volume) and increased blood volume)
Increased cardiac workloadIncreased cardiac workload(increased preload and afterload)(increased preload and afterload)
Vicious Cycle of Heart Failure
Initially Adaptive, Deleterious if SustainedInitially Adaptive, Deleterious if Sustained
ResponseShort-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
Neurohormonal Responses to ImpairedCardiac Performance
Jaski, B, MD: Jaski, B, MD: Basics of Heart Failure: A Problem Solving ApproachBasics 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
M-Mode EchoM-Mode Echo 2D Echo2D Echo
RARA
LALA
RVRVLVLV
SeptumSeptum
LV cavityLV cavity
LV WallLV Wall
Diagnostic Evaluation of New Onset Heart Failure
Current Treatment of Heart Failure
The Vicious Cycle of Heart Failure Management
Chronic HFChronic HF
MD’s OfficeMD’s Office
Emergency Emergency RoomRoom
HospitalizationHospitalization
SOBSOB
WeightWeight
PO LasixPO LasixIV Lasix IV Lasix or Admitor Admit
Diurese & Diurese & HomeHome
General Measures
Lifestyle Modifications:
• Weight reduction
• Discontinue smoking
• Avoid alcohol and other cardiotoxic substances
• Exercise
Medical Considerations:
• Treat HTN, hyperlipidemia, diabetes, arrhythmias
• Coronary revascularization
• Anticoagulation
• Immunization
• Sodium restriction
• Daily weights
• Close outpatient monitoring
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 1 Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult, 2001 p. 20.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。
阻阻阻阻阻阻阻阻阻
• 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 ManagementAldosterone 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
ATAT11 receptor receptor ATAT22 receptor receptor
• VasoconstrictionVasoconstriction
• Growth PromotionGrowth Promotion
• Anti-apoptoticAnti-apoptotic
• Pro-fibroticPro-fibrotic
• Pro-thromboticPro-thrombotic
• Pro-oxidantPro-oxidant
• VasodilationVasodilation
• Growth inhibitionGrowth inhibition
• Pro-apoptoticPro-apoptotic
• ? Fibrosis? Fibrosis
• ? Thrombosis? Thrombosis
• ? redox? redox
Angiotensin II Receptors
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 AStage A
At high risk, no At high risk, no structural diseasestructural disease
Stage BStage B
Structural heart Structural heart disease, disease,
asymptomaticasymptomatic
Stage DStage D
Refractory HF Refractory HF requiring requiring
specialized specialized interventionsinterventions
TherapyTherapy
• Treat HypertensionTreat Hypertension
• Treat lipid Treat lipid disordersdisorders
• Encourage regular Encourage regular exerciseexercise
• Discourage alcohol Discourage alcohol intakeintake
• ACE inhibitionACE inhibition
TherapyTherapy
• All measures All measures under stage Aunder stage A
• ACE inhibitors in ACE inhibitors in appropriate appropriate patientspatients
• Beta-blockers in Beta-blockers in appropriate appropriate patientspatients
TherapyTherapy
• All measures All measures under stage Aunder stage A
Drugs:Drugs:
• DiureticsDiuretics
• ACE inhibitorsACE inhibitors
• Beta-blockersBeta-blockers
• DigitalisDigitalis
• Dietary salt Dietary salt restrictionrestriction
TherapyTherapy
• All measures All measures under stages A,B, under stages A,B, and Cand C
• Mechanical assist Mechanical assist devicesdevices
• Heart Heart transplantationtransplantation
• Continuous (not Continuous (not intermittent) IV intermittent) IV inotropic infusions inotropic infusions for palliationfor palliation
• Hospice careHospice care
Stage CStage C
Structural heart Structural heart disease with disease with prior/current prior/current
symptoms of HFsymptoms of HF
Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult, 2001Chronic Heart Failure in the Adult, 2001
Cardiac Resynchronization Therapy
Increase the donkey’s (heart) efficiency
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
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. Note: CRT is adjunctive and is not intended to replace medical therapy. Patients will continue to be followed by HF Specialist and Physician Patients will continue to be followed by HF Specialist and Physician managing implantable devices.managing implantable devices.
1 Abraham, WT, et. Al. Cardiac Resynchronization in Chronic Heart Failure. 1 Abraham, WT, et. Al. Cardiac Resynchronization in Chronic Heart Failure. N Engl J MedN Engl J Med 2002;346:1845-53 2002;346:1845-53
• 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
Cardiac Resynchronization Therapy: Creating Realistic Patient Expectations
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.* 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