chd module.ppt

Congenital Heart Disease Modul

Edward Surjono, M.D.Pediatric Cardiology Division

Part 1: FETAL- NEONATAL CIRCULATIONPart 2: PHYSICAL EXAMINATIONPart 3: PLAIN FILM ANATOMYPart 4: PLAIN FILM INTERPRETATIONPart 5: CONGENITAL HEART DISEASES

Part 1: FETAL CIRCULATION

FETAL to NEONATAL CIRCULATION

Knowledge of FETAL and NEONATAL circulation is an integral part of understanding the pathophysiology and natural history of congenital heart disease (CHD)

Fetal circulation different from the adult circulation:

1. In the fetus = placenta for gas & nutrient exchange ; in the neonate/adult = lungs

2. In the fetus = right & left ventricles in parallel circuit; in the neonate / adult= series circuit

3. Three structures unique to the fetal circulation: ductus venosus, foramen ovale & ductus arteriosus

Course of Fetal Circulation

Placenta receives largest amount of ventricular output, RV&LV (55%) and has the lowest vascular resistance

SVC drains upper body & brain (15%); IVC drains lower body & placenta (70%); IVC has higher O2 sat (70%) than SVC

(40%); highest pO2 in the umbilical vein (32 mmHg)


Oxygenated blood from the placenta flows to the fetus thru the UV with Po2 of 30-35 mmHg; 50% of UV blood enters hepatic circ., whereas the rest bypasses the liver and joins the IVC via the ductus venosus


Most SVC blood goes to the RV; 1/3 of IVC blood w/ higher O2 sat is

directed to the LA thru foramen ovale;

Remaining 2/3 enters RV & PA and because pulmo. arterial circulation is vasoconstricted, only 10% goes to the lungs and majority flows thru the ductus arteriosus, to the desc.aorta to lower parts


The result is that the upper part of the fetal body, including the brain and coronaries receive blood w/ higher O2 sat

RV is larger and more dominant than LV; RV handles 55% while LV handles 45% of

combined ventricular output

Changes in Circulation After Birth

1. Interruption of umbilical cord results in: a. increase in systemic vasc. resistance as a result of removal of the low resistance placenta;

b. closure of the ductus venosus as a result of lack of blood return from placenta

2. Lung expansion result in the ff: a. reduction of PVR, increase in PBF &

fall in PA pressure;

Changes in circulation after birth

2. Lung expansion results in: b. functional closure of foramen ovale bec. of increase in LA pressure c. closure of PDA bec. of increased O2 sat

Part 2: PHYSICAL EXAMINATION

History Taking

1. Gestational and Natal History Infections, medications, excessive smoking or alcohol intake during pregnancy, birth weight

2. Postnatal/ Past History Weight gain, feeding pattern,

development,Cyanosis, “cyanotic spells”, squatting Tachypnea, dyspnea

History Taking

2. Postnatal History: Exercise intolerance

Heart murmur Joint symptoms Neurologic symptoms Chest pain Medications

History Taking

3. Family History Hereditary disease

CHD / RHD Sudden unexpected death Diabetes, atherosclerotic HD HPN

Physical Exam

I. INSPECTION Gen. appearance & nutritional state: in distress, malnourished, well nourished Chromosomal syndromes: Down syndHereditary / non-hereditary syndromesSystemic malformations

Color

Physical Exam

1. INSPECTION Color

Clubbing Retractions, Diaphoresis Inspection of the chest:

precordial bulge,Harrison’s groove

Physical Exam

2. PALPATION Peripheral pulses: weak, thready, bounding Chest: apical impulse, heaves, thrills Blood pressure: diff. sizes of cuffs

Physical Exam

3. AUSCULTATIONa. heart rate & regularity – fast, slow or

irregular, diff. rates for diff. ageb. heart sounds – intensity, quality shd

be evaluated; S1 & S2 shd be noted, S3 , gallop rhythm; muffled?

