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PLAIN X-RAY EVALUATION OF CONGENITAL HEART DISEASE

PLAIN X-RAY EVALUATION OF CONGENITAL HEART DISEASE. DR.SK. SAMSUZ ZAMAN 3 rd YEAR PGT MEDICAL COLLEGE KOLKATA. 1. INRODUCTION. Chest x-ray is an important, cost effective & simple investigation to diagnose various heart diseases.

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PLAIN X-RAY EVALUATION OF CONGENITAL HEART DISEASE

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  1. PLAIN X-RAY EVALUATION OF CONGENITAL HEART DISEASE DR.SK. SAMSUZ ZAMAN 3rd YEAR PGT MEDICAL COLLEGE KOLKATA 1

  2. INRODUCTION • Chest x-ray is an important, cost effective & simple investigation to diagnose various heart diseases. • Even though not the investigation of choice, it gives a lot of information regarding cardiac lesions. • The erect , frontal chest radiograph in full inspiration with an exposure showing peripheral pulmonary vessels ,rt & lt bronchi & location of aortic arch is most important. 2

  3. The right cardiac border is formed by the RA, IVC & SVC.The left cardiac border is normally the outflow tract of the LV. Above the LV convexity, there is prominence of the undivided portion of the pulmonary artery. The convexity above this is the aortic arch which displaces the trachea slightly to the right. FRONTAL PROJECTION 3

  4. RIGHT ANTERIOR OBLIQUE VIEW • The main advantage of this view is demonstration of left atrial enlargement • Enlargement of the left atrium will displace the esophagus to the right and posteriorly. • Also, a normal left aortic arch will produce indentation of the anterior border of the esophagus. 4

  5. The main advantage of this view is to evaluate right and left ventricular dilation. The anterior chamber is the RV, and the posterior chamber is the inflow tract of the LV. Increased convexity of the anterior cardiac chamber suggests RV dilation. A right aortic arch indenting the esophagus can be identified. LEFT ANTERIOR OBLIQUE VIEW 5

  6. LATERAL VIEW The RV constitutes the lower half to two-thirds of the anterior cardiac border, and lies behind the sternum. The upper third constitutes the right ventricular outflow tract and the main pulmonary artery. The upper half of the posterior cardiac border consists of the LA and the lower half is the LV. 6

  7. Congenital Heart diseases • 75% of all CHD are not detected or do not have signs or symptom at infancy. • Left to Right shunts , even large , rarely present with serious respiratory / cardiac difficulty in 1st month of life. 7

  8. classification-cyanotic • There are Nine congenital heart lesions causing severe cyanotic heart disease in children. Based upon pulmonary flow, these can be classified as follows : Group A: Lesions with  pulmonary blood flow 1. Pulmonary Atresia / severe PS with intact VSD 2. Tricuspid Atresia 3. Pulmonary malformation of tricuspid Atresia 4. TOF Group B: Lesions with  pulmonary blood flow 1. TGA 2. VSD with Coarctation of aorta Group C : Lesions with severe pulmonary venous hypertension 1.TAPVC 2.Hypoplastic left heart 3.Severe coarctation of aorta with intact VSD 8

  9. Classification-acyanotic • Acyanotic heart diseases 1.Atrial septal defect 2.Ventricular septal defect 3.Atrioventricular septal defect 4.Patent Ductus Arteriosus 5.Aortic Stenosis / Pulmonary Stenosis 6.Coarctation of aorta 7.Double aortic arch 9

  10. Diagnostic features • Pulmonary vascularity : The most important observation. • Size & shape of the heart. • Position, size & shape of ascending aorta & arch of aorta. • Situs of viscera & bronchi ( by inference of atria). • Presence of associated features, e.g. skeletal changes. 10

  11. LEFT TO RIGHT SHUNT(Acyanotic)  Enlarged Aortic knuckle --- Extra-cardiacshunt  Normal Aorta --- Intra-cardiac shunt  TYPES :1. Large Aorta 2. Normal aorta ( pre-tricuspid & post-tricuspid shunt) 11

