gagal-jantung (1)

Gagal Jantung

Dr.Pramudjo Abdulgani,Sp.JP,FIHA

Pekanbaru

Pendahuluan

Gagal jantung :

Sindroma klinis akibat jantung tidak mampu memompakan darah untuk mempertahankan kebutuhan metabo lisme jaringan atau mampu memenuhi rnetabolisme jaringan tetapi pada tekanan pengisian yang meningkat.

Definition of Heart Failure

HF is a complex clinical syndrome that canresult from any structural or functionalcardiac disorder that impairs the ability ofthe ventricle to fill with or eject blood.

“Heart Failure” vs. “Congestive Heart Failure”

Because not all patients have volume overload atthe time of initial or subsequent evaluation, theterm “heart failure” is preferred over the older term “congestive heart failure.”

1 World Health Statistics, World Health Organization, 1995.

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

Evolution of the Concept of Heart Failure 1950 to 2000

1950 2000 Aetiology Hypertension CHD

Valvular heart dis HypertensionDilated CMP

Natural Course Slowly progressive Slowly progressive (remodeling) or unpredictable and rapid

( coronary event )

Understanding Hemodynamicmodel Neurohormonal model

Common cause Pulmonary infection Sudden deathof death Pump failure

Arrhythmia Atrial Ventricular

Treatment goal Control edema Improve quality of life+ reduce mortality +

reduce hospitalization

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

Stages of Heart Failure

At Risk for Heart Failure:

STAGE A High risk for developing HF

STAGE B Asymptomatic LV dysfunction

Heart Failure:

STAGE C Past or current symptoms of HF

STAGE D End-stage HF


• Designed to emphasize preventability of HF

• Designed to recognize the progressive nature of LV dysfunction


COMPLEMENT, DO NOT REPLACE NYHA CLASSES

• NYHA Classes - shift back/forth in individual patient (in response to Rx and/or progression of disease)

• Stages - progress in one direction due to cardiac remodeling

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

Pathophysiology of Acute Heart Failure:

Determinants of stroke volume:• Contractility• Preload• Afterload• Note that the failing heart

is more afterload sensitive than normal hearts

SA

1. Systolic Dysfunction

2. Diastolic Dysfunction

3. Arrythmias

4. Dyssynchrony• Atrio-ventricular

• Inter-ventricular

• Intra-ventricular

5. High out put cardiac failure

PathomechanismsCO = SV × HR

1. Preload

2. After load

3. contractility

LVRV LARA

LungsPulmonary Artery

Pulmonary Vein

Aorta

The Cardiovascular Circulation:Right and Left Heart Failure:

IVC

SVC

Acute Left Heart Failure: Relative Preservation of RV Function Compared to LV function, and Sympathetic ActivationIncreased Preload and AfterloadDue to systolic or diastolic dysfunction of LV, or mitral or aortic valve stenosis or regurgitation, malignant hypertension

Afterload(sympathetic activation)Aorta

LVLA

Pulmonary Venous Pressure

LV EDP

LALungs

Pulmonary Edema

CHFIt’s a hemodynamic disease !

Preload

Afterload

Contractility

CHF

What is diastolic dysfunction?

Myocardial Dysfunction

Systolic Dysfunction

Left ventricle has reduced muscle contractility

Diastolic

Decreased left ventricular filling

Caused by ventricular stiffness, decreased rate of relaxation, or rapid heart rate

CHF

Dilated Normal Hypertrophic

Types of Heart Failureinclude left, right or both sides

left ventricular heart failure

most common

systolic failure: unable to contract

diastolic failure: unable to relax

right ventricular heart failure

usually occurs after left failure

less blood received causes right damage

less pumping by right side

venous pooling of blood in legs

Kriteria Gagal Jantung menurut Framingham Heart Study

(1)Kriteria Mayor

Paroxysmal Nocturnal Dyspnoe Dyspnoe On Effort Peningkatan Tekanan Vena Jugularis Ronkhi paru Kardiomegali Udema paru akut Gallop S3 Pemanjangan waktu sirkulasi (>25 detik) Refluks hepato jugular


(2)Kriteria minor

Udema pergelangan kaki Batuk malam Hepatomegali Efusi Pleura Takikardia (> 120 x / menit) Penurunan kapasitas vital paru (1/3 dan

maksimal)

Kriteria mayor atau minor Penurunan berat badan lebih dari 4,5 kg selama 5

hari perawatan.


