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Cardiac Failure

Clinicalsyndrome resulting from inability of myocardium to meet metabolicdemands of body.

Combination of tachypnea, tachycardia,cardiomegaly, and hepatomegaly is cardiac failure until proved otherwise.

In many cases, several mechanisms areresponsible for clinical picture of cardiac failure. These includeexcessive volume or pressure load, disturbance in myocardial function,and abnormal cardiac rhythm.

Principal Causes of Cardiac Failure

1. Excessivevolume load
   1. Left-to-rightshunt lesions
      1. Patentductus arteriosus
      2. Ventricular septal defect
      3. Atrial septal defect (ostium secundum)
      4. Atrioventricular canal defects
         1. Ostiumprimum defect
         2. Complete atrioventricular canal
      5. Aortic pulmonary window
      6. Total anomalous pulmonary venous connectionwithout obstruction
      7. Systemic arteriovenous fistulas
   2. Valvular incompetence
      1. Aorticincompetence
      2. Mitral incompetence
      3. Pulmonary incompetence
      4. Tricuspid incompetence
2. Excessive pressure load
   1. Left ventricularoutflow tract obstruction
      1. Hypertrophic cardiomyopathy
      2. Congenital valvar aortic stenosis
      3. Discrete subvalvar aortic stenosis
      4. Supravalvar aortic stenosis
      5. Aortic arch hypoplasia or interruption
      6. Localized juxtaductal coarctation ofthe aorta
   2. Right ventricular outflow tract obstruction
      1. Congenitalvalvar pulmonic stenosis
   3. Left ventricular inflow tract obstruction
      1. Pulmonaryvein stenosis
      2. Total anomalous pulmonary venous connectionwith obstruction
      3. Cor triatriatum
      4. Supravalvular stenosing ring of theleft atrium
      5. Tumor
      6. Mitral valve obstruction (atresia,stenosis, parachute mitral valve)
   4. Right ventricular inflow tract obstruction
      1. Systemicvenous obstruction
      2. Right atrium obstruction
      3. Tricuspid valve obstruction
      4. Ebstein anomaly
   5. Cor pulmonale
   6. Systemic hypertension
3. Disturbance in myocardial function
   1. Acuterheumatic fever and rheumatic heart disease
   2. Kawasaki disease
   3. Myocarditis
   4. Pericarditis
   5. Endocarditis
   6. Cardiomyopathy
   7. Myocardial infarction
      1. Anomalousleft coronary artery from the pulmonary artery
      2. Atherosclerosis
   8. Cardiac tumor
   9. Metabolic heart disease
      1. Perinatalasphyxia
      2. Hypocalcemia
      3. Hypoglycemia
      4. Severe anemia
   10. Drugs
4. Complex anatomic lesions
   1. Hypoplasticleft heart complex
   2. Transposition of the great arterieswith a large ventricular septal defect
   3. Double-outlet right ventricle
   4. Truncus arteriosus
   5. Univentricular atrioventricular connections
5. Abnormal cardiac rhythms
   1. Supraventriculartachycardia
   2. Atrial flutter
   3. Complete heart block

Clinical Features and Diagnosis

Excessive Volume Load

Left-to-Right Shunt Lesions

Patent Ductus Arteriosus

Fetal ductusarteriosus is open communication between upper descending aortaand junction of main and left pulmonary arteries.

Usually closes within 1–2days after birth but can remain open, especially in preterm infants whoweigh <1,500 g.

Development of cardiac failure, whichusually occurs in neonatal period, depends on size of communicationand relationship between pulmonary and systemic resistances.

Usual physical findings include enlargedheart with prominent LV and RV impulses, narrowly split S2, gradeII–IV/VI continuous or long systolic murmur withmaximum intensity at upper left sternal border, S3 at apex, hepatomegaly,and wide pulse pressure. Systolic ejection sounds may occasionallybe heard along left sternal border.

Chest radiography shows marked cardiomegaly,enlarged left atrium, prominent main pulmonary segment, increasedpulmonary vascular markings, and occasionally Kerley b lines.

ECG shows RV or biventricular hypertrophy.

Ductus can often be visualized with2-D echocardiographic techniques and Doppler methods.

Clinical diagnosis can be difficultin preterm infants with respiratory distress syndrome who requiremechanical ventilation. Murmur may not be heard, and heart may notbe enlarged on chest radiograph. Cardiac failure should be suspectedif arterial blood gas status deteriorates or need for mechanical ventilationis prolonged.

Most children do not need invasivestudies before surgical ligation unless other defects are suspected.Cardiac catheterization and angiography may be necessary with atypicalmurmur or if findings suggest increase in pulmonary artery pressure.

Ventricular Septal Defect

Definedas opening of variable size in ventricular septum, and >1defect can exist.

Cardiac failure occurs between 1 and2 mos of age in infants with medium to large defects.

Clinical manifestations include tachypnea,tiring with feeding, and poor weight gain. Hepatomegaly and sometimessplenomegaly occur. Lung crackles and pedal edema are unusual ininfants.

Cardiac exam reveals cardiac enlargementwith prominent RV and LV impulses. Usually S2 is narrowly splitand pulmonic component is louder than normal. S3 or S4 gallop orboth may be heard. Grade III–V/VI harsh, holosystolicmurmur is heard with maximum intensity at lower left sternal border withtransmission to apex, axilla, and back. Grade I–II/VIapical mid-diastolic rumble signifies increased blood flow acrossmitral valve.

Chest radiography shows marked cardiomegaly,large left atrium, prominent main pulmonary artery segment, increasedpulmonary vascular markings, and occasionally Kerley b lines.

ECG usually shows biventricular hypertrophy.

2-D echocardiography shows VSD.

Atrial Septal Defect (Ostium Secundum)

AlthoughASD does not usually lead to cardiac failure during infancy andchildhood, cardiac failure may occur if large left-to-right shuntexists. Cardiac failure also may occur with combination of moderatesize ASD and VSD.

Tachypnea, tachycardia, cardiomegaly,and usually hepatomegaly occur.

