Slide 1

Cardiovascular system and its disorder in children

Presented by:-Prerna sharmaM.Sc Nursing,3rd SemesterIntroductionThe circulatory system is composed of the heart and blood vessels, including arteries, veins, and capillaries. Our bodies actually have two circulatory systems: Thepulmonarycirculation is a short loop from the heart to the lungs and back again, and thesystemiccirculation(the system we usually think of as our circulatory system) sends blood from the heart to all the other parts of our bodies and back again.

The Heart

The heart is the key organ in the circulatory system. As a hollow, muscular pump, its main function is to propel blood throughout the body. It usually beats from 60 to 100 times per minute, but can go much faster when it needs to. It beats about 100,000 times a day, more than 30 million times per year, and about 2.5 billion times in a 70-year lifetime.

anatomyThe upper part of the heart is made up of the other two chambers of the heart, called therightandleft atria(pronounced: AY-tree-uh). The right and left atria receive the blood entering the heart. A wall called theinteratrial(pronounced: in-tur-AY-tree-ul)septumdivides the atria, and they're separated from the ventricles by theatrioventricular(pronounced: AY-tree-oh-ven-TRIK-yoo-lur)valves. Thetricuspid valveseparates the right atrium from the right ventricle, and themitral(pronounced: MY-trul)valveseparates the left atrium and the left ventricle.

ContdTwo other heart valves separate the ventricles and the large blood vessels that carry blood leaving the heart. These valves are called thepulmonic valve, which separates the right ventricle from thepulmonary arteryleading to the lungs, and theaortic valve, which separates the left ventricle from theaorta, the body's largest blood vessel.

Congenital heart disease

It is a structural malformation of heart or great vessel present at birth which may not be detected at the time of birth; CHD may represent an isolated heart disease or a combination of defect.

Etiology:-

It results either from abnormal embryonic development or persistence of fetal sturucture beyond the time of normal involution.A fetal and maternal infection occurring first trimester:-Rubella infectionTeratogenic effect of drugAlcohol taken during pregnancyMaternal dietary deficiencyGenetic defect(trisomes e.g. down syndrome)Maternal anomalies.

Classification of common congenital heart disease

Acyanotic heart disease:-

Left to right shuntObstructive lesionsVentricular septal defect(VSD)Aortic valvular stenosis(AVS)Arterial septal defect(ASD)Pulmonary stenosis(PS)Patent ductus arteriosis(PDA)Co-arcation of aortaCyanotic heart disease

Decreased pulmonary blood flowIncreased pulmonary blood flowTetrology of fallot(TOF)Transposition of great vesselsTricuspid atresiaTotal anomalous pulmonary venous connectionAcyanotic heart disease:- Left to right shunt

The three common left to right shunt are VSD,ASD AND PDA. VSD and PDA present in infancy while ASD present in later childhood. These lesions are present and characterized by:Absence of cyanosisRecurrent respiratory infectionCongestive heart failureCardiomegalyIncreased risk of infective endocarditis

Ventricular septal defect(VSD)

An abnormal opening in the septum between the right and left ventricle found in 25% of all congenital heart defects. It may vary in size from very small defect either the membraneous and vascular portion of the ventricle system90% are Located in the membraneous part of the ventricular septum with variable extension into the muscular septum.

Hemodynamics:-

The pressure in left ventricle is greater in right ventricle this promotes the flow of oxygenated blood from the left ventricle to this right ventricle shunt. This results in increased right ventricular pressure and increased blood flow in right ventricle.The flow of blood from left ventricle to right ventricles starts early in systole.When the defect is restrictive, a high pressure gradient is maintained between the two ventricles throughout the systole.The murmur starts early masking the first sound and continues throughout the systole with almost the same intensity appearing a pansystolic murmur on auscultation. As a thrill.Pulmonary artery and lungs as the disease progress long standing pulmonary arterial hypertension may result in increased pulmonary resistance.These results in diminished blood flow to the blood flow through the pulmonary artery and veins and markedly in this right ventricle pressure there by the right ventricle. Pressure raised by left ventricle pressure.[ventricular pressure lower than aortic pressure].The increased blood volume in left atrium may result in left atrial enlargement.passing through a normal mitral valve results in delayed diastolic murmur at the apex.ContdSince left ventricle has two outlets, the aortic valve allowing forward flow and the VSD result in backward leak, since the ejection into the right ventricle and pulmonary artery is increased because of left to right shunt.At this stage, the direction of shunt is reversed to right to left shunt. Cyanosis appears due to mixing and hypoxaemia. This condition results in eisenmenger complex. This indicates poor prognosis.

Fig 2 comparison of normal heart and VSDClinical manifestation

Small VSD usually closes spontaneously but higher VSD develop symptoms at 2-3 months of age. Premature babies with VSD can become symptomatic even earlier. i.e.PalpitationFrequent chest infectionHyperkinetic with a systolic thrill at left sterna border.Heart size is moderately enlarged with a left ventricular type apex.Murmur{the first and second sound is marked by pansystolic murmur which may be heard by left sterna border and third sound may be heard at apex of heart}Initially in ECG right ventricular hypertrophy is diagnosed. Weight gainFailure to thriveTachycardiaTachypneaFeeding problemsExsertional dyspneaSeating excessiveChild is pallor and suffers from respiratory tract syndrome.

Complication

Pulmonary artery hypertension or aortic regurgitation due to prolapsed of the right coronary or non coronary cusp of aortic valveInfective endocarditis.Pulmonary stenosis due to hypertrophy of right ventricular infundibulum.

Diagnostic evaluation

Diagnosis is confirmed by cardiac catheterization- an abnormal communication between ventricles and again increased blood oxygenation and pressure in right ventricle.Echocardiography shows increased left atrial and ventricular size as well as exaggerated mitral motion.Infundibulus stenosis.Chest Xray ranges from normal to cardiomegaly with associated pulmonary artery enlargement and increased pulmonary vascular marking.ECG is normal or show biventricular hypertrophy.On auscultation pansystolic murmur heart beat at the lower sternum (4th intercostals space)

Management

If it is small defect symptomatic treatment is conservative because spontaneously closure occurs between 1-2 yrs of age.If it is larger medical management is done.Medical management

Administration of diuretic and digoxinControl of anemia and infectionIf not treated by medical management; open heart surgery and cardio pulmonary bypass.Small systemic defect is closed with a purse string suture while larger defect needs a knitted dacroam patch swing over a opening. Surgery is contraindicated in patient with eisenmenger complex.After surgery heart size returns to normal and murmur and thrill disappear.

