my nidanam presentation

1. CONGENITAL HEART DISEASE

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)

26. SYSTEMIC HYPERTENSION

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.

30. ETIOLOGY & PATHOGENESIS
 A)Essential hypertension(90%)
1. Genetic factors
2. Racial & environmental factors
3. Risk factors modifying the course
 B)Secondary hypertension
1) Renal
I. Reno vascular
II. Renal parenchymal diseases

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.

34. CHRONIC VALVULAR
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.

36. COMMON VALVULAR DISEASES
 Rheumatic Heart Disease
 Mitral Valve Disease
 Aortic Valve Disease
 Tricuspid Valve Disease
 Pulmonary Valve Disease etc…

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.

41. 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.

43. INFECTIVE ENDOCARDITIS

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.

48. ETIOLOGY
 Infective agents
ABE – virulent strains of staphylococci ( staph.aureus )
SABE- streptococci with low virulence (streptococcus viridans)

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

55. INVESTIGATIONS
• Hemotological examination
• Angiogram
• Echo cardiography
• Chest radiograph
• ECG
• Tread miller test
• Dopplers

56. THANK YOU