Physical exam, radiographic, and ECGfindings are similar to those with ostium primum defect (see nextsection). Although frontal plane ECG axis of <–30degrees suggests AV canal defect, this pattern occurs in about 10% ofchildren with ostium secundum defects.

2-D echocardiography confirms diagnosis.

Atrioventricular Canal Defects

2 basictypes of AV canal defects are ostium primum and complete AV canaldefects.

In hearts with 2 ventricles, absenceor decrease in septal tissue immediately above and below normallevel of AV valves characterizes these defects.

Ostium Primum Defect

Clinicalpresentation is similar to that of ostium secundum defect, exceptthat mitral incompetence can occur with ostium primum defect becauseof cleft in mitral valve.

With presence of severe mitral incompetence,cardiac failure is more likely to occur.

Usual physical findings are enlargedheart, prominent RV impulse, normal or wide split of S2, grade II–III/VIsystolic ejection murmur with maximum intensity along upper leftsternal border, grade I–II/VI diastolic rumbleat lower left sternal border, and hepatomegaly. With significantmitral incompetence, murmur of mitral incompetence may be heardat apex.

Chest radiography shows cardiomegaly,prominent main pulmonary artery segment, and increased pulmonaryvascular markings.

ECG shows RV hypertrophy and QRS frontalplane axis that is more superior, especially in infants.

2-D echocardiography demonstrates defect.

Complete Atrioventricular Canal

Clinicalmanifestations are more diverse than those of other defects becauseof different hemodynamic situations that can exist. Lesion consistingof small VSD, large ostium primum defect, and normal mitral valvefunction presents like ostium primum defect. Lesion consisting oflarge VSD and normal mitral valve function presents like isolatedVSD. In either of these circumstances, if significant AV valve dysfunctionwith mitral or tricuspid incompetence exists, cardiac failure usuallyoccurs during first month of life.

Chest radiography shows marked cardiomegaly,enlarged main pulmonary artery segment, and increased pulmonaryvascular markings.

ECG shows RV or biventricular hypertrophyand frontal plane QRS axis of –40 to –150 degrees.

Defect may be seen with 2-D echocardiography.

Aortic Pulmonary Window

Due to failureof formation of base of spiral septum, which generally producescommunication between aorta and pulmonary artery just above semilunarvalves.

Cardiac failure occurs in early infancy.

Usual physical findings are markedcardiomegaly, accentuated pulmonary closure sound, long systolicmurmur of variable intensity along left sternal border in thirdand fourth intercostal spaces, hepatomegaly, and wide pulse pressure.

Radiographic and ECG findings are similarto those of large VSD or patent ductus arteriosus.

Usual method of diagnosis is 2-D echocardiography.

Total Anomalous Pulmonary Venous Connection without Obstruction

Severaltypes may occur. Most common is connection between pulmonary veinsand confluence behind left atrium. From this confluence, blood flowsvia anomalous vertical vein to left innominate vein and then toright superior vena cava and right atrium. Pulmonary veins alsomay connect at level of coronary sinus or posterior right atrium.

Clinical presentation and findingsare similar to those of large ASD, and cardiac failure may occurin infancy.

Chest radiography shows moderate cardiomegalywith increase in pulmonary vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography may show echo-freespace posterior to left atrium.

Cardiac catheterization and angiographyare frequently not needed.

Systemic Arteriovenous Fistulas

Usuallycongenital and can occur in cranium, liver, thorax, or extremity.

Clinical course is determined by amountof blood flow through fistula. If flow is large enough, increasein venous return produces increased volume load on heart.

Usual physical findings are markedcardiomegaly; normally split S2 with accentuated pulmonary component;continuous murmur over cranium, liver, or extremity; hepatomegaly;and wide pulse pressure. With intracranial fistula, neck veins aredistended and carotid pulses are bounding.

Chest radiography shows enlarged heartand increase in pulmonary vascular markings.

ECG shows RV or biventricular hypertrophy.

Head CT or MRI can help visualize anyintracranial pathology. Definitive diagnosis of intracranial orperipheral fistulas can be made by angiography.

Valvular Incompetence

Aortic Incompetence

Can be associatedwith unicuspid or bicuspid aortic valve, acute rheumatic fever,endocarditis, supracristal VSD, and Marfan syndrome.

Clinical course depends on acutenessof onset and severity of incompetence.

Mild aortic incompetence is asymptomatic,whereas acute severe aortic incompetence results in low cardiacoutput and hypotension. Chronic moderate-to-severe incompetenceproduces cardiac failure. Diastolic pressure of <50 mmHg and pulse pressure >50 mm Hg indicate significant incompetence.

When severe, LV impulse is increasedand displaced toward axilla. Pulse pressure is wide with boundingpulses. Murmur of aortic incompetence is diastolic decrescendo murmurthat begins with aortic closure. Its maximum intensity is at upperright sternal and left midsternal borders. The longer the murmur,the more severe the incompetence. Fluttering of anterior mitralvalve leaflet also can produce mid-diastolic apical murmur (AustinFlint murmur).

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG shows LV hypertrophy. Severe lesionmay produce subendocardial ischemia with ST depression and T-waveinversion.

2-D echocardiography with Doppler methodsis usually diagnostic.

Mitral Incompetence

Congenitalmitral incompetence is rare but may be due to underdevelopment ofvalve leaflets or short, thick chordae tendinae (parachute mitralvalve). Also may occur with AV canal defects and idiopathic hypertrophicsubaortic stenosis.

Acquired mitral incompetence is morecommon and can be seen with acute rheumatic fever or any cause ofLV failure, when there is dilatation of mitral valve annulus. Closedchest trauma, anomalous left coronary artery, Kawasaki disease,severe aortic stenosis, or coronary arterial disease may cause papillarymuscle infarction or rupture. Endocarditis may perforate valve orrupture chordae tendinae. Mitral valve also may undergo degenerationwith Marfan or Hurler disease. Another cause is prolapsing mitralleaflet syndrome, but severe incompetence is unusual with this lesion.

