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Bedside Approach to
common
Congenital Heart Diseases
The rule of Commonness
The uncommon manifestations
of common diseases
are much more commoner
than the
common manifestations
of uncommon diseases
When to suspect CHD ?
• Presentation in childhood or adolescence
• H/O murmur detected in newborn nursery or
school health cell
• Family history of congenital heart diseases
• Symptoms specific to CHD: Cyanosis, Spells,
Squatting, Recurrent respiratory infections
• Dysmorphic features
Cardinal Symptoms
Dyspnea Fatigue
Angina Resp. infection
Palpitation Cyanosis
Syncope Stroke/Embolism
Edema Hemoptysis
CARDIAC DYSPNEA - MECHANISMS
• INCREASED PULMONARY VENOUS PRESSURE
Stimulation of J receptors > Hering Breur reflex
Altered Lung Compliance > Respiratory muscle
length – tension mismatch
↑ Airway resistance : reflex broncho constriction
peribronchial &mucosal edema, intraluminal fluid
• DECREASED CARDIAC OUTPUT :
Fatigue of Respiratory & Exercising muscles
Increased O2 Extraction > Widened A-V O2 diff
• HYPOXIA : Right to Left shunts
Recurrent Respiratory Infections
• Respiratory infections that
are too frequent, more
severe and longer lasting.
• Arbitrarily, if respiratory
infections occur for more
than 6 times a year or
more than once in a
month, lasting for more
than a week or requiring
either iv antiobiotics or
hospitalizations.
SIMPLE
COMMUNICATIONS +
RESISTANCE TO PBF
MIXING
SITUATIONS
VSD, ASD, PDA +
PULMONARY PULMONARY
STENOSIS HYPERTENSION
Complete : TAPVC, COMMON
ATRIUM, SINGLE VENTRICLE,
TRUNCUS ARTERIOSUS
Incomplete : TGA
RA
RV
PV Ao
LV
LA
RV
RA LA
LV
TA
• Is it cyanotic or acyanotic
• Is the situation one of
↑ Pulmonary Blood Flow: Neonatal HF, LRTI
↓ Pulmonary blood flow: Cyanosis, Spell,
Squatting
or one of obstructive lesion: DOE, Angina,
Syncope
• Is it right heart disease or left heart disease
• Has the patient developed pulmonary hypertension
Ask yourself the following …..
CCHD - Age at Presentation
Neonatal life (< 1month) : most severe disease;
sickest children; markedly hypoxemic;
many don’t survive to see their first birthday.
a) Severe Obstruction to PBF with R>L shunt :
Severe TOF, Pulmonary Atresia with IVS
b) Incomplete Mixing:
TGA + IVS + restrictive IAC
c) Complete mixing but with obstruction to PBF
SV + PS, TA + small VSD or severe PS,
Obstructed TAPVC
CCHD - Age at Presentation
Infancy ( 1m – 1yr) :
1) Moderate to severe PS + R>L shunt :
TOF, Pulm Atresia + VSD, DORV + PS, TA
2) Small ( hypoplastic ) RV – R>L @ IAC
Hypoplastic RV, Ebstein’s anomaly
3) Unobstructed TAPVC
Childhood (1-12 yrs) Eisenmenger syndrome
Mode of Presentation
• Neonatal Heart Failure (feeding difficulty,
intercostal indrawing, tachypnea, sweating,
restless / dyspnea in recumbency)
Obstructive lesion, myocardial disease
• Heart failure at 4-6 weeks (regressing PVR)
Post tricuspid shunts (VSD,PDA)
• Cyanosis at birth: Complex defects
TGA, Truncus, TAPVC, SV, TA,
• Cyanosis 3-6 months: TOF, DORV PS, TA
• Cyanosis in late childhood: Eisenmenger
Squatting relieves dyspnea inTOF
↑ SVR / Early reflected waves > Central AoP
Cyanotic (hypoxic) Spells