Surgical management

Surgery is indicated if:-Congestive cardiac failure occurs in infancyLeft to right shunt is large.If there is associated pulmonary stenosis, pulmonary atrerial hypertension or aortic regurgitation

Fig 3 surgical managementOperative treatment

Consists in closure of VSD with the use of a patch.the operation is performed through the right atrium. Surgery can be done as early as diagnosed and also if medical management is not helpful.Catheter closure of VSD is best suited for muscular defects in relatively older children.Device closure is also a new technique for VSD closure but require expertise.Complication os surgery:-complete heart block,bifascicular block and residual VSD.

Arterial septum defect

ASD is an abnormal opening between the septum of left and right atrium. ASD accounts for 10% of congenital defect.

Fig 4 Normal V/S Atrial Septum DefectTypes

Ostium secundium typeASD:-The defect is located at the center of the atrial septum the site of foramen ovale.Ostium primumASD:-There is a large gap at the base of atrial septum and associated with deformity of mitral and tricuspid valve or a small or high VSD.Fossa ovalis ASD-They are located in the central portion of atrial septum, in the position of foramen ovale. These defects are amenable to closure in catheterization in laboratory.Sinus venosusASD-They are located at junction of superior vena cava and right atrium. These defects do not have a superior margin because superior vena cava straddles the defect.these defect is associated with anomalous drainage of one or more right pulmonary veins.Coronary sinus ASD-An unroofed coronary sinus is a rare communication between the coronary sinus and left atrium, which produces feature same as of other types ASD.

Hemodynamics

The pressure in left atrium is greater than the right atrium and promotes the flow of oxygenated blood from left to right atrium.Left to right shunt increased blood flows from the right atrium to right ventricle resulting in volume overload of right ventricle and its dilation.Overload of right ventricle results in prolong time required for emptying due to which hang out interval result and low resistance in pulmonary circulation occur.As a result blood flow increase in the pulmonary circulation but pulmonary hypertension is rare complication.

Fig 5 Hemodynamics in ASDClinical manifestation

ASD generally asymptomatic even when defected is large.Recurrent pneumonitis, mild activity intolerance and recurrent.Chest infection, cardiac enlargement is mild to moderate.

Diagnostic evaluation

On auscultation first sound , s2 is quietly splitChest X-ray reveal enlargement of pulmonary artery, right arterial and right ventricular enlargement and increase in vascular marking of lung and a relatively small aortic shadow and plethoric lung fields.ECG shows right ventricular volume overload.Cardiac catheterization shows defect in arterial septum, higher pressure on right side of chest.Echocardiogram shows increased size of right ventricle with paradoxical ventricular septal motion.

Management

Spontaneous closure occurs in patient with small ASD i.e. less than 6mm.Open heart surgery done in affected child before going to school even no symptoms present.For small purse string closure done by stitching around opening and pulling it closes.If surgery not done during childhood pulmonary hypertension, cardiac failure, arterial arrhythmia make operation more dangerous in adultIf defect is larger a knitted clacron patch is used to occult the aperature.

Fig 6 atrial septal defect closure using an expanding device.Patent Ductus Arteriosis(PDA)

PDA is the persistence of a fetal connection between pulmonary artery and aorta resulting in a left to right shunt. More common in females than males.

Fig 7 normal v/s PDAHemodynamics

During fetal life the ductus arteriosis allow most of the ventricular blood to bypass by non direction lung by direct in blood from pulmonary artery to aiota.After birth with the initiation of respiration the ductus arteriosis is no longer needed.It should functionally closed within several hrs after birth (24-72hrs) and anatomically within several days after birth.Degenerative changes occur in ductus arteriosis and it cause become fibrous connective tissue(ligamentum arteriosis)If ductus arteriosis remain patent, oxygenated blood from the higher systemic cercube flows to the lower pressure pulmonary cercube flow through PDA.This cause left to right shunt.{in premature infants ductus arteriosis may remain open because of lower oxygen level resulting from respiratory distress after birth}*Because of transfer of blood from aiota to pulmonary artery through the ductus systemic flow is compromised. The volume blood that the heart must pump meet demands of the peripheral tissue is increased. On the other side a greater volume burden is placed on the lungs and hence on the left side of the heart.

Fig 7 Normal V/S Abnormal CirculationClinical manifestation

Children may develop symptoms around 6-12 wks of life.Older children present effort intolerance, easy fatiguability, dyspnea on exertionIncrease respiratory infectionFrequent chest infectionHeart rate per over 150/mt, gallop rhythm due to rapid filling of ventricle.Large defect may be associated with congestive heart failure and pulmonary hypertension.Pulse is high volume and bounding pulse pressure is wide.

Assessment of severity

Larger the heart size the larger the left to right shunt.Absence of third sound and delayed diastolic murmur indicates small left to right shunt.Presence of third sound indicate moderate left to right shunt whereas an audible delayed diastolic murmur suggest a large left to right shunt.Wider the pulse pressure larger the shunt.

Diagnostic evaluation

Chest Xray reveals cardiomegaly and left ventricle enlargement.Aorta is prominent, lung feels plethoricEasy to reveal left ventricular hypertrophy.On auscultation continuous murmur is felt on the left intraclavicular area.A thrill may be palpable.Echocardiography shows atrial enlargement. Ascending aorta and aortic knuckle are prominent.

Fig 8 Abnormal Blood FlowDifferential diagnosis

Coronary arteriovenous fistulaRuptured sinus of valsalva fistulae into right sideSystemic arteriovenous fistula over the chest.Pulmonary arterialvenous fistulaBronchial collateral murmur

Management

Medical management:-Indomethazine or ibuprofen may be used to close the ductus in small new born preterm newborn; if diagnosis is made within 2 wks of life.Indomethzine causes inhibition of prostaglandin synthesis 12-18 hrs after medication, improvement in left or right shunt.Dose is 0.2 mg/l kg/dose, orally, every 12-24 hr for three doses(second and third dose is at 0.1 mg/kg/dose for 7 days old)Side effect of indomethazine:- it reduces amount of albumin bound serum bilirubin and may develop hyperbilirubinemia also a danger of transient and hyponetremia.

Surgical management

Consist of ligation of PDA, now a days device coil closure of PDA is possible without need of surgery in children more than 5 kg.Note: - since the right to left shunt through the PDA flows down the descending aorta, cyanosis is present in toes but not in fingers. This is called differential cyanosis and is a characteristic of PDA with pulmonary arterial hypertension and right to left shunt.

Fig 8 surgical repair of PDAObstructive lesions

These lesions are also acyanoti heart disease which may be right sided (pulmonary stenosis) or left sided (aiortic stenosis), co-arcation of stenosis.

