PEDIATRIC CARDIOLOGY

Jocelyn C. Banatao, MD, DPPS

HISTORY TAKING
Gestational and Natal History
1. Infections
a. Maternal rubella – 1st trimester results in multiple anomalies, cardiac defects
b. CMV, herpes virus, cocxsackievirus B
 teratogenic in early pregnancy
 may cause myocarditis later in pregnancy
2. Medications, including alcohol and smoking
 amphetamines – VSD, PDA, ASD, TGA
 anticonvulsants – PS, AS, COA, PDA
 progesterone/estrogen – VSD, TOF, TGA
 alcohol – featl alcohol syndrome, VSD, PDA,ASD, Tof
 cigarette smoking – IUGR (intrauterine growth retardation)
3. Maternal conditions
 diabetic mother – cardiomyopathy in infants, structural heart defects (TGA, VSD, PDA)
 maternal lupus erythematosus, mixed connective tissue disease – congenital heart block in off spring
 mother with CHD – incidence of CHD increases from about 1% in the general population to 15% even
if it is post-operative
4. Birth weight
 SGA indicates intrauterine infections
 high birth weight – seen in diabetic mothers, higher incidence of cardiac anomalies

Postnatal History
1. Weight gain and development, including feeding pattern
 delayed weight gain and general development in infants and children with CHD or severe cyanosis
 weight is more affected than height
 poor feeding – early sign of CHF in infants especially if it is the result of fatigue and dyspnea
2. Cyanosis, “Cyanotic spells”, and squatting
 Ask about the onset of cyanosis
 did it occur in the nursery or shortly after coming from home
 the severity, permanent or paroxysmal nature
 whether cyanosis becomes worse after feeding
 “cyanotic spells” – seen in infants with TOF
 ask about the time of its appearance ( in the morning on waking, after feeding)
 duration and frequency of the spell
 Breath-holding spell – breathing fast and deep during the spell or were holding their breaths
 History of squatting or knee-chest position - TOF
3. Tachypnea, dyspnea, puffy eyelids
 These are signs of CHF
 Left sided heart failure produces tachypnea with or without dyspnea
 Tachypnea becomes worse with feeding and results in poor feeding and poor weight gain
 Respiratory rate of >60bpm is abnormal
 Wheezing or persistent cough at night – early sign of CHF
 Puffy eyelids and sacral edema – systemic venous congestion

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Frequency of respiratory infections
 CHDs with large left-to-right shunts and increased pulmonary blood flow predispose to lower respiratory
tract infections.

Exercise intolerance
 Decrease exercise tolerance may result from any significant heart disease
 Obese children may be inactive and have decrease exercise tolerance in the absence of heart disease
 Does the child keep up with other children?
 How many blocks can the child walk or run?
 How many flights of stairs can the child climb without fatigue?
 With infants, ask the infant’s history of feeding pattern

Heart murmur
 Obtain information about the time of its first appearance and the circumstances of its discover
 Heart murmur at birth –indicates stenotic lesions (AS, PS), small left to right shunt lesions(VSD, PDA)
 Large left to right shunt lesions (VSD,PDA) - delayed because of slow regression of pulmonary vascular
resistance
 Stenotic lesions, onset of lesions is not affected by PVR, and the murmur is heard shortly after birth
 Febrile illness is associated with the discovery of murmur.

Chest pain
 Ask whether the pain is activity tolerated.
 Ask about the duration.
 Nature of pain(stabbing, squeezing)
 Radiation to other parts of the body (neck, left shoulder, left arm)
 Chest pain of cardiac origin is not sharp but rather deep, heavy pressure or the feeling of choking or a
squeezing sensation and triggered by exercise
 Ask whether deep breathing improves or worsens the pain
 Pain of cardiac origin is not affected by respiration except for pericarditis
 Ask for any recent cardiac death in the family
 3 most common noncardiac causes of chest pain in children: coctochondritis, trauma to the chest wall,
respiratory diseases ( bronchitis,pneumonia).
 Most children complaining of chest pain do not have a cardiac conditions.

Palpitation
 Subjective feeling of rapid heart beat.
 Children with MVP may first be taken to the physician due to palpitation.

Joint symptom
 When join pain is the primary complaint, rheumatic arthritis is a possibility.
 Ask about the number of joints involved, duration, migratory or stationary nature of the pain.
 Ask whether the joint was swollen, red, hot or tender.

