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Transcript
CHRONIC HEART FAILURE
Pathophysiology
Toni M. Aprami
Department of Cardiology and Vascular Medicine
Cardiovascular Subdivision, Department of Internal Medicine
Hasan Sadikin Hospital/Medical School, Padjadjaran University
Pulmonary
veins
Definition : Heart Failure
“The situation when the heart is incapable of
maintaining a cardiac output adequate to
accommodate metabolic requirements and the
venous return.“ Braunwald’s Heart Disease, 8 Ed, 2008
th
“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
CAUSES OF HEART FAILURE
Myocardial disease
Viral or other infectious agents
Coronary artery disease
Toxic or drug-induced damage
Myocardial infarction*
Disorders of rate and rhythm
Myocardial ischemia*
Chronic bradiarrhythmias
Chronic pressure overload
Chronic tachyarrhythmias
Hypertension*
Pulmonary heart disease
Obstructive valvular disease*
Cor pulmonale
Chronic volume overload
Pulmonary vascular disorders
Regurgitant valvular disease
High-output state
Intracardiac (left-to-right) shunting
Metabolic disorders
Extracardiac shunting
Nonischemic dilated cardiomyopathy
Familial/genetic disorders
Thyrotoxicosis
Nutritional disorders (beriberi)
Excessive blood flow requirements
Infiltrative disorders*
Systemic arteriovenosus shunting
Metabolic disorders*
Chronic anemia
*Indicates conditions that can also lead to HF with a preserved ejection fraction
Block diagram of left ventricular pump performance
PULMONARY VENOUS
PRESSURE
Input
Filling
ED volume
Emptying
x
EFeffective
Stroke
volume
x
Heart
rate
=
LV Distensibility
Relaxation
Left atrium
Mitral valve
Pericardium
Contractility
Afterload
Preload
Structure
Diastolic function
Systolic function
Output
(Little, 2001)
CARDIAC OUTPUT
Lung
SVC
Left
atrium
Pulmonal
vein
Pump
Container
Right
Atrium
Left
ventricle
Systemic
Vascular
Resistance
(SVR)
IVC
Right
ventricle
organ
Volume (blood within
circulatory system)
DETERMINANTS OF VENTRICULAR FUNCTION
CONTRACTILITY
PRELOAD
AFTERLOAD
STROKE
VOLUME
HEART RATE
- Synergistic LV contraction
- LV wall integrity
- Valvular competence
CARDIAC OUTPUT
Determinants of heart rate:
-balance of parasympathetic
and sympathetic tone
-sinus node function
-presence of an ectopic focus
-conduction system
COMPENSATORY MECHANISM
• Frank - Starling mechanism
• Neurohormonal stimulation
• Myocardial hypertrophy with or without chamber
dilatation
Myocardial Failure or Valvular Insufficiency
Reduced cardiac output
Reduced blood pressure
Decreased tissue perfusion
Activation of compensatory mechanisms:
-Sympathetic Nervous System (SNS)
-Frank-Starling Mechanism
-Renin-Angiotensin-System (RAS)
-Aldosterone
-Ventricular hypertrophy
-others… (anti-diuretic hormone, atrial natriuretic factor)
An effort to normalize tissue perfusion and blood pressure
Myocardial Failure or Valvular Insufficiency
Activates Compensatory
Mechanisms
SNS
Anti-diuretic Hormone
RAS
Angiotensin II
Vasoconstriction
Heart Rate
Aldosterone
Sodium and water retention
Increased Venous Return
and Increased Blood Pressure
F-S Mech.
Contractility
Augmentation of cardiac performance
CONCENTRIC HYPERTROPHY
PRESSURE
OVERLOAD
Thickened Ventricular Walls
Altered ventricular geometry
Myocardial
Failure
Valvular Insufficiency
Ischemia and Fibrosis
Elevated
Cardiac Filling Pressures
Diastolic Dysfunction
CONGESTIVE HEART FAILURE
- Myocardial Failure
- Valvular Insufficiency
-Moderate to large
L -> R shunt
VOLUME OVERLOAD
- Thick and Stiff Ventricular Walls
- Abnormal Ventricular Relaxation
- Ventricular Fibrosis
-Pericardial Disease
DIASTOLIC DYSFUNCTION
Elevated Cardiac Filling Pressures
CONGESTIVE HEART FAILURE
MECHANISM OF HEART FAILURE
Pressure
Normal pumping
function
overload
Volume
Compensatory
overload
mechanism
adequate
failed
Heart failure
 Myocardial
contractility
Classical Pathophysiology of HF
Primary
disease
state
Decreased
aortic
pressure
Decreased
cardiac
output
SNS
stimulation
Vasoconstriction
Ventricular
dilatation
Heart
Failure
symptoms
Release of
Renin /
angiotensin
aldosteron
Increased
vascular
volume
Increased
afterload
Increased
Preload
MI-INDUCED HEART FAILURE
Myocardial Damage
Contractility
Pump Performance
 Systolic Work Load
Vasoconstriction
RAAS SYSTEM
FLUID RETENTION
 SAS Drive
EVOLUTION OF CLINICAL STAGES
Normal
No symptoms
Asymptomatic
Normal exercise
LV Dysfunction
Normal LV fxn
No symptoms
Compensated
Normal exercise
CHF
Abnormal LV fxn
No symptoms
Decompensated
 Exercise
CHF
Abnormal LV fxn
Symptoms
Refractory
 Exercise
CHF
Abnormal LV fxn
Symptoms not controlled
with treatment
Stages in the evolution of HF and recommended therapy by stage
Stage A
Pts with :
• Hypertension
• CAD
• DM
• Cardiotoxins
• FHx CM
Stage B
Struct.
