All About CHF DR - Irwan

CHRONIC CONGESTIVE HEART
FAILURE
A Comprehensive Overview on Diagnosis and Treatment
Dr. Irwan, SpJP.

Faculty of Medicine of Riau University
Arifin Achmad Hospital,Pekanbaru
Introduction
Definition : Heart Failure

The situation when the heart is incapable of
maintaining a cardiac output adequate to
accommodate metabolic requirements and the
venous return. E. Braunwald
Pathophysiological state in which an
abnormality of cardiac function is responsible
for the failure of the heart to pump blood at a
rate commensurate with the requirements of
the metabolizing tissues. Euro Heart J; 2001. 22: 1527-1560
DEFINITION OF HEART FAILURE.

Criteria 1 and 2 should be fulfilled in all cases
1. Symptoms of heart failure

(at rest or during exercise)
And
2. Objective evidence of cardiac dysfunction
(at rest)
And
(in cases where the diagnosis is in doubt)
3. Response to treatment directed towards heart

failure
Task Force Report. Guidelines for the diagnosis and treatment of chronic heart failure.
European Society of Cardiology.2001
EPIDEMIOLOGY
Europe
The prevalence of symptomatic HF range from 0.4-2%.
10 million HF pts in 900 million total population
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560
USA
nearly 5 million HF pts.

500,000 pts are D/ HF for the 1st time each year.
Last 10 years number of hospitalizations has increased.
Nearly 300,000 patients die of HF each year.
ACC/AHA Guidelines for the
Evaluation and Management of Chronic Heart Failure in the Adult 2001
DESCRIPTIVE TERMS in HEART FAILURE

Acute vs Chronic Heart Failure
Systolic vs Diastolic Heart Failure
Right vs Left Heart Failure
Mild , Moderate, Severe Heart Failure

European Heart Journal (2001) 22, 1528
New York Heart Association (NYHA)

Classification of Heart Failure
Class I
No limitation : ordinary physical exercise does

not cause undue fatigue, dyspnoea or palpitations.
Class II
Slight limitation of physical activity : comfortable at rest but ordinary activity results in
fatigue, dyspnoea, or palpitation.
Class - III
Marked limitation of physical activity : comfortable at rest but less than ordinary activity
results in symptoms.
Class - IV
Unable to carry out any physical activity without discomfort : symptoms of heart failure are
present even at rest with increased discomfort
with any physical activity.
European Heart Journal (2001) 22, 1531
(Adapted from Williams JF et al., Circulation. 1995; 92 : 2764-2784)
ACC/AHA A New Approach To The Classification of HF

Stage
Descriptions
Examples
Patient who is at high risk for

developing HF but has no
structural disorder of the heart.
Hypertension; CAD; DM;

rheumatic fever; cardiomyopathy.
Patient with a structural disorder

of the heart but who has never
developed symptoms of HF.
LV hypertrophy or fibrosis;
LV dilatation; asymptomatic VHD;
MI.
Patient with past or current

symptoms of HF associated with
underlying structural heart
disease.
Dyspnea or fatigue ec LV systolic

dysfunction; asymptomatic
patients with HF.
Patient with end-stage disease
Frequently hospitalized pts ; pts

awaiting heart transplantation etc

Stages in the evolution of HF and recommended therapy by stage
Stage A
Stage B
Pts with :
Hypertension
CAD
DM
Cardiotoxins
FHx CM
Pts with :
Previous MI
LV systolic
dysfunction
Asymptomatic
Valvular disease
Struct.
Heart
Disease
THERAPY
Treat Hypertension
Stop smoking
Treat lipid disorders
Encourage regular
exercise
Stop alcohol
& drug use
ACE inhibition
THERAPY
All measures under
stage A
ACE inhibitor
Beta-blockers
Stage C
Stage D
Pts with :
Develop
Symp.of
HF
Struct. HD
Refract.
Shortness of
Symp.of
breath and fatigue,
HF at rest
reduce exercise
tolerance
THERAPY
All measures under
stage A
Drugs for routine use:
diuretic
ACE inhibitor
Beta-blockers
digitalis
Pts who have

marked symptoms
at rest despite
maximal medical
therapy.
THERAPY
All measures under
stage A,B and C
Mechanical assist
device
Heart transplantation
Continuous IV
inotrphic infusions for
palliation

EVOLUTION OF
CLINICAL STAGES
NORMAL
Asymptomatic
LV Dysfunction
No symptoms
Compensated
Normal exercise
CHF
Abnormal LV fxn
No symptoms
Decompensated
Exercise
CHF
Abnormal LV fxn
Symptoms
Refractory
Exercise
CHF
Abnormal LV fxn
No symptoms
Normal exercise
Normal LV fxn
Symptoms not controlled

with treatment
Patophysiology of C H F
PULMONARY VENOUS
PRESSURE
Input
Filling
Emptying
Stroke
EF
ED volume x
effective = volume
LV Distensibility
x
Contractility
Relaxation
Afterload
Heart
Left atrium
Preload
rate
Mitral valve
Pericardium
Structure
Diastolic function Systolic function