( 3 )Disebut gagal jantung kongestif

bila memenuhi 2 kriteria mayor

atau 1 mayor dengan 2 minor.

Sensitivity (%) Specificity (%) Positive* predictive

value (%)SymptomDyspnoea 66 52 23

Orthopnoea 21 81 2Paroxysmal nocturnal dyspnoea 33 76 26History of oedema 23 80 22

SignHeart rate>100/minute at rest 7 99 8Pulmonary crackles 13 91 27Oedema by examination 10 93 3Third heart sound 31 95 61Jugular venous distension 10 97 2

*proportion of patients in whom heart failure was correctly diagnosed

Sensitivity (%) Specificity (%) Positive* predictive

value (%)SymptomDyspnoea 66 52 23

Orthopnoea 21 81 2Paroxysmal nocturnal dyspnoea 33 76 26History of oedema 23 80 22

SignHeart rate>100/minute at rest 7 99 8Pulmonary crackles 13 91 27Oedema by examination 10 93 3Third heart sound 31 95 61Jugular venous distension 10 97 2

*proportion of patients in whom heart failure was correctly diagnosed

Tujuan pengobatan

Jangka pendek : menghilangkan keluhan dan gejala klinik

Jangka panjang :memperbaiki kualitas hidup dan masa harapan hidupmengurangi kekerapan masuk rumah sakitmencegah kematian dengan mencegah perbu rukan fungsi ventrikel.

SurvivalMorbidityExercise capacityQuality of lifeNeurohormonal changes Progression of CHFSymptoms


TREATMENT OBJECTIVESTREATMENT OBJECTIVES

GAGAL JANTUNG AKUT

Secara klinis dibagi dalam 3 kelompok yaitu:

1. udema paru akut kardiogenik

2. syok kardiogenik

3. dekompensasi akut pada gagal jantung kronik

diagnostik dini

1.Riwayat penyakit dan pemeriksaan fisik

2.EKG 12 sandapan & monitoring EKG

3.Pemeriksaan darah: rutin, elektrolit, urea-N,

kreatinin dan enzim jantung

4.Pulse oximetry/analisa gas darah

5.Rontgen dada

6.Ekokardiografi transtoraks

The Donkey Analogy

Ventricular dysfunction limits a patient's ability to perform the routine activities of daily living…

30%

70%

Diastolic DysfunctionSystolic Dysfunction

(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. 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

StrokeVolume

Preload Afterload

Contractility

Cardiac Output

Heart Rate• Synergistic LV Contraction• Wall Integrity• Valvular Competence

Determinants of Ventricular Function

Hemodynamic Basis for Heart Failure Symptoms

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

Compensatory Mechanisms

• Frank-Starling Mechanism

• Neurohormonal Activation

• Ventricular Remodeling


Frank-Starling Mechanism

a. At rest, no HF

b. HF due to LV systolic dysfunction

c. Advanced HF


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 = (SV x HR) x TPR

Sympathetic Nervous System

Contractility Tachycardia Vasoconstriction

Compensatory Mechanisms: Sympathetic Nervous System

Decreased MAP

Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.

CNS sympathetic outflow

Disease progression

Cardiac sympatheticactivity

1-receptors

2-receptors

1-receptors

VasoconstrictionSodium retention

Myocardial toxicityIncreased arrhythmias

Sympatheticactivity to kidneys

+ peripheral vasculature

Activationof RAS

1- b1-

Sympathetic Activation in Heart Failure

Vasoconstriction

Oxidative Stress

Cell Growth Proteinuria

LV remodeling

Vascular remodeling

Angiotensinogen

Angiotensin I

Angiotensin II

AT I receptor

Renin

AngiotensinConverting

Enzyme

Compensatory Mechanisms: Renin-Angiotensin-Aldosterone (RAAS)

MAP = (SV x HR) x TPR

Renin-Angiotensin-Aldosterone( renal perfusion)

