Congenital heart disease


Published on

Published in: Education, Health & Medicine
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Congenital heart disease

  2. 2. INCIDENCE: The overall incidence of congenital heart diseases is about 8 – 10 percent per 1000 live births Defect VSD PDA ASD Coarctation of aorta TOF Percentage 25 – 30 % 10 % 10 % 6% 5- 9 %
  3. 3. ETIOLOGY AND INCIDENCE    Hereditary factors  CHD affects 8 – 12 of every 1000 neonates  Associated factor for CHD include Ø Fetal or Maternal infection during the first trimester (Rubella) Ø Chromosomal abnormality (Trisomy 21, 18, 13) Ø Maternal diabetes Ø Teratogenic effects of drugs and alcohol  Syndromes that include CHD Ø Ø Ø Ø Marfan`s syndrome Turner’s syndrome William’s syndrome Down syndrome : Mitral value prolapse : Aortic value stenosis, COA : Dysplastic pulmonary value : Triosomy
  4. 4.  Congenital Heart diseases Cyanotic heart Acyanotic heart Obstructive diseases ( R to L shunt ) diseases ( L to R ) .Coarctation of aorta  Fallots tetrology . VSD . Vascular ring  Transposition of greater . ASD . Pulmonary stenosis vessels   Tricuspid atresia . PDA . Aortic stenosis
  5. 5. VENRICULAR SEPTAL DEFECT (VSD) Definition VSD is an abnormal communication between the two ventricles
  6. 6. Pathophysiology Blood is shunted from the left to the right ventricles in most of the cases due to the relatively high pressure of the left ventricles chamber If the defect is large, the amount of blood shunted in to the right ventricles may be quite large resulting in increased workload for both ventricles Right ventricles increased pulmonary enlargement develops right ventricular out put and Blood increased return to the left atrium, thus increasing the work of the left ventricles, resulting in bi – ventricular hypertrophy Pulmonary over circulation cause a change in the pulmonary arterial bed, leading to increased pulmonary artery vascular resistance
  7. 7. Clinical manifestation Small VSD`s : usually a symptomatic; High spontaneous closure rate during the first year of life Large VSD`s:  CHF – tachypnea, tachycardia, excessive sweating  Frequent URI  Poor weight gain, Failure to thrive  Feeding difficulties  Murmur present  Pulmonary vascular obstructive diseases
  8. 8. Investigation X. - ray chest - ventricular hypertrophy  Small -Normal  Moderate VSD - shunt vascularity (pulmonary plethora) Ventricular hypertrophy o Pulmonary artery increased size.  Large VSD - Biventricular hypertrophy  Increased pulmonary trunk  Left arterial enlargement. – Enlarged main pulmonary artery --- Right ventricular hypertrophy --- Peripheral pruning with apparent decrease in shunt --- vascularity.
  10. 10.  ECG  Echo and Doppler study  Cardiac cauterization study  Angiocardiography
  11. 11. Management of VSD: Aims: 1.     To achieve normal growth by controlling ccf 2. Prevention and treatment of anemia 3. Prevention and treatment of infective endocarditis
  12. 12. 1. Medical management : 1. CHF management :digoxin and diuretics(furasemide, spironolactone) and after reduction 2. Avoid oxygen : - oxygen is a potent pulmonary vasodilator and will increase blood flow in to the P.A 3. Increase caloric intake: fortify formula or breast milk to make 24 to 30 caloz formula, supplemental nasogastric feeds as needed. 4. Ineffective endocarditis prophylaxis for 6 months after surgery. 2.Surgical treatment: Corrective surgery done in first 2 years of life prevents progression of pulmonary hypertension
  13. 13. Surgeries: 1. Corrective surgery –patch graft – Dacron / Natural 2. Palliative surgery – Pulmonary artery banding Complication:  C.H.F  Recurrent respiratory tract infection  Ineffective endocarditis  Failure to thrive: poor weight gain  Pulmonary arterial hypertension elsenmengerisation  Aortic or tricuspid regurgitation  Right ventricular outflow tract obstruction. and
  14. 14. ATRIAL SEPTAL DEFECT(ASD ) Definition: Atrial septal defect is an abnormal communication between the two atria.
  15. 15. Pathophysiology: Blood flows from the higher pressure left atrium across the ASD in to the lower pressure right atrium.  Increased blood return to the right heart leads to right ventricular volume over load. Right ventricular dilatation Increased pulmonary blood flow leads to elevated pulmonary artery pressure.