Output
CARDIAC OUTPUT
Block diagram of left ventricular pump performance

(Little, 2001)
DETERMINANTS OF
VENTRICULAR FUNCTION
CONTRACTILITY
PRELOAD
AFTERLOAD
STROKE
VOLUME
- Synergistic LV contraction
- LV wall integrity
- Valvular competence
CARDIAC OUTPUT
HEART
RATE
Frank-Starling Law
Normal
Cardiac Output
Compensated
Normal C.O.
CHF
LVEDP
The Pathophysiology of Heart Failure
Hurst. The Heart. Diagnosis and Management of Heart Failure.10th ed. 688
Pathophysiological Sequence of CHF

Heart Failure
Inadequate Cardiac Output
( ) O2 Delivery (rest and/or exercise)

Systemic Vasoconstriction
SAS (NE))
RAAS (A-II)
() Flow to Skin, Gut,
and Renal Circulations
Neurohormonal Activation
Activation of
RAS and ANS
Hurst. The Heart. Diagnosis and Management of Heart Failure.10th ed. 688
SNS
Preload
Afterload
Renin release
Angiotensin II
Growth
factors
ALDO
Vasoconstriction
Hypertrophy
Apoptosis
Fluid
accumulation
Collagen
deposition
Myofibril
necrosis
Perfusion of Vital Organs

RBF
Na filtered
Renin release
Angiotensin II
Growth
factors
ALDO
Vasoconstriction
Hypertrophy
Apoptosis
Fluid accumulation
Afterload
Collagen deposition
Myofibril necrosis
Sympathetic nervous system up-regulation

Increased
Norepinephrine levels
Activation of the
RAA system
Increased
Angiotensin II &
Aldosteron
Na+
& water
retention
Vasoconstriction
Direct
Myocardial toxicity
Decreased
Renal blood
flow
Myocyte dysfunction
Increased HR, PVR &
arteriolar vasoconstriction
Increased myocardial
oxygen demand
Cardiac remodeling
Myocyte
necrosis
Intracellular
Ca2+ overload/
Energy depletion
Apoptosis
Cesario et.al; Reviews in cardiovascular medicine, vol 3, no.1, 2002
Causes of Heart Failure

Myocardial Damage or Disease
Infarction (Acute) / Ischemia
Myocarditis
Hypertrophic Cardiomyopathy
Excess Load on Ventricle

Volume/ Pressure Overload
Resistance to Flow into Ventricle

Cardiac Arrhythmias
MI-INDUCED HEART FAILURE

Myocardial Damage
Contractility
Pump Performance
() Systolic Work Load
Vasoconstriction
RAAS SYSTEM
FLUID RETENTION
() SAS Drive
Diagnosis of C H F
IDENTIFICATIONS OF HF PATIENTS
With a Syndrome of Decrease Exercise
Tolerance
With a Syndrome of Fluid Retention
With No Symptoms or Symptoms of
Another Cardiac or Non Cardiac
Disorder
(MI, Arrythmias, Pulmonary or
Systemic Thromboembolic Events)
SYMPTOMS AND SIGN

Breathlessness, Ankle Swelling, Fatique
Characteristic Symptoms
Peripheral Oedema, JVP , Hepatomegaly
Signs of Congestion of Systemic Veins
S3 , Pulmonary Rales , Cardiac Murmur
ECG
A low Predictive Value
LAH and LVH May Be Associated wit LV Dysfunction
Anterior Q-wave and LBBB a good predictors of EF
Detecting Arrhytmias as Causative of HF
CHEST X-RAY
A Part of Initial Diagnosis of HF
Cardiomegaly, Pulmonary Congestion
Relationship Between Radiological Signs and
Haemodynamic Findings may Depend on the Duration
and Severity HF
HAEMATOLOGY & BIOCHEMISTRY

A Part of Routine Diagnostic
Hb, Leucocyte, Platelets
Electrolytes, Creatinine, Glucose, Hepatic Enzyme,
Urinalysis
TSH, C-RP, Uric Acid
ECHOCARDIOGRAPHY
The Preferred Methods
Helpful in Determining the Aetiology
Follow Up of Patients Heart Failure
INVASIVE INVESTIGATION
Elucidating the Cause and Prognostic Informations
Coronary Angiography :
in CADs Patients
Haemodynamic Monitoring :
To Assess Diagnostic and Treatment of HF
Endomyocardial Biopsy :
in Patients with Unexplained HF
NATRIURETIC PEPTIDES
Cardiac Function (LV Function )
Plasma Natriuretic Peptide Concentration
(Diagnostic Blood Use for HF)
Natriuretic Peptide :
Greatest Risk of CV Events
Natriuretic Peptide :
Improve Outcome in Patients with
Treatment
Identify Pts. With Asymptomatic LV
Dysfunction (MI, CAD)
ALGORITHM FOR THE DIAGNOSIS OF THE HF

