heart conditions inn children

8/6/2019 Heart Conditions Inn Children

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HEART CONDITIONS IN

CHILDREN

noa nyaberi1


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Inntroduction

Results in blood flow (hemodynamic) changes, which eventuallyaffect the heart, bld vessels and other organs.

FETAL CIRCULATION Fetal lungs are non-functional in utero; Fetal O2 depends on

placental circulation. Bld from I.V.C returns to the R.A straight thru the L.A via

foramen ovale. Then to the L.V from where it is pumped mainly to the vessels of

the head & forelimbs. Bld from the S.V.C, mainly deoxygenated, returns to R.V thru

the R.A, then to the pulmonary artery, and eventually to the

aorta via the ductus arteriosus. Only 12% of fetal blood circulates thru the lungs Deoxygenated bld from the aorta circulates to the umbilical

arteries, where it is eventually oxygenated.

I.V.C = Inferior Vena Cava

S.V.C = Superior Vena Cava 2


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CONGENITAL HEART DISEASE

(CHD) Genetic and environmental factors Increased risk in the followings:

Maternal factors

1. diabetes mellitus (DM), phenylketonuria (PKU)2. medication, alcohol or drug use3. infection (e.g. rubella, cytomegalovirus (CMV)) Infant factors

1. prematurity (e.g. patent ductus arteriosus (PDA))2. chromosomal abnormalities (e.g. Down syndrome -

AVSD)3. positive family history (2-4% risk)

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CHDs are described according to the anatomical abNs

Non closure of the foramen ovale

Non closure of the ductus arteriosus

Communication btn the ventricles

Misplacement of the great vessels

Tissue oxygenation may also get compromised after birth.

This is the basis for classification as ACYANOTIC or

CYANOTIC.

NOTE: Even in acyanotic conditions, there may be cyanosis

as one clinical sign.

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A. ACYANOTIC CHD

1.Lft-to-rt shunt lesions

ASD,VSD,PDA,AVC2.Obstructive Lesions

Coarctation of aorta

Aortic stenosisPulmonary stenosis

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1. LEFT TO RIGHT SHUNT

LESIONS extra bld is displaced thru a

communication from the lft to the rt side ofthe heart, resulting in sed pulmonary bld

flow shunt volume dependent upon three

factors: size of defect, pressure gradient btnchambers or vessels, peripheral outflow

resistance untreated shunts can result in pulmonary

vascular disease, right ventricularhypertension (RVH), & revert to R to L shunts

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Atrial Septal Defect (ASD)

An opening btn the Left and Right atria

Of three types

ostium primum ; ostium secundum ;sinus venosus

often asymptomatic in childhood murmur: often grade 2/6-3/6 pulmonic outflow murmur with

widely split and fixed S2

ECG: right axis deviation, mild RVH, Rt bundle branch block.

CXR: increased pulmonary vasculature

natural Hx: 80-100% spontaneous closure rate

if remains patent, CHF & pulm. hypertension can dvp later

Mx: elective surgical or catheter closure btn 2-5 years of age

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Atrial Septal Defect

Unn Figure 25-1 Atrial septal defect

http://www.youtube.com/watch?v=kPfH-

D2O9mA go to 2:18


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Ventricular Septal Defect

(VSD)A communication btn the rt and lft ventricular compartments most common congenital heart defect (30-50%) small VSD (majority) asymptomatic, normal growth and development murmur: early systolic to holosystolic, best heard at left lower sternal border (LLSB) ECG and CXR are normal most close spontaneously without surgical intervention moderate to large VSD cause Lft to Rt shunt thus increasing pulmonary circuln When pulmonary hypertension occurs, the shunt reverses to a rt-to-lft

shunt(Eisenmenger syndrome) delayed growth and development, decreased exercise tolerance, recurrent URTIs or

"asthma" episodes, CHF murmur: holosystolic at LLSB with thrill, mid-diastolic rumble at apex ECG: left ventricular hypertrophy (LVH), left atrial hypertrophy (LAH), RVH CXR: increased pulmonary vasculature, cardiomegaly, CHF natural history: secondary pulmonary hypertension, CHF by 2 months of age management: treatment of CHF; surgical closure

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Patent Ductus Arteriosus(PDA)

Failure of the ductus arteriosus (btn descending aorta & pulmonary artery) to closewithin the 1st wks

