1. Heart Failure
- C.S.N.Vittal

2. Definition
• HEART FAILURE IS A CLINICALHEART FAILURE IS A CLINICAL
SYNDROME IN WHICH HEART CANNOTSYNDROME IN WHICH HEART CANNOT
PUMP AT A RATE COMMENSURATEPUMP AT A RATE COMMENSURATE
• WITH REQUIREMENTS OFWITH REQUIREMENTS OF
• TISSUE METABOLISM.TISSUE METABOLISM.

3. Possible types
Excessive work load on myocardium
(pressure and volume loading)
Primary alterations in myocardial
performance (inflammatory disease)
Metabolic derangements
Combinations of these

4. Pathophysiology
HEART IS A PUMP WITH OUTPUTHEART IS A PUMP WITH OUTPUT
PROPORTIONAL TO FILLING VOLUME &PROPORTIONAL TO FILLING VOLUME &
INVERSELY PROPORTIONAL TOINVERSELY PROPORTIONAL TO
RESISTANCE AGAINST WHICH IT PUMPS .RESISTANCE AGAINST WHICH IT PUMPS .
SYSTEMIC OXYGEN TRANSPORT ISSYSTEMIC OXYGEN TRANSPORT IS
PRODUCT OF COP AND SYSTEMIC OXYGENPRODUCT OF COP AND SYSTEMIC OXYGEN
CONTENTCONTENT

5. Cardiac output is determined by...
• PRELOAD
• AFTERLOAD
• CONTRACTILITY
• HEART RATE
Systemic oxygen content is...
•DECREASED IN ANEMIA &
HYPOXIA
•INCREASED IN HYPERMETABOLIC
STATES

6. General manifestations
Pulmonary and systemic venous congestion
Decreased systemic perfusion
Operation of several potentially adaptive
mechanisms
increased adrenal activity
fluid retention
ventricular dilatation and hypertrophy

7. Aetiology
Fetus
Severe anemia
SVT
Complete heart block
CHD
High output failuers (A-V malformations,
teretoma)

8. Aetiology
Preterm
Fluid overload
Bronchopulmonary dysplasis
Full term neonate
Asphyxia
AV - malformations
Lt. sided obstructive lesions
TGA
Large shunt diseases
Viral myocarditis

9. Aetiology
Infant or Toddler
Lt to Rt Shunts
AV malformations
Metabolic cardiomyopathy
Acute hypertension (hemolytic
uremic syndrome
SVT
Kawasaki disease
Post operative repair of CHDs

10. Aetiology
Children & Adolescents
Rheumatic fever
Acute hypertension ( glomerulonephritis)
Viral myocarditis
Thyrotoxicosis
Anemias Eg. Sickle cell disease
Infective Endocarditis
Cor pulmonale ( cystic fibrosis)
Cardiomyopathy
Cancer therapy (radiation, adriamycin)

11. Compensatory mechanisms
•SYMPATHETIC STIMULATION
•INCREASED HEART RATE
•INCREASED CONTRACTILITY
•REDISTRIBUTION OF BLOOD
DUE TO PERIPHERAL
VASOCONSTRICTION

12. Prolonged sympathetic
stimulation may lead to..
INCREASED OXYGEN DEMAND
INCREASED AFTER LOAD
HYPERMETABOLISM
MYOCARDIAL TOXICITY
DECREASED GIT RENAL HEPATIC
FLOW

13. Precipitating Causes of
CHF
INFECTIONS
ANEMIA
INFECTIVE ENDOCARDITIS
EXCESSIVE PHYSICAL ACTIVITY
SODIUM OVER LOAD
ARRHYTHMIAS

14. TYPES OF HEART FAILURE
SYSTOLIC OR DIASTOLICSYSTOLIC OR DIASTOLIC
ACUTE OR CHRONIC
RIGHT OR LEFT
FORWARD OR BACKWARD
HIGH OUTPUT OR LOW
OUTPUT

15. Clinical Features
HISTORY
• INFANTS
• POOR FEEDING
• POOR WEIGHT GAIN
• DYSPNOEA WHILE
SUCKING
• PERSPIRATION

16. Clinical Features
HISTORY
• OLDER CHILDRE
BREATHLESSNESS
ORTHOPNEOEA
EASY FATIGABILITY
EDEMA
ABDOMINAL PAIN
ANOREXIA
COUGH

17. PULMONARY
VENOUS
CONGESTION
TACHYPNEA
DYSPNEA
ORTHOPNEA
COUGH
WHEEZING
SYSTEMIC
VENOUS
CONGESTION
• EDEMAHEPAT
OMEGALYRAIS
ED
JVPANOREXI
AABDOMINAL
PAIN

18. Clinical Signs of CHF
Cardiomegaly
Gallop sounds
Coarse rales in the lung bases
Sputum frothy and blood tinged
Hydrothorax
Hepatojugular reflux (Pasteur-Randot
reflux)
Ascites

19. Framingham Criteria for CHF
Major Criteria
PND/ orthopnoea
JVP
Rales
Cardiomegaly
Ac. pul. edema
S3 gallop
CT > 25 sec.
Hepatojugular reflux
Minor Criteria
Ankle edema
Night cough
Dyspnoea on exertion
Hepatomegaly
Pleural effusion
Vital capacity  to 1/3 max.
Tachycardia( > 120/m)
Major or Minor : Wt. loss > 4.5 kg in 5 days with treatment
Diagnosis of CHF : 2 major OR 1 major + 2 minor

20. DIAGNOSIS
CXR Cardiomegaly
ECG
Chamber hypertrophy, arrhythmias,
myocarditis
ECHO Detection of actual lesion
Ventricular
Function
BNP

21. Management of CHF - General
Rest Reduces COP
Oxygen Improves oxygenation in pulm. edema
Na and Fluid
restriction
Decreases vascular congestion and preload
Diuretics -
frusemide
Reduces preload, vasodialatation
Combination
DCT diuretic
Better salt excretion

22. Management of CHF -
Inotorpes
Digoxin
Inhibits membrane Na+K+ ATPase,
Increases intracellular Ca++, Improves cardiac
contractility and myocardial O2 consumption
Dopamine
Reduces myocardial norepinephrine,
direct beta receptor action - increase in systemic
BP
Dobutamine Beta 1 agonist, often used with dopamine
Amrinone
Non-sympathomimetic, non-cardiac glycoside with
inotropic effect, also - vasodialatation

23. Management of CHF - Afterload reducing agents
Hydralazine Arterial vasodialatation
Nitroprusside Arterial & venous relaxation, reduces preload also
Captopril/
enalapril
ACE Inhibitors, reduce Angiotensin II
production
Prazosin
Oral alpha adrenergic blocker, arterial & venous
dialatation, reduces preload also
Mechanical
Counter
pulasations
Improves coronary flow, afterload
Partial Lt.
ventriculotomy _
mitral valve
Improves Laplace relationship by less wall
tension

24. Digitalization
PO : Half initially followed by 1/4th
every 8 - 12 hrs X 2
Dose:
Preterm : 20 microG/kg
Term neonate: 2-=30 mcg/kg
Adolescent : 0.5 - 1.0 mg in div doses
IV : 75% of oral dose