c. systolic or diastolic sounds: clicksd. murmurs

Murmurs Evaluate as to: 1. Timing – systolic, diastolic or continuous

2. Location – LUSB, LMSB, LLSB,apical et 3. Transmission- to the back, neck, apex

4. Type – ejection, regurgitant 5. Quality – soft, blowing, rumbling, vibratory 6. Intensity - Grade I to 6

Intensity

Grade 1 barely audibleGrade 2 soft, but easily audibleGrade 3 moderately loud, but not

accompanied by a thrillGrade 4 louder and associated with a thrillGrade 5 audible with the stethoscope barely

on the chestGrade 6 audible w/ the stethoscope off the

chest

Murmurs

1. Systolic – may be A. innocent – venous hum, pulmonary

flow murmur B. pathologic- AS, PS, MR, VSD, ASD2. Diastolic- are usually all pathologic; AI,

MS, PR 3. Continuous – may be

A. innocent - venous hum B. pathologic- PDA, coronary fistula

Laboratory Evaluation

1. Radiologic assessment (CXR)* cardiac size – CT ratio* cardiac shape- “boot-shaped”,” egg on side”, “snowman” appearance* chamber enlargement – LVH, RVH, LAE, RAE etc* pulmonary vascularity – increased, decreased, or normal* others: lungs, skeletal abnormalities


2. Electrocardiography (ECG / EKG)different in pediatrics : 15 leadsnormal in NB & 1st few days/months

of life to have RAD, RV dominance

evaluate for any chamber hypertrophy, rhythm disturbances, etc


3. Echocardiographyvery useful & important tool to the ped

cardiologist; non-invasive procedureevaluates: cardiac anatomic defect,

estimates pressures/gradients across stenotic valves, vessels;quantitate contractile function; vegetations, fluids


4. Cardiac Catherizationan invasive procedurehas both diagnostic and therapeutic

use (interventional procedure)measures O2 sat, shunt volumes,

pressuresballoon angioplasty,valvotomy,

septostomy, stents, occlude PDA, ASD, VSD

Part 3: PLAIN FILM ANATOMY

Postero-Anterior (PA) View

SVC

IVC


RA


RV


PA


LA


LV


Aorta


Right border Superior vena cava Right atrium Inferior vena cava


Right border Superior vena cava Right atrium Inferior vena cava

Left border Aortic knob Main pulmonary trunk Left ventricle


Pulmonary Arteries Right


Pulmonary Arteries Right Left


Pulmonary Arteries Right Left

Pulmonary VeinsLA

Lateral View

RA

SVC

IVC

Lateral View

RV

Lateral View

PA

Lateral View

LA

Lateral View

LV

Lateral View

Aorta

Lateral View

Lateral View

Left atrium Left ventricle

Lateral View

Left atrium Left ventricle

Right ventricle

Lateral View

Aorta

Main Pulmonary Artery

Inferior vena cava

Lateral View

Pulmonary Arteries Left Right

Pulmonary Veins

Part 4: PLAIN FILM INTERPRETATION

Systemic Approach

Overview or overall glance at the film Check cardiac position and situs Cardiac size Pulmonary vascularity Chamber enlargement Great vessels Thoracic musculo- skeletal structures Lungs Ancillary findings

Overview or overall glance at the film

Is it adequate

or optimal forcardiac evaluation?


Things to consider: Position Inspiration Exposure


Things to consider: Position

slight degrees of rotation or obliquity will substantially affect the cardiac contour and may alter the apparent size as well


Things to consider: Inspiration

Should be in full inspiration In suboptimal inspiration or supine chest

radiographs, the lower lobe markings are crowded and may obscure the possibility of early pulmonary edema


Things to consider: Exposure

underexposure may simulate the appearance of pulmonary congestion

overexposure may simulate diminished pulmonary blood flow

Cardiac Position and Situs

Cardiac Positions: Levocardia: the heart is predominantly in the

left chest, and the cadiac apex points leftward Dextrocardia: the heart is predominantly in

the right chest, and the cardiac apex points rightward

Mesocardia: the heart is positioned in the midline, and the cardiac apex points directly inferiorly


Cardiac Positions: Dextroposition (dextroversion): the cardiac

apex points leftward, but the heart is located predominantly in the right chest (typically due to extrinsic forces)


Visceroatrial Situs: “SITUS” refers to the pattern of anatomic

arrangement. atrial situs is usually concordant with visceral

situs; hence these two are described together


Visceroatrial Situs: Situs solitus:

the morphologic right atrium is to the right of the morphologic left atrium

the gastric air bubble is on the left side, and the liver is on the right

Situs inversus: the morphologic right atrium is to the left of the

morphologic left atrium the gastric air bubble is on the right side, and the

liver is on the left


Visceroatrial Situs: Situs ambiguous:

this term is used when identification of visceroatrial situs is not possible due to paucity of anatomic markers