Due to great press in the aorta, blood shunts to the pulmonary arteries thusoverloading the LFT atrium. The pulmonary resistance continues to increaese

common in premature infants (1/3 of infants < 1750 grams)

may be asymptomatic or have apneic or bradycardic spells, poor feeding, accessorymuscle use

Associated tachycardia, bounding pulses, hyperactive precordium, wide pulsepressure

murmur: continuous "machinery" murmur, in left infraclavicular area

ECG: may show LVH, RVH

CXR: normal to mildly enlarged heart, increased pulmonary vasculature

diagnosis by echocardiography (ECHO)

natural history: spontaneous closure common in premature infants, less common interm infants

management: indomethacin(a pg inhibitor), surgical ligation, or catheter closure

high risk of SBE, antibiotic prophylaxis required until 6 months after closure

SBE = subacute bacterial endocarditis 10


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Patent Ductus Arteriosus

Unn Figure 25-4 Patent ductus arteriosus


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Endocardial Cushion Defect

(Atrioventricular (AV) Canal)

Endocardial cushions fails to grow, resulting in abnormalitiesin the septa i.e. separation btn atria & ventricles.

Since the endocardial cushion is where the tricuspid & mitralvalves grow, abnormalities in the formation of theatrioventricular valves also present.

commonly associated with Down syndrome natural history depends on size of defect and valvular

involvement may miimic changes seen in ASD or VSD & may result in

enlargement of all cardiac chambers Regurgitation of blood to the atria causing a systolic murmur surgical correction to close septal defects & repair valvular

defects before age 1 yr to prevent pulmonary complications

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Atrioventricular Canal

Defect

Unn Figure 25-3 Atrioventricular canal defect


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2. OBSTRUCTIVE LESIONS

present with pallor, decreased urineoutput, cool extremities and poor pulses

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Coarctation of the Aorta

narrowing of aorta; commonly at the level of the ductus arteriosus causes higher pressures above the site or low press below it few have high BP in infancy (160-200 mmHg systolic) but this

decreases as collaterals develop

if severe, presents with shock in the neonatal period when theductus closes often asymptomatic with upper extremity systolic pressures of 140-

145 mm Hg weak pulses, sed bld pressure in lower extremities, radial-femoral

delay if associated with other lesions (e.g. PDA, VSD), can cause CHF ECG: RVH early in infancy, LVH later in childhood murmur: absent or systolic with late peak at apex, left axilla, left

back management: balloon arterioplasty or surgical correction complications: essential hypertension

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Coarctation of the Aorta*

Unn Figure 25-5 Coarctation of the aorta


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Aortic Stenosis

Narrowing of the aortic valve or aortic outflow tract valvular (75%), subvalvular (20%), supravalvular and idiopathic

hypertrophic subaortic stenosis (IHSS) (5%)

Results in LVH & increaesed left atrial pressure

often asymptomatic but may be associated with CHF,exertional chest pain, syncope or sudden death

murmur: systolic ejection murmur (SEM) at upper rightsternal border (URSB) with aortic ejection click at the

apex management: surgical or balloon valvuloplasty, repeated

interventions and valve replacement may be necessary

SBE prophylaxis and exercise restriction required

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Aortic Stenosis

Unn Figure 25-6 Aortic stenosis


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Pulmonary Stenosis

narrowing of pulmonary outflow tract Thus rt ventricle may hypertrophy & eventually cause Rt atrium

hypertrophy. usually part of other congenital heart lesions (e.g. Tetralogy

of Fallot) or in association with other syndromes (e.g. congenitalrubella, Noonan syndrome)

critical pulmonic stenosis: inadequate pulmonary blood flow,dependent on ductus for oxygenation, progressive hypoxia andcyanosis

presentation varies from asymptomatic to CHF murmur: wide split S2 maximal on expiration, SEM at ULSB,

pulmonary ejection click ECG: RVH CXR: dilated post-stenotic pulmonary artery management: balloon valvuloplasty, surgical valvotomy

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Pulmonic Stenosis*

Unn Figure 25-7 Pulmonic stenosis


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B.CYANOTIC CONGENITAL HEARTDISEASE

systemic venous return re-enters systemiccirculation directly

most prominent feature is cyanosis (O2 sat< 75%) differentiate between cardiac and othercauses of cyanosis with hyperoxic test (if

improvement of PaO2, less likely cardiaccause) survival depends on mixing via shunts (e.g.ASD, VSD, PDA)

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1. LESIONS ASSOCIATED WITH

DECREASED PULMONARY BLOOD FLOW

Tetralogy of Fallot Common cyanotic heart defect beyond infancy consists of four defects

ventricular septal defect (VSD) right ventrical (RV) outflow tract obstruction (RVOTO) overriding aorta right venticular hypertrophy (RVH)

infants may initially have a left to right shuntand therefore are not cyanotic but the RVOTO isprogressive, resulting in increasing right to leftshunting with hypoxemia and cyanosis.

