Russian Call Girls in Jaipur Riya WhatsApp ❤8445551418 VIP Call Girls Jaipur
Acyanotic chd
1. 05/31/15 DR. M. S. PRASAD 1
Acyanotic Congenital Heart DiseaseAcyanotic Congenital Heart Disease
Dr. M. S. Prasad
Professor & HOD
Dept. of Pediatrics
SGT Medical College
2. 05/31/15 DR. M. S. PRASAD 2
ObjectivesObjectives
• By the end of this class, the students will be able
– to define Congenital Heart Disease (CHD), and
– to describe common types of Acyanotic CHD.
7. 05/31/15 DR. M. S. PRASAD 7
Cardiovascular DiseasesCardiovascular Diseases
• Congenital Heart Disease
– Acyanotic CHD (L R shunt)
– Cyanotic CHD (R L shunt).
• Acquired Heart Diseases:
– Kawasaki Disease,
– Myocarditis,
– Rheumatic Heart Disease.
8. 05/31/15 DR. M. S. PRASAD 8
Congenital Heart Disease (CHD)Congenital Heart Disease (CHD)
• Con = Together.
• Genitus = Born.
9. 05/31/15 DR. M. S. PRASAD 9
Definition
• A structural or functional deficiency in heart or
its appendages which originates during foetal
life is known as ‘Congenital Heart Disease’Congenital Heart Disease’
(CHD).
• It may or may not manifest at birth.
• Congenital Bicuspid Aortic Valve is normal at birth but may take 2,
3, or more decades to stiffen, calcify and present as overt Aortic
Stenosis.
13. 05/31/15 DR. M. S. PRASAD 13
Acyanotic CHDAcyanotic CHD
• Shunt Lesions (Left Right),
• Obstructive Lesions,
• Regurgitant Lesions, and
• Mixed (combination)
14. 05/31/15 DR. M. S. PRASAD 14
LL R Shunt LesionsR Shunt Lesions
• ASD (Atrial Septal Defect),
• AVSD (Atrio-ventricular Septal Defect),
• VSD (Ventricular Septal Defect),
• PDA (Patent Ductus Arteriosus).
15. 05/31/15 DR. M. S. PRASAD 15
Obstructive LesionsObstructive Lesions
• AS (Aortic Stenosis),
• COA (Coarctation of Aorta)
• HLHS (Hypoplastic Left Heart Syndrome),
• PS (Pulmonary Stenosis),
• Mitral Stenosis,
• Tricuspid Stenosis
16. 05/31/15 DR. M. S. PRASAD 16
Regurgitant LesionsRegurgitant Lesions
• AR (Aortic Regurgitation),
• MR (Mitral Regurgitation),
• MVP (Mitral Valve Prolapse),
• TR (Tricuspid Regurgitation),
• PI (Pulmonary Incompetence)
17. 05/31/15 DR. M. S. PRASAD 17
Patent Foramen OvalePatent Foramen Ovale
(PFO)(PFO)
&&
Atrial Septal DefectAtrial Septal Defect
(ASD)(ASD)
18. 05/31/15 DR. M. S. PRASAD 18
PFOPFO
• An isolated patent foramen (PFO) is a common
finding during infancy and it usually closes.
• It is not considered abnormal, even if it persists
throughout life.
• It is usually of no hemodynamic significance and
is not considered an ASD.
May play an important role if other structural heart defects are
present.
19. 05/31/15 DR. M. S. PRASAD 19
Atrial Septal Defect (ASD)Atrial Septal Defect (ASD)
• A defect in the wall between left and right atrium
is known as Atrial Septal Defect (ASD).
• This is one of the Acyanotic CHD with L R
shunt.
• More common in females than in males.
[M:F = 1:2].
21. 05/31/15 DR. M. S. PRASAD 21
Types of ASDTypes of ASD
• Ostium Secundum Defect
(5-10% of CHD)
• Sinus Venosus ASD.
(10% of ASD)
• Ostium primum ASD
22. 05/31/15 DR. M. S. PRASAD 22
SVC
IVC
TV
Ostium primum
Ostium secundum
Superior Sinus Venosus
Inferior Sinus Venosus
23. 05/31/15 DR. M. S. PRASAD 23
• Ostium secundum ASD constitutes 5-10%
of CHD.
• Ostium Secundum Defect is 3 times more
common in girls than in boys.
• PAPVR may be present.
24. 05/31/15 DR. M. S. PRASAD 24
Secundum ASDSecundum ASD
• Spontaneous closure up to 2-3 years may
occur.
• Symptoms in childhood are rare.
• Life expectancy virtually normal if closure
undertaken in childhood.