Clinical course depends on how severethe lesion is. Mild incompetence is asymptomatic, and moderate incompetencemay be tolerated for many years before cardiac failure occurs. Classicmurmur of mitral incompetence is grade III–IV/VIhigh pitched holosystolic murmur with maximum intensity at apexand transmission to left axilla and back. In severe mitral incompetence,prominent LV impulse, S3, and diastolic rumble at apex are commonfindings.

Chest radiography shows marked cardiomegalywith enlarged left atrium and pulmonary venous congestion.

ECG shows left atrial enlargement andmay show LV hypertrophy.

2-D echocardiography can assess anatomyof valve and its attachments as well as any associated abnormalities.Doppler methods can assess severity of incompetence.

Pulmonary Incompetence

Most commoncause is surgical valvotomy. Other causes include isolated congenital incompetenceof pulmonic valve, bicuspid pulmonic valve, and idiopathic dilatationof main pulmonary artery. Absence of pulmonic valve, which is usuallyassociated with VSD and infundibular pulmonic stenosis, causes severeincompetence.

Usual physical findings with moderate-to-severeincompetence include prominent RV impulse, delayed or absent pulmoniccomponent of S2, and characteristic grade II–IV/VImedium-pitched diastolic decrescendo murmur heard with maximum intensityat upper and middle left sternal border.

Chest radiography shows marked cardiomegaly.

ECG shows RV hypertrophy.

2-D echocardiography and Doppler methodsare usually diagnostic.

Tricuspid Incompetence

Congenitaland acquired cardiac lesions may produce tricuspid incompetence.Occasionally, valve leaflets do not form and cardiac failure mayoccur in utero. Isolated tricuspid incompetence may be due to dysmorphicvalve, cleft in valve, or abnormal chordae tendinae. Incompetenceof tricuspid valve also may occur with AV canal defects and Ebsteinanomaly. Acquired causes include severe perinatal asphyxia, acuterheumatic fever, and endocarditis.

Physical exam can establish diagnosisof significant tricuspid incompetence. Typical murmur is grade III/VIhigh-pitched holosystolic murmur that is louder on inspiration andheard with maximum intensity at lower left sternal border. Livermay be enlarged and show systolic pulsations. Jugular venous pulseshows prominent v wave followed by deep y descent. Mid-diastolicrumble that reflects increased blood flow across tricuspid valvealso may be heard at lower left sternal border. Other findings can includecyanosis, peripheral edema, and ascites.

Chest radiography shows cardiomegaly,which is due to large right atrium.

ECG findings depend on associated lesions,but large P waves indicate right atrial enlargement.

2-D echocardiography can assess anatomy,whereas Doppler methods can be helpful in estimating severity ofincompetence.

Excessive Pressure Load

Left Ventricular Outflow Tract Obstruction

Hypertrophic Cardiomyopathy

Genetictransmission is usually autosomal-dominant.

Some individuals have obstructive form,with massive hypertrophy of ventricular musculature, especiallyventricular septum. Abnormal systolic anterior motion of anteriormitral leaflet also produces dynamic subaortic obstruction. Besidescardiac failure, angina and syncope also may occur.

Usual physical findings include sustainedthrusting single or bifid apical pulse, variable splitting of S2depending on how severe obstruction is, grade II–III/VIsystolic ejection murmur with maximum intensity along left midsternalborder, jerky pulse with rapid upstroke, and hepatomegaly. Occasionally,murmur of mitral incompetence is heard at apex.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG shows LV or biventricular hypertrophy.

2-D echocardiography can effectivelydelineate extent of hypertrophy.

Congenital Valvar Aortic Stenosis

Due to imperfectcusp development and leaflet thickening.

Severe stenosis can cause cardiac failurein early infancy.

Usualphysical findings include ejection click and systolic ejection murmur,which may be heard with maximum intensity at upper right and middleleft sternal borders. If cardiac output is reduced, murmur may besoft or absent.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG often shows RV forces in infants <1mo of age. In infants with critical aortic stenosis, ST depressionand T-wave inversion may be seen in left precordial leads.

2-D echocardiography usually showsabnormal aortic valve and poorly contractile LV.

Other manifestations in older childrenare angina, dyspnea on exertion, and syncope.

There is usually prominent LV impulseat apex, narrowly or paradoxically split S2, grade II–IV/VIharsh systolic ejection murmur with maximum intensity at upper rightsternal border, aortic ejection click, sometimes S3 and S4 at apex,and pulse with slow upstroke and narrow pulse pressure.

Chest radiography shows enlarged heartwith prominent ascending aorta and pulmonary venous congestion.

ECG usually shows LV hypertrophy withor without ST depression and T-wave inversion.

2-D echocardiography shows abnormalaortic valve, and Doppler methods can estimate pressure differenceacross valve.

Discrete Subvalvar Aortic Stenosis

Obstructionbelow aortic valve may be due to thin membrane diaphragm or thickfibromuscular tissue. Diaphragm also may be associated with aorticinsufficiency.

Clinical findings are similar to thosewith valvar aortic stenosis, except that aortic ejection click isless common and aortic dilatation is less prominent.

2-D echocardiography usually demonstratestype and location of obstruction. Otherwise, cardiac catheterizationand angiography are diagnostic.

Supravalvar Aortic Stenosis

Definedas localized or diffuse narrowing of ascending aorta just abovelevel of coronary arteries.

Can occur as familial or sporadic isolatedlesion but is often associated with Williams syndrome, whose featuresinclude elfin facies and mental retardation. Many individuals, especiallyif they have Williams syndrome, usually have RV outflow tract obstruction,which can occur at valvar, supravalvar, and peripheral pulmonaryartery levels.

Clinical findings are similar to thoseof congenital valvar aortic stenosis, except that murmur is heardhigher on chest wall and ejection click is unusual. Suprasternalnotch thrill is common.

BP in right arm may be 20 mm Hg higherthan that in left arm because of stenosis at origin of left subclavianartery or jet effect of blood with ejection from LV into ascendingaorta.

Chest radiography shows enlarged heartwithout poststenotic dilatation of ascending aorta.

ECG shows LV hypertrophy and, if stenosisis severe, T-wave inversion in left chest leads.