  12. LEFT TO RIGHT SHUNT(Acyanotic) – Large Aorta Enlarged Aortic knuckle & Plethora (Enlarged Ascending Aorta) – 1.PDA  Normal Aortic knuckle & Plethora (Enlarged Ascending Aorta) - 1. Ruptured aneurysm of the sinus of valsalva 2. Aortopulmonary window 3.Coronary A-V fistula 12

  13. LEFT TO RIGHT SHUNT(Acyanotic) – Normal Aorta • Normal or small aortic knuckle / ascending aorta with plethora. Pre-tricuspid shunt : 1.ASD 2.PAPVC Post-tricuspid Shunt : 1.VSD 13

  14. RIGHT TO LEFT SHUNT • Cyanosis 14

  15. Cyanosis with decreased vascularity(Oligaemia) ( But LARGE AORTA)- Right to Lt shunt 1.TOF 2.Pulmonary Artesia with VSD 3.Hypoplastic RV4.Tricuspid Artesia5.D-TGA,VSD with Pulmonary Stenosis • Cyanosis and increased vascularity(Plethora) (But SMALL AORTA)- Right to Lt shunt 1.D-TGA 15

  16. Cyanosis with decreased vascularity(Oligaemia) ( But NORMAL AORTA)-Right to Lt shunt 1.Ebstein Anomaly 2. Vulvular Pulmonary Stenosis • Cyanosis and increased vascularity(Plethora) (But LARGE PEDICLE)-Right to Lt shunt 1.Truncus Arteriosus 2.TAPVC 16

  17. Acyanotic with Normal Vascularity- 1. Coarctation of Aorta 2.Aortic Stenosis 3.Aortic insufficiency 4.Pulmonic Stenosis/insufficiency 17

  18. Sequential segmental analysis • In complex congenital defects the identification of cardiac chambers can’t be done by geographic position but by their intrinsic anatomical & morphological characteristics. • The nomenclature is based on Sequential segmental analysis in following steps– • Atrial situs • Atrioventricular connection • Ventriculoarterial connection • Identification of other abnormalities 18

  19. How the heart chambers are named • Anatomic right atrium is on the side of the trilobed lung and liver & the anatomic left atrium is on the side of the bilobed lung and spleen. • The atrial appendages are the best method of atrial identification. • Rt atrial appd. is triangular with a wide base ‘Dog ear configuration’. Terminal crest & pectinate muscle is present within. • Lt atrial appd. is a tubular structure. • The AV valves belong to the anatomic ventricles not atria 19

  20. The anatomic RV is the coarsely trabeculated with a muscular pulmonic infundibulum & a mid ventricular ‘Moderator band’. Outflow portion is separated from inflow tract by crista supraventricularis. • The anatomic LV is the smooth-walled ventricle. Fibrous continuity between: mitral valve anterior leaflet and aortic valve. • The pulmonic valve is part of pulmonary artery not anatomic RV & the aortic valve is part of aorta not anatomic LV. • The aorta & pulmonary arteries are identified by their typical branching patterns. 20

  21. LARGE AORTA1.Patent Ductus Arteriosus (PDA) • 9-12% of all CHDs ( Enlarged ascending aorta , aortic knuckle & plethora). Ductus Arteriosus – communicate between the PA and the descending aorta distal to the origin of left subclavian artery. • Infants with prematurity, patients exposed to hypoxemia, birth at high altitudes, female sex and exposure to rubella particularly in the first 4 weeks of pregnancy are all associated with increased incidence. 21

