Congenital heart disease (1)


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Congenital heart disease (1)

  2. 2.  Abnormality of heart present from birth. Most common & important form of hd in early stages of life. Higher incidence in premature infants.
  3. 3. AETIOLOGY • Maternal infection or exposure to drugs • Maternal rubella infection • Maternal alcohol misuse • Maternal lupus erythematosus • Genetic and chromosomal abnormalities
  4. 4. PRESENTATION THROUGHOUT LIFE Infancy and childhoodBirth and neonatal period  Cyanosis Cyanosis  Heart failure  Arrhythmia Heart failure  Murmur  Failure to thrive
  5. 5. Adolescence and adulthood• Heart failure• Murmur• Arrhythmia• Cyanosis due to shunt reversal (Eisenmenger’s syndrome)• Hypertension• Late consequences of previous cardiac surgery
  6. 6. CLASSIFICATION MALPOSITIONS OF HEART SHUNTS(CYANOTIC CHD) 1)LEFT TO RIGHT SHUNTS: Ventricular septal defect Atrial septal defect Patent ductus arteriosus 2)RIGHT TO LEFT SHUNTS: TETROLOGY OF FALLOT Transposition of great arteries Persistent truncus arteriosus Tricuspid atresia & stenosis
  7. 7.  OBSTRUCTIONS Coarctation of aorta Aortic stenosis & atresia Pulmonary stenosis & atresia1.MALPOSITIONS OF THE HEART Dextrocardia: condition when the apex of the heart points to the right side of the chest. Accompanied by sinus inversus. Associated with major anomalies of heart.
  8. 8. 2.SHUNTS(CYANOTIC CHD)A. left to right shunts (acyanotic/late cyanotic gp) Volume overload on right  pulmonary hypertensionand right ventricular hypertrophy. Ventricular Septal Defect. Atrial Septal Defect. Patent Ductus Arteriosus.
  9. 9.  Ventricular Septal Defect Most common congenital anomaly Recognized early in life Result of incomplete septation of ventricles Acquired VSD result from rupture as a complication of acute MI or traumaClinical features Volume hypertrophy of right ventricle Enlargement and hemodynamic changes in tricuspid,mitral,pulmonary & aortic valves
  10. 10.  Endocardial hypertrophy of the right ventricle. Pressure hypertrophy of right atrium. Volume hypertrophy of left atrium and left ventricle Eisenmenger’s syndrome in cases immediately after birth, while pulmonaryvascular resistance remains high or when the shunt isreversed. Prominent parasternal pulsation, tachypnoea & indrawing of lower ribs on inspiration.
  11. 11.  Atrial Septal Defect Occurs twice as frequently in females Remains unnoticed in infancy & childhood till pulmonary hypertension is induced causing late CHD & right -sided HF Depending upon the location of defect,3 types of ASD: i)Fossa ovalis type ii)Ostium primum type iii)Sinus venous type
  12. 12. Morphologic features Volume hypertrophy of right atrium & right ventricle Enlargement & hemodynamic changes of tricuspid & pulmonary valves Focal or diffuse endocardial hypertrophy of right atrium & right ventricle Volume atrophy of left atrium & left ventricle Small sized mitral & aortic orificesClinical features Dyspnea, chest infections, cardiac failure & arrhythmias
  13. 13. Characteristic physical signs Wide fixed splitting of 2nd heart sound wide because of delay in right ventricular ejection fixed because septal defect equalizes left & right atrialpressures throughout respiratory cycle Systolic flow murmur over the pulmonary valve
  14. 14. b)Right to left shunts(cyanotic gp) Shunting of blood from right side to left side of the heart. Entry of poorly oxygenated blood into systemic circulationresulting in early cyanosis. Tetralogy of Fallot. Transposition of great arteries. Persistent truncus arteriosus. Tricuspid atresia & stenosis.