Neurologic symptoms
 History of stroke suggest embolization or thrombosis 2’ to cyanotic CHD with polycythemia or infective
endocarditis
 History of headache – cerebral hypoxia with cyanotic heart disease, severe polycythemia, or brain abscess
in cyanotic children.
 Choreic movement suggests arrhythmia.
Medication
 Note the name, dosage, timing, and duration of cardiac and noncardiac medications.
 Tachycardia and palpitation – caused by cold medications or antiasthmatic drugs (aminophylline)

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Family History
 Hereditary diseases – associated with certain forms of CHDs
 Congenital heart disease – incidence is 8-12 of 1000 live births
 history of CHDs in close relatives increases the chance of CHD in a child
 Rheumatic Fever – occurs in more than one family member
 higher incidence among relatives of rheumatic children (INHERITED SUSCEPTIBILITY to
acquiring RF).

PHYSICAL EXAMINATION
1. Inspection
a. General Appearance and Nutritional State
 child is in distress
 Well-nourished or undernourished
 Happy or cranky
b. Chromosomal abnormalities
CONDITIONS INCIDENCE OF CHD DEFECTS
Cri du chat syndrome 25% VSD, PDA, ASD
Tri 13 90% VSD, PDA, dextrocardia
Tri 18 99% VSD, PDA, PS
Tri 21 50% ECD, VSD
Turner’s syndrome 35% COA, AS, ASD
Klinefelter’s variant 15% PDA, ASD

c. Color
 Note whether the child is cyanotic, pale or jaundiced
 If cyanotic, the degree and distribution should be noted
 Arterial saturation is <85% before cyanosis is detectable in pts with normal hemoglobin levels.
 Children with cyanosis do not always have cyanotic CHD
 Cyanosis may result from respiratory disease or CNS disease.
 Peripheral cyanosis- normal arterial saturation
 Central cyanosis – with arterial desaturation
d. Clubbing
 Long standing arterial desaturation, longer than 6 months
 Widening and thickening of the ends of the fingers and toes, convex fingernails and loss of angle
between the nail and nail bed.

Respiratory rate, dyspnea and retraction

 If the infant breathes irregularly, count for a minute
 Most reliable RR taken during sleep.
 >60bpm is abnormal at any age.
 Tachypnea along with tachycardia is the earliest sign of left-sided heart failure.

Sweat on the forehead

 Infants with CHF often have cold sweat on their forehead
 Sympathetic over activity as a compensatory mechanism for the decreased cardiac output

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Inspection of the chest
 Precordial bulge – chronic cardiac enlargement
 Pectus excavatum – undue depression of the sternum, rarely causes cardiac embarrassment
 Harrison’s groove – line of depression in the bottom of the rib cage along the attachment of the
diaphragm, indicates poor lung compliance of long duration
2. Auscultation
 Provides more valuable information than other methods of heart examination
 Normal heart rates:
 Newborn – 110-150bpm
 2 years – 85-125
 4 years – 75 – 115
 >6 years – 60 -100

Intensity of the murmur

 Grade 1 - barely audible
 Grade 2 – soft, but easily audible
 Grade 3 – moderately loud, not accompanied by thrill
 Grade 4 – louder and associated by thrill
 Grade 5 – audible with stethoscope barely on the chest
 Grade 6 – audible with the stethoscope off the chest

CYANOTIC CONGENITAL HEART DISEASE – RIGHT-TO-LEFT SHUNTS

CONSEQUENCES AND COMPLICATIONS
1. Polycythemia – increase number of red blood cells
 low arterial oxygen content stimulate bone marrow through erythropoietin release from the kidneys
 increase oxygen carrying capacity, benefits cyanotic children
 hematocrit >65% - increase in viscosity of blood (polycythemic response is disadvantageous
2. Clubbing
 Does not appear until a child is 6 months or older
3. Hypoxic spells and squatting
 Hypoxic spells – period of uncontrollable crying, rapid and deep breathing, deepening of cyanosis,
limpness or convulsions, and occasionally death.
 Squatting – seen in children with right-to-left shunt, increases arterial oxygen saturation, by temporary
trapping desaturated blood in the lower extremities.
4. Central nervous system complications
 Cyanotic infants are prone to develop disorders of the CNS, such as brain abscess or cerebrovascular
accidents.
 Right-to- left shunts may bypass the normally effective phagocytic filtering actions of the pulmonary
capillary bed
 Polycythemia and high viscosity of blood lead to tissue hypoxia and microinfarction of the brain,
complicated by bacterial colonizations
5. Bleeding disorders
 Disturbances in hemostasis, noted as thrombocytopenia and platelet aggregation.
 Easy bruising, petechiae, epistaxis, gingival bleeding
6. Depressed intelligent quotient
 Poorer perceptual and gross motor function even after surgical repair of cyanotic heart disease.
7. Scoliosis – particularly girls and patients with TOF.
8. Hyperuricemia and gouts
1. COMPLETE TRANSPOSITION OF THE GREAT ARTERIES

