Pathophysiology of congestive heart failure

PATHOPHYSIOLOGY OF CONGESTIVE HEART FAILURE

OBJECTIVES

Definition Epidemiology Etiology Pathophysiology Clinical manifestations Diagnosis Principle of management

Definition

Heart failure results when cardiac output is insufficent to meet the metabolic demand of the body.

Epidemology

Etiology

The larger burden comes from children born with congenital malformation.

15%-25% of children who have structural defect develop heart failure.

Although cardiomyopathy is rare, approxiamtely 40% of pateints who experince cardiomyopathy develop severe heart failure.

Frank Starling Principle

As the Ventricular End Diastolic volume increases, a healthy heart increases its Cardiac output until maximum is reached.

Pathophysiology

Any condition which brings change in systemic oxygen transport leads to HF.

Systemic Oxygen transport= CO*Systemic Oxygen consumption

CO= SV*HR SV depends on: preload(volume work) afterload(pressure work) contractility

Patho…..

>HR depends on: ANS Temperature Metabolism >Systemic oxygen content

a) Decreased systemic content- anemiab) Increased oxygen demand- hyperventilation,

hyperthyroidism, hyper metabolismc) Arteriovenous fistulas

Patho...

Common causes of heart failure in pediatrics is classified as congenital heart disease or acquired heart disease.

There are some rare miscellaneous causes of HF Heart failure in children can also be categorized

as a result of *excessive preload *excessive afterload *abnormal rhythm *decreased contractility

Congenital heart diseases

The most common cause of heart failure in pediatric age group.

The ighly dependent on age. That results in Excessive preload are: left to right shunt: VSD PDA Valvular Regurgitation: MR AR

Congenital….

that result in Excessive afterload: left side obstruction: AS COA right side obstruction: PS

Congenital…

There are some rare complex congenital heart diseases that result in HF.

single ventricle: hypoplastic left heart syndrome unbalanced AV septal defect systemic right ventricle: TGA

Acquired Heart Diseases

*Cardiomyopathy: dialted CM Hypertrophic CM Restrictive CM( rare) Arrymogenic CM (rare) *Rheumatic valvular diseases results in volume

overload lesions such as MR or AR in older children.

*Rheumatic heart disease can also be a proposing factor for infective endocarditis.

*Myocarditis *Rheumatic carditis (rare)

Miscellaneous causes of HF

Metabolic abnormalities Hyperthyroidism Complete heart block Severe anemia Cor pulmonale Acute systemic hypertension

Cause by age

FETAL Severe anemia (hemolysis, fetal-maternal transfusion,

parvovirus B19–induced anemia, hypoplastic anemia) Supraventricular tachycardia Ventricular tachycardia Complete heart block

PREMATURE NEONATE Fluid overload Patent ductus arteriosus Ventricular septal defect Cor pulmonale (bronchopulmonary dysplasia) Hypertension

PREMATURE NEONATE Fluid overload Patent ductus arteriosus Ventricular septal defect Cor pulmonale (bronchopulmonary

dysplasia) Hypertension

In full term neonate

Left-sided obstructive lesions (coarctation of aorta, hypoplastic left heart syndrome)

Large mixing cardiac defects (single ventricle, truncus arteriosus)

Viral myocarditis

Infants

Left-to-right cardiac shunts (ventricular septal defect)

Metabolic cardiomyopathy Acute hypertension (hemolytic-uremic

syndrome) Supraventricular tachycardia Kawasaki disease Viral myocarditis

Child-Adolescent

Rheumatic fever Acute hypertension (glomerulonephritis) Viral myocarditis Thyrotoxicosis Hemochromatosis-hemosiderosis Cancer therapy (radiation, doxorubicin) Sickle cell anemia Endocarditis Cor pulmonale (cystic fibrosis) Cardiomyopathy (hypertrophic, dilated)

Compensatory mechanisms

It could be at molecular/cellular level or neurohormonal level.

Unmet tissue demands for CO results in activation of RAAS, SNS, Cytokine-induced inflammation & recently appreciated ‘’signaling’’ cascades that triggers Cachexia.