(ESC, 2001)
Suspected Heart Failure Because
of symptoms and signs
Assess Presence of Cardiac Disease by ECG, X-Ray

or NatriureticPeptides (Where Available)
If Normal
Heart Failure
Unlikely
Tests Abnormal
Imaging by Echocardiography (Nuclear

Angiography or MRI Where Available)
If Normal
Heart Failure
Unlikely
Tests Abnormal
Assess Etiology, Degree, Precipitating

Factors and Type of Cardiac Dysfunction
Choose Therapy
Additional Diagnosis Tests

Where Appropriate (e.g.
Coronary Angiography)
Treatment of C H F
Aims of Treatment
1. Prevention
a) Prevention and/or controlling of diseases leading
to cardiac dysfunction and heart failure
b) Prevention of progression to heart failure once
cardiac dysfunction is established
2. Morbidity
Maintenance or improvement in quality of life
3. Mortality
Increased duration of life
Management Outline
Establish that the patient has HF.
Ascertain presenting features: pulmonary oedema, exertional
breathlessness, fatigue, peripheral oedema
Assess severity of symptoms
Determine aetiology of heart failure
Identify precipitating and exacerbating factors
Identify concomitant diseases
Estimate prognosis
Anticipate complications
Counsel patient and relatives
Choose appropriate management
Monitor progress and manage accordingly
TREATMENT
Correction of aggravating factors

Pregnancy
Endocarditis
Arrhythmias (AF)
Infections
Obesity
Hypertension
Hyperthyroidism
Thromboembolism
Physical activity
Dietary excess
MEDICATIONS
Treatment options
Non-pharmacological management
General advice and measures
Exercise and exercise training
Pharmacological therapy
Angiotensin-converting enzyme (ACE) inhibitors
Diuretics
Beta-adrenoceptor antagonists
Aldosterone receptor antagonists
Angiotensin receptor antagonists
Cardiac glycosides
Vasodilator agents (nitrates/hydralazine)
Positive inotropic agents
Anticoagulation
Antiarrhythmic agents
Oxygen
Devices and surgery

Revascularization (catheter interventions and surgery), other forms of
surgery
Pacemakers
Implantable cardioverter defibrillators (ICD)
Heart transplantation, ventricular assist devices, artificial heart
Ultrafiltration, haemodialysis
ACC/AHA & EUROPE (ESC) 2001

GUIDELINES FOR THE MANAGEMENT
OF HEART FAILURE
ACE-inhibitor
Use as first line therapy
Should be up titrated to the dosages shown in the large
clinical trial, and not titrated based on symptomatic
improvement
DIURETIC to control fluid overload
-BLOCKER
For all patients with stable mild-severe HF on
standard treatment
ACC/AHA & EUROPE (ESC) 2001

GUIDELINES FOR THE MANAGEMENT
OF HEART FAILURE
Aldosteron Receptor Antagonis
in advance HF ( NYHA III-IV )
DIGOXIN
in AF
May be added for symptom relief

ARB
Considered in patients not tolerate ACE
inhibitors and not on - blocker
TREATMENT
Normal
Asymptomatic
LV dysfunction
EF <40%
Symptomatic CHF
ACEI
NYHA II Symptomatic CHF
NYHA - III
Diuretics mild
Neurohormonal
Symptomatic CHF
Loop
inhibitors
NYHA - IV
Diuretics
Digoxin?
Inotropes
Specialized therapy
Transplant
Secondary prevention
Modification of physical activity
Pharmacological therapy
Stages in the evolution of HF and recommended therapy by stage
Stage A
Stage B
Pts with :
Hypertension
CAD
DM
Cardiotoxins
FHx CM
Pts with :
Previous MI
LV systolic
dysfunction
Asymptomatic
Valvular disease
Struct.
Heart
Disease
THERAPY
Treat Hypertension
Stop smoking
Treat lipid disorders
Encourage regular
exercise
Stop alcohol
& drug use
ACE inhibition
THERAPY
All measures under
stage A
ACE inhibitor
Beta-blockers
Stage C
Stage D
Pts with :
Develop
Symp.of
HF
Struct. HD
Refract.
Shortness of
Symp.of
breath and fatigue,
HF at rest
reduce exercise
tolerance
THERAPY
All measures under
stage A
Drugs for routine use:
diuretic
ACE inhibitor
Beta-blockers
digitalis
Pts who have

marked symptoms
at rest despite
maximal medical
therapy.
THERAPY
All measures under
stage A,B and C
Mechanical assist
device
Heart transplantation
Continuous IV
inotrphic infusions for
palliation