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  Clinical Manifestations:
 Cyanosis from birth
 Signs of CHF with dyspnea and feeding difficulties during the newborn period.
 Hepatomegaly
 Laboratory studies:
 Severe arterial hypoxemia – does not respond to 02 inhalation.
 Hypoglycemia and hypocalcemia
 X-ray studies
 cardiomegaly with increase vascularity
 egg- shaped cardiac silhouette
 Management :
 supportive therapy
 digoxin and diuretics – CHF
 surgery

2. TETRALOGY OF FALLOT
 Incidence: 10% of all CHD
 Most common cyanotic heart defect in
children beyond infancy
 Components:
 Large VSD
 RV outflow tract obstruction
 RVH (right ventricular hypertrophy)
 Overriding of the aorta
 Clinical manifestations:
 Heart murmur is audible at birth.
 Most patients are symptomatic with cyanosis at birth, dyspnea on exertion; squatting or hypoxic spells
develop later in mildly cyanotic infants.
 Failure to thrive
 Frequent respiratory tract infections
 PE:
 Blowing systolic murmur
 X-Ray: boot – shaped heart
 Natural history:
 Hypoxic spells for <2yr
 Infective endocarditis
 Brain abscess or CVA
 polycythemia
 Management:
 Prevent iron deficiency
 Avoid dehydration
 Propranolol for anoxic spells as temporary measure
 Classical or modified Blalock-Taussig shunt – palliative procedure
 Corrective surgery-optimal age 2-3 years

3. TRICUSPID ATRESIA
 Tricuspid valve is absent, RV is hypoplastic
 Clinical manifestations:
 Cyanosis is severe from birth.
 Tachypnea and poor feeding usually manifest
 History of hypoxic spells
 X-ray:

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  Mild to moderate cardiomegaly with enlarged right and left atria
 Prognosis:
 Death occurs within the 1st 6mos of life from severe anoxic spells and CHF
 Large septal defects survive up to the age of 3-6years
 Management :
 Prostaglandin E- to maintain the patency of the ductus before planned cardiac catheterization or
surgery
 Surgery – shunt operation (blalock-taussig shunt)

4. PERSISTENT TRUNCUS ARTERIOSUS

 Only a single arterial trunk with a truncal valve leaves the heart and gives rise to the pulmonary, systemic
and coronary circulation.
 Clinical manifestations:
 Cyanosis seen immediately at birth
 Signs of CHF develop within several days or weeks after birth
 History of dyspnea with feeding, FTT, and frequent respiratory infections
 X-ray :
 Cardiomegaly with increased pulmonary vascular markings
 Natural history:
 Most infant die of CHF within 6-1 months, longer survival in types with normal PBF
 Truncal valve insufficiency worsens with time
 Management :
 Vigorous anticongestive measures with diuretics and digitalis
 Surgery: Rastelli procedure

LEFT- TO- RIGHT SHUNT(ACYANOTIC)

1. ATRIAL SEPTAL DEFECT
 3 types:
 Ostium secundum – MC type
 Ostium primum
 Sinus venosum
 History:
 Infants and children are usually asymptomatic
 PE:
 Slender body built is typical (BW is <10th %)
 Typical auscultatory findings may be absent in infants
 X-ray:
 Cardiomegaly with RAE and RVE are visible
 Natural history:
 Spontaneous closure of the secundum defect occurred
in 40% of cases in the 1st 4yrs of life, some may
decrease in size, and spontaneous closure is 87%.
 Spontaneous closure is 100% in patients with defect <3mm at 1 ½ years of age
 Closure is 80% with defects 3-8mm before 1 ½ years
 >8mm rarely closes spontaneously
 Most children with ASD remain active and asymptomatic, although CHF develops in infancy
 If untreated, CHF and pulmonary hypertension develop in adults in their 20s and 30s
 With or without surgery, atrial arrhythmias may occur as an adult.
 Cerebrovascular accident, through ASD is a rare complication