2-D echocardiography demonstrates narrowing,and Doppler methods can assess pressure gradient across ascendingaorta.

Cardiac catheterization and angiographyare usually performed because of high incidence of associated abnormalities,which include patent ductus arteriosus, coarctation of aorta, pulmonarystenosis, and mitral insufficiency.

Aortic Arch Hypoplasia or Interruption

Most commonlyoccurs in aortic isthmus but may occur anywhere in aortic arch.Most extreme form is interruption of arch, which can occur proximalto left carotid artery, distal to left subclavian artery, or betweenleft subclavian and left carotid arteries.

In almost all cases, patent ductusarteriosus provides blood flow to lower part of body.

With rare exceptions, there are associateddefects (e.g., VSD, double outlet RV, AV canal defect, and tricuspidatresia with aortopulmonary transposition).

Clinical findings depend on severityof intracardiac defects, pulmonary vascular resistance, and sizeof ductus arteriosus. Almost all infants develop severe cardiacfailure during first week of life.

Differential cyanosis of extremitiesdepends on degree of ventricular shunting and is variable finding.

Femoral pulses are diminished or absent.No murmur is specific.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG may show RV or biventricular hypertrophy.

Although 2-D echocardiography may bediagnostic, cardiac catheterization and angiography are definitive.

Localized Juxtaductal Coarctation of Aorta

Definedas congenital narrowing of upper descending aorta that is usuallylocated near ductus arteriosus.

Primary coarctation of aorta occurswith or without patent ductus arteriosus but without other majorcardiac defects.

Complex coarctation is associationof other cardiac defects with coarctation [e.g., VSD, aorticvalvar stenosis, or mitral stenosis (Shone syndrome)].

Severe primary coarctation of aortausually presents with cardiac failure during first month of life.Delay in onset is possibly related to ductal closure at aortic end.With complex coarctation, cardiac failure usually appears duringfirst week of life.

Usual physical findings in child withprimary coarctation of aorta are arm BP that is ≥20 mm Hg higherthan pressure in legs, diminished or absent femoral pulses, andgrade II–III/VI systolic ejection murmur withmaximum intensity along left sternal border or over scapula in leftback. Arm BPs may be unequal if anomalous right subclavian arteryis present below coarctation or left subclavian artery is narrowedat origin of coarctation. Clinical findings with complex coarctationdepend on presence of associated lesions. Murmurs of VSD, valvaraortic stenosis, or mitral incompetence usually can be heard ifthese defects are present.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

In early infancy, ECG usually showsRV hypertrophy. In later infancy and childhood, it usually showsLV or biventricular hypertrophy, which is usual finding with complexcoarctation.

In neonates 2-D echocardiography canoften visualize coarctation, and Doppler methods can estimate itsseverity.

MRI can help define anatomy in somecases. If precise diagnosis of coarctation and associated lesionscan be accurately made, cardiac catheterization may not be necessary.

Right Ventricular Outflow Tract Obstruction

Can occurat level of pulmonary valve or above or below valve leaflets.

Valvar pulmonic stenosis is most commonform.

Congenital Valvar Pulmonic Stenosis

Neonateswith critical pulmonary valvar stenosis develop cardiac failurein immediate postnatal period.

Often infundibular hypertrophy occurswith valvar stenosis and tends to be progressive. Asymptomatic infantsand children may develop progressive severe pulmonary stenosis withonset of cardiac failure in adulthood.

Usual physical findings are prominentRV impulse; normal or diminished pulmonary component of S2; gradeII–IV/VI systolic ejection murmur with maximumintensity at upper left sternal border; and hepatomegaly. Severestenosis produces delay in peak intensity of murmur and delay in pulmonaryvalve closure. Occasionally, continuous murmur of patent ductusarteriosus or pansystolic murmur of tricuspid incompetence is heard.

Chest radiography shows cardiomegalyand decreased pulmonary vascular markings.

ECG usually shows RV hypertrophy, unlessRV is hypoplastic. T-wave inversion is sometimes seen in right precordialleads.

2-D echocardiography can visualizethickened, stenotic valve and narrowed infundibulum. Doppler methodsindicate severity of obstruction.

Left Ventricular Inflow Tract Obstruction

Pulmonary Vein Stenosis

Obstructionof normally connected pulmonary veins may be due to intrinsic narrowing(diffuse hypoplasia, localized diaphragm, narrowing on entry toleft atrium) or occasionally by external compression by posteriormediastinal mass.

Presentation is similar to that oftotal anomalous pulmonary venous connection with obstruction. Usualphysical findings are prominent RV impulse and accentuated pulmonaryclosure sound. No specific murmurs are heard.

Chest radiography shows near-normalheart size with increase in pulmonary venous vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography can sometimesview stenoses directly.

Cardiac catheterization and angiographyare definitive.

Total Anomalous Pulmonary Venous Connection with Obstruction

Pulmonaryvenous drainage below diaphragm to ductus venosus with venous return viainferior vena cava produces pulmonary venous obstruction.

Supracardiac or cardiac connectionsof pulmonary veins can cause pulmonary venous obstruction, but thisis uncommon.

Severe obstruction produces severecyanosis and respiratory distress in neonatal period.

Usual physical findings are prominentRV impulse, narrowly split S2, and hepatomegaly. These murmurs aresometimes heard: murmur of tricuspid incompetence; continuous murmuralong left sternal border, which reflects blood flow through anomalouschannel; and systolic ejection murmur along upper left sternal border,which reflects blood flow across pulmonary valve.

Chest radiography usually shows mildcardiomegaly and intense increase in pulmonary vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography shows enlargedRV, and no pulmonary veins are seen entering left atrium. If pulmonaryveins empty into coronary sinus or into large channel behind atria,these structures can be seen.

Cardiac catheterization and angiographyare definitive.

Cor Triatriatum

Failureof resorption of common pulmonary vein results in cor triatriatumwith division of left atrium into upper and lower chambers usuallyconnected by restrictive opening.

Clinical presentation is same as pulmonaryvenous obstruction. Usual physical findings are prominent RV impulseand accentuated pulmonary closure sound. No specific murmurs are heard.

