This document discusses several types of congenital heart diseases including their etiology, pathophysiology, clinical manifestations, diagnostic evaluation, and management. It covers tetralogy of fallot, persistent ductus arteriosus, atrial septal defect, and ventricular septal defect. For each condition, it provides details on the anatomical defects involved, characteristic signs and symptoms, relevant test findings, and treatment options including surgical repair when indicated.

1. HYPERCALCEMIA
AND
HYPOCALCEMIA
ROLL NO. 113-117

17. CLINICAL MANIFESTATION
OF HYPERCALCEMIA
 Renal stones
 Nephrolithiasis
 Nephrogenic Diabetes Insipidus
 Dehydration
 Nephrocalcinosis
 Skeleton bones
 Bone pain
 Arthritis
 Osteoporosis
 Osteitis fibrosis cystica in hyperparathyroidism
 Gastrointestinal
 Nausea, vomiting
 Anorexia
 Constipation
 Abdominal Pain

18.  Neuromuscular
 Impaired concentration and memory
 Confusion, stupor, coma
 Lethargy and fatigue
 Muscle weakness
 Corneal calcification
 Cardiovascular
 Hypertension
 Shortened QT interval in ECG
 Cardiac Arrhythmias
 Vascular Calcification

48. Cyanotic congenital
Heart disease

49. Classification
• Pulmonary blood flow – tetralogy of fallot
• —Tricuspid atresia
• Mixed blood flow — transposition of great
arteries
• —total anomalous
pulmonary venous return
• — hypoplastic left heart
syndrome

50. Tetralogy of fallot
• It is the most common type of cyanotic
congenital heart disease .
• Classical form includes 4 defects i.e.
• Ventricular septal defect
• Pulmonary stenosis
• Overriding aorta
• Right ventricular hypertrophy

51. Pathophysiology
• Blood normally returns from systemic circulation
to right atrium and right ventricles .
• Outflow of the blood from right ventricle is
resisted by pulmonary stenosis so that blood
flows through ventricular septal defect into the
aorta .
• There is right to left shunt , hypertrophy of right
ventricles occur .
• Due to this unoxygenated blood from right
ventricles cyanosis occurs .

52. Clinical manifestations:
• Cyanosis of lips , fingers and toes
• Bluish skin during episodes of crying and feeding
• Clubbing of fingers and toes
• Squatting posture
• Dyspnea on exertion
• Hypoxic spells
• Transient cerebral ischemia
• Pan systolic murmur
• Poor growth

53. Diagnostic evaluation :
• On Auscultation – loud harsh systolic murmur may be
heard at left middle to lower sternal border .
• Radiography – The heart shows enlarged ventricle on
right side , large aorta and decrease in size of
pulmonary artery . Unusual shape of heart – wooden
shoe or boot shaped heart .
• ECG : shows evidence of right ventricular
hypertrophy.
• Echocardiography: shows evidence of aortic override
, thick anterior right ventricular wall and large aorta .

54. Management :
• Oxygen administration for cyanosis .
• Surgical management:
• Palliative shunt – if pulmonary arteries
are too hypoplastic then preferred
procedure is modified Blalock Taussig shunt ,
with an anastomoses created between
pulmonary artery and subclavian artery .

55. • Complete repair : Elective repair is usually
performed in the first year of life . Indications
for repair includes increasing cyanosis and
valve closure of the VSD and resection of
infundibular stenosis with a pericardial patch
to enlarge the right ventricular outflow tract .

56. • Normally ductus atreriosus closes soon after birth
but in this anomaly it fails to do so due to which
there is continuous AV shunt from aorta to
pulmonary artery .
• Clinical features — dyspnoea , machinery murmur.
( maximum in 2nd left inter coastal space below
clavicle) , accompanied her thrill , pulse is increased
in volume .
• Investigations – echocardiogram is IOC . Enlargement
of pulmonary artery may be detected radiologically .
• ECG – evidence of right ventricular hypertrophy.
Persistent ductus atreriosus

57. Management:
• Persistent ductus can be closed at cardiac
catheterisation with an implantable occlusive
device
• Closure should be undertaken in infancy if
shunt is significant otherwise it can be
delayed until childhood.
• When ductus is structurally intact ,
prostaglandin synthetase inhibitor may be
used in first week of life to induce closure .

58. ATRIAL SEPTAL DEFECT
.

59. ETIOPATHOGENESIS
• One of most common CHD.
• FREQUENCY: twice in females
• Due to defect in ‘ostium secundum ’ involving fossa ovalis
• Large volume of blood shunts through defect from LA to RA
• From RA to pulmonary arteries

60. CLINICAL FEATURES
• Mostly asymptomatic for years & detected at routine
examination.
• Dyspnea
• Chest infection
• Arrythmias esp. atrial fibrillation
• characteristic physical signs are result of volume
overload of RV
• In children with large shunt : have diastolic murmur
over tricuspid valve.

61. .

62. INVESTIGATIONS
• CHEST X- Ray : enlargement of heart , pul. Artery & pul.
Plethora
• ECG: incomplete right bundle branch block
• Echocardiography: demonstrate defect and RV dilation,
RV hypertrophy and pul. Artery dilation
• Transesophageal Echocardiography: show precise size
and location of defect

63. MANAGEMENT
• ASD with pul. Flow is increased by
50% above systemic flow : closed
surgically
• Closure can accomplished at cardiac
catheterization using implant closure
devices
• Contraindication to surgery: Shunt
reversal and severe pul. Hypertension

64. VENTRICULAR SEPTAL
DEFECT
•
.

65. ETIOPATHOGENESIS
• It is most common congenital cardiac defect
• Defect may be isolated or part of compex congenital
heart dis.
• Occurs as result of incomplete septation of ventricles.
• Most defects are perimembranous (junction of
membrane & muscular portion)
• Acquired defect may occur due to rupture as in acute
MI or rarely trauma

66. CLINICAL FEATURES
• Pansystolic murmur
• Prominent parasternal pulsation
• tachypnea
• Indrawing of ribs on inspiration
• May present as: cardiac failure in infants
As murmur with only minor hemodynamic
disturbance in older children & adults

67. DIAGNOSIS
• CHEST X-Ray : shows pul. Plethora
• ECG: bilateral vent. hypertrophy

68. MANAGEMENT
• Small defect : no specific treatment
• Cardiac failure in infancy: treated with digoxin and
diuretics
• Persistent failure indication for surgical repair of defect.
• Except in Eisenmenger’s syndrome ,long term
prognosis is very good in VSD