Aiortic stenosis

There is obstruction to the left ventricle outflow tract at the level of aiortic valve.This is the most common form of aiortic stenosis. Other being hypertrophic subvascular stenosis, supravascular stenosis.

Fig 9 aortic valve stenosisHemodynamics

Valve obstruction is overcome by raising the systolic pressure of the left ventricle. This cause hypertrophy of left ventricle.Ventricular hypertrophy cause rise in left ventricular diastolic pressure.Blood flows from the left ventricle to the obstructed aortic valves into the aorta. This results in increased left ventricular pressure to overcome the resistance offered by obstructed valve.Myocardial ischemia may occur in late stages as a result of the hypertrophied left ventricle and the amount of oxygen that can be supplied to the myocardium.Left ventricle may fail resulting in pulmonary edema.The disorder rarely presence in neonatal period or during evidence with evidence of decreased cardiac output like fainting, peripheral pulses, pallor, cool skin.In older children it present as chest pain, dyspnea, syncope attack, exercise intolerance.Complication include:- congestive heart failure and bacterial endocarditis

Fig 10 pathophysiology of aortic stenosisClinical features

Dyspnea on exertionMay have history of angina on effort and syncope.Cardiac size is normal unless left ventricular failure is present.Systolic thrill may be palpable at the second right interspace, suprasternal notch and carotid arteries.

Diagnosis

Pulse is low in volume and there is thrill in the super sterna notch.Chest X-ray detects dilating ascending aorta and varying degree of left ventricular enlargement.ECG reveals normal and left ventricular hypertrophy.

Management

If heart failure occurs in infancy management is carried out by surgical intervention.Surgical management consist of balloon dilatation, aiotic valvotomy or aiortic valve replacement.[valvotomy is done to divide the fused cusps if the stenosis is at the valvular level, supravalvular or subaiortic stenosis is corrected through the excision of the obstructive tissue.]

Pulmonary stenosis

There is an obstruction to flow of blood from right ventricle to lungs. It accounts for 8% of congenital heart defect.90% of the obstruction occurs at the level of pulmonary valve other outside subvavlvular and supravalvular pulmonary stenosis.

Contd..Infundibular stenosis,there is a muscular or fibrous stenosis, valvular stenosis caused by the failure of involution. This obstruction may close to pulmonary artery or venoid. If pressure from other valvular or infundibular obstruction greatly increased blood back up in the left atrium resulting present foramen ovale in neonate allow blood to be shunted in left atrium.If the right ventricle cannot eject necessary amount of venous blood in pulmonary circulation, systemic if patent ductus arteriosus. Pressure blood shunted in aiota to pulmonary artery and then lungs partially compensating with obstruction with severe defect persistence is to return of blood to heart and congestive heart failure.

Fig 12 Normal Heart V/S Pulmonary StenosisContd..Infundibular stenosis can be distinguished from pulmonary stenosis by:-absence of clickabsence of post stenotic dilatationRelatively lower point of maximum intensity of systolic murmur in 3-4 th left interspaceHemodynamics

Blood flows from the right ventricle through obstructive pulmonary valve into right ventricle pressure increases to maintain normal cardiac output and right ventricular hypertrophy occurs in several cases.Right sided ventricular failure occurs in severe cases.

Clinical manifestation

Child is generally asymptomatic.Poor exercise tolerance; child become fatigue with exertional dysphagia, precordial pain.Presence of murmur in mild stenosis, cyanosis and cardiac failure may occur with the severe defect with severe symptoms of severe stenosis.Complication-anoxic spell in infant, bacterial endocarditis, congestive heart failure and sudden death.

Fig 13 Complication of Pulmonary StenosisDiagnostic evaluation

Auscultation reveals systolic ejection, murmur over pulmonary area.Chest X-ray reveals enlargement of ventricle and main pulmonary artery.ECG shows right ventricular hypertrophy.

Management

Pre congestive heart failure is present, surgery is done like valvotomy, ballon dilatation of pulmonary obstruction.Open heart surgery is needed because right ventricle centred to reach this structure.If obstruction at ventricular level leaflet of valve are separated by incision at fused commisure.If stenosis is infundibular , resection of excess muscular fibrous tissue is done, if there is ASD it is closed.Balloon pulmonary valvuloplasty is the treatment of choice for isolated valvar pulmonary stenosis.

Coarctation of aorta.

It is a narrowing or constriction of aiorta at any point most commonly the constriction is located distal to origin of the left subclavin artery in the vignity of the ductus arteriosis.

Fig 14 Coarctation of AortaHemodynamics

In fetal life the portion of the aorta distal to the left subclavian and before the portion where the ductus arteriosus join is called Isthmus. At birth, isthmus is the narrowest part of the aorta.Following closure of ductus arteriosus, the descending aorta must receive its total supply from left ventricle via ascending aorta.The exact mechanism for the production of systemic hypertension in coarcation is not known.The narrowing of aorta obstructs the blood flow through constricted segment of aorta thus increasing left ventricle pressure and work load.Collateral vessel develops arise in chiefly between the branches of subclavin and intercostals artery by passing the coarcation segment of aorta and subclavin circulation to the lower extremity.Palpable collaterals are also felt at medial and inferior angel of scapula.Because of the decompression of the upper segment by collaterals, the resting blood pressure in upper extremity may even be normal, but rises on exercise.

Clinical manifestation

Children are usually asymptomatic in early year. Growth and development is normal.Sometime they develop occasional fatigue, headache,dizziness, nose bleeding and leg cramps.Femoral pulse absent or greatly reduces. Carotid pulse is bounding, Blood Pressure reduce hypertension in upper extremity and diminished in lower extremity.

Contd.Severe lesions present in infancy with symptoms of poor feeding growth failure, tachypnea, peripheral edema, acidosis, low cardiac output and severe congestive heart failure.Claudication, pain and weakness of legs and dyspnea on running.Systolic thrill may be palpable in suprasternal notch.

Fig 15 clinical symptom of coarctation of aortaDiagnostic evaluation

Reversal of normal blood pressure determination in arms and legs.Chest X-ray shows a prominent aorta, rib notching is common, findings in children older than 6 years.ECG shows varying degree of ventricular hypertrophy.st and t waves changing below the age of 15 yrs suggest additional aortic stenosis.

Management

Either surgical or non surgical ballon dilatation or stunting of coarcation depends on age.Control of congestive heart failure by an appropriate drug.Removal of narrowed portion of aorta with anastomosis at the end.Prostaglandlin E1 is used to maintain a ductal patency prior to surgery in first few weaks of life.In some cases the graft of transplanted aorta is inserted.Age 3-6yrs of age if child condition promotes, not during infancy.