1. ACE INHIBITOR
Angiotensin-converting enzyme inhibitors

Recommended as first-line therapy.
Should be uptitrated to the dosages shown to be

effective in the large, controlled trials, and not
titrated based on symptomatic improvement.
Moderate renal insufficiency and a relatively low blood
pressure (serum creatinine 250 mol.l-1 and systolic
BP 90 mmHg) are not contraindications.
Absolute contraindications: bilateral renal artery
stenosis and angioedema.
ACEI
MECHANISM OF ACTION
VASOCONSTRICTION
ALDOSTERONE
VASOPRESSIN
SYMPATHETIC
VASODILATATION
PROSTAGLANDINS
Kininogen
tPA
Kallikrein
Angiotensinogen
RENIN
Angiotensin I
A.C.E.
ANGIOTENSIN II
Inhibitor
BRADYKININ
Kininase II
Inactive Fragments
ACEI
UNDESIRABLE EFFECTS
Inherent in their mechanism of action
- Hypotension
- Hyperkalemia
- Angioneurotic edema
- Dry cough
- Renal Insuff.
Due to their chemical structure

- Cutaneous eruptions
- Neutropenia,
thrombocytopenia
- Digestive upset
- Dysgeusia
- Proteinuria
ACEI
CONTRAINDICATIONS
Renal artery stenosis

Renal insufficiency
Hyperkalemia
Arterial hypotension
Intolerance (due to side effects)
ACE-Inhibitors in Asymptomatic Heart Failure
Development of symptomatic HF
Hospitalization of HF
SAVE & TRACE Study

ACE-Inhibitors in Symptomatic Heart Failure

All patients symptomatic Heart Failure should receive ACE-I.
A) No fluid retention, ACE-I should be given first.
B) With fluid retention, ACE-I + Diuretic
ACE-I : A) improves survival and symptoms.
B) reduces hospitalization.
2. DIURETICS
Diuretics
Essential for symptomatic treatment when

fluid overload is present and manifest.
Always be administered in combination

with ACE inhibitors if possible.

DIURETICS
Thiazides
Inhibit active exchange of Cl-Na
in the cortical diluting segment of the
ascending loop of Henle
Cortex
K-sparing
Inhibit reabsorption of Na in the
distal convoluted and collecting tubule
Medulla
Loop of Henle
Loop diuretics
Inhibit exchange of Cl-Na-K in
the thick segment of the ascending
loop of Henle
Collecting tubule
THIAZIDES
MECHANISM OF ACTION
Excrete 5 - 10% of filtered Na+
Elimination of K
Inhibit carbonic anhydrase:
increase elimination of HCO3
Excretion of uric acid, Ca and Mg
No dose - effect relationship
LOOP DIURETICS
MECHANISM OF ACTION
Excrete 15 - 20% of filtered Na+
Elimination of K+, Ca+ and Mg++
Resistance of afferent arterioles

-
Cortical flow and GFR
Release renal PGs
NSAIDs may antagonize diuresis
K-SPARING DIURETICS
MECHANISM OF ACTION
Eliminate < 5% of filtered Na+
Inhibit exchange of Na+ for K+ or H+

Spironolactone = competitive
antagonist for the aldosterone receptor
Amiloride and triamterene block
Na+ channels controlled by aldosterone
3. ALDOSTERONE INHIBITORS
ALDOSTERONE INHIBITORS
Spironolactone
ALDOSTERONE
Competitive antagonist of the

aldosterone receptor
(myocardium, arterial walls, kidney)
Retention Na+
Retention H2O
Edema
Excretion K+
Arrhythmias
Excretion Mg2+
Collagen
deposition
Fibrosis
- myocardium
- vessels
ALDOSTERONE INHIBITORS
INDICATIONS
FOR DIURETIC EFFECT
Pulmonary congestion (dyspnea)
Systemic congestion (edema)
FOR ELECTROLYTE EFFECTS
Hypo K+, Hypo Mg+
Arrhythmias
Better than K+ supplements
FOR NEUROHORMONAL EFFECTS
Please see RALES results,
N Engl J Med 1999:341:709-717
Aldosterone receptor antagonists - spironolactone
Recommended in advanced HF (NYHA III-IV),

in addition to ACE inhibition and diuretics to
improve survival and morbidity

4. -Blockers
Start Low Go Slow
Activation and Blockade of Neurohumoral

System in CHF
RAA System
SNS System
Angiotensin II
Noradrenalin
ACE-I
-Blocker
Hypertrophy, apoptosis, ischaemia,

arrhytmia, remodeling, fibrosis
ADRENERGIC ACTIVATION
CNS Sympathetic
Outflow
Sympathetic
activity to kidneys
& blood vessels
Cardiac
Sympathetic activity
1-receptors
2-receptors
1-receptors
Mycocyte hypertrophy & death,

dilatation, ischaemia & arrhytmias
Vasoconstriction
Sodium Retention
Packer, AHA 2000
Benefits of Add-on -Blocker