  22. X-ray findings • A small PDA may be asymptomatic & not detected on X-ray. Sometimes seen as an inconspicuous soft convexity b/w aortic knob & PA. • In mod to large PDA : ( L  R shunt – blood shift from aorta to PA – more blood at PA & pulmonary circulation causing plethora – more blood at pulmonary vein – more blood at LA – more blood at LV – more blood at aorta – enlarged ascending aorta - large aortic knuckle due to shifting of blood occours distal to left subclavian artery) • LA, LV, PA & its branches(plethora) ,ascending aorta & aortic knuckle are enlarged. • The main PA may become calcified s/o chronic PAH • PDA with reversalexhibits reduced pulmonary vascularity , dilatation of pulmonary trunk, a normal LV & hypertrophied RV. 22

  23. The heart is slightly enlarged, the main pulmonary artery convex, and the aortic arch prominent above the MPA. There are increased pulmonary vascular markings. RAO view demonstrates the esophagus to be indented by a large left aortic arch in addition to posterior displacement by the dilated left atrium. 23

  24. …LARGE AORTA • If the ascending aorta is enlarged disproportionate to the aortic knuckle, the LR shunt is at the aortic root level (Enlarged ascending aorta & plethora but normal aortic knuckle). • TYPES : 1. Ruptured aneurysm of the sinus of valsalva(RSOV) 2. Aortopulmonary window 3.Coronary A-V fistula 24

  25. 2.Ruptured Aneurysm of the Sinus of Valsalva(RSOV) • Rare congenital heart disease(MC- right coronary sinus rupture into RV). May be acquired (endocarditis ,TB ,atherosclerosis ,mycotic) • Pathophysiology : Defect in elastic lamina valsalva sinus (aortic sinus/right coronary sinus) – formation of aneurysm & rupture – rupture into RV( most common) or RA ( common) or RV outflow tract (less common) – more blood in RV – more blood in PA & pulmonary circulation causing plethora – more blood in LA – more blood in LV – more blood through ascending aorta – shunting of blood into RA/RV at aortic root level before origin of Brachiocephalic trunk – enlarged ascending aorta below the sinus part – small aortic knuckle due to shunting.  Heart size enlarged ( LV /Biventricular type),pulmonary plethora ,PVH , enlarged ascending aorta , normal aortic knuckle 25

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  27. 3.Aortopulmonary Window • Rare CHD(<1%) • Aorta & PA do not divide normally – connection present at aortic root level. • Pathophysiology : As aortic pressure > PA pressure -more blood in PA & pulmonary circulation causing plethora – more blood in LA – more blood in LV – more blood through ascending aorta – shunting of blood from aorta to PA– enlarged part of ascending aorta – small aortic knuckle due to shunting.  Heart size enlarged ( LV type),pulmonary plethora ,PVH , enlarged part of ascending aorta , normal aortic knuckle 27

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  29. 4.Coronary A-V fistula • Rare congenital heart disease where coronary artery most commonly communicate with right sided cardiac circulation. • Usually asymptomatic or may present with dyspnoea/angina on exertion. • MC type- RCA(50%) , LAD(42%) drain at RV(41%) ,RA(26%), PA(17%) • Pathophysiology: MORE blood at RA/RV- more blood in PA & pulmonary circulation causing plethora – more blood in LA – more blood in LV – more blood through ascending aorta – shunting of blood from aorta to PA– enlarged part of ascending aorta – small aortic knuckle due to shunting.  Heart size may be normal/ biventricular/LV type , pulmonary plethora , enlarged part of aorta. 29

  30. Normal aorta ,LR shunt ,pre-tricuspid 1.Atrial Septal Defect (ASD) • 6-8% of all CHDs. The most common CHD detected in adults. • An ASD is defined as any communication within the atrial septum which results in shunting between the atria. • Holt-Oram syndrome is as/d with autosomal dominant inherited ASDs with absent or hypoplastic radii, and ECG findings of 1st degree AV block and RBBB. 30