• TOF, Pulm Atresia with VSD, DORV PS
• 2 m – 2 yrs, early hours (activity, feeding,
defecation), worse in summer / during respiratory
infections, Cath may precipitate
Increased C.O / Lowered SVR > ↑ R-L shunt
Hyperpnea ↑Hypoxia
Tachycardia
Catecholamines R V contractility ↓RV size
General Examination
• ↓ weight + normal height - ↓ PBF
• ↓ weight + ↓ height - ↑ PBF
• Ellis van Creveld: Common atrium
• TOF : Down & Poland syndrome, CHARGE,
CATCH 22
• Trisomy 18 : DORV
• Cat eye syndrome : Tricuspid atresia
6-10% of CHDs
1 out of 1500 live births
5-10%
15-20%
75%
ATRIAL SEPTAL DEFECT
E I
E I
Variable split of S2
Small ASD /PAPVC; Pulmonary Hypertension
Absent flow murmur
Pulmonary Hypertension/Small ASD
ASD - Differential Diagnosis
• MILD PULMONARY STENOSIS
No RV Volume overload features,
Ejection sound, Harsh MSM, S2 split
varies with respiration, P2 N, No MDM
• IDPA
Normal S2 split & P2, No MDM
• Straight back
A.S.D with Cyanosis
• PH with shunt
reversal
• Deroofed
Coronary sinus
• LSVC into LA
• Common Atrium
• TAPVC
A.S.D with Pulmonary Ejection Sound
• ASD with Pulmonary Hypertension
• ASD with Pulmonary Stenosis
• ASD with large L > R shunt
A.S.D with Mitral Regurgitation
• Cleft Mitral Valve in Primum ASD
• Mitral Valve Prolapse
• Rheumatic
A.S.D with systolic thrill in L II ICS
ATRIAL SEPTAL DEFECT
WITH PULMONARY STENOSIS
WITH MITRAL STENOSIS
LARGE L > R SHUNT
ECG in Atrial Septal Defect
• Left axis deviation of QRS: Primum ASD
• Left axis deviation of P: SVC ASD
• Left axis deviation of P & QRS: C.A
Ventricular Septal Defect
Ventricular Septal Defect
• Brisk upstroke of arterial pulse
• Hyperdynamic apex, RV impulse, Systolic thrill
• S2 split wide (L>R) Single (↑PVR), S3, MDM
• Restrictive VSD: High pitched, S2 normal
• Moderate sized VSD: Harsh, S2 wide
• Large VSD with ↑ PVR: Murmur shorter & fainter
S2 single & loud
What are the other two occasions
in which the murmur of VSD
is not holosystolic ?
What are the other two occasions
in which the murmur of VSD
is not holosystolic ?
• Muscular VSD
• Closing VSD
DD of Precordial Holo Systolic Murmur
VSD LV-RAF TR MR
Location L IV ICS RLSB LLSB APEX
Pulse Brisk Brisk Low Vol Brisk
JVP -- -- ↑v --
API RV
Precordium BiV BiV RV LV
Murmur Loud 3-4/6 2-3/6 3-4/6
harsh soft, high ptiched
Inspiration - - ↑ -
Patent Ductus Arteriosus
• Wide pulse pressure
• Hyperdynamic API
• S1 N; S2 paradoxical
• Continuous murmur
machinery, peaks around S2, eddy sounds
• S3, MDM at apex
DD of Continuous Murmur
• Patent Ductus
Arteriosus
• Coronary Arterial
Fistula
• Ruptured aneurysm
of sinus of Valsalva
• Anomalous origin of
LCA from from PA
• Venous hum, Mammary souffle, MS with PFO
SITE NATURE CONFIGURATION
PDA L II,I ICS Machinery
Eddies
CAF L II, III IS Soft high pitched
RSB, LLSB
RSOV L III ICS Loud, harsh, sawing
RSB, LSB Superficial
ALCOPA L II ICS Soft, high pitched
VENOUS NECK Soft / Rough
HUM URSB noisy
VALVULAR PULMONARY STENOSIS
• Prominent ‘a’ in neck
• ↑ RV Impulse, RV S4
• ESM L II ICS > LSB, Delayed soft P2
RV OUTFLOW OBSTRUCTION
Which right sided
auscultatory event
is prominent in expiration
& Why ?
Which right sided auscultatory event
is prominent in expiration & Why ?