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  Management:
 medical:
 Exercise restriction is unnecessary.
 Prophylaxis for infective endocarditis is not indicated unless the patient has associated MVP.
 In infants with CHF medical management is recommended because of its possibility of
spontaneous closure of the defect.
 Surgical
 Surgery is delayed until 3-4years of age because of the possibility of spontaneous closure
 Surgery is performed during infancy if CHF does not respond to medical management

2. VENTRICULAR SEPTAL DEFECT

 Most common form of CHD
 Clinical Manifestations:
 History:
 Small VSD, the patient is asymptomatic with normal growth and development
 Moderate to large VSD, delayed growth and development, decrease exercise tolerance, repeated
pulmonary infections and CHF during infancy
 With long standing pulmonary hypertension, cyanosis and decreased level of activity may be
present
 Physical Examination:
 Infants with small VSD are well-developed and acyanotic
 Before 2-3 mos, infants with large VSD may have poor weight gain
 X-ray: cardiomegaly
 Natural History
 Spontaneous closure in 30-40% with membranous VSD and vascular VSDs during the first 6mo of life.
 CHF develops in infants with large VSDs but usually not until 6-8 weeks of age.
 Infective endocarditis rarely occurs
 Management
 Medical
 CHF - Digoxin and diuretics for 2-4 months to see if growth failure could be improved
 Frequent feedings of high calorie formulas
 Oral iron therapy for anemia
 No exercise restriction is required in the absence of pulmonary hypertension
 Maintenance of good dental hygiene and prophylaxis against infective endocarditis
 Surgical
 Large VSD with CHF and growth retardation are managed first with digoxin and diuretics
 If growth failure cannot be improved by medical therapy, VSD should be operated within the first
6mos of life
 Delayed for infants who respond to medical therapy

3. PATENT DUCTUS ARTERIOSUS

 More common in females
 Common problem in premature infants
 Pathology:
 Persistent patency of a normal fetal structure between the left PA and the descending aorta
 Clinical manifestations:
 Patient is usually asymptomatic when the ductus is small
 A large shunt PDA may cause lower RTI, atelectasis and CHF ( accompanied by tachypnea and poor
weight gain)
 Physical examination:
 Tachycardia and exertional dyspnea in infants with large-shunt PDA
 Precordium is hyperactive

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  Bounding peripheral pulses with wide pulse pressure
 X-ray:
 Normal with a small shunt PDA
 Cardiomegaly with large shunt
 Natural history
 Spontaneous closure of PDA among premature infants do not occur
 CHF and/or recurrent pneumonia develop if the shunt is large
 Management :
 Medical
 Indomethacin is ineffective in term infants with PDA, therefore it should not be used
 No exercise restriction is needed in the absence of pulmonary hypertension
 Surgical
 Anatomic existence of the PDA, regardless of the size, is an indication for surgery
 Surgery is performed between 6 months and 2 years of age
 Infants with CHF, pulmonary hypertension, or recurrent pneumonia, surgery is performed on an
urgent basis

OBSTRUCTIVE LESIONS
1. COARCTATION OF THE AORTA
 More common in males
 Of patients with Turner’s syndrome, 30% have COA
 Localized narrowing of the aorta
 Clinical manifestations: (symptomatic children)
 Poor feeding, dyspnea, poor weight gain or signs of acute circulatory shock may develop in the first 6
weeks of life
 Diminished pulses in the lower extremities, they may be left undiagnosed
 Pulses in the upper extremities are full with elevated systolic pressure in the arms more than in the
legs, resulting in coldness of the feet
 Diastolic pressure in both extremities are equal
 Systolic pressure varies from 110 to 220mmhg in the arms and 60-100mmhg in the legs
 Headache, epistaxis and cerebral hemorrhages may occur as a result of the hypertension
 Clinical manifestations: (asymptomatic children)
 Most children are asymptomatic
 Occasionally, a child complains of weakness and/or pain in the legs after exercise
 Patients grow and develop normally
 Arterial pulses in the legs are either absent, weak and delayed
 X-ray:
 Heart size may be normal or slightly enlarged
 E-shaped indentation on the barium filled esophagus or “3” sign on over penetrated film
 Rib notching between the 4th and 8th rib in older children
 Natural history:
 Most patients do well during the first 2 decades
 Complications: subacute bacterial endocarditis and hypertensive encephalopathy
 Management
 Medical
 Good dental hygiene and prophylaxis against SBE
 Watched closely for hypertension in the armsions or for increasing pressure differences between
the arms and legs
 Prostaglandin E1 infusion to reopen the ductus arteriosus and establish flow to the descending
aorta and the kidneys during the first week of life
 Short acting inotropics (dopamine, dobutamine), diuretics, and oxygens