  16. 16. Clinical manifestation: 1.     Usually a symptomatic 2.     CHF 3.     Frequent upper respiratory tract infection 4.     Poor weight gain 5.     Decreased exercise tolerance. Diagnostic evaluation:  X-Ray Right atrial and ventricular enlargementenlargement of pulmonary artery  E.C.G  Auscultation: soft systolic ejection murmur heard best at the left upper sternal border.  Cardiac caterization
  17. 17. Management: 1.Medical management a).Monitor and reassess b).Treatment with anticongestive therapy (digoxin and lasix) may be necessary. if signs of CHF are present c).Infective endocarditis prophylaxis for 6 months after surgery or atrial occlusion devise is used.  2. Cardiac catherisation for placement of an atrial occlusion device for ostium secundam defects. 3.Surgical intervention: a)     Primary repair suture closure of the ASD. b)     Patch repair of the ASD.
  18. 18. Complication:  CHF  Infective endocarditis  Pulmonary hypertension  Atrial arrhythmias.  
  19. 19. Patent ductus arteriosus (PDA) Definition This defect, which normally occurs during fetal life, short circuits the normal pulmonary vascular system and allows blood to mix between the pulmonary artery and the aorta. Prior to birth, there is an open passageway between the two blood vessels, which closes soon after birth. When it does not close, some blood returns to the lungs. Patent ductus arteriosus is often seen in premature infants.
  20. 20. Pathophysiology: During fetal life, the ductus arteriosus allows blood to by pass the pulmonary circulation and flow directly in to the systemic circulation. After birth, the ductus arteriosus is no longer needed. Functional closure usually occurs within 48 hrs after birth. When the ductus arteriosus fails to close blood from the aorta ( high pressure) flows in to the lower pressure PA.   Resulting in pulmonary over circulation  Increased pulmonary blood flow leads to a volume- loaded LV.
  21. 21. Clinical manifestation: 1.     Growth retardation 2.     External dyspnea 3.     CCF 4.     Pericardial pain 5.     Cough 6.     Dyspnoea 7.     Tachypnoea. 8.     Dyspnoea 9.     Tacycardia 10. Hepato splenomegali 11. Machinery murmur. It is harsh and may be localized to second left intercostals space or transmitted to left clavicle to lower down (ie) left sternal border. It is accomplished by a thrill .
  22. 22. Diagnostic evaluation : Chest X-Ray- cardiomegaly ECG ECHO Cardiac catherization; raised pressure in right ventricles and pulmonary artery. Management: 1.In the symptomatic premature neonate; Indomethacin. Given IV. 2.Medical management: a)      Monitor growth and development b)     Reassures for spontaneous PDA closure c)      Increase caloric intake as needed for normal weight gain d)     Diuretics: furusemide (lasix), spironolactone (Aldactone). e)      Ineffective endocarditis prophylaxis for 6 months after surgery.
  23. 23. 3.Cardiac catherization: a)      For small PDAs coil occlusion b)     For large PDAs closure device may be used. 4.Surgical management through PDA ligation.   Complication: 1.     CHF, pulmonary oedema 2.     Infective endocarditis 3.     Pulmonary hypertension 4.     Recurrent pneumonia.  
  25. 25. PATHOPHYSIOLOGY The blood normally returns from the systemic circulation to the systemic circulation to the right atrium and right ventricles     The outflow of blood from the right ventricles is resisted by the pulmonary stenosis so that the blood flows through the ventricular septal defect in to the aorta There is right to left shunt. Hypertrophy of the right ventricles occurs as a result of the pressure exerted against the pulmonary stenosis. Because, the blood from the right ventricles is unoxygenated, cyanosis results.
  26. 26. Clinical manifestation: 1. Cyanotic episodes: cyanotic spells may occur while crying and after feeding. After cyanotic spells, there may be limpness, fatigue and fainting. 2. Dyspnoea 3. Delayed physical growth and development 4. Pansystolic murmur may be heard at the middle to lower sternal borders 5. Cyanosis- may be seen mucous membrane of the lips, mouth and pharynx and in fingernails and toe- nails. 6. Clubbing of the fingers 7. Paroxysmal dyspneic attacks (anoxia, “ blue “ spells) occur during the first 24 months of life and last for a few minutes to hours .