Pulmonary Ejection sound of VPS
R II ICS
L III ICS
L III IV
ICS
L I ICS
LVOT OBSTRUCTION
How does the murmur of
Aortic stenosis
differ from that of
Pulmonary Stenosis ?
TETRALOGY OF FALLOT
Post VPD ↑↑ ---
Prominent ‘a’ JVP yes no
Parasternal impulse ++ no
VSD PS Physiology
• Tetralogy of Fallot 3-6 m, Rt Ao Arch, QRS 90-1500
• DORV with P.S Longer louder murmur, QRS > 1500,
Counterclockwise rotation
• CTGV with PS Pulsation L III ICS, Apical HSM
• Tricuspid atresia /VSD /PS ↑a JVP, ↓RV impulse,
LAD + LVH
• TGA PS Intense cyanosis from birth
• Single ventricle PS Precordial QRS
Eisenmenger Syndrome
ASD VSD PDA
• Age 4th decade 2nd decade
• Neonatal HF No +++ ++
• Effort syncope Yes Yes No
• Cyanosis Uniform Uniform Differential
• ‘a’ JVP No Yes Yes
• S2 split wide fixed Single Normal
• PR murmur ± ± ++
• ↑ CTR +++ No No
• Aorta -- -- ++
Be inquisitive !
Learn from
Textbooks / online
Teachers
Patients
Colleagues
Students
by yourself
Learning is a
life long commitment…
LVOT Obstruction – Causes & Differentials
`
Cyanosis in Congenital Heart Diseases
High resistance to PBF due
to PS / PH
R > L shunting across
ASD,VSD,PDA
Mixing of venous &
arterial blood
Adequate : TAPVC, T At, CA, SV, TA,
Inadquate: TGA
Atrial Septal Defect
Age at Presentation
1 month to 1 year :
TOF, VSD+PS, DORV+PS, PS + ASD,
Pulmonary Atresia + VSD + MAPCAs,
Pulmonary AV fistula, Mixing situations
with good mixing
1 year to 12 years :
Eisenmenger syndrome

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bedside approach to common congenital heart diseases

  • 2. The rule of Commonness The uncommon manifestations of common diseases are much more commoner than the common manifestations of uncommon diseases
  • 3.
  • 4. When to suspect CHD ? • Presentation in childhood or adolescence • H/O murmur detected in newborn nursery or school health cell • Family history of congenital heart diseases • Symptoms specific to CHD: Cyanosis, Spells, Squatting, Recurrent respiratory infections • Dysmorphic features
  • 5. Cardinal Symptoms Dyspnea Fatigue Angina Resp. infection Palpitation Cyanosis Syncope Stroke/Embolism Edema Hemoptysis
  • 6. CARDIAC DYSPNEA - MECHANISMS • INCREASED PULMONARY VENOUS PRESSURE Stimulation of J receptors > Hering Breur reflex Altered Lung Compliance > Respiratory muscle length – tension mismatch ↑ Airway resistance : reflex broncho constriction peribronchial &mucosal edema, intraluminal fluid • DECREASED CARDIAC OUTPUT : Fatigue of Respiratory & Exercising muscles Increased O2 Extraction > Widened A-V O2 diff • HYPOXIA : Right to Left shunts
  • 7. Recurrent Respiratory Infections • Respiratory infections that are too frequent, more severe and longer lasting. • Arbitrarily, if respiratory infections occur for more than 6 times a year or more than once in a month, lasting for more than a week or requiring either iv antiobiotics or hospitalizations.
  • 8. SIMPLE COMMUNICATIONS + RESISTANCE TO PBF MIXING SITUATIONS VSD, ASD, PDA + PULMONARY PULMONARY STENOSIS HYPERTENSION Complete : TAPVC, COMMON ATRIUM, SINGLE VENTRICLE, TRUNCUS ARTERIOSUS Incomplete : TGA RA RV PV Ao LV LA RV RA LA LV TA
  • 9. • Is it cyanotic or acyanotic • Is the situation one of ↑ Pulmonary Blood Flow: Neonatal HF, LRTI ↓ Pulmonary blood flow: Cyanosis, Spell, Squatting or one of obstructive lesion: DOE, Angina, Syncope • Is it right heart disease or left heart disease • Has the patient developed pulmonary hypertension Ask yourself the following …..
