2. Abnormality of heart present from
birth.
Most common & important form of hd
in early stages of life.
Higher incidence in premature infants.
3. AETIOLOGY
• Maternal infection or exposure to drugs
• Maternal rubella infection
• Maternal alcohol misuse
• Maternal lupus erythematosus
• Genetic and chromosomal
abnormalities
4. PRESENTATION THROUGHOUT LIFE
Infancy and childhood
Birth and neonatal period Cyanosis
Cyanosis Heart failure
Arrhythmia
Heart failure
Murmur
Failure to thrive
5. Adolescence and adulthood
• Heart failure
• Murmur
• Arrhythmia
• Cyanosis due to shunt reversal
(Eisenmenger’s syndrome)
• Hypertension
• Late consequences of previous cardiac surgery
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. OBSTRUCTIONS
Coarctation of aorta
Aortic stenosis & atresia
Pulmonary stenosis & atresia
1.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. 2.SHUNTS(CYANOTIC CHD)
A. left to right shunts (acyanotic/late cyanotic gp)
Volume overload on right pulmonary hypertension
and right ventricular hypertrophy.
Ventricular Septal Defect.
Atrial Septal Defect.
Patent Ductus Arteriosus.
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 trauma
Clinical features
Volume hypertrophy of right ventricle
Enlargement and hemodynamic changes in
tricuspid,mitral,pulmonary & aortic valves
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 pulmonary
vascular resistance remains high or when the shunt is
reversed.
Prominent parasternal pulsation, tachypnoea & indrawing of
lower ribs on inspiration.
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. 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 orifices
Clinical features
Dyspnea, chest infections, cardiac failure & arrhythmias
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 atrial
pressures throughout respiratory cycle
Systolic flow murmur over the pulmonary valve
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 circulation
resulting in early cyanosis.
Tetralogy of Fallot.
Transposition of great arteries.
Persistent truncus arteriosus.
Tricuspid atresia & stenosis.
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. Clinical features
Depend on 2 factors :
I. Extent of pulmonary stenosis
II. Size of VSD
2 forms:
Cyanotic
Acyanotic
17. Features
Displacement of
Ventricular septal defect
aorta to right
Right ventricular
Pulmonary stenosis hypertrophy
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. 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. 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. 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. 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. 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. 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)
27. Definition
A disorder characterized by sustained elevation of
systemic arterial BP, usually above a diastolic level of
90 mm of Hg & a systolic level of 140 mm of Hg.
28. CLASSIFICATION
Generally :
I. Primary or essential hypertension
II. Secondary hypertension
Clinical course:
i. Benign
ii. Malignant
29. 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 & hypertensive
encephalopathy.
31. 2. Endocrine
i. Adrenocortical hypertension
ii. Hyperparathyroidism
iii. Oral contraceptives
3) Coarctation of aorta
4) Neurogenic
Normal BP regulated by 2 hemodynamic forces
• Cardiac output
• Total peripheral vascular resistance
32. 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.
35. 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 types
a) Stenosis.
b) Insufficiency/incompetence/regurgitation.
37. 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
38. 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.
39. JONE’S CRITERIA
Major 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
40. 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.
44. ENDOCARDITIS
Is the inflammatory involvement of the
endocardial layer of the heart.
45. 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.
46. INFECTIVE(BACTERIAL)ENDOCARDITIS
Serious infection of the valvular & mural
endocardium caused by different forms of micro organisms
and is characterized by typical infected and friable
vegetation's.
Depending on severity of infection, BE is of 2 forms:-
A. Acute bacterial endocarditis.
B. Sub acute bacterial endocarditis or endocarditis lenta.
47. 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.
49. Predisposing factors
3 main factors:
I. Conditions initiating transient bacteremia,
septicemia & pyaemia.
II. Underlying heart disease.
III. Impaired host defenses.
50. PATHOGENESIS
Implant on
Bacteria
cardiac valves Inflammation
enter
or mural results
bloodstream
endocardium
51. 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.
52. 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.
53. 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