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

Definition

• HEART FAILURE IS A CLINICAL HEART FAILURE IS A CLINICAL

SYNDROME IN WHICH HEART CANNOT SYNDROME IN WHICH HEART CANNOT

PUMP AT A RATE COMMENSURATE PUMP AT A RATE COMMENSURATE

• WITH REQUIREMENTS OFWITH REQUIREMENTS OF

• TISSUE METABOLISM.TISSUE METABOLISM.

Possible types

Excessive work load on myocardium (pressure and volume loading)

Primary alterations in myocardial performance (inflammatory disease)

Metabolic derangements

Combinations of these

Pathophysiology

HEART IS A PUMP WITH OUTPUT HEART IS A PUMP WITH OUTPUT PROPORTIONAL TO FILLING VOLUME & PROPORTIONAL TO FILLING VOLUME & INVERSELY PROPORTIONAL TO INVERSELY PROPORTIONAL TO RESISTANCE AGAINST WHICH IT PUMPS .RESISTANCE AGAINST WHICH IT PUMPS .

SYSTEMIC OXYGEN TRANSPORT IS SYSTEMIC OXYGEN TRANSPORT IS PRODUCT OF COP AND SYSTEMIC PRODUCT OF COP AND SYSTEMIC OXYGEN CONTENTOXYGEN CONTENT

Cardiac output is determined by...

• PRELOAD

• AFTERLOAD

• CONTRACTILITY

• HEART RATE

Systemic oxygen content is...

•DECREASED IN ANEMIA &

HYPOXIA

•INCREASED IN HYPERMETABOLIC

STATES

General manifestationsPulmonary and systemic venous congestion

Decreased systemic perfusion

Operation of several potentially adaptive mechanisms

increased adrenal activity

fluid retention

ventricular dilatation and hypertrophy

Aetiology

FetusSevere anemia

SVT

Complete heart block

CHD

High output failuers (A-V malformations, teretoma)

AetiologyPreterm

Fluid overload

Bronchopulmonary dysplasis

Full term neonateAsphyxia

AV - malformations

Lt. sided obstructive lesions

TGA

Large shunt diseases

Viral myocarditis

AetiologyInfant or Toddler

Lt to Rt ShuntsAV malformationsMetabolic cardiomyopathyAcute hypertension (hemolytic uremic syndromeSVTKawasaki diseasePost operative repair of CHDs

AetiologyChildren & 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)

Compensatory mechanisms

•SYMPATHETIC STIMULATION

•INCREASED HEART RATE

•INCREASED CONTRACTILITY

•REDISTRIBUTION OF BLOOD DUE TO PERIPHERAL VASOCONSTRICTION

Prolonged sympathetic stimulation may lead to..

INCREASED OXYGEN DEMAND

INCREASED AFTER LOAD

HYPERMETABOLISM

MYOCARDIAL TOXICITY

DECREASED GIT RENAL HEPATIC FLOW

Precipitating Causes of CHF

INFECTIONS

ANEMIA

INFECTIVE ENDOCARDITIS

EXCESSIVE PHYSICAL ACTIVITY

SODIUM OVER LOAD

ARRHYTHMIAS

TYPES OF HEART FAILURE

SYSTOLIC OR DIASTOLICSYSTOLIC OR DIASTOLIC

ACUTE OR CHRONIC

RIGHT OR LEFT

FORWARD OR BACKWARD

HIGH OUTPUT OR LOW OUTPUT

Clinical FeaturesHISTORY

• INFANTS

• POOR FEEDING

• POOR WEIGHT GAIN

• DYSPNOEA WHILE SUCKING

• PERSPIRATION

Clinical FeaturesHISTORY

• OLDER CHILDRE

BREATHLESSNESS

ORTHOPNEOEA

EASY FATIGABILITY

EDEMA

ABDOMINAL PAIN

ANOREXIA

COUGH

PULMONARY VENOUS CONGESTION

TACHYPNEA

DYSPNEA

ORTHOPNEA

COUGH

WHEEZING

SYSTEMIC VENOUS

CONGESTION

• EDEMAHEPATOMEGALYRAISED JVPANOREXIAABDOMINAL PAIN

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

Framingham Criteria for CHF

Major CriteriaPND/ orthopnoea

JVP

Rales

Cardiomegaly

Ac. pul. edema

S3 gallop

CT > 25 sec.

Hepatojugular reflux

Minor CriteriaAnkle 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

DIAGNOSIS

CXR Cardiomegaly

ECGChamber hypertrophy,

arrhythmias, myocarditis

ECHO Detection of actual lesion

Ventricular Function

BNP

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

Management of CHF - Inotorpes

DigoxinInhibits membrane Na+K+ ATPase,

Increases intracellular Ca++, Improves cardiac contractility and myocardial O2 consumption

DopamineReduces myocardial norepinephrine,

direct beta receptor action - increase in systemic BP

Dobutamine Beta 1 agonist, often used with dopamine

AmrinoneNon-sympathomimetic, non-cardiac glycoside with inotropic effect, also -

vasodialatation

Management of CHF - Afterload reducing agents

Hydralazine Arterial vasodialatation

NitroprussideArterial & venous relaxation, reduces

preload also

Captopril/ enalapril

ACE Inhibitors, reduce Angiotensin II production

PrazosinOral alpha adrenergic blocker, arterial & venous dialatation, reduces preload also

Mechanical Counter

pulasationsImproves coronary flow, afterload

Partial Lt. ventriculotomy _ mitral valve

Improves Laplace relationship by less wall tension

DigitalizationPO : 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