  27. 27. Diagnosis: 1. Blood studies. 2. X-Ray chest 3. ECG- right ventricular hypertrophy. 4. Echo- evidence of the aortic override, thick anterior right ventricular wall and large aorta. Medical and Nursing management :  Palliative and corrective surgery for tetrology of fallot is being done in infants and children of all ages.
  28. 28. Transposition of the great arteries  This congenital heart defect, the positions of the pulmonary artery and the aorta are reversed, thus: o The aorta originates from the right ventricle, so most of the blood returning to the heart from the body is pumped back out without first going to the lungs. o The pulmonary artery originates from the left ventricle, so that most of the blood returning from the lungs goes back to the lungs again
  29. 29. Pathophysiology : In this anomaly the aorta has its origin in the right ventricles and pulmonary artery has its origins in the left ventricles. Hence, the aorta carries unoxygenated blood to the systemic circulation and the pulmonary circuit carries oxygenated blood back to the lungs.    The pulmonary venous return is to the left atrium and the systemic veins returns to the right atrium. There is two separate circulatory systemic exist, one pulmonary and one systemic. An infant can survive with this malformation initially only if an associated with defect or PDA is present  There co-existing lesions provide a means for mixing venous and
  30. 30. Clinical manifestation : 1.     Cyanosis from neonatal period and polycythemia 2.     Congestive cardiac failure 3.     Hypercapnoea due to low arterial oxygen 4.     Delayed growth and development 5.     Metabolic acidosis 6.     Clubbing of the finger and toes. Diagnostic evaluation : 1.     Physical examination – if defect is there murmur can be heard 2.     X-ray- cardiomegaly and increased pulmonary vasculature 3.     Fluoroscopy- egg shaped” cardiac contour can be identified 4.     Echo- Right ventricular hypertrophy 5.     ECG 6.     Angiocardiography Cardiac catherization
  31. 31. Treatment:  Procedure used for the treatment of transposition of the great vessels are palliative and corrective.
  32. 32. Coarctation of the aorta Aortic coarctation is a narrowing of part of the aorta (the major artery leading out of the heart). It is a type of birth defect. Coarctation means narrowing. It accounts for 8 -10% of CHD and is 2 to 5 time more common in male.
  33. 33. Obstructive
  34. 34. Causes The aorta carries blood from the heart to the vessels that supply the body with blood and nutrients. If part of the aorta is narrowed, it is hard for blood to pass through the artery. Aortic coarctation is more common in Turner syndrome. Coarctation of the aorta may be seen with other congenital heart defects, such as: Bicuspid aortic valve Defects in which only one ventricle is present Ventricular septal defect
  35. 35. Clinical manifestation Asymptomatical until the PDA begin to close After PDA closure:Sever CHF Tachypnea Acidosis Prograsive circulatory shock Absent femoral and pedal pulses
  36. 36. Chest pain Cold feet or legs Dizziness or fainting Decreased ability to exercise Failure to thrive Leg cramps with exercise Nosebleed Poor growth Pounding headache
  37. 37. Diagnostic evaluation 1.     Physical examination –The pulse in the groin (femoral) area or feet will be weaker than the pulse in the arms or neck (carotid). Sometimes, the femoral pulse may not be felt at all and murmur sound can be heard , 2.     X-ray- cardiomegaly 3.    ECG 4. Echo- Right ventricular hypertrophy 5.     Angiocardiography 6. Cardiac catherization 7. Heart CT may be needed in older children 8. MRI or MR angiography of the chest may be needed in older children  
  38. 38. Management 1. Medical Menagement  Resuscitation and stabilization with Prostaglandin E1 infusion  Intubation and ventilation as needed  Infective endocarditis prophylaxis  Anticongestive theraphy( digixin and lasix)  Assessment of renal ,hepatic,and nurologic function. 2. Ballon angioplasty may be indicated for infants who are a high surgical risk. 3. Surgical intervention: usually performed as soon as the diagnosis is made  Subclavian flap repair  End to end anastomosis  Dacron patch repair 4. hypertention management is needed for the older children
  39. 39. Complication Aortic aneurysm Endocarditis (infection in the heart) Heart failure Kidney problems Paralysis of the lower half of the body (a rare complication of surgery to repair coarctation) Severe high blood pressure
  40. 40. Pulmonary stenosis Pulmonary valve stenosis is a heart valve disorder that involves the pulmonary valve. This valve separates the right ventricle (one of the chambers in the heart) and the pulmonary artery. The pulmonary artery carries oxygen-poor blood to the lungs. Stenosis, or narrowing, occurs when the valve cannot open wide enough. As a result, less blood flows to the lungs.