Fig 16 anastomosisCyanotic heart disease

Right to left shunt is in two groups:-

Decreased pulmonary blood flow:-Tetralogy of fallot(TOF)Tricuspid atresia

Increased pulmonary blood flow:-Transposition of great vesselTotal anomalous pulmonary venous return.

Tetralogy of fallot

It account for 6-10% congenital heart disease and consist of four abnormality:-Pulmonary stenosisVentricular septum defectOverriding of aorta(dextra position of aorta)Right ventricular hypertrophy.

Fig 17 Tetralogy Of FallotHemodynamics

Due to pulmonary stenosis there is obstruction of blood flow from the right ventricle to pulmonary artery. Pressure thus rises in the right ventricle increases. So as to become equal to the ventricle. Deoxygenated blood is shunted from right ventricle through the VSD to left ventricle directly into aorta (right to left shunt)

Fig 17 Hemodynamic Of TOFClinical manifestation

Clinical features depends upon primarily on degree of pulmonary stenosis and right ventricle outflow obstruction(many infant with this defect are not cyanosed at birth they develop cyanosis as stenosis become relatively more severly)Cyanosis initially observed while crying and only on exertion then later even at rest.In some children infundubular stenosis may be minimal, so that cyanosis never develop pink tetrology

Contd..Hypercyanotic spells(hypoxic or anoxic spell)- It is characterized by episodes of intend cyanosis that occur predominantly in morning after awakening from sleeping, during or after defecation during or immediately following feeding. Child start crying,get cyanosed and may have convulsionor become unconsciousness.Cyanosis can be seen in mucous membrane, lips, mouth, pharynx and toe nail.

Fig 18 Child with CyanosisContdClubbing of fingers, toe nails occur by 2-4 yr of age.Exercise cause severe dyspnea.Infant take knee chest position rather than expanding their extremities when they lie down.Child assumes squatting position to increase pulmonary blood flow squatting act by increasing systemic resistance and defecating blood flow to relatively low resistance pulmonary circuit.Infant becomes cyanotic and gasp for breath, convulsion or hemeparesis even death may present.Slow weight gain, failure to thrive, associated with dyspnea on exertion.

ContdShort episodes of unconsciousness followed by sleep may persist.Murmur shortens and cyanosis increased with increasing severity of right ventricular outflow tract obstruction.

Complication

Infective endocarditisCerebrovascular accidentsParadoxical embolismAnoxic infarction due to anoxic spell.Brain abscess-Polychythemia develops because of body attempts to compensate for unoxygenated blood. The resulting increase viscosity of the blood causes slowing of the circulation and possibly thrombophlebitis, embolism and cerebrovascular defect may occur.

Diagnostic evaluation

Cyanosis, clubbing, polychythemiaChest X ray reveals heart size is normal and shape like shoe(boot shaped heart)Pulmonary segment appear small and concave.Lung margin is diminishedECG reveals right axis deviation and left ventricular hypertrophy.Lab investigation shows degree of polychythemia, arterial oxygen desaturation.Medical management

Child should be treated for cyanosis and hypoxic spell.Oral B-blocker helps to prevent cyanotic spells. Maximally tolerated dose of propranol ranging from 0.5-1.5 mg/kg/dose should be administered.Treat for dehydration and anemia.Iron supplementation.Treatment for congestive heart failure vigorously.Surgical management

Palliative shunt this is used to infant who cannot undergo primary repair. In this palliative procedure to increase pulmonary blood flow and increased oxygen saturation may be performed.The types of surgery depend upon condition nof child and on the severity of right ventricular outflow obstruction.

blalock tausing shuntPreferred procedure is blalock tausing or modified blalock tausing shunt.Artificial ductus is created by anastomosis of branch of aorta(subclavian artery) to pulmonary artery. This shunt provide blood flow to the pulmonary artery from the left to right subclavian artery.A side to side anastomosis of presenting aorta and right pulmonary artery in neonate(water stent shunt)

Fig 19 patch repairContd..Anastomosis of upper descending aorta and left pulmonary artery(potts procedure):-The particular blood vessel i.e. used to create a systemic pulmonary anastomosis depends on the childs size because one i.e too large may result in congestive heart failure.

Fig 20 AnstomosisContdMustard procedure is definitive repair by arterial switch operation or by redirecting blood flow.Complete repair(elective surgery); it includes closure of VSD and resection of infundibular stenosis with a pericardial patch to enlarge the right ventricular outflow tract. The procedure requires a medial sternotomy and a use of cardio pulmonary bypass.Corrective surgery at an early stage prevent children from continuing to be crippled by defect even after previous surgery has been a success.

Tricuspid atresia

Failure of tricuspid valve to develop, so that there is no communication from right atrium to right ventricle.In this condition blood flows through on ASD or a patent foramen ovale, to the left side of the heart and through a VSD to the right ventricle and out to lungs.It is associated with pulmonary stenosis and transposition of great artery.There is complete mixing of unoxygentaed and oxygenated blood in left side of heart resulting in systemic desaturation and pulmonary obstruction which result in decreased pulmonary blood flow.

Fig 21 Normal Heart V/S Tricuspid AtresiaClinical manifestationLeft ventricular type of apical pulseProminent large wave in jugular venous pulseEnlarged liverCyanosis of lip, skin ,nailsTachycardia Dyspnea or laboured breathingCool calmy skinChronic hypoxiemia with clubbing.

Diagnostic evaluation

Chest X-rayECG left ventricular hypertrophy.Cardiac catheterization

Pathophysiology

At birth presence of patent foramen ovale is required to permit blood flow across the septum into the left atrium.The PDA allows blood to flow to pulmonary artery into the lungs for oxygenation.VSD allows some amount of blood to enter right ventricle and pulmonary artery for oxygenation. In this condition blood flow is decreased.

Fig 22 changes in tricuspid atresiaManagement

In neonate whose pulmonary blood flows depend upon the patency of ductus arteriosis in continuous infusion of prostaglandlin-E, started at 0.1 mg/kg of body weight/min until surgical treatment not done.

Surgical management

Palliative treatment is the placement of the shunt(pulmonary tube systemic artery anastomosis):-To decrease blood flow to lungs.If ASD is small than atrial septostomy is done during cardiac catheterisation.A direction glnn shunt(cardio pulmonary anastomosis) may be performed at 6-7 month at the 2nd stage.