Chest radiography shows mild cardiomegalyand increase in pulmonary venous vascular markings.

ECG shows RV hypertrophy.

2-D echocardiography or MRI can bediagnostic.

Supravalvular Stenosing Ring of Left Atrium

Fibrousring located on atrial side of mitral annulus sometimes protrudesinto mitral orifice, causing inflow obstruction of LV. Occurs asisolated lesion or in association with parachute mitral valve, subaorticstenosis, and coarctation of aorta (Shone syndrome).

Clinical presentation and findingsare similar to those for cor triatriatum.

Although this lesion can be visualizedby 2-D echocardiography, cardiac catheterization and angiographyare definitive.

Tumor

Tumor withinleft atrium, usually myxoma, can produce findings similar to mitral stenosis,but if tumor is on pedicle that sometimes protrudes into mitralvalve orifice, findings may be intermittent.

2-D echocardiography and MRI revealtumor mass.

Mitral Valve Obstruction (Atresia, Stenosis, Parachute Mitral Valve)

Most severeform is mitral atresia, which is discussed later in section Hypoplastic Left Heart Complex.

Mitral stenosis is prototype lesionof LV inflow tract obstruction. Congenital mitral stenosis occursas isolated lesion or in association with other lesions (e.g., aorticstenosis, VSD, ASD, coarctation of aorta, or endocardial fibroelastosis).Cusps may be abnormal, commissures may fuse, or chordae tendinaemay join below valve ring. Parachute valve with chordae tendinaeattached to single papillary muscle also may cause obstruction toblood flow at mitral valve level.

Congenital forms of mitral stenosisare usually severe, and infants present with cardiac failure. Usualphysical findings are prominent RV impulse, loud S1, and accentuatedpulmonic component of S2. Apical mid-diastolic murmur with presystolicaccentuation may not be heard with severe cardiac failure but maybe heard once failure is controlled. Opening snap of mitral valvemay not be heard because of thickness and immobility of valve. Variousdegrees of mitral incompetence may occur, and typical apical murmurof mitral insufficiency may be heard. With severe pulmonary arteryhypertension and RV dilatation, murmur of tricuspid insufficiencyalso may be heard.

Chest radiography shows left atrialenlargement out of proportion to cardiac enlargement, large pulmonaryartery segment, and pulmonary edema in severe cases.

ECG shows hypertrophy of RV and bothatria.

2-D echocardiography shows anatomyand function of valve and presence of any other abnormalities. Dopplermethods can also estimate flow and pressure difference across valve.

Diagnosis rarely needs confirmationby cardiac catheterization and angiography.

Right Ventricular Inflow Tract Obstruction

Systemic Venous Obstruction

May be dueto obstruction of venous return in superior or inferior vena cavaby thrombus, mediastinal mass, or secondary to atrial baffle procedurefor aortopulmonary transposition.

Venous distension and edema of thatportion of body drained by obstructed vessel usually occurs.

Right Atrium Obstruction

Thrombusformation may produce obstruction and can be complication of indwelling cathetersin vena cava or right atrium.

Right atrial myxoma and extension ofWilms tumor or hepatic tumor also may produce obstruction.

Tricuspid Valve Obstruction

Tricuspidatresia is most severe form of tricuspid valve obstruction. See Chap. 12, Cyanosis.

Isolated tricuspid stenosis is rare,and if atrial septum is intact, findings are those of venous obstruction.If stenosis is severe, there is mid-diastolic rumbling murmur atlower left sternal border, and prominent S3 and S4.

ECG shows tall peaked P waves indicativeof right atrial enlargement. Right atrium is also enlarged on chestradiograph.

2-D echocardiography is diagnostic.

Ebstein Anomaly

Septal andinferior leaflets of tricuspid valve are displaced into RV withanomalous attachments to wall of RV.

Depending on specific anatomy, widespectrum of clinical presentations occurs. With severe RV dysfunctionand increased pulmonary vascular resistance, intense cyanosis andcardiac failure can occur in neonatal period. Usual physical findingsare wide splitting of S2, prominent S3 and S4, murmur of tricuspidincompetence, and hepatomegaly.

Chest radiography shows marked cardiomegalywith enlargement of right atrium (heart shape is globular) and usuallydecreased pulmonary vascular markings.

ECG commonly shows right atrial hypertrophy,prolonged PR interval, right bundle branch block, and sometimesWolff-Parkinson-White syndrome.

2-D echocardiography is diagnostic.

When specific anatomic details needto be evaluated, cardiac catheterization and angiography are necessary.

Cor Pulmonale

Definedas pulmonary hypertension complicating lung disease.

Most common causes in pediatric populationare bronchopulmonary dysplasia, cystic fibrosis, and chronic upperairway obstruction.

Patients may experience dyspnea, fatigue,exercise intolerance, chest pain, syncope, and cyanosis. Physicalfindings include RV heave, increase in intensity of S2 with narrowor fixed splitting, jugular venous distension, hepatomegaly, andperipheral edema.

Chest radiographic findings may showevidence of chronic lung disease with RV enlargement and dilatedcentral pulmonary arteries.

ECG usually shows RV hypertrophy.

Systemic Hypertension

Althoughcommon cause of cardiac failure in adults, children with hypertensiondo not usually develop failure unless onset is acute or hypertensionis extremely severe.

Most common cause of acute severe hypertensionin childhood is acute glomerulonephritis.

BP should always be measured in anyonewith cardiac failure.

See Chap.32, Hypertension.

Disturbance in Myocardial Function

Acute Rheumatic Fever and Rheumatic Heart Disease

Acute andchronic cardiac failure can result from rheumatic heart disease.Most common valve lesions are mitral and aortic incompetence.

See Chap.37, Limp.

Kawasaki Disease

Most seriouscomplications are coronary artery aneurysm, coronary thrombosis,myocarditis, mitral valve incompetence, pericardial effusion, andarrhythmias.

Indications of cardiac involvementare murmur of mitral incompetence, pericardial friction rub, chestradiographic findings of cardiomegaly and pulmonary venous congestion,ST and T-wave changes on ECG, and coronary aneurysms as shown by2-D echocardiography.