  31. Classification • Patent foramen ovale -25-30% of normal hearts has incomplete fusion of septum primum & secundum with a potential for right to left shunt. • Ostium secundum defect - 80% of all ASDs. located in the fossa ovalis. • Ostium primum defect - prev. Regarded as ASD but actually is an AVSD . • Sinus venosus defect - found at the junction of caval veins & the right atrium. • Pathophysiology : LA pressure>RA pressure – more blood in RA/RV – more blood through PA causing plethora(more on right side) – normal aorta 31

  32. X-ray findings (Pulmonary Plethora – normal aorta – acyanotic ) • Cardiomegaly with enlargement of RA & RV- pulmonary plethora – normal aorta. • Gross enlargement of pulmonary artery (calcified in chronic cases). • Ampullary sign : bulging of SVC in sinus venosus defect 32

  33. PA chest film showing cardiomegaly with dilation of the main pulmonary artery segment, which obscures the left pulmonary artery, and the prominent right pulmonary artery and branches -secundum atrial septal defect (ASD) 33

  34. Normal aorta ,LR shunt ,pre-tricuspid2.Partial anomalous pulmonary venous connection (PAPVC) • Rare congenital anomaly in which some pulmonary veins (not all) drain into systemic circulation rather than in the left atrium. • Types : Supra-cardiac : Veins drain into right SVC(MC) , persistent left SVC , brachiocephalic vein. Cardiac : Veins drain into RA , coronary sinus Infra-cardiac : veins drain into portal vein, hepatic vein , IVC ( scimitar syndrome) mixed : combination of two or more 34

  35. PAPVC cont... • Right sided PAPVC common – children. • Left sided PAPVC common – adult. • Left upper lobe vein anomaly MC. • Association – ASD (40%). • Abnormal vein rarely identified except scimitar sydrome . • Suspected radiographic features of ASD with abnormally enlarged shadow of SVC or abnormally directed pulmonary veins. • Pathophysiology : Abnormally directed pulmonary veins in SVC/RA/IVC – more blood in RA – more blood in RV – enlarged PA causing plethora – normal aorta 35

  36. PAPVC- infracardiac 36

  37. Normal aorta, LR shunt , Post-tricuspid1.Ventricular Septal Defect (VSD) • VSDs represent the commonest ,acyanotic form of CHDs. Classification: • Supracristal VSD (type I): occur beneath the pulmonary valve and communicate with the RV outflow tract. • Perimembranous VSD (type II): (80% ) occur infracristal . 3 groups related to anatomical position; Perimembranous inlet, perimembranous trabecular (commonest) perimembranous outlet. 37

  38. AV canal VSD (type III): (10%) occur beneath the tricuspid valve, in the posterior region of the septum. • Muscular VSD (type IV): occur within the muscular septum and are subclassified as inlet, trabecular and infundibular. Trabecular defects may be multiple and described as Swiss cheese defects. • Small membranous defects close spontaneously but muscular defects rarely do. • COA & AS are most important ASD cardiac anomaly . • Left to right shunt through VSD – more blood in RV – more blood through PA causing plethora & PAH –normal aorta. • Cardiomegaly with LV / Bi-ventriculer configuration with plethora & PAH. 38

  39. X-ray findings • Small defects show normal sized heart and PA & its branches. Large defects are associated with- • Hyperinflated lung fields with flat hemidiaphragms. • Enlargement of LA & volume overload of LV. • RA enlargement indicates CHF. • Increase in size of PA & branches. • Small sized aorta. 39

  40. PA chest radiograph demonstrates a slight increase in pulmonary arterial markings with a normal sized heart. The main pulmonary artery segment is convex. Small asymptomatic VSDs - "maladie de Roger". 40

  41. PA chest radiograph demonstrates moderate cardiomegaly with the left ventricular apex extending to the left chest wall. The pulmonary vascular markings are bilaterally symmetrically increased and the pulmonary outflow tract is convex. RAO film and barium swallow demonstrates compression of the esophagus confirming left atrial dilation - VSD 41