Fig 23 surgical repairModified fontan procedure

In this procedure systemic venous return directed to the lungs without ventricular pump through surgical connection between right atrium and pulmonary artery.A fenestration(opening) in the right atrial baffle is sometimes done to relieve pressure.The patient must have normal ventricular pressure and low pulmonary vascular procedure to be successful.The modified fanton procedure separate oxygenation and unoxygentaed blood inside the heart and eliminate the excess volume load on ventricle but does not restore normal antomy.

Fig 24 fontan procedureTransposition of great vessel(TGA)

TGA occurs when the pulmonary arteries originate from the left ventricle and aorta originates from the right ventricles.

Hemodynamics

This result in two separate circulations the right heart manages the systemic circulation and left heart manages the pulmonary circulation.This is just opposite of normal circulation.Aorta carries unoxygenated blood to the systemic circulation and pulmonary circuit circulation carries oxygenated blood back to lungs. Pulmonary vessels return back to atrium.

Fig 25. Normal heart V/S transposition of great vesselContdTwo circulatory systems exists one pulmonary and one systemic to sustain life there must be an accompanying and unoxygenated blood between the two circulations.Mixing of oxygenated and unoxygenated blood through one or more of the following shunt through ASD, VSD and PDA(these existing lesions provide a means for mixing venous and atrterial blood.PDA crosses functionally and anatomically in neonatal period.) ASD(foramen ovale) VSD remain open causing increased blood flow through lung.

Fig 26 changes in transposition of great vesselClinical manifestation

These manifestations are influenced by extent of intercirculatory mixing. These children present with cyanosis and unable to suck.Rapid breathing and hypoxemia within first weak of life.Murmur sound presentClubbing of fingers and toesEasy fatiguabilitySlow weight gainMetabolic acidosisFailure to thriveHypopnea, tachypnea Cardiomegaly.

Complication

Infective endocarditisBrain abscessCerebro vascular accident due to thrombosisSevere hypoxia.

Diagnostic evaluation

Chest X-ray shows cardiomegaly with a typical egg on site. The right upper lung fields appear more plethoric than other areas.cardiomegaly present.Pulmonary vascular markings are increasedECG shows right axis deviation and right or bi-ventricular hypertrophy.

Medical management

Treating CHF vigorously palliative and corrective procedureProstaglandlin E1 can help to reduce cyanosis in selected cases by keeping the PDA openPalliative procedure-This include the non surgical technique of enlarging of existing foramen ovale or ASD so that interarterial mixing of blood can occur by pulling a balloon through the defect. Balloon septostomy during cardiac catheterization RASKIN PROCEDURE.

Surgical technique

Palliative creating atrial septum defect (blalock hanlon operation)Pulmonary artery bending done to decrease pulmonary hypertension to presence of ventricular septum defect.

ContdSurgical creation of ductus arteriosus if pulmonary stenosis and VSD exist. Total creation or definitive repair by atrial stich operation or by redirecting the blood flow by mustard or senning procedure.in this a new arterial septum is created from pericardium or with a prosthesis with result that two separate function correct atria are formed. Systemic venous deoxygenated blood returning to right atrium is redirected to mitral valve into the left ventricle and into the pulmonary artery and to lung oxygenated blood that returns to its ventricle is redirect to tricuspid valve to right atrium and then into the systemic circulation to the aorta this procedure reverse the function of aorta but does not transplant the transverse position.

Fig 27 senning operationContdArterial switch operation is now established as treatment of choice in TGA in which pulmonary artery and aorta are transected.Systemic improvement after surgeries i.e. exercise tolerance improves, cyanosis and clubbing disappear.

Fig 28 Arterial Switch OperationTotal anomalous pulmonary venous connection (TAPVC)

All the pulmonary veins instead of joining the left atrium are connected anomalously to result in the total pulmonary venous blood reaching the right atrium. The anatomical classification of TAPVC is into supracardiac, cardiac, ifracardiac and mixed varieties.

Fig 29 normal V/S TAPVCHemodynamics

TAPVC results in pulmonary venous blood reaching the right atrium, which also receives the systemic venous blood.This results in almost complete mixing of the two venous returns.The blood flow to the left atrium is the right to left through a patient foramen ovale or atrial septal defect.The oxygen saturation of the blood in the pulmonary artery is often identical to that in the aorta because of mixing of blood in right atrium.Physiologically TAPVC cann be divided into { patient with pulmonary venous obstruction and patient without pulmonary venous obstruction}Pulmonary venous obstruction results in pulmonary arterial hypertension and as well as restriction in blood flow.In absence of pulmonary obstruction blood flow is large and result in cardiac failure between 4-10 weak of age.

Fig 30 changes in TAPVCClinical feature

CyanosisFailure to thriveCardiomegalyHyperkinetic precordium normal or accentuated pulmonic component. A grade two to four pulmonary ejection systolic murmur and a tricuspid flow murmur.tricuspid regurgitation

Diagnostic investigation

ECG shows right axis deviation and right ventricular hypertrophy.X-ray of obstructive TAPVC shows normal heart size with severe pulmonary venous hypertension resulting in ground glass appearance of lungs very much like hyaline membrane disease.

Management

Operation is indicated as soon as possible in 80% cases of infants die within first 3 months of life without surgical help.Obstructed TAPVC need surgery in short notice.Long time recovery time is needed.These patients are prone to develop pulmonary hypertensive crisis in the postoperative period.

Acute rheumatic fever

Acute rheumatic fever (ARF); is the leading cause of acquired heart disease in pediatric patient. The school age children are more susceptible to disease more common in children related to poor socio economic status.Rheumatic fever is a group of bodily response to streptococcus.

Etiology

This is an immunological disorder caused by damage to the heart by antibodies. These antibodies are produced in response way primary infection to throat or skin by a group of b-hemolytic streptococci.History of sore throat may present.Following untreated throat streptococcal sore throat is in latent period last from 10 days-7 weak. During this period antibodies formed to streptococcal antigen. These antigens have capacity to reactive with connective tissue.This antigen antibody reaction result in rheumatic fever.

Fig 32 Causes Of Acute Rheumatic FeverPathophysiology

During acute stage there is exudates influence reaction in connective tissue of joints, heart and skin.There is edema and lymphatic infiltrationAll layers of heart are affected.In joints there is edema, articular and periarticular infiltration of synovial membrane and effusion.Histopathology aschaff body which is pathogenic of rheumatic disease chacterized by large multinucleated.Cells arranged in pervascular area around and avascular fibrinoid material.

Clinical features(Major clinical manifestation)

Fever(range 102-1040F)Polyarthritis i.e. joints shows limited range of motion, inflammation , tenderness, swelling(generally in large joints,knees,wrist,elbow,shoulder and hip)Other chacteristics:-Migrating and reversible nature of progress helps to differentiate from other of arthritis.