Dextrocardia Situs solitus


Dextrocardia Situs inversus


Situs ambiguous

Heart Size

CT ratio – simplest way to estimate heart size

measure by relating the widest diameter of the heart to the widest diameter of the chest. CT ratio = A + B C

A & B – maximum cardiac dimension to the right and left from the midline

Normal cardio thoracic ratio is 0.5 > 0.5 this is considered cardiomegaly CT ratio is not reliable in newborn

and infant. normal CT ratio in the newborn is approximately 0.65

PLAIN FILM ANALYSIS IN CARDIO-VASCULAR DISEASE

PULMONARY VASCULAR PATTERN

• Normal• Increased• Diminished

Pulmonary Vascular Marking

Normal Pulmonary Vasculature≈ Uniform diminution in the

caliber of the sharp-edged PAs, from the hilus of the

lung to its periphery

Pulmonary Vascular Pattern

NORMAL

Pulmonary Vascular Marking

Normal Vasculature Prominent Apical & Peripheral Vascular

Markings

Pulmonary Arterial Hypertension


Increased Pulmonary Vascularity

1. Pulmonary vascular engorgement which is uniform throughout both upper and

lower lobes


2. Individual vessels are dilated and

tortuous extending farther into the

periphery than usual


3. Bigger pulmonary artery than the

accompanying bronchus of the same level when seen caught on end.


4. Diameter of the RDPA bigger than the diameter of the trachea. (Coussement, A.M., Gooding G.A., Radiology, 1973)

VSD

Increased Pulmonary Vascular

Markings


Increased Pulmonary Vascularity

Pulmonary Vascular Marking Decreased Pulmonary

Vasculature SIGNS:

1. hilum appears small 2. concave main pulmonary

artery segment3. stringy peripheral

pulmonary vascular markings

TOF

Concave MPA

PVM

PS

PVM

Prominent MPA


Diminished Pulmonary Vascularity

1. Generalized hyperlucent lungs

2. Thin, stringy blood vessels giving the lungs a ratty appearance.


Diminished P. Vascularity

NORMAL


INCREASED

NORMAL INCREASED


NORMAL


DECREASED

NORMAL


VENOUSCONGESTION


VENOUSCONGESTION

INCREASEDARTERIAL

BLOOD FLOW


VENOUSCONGESTION

Kerley’s B lines


VENOUSCONGESTION

Perihilar Haziness


VENOUSCONGESTION

Peribronchial Cuffing


VENOUSCONGESTION

Redistribution: equalization


Redistribution: cephalization

VENOUSCONGESTION


Redistribution: cephalization


VENOUSCONGESTION Interstitial Edema

Kerley B Lines


VENOUSCONGESTION Interstitial Edema

Kerley B LinesKerley A Lines


VENOUSCONGESTION

Alveolar Edema

Specific Cardiac Chamber Enlargement

Right Atrial Enlargement

Best seen in PA view as increased prominence of right lower cardiac border

RA Enlargement in PA View

Chamber Enlargement

Right Atrial Enlargement lateral bulging of the right

heart border elongation of the right

heart border (length of right heart border exceeds 50% of the mediastinal cardiovascular shadow)

Right Ventricular Enlargement PA view

Lateral and upward displacement of the cardiac apex

Lateral view Fullness of the retrosternal space


Chamber Enlargement

Right Ventricular Enlargement PA View: Rounding and

upliftment of cardiac apex

Chamber Enlargement

Right Ventricular Enlargement PA View: Rounding and

upliftment of cardiac apex Lateral View:

Retrosternal fullness (contact of anterior cardiac border greater than 1/3 of the sternal length


Left Atrial Enlargement PA view

1. Double density2. Prominence of LA appendage on the left

upper cardiac border3. Widening of carinal angle, secondary to

elevation of left main stem bronchus

Signs of LA Enlargement In PA View

Signs of LA Enlargement in

Lateral View


Left Atrial Enlargement

Chamber Enlargement

Left Atrial Enlargement PA view:

Double density Enlargement of LA

appendage Upliftment of left mainstem

bronchus Widening of carinal angle

Chamber Enlargement

Left Atrial Enlargement Lateral view:

Prominent posterosuperior cardiac border

Posterior displacement and upliftment of left mainstem bronchus


LV Enlargement PA view

Downward displacement (drooping or sagging) of cardiac apex

LATERAL VIEW Lower posterior cardiac border is posteriorly

displaced. It meets the IVC line below the level of the diaphragm (Normally, above the diaphragm).