Systematic activation HF

RAAS in HF

Compensatory…

>>>Increased SNS-> Increased cathecolamines: positive inotorpic increase in HR

However, chronic adrenergic stimulation eventually leads to adverse myocardial effects: including increased afterload,

hypermetabolism arrhythmogenesis direct myocardial toxicity>>>increase in renin output, and formation of angiotensin II

Due to decresed blood flow to the kidneys Angiotensin II leads to further increase in reabsorption of both water and

salt from the renal tubules Angiotensin II may cause a trophic response in vascular smooth muscle

(with vasoconstriction) and myocardial hypertrophy However, angiotensin II plays a maladaptive role in CHF by initiating

fibrosis and altering ventricular compliance

Compensatory…

Cardiac remodeling results in increased cardiac mass (maladaptive cardiac hypertrophy). Taken together, these processes produce a poorly contractile and less compliant heart, resulting in increased filling pressures, pulmonary or systemic edema, hypoxia, redistribution of blood flow away from skeletal muscle and the splanchnic circulation, tissue lactic acidosis, and loss of lean body mass (cachexia).

Clinical manifestation

Because HF has multiple causes, it has a variety of age dependent clinical presentations.

* IN INFANTS Tachypnea, feeding difficulties, poor weight gain,

excessive perspiration, irritability, weak cry, noisy, labored respirations with intercostal and

subcostal retractions, as well as flaring of the alae nasi

Hepatomegaly , cardiomegaly , gallop rhythm, underlying cardiac lesion (auscultatory)

Edema may be generalized and usually involves the eyelids as well as the sacrum and less often the legs and feet.

jugular venous pressure in infants may be difficult

In children

similar to those in adults and include : fatigue, effort intolerance, anorexia, abdominal

pain, dyspnea, and cough. abdominal symptoms jugular venous pressure and liver enlargement Orthopnea edema in dependent portions of the body, or

anasarca may be present Cardiomegaly , A gallop rhythm is common; when ventricular dilatation is advanced, the

pansystolic murmur of mitral or tricuspid valve regurgitation may be heard.

Diagnosis

History, PE , investigations History *Poor feeding of recent onset, tachypnea that

worsens during feeding, poor weight gain, and cold sweat on the forehead suggest CHF in infants.

*Older children may complain of shortness of breath, especially with activities, early fatigability, puffy eyelids, or swollen feet.

*History of congenital and acquired heart disease

P/E

Tachypnea Gallop rhythm Weak & thready pulse Cardiomegaly Growth failure perspiration

Diagnostic investigations

CBC: WBC/Differential, Hct, Hgb,ESR Show increased ANP & BNP

CXR: Cardiomegaly increased PBF Venous congestion Pulmonary edema Echocardiogram: Function, caliber, flow and valves ECG: Causes- hypertrophy, arrhythmia Blood culture: IE – 3-5 bottles ASO titer, throat swab culture Electrolyte Cardiac cathterization: underlying causes( inflammatory

disease, infectious process or metabolic disorder) Pulse oximetry: cyanosis

cardiothoracic (CT)=dividing the largest horizontal diameter of the heart (A + B) by the longest internal diameter of the chest (C).

CT ratio = (A + B) ÷ C

Principle of management

The treatment of CHF consists of (1) elimination of the underlying causes, (2) treatment of the precipitating or

contributing causes (e.g., infection, anemia, arrhythmias, fever), and

(3) control of the heart failure state. general measures drug therapy

Treatment of underlying cause or contributing factor

Timely surgical repair of structural anomalies Afterload reduction: ACEIs Angiotensin release blockers Nitrates Preload reduction: Diuretics BNP ( Brain Natriuretic Peptide) Sympthatic inhibition: B blockers BNP Digoxin Cardiac remodeling prevention: Mineralocorticiods Inotrophy: Digoxin

References

Nelson text book of pediatrics 18th edition

Pediatric cardiology May 19, 2013 edition article about Heart

Failure in Infants and Children by American Academy of Pediatrics.

May 19, 2013 edition article about Circulation Heart Failure by American Heart Association.

Thank you!