25. 05/31/15 DR. M. S. PRASAD 25
Sinus VenosusSinus Venosus
• Spontaneous closure does not occur.
• Natural history same as secundum ASD.
26. 05/31/15 DR. M. S. PRASAD 26
ASD
• History: Usually asymptomatic.
• Physical Examination:
– Thin built.
– There is absence of sinus arrhythmia.
– Wide & fixed splitting of 2nd
Heart Sound.
– Ejection Systolic Murmur.
• ECG
• CXR
• Echocardiogram
27. 05/31/15 DR. M. S. PRASAD 27
ASD
• ECG:
– Features of RBBB
– rsR/
pattern V1
– Mild RVH
– RAD
• CXR:
– Cardiomegaly
– Prominent Pulmonary Conus.
– Increased Pulmonary Vascular Markings.
• Echocardiography
– Diagnostic,
– shows exact location.
28. 05/31/15 DR. M. S. PRASAD 28
Atrio-ventricular Septal DefectAtrio-ventricular Septal Defect
29. 05/31/15 DR. M. S. PRASAD 29
Atrio-Ventricular Septal DefectAtrio-Ventricular Septal Defect
• Partial (ostium primum) AVSD
– Atrial Shunting,
– Mitral Valve is always defective,
– LV RA shunting may occur.
• Complete AVSD
– Strong association with Down’s Syndrome,
– Atrial and Ventricular shunting,
– AV regurgitation.
30. 05/31/15 DR. M. S. PRASAD 30
Clinical FeaturesClinical Features
• FTT
• Clinical signs of CHF,
• Signs of the most prominent lesion
(ASD, Regurgitation, others)
31. 05/31/15 DR. M. S. PRASAD 31
ManagementManagement
• Management of CHF,
• Corrective surgery.
35. 05/31/15 DR. M. S. PRASAD 35
Types of VSD
•Membranous.
•Muscular.
•Swiss Cheese Septum.
36. 05/31/15 DR. M. S. PRASAD 36
VSD: PathopyhsiologyVSD: Pathopyhsiology
• LV pressure higher than RV.
• Blood passes through the defect to RV.
• RV load is increased.
• PA receives more volume than expected.
• This extremely large pulmonary blood flow results
into Pulmonary Hypertension.
37. 05/31/15 DR. M. S. PRASAD 37
Clinical ManifestationsClinical Manifestations
38. 05/31/15 DR. M. S. PRASAD 38
Small VSDSmall VSD
• Asymptomatic.
• Cardiac lesion is usually found during
routine physical examination.
• A loud, harsh, or blowing systolic murmur
best heard over the lower left sternal
border.
39. 05/31/15 DR. M. S. PRASAD 39
Large VSDLarge VSD
• Patients with large defects typically
develop CHF.
• Excessive pulmonary blood flow and
Pulmonary Hypertension
• Dyspnoea or effort intolerance.
• Poor Growth.
40. 05/31/15 DR. M. S. PRASAD 40
Large VSDLarge VSD (continued)
• Profuse Perspiration (Sweating).
• Recurrent RTI.
• Feeding difficulty,
• Systolic Murmur: less harsh, more blowing
• Loud P2
41. 05/31/15 DR. M. S. PRASAD 41
VSD:VSD: DiagnosisDiagnosis
• Most common Acyanotic CHD.
• CXR:
– Small VSD: Normal.
– Large VSD:
• Cardiomegaly.
• Increased Pulmonary Vascular Markings.
• ECG:
– Small VSD: Normal.
– Large VSD: Biventricular Hypertrophy.
• Echocardiogram
• Cardiac Catheterization.
42. 05/31/15 DR. M. S. PRASAD 42
Natural HistoryNatural History
• 65% of VSD present at birth close
spontaneously.
• Remaining cases:
– FTT,
– Feeding difficulty,
– Signs of VSD and CHF.
43. 05/31/15 DR. M. S. PRASAD 43
ManagementManagement
• Manage CHF,
• Surgical closure.
44. 05/31/15 DR. M. S. PRASAD 44
Patent Ductus ArteriosusPatent Ductus Arteriosus
(PDA)(PDA)
45. 05/31/15 DR. M. S. PRASAD 45
Patent DuctusPatent Ductus
arteriosus (PDa)arteriosus (PDa)
Patent DuctusPatent Ductus
arteriosus (PDa)arteriosus (PDa)
PA
Aorta
RA
RV
LA
LV
PVIVC & SVC
48. 05/31/15 DR. M. S. PRASAD 48
PDAPDA
• More in females [2:1]
• Maternal Rubella in early pregnancy.
• Common in premature infants.
• 10% of PDA is associated with other CHD.