Short-term :
1. Improvement of symptoms (LVEF )
2. Improvement of NYHA class
3. Improvement of daily activities
4. Reduction of hospitalization rate & length of
hospital stay (financial & psychological burden)
Long-term :
1. Slowing the progression of CHF

2. Increase of survival rate
Beta-adrenoceptor antagonists
Recommended for the treatment of all pts

with stable, mild, moderate and severe heart
failure on standard treatment, unless there is
a contraindication.
Patients with LV systolic dysfunction, with or

without symptomatic HF, following an AMI
long-term betablockade is recommended
in addition to ACE inhibitor.
THE RECOMMENDED PROCEDURE FOR

STARTING -BLOCKER
1. Patient should be on standard therapy
(ACE inhibitor +/- diuretic)
2. Patient in stable conditions
No iv inotropic therapy
Without signs of marked fluid retention
3. Start initial low doses and titrate to maintenance dose
(the dose may be doubled every 1 2 weeks)

(ESC.Guidelines for HF, 2001)
DOSES OF -BLOCKER
BLOCKER
FIRST DOSE
TARGET DOSE
TITRATION
PERIOD
Bisoprolol
1.25 mg
10 mg
Weeks Month
Metoprolol
Tartrate
5 mg
150 mg
Weeks Month
Metoprolol
Succinate
12.5 mg
200 mg
Weeks Month
Carvedilol
2 x 3.125 mg
2 x 25 mg
Weeks Month
(European Heart Journal, vol. 22, Sept. 2001)
CONTRAINDICATIONS OF
-BLOCKER IN PATIENT H F
Asthma Bronchial
Severe Bronchial Desease

Symptomatic Bradycardia and
Hypotension
INTOLERANCE OF -BLOCKER
Symptomatic
Bradycardia
Worsening HF
Hypotension
5. Angiotensin II receptor
antagonists
ANGIOTENSIN II INHIBITORS
MECHANISM OF ACTION
RENIN
Angiotensin I
Angiotensinogen
ACE
Other paths
ANGIOTENSIN II
AT1
RECEPTOR
BLOCKERS
AT1
Vasoconstriction
RECEPTORS
Proliferative
Action
AT2
Vasodilatation Antiproliferative
Action
AT1 RECEPTOR BLOCKERS

DRUGS
Losartan
Valsartan
Irbersartan
Candesartan
Competitive and selective
blocking of AT1 receptors
Angiotensin II receptor antagonists

ARBs could be considered in patients who do not
tolerate ACE inhibitors for symptomatic
treatment.
It is unclear whether ARBs are as effective as

ACE inhibitors for mortality reduction.
In combination with ACE inhibition, ARBs may
improve heart failure symptoms and reduce
hospitalizations for worsening heart failure.
6. Cardiac glycosides
DIGOXIN
Na-K ATPase
Na+
K+
K+ Na+
Na-Ca Exchange
Na+
Myofilaments
Ca++
Ca++
CONTRACTILITY
DIGOXIN
DIGITALIZATION STRATEGIES
Loading dose (mg)
i.v
0.5 + 0.25 / 4 h
ILD: 0.75-1
oral 12-24 h
oral 2-5 d
0.75 + 0.25 / 6 h 0.25 / 6-12 h

1.25-1.5
1.5-1.75
Maintenance
Dose
(mg)
0.125-0.5 / d
0.25 / d
ILD = average INITIAL dose required for