  41. 41. Causes Narrowing of the pulmonary valve is usually present at birth (congenital). It is caused by a problem that occurs when the unborn baby (fetus) is developing. The cause is unknown, but genetics may play a role. Pulmonary valve stenosis is a rare disorder. In some cases, pulmonary valve stenosis more in families.
  42. 42. Clinical manifestation  These infants are usually found to have a murmur on a routine heart examination.  When the valve narrowing (stenosis) is moderate to severe, the symptoms include:  Bluish color to the skin (cyanosis) in some patients  Chest pain  Fainting  Fatigue  Poor weight gain or failure to thrive in infants with severe blockage  Shortness of breath  Sudden death  Symptoms may get worse with exercise or activity.
  43. 43. Diagnostic evaluation Physical examination:- The health care provider may hear a heart murmur when listening to your heart using a stethoscope. Murmurs are blowing, whooshing, or rasping sounds heard during a heartbeat. Tests used to diagnose pulmonary stenosis may include: Cardiac catheterization Chest x-ray ECG Echocardiogram MRI of the heart
  44. 44. Treatment  Sometimes, treatment may not be needed if the disorder is mild.  When there are also other heart defects, medications may be used to:  Help blood flow through the heart (prostaglandins)  Help the heart beat stronger  Prevent clots (blood thinners)  Remove excess fluid (water pills)  Treat abnormal heartbeats and rhythms  Percutaneous balloon pulmonary dilation (valvuloplasty) may be performed when no other heart defects are present.  This procedure is done through an artery in the groin.  The doctor sends a flexible tube (catheter) with a balloon attached to the end up to the heart. Special x-rays are used to help guide the catheter.  The balloon stretches the opening of the valve.  Some patients may need heart surgery to repair or replace the pulmonary valve. The new valve can be made from different materials. If the valve cannot be repaired or replaced, other procedures may be needed.
  45. 45. Complications Abnormal heartbeats (arrhythmias) Death Heart failure and enlargement of the right side of the heart Leaking of blood back into the right ventricle (pulmonary regurgitation) after repair
  46. 46. NURSING CARE OF THE CHILD WITH CONGENITAL HEART DISEASES. Nursing Assessment:  Obtain a through nursing history  Discuss the care plan with the health care team (cardiologist, cardiac surgeon, nursing care manager, social worker, nutrition list)  Measure and record height and weight plot on a growth chart  Record vital signs and oxygen saturations.    Measure vital signs at a time when the infant / child is quit.   Choose appropriate size blood pressure cuff   Check four extremities BPxl. Assess and record.        Skin color, pink, cyanotic, mottled        Mucous membranes; moist, dry, cyanotic    Extremities: check peripheral pulses for quality and symmetry, dependent edema, capillary refill, color and temperature.
  47. 47. Assess for clubbing (cyanotic heart disease0 Assess chest wall for deformities; prominent pericardial activity.  Assess respiratory pattern  Before disturbing the child, stand back on count the respiratory rate.  Loosen or remove clothing to directly observe chest movement  Assess for signs of respiratory distress; increased respiratory rate, granting, retraction, nasal flaring.  Αuscultate for crackles, wheezing, congestion, and strider. Assess heart sounds.  Determine rate (bradycardia, tachycardia) and rhythm( regular or irregular)  Identity murmur (type, locations, and grade)
  48. 48.      Assess fluids status. •      Daily weights •   Strict intake and output (number of wet diaper, urine output)        Assess and record the child’s level of activity       Observe the infant while feeding, does the infant need frequent breaks or child asleep during feeding, assess for sweating, color change, or respiratory distress while feeding.    Observe the child at play, is play interrupted to rest    Assess and record findings relevant to the child’s development level, age appropriate behavior, cognitive skill, gross and fine motor skills.
  49. 49. Summary:  So far we have discussed about congenital heart diseases, cyanotic heart disease like fallots tetrology, transposition of great arteries and acynotic heart disease like VSD, ASD, PDA and Nursing care of the child with congenital heart disease.