See Chap.21, Fever.

Myocarditis

Usual causeis enteroviral infection. Isolation of pathogen from myocardiumis most reliable way to determine etiology; however, this is notalways possible. Isolation from other tissues or body fluids orserologic tests can be used.

Clinical manifestations include fatigue,dyspnea, chest pain, and tachypnea. Cardiac failure with pulmonaryedema and shock also may occur.

Chest radiography shows marked cardiomegalyand pulmonary venous congestion.

ECG findings suggestive of myocarditisare generalized low-voltage QRS complexes, T-wave inversion, andarrhythmias (e.g., ventricular extrasystoles and atrial tachycardia).

2-D echocardiography shows dilatationof chambers and poor contractility.

Pericarditis

Acute pericarditisis inflammation of parietal pericardium, which can be associated withinfectious or noninfectious disorder.

Infectious causes include viruses (enterovirusesmost commonly), pyogenic bacteria (S. aureus, S. pneumoniae, N.meningitidis, and H. influenzae type b most commonly), M. tuberculosis, andfungi (Candida and Aspergillus species).

Noninfectious causes include acuterheumatic fever, juvenile rheumatoid arthritis, Kawasaki disease,and postpericardiotomy syndrome.

Can occur in asymptomatic individualwith mild pericardial effusion or as life-threatening process inwhich large effusion may compromise cardiac function (cardiac tamponade).Chest pain is most common symptom of pericarditis, but exerciseintolerance and fever also may occur. Cardiac exam reveals muffledheart sounds, tachycardia, and friction rub if effusion is smallvolume. Rub is grating to and fro sound heard best in inspirationwith patient leaning forward. Manifestations of tamponade includetachycardia, reduced BP, and pulsus paradoxus with >10mm Hg decrease in systolic BP during inspiration as result of decreasedcardiac filling.

Chest radiography shows increase insize of cardiac shadow.

ECG shows low-voltage QRS complexesand generalized ST segment elevation.

2-D echocardiography can demonstrateeffusion.

Specific etiology of infectious pericarditisis best determined by evaluation of pericardial fluid obtained bypericardiocentesis. Appropriate viral, bacterial, mycobacteria,and fungal cultures should be performed. Serologic tests may benecessary for diagnosis of viral disease.

Endocarditis

Infectionof cardiac endothelial surface signifies endocarditis.

In pediatric population, usually occursas complication of congenital or rheumatic heart disease, valvehomografts, or artificial heart valves. Most frequent pathogensin childhood are viridans streptococci and S. aureus.

Common findings include fever, malaise,anorexia, and weight loss. New or changed murmur, splenomegaly,petechiae, and embolic phenomena are often found, but Osler nodes,Roth spots, Janeway lesions, and splinter hemorrhages are uncommon.

Although clinical findings suggestdiagnosis, positive blood culture confirms specific pathogen involved.2-D echocardiography can show characteristic vegetations.

Cardiomyopathy

Chronicmyocardial diseases can be classified as dilated, hypertrophic,or restrictive cardiomyopathies.

Dilated cardiomyopathy is thought to be primaryor result from viral myocarditis.

Hypertrophic cardiomyopathy is oftengenetic and may be associated with neuromuscular disorders.

Restrictive cardiomyopathy may be associatedwith infiltrative disorders.

Chest radiography usually shows enlargedheart.

ECG often shows LV hypertrophy, STsegment flattening, and T-wave inversion.

Echocardiography shows marked ventricularenlargement and poor contractile function with dilated cardiomyopathy,massive septal hypertrophy with hypertrophic cardiomyopathy, andlarge dilated atria with reduced ventricular filling with restrictivecardiomyopathy.

Cardiac biopsy is only occasionallyuseful in making specific diagnosis.

Myocardial Infarction

Anomalous Left Coronary Artery from Pulmonary Artery

May presentwith acute myocardial infarction and cardiac failure in infancy.Murmur of mitral incompetence may be heard.

Chest radiography shows cardiomegalyand pulmonary venous congestion.

ECG shows anterior or anteroseptalmyocardial infarction with deep Q waves and T-wave inversion inleads 1, aVL, and left precordial leads.

2-D echocardiography with Doppler methodsis almost always diagnostic.

Cardiac catheterization and angiographyare definitive.

Older children are usually asymptomaticand may only present with murmur of mitral incompetence or continuousmurmur at upper left or mid-sternal border. Presence of deep Q wavesin leads 1, aVL, and V4–V6 suggests diagnosis.

Atherosclerosis

Familialhypercholesterolemia (familial hyperlipoproteinemia type II) cancause atherosclerosis and myocardial infarction in childhood.

Genetic transmission is autosomal-dominant.

Tendon and tuberous xanthomas are common.

Plasma cholesterol is high (600–1,000mg/dL), plasma triglycerides are normal, and low-densitylipoproteins are elevated.

Cardiac Tumor

Mass withinchamber can cause inflow or outflow tract obstruction. Involvementof myocardium can cause cardiac failure.

Benign tumors include rhabdomyoma,fibroma, myxoma, and teratoma, whereas malignant tumors includerhabdomyosarcoma and teratoma. Leukemia and lymphoma can involvepericardium and cause pericardial compression.

Clinical manifestations vary dependingon location and histologic type.

2-D echocardiography and MRI locateand define extent of mass lesion.

Histologic diagnosis is definitive.

Metabolic Heart Disease

Severalcommon metabolic problems that affect myocardial function are discussedin this section.

See Garson et al. (1998) for detaileddiscussion of metabolic disorders affecting heart.

Perinatal Asphyxia

Can producetransient ischemia of myocardium and cardiac failure.

Gallop rhythm and murmurs of mitralor tricuspid incompetence may be heard.

Chest radiography shows cardiomegalywith pulmonary venous congestion.

ECG shows RV hypertrophy, ST depression,and T-wave flattening. Abnormal Q waves in limb and chest leadssuggest anterior or inferior myocardial infarction.

2-D echocardiography sometimes showsdecreased myocardial contractility.