digoxin loading
DIGOXIN
HEMODYNAMIC EFFECTS
Cardiac output
LV ejection fraction
LVEDP
Exercise tolerance
Natriuresis
Neurohormonal activation
DIGOXIN
NEUROHORMONAL EFFECTS
Plasma Noradrenaline
Peripheral nervous system activity
RAAS activity
Vagal tone
Normalizes arterial baroreceptors
DIGOXIN
CLINICAL USES
AF with rapid ventricular response
CHF refractory to other drugs
Other indications?
Can be combined with other drugs
DIGOXIN
CONTRAINDICATIONS
ABSOLUTE:
- Digoxin toxicity
RELATIVE
- Advanced A-V block without pacemaker
- Bradycardia or sick sinus without PM
- PVCs and TV
- Marked hypokalemia
- W-P-W with atrial fibrillation
DIGOXIN TOXICITY
CARDIAC MANIFESTATIONS
ARRHYTHMIAS :
- Ventricular (PVCs, TV, VF)
- Supraventricular (PACs, SVT)
BLOCKS:
- S-A and A-V blocks
CHF EXACERBATION
DIGOXIN TOXICITY
EXTRACARDIAC MANIFESTATIONS
GASTROINTESTINAL:
- Nausea, vomiting, diarrhea
NERVOUS:
- Depression, disorientation, paresthesias
VISUAL:
- Blurred vision, scotomas and yellow-green
vision
HYPERESTROGENISM:
- Gynecomastia, galactorrhea
Cardiac glycosides
indicated in atrial fibrillation and any degree of
symptomatic heart failure.
A combination of digoxin and beta-blockade
appears superior than either agent alone.
In sinus rhythm, digoxin is recommended to
improve the clinical status of patients with
persisting heart failure despite ACE inhibitor and
diuretic treatment.
7. Vasodilator agents
Vasodilator agents in chronic heart failure

No specific role for vasodilators in the treatment of HF
Used as adjunctive therapy for angina or concomitant
hypertension.
In case of intolerance to ACE inhibitors ARBs are
preferred to the combination hydralazinenitrates.
HYDRALAZINE-ISOSORBIDE DINITRATE
Hydralazine (up to 300 mg) in combination with ISDN (up to 160
mg) without ACE inhibition may have some beneficial effect on
mortality, but not on hospitalization for HF.
Nitrates may be used for the treatment of concomitant angina or
relief of acute dyspnoea.
8. Positive inotropic therapy
POSITIVE INOTROPES
CARDIAC GLYCOSIDES
SYMPATHOMIMETICS
Catecholamines
-adrenergic agonists
PHOSPHODIESTERASE INHIBITORS
Amrinone
Enoximone
Others
Milrinone
Piroximone
DOPAMINE AND DOBUTAMINE

EFFECTS
DA (g / Kg / min)
Dobutamine
<2
DA1 / DA2
2-5
1
>5
1 +
Contractility
++
++
++
Heart Rate
++
Arterial Press.
++
++
++
++
Receptors
Renal perfusion
Arrhythmia
POSITIVE INOTROPES
CONCLUSIONS
May increase mortality
Safer in lower doses
Use only in refractory CHF
NOT for use as chronic therapy
10. Anticoagulation
11. Antiplatelet Drugs
ANTICOAGULANTS
PREVIOUS EMBOLIC EPISODE
ATRIAL FIBRILLATION
Identified thrombus
LV Aneurysm (3-6 mo post MI)
Class III-IV in the presence of:
- EF < 30
- Aneurysm or very dilated LV
Phlebitis
Prolonged bed rest
Anticoagulation
Recommendation
1. All pts with HF and AF should be
treated with warfarin unless
contraindicated.
2. Patients with LVEF 35% or less.
HFSA Guidelines for Management of Patients With Heart Failure Caused by Left
Ventricular Systolic Dysfunction - Pharmacological Approaches 2000
Chronic heart failure choice of

pharmacological therapy
LV systolic dysfunction
ACE inhibitor
Diuretic
Beta-blocker
Aldosterone
Antagonist
Asymptomatic LV
dysfunction
Indicated
Not indicated
Post MI
Not indicated
Symptomatic HF (NYHA II)
Indicated
Indicated if
Fluid retention
Indicated
Not indicated
Worsening HF (NYHA III-IV)
Indicated
Indicated
comb. diuretic
Indicated
End-stage HF (NYHA IV)
Indicated
Indicated
comb. diuretic
Indicated
Indicated
Indicated

Chronic heart failure choice of

pharmacological therapy
LV systolic dysfunction
Angiotensin
II receptor
antagonists
Asymptomatic LV
dysfunction
Not indicated
Symptomatic HF (NYHA II)
Worsening HF (NYHA III-IV)
End-stage HF (NYHA IV)
Vasodilator
(hydralazine/ Potassium -sparing
Cardiac glycosides
isosorbide
diuretic
dinitrate)
Not indicated
With AF
(a) when AF
If ACE inhibitors
If ACE inhibitors
and angiotensin
are not tolerated (b) when improved
from more severe II antagonists
and not on betaare not
HF in sinus
blockade
tolerated
rhythm
If ACE inhibitors
If ACE inhibitors
and angiotensin
are not tolerated
indicated
II antagonists
blockade
tolerated
If ACE inhibitors
If ACE inhibitors
and angiotensin
are not tolerated
indicated
II antagonists
blockade
tolerated
Not indicated
If persisting
hypokalaemia
If persisting
hypokalaemia
If persisting
hypokalaemia