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Tetralogy of Fallot

Unn Figure 25-8 Tetralogy of Fallot


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hypoxic tet spells

primary pathophysiology is hypoxia, leading to increased pulmonary vascularresistance (PVR) and decreased systemic resistance, occurring in exertionalstates (e.g. crying, exercise)

paroxysm of rapid and deep breathing, irritability and crying hyperpnea, increasing cyanosis often leading to deep sleep and decreased

intensity of murmur

peak incidence at 2-4 months of age if severe may lead to seizures, loss of consciousness (LOC), death (rare) management: O2, knee-chest position, fluid bolus, morphine sulfate,

propanolol

murmur: single loud S2 due to severe pulmonic stenosis ECG: right axis deviation, RVH CXR: boot shaped heart, decreased pulmonary vasculature,

right aortic arch management: surgical repair including closure of VSD and

widening of RVOTO

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Knee-chest Position

Child with a cyanotic heart

defect squats (assumes a knee-chest position) to relieve

cyanotic spells. Some times called tet spells. Ball & Bindler

Nurse puts infant in knee-chest

position. Whaley & Wong


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Clubbing of Fingers

Clubbing of Fingers

Whaley & Wong Bowden text


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2. LESIONS ASSOCIATED WITH

INCREASED PULMONARY BLOOD FLOW

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Transposition of the Great

Arteries (TGA)

Pulmonary artery becomes the outflow tract of Lft ventrilce & aorta for thert ventricle.

Bld from the L.V repeatedly circulates into pulmonary circulation. Oxygenatedbld does not reach the systemic circulation.

newborn presents with progressive cyanosis unresponsive to O2 therapy as the

ductus arteriosus closes and mixing between the two circulations diminishes;severe hypoxemia, acidosis, and death can occur rapidly if VSD present, cyanosis is not prominent, infant presents with CHF after a

few weeks of life murmur: none if no VSD ECG: RAD, RVH CXR: egg-shaped heart with narrow mediastinum ("egg on a string") management

prostaglandin E1 (PGE1) infusion to keep ductus open until septotomy or surgery balloon atrial septostomy with catheter surgical correction: arterial switch procedure

infants without VSD must be repaired within 2 weeks to avoid weak LV muscle

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Transposition Of The Great

Arteries, Or Transposition Of The

Great Vessels*

Unn Figure 25-11 Transposition of great vessels


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Hypoplastic Left Heart

Syndrome

a spectrum of hypoplasia of left ventricle, atreticmitral and/or aortic valves,

small ascending aorta, coarctation of the aorta withresultant systemic hypoperfusion

most common cause of death from congenital heartdisease in first month of life presents with circulatory shock and metabolic acidosis

on closure of the ductus management

intubate and correct metabolic acidosis IV infusion of PGE1 to keep ductus open surgical correction (overall survival 50% to late childhood) transplantation palliative

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Hypoplastic Left-Sided Heart

Syndrome

Unn Figure 25-14 Hypoplastic left-sided heart syndrome


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Nursing management of CHD

Goal of nursing care inuncorrected cardiac abN centre

on promoting cardiac output,diminishing respiratorydistress, maintaining fluidbalance, and promoting growth &development.