Hypocalcemia

Can causedilated cardiomyopathy in neonates and older children.

Cardiac failure usually resolves withrepletion of calcium.

Hypoglycemia

In neonateshypoglycemia may cause cardiomegaly and cardiac failure.

Risk factors include maternal diabetesmellitus, low birth weight, and septicemia.

Severe Anemia

Any severe chronic anemia with hemoglobinconcentration <5 g/dL may produce cardiac failure.

Drugs

Anthracyclineantibiotics doxorubicin and daunomycin are cancer chemotherapeutic agentsthat can damage myocardium. Development of cardiac failure is relatedto cumulative dose.

Echocardiographic ejection fractionmeasurements are useful for monitoring individuals who are takingthese drugs.

Complex Anatomic Lesions

5 lesionsin this section involve intracardiac or ductal right-to-left shunts.

Cardiac failure is most obvious manifestation,and cyanosis is not often clinically visible.

Hypoplastic Left Heart Complex

2 basic types of hypoplastic left heart complexare (a) aortic and mitral atresia with absent or slitlike LV, and(b) aortic and mitral stenosis with small LV.

Aortic and Mitral Atresia

Usuallypresent within 48 hrs of birth with cardiac failure and mild cyanosis.Usual physical findings are prominent RV impulse, single loud S2,grade II/VI systolic ejection murmur along left sternalborder, hepatomegaly, and diminished peripheral pulses.

Chest radiography shows moderate cardiomegalyand pulmonary venous congestion.

ECG shows RV hypertrophy.

2-D echocardiography shows large RV,small or absent LV, mitral and aortic atresia, and hypoplastic ascendingaorta.

Aortic and Mitral Stenosis

Usuallypresent with cardiac failure in first or second week after birth.Usual physical findings are prominent RV impulse or LV impulse dependingon size of LV, single or narrow split of S2, murmur of aortic stenosis,hepatomegaly, and diminished pulses.

Chest radiography shows enlarged heartand pulmonary venous congestion.

ECG usually shows LV hypertrophy withoccasional ST depression and T-wave flattening or inversion in leftprecordial leads.

2-D echocardiography is usually diagnostic.

Transposition of Great Arteries with Large Ventricular SeptalDefect

The aortarises from RV, while pulmonary artery arises from LV. Large communicationexists at ventricular level and also may occur at ductal level.

Cardiac failure and mild cyanosis occurat 2–4 wks of age. Murmur of VSD can be heard. S2 is narrowwith accentuated pulmonary component.

Chest radiography shows cardiomegaly,increase in pulmonary vascular markings, an absent pulmonary arterysegment.

ECG shows RV or biventricular hypertrophy.

2-D echocardiography is diagnostic.

Double-Outlet Right Ventricle

Both aortaand pulmonary artery arise entirely or in large part from RV. VSDis part of this lesion and can be subaortic, subpulmonic, doublycommitted, or noncommitted. Subaortic and subpulmonic defects aremost common.

Clinical presentation of subaorticdefect is similar to that of isolated large VSD, whereas clinicalpresentation of subpulmonic defect is similar to that of transpositionof great arteries with intact ventricular septum.

2-D echocardiography is usually diagnostic.

Cardiac catheterization and angiographyare important in planning of surgery.

Truncus Arteriosus

1 greatartery with single semilunar valve arises from base of heart. Systemic,coronary, and 1 or 2 pulmonary arteries arise from this artery.Beneath valve is VSD. Usually presents during neonatal period withcardiac failure and mild cyanosis.

Usual physical findings are diffuseprominent impulse at lower left sternal border, occasional ejectionclick, grade II–IV/VI systolic ejection murmuralong left sternal border, wide pulse pressure, and hepatomegaly.Other possible findings are early diastolic murmur along left sternalborder, which signifies truncal incompetence, or continuous murmurat 1 or both upper sternal borders, which reflects stenosis of originof 1 or both pulmonary arteries. Stenosis of truncal valve may produceharsh systolic ejection murmur at upper right sternal border.

Chest radiography shows cardiomegaly,increase in pulmonary vascular markings, deficient main pulmonaryartery segment, and frequently right aortic arch.

ECG shows RV hypertrophy and frequentlybiventricular hypertrophy.

2-D echocardiography is diagnostic.

Cardiac catheterization and angiographycan define anatomy of pulmonary arteries, aortic arch, truncal valve,and hemodynamic state.

Univentricular Atrioventricular Connections

Definedas malformations in which both AV valves or common AV valve openinto same ventricle.

In absence of pulmonary stenosis oratresia, clinical presentation of this lesion is similar to thatof large VSD.

Chest radiography shows cardiomegalywith increase in pulmonary vascular markings.

ECG may show increased voltage in eitherright or left precordial leads.

2-D echocardiography and cardiac catheterizationand angiography are diagnostic.

Abnormal Cardiac Rhythms

Supraventricular Tachycardia

Most childrenhave structurally normal heart; however, some may have Wolff-Parkinson-Whitesyndrome.

Mechanisms include reentry using accessorypathway, reentry without accessory pathway, and automatic tachycardia.

In infants <1 yr of age, ventricularrate varies from 220 to 280 bpm, whereas in older children it variesfrom 180 to 240 bpm. RR interval is regular, and onset and terminationof rhythm are usually sudden. P waves may or may not be visible.They follow or precede each QRS or are unrelated (AV dissociation).

In infants left bundle branch blockpattern with aberrant conduction is common. Neonates may developcardiac failure if arrhythmia lasts only few hours. Infants whohave this abnormal rhythm for >24 hrs are at risk for developmentof cardiac failure.

ECG confirms diagnosis. Fetal echocardiographymay confirm diagnosis in utero.

Atrial Flutter

Can occurin individuals with normal heart, in those with structural defects,and after surgery for congenital heart defects.

Can cause cardiac failure, especiallyin young infant.

Atrial rate varies from 250 to 500bpm. With 1:1 conduction, ventricular rate is too fast for ventriclesto fill in diastole, and low cardiac output occurs. With some degreeof AV block such that conduction is 2:1, assuming atrial rate of300 bpm and ventricular rate of 150 bpm, cardiac failure is unlikely. RRinterval is usually regular, but it can be irregular in presenceof AV block.