  42. Large aorta, Rt to Lt shunt , pulmonary oligaemia1.Tetralogy of Fallot ( TOF) • TOF is the commonest cyanotic CHD after age of 2 years. • Pathophysiology : PS(small pulmonary conus) with VSD causing pulmonary oligaemia – Rt to Lt shunt causing cyanosis-more blood in LV- more blood in aorta – large aorta. • Pseudotruncus Arteriosus : Tetralogy with pulmonary Atresia . • Pentalogy of Fallot : Tetralogy with ASD • Association: 1.Right sided aortic arch(25%) 2.Anamalous coronary artery 3. AVSD 4.MS / AS 5.Absent pulmonary artery ( lt>rt) 6.Rib notching may be due to collateral 7.Cardiomegaly - in PR/TR , absent pulmonary valve, anemia ,endocarditis 8.Absent pulmonary valve 42

  43. RV outflow tract obstruction ( infundibuler pulmonary stenosis) • Sub-aortic large VSD • Overriding of the aorta • RV hypertrophy 43

  44. X-ray findings • Normal-sized heart with abnormal shape. The vascular pedicle is narrow and there is uplifting of the ventricular apex due to rotation of the heart secondary to right ventricular enlargement. • There is concavity in the region of the main PA segment due to infundibular stenosis. • This leads to a characteristic boot-shaped heart. “Coeur en sabot” appearance. • The pulmonary vascularity is usually decreased. 44

  45. PA chest radiograph shows normal heart size which is "boot-shaped“. There is elevation of the cardiac apex, concavity of the main PA segment There are diminished pulmonary vascular markings and a prominent left sided aortic arch. 45

  46. The heart is of normal size with an upturned RV apex, reduced pulmonary arterial markings and there is a right sided aortic arch. Pulmonary atresia with ventricular septal defect (Pseudotruncus). 46

  47. Large aorta, Rt to Lt shunt , pulmonary oligaemia 2.Tricuspid atresia • The third commonest form of cyanotic CHD • There is an obligatory ASD. • Pathophysiology : Though LA pressure > RA pressure , due to stenosis of tricuspid valve / rt ventriculer inlet , blood is shifted RA to LA through ASD / patent foramen ovale to complete circulation – enlarged LA & LV – straightening of left heart border – more blood through aorta – enlarged aorta Less blood through PA(normal) / associated PS –small pulmonary conus – pulmonary oligaemia. • Association: 1.rt sided aortic arch -33 % 2.TGA 3. small VSD 4. absent spleen 47

  48. X-ray findings (Tricuspid Atresia) • RA enlargement • LV hypertrophy • The RV area is receding or flat. • Varying degrees of lung perfusion. 48

  49. Large aorta, Rt to Lt shunt , pulmonary oligaemia 3.Pulmonary atresia with VSD • Congenital cyanotic heart disease • Pathophysiology : Pulmonary atresia – small pulmonary conus – pulmonary oligaemia – rt to lt shifting of blood through VSD due to pulmonary atresia through LV pressure > RV pressure – enlarged aorta – mild cardiomegaly with RV configuration. Association : 1. rt sided aortic arch (30-40%) 2. frequent bronchial collateral circulation 3. rib notching 49

  50. Large aorta, Rt to Lt shunt , pulmonary oligaemia4.D-TGA,VSD with PS • Rare congenital cyanotic heart disease. • Aorta arise from RV – receive venous blood – cyanosis. • PA arise from LV with PS – less blood through PA – pulmonary oligaemia. • VSD with PS – lt to rt shunt – more blood in the RV/Aorta –enlarged aortic knuckle to supply more oxygen to tissue. • PS small – child can survive for many month / year – later PAH developed – surgery required. • Severe PS – early PAH – early surgery • Surgery (Rastelli operation) – 1.A patch in the RV to prevent blood passing from RV to aorta but blood can pass from LV to aorta. 2.A artificial tube conduit is connected between RV to PA 50

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