  15. 15.  Tetralogy of Fallot Most common cyanotic CHD Abnormal development of bulbar septum which separates ascending aorta from pulmonary artery,& which normally aligns & fuses with the outflow part of IV septum
  16. 16. Clinical features Depend on 2 factors :I. Extent of pulmonary stenosisII. Size of VSD 2 forms:CyanoticAcyanotic
  17. 17. Features Displacement ofVentricular septal defect aorta to right Right ventricularPulmonary stenosis hypertrophy
  18. 18. o Cyanotic tetralogy Pulmonary stenosis is greater VSD is mild More resistance to outflow of blood from right ventricle Right to left shunt at the ventricular level and cyanosis
  19. 19. Effects on the heart Pressure hypertrophy of the right atrium & right ventricle Smaller and abnormal tricuspid valve Smaller left atrium and left ventricle Enlarged aortic orifice
  20. 20. o Acyanotic tetralogy VSD is larger Pulmonary stenosis is mild Left-to-right shunt with increased pulmonary flow Increased volume in the left heart No cyanosis
  21. 21. Effects on heart Pressure hypertrophy of the right ventricle and right atrium Volume hypertrophy of the left atrium and left ventricle Enlargement of mitral and aortic orifices
  22. 22. Clinical features Children are usually cyanosed not neonates Only when right ventricular press rises to equal or exceeds left ventricular pressure Subvalvular component of RV outflow obstruction is dynamic, may increase suddenly under adrenergic stimulation Affected child suddenly becomes cyanosed, may become apnoeic & unconscious Attack known as FALLOT’S SPELLS
  23. 23.  In older children, cyanosis become increasingly apparent, with stunting growth, digital clubbing and polycythemia Most characteristic feature- combination of cyanosis with a loud ejection systolic murmur in the pulmonary area
  24. 24. 3)OBSTRUCTIONS(OBSTRUCTIVE CHD) Obstruction in the aorta due to narrowing (COARCTATION OF AORTA) Obstruction to outflow from the lt ventricle (AORTIC STENOSIS & ATRESIA) Obstruction to outflow from the right ventricle (PULMONARY STENOSIS & ATRESIA)
  26. 26. Definition A disorder characterized by sustained elevation ofsystemic arterial BP, usually above a diastolic level of90 mm of Hg & a systolic level of 140 mm of Hg.
  27. 27. CLASSIFICATION Generally :I. Primary or essential hypertensionII. Secondary hypertension Clinical course:i. Benignii. Malignant
  28. 28.  Primary hypertension unknown cause of increase in BP. 80-95% Secondary hypertension due to diseases of kidneys, endocrines, etc. 5-20% Benign moderate elevation of BP & rise is slow. 90-95% Malignant marked & sudden increase of BP to 200/140mm Hg develop papilledema, retinal hemorrhages & hypertensiveencephalopathy.
  29. 29. ETIOLOGY & PATHOGENESIS A)Essential hypertension(90%)1. Genetic factors2. Racial & environmental factors3. Risk factors modifying the course B)Secondary hypertension1) RenalI. Reno vascularII. Renal parenchymal diseases
  30. 30. 2. Endocrinei. Adrenocortical hypertensionii. Hyperparathyroidismiii. Oral contraceptives3) Coarctation of aorta4) NeurogenicNormal BP regulated by 2 hemodynamic forces• Cardiac output• Total peripheral vascular resistance
  31. 31. EFFECTS OF HYPERTENSION Major effects in 3 main organs:- Heart & Blood vessels, Nervous system & Kidneys. Renal effects:I. Benign nephrosclerosis.II. Malignant nephrosclerosis. Cerebrovascular shock. Hypertensive heart disease.
  33. 33.  Various forms of congenital & acquired diseases causing valvular deformities Result in cardiac failure Rheumatic heart disease – most common Valves of left side- more involved Valvular deformities-2 typesa) Stenosis.b) Insufficiency/incompetence/regurgitation.
  34. 34. COMMON VALVULAR DISEASES Rheumatic Heart Disease Mitral Valve Disease Aortic Valve Disease Tricuspid Valve Disease Pulmonary Valve Disease etc…
  35. 35. RHEUMATIC HEART DISEASE RF:- Systemic, post-streptococcal, non-suppurative inflammatory disease, principally affecting the heart, joints, CNS, skin & subcutaneous tissues RHD :- Major cardiac sequale caused in chronic stage of RF involving all layers of the heart
  36. 36.  ACUTE RHEUMATIC FEVER Most common cause of acquired heart disease in childhood & adolescence. Triggered by an abnormal response to infection with specific strains of group A streptococci. Antibodies produced against streptococcal antigens mediate inflammation in endocardium, myocardium & pericardium as well as the joints & skin.