  • 10. CCHD - Age at Presentation Neonatal life (< 1month) : most severe disease; sickest children; markedly hypoxemic; many don’t survive to see their first birthday. a) Severe Obstruction to PBF with R>L shunt : Severe TOF, Pulmonary Atresia with IVS b) Incomplete Mixing: TGA + IVS + restrictive IAC c) Complete mixing but with obstruction to PBF SV + PS, TA + small VSD or severe PS, Obstructed TAPVC
  • 11. CCHD - Age at Presentation Infancy ( 1m – 1yr) : 1) Moderate to severe PS + R>L shunt : TOF, Pulm Atresia + VSD, DORV + PS, TA 2) Small ( hypoplastic ) RV – R>L @ IAC Hypoplastic RV, Ebstein’s anomaly 3) Unobstructed TAPVC Childhood (1-12 yrs) Eisenmenger syndrome
  • 12. Mode of Presentation • Neonatal Heart Failure (feeding difficulty, intercostal indrawing, tachypnea, sweating, restless / dyspnea in recumbency) Obstructive lesion, myocardial disease • Heart failure at 4-6 weeks (regressing PVR) Post tricuspid shunts (VSD,PDA) • Cyanosis at birth: Complex defects TGA, Truncus, TAPVC, SV, TA, • Cyanosis 3-6 months: TOF, DORV PS, TA • Cyanosis in late childhood: Eisenmenger
  • 13. Squatting relieves dyspnea inTOF ↑ SVR / Early reflected waves > Central AoP
  • 14. Cyanotic (hypoxic) Spells • TOF, Pulm Atresia with VSD, DORV PS • 2 m – 2 yrs, early hours (activity, feeding, defecation), worse in summer / during respiratory infections, Cath may precipitate Increased C.O / Lowered SVR > ↑ R-L shunt Hyperpnea ↑Hypoxia Tachycardia Catecholamines R V contractility ↓RV size
  • 15. General Examination • ↓ weight + normal height - ↓ PBF • ↓ weight + ↓ height - ↑ PBF • Ellis van Creveld: Common atrium • TOF : Down & Poland syndrome, CHARGE, CATCH 22 • Trisomy 18 : DORV • Cat eye syndrome : Tricuspid atresia
  • 16. 6-10% of CHDs 1 out of 1500 live births 5-10% 15-20% 75% ATRIAL SEPTAL DEFECT
  • 17. E I
  • 18. E I Variable split of S2 Small ASD /PAPVC; Pulmonary Hypertension Absent flow murmur Pulmonary Hypertension/Small ASD
  • 19. ASD - Differential Diagnosis • MILD PULMONARY STENOSIS No RV Volume overload features, Ejection sound, Harsh MSM, S2 split varies with respiration, P2 N, No MDM • IDPA Normal S2 split & P2, No MDM • Straight back
  • 20.
  • 21. A.S.D with Cyanosis • PH with shunt reversal • Deroofed Coronary sinus • LSVC into LA • Common Atrium • TAPVC
  • 22. A.S.D with Pulmonary Ejection Sound • ASD with Pulmonary Hypertension • ASD with Pulmonary Stenosis • ASD with large L > R shunt
  • 23. A.S.D with Mitral Regurgitation • Cleft Mitral Valve in Primum ASD • Mitral Valve Prolapse • Rheumatic
  • 24. A.S.D with systolic thrill in L II ICS ATRIAL SEPTAL DEFECT WITH PULMONARY STENOSIS WITH MITRAL STENOSIS LARGE L > R SHUNT
  • 25. ECG in Atrial Septal Defect • Left axis deviation of QRS: Primum ASD • Left axis deviation of P: SVC ASD • Left axis deviation of P & QRS: C.A
  • 27. Ventricular Septal Defect • Brisk upstroke of arterial pulse • Hyperdynamic apex, RV impulse, Systolic thrill • S2 split wide (L>R) Single (↑PVR), S3, MDM • Restrictive VSD: High pitched, S2 normal • Moderate sized VSD: Harsh, S2 wide • Large VSD with ↑ PVR: Murmur shorter & fainter S2 single & loud
  • 28. What are the other two occasions in which the murmur of VSD is not holosystolic ?
