DR SARIKA GUPTA (MD,PHD) ASST. PROFESSOR CLINICAL APPROACH & MANAGEMENT OF CHF.

DR SARIKA GUPTA (MD,PHD) ASST. PROFESSOR

CLINICAL APPROACH & MANAGEMENT OF CHF

DEFINITION

A clinical syndromeOccurs when The heart is unable to pump enough blood to the

body to meet its needs The heart is unable to dispose of systemic or

pulmonary return adequately Or a combination of the two

PATHOPHYSIOLOGY

Systemic oxygen transport = cardiac output X systemic oxygen content

Cardiac output = heart rate X stroke volume The primary determinants of stroke volume: afterload (pressure work) preload (volume work) contractility (intrinsic myocardial function)

PATHOPHYSIOLOGY

The heart can be viewed as a pump with an output proportional to its filling volume and inversely proportional to the resistance against which it pumps

PATHOPHYSIOLOGY

As ventricular end-diastolic volume increases, a healthy heart increases cardiac output until a maximum is reached

The increased stroke volume obtained in this manner is due to stretching of myocardial fibers

Resulting in increased wall tension, elevating myocardial oxygen consumption

Cardiac muscle with compromised intrinsic contractility requires a greater degree of dilatation to produce increased stroke volume & does not achieve the same maximal cardiac output as normal myocardium does

PATHOPHYSIOLOGY

Lesion causing increased preload (left-to-right shunt or valvular insufficiency)

Cardiac chamber is already dilated

Little room for further dilatation as a means of augmenting cardiac output

Lesions that result in increased afterload to the ventricle (aortic or pulmonic stenosis, coarctation of the aorta)

decreases cardiac performance

PATHOPHYSIOLOGY

Abnormalities in heart rate: compromise cardiac output

Tachyarrhythmias shorten the diastolic time interval for ventricular filling.

High-output failure: NO basic abnormality in myocardial function Cardiac output is greater than normal Alterations in the oxygen-carrying capacity of

blood (anemia or hypoxemia) & increased oxygen demands (secondary to hyperventilation, hyperthyroidism, or hypermetabolism)

PATHOPHYSIOLOGY

ETIOLOGY

FETAL

Severe anemia (hemolysis, fetal-maternal transfusion, parvovirus B19–induced anemia,

hypoplastic anemia)

Supraventricular tachycardia

Ventricular tachycardia

Complete heart block

Severe Ebstein anomaly or other severe right-sided lesions

Myocarditis

ETIOLOGY

PREMATURE NEONATE

Fluid overload

Patent ductus arteriosus

Ventricular septal defect

Cor pulmonale (bronchopulmonary dysplasia)

Hypertension

Myocarditis

Genetic cardiomyopathy

ETIOLOGY

FULL-TERM NEONATE

Asphyxial cardiomyopathyArteriovenous malformation (vein of Galen,

hepatic)Left-sided obstructive lesions (coarctation of

aorta, hypoplastic left heart syndrome)Large mixing cardiac defects (single ventricle,

truncus arteriosus)Myocarditis

Genetic cardiomyopathy

ETIOLOGY

INFANT-TODDLER

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

Hemangioma (arteriovenous malformation)Anomalous left coronary artery

Genetic or metabolic cardiomyopathyAcute hypertension (hemolytic-uremic syndrome)

Supraventricular tachycardiaKawasaki disease

Myocarditis

ETIOLOGY

CHILD-ADOLESCENT

Rheumatic feverAcute hypertension (glomerulonephritis)

MyocarditisThyrotoxicosis

Hemochromatosis-hemosiderosisCancer therapy (radiation, doxorubicin)

Sickle cell anemiaEndocarditis

Cor pulmonale (ILD, cystic fibrosis)Genetic or metabolic cardiomyopathy

CLINICAL FEATURES

Depend on the degree of the child's cardiac reserve

A critically ill infant or child who has exhausted the compensatory mechanisms- symptomatic at rest

Other patients may be comfortable when quiet but are incapable of increasing cardiac output in response to even mild activity without experiencing significant symptoms

CLINICAL FEATURES

History: Poor feeding, poor weigh gain, tachypnea

(worsening during feeding), cold sweat on the forehead- CHF in infants

Shortness of breath, specially with activities, easy fatigability, puffy eyelids or swollen feet-older children