Fig 34 clinical feature of acute rheumatic feverContd..Carditis- Inflammatory hemorrhagic blue lesion known as aschaff body or nodules present in interstitial tissue of the heart in response of rheumatic myocarditis, vegetation also form as result of myocarditis. The vegetation occurs mainly on the mitral aiortic valve and become scar, when fibrous area healed. Carditis often seems as CHF, cardiomegaly, pericardiac effusion, pericarditis.Sign and symptoms- Tachycardia, Murmur,Prediastolic gallop, Precardia friction rub, Precardial pain.

ContdStenosis- stenosis of the leaflets (valves) or cusp occurs because of their fusing together. This process causing obstruction to the fl;ow of blood to left ventricle for aiorta or both valves. Become scarded that may cannot completely close causing a back flow or regurgitation (valvular insufficiency) when the valve closed.

ContdChorea(syndenhens chorea)- saint witus danee children have involuntary, sudden random movement of extremity, emotional liability, sleep disturbance and severe muscle weakness, facial grimaces(involuntary)Erythema marginatum-Rash is reddish; lesions are non pruritic and appear as undifferentiated macule on trunk and inner aspect of extremity. These macule join together in a connective pattern giving chicken wire appearance on skin.

ContdSubcutaneous nodules- These are present on elbow, knees, ankles, over scalp, occiput over long prominence and skin. Careful observation of prominence is must because the nodules of rheumatic fever are seen than palpated.

Minor complication

Low grade fever(high in afternoon)Weakness, fatigue, weight loss, epistaxis with no known cause and abdominal pain.Prolonged PR interval in ECG

Course of disease

Cardiac involvement may result in permanent damage to valves causing long lasting heart lesion aortic or mitral regurgitation, mitral stenosis, tricuspid regurgitation i.e. classified and referred as rheumatic heart disease.

Diagnostic evaluation

ASO(antistreptolysin Otitre):-ASO titer is antibody reaction to streptococcal infection. Children over 5 years of age a titre of 333 todd unit is considered indicative other test can be used to determine serologic evidence of streptococcus infection.CRP(C-reactive protein):-CRP is absent in sera of normal individual. One positive culture is firm, 3 throat swabs at varying time interval for confirm of group A, B-hemolytic streptococci. These cultures should be taken atleast 2 before starting antibiotic therapy.Throat culture.ESR

Essential criteria

Increase ASO titerScearlet feverPositive throat culture

Medical management

Focus of treatment is:-Suppression of acute inflammatory process.Eradication of streptococcal infection.Prevention of disease recurrence.

Management

Start steroid and aspirin:-If heart involvement is present prednisolone 1.5 mg/kg/day in 3 divided doses is given for 3 weeks. Taper the dose by 5 mg/wk and discontinue after 12 wks simultaneously start.Start aspirin 100 mg/kg/day in 3 divided doses in uncompleted Rh Fever and before 12 weeks. Always give aspirin after meal to avoid gastritis and watch for side effect.

ContdPenicillin:-Give proclaimed penicillin 4 lakhs unit IM BD for 10 days to avoid streptococci.Start benzoteine penicillin 12 lakhs IM or IV on 8th day of proclaimed penicillin therapy. These infections are painful. If the child is sensitive to penicillin erythromycin therapy to reduce streptococcal infection.Steroid therapy may result in cushingoid features, hurshitism, and increased susceptibility to infection.

Nursing management

Bed rest:-Assist child and parent to understood need for amount of bed rest i.e. complete bed rest till the rheumatic activity subsides. Exertion can aggrevate symptoms. Bed rest to be continued from 2-3 wks to 2-3 months very strictly, if cardiac involvement is there.Diet:-Restrict salt intake only if feature of CHF present otherwise normal diet rich in iron prevent anemia. Due to fever child may be anorexic. Encourage fluid intake to prevent dehydration. Over feeding has to be avoided.

ContdAccident prevention:-Warm and cool alternative day to affect joint to reduce swelling and inflammation to reduce pain.Bed cradle to minimize pressure on affected joints.Use side rails to prevent falling, padded side of bed or chair to prevent injury; when involuntary jerking and violent movement occurs.Clothing according to weather.

ContdIf child develops chorea and behavioral changes occur learning difficulty should be discussed with teacher, classmates.Monitor daily weight, intake output chart, resting and sleeping heart rate in absence of febrile state. Nurse must encourage parent and child continue follow up care even when condition of child is improved.

Prevention

Primary prevention:-Diagnosis and treat all cases of sore throat by penicillin or erythromycin for 10 days to prevent Rh fever.Secondary prevention:-After Rh fever occur start child on 3wkly benzathine penicillin. Continue for atleast 5 yrs if there is no heart involvement. Treatment need to be taken lifelong if cardiac involvement is there, this prevent recurrence of Rh fever.

Rheumatic heart diseaseRheumatic heart disease is permanent damage to the heart following rheumatic fever. It can lead to heart failure and sometimes the need for cardiac surgery. Rheumatic heart disease is the most common form of heart disease in children in the world.A heart valve acts like a one-way door. It makes sure that blood pumped by the heart flows in one direction. When the heart is damaged, the heart valves are unable to function adequately.

Symptoms

People who get rheumatic heart disease sometimes end up very sick because the blood stopsflowing the right way, making them tired and short of breathChest painHeart palpitationsBreathlessness on exertionBreathing problems when lying downWaking from sleep with the need to sit or stand upSwellingFainting

Mitral regurgitation (MR)This occurs when the mitral valve allows reversal of blood flow from the left ventricle (LV) to the left atrium.

Pathophysiology

Normal blood flow from the left atrium to the LV and, subsequently, to the systemic circulation, is altered in mitral regurgitation. In the presence of mitral regurgitation, blood flows antegrade from the LV into the aorta, and the regurgitant volume flows retrograde from the LV into the left atrium. This causes a proportionate increase in LV ejection volume. The regurgitant fraction reenters the LV, producing left ventricular volume overload. The LV compensates via the Frank-Starling mechanism, resulting in a greater ventricular stroke volume.

ContdThe volume of the regurgitant fraction depends on several factors, including size of the orifice allowing regurgitation and the pressure gradient between the left ventricle and left atrium. This volume also depends on ventricular systolic pressure; therefore, the regurgitant volume increases in situations that increase afterload, such as hypertension or aortic stenosis.

Complications

In patients with mechanical prostheses, too much warfarin may result in excessive bleeding, whereas insufficient anticoagulation may lead to thromboembolism.

