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Congenital heart disease (1)

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Congenital heart disease (1) Congenital heart disease (1) Presentation Transcript

  • CONGENITAL HEART DISEASE
  •  Abnormality of heart present from birth. Most common & important form of hd in early stages of life. Higher incidence in premature infants.
  • AETIOLOGY • Maternal infection or exposure to drugs • Maternal rubella infection • Maternal alcohol misuse • Maternal lupus erythematosus • Genetic and chromosomal abnormalities
  • PRESENTATION THROUGHOUT LIFE Infancy and childhoodBirth and neonatal period  Cyanosis Cyanosis  Heart failure  Arrhythmia Heart failure  Murmur  Failure to thrive
  • Adolescence and adulthood• Heart failure• Murmur• Arrhythmia• Cyanosis due to shunt reversal (Eisenmenger’s syndrome)• Hypertension• Late consequences of previous cardiac surgery
  • 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
  •  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.
  • 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.
  •  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
  •  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.
  •  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
  • 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
  • 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
  • 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.
  •  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
  • Clinical features Depend on 2 factors :I. Extent of pulmonary stenosisII. Size of VSD 2 forms:CyanoticAcyanotic
  • Features Displacement ofVentricular septal defect aorta to right Right ventricularPulmonary stenosis hypertrophy
  • 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
  • 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
  • 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
  • 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
  • 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
  •  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
  • 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)
  • SYSTEMIC HYPERTENSION
  • 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.
  • CLASSIFICATION Generally :I. Primary or essential hypertensionII. Secondary hypertension Clinical course:i. Benignii. Malignant
  •  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.
  • 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
  • 2. Endocrinei. Adrenocortical hypertensionii. Hyperparathyroidismiii. Oral contraceptives3) Coarctation of aorta4) NeurogenicNormal BP regulated by 2 hemodynamic forces• Cardiac output• Total peripheral vascular resistance
  • 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.
  • CHRONIC VALVULAR DISEASE
  •  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.
  • COMMON VALVULAR DISEASES Rheumatic Heart Disease Mitral Valve Disease Aortic Valve Disease Tricuspid Valve Disease Pulmonary Valve Disease etc…
  • 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
  •  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.
  • 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
  •  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.
  • 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.
  • INFECTIVE ENDOCARDITIS
  • ENDOCARDITIS Is the inflammatory involvement of theendocardial layer of the heart.
  • 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.
  • 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.
  • 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.
  • ETIOLOGY Infective agents ABE – virulent strains of staphylococci ( staph.aureus ) SABE- streptococci with low virulence (streptococcus viridans)
  •  Predisposing factors 3 main factors:I. Conditions initiating transient bacteremia, septicemia & pyaemia.II. Underlying heart disease.III. Impaired host defenses.
  • PATHOGENESIS Implant on Bacteria cardiac valves Inflammation enter or mural resultsbloodstream endocardium
  • 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.
  • 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.
  • 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
  • INVESTIGATIONS • Hemotological examination • Angiogram • Echo cardiography • Chest radiograph • ECG • Tread miller test • Dopplers
  • THANK YOU