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  Surgical:
 Infants with severe coarctation who do not respond to medical management should be operated
immediately
 If the child is well, active and free from complicating defects, surgery can wait until 7 or 8 years of
age
 Optimal age of operation is between 7 and 20 years

2. AORTIC STENOSIS
 M:F = 4:1
 Stenosis may be at the valvular, subvalvular, supravalvular
 Clinical manifestations:
 Mild to moderate AS are asymptomatic. Exercise intolerance may be present
 Exertional chest pain, fatigability or syncope may occur with a severe degree of obstruction
 Patients are acyanotic and have developed normally
 Narrow pulse pressure in severe AS
 Newborn with critical AS may develop CHF. Heart murmur may be absent, peripheral pulses are weal
and thready
 Heart murmur becomes louder when CHF improves
 X-ray:
 Heart size is normal in children
 Cardiomegaly in patients with CHF
 Newborns with critical AS have generalized cardiomegaly with pulmonary venous congestion
 Natural history:
 Chest pain, syncope and even sudden death with severe AS
 Heart failure with severe AS during the newborn period or later in adult life
 Stenosis may worsen with aging
 Medical management:
 Maintenance of good oral hygiene and antibiotic prophylaxis against bacterial endocarditis regardless
of the degree of stenosis
 Surgical management:
 closed aortic valvotomy using calibrated dilators or balloon catheters without cardiopulmonary bypass
 Neonates and young infants with CHF from critical AS require urgent surgery
 Asymptomatic children with systolic pressure <50mmhg do not usually require surgery

3. PULMONARY STENOSIS
 Valvular PS – pulmonary valve is thickened with fused or absent commissures and a small orifice
 Infundibular PS – associated with large VSD
 Supravalvular PS – stenosis of the main PA, seen in rubella syndrome
 Clinical manifestations:
 Mild PS are completely asymptomatic
 Exertional dyspnea and fatigability with moderately severe cases
 Heart failure or exertional chest pain may develop in severe cases
 Physical examination:
 Most patients are acyanotic and well developed
 Newborns with critical PS are cyanotic and tachypneic
 X-ray:
 Heart size is usually normal
 Cardiomegaly if CHF develops
 Management:
 Medical:
 Restriction of activity is not necessary, except in cases of severe PS
 Prophylaxis against SBE when indications arise

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  Newborn with critical PS and cyanosis may improve by prostaglandin E1 infusion which reopen
the ductus
 Surgical management:
 Children with valvular PS and RV pressure >80mmhg require surgery on elective basis

CADIOVASCULAR INFECTIONS
1. INFECTIVE ENDOCARDITIS
 About 90% of children with IE have underlying CHD or RHD
 Etiology:
 Strep viridans – 46%
 Staph aureus – 32%
 Others: S. Fecalis, strep pneumonia, H. Influenza, gr (-) organism, enterococci, fungi
 Clinical manifestations:
 Prolonged fever – most consistent
 splenomegaly, petechiae, arthritis
 anorexia, weight loss, chills, weakness, arthralgia
 Osler’s nodes, janeway’s lesions and linear splinter hemorrhages
 Heart murmur (98%)
 anemia
 Osler’s nodes –tender red nodes at the end of the fingers
 Janeway’s lesions – small, painless, hemorrhagic areas on the palms or soles
 Splinter hemorrhage – linear hemorrhagic streaks beneath the nails
 Diagnostics:
 CBC – leukocytosis
 2D-echo – vegetative lesions
 Blood culture - 85-95% + when 3 separate cultures are obtained
 ESR – elevated
 Urinalysis – microscopic hematuria
 Complications:
 CHF
 Progressive cardiac destruction
 Diffuse glomerulonephritis and renal failure
 Neurologic from mycotic, embolic, and cerebral abscesses
 Management:
 Stabilize cardiorespiratory status immediately
 Treat CHF
 Antibiotics – treatment course 6-8 wks