Signs of LV Enlargement in PA

View

Signs of LV Enlargement in

Lateral View


LV Enlargement

Chamber Enlargement

Left Ventricular Enlargement PA View: lateral and

downward displacement of the cardiac apex

Chamber Enlargement

Left Ventricular Enlargement Lateral view:

posterior displacement of the posterior inferior border of the heart

Hoffman-Rigler Sign: measured 2 cm above the intersection of the diaphragm & IVC; (+) if posterior border extends more than 1.8 cm of IVC

The Great Arteries

Are they in normal position? Are they of normal size?

The Great Arteries

Aorta normal prominent diminutive

Main pulmonary artery normal prominent concave

Ancillary Findings

calcifications bone deformities others

Part 5: CONGENITAL HEART DISEASES

CONGENITAL HEART DISEASES

anatomic malformation of the heart and or its vessels, which occurs during the intrauterine development

Incidence: 8/1000 live births Most common congenital

malformation 13% will have more than one

cardiac defect 25% will have associated non-

cardiac deformity


Etiology: Unknown Multifactorial

Hereditary Chromosomal

abnormality Maternal infection Teratogenic drugs Maternal factors Environmental

RADIOLOGIC INTERPRETATION OF CONGENITAL HEART DISEASE

1. Cyanotic or Non-cyanotic? 2. Vascularity 3. Specific chamber enlargement 4. Great Vessels 5. Ancillary findings


Increased Venous

Vascularity

Decreased Vascularity

Increased Vascularity

Cyanotic:

• dTGA

• TAPVR without obstruction

• PTA

• Single ventricle

• DORV without pulmonary stenosis

Non-cyanotic:

• ASD

• VSD

• PDA

• AV canal defect

Normal Vascularity

• TOF• Ebstein’s Anomaly• Severe Pulmonary Stenosis• Pulmonary Atresia • Tricuspid Atresia with pulmonary stenosis• DORV with pulmonary stenosis

• Coarctation of Aorta• Aortic Stenosis• Pulmonary stenosis

• Hypoplastic Left Heart• Pulmonary vein stenosis• TAPVR with obstruction

A tr ial S eptal Def ectL to R S hunt with PH PN

PA PVR

RVH

Ventr icular S eptal Def ectPatent Ductus A rter iosus

A VS D

LVH or CVH

I ncrease PBF

A cyanot ic

Pulmonary S tenosisM itral S tenosis

RVH

Mitral Regurgitat ionA ort ic S tenosis

Coarctat ion of A ortaPrimary Myocardial Disease

LVH

N ormal PBF

A cyanot ic

T A PVRH ypoplast ic S yndrome

T GA

RVH

T GA with VS DS ingle Ventr icle

T runcus A rter iosusPVO D

Bidirect ional S hunt

LVH or CVH

I ncrease PBF

Cyanot ic

VS D with PS

T etralogy of Fallot

Ebstein A nomaly

Eisenmenger

RVH

T ricuspid A tresia

Pulmonary A tresiaHypoplastic RV

LVH

T A with hypoplast ic PA s

T GA with PS

S ingle Ventr icle with PS

LVH or CVH

Decrease PBF

Cyanot ic

Ventricular Septal Defect

VSD: Clinical Manifestations

History: 1. with small VSD, patient is asymptomatic w/ normal growth &dev2. with moderate to large size VSD, patient has failure to thrive, frequent RTI, PAH, CHF common in infancy3. with severe PAH, cyanosis & dec.activity (Eisenmenger syndrome)

VSD: Physical exam

Infants w/ small VSD: well developed, acyanotic.

Infants w/ large VSD: poor weight gain, signs of CHF; precordial bulge, Harrison’s, hyperactive precordium; systolic thrill

Grade 2-5/6 PSM at the LLSB P2 accentuated w/ PAH w/ PVOD: cyanosis, clubbing

(Eisenmenger), loud single S2

VSD: Laboratory Exam

ECG: small VSD – normal ECG moderate size- LVH, LAE large VSD – CVH , +/- LAE

CXR

Ventricular Septal Defect

Increased vascularity Normal or enlarged

cardiac size Chamber prominence:

either or both ventricles left atrium

Enlarged main and central pulmonary arteries

Normal or small aorta

VSD: NATURAL HISTORY

Spontaneous closure in 30-40% with small VSD, esp. muscular type, within 6mos – 2 yrs.