Salt-water retentionThirst

Sympatheticaugmentation

Vasoconstriction

Compensatory Mechanisms: Renin-Angiotensin-Aldosterone (RAAS)

Decreased systemic blood pressure

Central baroreceptors

Stimulation of hypothalamus, which producesvasopressin for release by pituitary gland

Release of vasopressin by pituitary glandVasoconstriction

Increased systemic blood pressure

-

Compensatory Mechanisms: Neurohormonal Activation – Vasopressin

Compensatory Neurohormonal Stimulation: Summary

Decreased Cardiac Output

Sympatheticnervous system

Renin-angiotensinsystem

Antidiuretic hormone(vasopressin)

Heartrate

Contractility Vasoconstriction Circulating volume

Anteriolar

Maintainblood

pressure

Cardiacoutput

Strokevolume

+

-+

Venous

Venous return to heart

( preload)

Peripheral edemaand pulmonary

congestion

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.


Ventricular Remodeling

Alterations in the heart’s size, shape, structure, and function brought about by the chronic hemodynamic stresses experienced by the failing heart.

LV Dysfunction

Decreased cardiac outputand

Decreased blood pressure

Frank-Starling MechanismRemodeling

Neurohormonal activation

Increased cardiac output (via increasedcontractility and heart rate)

Increased blood pressure (via vasoconstriction and increased blood volume)

Increased cardiac workload(increased preload and afterload)

Vicious Cycle of Heart Failure

Initially 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: Basics of Heart Failure: A Problem Solving Approach

Part II: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


Initial Work-up:

• ECG

• Chest x-ray

• Blood work

• Echocardiography

diagnostik dini





4.Pulse oximetry/analisa gas darah• 5.Rontgen dada


CHF

Normal Heart Enlarged Heart

M-Mode Echo 2D Echo

RA

LA

RVLV

Septum

LV cavity

LV Wall


Part III: Current Treatment

of Heart Failure

The Vicious Cycle of Heart Failure Management

Chronic HF

MD’s Office

Emergency Room

Hospitalization

SOB

Weight

PO LasixIV Lasix or Admit

Diurese & Home

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


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


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


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


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


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

AT1 receptor AT2 receptor

• Vasoconstriction

• Growth Promotion

• Anti-apoptotic

• Pro-fibrotic

• Pro-thrombotic

• Pro-oxidant

• Vasodilation

• Growth inhibition

• Pro-apoptotic

• ? Fibrosis

• ? Thrombosis

• ? redox

Angiotensin II Receptors

Treatment Approach for the Patient with Heart Failure

Stage A

At high risk, no structural disease

Stage B

Structural heart disease,

asymptomatic

Stage D

Refractory HF requiring

specialized interventions

Therapy

• Treat Hypertension

• Treat lipid disorders

• Encourage regular exercise

• Discourage alcohol intake

• ACE inhibition

Therapy

• All measures under stage A

• ACE inhibitors in appropriate patients

• Beta-blockers in appropriate patients

Therapy

• All measures under stage A

Drugs:

• Diuretics

• ACE inhibitors

• Beta-blockers

• Digitalis

• Dietary salt restriction

Therapy

• All measures under stages A,B, and C

• Mechanical assist devices

• Heart transplantation

• Continuous (not intermittent) IV inotropic infusions for palliation

• Hospice care

Stage C

Structural heart disease with prior/current

symptoms of HF

Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult, 2001

Tujuan pengobatan

Jangka pendek : menghilangkan keluhan dan gejala klinik

Jangka panjang :memperbaiki kualitas hidup dan masa harapan hidupmengurangi kekerapan masuk rumah sakitmencegah kematian dengan mencegah perbu rukan fungsi ventrikel.