2. MYOCARDITIS
 Incidence: not rare
 Etiology:
 infections: viral(coxsackie A/B), rarely bacterial
 Acute RF
 Collagen disease
 Toxic myocarditis
 Clinical manifestations:
 History of previous URTI
 Sudden onset of illness in NB and small infants

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  PE:
 CHF signs, soft systolic murmur, gallop rhythm, irregular cardiac rhythm, cardiomegaly, poor
peripheral perfusion, hypotension
 Diagnostics:
 CXR – cardiomegaly
 SGOT/CPK-MB/LDH – elevated
 ECG – low QRS complexes, prolonged QT interval, arrhythmia
 ESR/CRP elevated
 Management:
 Anti CHF regimen
 BP control
 Supportive measures
 fluid and caloric maintenance
 electrolyte imbalance correction
 anemia correction
 acid-base balance correction
 temperature control

3. RHEUMATIC FEVER
 Major Criteria:
a. Arthritis (70%) involves large joints, >1 joint, migratory with swelling, heat, redness, severe pain
tenderness and limitation of motion
 dramatic response to salicylates, if do not respond to ASA in 48hrs, RF is unlikely, probably
“poststreptococcal reactive arthritis”
b. Carditis (50%) signs:
 Tachycardia – out of proportion to degree of fever, if absent, myocarditis is unlikely the diagnosis
 Murmur (MR/AR) – carditis is not diagnosed if absent
 Pericarditis – friction rub, pericardial effusion, chest pain, and ECG changes
 Cardiomegaly – on CXR indicates pericarditis, pancarditis or CHF
 CHF signs – gallop rhythm, distant heart sound, cardiomegaly, indicates severe carditis
c. Erythema marginatum (<10%)
 non-pruritic, serpiginous or annular erythematous rashes, prominent on the trunk and inner
parts of the extremities, never seen on the face, avanescent, disappear on cold exposure,
reappears after hot shower
d. Syndenham’s chorea (15%)
 Often in pre-pubertal girls(8-12 yo) than boys
 Begin with emotional lability and personality changes, then loss of motor coordination
 With spontaneous, purposeless movement followed by motor weakness
 May persist for 7 -17 mos then slowly wanes
e. Subcutaneous nodules (2-10%)
 hard, painless, non-pruritic freely movable swelling, 0.2-2 cm diameter, symmetrical found
singly/clusters on extensor surfaces of small and large joints, scalp or spine, may last for weeks
 Minor criteria:
a. arthralgia – joint pain without objective changes of arthritis, not considered as minor criteria when
arthritis is present
b. Fever - <39’C
 Laboratory Findings:
c. Elevated acute phase reactants (ESR erythrocyte sedimentation rate, R- reactive protein) – objective
evidence of inflammatory process
d. Prolonged PR interval – not specific for RF
 Plus....
 Supportive evidence of antecedent group A streptococcal infection

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 a. Positive throat culture or rapid streptococcal antigen test
b. Elevated or rising streptococcal antibody titer
 ASO
 antideoxyribonuclease B test
 streptozyme test
 Diagnosis
 2 major; or
 1 major + 2 minor
 Plus evidence of a previous group A streptococcal infection
 Exceptions:
 Chorea – may be the only manifestations of RF
 Carditis may be the only manifestations in patients who come to medical attention months after
the onset of RF
 Clinical course:
 Only carditis can cause permanent cardiac damage. Mild carditis rapidly disappears in weeks,
severe carditis in 2-6 months
 Arthritis subsides in a few days – several weeks even without treatment, with no permanent
damage
 Chorea gradually subsides in >6-7 mos, no permanent neurologic sequelae

4. RHEUMATIC HEART DISEASE

 RHD is a sequelae of RF and is present if:
 MR/MS is appreciated on PE
 LVH/RVH on ECG
 Irregular cardiac borders on CXR
 In RF, there is also cardiomegaly but with normal ECG findings

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