Congestive heart failure (CHF) in infants w/ large VSD may set in bet. 6-8 wks of age

Pulmonary HPN may develop as early as 6-12 mos & progress to PVOD later

Infundibular stenosis or AI may develop in some

Infective endocarditis may be a risk

VSD: MANAGEMENT

MEDICAL:1. Treat CHF if present :Digoxin,diuretics

2. Frequent feedings w/ high calorie formula for those malnourished infants 3. Anemia may be corrected w/ iron therapy 4. Good dental hygiene , antibiotic prophylaxis against IE5. “Umbrella” device for selected VSD

VSD: MANAGEMENT

2. SURGICAL: *Small infants with large VSD & CHF may be

managed first w/ digoxin & diuretics *If growth failure &/or CHF not improved

medically, surgery may be done w/in 1st 6mos. of life *With PAH but no CHF, cath shd be done at 6- 12 mos & surgery shd follow soon* Surgery contraindicated in those w/ PVOD

Patent Ductus Arteriosus

PATENT DUCTUS ARTERIOSUS

PATHOLOGY: persistence of a normal fetal structure bet. the LPA & desc. aorta

CLINICAL MANIFESTATIONS: History: Asymptomatic with small PDA Large PDA may cause lower RTI,atelectasis, CHF

PDA: Physical Exam

Tachycardia & exertional dyspnea seen in those children w/ large PDA

a right to left ductal shunt results in cyanosis only in the LE (differential cyanosis)

Hyperactive precordium; systolic thrill at the LUSB

Bounding pulses, wide pulse pressure

PDA: Physical Exam

Grade 2-4/6 continuous, “ machinery” murmur best audilble at the LUSB, infraclavicular area

Murmur may be a crescendo systolic murmur at the LUSB in small infants or in those w/ PAH

P2 usually normal but may be accentuated w/ PAH

PDA: Laboratory Exam

ECG: Similar to those of VSD Small PDA may have normal ECG

Moderate PDA- LVH Large PDA – CVH With PVOD – RVH


CXR: May be normal in small PDA

Cardiomegaly with LAE, LVH & prominent aorta

Increased pulmonary vascularity Prominent MPA with PAH

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Echocardiography: visualizes PDA at the parasternal and suprasternal viewsColor and doppler studies performedSize of PDA as well as chambers and pulmonary pressures are measured

PDA: Natural History

Spontaneous closure of PDA does not usually occur in term infants unlike in premature infants

CHF & recurrent pneumonia develop with large PDA

Infective endocarditis may be frequent PVOD may develop if PDA is large &

PAH untreated

PDA: Management

Medical: *Indomethacin is ineffective in term infant

* No exercise restriction is needed in the absence of PAH

* Prophylaxis for IE * Non-surgical closure with occluding

device * Treat CHF

PDA: Management

Surgical: Anatomic existence of a PDA, regardless

of size is an indication for surgery Presence of PVOD is contraindication Surgery performed at any time bet. 6

mos to 2 yrs In infants w/ CHF & PAH, surgery is performed on an urgent basis

Patent Ductus Arteriosus

Increased vascularity Normal or enlarged

cardiac size Chamber prominence:

left ventricle left atrium


Prominent aortic knob

Atrial Septal Defect

ATRIAL SEPTAL DEFECT

PATHOLOGY:

3 Types of ASD – secundum, ostium primum, sinus

venosus Associated defects may be:

PAPVR, MVP

ASD: CLINICAL MANIFESTATIONS

HISTORY: Infants & children usually asymptomatic, rarely w/ CHF

PHYSICAL EXAM: 1. slender body built

2. SEM grade 2-3/ 6 characteristic finding; but may be absent in infants

3. fixed & widely split S2

ASD: LABORATORY EXAM

ECG: RAD, RVH or RBBB (rSR’ pattern) CXR: cardiomegaly w/ RAE & RVH increased pulmonary vascularity

prominent MPA w/ PAH may be seen

Echocardiography: visualize size & position of the ASD, other assoc. defects

ASD: Natural History

Spontaneous closure of secundum ASD occur in 40% of pxs in the first 4yrs of life, if size bet. 3-8 mm