  • 29. What are the other two occasions in which the murmur of VSD is not holosystolic ? • Muscular VSD • Closing VSD
  • 30. DD of Precordial Holo Systolic Murmur VSD LV-RAF TR MR Location L IV ICS RLSB LLSB APEX Pulse Brisk Brisk Low Vol Brisk JVP -- -- ↑v -- API RV Precordium BiV BiV RV LV Murmur Loud 3-4/6 2-3/6 3-4/6 harsh soft, high ptiched Inspiration - - ↑ -
  • 31. Patent Ductus Arteriosus • Wide pulse pressure • Hyperdynamic API • S1 N; S2 paradoxical • Continuous murmur machinery, peaks around S2, eddy sounds • S3, MDM at apex
  • 32. DD of Continuous Murmur • Patent Ductus Arteriosus • Coronary Arterial Fistula • Ruptured aneurysm of sinus of Valsalva • Anomalous origin of LCA from from PA • Venous hum, Mammary souffle, MS with PFO
  • 33. SITE NATURE CONFIGURATION PDA L II,I ICS Machinery Eddies CAF L II, III IS Soft high pitched RSB, LLSB RSOV L III ICS Loud, harsh, sawing RSB, LSB Superficial ALCOPA L II ICS Soft, high pitched VENOUS NECK Soft / Rough HUM URSB noisy
  • 34. VALVULAR PULMONARY STENOSIS • Prominent ‘a’ in neck • ↑ RV Impulse, RV S4 • ESM L II ICS > LSB, Delayed soft P2
  • 36. Which right sided auscultatory event is prominent in expiration & Why ?
  • 37. Which right sided auscultatory event is prominent in expiration & Why ? Pulmonary Ejection sound of VPS
  • 38. R II ICS L III ICS L III IV ICS L I ICS LVOT OBSTRUCTION
  • 39. How does the murmur of Aortic stenosis differ from that of Pulmonary Stenosis ?
  • 40.
  • 41.
  • 42. TETRALOGY OF FALLOT Post VPD ↑↑ --- Prominent ‘a’ JVP yes no Parasternal impulse ++ no
  • 43. VSD PS Physiology • Tetralogy of Fallot 3-6 m, Rt Ao Arch, QRS 90-1500 • DORV with P.S Longer louder murmur, QRS > 1500, Counterclockwise rotation • CTGV with PS Pulsation L III ICS, Apical HSM • Tricuspid atresia /VSD /PS ↑a JVP, ↓RV impulse, LAD + LVH • TGA PS Intense cyanosis from birth • Single ventricle PS Precordial QRS
  • 44.
  • 45. Eisenmenger Syndrome ASD VSD PDA • Age 4th decade 2nd decade • Neonatal HF No +++ ++ • Effort syncope Yes Yes No • Cyanosis Uniform Uniform Differential • ‘a’ JVP No Yes Yes • S2 split wide fixed Single Normal • PR murmur ± ± ++ • ↑ CTR +++ No No • Aorta -- -- ++
  • 46. Be inquisitive ! Learn from Textbooks / online Teachers Patients Colleagues Students by yourself Learning is a life long commitment…
  • 47.
  • 48.
  • 49.
  • 50. LVOT Obstruction – Causes & Differentials
  • 51.
  • 52.
  • 53. `
  • 54. Cyanosis in Congenital Heart Diseases High resistance to PBF due to PS / PH R > L shunting across ASD,VSD,PDA Mixing of venous & arterial blood Adequate : TAPVC, T At, CA, SV, TA, Inadquate: TGA
  • 55.
  • 56.
  • 58.
  • 59.
  • 60. Age at Presentation 1 month to 1 year : TOF, VSD+PS, DORV+PS, PS + ASD, Pulmonary Atresia + VSD + MAPCAs, Pulmonary AV fistula, Mixing situations with good mixing 1 year to 12 years : Eisenmenger syndrome