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ACQUIRED CARDIOVASCULAR

DISORDERSInfectious and InflammatoryCardiac Disorders

Occur after birth & may result from congenital heartdefects or other environmental factors.Include CHF, 10 Hypertension, Rh Heart Disease, &Kawasaki Disease


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CONGESTIVE HEART FAILURE

(CHF)

Etiology congenital heart defects (CHD) ; arteriovenous malformations (AVMs); cardiomyopathy; arrhythmias; acute hypertension; anemia; corpulmonale; myocarditis

Symptoms

infant: feeding difficulties, easy fatiguability, exertionaldyspnea, diaphoresis when sleeping or eating, respiratorydistress, vomiting, lethargy, cyanosis

child: decreased exercise tolerance, fatigue, decreased

appetite, failure to thrive, respiratory distress, syncope,frequent URTIs or "asthma" episodes

orthopnea, paroxysmal nocturnal dyspnea, edema are alluncommon in children

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Physical Findings

4 key features: tachycardia, tachypnea, cardiomegaly,hepatomegaly (2 tachys, 2 megalys) failure to thrive (FTT) respiratory distress, gallop rhythm, wheezing, crackles,

cyanosis, clubbing (with CHD)

alterations in peripheral pulses, four limb bloodpressures dysmorphic features associated with congenital

syndromes Management correction of underlying cause general: sitting up, O2, sodium and water restriction,

increased caloric intake pharmacologic: diuretics, inotropic agents, afterload

reduction

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Acute rheumatic fever

Rheumatic fever is the most commoncause of acquired heart disease inchildren in developing countries.

A complication of pharyngitis (a throatinfection) caused by Streptococcusbacteria; Group A beta haemolytic

Streptococcus

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clinical features of acute

rheumatic fever Develops 23 weeks after a Streptococcal

pharyngitis. Classical features Fever A flitting polyarthritisusually large jts Carditis Eythema marginatum --- A short-lived

erythematous (pink) rash which forms irregularpatterns on the trunk.

Subcutaneous nodulesover the elbows,knuckles,wrists, knees and spine

Chorea

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signs of carditis

Carditis is an inflammation of the heart.The heart muscle, valves andpericardium are involved.

A heart murmur

Tachycardia

An enlarged heart A rubbing noise (friction rub) heard on

auscultation

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clinical diagnosis of acute

rheumatic fever

A Streptococcal infection plus 2 major or 1 majorand 2 minor criteria.

The major criteria are: Flitting polyarthritis Carditis Erythema marginatum Nodules Chorea

The minor criteria are: Fever Arthralgia Blood tests indicating inflammation An abnormal ECG esp a prolonged PR interval

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Treatment

Bed rest

Amoxycillin 10 mg/kg QID P.O X 10/7

Or a single dose of benzathine penicillin1.2 MU IM

Aspirin for symptomatic relief of fever

and joint pain. Observe closely for signs of heart

failure.

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Preventing repeated attacks

of acute rheumatic fever

Benzathine penicillin 1.2 million unitsintramuscularly every 4 weeks (600 000units if the child weighs less than 30kg).

This must be continued until adulthoodwhen it should be reviewed

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INFECTIVE ENDOCARDITIS

Serial +ve cultures are needed for definitive diagnosis,but rely on clinical suspicion and other investigations.

5% of cases are culture ve ---- a risk factor for poorprognosis

Osler's nodes, Janeway's lesions, splinter hemorrhagesare late findings in children antibiotic prophylaxis for prevention is necessary for

all patients with congenital heart disease (except for isolated secundum ASD) rheumatic valve lesions prosthetic heart valves surgical shunts previous endocarditis pacemaker leads

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DYSRHYTHMIAS

Can be transient or

permanent, congenital(structurally normal or

abnormal) or acquired (toxin,infection)

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Sinus Arrhythmia phasic variations with respiration

in almost all normal children Premature Atrial Contractions (PACs) may be normal variant or can be caused by

electrolyte disturbances, hyperthyroidism, cardiac surgery, digitalis toxicity Premature Ventricular Contractions (PVCs) common in adolescents

benign if single, uniform, disappear withexercise, no associated structural lesions if not benign, may degenerate into more severe

dysrhythmias

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Supraventricular Tachycardia (SVT)

most frequent sustained dysrhythmia in children not life-threatening but can lead to symptoms caused by re-entry via accessory connection

(atrioventricular (AV) node most common site) characterized by a rate of greater than 210 bpm

treatment: vagal maneuver, adenosine, digoxin (exceptin Wolfe-Parkinson-White (WPW)) or B-blockers Complete Heart Block congenital heart block can be caused by maternal Rho

antibody formed in mothers with CVD clinical symptoms related to level of block

the lower the block, the greater the symptoms ofinadequate cardiac output (CO)

symptomatic patients need a pacemaker

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heart conditions inn children

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