Most infants & children are asymptomatic & active; CHF is rare

With large ASD, untreated, may develop CHF and PAH in adulthood (20-30 yrs)

With/-out surgery: atrial arryhthmias may occur in adulthood (flutter, fibrillation)

Infective endocariditis does not occur

ASD: Management

MEDICAL: * Exercise restriction NOT necessary

* Infective endocarditis prophylaxis NOT indicated unless associated with MR, MVP

* Non-surgical closure with occluder device (Amplatzer, Clamshell, Cardioseal)

Device

ASD: Management

SURGICAL:Usually delayed till age 3-4 yrsHowever, surgery may be

performed during infancy if CHF does not respond to medical Tx

Atrial Septal Defect

Increased vascularity Cardiomegaly Chamber prominence:

right atrium right ventricle


Small aortic knob

Pulmonary Stenosis

Pulmonary Stenosis

Normal to decreased vascularity

Normal or enlarged cardiac size

right ventricular prominence

Post-stenotic dilatation of the main pulmonary artery

Aortic Stenosis

Aortic Stenosis

Normal vascularity Cardiomegaly Left ventricular

prominence Dilated ascending

aorta

Coarctation of the Aorta



prominence “3” sign



prominence “3” sign Rib notching

Transposition of the Great Arteries (d-TGA)

Transposition of the Great Arteries (d-TGA)

Increased vascularity Cardiomegaly Cardiac silhouette:

“Egg on its side” “Apple on a stem”

Narrow vascular pedicle

Persistent Truncus Arteriosus


Increased vascularity Pulmonary venous

congestion or edema is frequent in Type I

Cardiomegaly Chamber prominence:

either or both ventricles left atrium

Concave main pulmonary artery segment (Prominent in Type I)


wide mediastinum due to large “aortic shadow”

right aortic arch (in 35%)

Total Anomalous Pulmonary Venous Return


Increased vascularity Cardiomegaly Chamber prominence:

right atrium right ventricle

Enlarged systemic vein into which drainage occurs


Type I (Supracardiac)

left-sided vertical vein connects pulmonary venous confluence to the left innominate vein, right SVC or azygos vein

“Snowman appearance”


Type II (Intracardiac)

connections to the right atrium or coronary sinus

radiographic findings are similar to ASD


Type III (Infracardiac) Connection is below the

diaphragm; to the portal vein, ductus venosus or hepatic vein

Pulmonary edema Normal sized heart Prominence of the right

atrium & less often the right ventricle


Mixed type with various connections

to the right side of the heart

Ebstein’s Anomaly

Ebstein’s Anomaly

Decreased vascularity Marked cardiomegaly right atrial prominence “Balloon-” or “box-

shaped”

Tetralogy of Fallot

Natural History

Cyanotic Polycthemia Relative iron deficiency Hypoxic spell/Tet spell Growth retardation Brain abscess coagulopathy

Clinical manifestation

Heart murmur audible at birth Tachypnea, Cyanosis, clubbing Dyspnea squatting; hypoxic spell Acyanotic TOF may asymptomatic

Hypoxic spell

Paroxysm of hyperpnea Irritability, prolonged crying Increasing cyanosis Decreasing intensity of murmur

What should we do? Infant should be picked up, knee-chest

position Morphine sulfate 0.2 mg/kg sc/IM O2 Sodium bicarbonate Phenylephrine 0.02 mg/kg Ketamine 1-3 mg/kg IV 60 sec. Propanolol 0.01-0.25 mg/kg slow iv push

Management : medical

Propanolol therapy 0.5-1.5 mg/kg q 6 hr

Baloon dilatation Good dental hygiene, antibiotics

prophylaxis Fe for relative iron deficiency anemia Prostaglandin to maintain PDA

Management : surgical

Classic Blalock - Taussig Gore-Tex The Waterson shunt Potts operation

Tetralogy of Fallot

Decreased vascularity Normal or enlarged

cardiac size right ventricular

prominence Concave main

pulmonary artery segment

Prominent aorta right aortic arch (in 20-

25%)

THAT’S ALL… THANK YOU!

“Filled With Knowledge About the Heart!”

chd module.ppt

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