49. 05/31/15 DR. M. S. PRASAD 49
PDA: Clinical ManifestationsPDA: Clinical Manifestations
• Wide Pulse Pressure.
• Bounding Peripheral Pulses.
• Cardiac Enlargement.
• Thrill.
LSB & below left clavicle.
• Machinery Murmur.
• CHF
50. 05/31/15 DR. M. S. PRASAD 50
PDA: DiagnosisPDA: Diagnosis
• ECG: Normal/LVH/BVH
• CXR: Prominent PA & Increased PVM.
• Echocardiogram: from the suprasternal notch.
• Colour & Pulsed Doppler Examination.
• Cardiac Catheterization.
53. 05/31/15 DR. M. S. PRASAD 53
COA
• COA is a localized or segmental
constriction [narrowing] of aorta
• The size of constriction may vary.
54. 05/31/15 DR. M. S. PRASAD 54
COACOA
• It may be at one point or multiple points.
• It may involve a long segment continuously.
• Involvement of long segment is known as
“Tubular Hypoplasia”.
• Sometimes, the the aorta becomes
completely atretic and results in an
“Interrupted Aortic Arch”.
55. 05/31/15 DR. M. S. PRASAD 55
COACOA
• The COA may occur at any point from the
Transverse Arch to the iliac bifurcation.
• 98% occur just below the origin of the left
subclavian artery at the origin of the ductus
arteriosus [juxtaductal COA].
56. 05/31/15 DR. M. S. PRASAD 56
Coarctation of Aorta
• Two times more common in males.
• M:F = 2:1
57. 05/31/15 DR. M. S. PRASAD 57
Types of COATypes of COA
o Infantile Type.
COA associated with arch hypoplasia was
referred to as Infantile Type because its
severity led to its recognition in early infancy.
o Adult Type.
Adult Type referred to isolated juxtaductal COA,
which if mild, was not usually recognized until
later childhood.
58. 05/31/15 DR. M. S. PRASAD 58
COA: Clinical Manifestations
• Weakness and pain after exercise.
• Hypertension on routine physical examination.
• Classis Sign: Disparity in pulsation and B. P. in
the arms and legs.
59. 05/31/15 DR. M. S. PRASAD 59
COA: Diagnosis
• Mainly on clinical grounds.
• CXR & ECG: not much
helpful.
• Pulsed and continuous wave
Doppler studies are helpful.
60. 05/31/15 DR. M. S. PRASAD 60
Typical clinical findings in common CHD
Lesion Pulse
Ventricular
dominance
Heart
Sounds
Murmur
Radiation
of murmur
VSD Normal Both N/↑P2 PSM
Apex &
Back
ASD Normal RVH
wide &
fixed 2nd
sound
ESM Back
PDA Collapsing RVH ↑ P2 Continuous Back
COA
Delayed
Femoral
LVH Normal ESM Back
PS Normal RVH Normal ESM Back
61. 05/31/15 DR. M. S. PRASAD 61
या देवी सवरभूतेषु िवदारपेण संिसथता,
नमसतसयै नमसतसयै नमसतसयै नमो नमः ||
62. 05/31/15 DR. M. S. PRASAD 62
Did you meet your objectives?Did you meet your objectives?
• Can you define Congenital Heart
Disease (CHD)? and
• Can you describe common types
of Acyanotic CHD?
• Yes, very good.
• No, discuss again next time.
Editor's Notes
<number>
The oval foramen ("foramen ovale"), labeled FO, is covered by a "flap" that allows "red", oxygenated blood from the placenta to enter the left atrium (LA).
The duct ("ductus arteriosus") is a bypass, so that "blue", less oxygen rich blood from the veins does not enter the lungs, but returns to the placenta.
At birth, a baby takes its first breath, the lungs inflate and the duct slowly closes to allow the lungs to take over the oxygenation of blood.
After birth, the FO flap closes due to lack of flow from the placenta and high pressure in the left atrium.
If the FO flap fails to close after birth (or has a defect so that it cannot seal the FO) this is known as an atrial septal defect (ASD), and results in mixing of red and blue blood.
The oval foramen ("foramen ovale"), labeled FO, is covered by a "flap" that allows "red", oxygenated blood from the placenta to enter the left atrium (LA).
The placenta supplies nutrition and oxygen as "red", oxygenated blood from the mother and also removes waste as "blue", less oxygenated blood.
After birth the umbilical cord to the placenta is cut and baby is no longer reliant on mother's blood supply.
The fetal heart works at much lower pressure than the heart after birth and there is much more mixing of "red" and "blue" blood through the FO flap and duct.
This mixing allows a baby to survive even if there is heart disease blocking a valve or a problem with the connections of the chambers and vessels.