TREATMENT OBJECTIVESTREATMENT OBJECTIVES

GAGAL JANTUNG AKUT

Secara klinis dibagi dalam 3 kelompok yaitu:

1. udema paru akut kardiogenik

2. syok kardiogenik

3. dekompensasi akut pada gagal jantung kronik

diagnostik dini





4.Pulse oximetry/analisa gas darah

5.Rontgen dada


Penatalaksanaan Gagal Jantung Akut (1)

Tindakan umumObat-obatan :

1. Diuretik, paling baik furosemid (lasix) dosis 40- 80 mg secara intravena

2. Morfin sulfat (3 - 5 mg/iv) 3. Nitroglisenin sublingual (0,4-0,6 mg, dapat

diulang 4 kali setiap 5-10 menit), I.V. mulai dengan dosis 0,3-0,5 mikrogram/kg/BB/ menit, atau dengan ISDN I.V. 2-4 mg per jam


4.Penghambat ACE :

kaptopril 2 kali 6,25-12.5 mg

5.Pada kasus-kasus berat dimana curah jantung tetap rendah perlu inotropik, seperti dobutamin, dopamin

6.Aminophilin jarang digunakan pada terapi gagal jantung akut


7.Terapi trombolitik dan revaskularisasi segera (angioplasti atau bedah pintas) untuk infark miokard akut/injury

8.Intubasi dan pemasangan ventilator

9 Koreksi penyebab/penyakit dasar

EVOLUTION OF CLINICAL STAGESEVOLUTION OF

CLINICAL STAGES

NORMALNORMAL

Asymptomatic LV DysfunctionAsymptomatic LV Dysfunction

CompensatedCHF

CompensatedCHF

DecompensatedCHF

DecompensatedCHF

No symptomsNormal exerciseNormal LV fxn

No symptomsNormal exerciseNormal LV fxn

No symptomsNormal exerciseAbnormal LV fxn

No symptomsNormal exerciseAbnormal LV fxn

No symptoms ExerciseAbnormal LV fxn

No symptoms ExerciseAbnormal LV fxn

Symptoms ExerciseAbnormal LV fxn

Symptoms ExerciseAbnormal LV fxn

RefractoryCHF

RefractoryCHF

Symptoms not controlled with treatmentSymptoms not controlled with treatment

Chronic Congestive Heart Failure

TREATMENTTREATMENT

NormalNormal

AsymptomaticLV dysfunctionEF <40%

AsymptomaticLV dysfunctionEF <40%

Symptomatic CHFNYHA II

Symptomatic CHFNYHA II

InotropesSpecialized therapyTransplant

InotropesSpecialized therapyTransplant

Symptomatic CHFNYHA - IV

Symptomatic CHFNYHA - IV

Symptomatic CHFNYHA - III

Symptomatic CHFNYHA - III

Secondary preventionModification of physical activitySecondary preventionModification of physical activity

ACEIACEI

Diuretics mild

Neurohormonal inhibitors Digoxin?

Diuretics mild

Neurohormonal inhibitors Digoxin?

Loop DiureticsLoop Diuretics

TREATMENTCorrection of aggravating factors


MEDICATIONSMEDICATIONS

Endocarditis

Obesity

Hypertension

Physical activity

Dietary excess

Endocarditis

Obesity

Hypertension

Physical activity

Dietary excess

Pregnancy

Arrhythmias (AF)

Infections

Hyperthyroidism

Thromboembolism

Pregnancy

Arrhythmias (AF)

Infections

Hyperthyroidism

Thromboembolism

TREATMENTPHARMACOLOGIC THERAPY


DIURETICS

INOTROPES

VASODILATORS

NEUROHORMONAL ANTAGONISTSOTHERS (Anticoagulants, antiarrhythmics, etc)

DIURETICS

INOTROPES

VASODILATORS


Gagal Jantung Kronik

1.Anjuran Umum

2.Tindakan Umum

3.Obat-obatan1.Diuretik:

2.penghambat enzim konversi angiotensin (EKA)

3.penyekat beta .

4.Digitalis

5.antagonis reseptor angiotensin II

3.Obat-obatan (lanjutan)