CLINICAL FEATURES

Examination: Tachycardia, gallop rhythm, weak & thready pulsesGrowth failure, perspiration, cold & wet skinCardiomegaly

TachypneaDyspnea on exertionOrthopneaWheezing & pulmonary crackles

COMPENSATORY RESPONSE

PULMONARY VENOUS CONGESTION

CLINICAL FEATURES

Examination: HepatomegalyPuffy eyelidsDistended neck veins Ankle edema

SYSTEMIC VENOUS CONGESTION

Clinical assessment of jugular venous pressure in infants may be difficult because of the shortness of the neck & the difficulty of observing a relaxed state; palpation of an enlarged liver is a more reliable signEdema may be generalized & involves the eyelids & sacrum & less often the legs and feet

CLINICAL FEATURES

INVESTIGATION

X-RAY Study:

INVESTIGATION

X-RAY Study:

INVESTIGATION

ECG: not helpfulECHO: Standard technique for assessing ventricular functionThe most commonly used parameter in children is

fractional shortening (impaired LV systolic function)

Difference between end-systolic & end-diastolic diameter divided by end-diastolic diameter (N=28%-42%)

Ejection fraction (impaired LV systolic function)Enlargement of ventricular chambersDoppler tissue imaging (impaired LV systolic &

diastolic function)

INVESTIGATION

Magnetic resonance angiographyCardiac catheterization-evaluation of biopsy

specimensDecreased arterial oxygen levels; respiratory or

metabolic acidosisHyponatremia Serum B-type natriuretic peptide (BNP) Cardiac neurohormone released in response to

increased ventricular wall tensionElevated in patients with heart failure due to

systolic dysfunction (cardiomyopathy) Elevated in children with volume overload (left-to-

right shunts such as ventricular septal defect)

MANAGEMENT

PRINCIPAL:Elimination of the underlying causesTreatment of the precipitating or contributing

causes (infection, anemia, arrhythmias, fever)Control of the heart failure state

MANAGEMENT

Control of the heart failure– GENERAL MEASURESBed rest Humidified oxygenAdequate calories & fluid 1. Calorie dense food 2. Frequent small feeding 3. Nasogastric feeding 4. Salt restrictionsPatients with pulmonary edema- positive pressure

ventilation Daily weight measurement in hospitalized children

MANAGEMENT

Control of the heart failure state- Drug therapy Inotropic agentsDiureticsAfterload reducing agents DIURETICS: interfere with reabsorption of water & sodium by

the kidneys results in a reduction in circulating blood volume thereby reduces preload & control pulmonary &

systemic venous congestive symptoms

MANAGEMENT

INOTROPIC AGENTS: Rapidly acting Inotropic agents Dopamine, dobutamine, isoproterenol, epinephrine

& amrinone Additional vasodilator actions Used for critically ill infants with CHF, those with

renal dysfunction & postoperative cardiac patients with CHF

Digoxin

MANAGEMENT

AFTERLOAD REDUCING AGENTS: Arteriolar vasodilator Augments cardiac output by acting primarily on the

arteriolar bed Reduction of afterload HydralazineVenodilators Dilate systemic veins & redistribute blood from the

pulmonary to the systemic circuits Decrease in pulmonary symptoms Nitriglycerine, isosorbide dinitrate

MANAGEMENT

AFTERLOAD REDUCING AGENTS: Mixed vasodilator Act on both arteriolar & venous beds ACE inhibitors, nitroprusside & prazosin ACEIs have additional beneficial effects on cardiac

structure & function that may be independent of their effect on afterload

MANAGEMENT

AFTERLOAD REDUCING AGENTS: Afterload reducers: especially useful in children

with heart failure secondary to cardiomyopathy & in patients with severe mitral or aortic insufficiency

Effective in patients with heart failure caused by left-to-right shunts

Not used in the presence of stenotic lesions of the left ventricular outflow tract because of concern over coronary perfusion

MANAGEMENT

β-ADRENERGIC BLOCKERS: β-Blockers are used for the chronic treatment of

patients with heart failure who were symptomatic despite being treated with standard anticongestive drugs

MANAGEMENT

MANAGEMENT