Heart
Disease
THERAPY
• Treat Hypertension
• Stop smoking
• Treat lipid
disorders
• Encourage regular
exercise
• Stop alcohol
& drug use
• ACE inhibition
Stage C
Pts with :
• Previous MI
Develop
• LV systolic
dysfunction
Symp.of
• Asymptomatic
HF
Valvular disease
THERAPY
• All measures under
stage A
• ACE inhibitor
• Beta-blockers
Stage D
Pts with :
• Struct. HD
• Shortness of
breath and
fatigue, reduce
exercise tolerance
Refract.
Symp.of
HF at rest
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
ACC/AHA Guidelines for the
Evaluation and Management of Chronic Heart Failure in the Adult 2005
Pregnancy
Arrhythmias (AF)
Endocarditis
Obesity
Infections
Hyperthyroidism
Hypertension
Physical activity
Thromboembolism
Dietary excess
Diagnosis of C H F
IDENTIFICATIONS OF HEART FAILURE PATIENTS
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.2005
SYMPTOMS AND SIGN
 Breathlessness, Ankle Swelling, Fatique
→ Characteristic Symptoms
 Peripheral Oedema, JVP ↑, Hepatomegaly
→ Signs of Congestion of Systemic Veins
 S3  , Pulmonary Rales , Cardiac Murmur 
Physical Examinations of Heart Failure patient
Vital Signs
Abdominal
• Positional blood pressure
• Ascites
• Pulse rate, rhythm, pulse pressure
• Respiratory rate and pattern
• Temperature
• Hepatosplenomegaly
• Pulsatile liver
• Decreased bowel sounds
• Obesity
Neurologic
• Mental status abnormalities
Pulmonary
Cardiovascular
• Rales
• Neck vein distention
• Rhonchi
• Prolonged expiration
• wheezes
• dullness to chest percussion
• Friction rubs
• Abdominal-jugular neck vein reflux
• Cardiomegaly
• Displaced, sustained, or hyperkinetic apical impulse
• Chest wall pulsatile activity (Right ventricular lift)
• Gallop rhythms
• Heart murmurs (especially aortic, mitral, tricuspid,
and pulmonic insufficiency or stenosis murmurs)
• Diminished S1 or S2
• Friction rub
• Peripheral venous insufficiency
Systemic
• Acrocyanosis
• Edema
• Temporal muscle wasting
• Cachexia
CHEST X-RAY
 A Part of Initial Diagnosis of HF
→ Cardiomegaly, Pulmonary Congestion,
pulmonary disease
 In pts CHF, CTR > 0.50 and pulmonary congestion →
indicators of abnormal cardiac func. with ↓ EF
 Relationship Between Radiological Signs and
Haemodynamic Findings may Depend on the
Duration and Severity HF
ECG
A normal ECG suggests that the diagnosis of CHF
should be carefully reviewed
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
Value of electrocardiography* in identifying heart failure
Resulting from left ventricular systolic dysfunction
Sensitivity
Specificity
Positive predictive value
Negative predictive value
94%
61%
35%
98%
*Electrocardiographic abnormalities are defined as atrial fibrillation, evidence of
Previous myocardial infarction, left ventricular hypertrophy, bundle branch block,
and left axis deviation.
HAEMATOLOGY & BIOCHEMISTRY
A Part of Routine Diagnostic
 Hb, Leucocyte, Platelets
 Electrolytes, Creatinine, Glucose, Hepatic Enzyme,
Urinalysis
 TSH, hs-CRP, Uric Acid
ECHOCARDIOGRAPHY
 The Preferred Methods
 Helpful in Determining the Aetiology
 Follow Up of Patients Heart Failure
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)
PULMONARY FUNCTIONS
 A Little Value in Diagnosis Heart Failure
 Usefull in Excluding Respiratory Diseases
EXERCISE TESTING
 Focused on Functional, Treatment
Assessment and Prognostic
STRESS ECHOCARDIOGRAPHY
 For Detecting Ischaemia
 Viability Study
NUCLEAR CARDIOLOGY
 Not Recommended as a Routine Use
CMR
( CARDIAC MAGNETIC RESONANCE IMAGING)
 Recommended if Other Imaging Techniques not
Provided Diagnostic Answer
INVASIVE INVESTIGATION
Elucidating the Cause and Prognostic Informations
– Coronary Angiography :
in CAD’s Patients
– Haemodynamic Monitoring :
To Assess Diagnostic and Treatment of HF
– Endomyocardial Biopsy :
in Patients with Unexplained HF
Terima Kasih