Intervention
Surgical
Revascularization
Non Surgical
Pts with heart failure of ischaemic origin revascularization
symtomatic improvement.
A strong negative correlation of operative mortality and LVEF,
a low LVEF (<25%) was associated with increased
operative mortality. Advance HF symptoms (NYHA IV)

resulted in a greater mortality rate.
Off pump coronary revascularization may lower the surgical
risk for HF.
Heart Transplantation is an accepted mode of treatment for
end-stage HF.
Care and Follow-up

Recommended components of programs
use a team approach

vigilant follow-up, first follow-up within 10 days of
discharge
discharge planning
increased access to health care
optimizing medical therapy with guidelines
intense education and counselling inpatient and
outpatient
strategies address barriers to compliance
early attention to signs and symptoms
flexible diuretic regimen
Future treatment
Neurohormonal modulation
1.
2.
3.
4.
5.
6.
7.
Sympathetic nervous system

The RAA system
Atrial and brain natriuretic peptides
Arginin vasopressin
Endothelin
Growth hormone
Calcitonin gene related peptide
Cardiac reparation: fixing the heart

with cells, new vessels and genes (1)
Cell based
interventions
Aims: to repopulate fibrous scars with new
contractile cells
1. Multiplication of residual myocytes
(forcing the cells to enter mytotic cycle)
2. Transforming fibrablasts in the scar
3. Implanting exogenous contractiles cells
(foetal cardiomyocites, skeletal
myoblasts, stem cells)
Eur Heart J 2002;4: D73-81
CONT (2)
Angiogenesis
Aims: to provides new blood supply to
the diseased heart
1. Administration of angiogenic growth factors
VEGF, basic FGF
2. Problems: nature of compound , dose, route,
and adverse events (abnormal blood vessels,
proliferative retinopathy, etc)
Eur Heart J 2002;4: D73-81
CONT(3)
Gene therapy
Aims: to improve the function of the failing
heart
1. Gene manipulation of 3 majors areas: Ca
handling, beta-adenergic signalling and
apoptosis
2. Inducing expression of silent genes
Safety problems: control of targeted protein

expression, inflammation, autoimmunity
and oncogenesis (basically irreversible)
Eur Heart J 2002;4: D73-81
Dual-chamber pacemakers are

beneficial
Drug-resistant CHF
Intact sinus rhythm
Absence of chronic atrial dysrhythmias
EF <20%
Viable myocardium
No or stable angina
DMC and PR >, MR and TR, QRS >, QRS
PR + QRS > 350 ms.
QRS >140 ms, MR > 450 ms, and LV filling
time <200 ms
HOCM
Resume
Pharmacological Treatment :
I.
Asymptomatic Systolic LV dysfunction :
II.
ACE Inhibitor
-Blocker (in CAD)
Symptomatic Systolic LV dysfunction

A.
No fluid retention
ACE Inhibitor
-Blocker
If ischaemia (+) nitrate / revascularization
B.
Fluid retention
Diuretic
ACE Inhibitor (ARBs if not tolerated)
-Blocker
Digitalis
Resume
III.
Worsening HF
IV.
Standard treatment : ACE Inhibitor, -Blocker

Diuretic : doses + loop diuretic
Low dose spironolactone
Digitalis
Consider :
Revascularization
Valve surgery
Heart transplant
End-stage HF
Intermittent inotrophic support

Circulatory support (IABP, Ventr.Assist Devices)
Haemofiltration on dialysis
briddging to heart transplantation
Conclusion
Management of HF must be starting from
the earlier stage (AHA/ACC stage A).
Treatment at each stage can reduce
morbidity and mortality.
Before initiating therapy :
Established the correct diagnose.
Consider management outline.
Conclusion
Non pharmacolgical intervention are helpfull in :
improving quality of life
reducing readmission
lowering cost.
Organize multi-disciplinary care :

HF clinic, HF nurse specialist, pts telemonitoring.
Health care system.
To optimize HF management
Treatment should be according to the Guidelines,
intensive education, and behavioral change efforts.
Thank YoU
DIASTOLIC HEART
FAILURE
SCOPE OF THE PROBLEM

Epidemiological studies of HF have
suggested that 30-50% of cases of HF
have preserved LV systolic function.
DHF has mortality rate equal as
systolic heart failure
No guideline yet regarding the
treatment of DHF
Greenberg & Hermann 2004
Defining Diastolic Heart Failure