Optimal medical therapy Diuretics are also helpful in decreasing the total volume and may alleviate the pulmonary edema and congestion that may be present.Digoxin is useful in patients with left heart failure because it allows the heart to pump more efficiently.Vasodilators, such as nitroprusside, are very effective; however, preexisting hypotension may be exacerbated.Anticoagulation may be needed if diminished left ventricular function or atrial fibrillation or evidence of thromboembolism.

ContdInotropic agents may improve systolic blood pressure. Intra-aortic balloon counterpulsation or immediate surgical intervention (valvuloplasty) may be necessary in severe cases.In patients who stabilize but remain symptomatic, early semielective surgery should be considered to reduce the risk of irreversible ventricular dysfunction.Patients who become asymptomatic with medical therapy can be treated in the same manner as those with chronic mitral regurgitation.

Surgical Care

Transcatheter management, mitral valve clips may be a therapeutic option.Surgical repair of the regurgitant mitral valve can be classified into 3 major groups depending on the leaflet motion, namely, normal, prolapsing, and restricted. If the mitral annulus is dilated, an annuloplasty may be successful in alleviating the degree of regurgitation. The annuloplasty may involve the use of a ring prosthesis. In younger patients (in whom restriction of valve growth is undesirable), resection of a portion of the leaflet and annular plication may be performed.Shortening of the chordae and/or papillary muscles may repair prolapsed leaflets. Lengthening may be required in cases where there are short chordaeMitral regurgitation with restricted leaflet motion is observed in parachute and hammock valves and, along with a valvuloplasty, can be improved by incising the valve leaflets at an appropriate location.

ContdQuadrilateral resection of a prolapsing leaflet with sliding annuloplasty may be helpful in cases with mitral valve prolapsedE-to-E mitral valve repair is help in some cases in which an opposition suture in placed in the center of the anterior and posterior leaflets producing a double orificeMitral valve replacement is the final option in the treatment of mitral regurgitation. The choice of which valve to use (mechanical vs bioprosthesis) can be difficult.Bioprosthetic valves resolve the anticoagulation issue but raise problems of their own. Bioprostheses may degenerate rapidly and may become calcified and dysfunctional as early as 6 months after insertion. Mitral stenosis

Mitral stenosis is a disorder in which the mitral valve does not fully open. This restricts the flow of blood.

Causes

Mitral stenosis means that the valve cannot open enough. As a result, less blood flows to the body. The upper heart chamber swells as pressure builds up. Blood and fluid may then collect in the lung tissue (pulmonary edema), making it hard to breathe.The valve problems develop 5 - 10 years or more afterhavingrheumatic fever. Symptoms may not show up for even longer. Children may be born with mitral stenosis (congenital) or other birth defects involving the heart that cause mitral stenosis. Mitral stenosis may run in families.

Symptoms

Chest discomfort that increases with activity and extends to the arm, neck, jaw or other areas (This is rare)Cough, possibly with bloody phlegmDifficulty breathing during or after exercise, or when lying flat;Waking up due to breathing problems (This is the most common symptom)FatigueFrequent respiratory infections, such as bronchitisFeeling of pounding heart beat (palpitations)Swelling of feet or anklesIn infants and children, symptoms may be present from birth (congenital). It will almost always develop within the first 2 years of life. Symptoms include:CoughPoor feeding, or sweating when feedingPoor growthShortness of breath

Exams and Tests

The health care provider will listen to the heart and lungs with a stethoscope. A murmur, snap, or other abnormal heart sound may be heard. The typical murmur is a rumbling sound that is heard over the heart during the resting phase of the heartbeat. The sound often gets louder just before the heart begins to contract.The exam may also reveal an irregular heartbeat or lung congestion. Blood pressure is most often normal.Narrowing or blockage of the valve or swelling of the upper heart chambers may be seen on:Chest x-rayCT scan of the heartEchocardiogramECG (electrocardiogram)MRI of the heartTransesophageal echocardiogram (TEE)

Treatment

Diuretics (water pills)Nitrates, beta-blockersCalcium channel blockersACE inhibitorsAngiotensin receptor blockers (ARBs)DigoxinAnticoagulants (blood thinners) are used to prevent blood clots from forming and traveling to other parts of the body.Antibiotics may be used in some cases of mitral stenosis. People who have had rheumatic fever may need long-term preventive treatment with the antibiotic penicillin.In the past, most patients with heart valve problems were given antibiotics before dental work or invasive procedures, such as colonoscopy. The antibiotics were given to prevent an infection of the damaged heart valve. Surgical treatmentPercutaneous mitral balloon valvotomy (also calledvalvuloplasty). During this procedure, a tube (catheter) is inserted into a vein, usually in the leg. It is threaded up into the heart. A balloon on the tip of the catheter is inflated, widening the mitral valve and improving blood flow. This procedure may be tried instead of surgery in people with a less damaged mitral valve. Surgery to repair orreplacethe mitral valve. Replacement valves can be made from different materials. Some may last for decades, and others can wear out and need to be replaced.

(Prognosis)

The outcome varies. The disorder may be mild, without symptoms, or may be more severe and become disabling over time. Complications may be severe or life-threatening. In most cases, mitral stenosis can be controlled with treatment and improved with valvuloplasty or surgery.

Possible Complications

Atrial fibrillation and atrial flutterBlood clots to the brain (stroke), intestines, kidneys, or other areasCongestive heart failurePulmonary edemaPulmonary hypertension

Tricuspid regurgitation

The valve is leaky or doesn't close tight enough, causing blood to leak backwards across the valve

Fig 35 Tricuspid RegurgitationetiologyInfection, such as rheumatic fever orinfective endocarditisA dilated right ventricle, causing the annulus (a ring of tough fibrous tissue which is attached to and supports the leaflets of the valve) of the tricuspid valve to enlargeIncreased pressure through the tricuspid valve (seen with pulmonary hypertension)Less common causes include congenital defects, trauma, carcinoid heart disease, tumor, tricuspid valve prolapse, Ebstein's anomaly, systemic lupus, and trauma.Tricuspid valve disease, if caused by rheumatic fever, is often combined with mitral and/or aortic valve disease.

Symptoms may include:

Irregular heart rhythm (atrial fibrillation)Easily tired (fatigue)A fluttering discomfort in the neckWith severe disease, heart failure symptoms (right abdominal pain, shortness of breath, swelling in the legs or abdomen, cold skin)

How is tricuspid valve disease diagnosed?