6.Antagonis aldosteron 7.Vasodilator hidralazin sampai 300 mg +

ISDN 160 mg 8.Antikoagulan: 9.Antiaritmia pada fibrilasi atrial dan VT

Pathophysiology of Heart Failure

Initial Event

Myocardial Infarctwith

Excessive load

LV Remodeling

Ang II

Mitralregurgitation

Direct WaIIStress

Energy Supply

ClinicalSyndrome

Loss ofCardiac

Myocytes

Sodium Retention

Chamber enlargement &

Hypertrophy

Oedema

CHF

Cohn et al,N Engl J Med,1996 ; LeJemtel et al,Circulation,1993;87

Ventricular Remodeling and Ventricular Dysfunction

Coronary artery disease

Hypertension

Cardiomyopathy

Valvular disease

Left ventricular

dysfunction

Lowejectionfraction

Non- cardiacfactors

Remodeling

Symptoms

Arrhythmia

Death

Pump failure

Cohn, N Engl J Med, 1996;335

ChronicHeartfailure

catecholamineRAAS

endothelinnatriuretic peptide

cytokinegrowth factor

Changes in the Renin-Angiotensin System in CHF

Increased release of renin by the kidneysIncreased production of angiotensin II

- Stimulates smooth muscle cells- Increases extracellular matrix

production by smooth muscle cells and

cardiac fibroblasts- Causes hypertrophy of cardiac

myocytes

Angiotensin II Formation

Alternate Pathways*

Adapted from Dzau VJ et al. J Hypertens. 1993: 11(suppl 3).

* The clinical significance of the alternate pathway is unknown

Renin

ARB site of action

• CAGE• Cathepsin G• Chymase

Angiotensin II receptors

Angiotensin II

Angiotensin I

Angiotensinogen

ACE

• t-PA• Cathepsin G• Tonin

Renin Angiotensin SystemSELECTIVE MECHANISM OF ACTION

CHYMASE

ANGIOTENSIN I

ANGIOTENSINOGEN(LIVER)

AT1 AT2

ANGIOTENSIN II

ACE INHIBITOR

AT1 RECEPTOR BLOCKER

RENIN INHIBITOR

BRADYKININ

PEPTIDES

Other enzymese.g.

Summary of Key Heart Failure Studies (1)

Trial Scope Mission Result

V-Heft (1986) - n = 642 CCHF Improvement- Impaired cardiac Vasodilator therapy: function - placebo, prazosin

- ISDN + Hydralazine

CONSENSUS (1988) - n = 253 - Enalapril - Mortality reduced- Several CHF - Improved symptoms

SOLVD (1991) - n = 2569 - Enalapril Reduced hospt. - HF w/ conven- - Hospt. & Mortality and mortality tional Th/ - EF< 0.35

ATLAS (1991) - n = 3164 Low, medium, high dose High dose more- HF lisinopril on mortality effective in

reducing mortality

Trial Scope Mission Result

RESOLVD (1999) - 769 HF patient - Candesartan alone Combination therapy - Enalapril alone more effective- Combination-QOL Increased mortality w/

candesartan aloneELITE II (1999) - 3,152 CHF Losartan vs Captopril Losartan failed to show

- > 60 years superiority

CIBIS II (1999) - 2647 NYHA III/IV Efficacy of 1,25 mg Significant mortality - EF < 35% bisoprolol in HF benefit - trial stopped

receiving ACE + D

MERIT-HF (1999) - 3,991 HF patients Metoprolol CR/XL All cause mortality wasNYHA II-IV; EF < 40% lower - trial stopped

CARVEDILOL HF - 1,094 patients CHF Mortality & morbidity Trial stopped early,STUDY (1999) effects carvedilol to reduced risk or death

standard therapy

Summary of Key Heart Failure Studies (2)



MEDICATIONSMEDICATIONS

Endocarditis

Obesity

Hypertension

Physical activity

Dietary excess

Endocarditis

Obesity

Hypertension

Physical activity

Dietary excess

Pregnancy

Arrhythmias (AF)

Infections

Hyperthyroidism

Thromboembolism

Pregnancy

Arrhythmias (AF)

Infections

Hyperthyroidism

Thromboembolism



DIURETICS

INOTROPES

VASODILATORS


DIURETICS

INOTROPES

VASODILATORS


CAUSES OF HEART FAILURE:

• Final common pathway of many kinds of heart diseases– Ischemic, alcoholic, restrictive, hypertrophic– Optimal treatment requires identification of

primary & secondary factors leading to CHF– HELPFUL RESULT of dilatation: increases cardiac

output– HARMFUL RESULT of dilation: more wall tension,

more oxygen is needed to produce any given stroke volume

Effect on Cardiac Output

Overall decrease in Frank-Starling curve with CHF

Documents

gagal-jantung (1)