  37. 37. JONE’S CRITERIAMajor manifestations Minor manifestations  Fever Carditis  Arthralgia Polyarthritis  Previous RF Chorea  Raised ESR or C-reactive protein Erythema margination  Leukocytosis Subcutaneous nodules  First or second degree AV block
  38. 38.  CHRONIC RHD Develops in at least half of those affected by RF with carditis. Two-thirds of cases occur in women. Mitral valve affected more. Mostly asymptomatic.
  39. 39. Pathology Main process- progressive fibrosis. Heart valves predominantly affected. Involvement of pericardium & myocardium heart failure & conduction disorders. Fusion of mitral valve commissures &chordae tendinae shortening mitral stenosis. Valve damage  altered hemodynamic stress popetuate  extend the damage.
  41. 41. ENDOCARDITIS Is the inflammatory involvement of theendocardial layer of the heart.
  42. 42. CLASSIFICATION OF ENDOCARDITIS NON-INFECTIVE INFECTIVE Rheumatic endocarditis.  Bacterial endocarditis. Atypical  Other infective types verrucous(Libman-Sacks) (tuberculosis endocarditis. , syphilitic, fungal, viral, ri Non-bacterial ckettsial). thrombotic(cachectic, mar antic) endocarditis.
  43. 43. INFECTIVE(BACTERIAL)ENDOCARDITIS Serious infection of the valvular & muralendocardium caused by different forms of micro organismsand is characterized by typical infected and friablevegetations. Depending on severity of infection, BE is of 2 forms:-A. Acute bacterial endocarditis.B. Sub acute bacterial endocarditis or endocarditis lenta.
  44. 44. ABE SABE Fulminant & destructive  Caused by less virulent acute infection of the bacteria in a previously endocardium by highly diseased heart & has a virulent bacteria in a gradual downhill course in previously normal heart and a period of 6 weeks to a almost invariably runs a few months and sometimes rapidly fatal course in a years. period of 2-6 weeks.
  45. 45. ETIOLOGY Infective agents ABE – virulent strains of staphylococci ( staph.aureus ) SABE- streptococci with low virulence (streptococcus viridans)
  46. 46.  Predisposing factors 3 main factors:I. Conditions initiating transient bacteremia, septicemia & pyaemia.II. Underlying heart disease.III. Impaired host defenses.
  47. 47. PATHOGENESIS Implant on Bacteria cardiac valves Inflammation enter or mural resultsbloodstream endocardium
  48. 48. Development of bacterial implants by:I. lodging of circulating bacteria on previously damaged valves.II. Conditions producing hemodynamic stress.III. Occurrence of non-bacterial thrombic endocarditis from prolonged stress followed by bacterial contamination.
  49. 49. CLINICAL FEATURES SABE ABE Persistent fever, night sweats, weight loss.  Severe febrile illness with prominent & changing heart Embolic stroke or peripheral murmurs & petechiae. arterial embolism.  Embolic events common. Purpura & petechial hemorrhages and splinter  Rapid development of cardiac hemorrhages. or renal failure. Osler’s nodes.  Abscesses in echo. Digital clubbing- late sign. Splenomegaly.
  50. 50. Distinguishing features of ABE & SABE FEATURE ABE SABE Duration < 6 weeks  > 6 weeks Most common Staphylococcus  Streptococcus organisms aureus viridans Virulence of Highly virulent  Less virulent organisms Previous condition Usually previously  Usually previously of valves normal damaged Lesion on valves Invasive,  Usually not invasive destructive, or suppurative suppurative Clinical features Features of acute  Splenomegaly, systemic infection clubbing of fingers , petechiae
  51. 51. INVESTIGATIONS • Hemotological examination • Angiogram • Echo cardiography • Chest radiograph • ECG • Tread miller test • Dopplers
  52. 52. THANK YOU