Tricuspid valve disease may first be diagnosed during aphysical exam. The doctor will often hear a murmur (abnormal blood flow through the valve). Other signs your doctor may find are an irregular pulse and a fluttering or abnormal pulsation in your neck (jugular vein).Tests used to diagnose valve disease may include:Electrocardiography (ECG)Chest X-rayEchocardiographyTransesophageal echocardiographyCardiac Catheterization(cardiac cath or angiogram)Radionuclide scans

Fig 36 Lanyard and template handle assists with placement of ringSurgical ManagementTricuspid Valve RepairWhen valve disease is severe, it may be necessary to repair or replace the diseased valve. Tricuspid valve repair using an annuloplasty ring is the preferred surgical approach for tricuspid regurgitation and may be performed for primary tricuspid disease or for combined cases with other valve surgery (mitral, aortic).

Fig 37 Anatomically correct design conforms to the 3-D tricuspid valve opening.Aortic Regurgitation

Aortic regurgitation in children is usually found in association with a bicuspid aortic valve. The aortic valve connects the left ventricle to the aorta. As the ventricle starts to contract to pump blood to the body, pressure builds. This increase in pressure causes the aortic valve to open, allowing blood to pass from the left ventricle into the aorta. As the heart then starts to relax, pressure falls and the valve closes.

ContdAortic regurgitation refers to a leak of blood backwards from the aorta into the left ventricle because of inadequate or incomplete closure of the aortic valve. Aortic regurgitation is also called aortic valve insufficiency, or simply an aortic valve leak.

causesAortic regurgitation in children is usually the result of abicuspid aortic valve. Normally the aortic valve typically has 3 separate pieces or leaflets. A bicuspid aortic valve is a valve which has only two leaflets instead of the normal three. Typically 2 out of the 3 leaflets have fused together during development in the womb. Contd.Aortic regurgitation can also happen in children who have enlarged aortas from any cause. As the aorta enlarges, it may actually pull the valve leaflets apart. This can lead to an open space in the middle of the valve where blood can then flow backwards into the left ventricle while the valve is trying to close. Enlarged aortas are often seen in the setting of Marfan syndrome or other connective tissue disorders. ContdAortic regurgitation in children can also be seen in the setting of aventricular septal defect. VSDs that are positioned very close to the aortic valve may create a jet effect that can actually distort and deform the valve. Over time, this may result in the development of aortic regurgitationyContdLess common causes of aortic regurgitation include infections and other inflammatory conditions. Rarely bacteria may attack the aortic valve causing endocarditis. The valve gets destroyed or damaged by the infection and therefore does not work properly.Symptoms

Aortic regurgitation is a potential problem in that it creates an extra workload or stress on the heart. The left ventricle is forced to pump the normal amount of blood coming forward into it, plus any additional blood that leaks backwards. Over time, this can creates an extra burden and workload on the heart that may tire it out over the course of several years. This is usually only a problem with a significant degree of aortic regurgitation. Symptoms caused by aortic regurgitation are variable. Many children are identified by the presence of an asymptomaticheart murmur. Other children may present with symptoms of fatigue or decreasing exercise tolerance. Symptoms such aschest pain,palpitations, orsyncopeare unusual in the setting of aortic regurgitation. Infants with aortic valve insufficiency may haverapid breathing,sweating, ortachycardia.

Treatment

When aortic regurgitation is significant, it usually must be addressed by surgery. Medication may assist the heart in tolerating the extra workload but does not do anything to decrease or lessen the degree of leaking in most cases. The most common indication for surgery in pediatric patients is the development of symptoms or evidence of a progressively enlarging heart size. Surgery usually involves completely replacing the aortic valve, although in some instances the valve may be able to be successfully repaired without needing to be replaced.

Nursing management of a child with heart disorder

Nursing assessment

Complete thorough history of child and family should be taken.Child growth and development pattern, exercise intolerance.Observe childs skin, mucous membrane for colour and temperature change.Extremities-Are extremities cold? is their difference present between upper and lower extremity, check quality of pulse in all limbs, check edema in extremity.Observe for clubbing increase in soft tissue around terminal phlenges of finger especially thumb nail. This may occur in cyanotic children one year of age.Observe for any chest deformity and precordial pulse.Auscultate apical pulse rate for full one minute.Determine cardiac rhythm or any changeRecord vital signsLook for any other congenital defect, abnormal fascia or relevant history.Relieving respiratory distress

Determine the degree of respiratory distress.Observe pattern of regularity of respiratory pattern.Observe for nasal flaring, listen for grunting and observe any response to change of positioning.Raise the head end upto 45o degree angle to increase the pressure of viscera from the diaphragm and increase lung volume.Feed slowly allowing frequent resting period. To reduce the risk of aspiration.Observe for abdominal distension which may increase respiratory difficulty, if distension present inserts NG tube for the relief.Suction nose and mouth if the child is not able cough out the secretion.Provide oxygen therapy as required.Administer diuretics as ordered to reduce lung congestion, monitor intake output chart; monitor effectiveness, specific gravity of urine and restrict fluid as required.

Improving cardiac output

Organize nursing care to provide period of uninterrupted rest.Prevent excessive crying.Provide diversion activities. Proper medication should be given as per prescription.Avoid excessive temperature.Prevent constipation.

Improving oxygenation and activity tolerance

Provide oxygen therapy.Observe child response to oxygen.Observe child response while weaned off from oxygen.

Provide adequate nutrition

Feed slowly in semierect position.Burp infants after each ouns to decrease compression of stomach on heart and lungs.Provide small and frequent feed.Monitor strict intake and output chart.Monitor daily weight.Proper diet chart should be maintained to follow high nutritive value.

Prevent the infectionPrevent exposure to communicable disease including exposure to children with upper respiratory infection.Ensure that child is completely immunized.Prevent cold stress.Report any symptoms of fever, diarrhoea and vomiting.Be specific that child receive prophylactic antibiotics for endocarditis before any dental procedure or urinary instrumentation.

Reduce fear and anxiety of parents as well as child

Prepare child and parent for corrective surgery.Refer family to appropriate resources concerned with the financial or emotion aspect of caring child with CHD.

Summary

The human heart is an astonishing organ. A muscle onlyabout the size of your fist, it sits just to the left of thecenter of your chest contracting and relaxing to pumpbloodroughly five liters of it a minutethroughoutyour body. It is an involuntary muscle. commonlycalled heart disease (though, more accurately known ascoronary artery disease) is, interestingly enough, not adisease of the heart at all. Its a disease of the large arteries outside the heart that supply thesmaller vessels that feed the heart muscle with blood richin nutrients and oxygen that the heart needs to keepworking. Coronaryarteries, the large arteries carrying blood to the heartmuscle, are like the huge pipes that carry water from areservoir to a big city, to be distributed to streets, individual houses, and then specific faucets before being carried away again through drains.