Diastolic dysfunction refers to a condition in which
abnormalities in mechanical function are presenting
during diastole.
Diastolic dysfunction is a condition in which higher
than normal LV filling pressure are needed to maintain
a normal cardiac output.
Diastolic heart failure is a clinical syndrome
characterized by the symptoms and signs of heart
failure, a preserved EF and abnormal diastolic
function.
(Vasan & Levy 2000)
(Mandinov,Eberli,Seiler,Hess.Cardiosvasc Res 2000)
Other Methods in diagnosing DHF
Plasma Brain Natriuretic Peptide

Doppler tissue imaging
Magnetic resonance imaging
Radionuclide angiography
Cardiac catheterization
Greenberg & Hermann 2004
Treatment of Diastolic Heart Failure

The guidelines are based on :
Clinical investigations in relatively small
groups of patients
Clinical experience
Concepts based on pathophysiology
mechanisms
Treatment of Diastolic Heart failure

symptom targeted treatment
disease / pathological targeted treatment
the underlying mechanism targeted

treatment
( Zile & Brutsaert, 2002 )
Diastolic Heart Failure: Treatment

Symptom targeted treatment
Decrease pulmonary venous pressure

Reduce LV volume
Maintain atrial contraction
Prevent tachycardia
Improve exercise tolerance
Use positive inotropic agents with caution
Diastolic Heart Failure: Treatment

Symptom targeted treatment
Nonpharmacological treatment
Restrict sodium to prevent volume overload

Restrict fluid to prevent volume overload
Perform moderate aerobic exercise to improve cardiovascular
conditioning, decrease heart rate and maintain skeletal muscle
function
Pharmacological treatment
Diuretics including loop diuretics thiazides, spironolactone
Long-acting nitrates, -Adrenergic blockers

Calcium channel blockers
Renin angiotensin-aldosterone antagonists including ACE
inhibitors, angiotensin II receptor blockers and aldosterone
antagonists
Diastolic Heart Failure

Disease-targeted treatment
Prevent/treat myocardial ischemia
Prevent/regress ventricular hypertrophy
Mechanisms targeted treatment
Modify myocardial and extramyocardial mechanisms
Modify intracellular and extracellular mechanisms
An ideal therapeutic agent.
- Should target the underlying mechanisms

- Improve calcium homeostasis and energetics
- Blunt neurohumoral activation
- Prevent and regress fibrosis

All About CHF DR - Irwan

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CHRONIC CONGESTIVE HEART

Dr. Irwan, SpJP.

Definition : Heart Failure

DEFINITION OF HEART FAILURE.

1. Symptoms of heart failure

(in cases where the diagnosis is in doubt)

3. Response to treatment directed towards heart

nearly 5 million HF pts.

DESCRIPTIVE TERMS in HEART FAILURE

Mild , Moderate, Severe Heart Failure

New York Heart Association (NYHA)

No limitation : ordinary physical exercise does

ACC/AHA A New Approach To The Classification of HF

Patient who is at high risk for

Hypertension; CAD; DM;

Patient with a structural disorder

Patient with past or current

Dyspnea or fatigue ec LV systolic

Patient with end-stage disease

Frequently hospitalized pts ; pts

ACC/AHA Guidelines for the

Stages in the evolution of HF and recommended therapy by stage

Pts who have

ACC/AHA Guidelines for the

Symptoms not controlled

Diastolic function Systolic function

Block diagram of left ventricular pump performance

The Pathophysiology of Heart Failure

Pathophysiological Sequence of CHF

( ) O2 Delivery (rest and/or exercise)

Perfusion of Vital Organs

Sympathetic nervous system up-regulation

Cesario et.al; Reviews in cardiovascular medicine, vol 3, no.1, 2002

Causes of Heart Failure

Excess Load on Ventricle

Resistance to Flow into Ventricle

MI-INDUCED HEART FAILURE

SYMPTOMS AND SIGN

S3 , Pulmonary Rales , Cardiac Murmur

HAEMATOLOGY & BIOCHEMISTRY

ALGORITHM FOR THE DIAGNOSIS OF THE HF

Assess Presence of Cardiac Disease by ECG, X-Ray

Imaging by Echocardiography (Nuclear

Assess Etiology, Degree, Precipitating

Additional Diagnosis Tests

Correction of aggravating factors

Devices and surgery

ACC/AHA & EUROPE (ESC) 2001

ACC/AHA & EUROPE (ESC) 2001

May be added for symptom relief

Stages in the evolution of HF and recommended therapy by stage

Pts who have

ACC/AHA Guidelines for the

Angiotensin-converting enzyme inhibitors

Should be uptitrated to the dosages shown to be

Due to their chemical structure

Renal artery stenosis

ACE-Inhibitors in Asymptomatic Heart Failure

SAVE & TRACE Study

Guidelines for the diagnosis and treatment of chronic heart failure

ACE-Inhibitors in Symptomatic Heart Failure

Essential for symptomatic treatment when

Always be administered in combination