Sawtooth flutter waves are diagnostic.

Complete Heart Block

Congenitalcomplete heart block can occur in infants with otherwise normalheart, in some neonates whose mothers have systemic lupus erythematosus,and in infants with ventricular inversion and transposition of greatarteries.

May occur following surgical correctionof congenital heart defects.

Cardiac failure occurs only if ventricularrate is too slow to maintain normal cardiac output. In neonates,ventricular rate of <40 bpm usually results in cardiacfailure, whereas infants with ventricular rate of >50 bpmare usually asymptomatic.

ECG shows lack of conduction of atrialimpulses to ventricles with faster atrial rate and slower ventricularrate.

Diagnostic Approach

Diagnosis of Cardiac Failure

Diagnosisof cardiac failure is clinical and is based on history and physicalexam findings.

Most cardiac disease produces LV orbiventricular failure. Pure right heart failure is uncommon.

Manifestations of cardiac failure ininfants are increased work of breathing, tiring with feedings, andpoor weight gain.

Tachycardia, sweating, gallop rhythm,and cardiac enlargement indicate impaired myocardial performance.

Tachypnea, dyspnea, wheezing, cough,crackles, and cyanosis are manifestations of pulmonary venous congestion.

Signs of systemic venous congestionare hepatomegaly, neck vein distension, peripheral edema, splenomegaly,and ascites.

Diminished peripheral pulses and hypotensionreflect decreased cardiac output.

In infancy, crackles may not be heard,neck vein distension is difficult to evaluate, and peripheral edemais uncommon.

Once diagnosis is made, next task isto determine specific cause.

Age of Onset of Cardiac Failure

Often providesclue to specific cause of cardiac failure.

Birth–1 wk: Causes of cardiacfailure include perinatal asphyxia, severe anemia, complete heartblock, supraventricular tachycardia, hypoplastic left heart syndrome,critical aortic stenosis, critical pulmonary stenosis, complex coarctationof aorta, VSD with absent pulmonary valve, aortic incompetence (aorta–LVtunnel syndrome), isolated tricuspid incompetence, and Ebstein anomaly.

1–6 wks: Common causes ofcardiac failure include patent ductus arteriosus, VSD, complete AVcanal, double-outlet RV, truncus arteriosus, transposition of greatarteries with large VSD or patent ductus arteriosus, univentricularAV connections, simple or complex coarctation of aorta, total anomalous pulmonaryvenous connection with obstruction, severe aortic stenosis, anycause of pulmonary venous obstruction, myocarditis, anomalous leftcoronary artery, and any cause of severe anemia.

Common acquired causes of cardiac failureare myocarditis, cardiomyopathy, pericarditis, acute rheumatic fever,endocarditis, postcardiac surgery for complex lesions, and arrhythmias.

Diagnostic Categories

Many cardiaclesions can be grouped together in diagnostic categories based onpresence or absence of cyanosis, physical exam findings, and chestradiographic findings (Table 7.1 ).

Other tests (e.g., ECG, 2-D echocardiographywith Doppler methods and cardiac catheterization with angiography)can be used to make definitive diagnosis.

Table 7.1. Diagnostic Classification of Common Causes of CardiacFailure

Group	Findings	Possible Causes
I	Acyanotic	Left-to-right shunt lesions
	Cardiomegaly
	Increased pulmonary vascular markings
II	Acyanotic	Left-sided obstructive lesions
	Cardiomegaly
	Pulmonary venous congestion
III	Acyanotic usually	Myocarditis
	Cardiomegaly	Cardiomyopathy
	Pulmonary venous congestion	Anomalous coronary artery
	No heart murmur frequently
IV	Mild cyanosis	Transposition with large VSD
	Cardiomegaly	Hypoplastic left heart syndrome
	Increased pulmonary vascular markings	Double-outlet RV
		Truncus arteriosus
		Univentricular AV connections
V	Marked cyanosis	Pulmonary venous obstruction
	Normal-sized heart or mild cardiomegaly
	Pulmonary venous congestion
VI	Cyanosis	Critical pulmonic stenosis
	Cardiomegaly	Ebstein anomaly
	Decreased pulmonary vascular markings

Evaluation

These testsshould generally be performed in any infant or child with cardiacfailure: chest radiography; ECG; CBC with differential; analysisof serum electrolytes, glucose, creatinine; blood urea nitrogen;pulse oximetry; and 2-D echocardiography.

Chest radiography shows presence ofcardiomegaly and whether pulmonary vascular markings are normal,increased, or decreased.

ECG indicates presence of hypertrophyof chambers and permits diagnosis of arrhythmias.

Hyponatremia is common and reflectsincrease in water retention in excess of sodium.

2-D echocardiography with Doppler methodsis often diagnostic or at very least provides useful informationin many cases of cardiac failure. Cardiac catheterization with angiographyprovides definitive diagnosis for selected heart lesions.

References

1. Garson A Jr, et al., eds. The scienceand practice of pediatric cardiology, 2nd ed. Baltimore: Williams & Wilkins,1998.
2. Kirklin JW, Barratt-Boyes BC. Cardiac surgery. NewYork: John Wiley & Sons, 1986.
3. Long SS, et al., eds. Principles and practice of pediatricinfectious diseases. New York: Churchill Livingstone, 1997.
4. Rudolph AM. Congenital diseases of the heart. Chicago:Year Book Medical, 1974.
5. Rudolph AM, ed. Rudolph's pediatrics, 20thed. Stamford, CT: Appleton & Lange, 1996.

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Book Source Details

• Book Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics
• Author(s): Paul S. Bellet
• Year of Publication: 2006
• Copyright Details: The Diagnostic Approach to Symptoms and Signs in Pediatrics, Copyright © 2006 Lippincott Williams & Wilkins.

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More About This Book: Title: The Diagnostic Approach to Symptoms and Signs in Pediatrics Authors: Paul S. Bellet Publisher: Lippincott Williams & Wilkins Copyright: 2006 ISBN: 0-78172-899-1

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