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Congenital heart disease

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Congenital heart disease
Congenital heart disease
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Congenital heart disease

  1. 1. Congenital heart disease for year II Anesthesia students Tazebew T.(MD)
  2. 2. OUTLINE • Prevalence • Etiology • Evaluation of the patient • Specific lesions – Pathophysiology – Clinical manifestations – Diagnosis – Management – complications – prognosis
  3. 3. Overview of fetal circulation
  4. 4.  PREVALENCE.  In live births (0.5–0.8%)  In premature infants 2% excluding patent [PDA]  In stillborns (3–4%)  In spontaneous abortuses (10–25%)  This does not include mitral valve prolapse, PDA of preterm infants, and bicuspid aortic valves (present in 1–2% of adults).  and this incidence increases to 2–6% for a 2nd pregnancy after birth of a child with CHD or if a parent is affected.  Recurrence is highly depend on the type of lesion in the 1st child.
  5. 5. … • Most congenital defects are well tolerated in the fetus because of the parallel nature of the fetal circulation. • Even the most severe cardiac defects (hypoplastic left heart syndrome) can usually be well compensated for by the fetal circulation. • One notable exception is the Episten Anomaly • In utero heart failure often (nonimmune hydrops fetalis) may occur.
  6. 6. Etiology • Maternal  seizure disorder w/intake of medications  lithium given for depression  uncontrolled IDDM  Lupus  maternal Rubella • Paternal • Chromosomal trisomes(chromosome 21,18,13) ,turners syndrome • For majority cause is unkown
  7. 7. Evaluation  by pulse oximetry.  Acyanotic ‘’ Hyperoxia test’’  Cyanotic  By chest radiograph  increased  Normal  decreased pulmonary vascular markings – byelectrocardiogram can be used to determine whether : • right • left hypertrophy exists. • biventricular  The final diagnosis is then confirmed by echocardiography, CT ,MRI or cardiac catheterization.
  8. 8. Acyanotic Congenital Heart Disease(CHD) 1) lesions that cause a volume load A) left-to-right shunt lesions. • ASD • VSD • PDA • AVSD • PAPVR • Aorticopulmonary Window Defect • Ruptured Sinus of Valsalva Aneurysm • Coronary- Arteriovenous Fistula (Coronary-Cameral Fistula)
  9. 9. B) Regurgitant lesions • PR=common • MVP • MR • TR • AR C) some of the cardiomyopathies
  10. 10. 2) lesions that cause a pressure load (The Obstructive Lesions) • ventricular outflow obstruction – Pulmonic valve stenosis – aortic valve stenosis • narrowing of one of the great vessels – coarctation of the aorta Rarely • MS • TS The CXR and ECG are useful tools for differentiating between volume and pressure overload lesions.
  11. 11. ASD • can occur in any portion of the atrial septum – 4 types • secundum(OS)- the most common type • primum(OP)-ECD • sinus venosus(SV) • Coronary sinus defect • Less commonly, the atrial septum may be nearly absent, with the creation of a functional single atrium. • An isolated valve-incompetent patent foramen ovale (PFO) is a common echocardiographic finding during infancy. It is usually of no hemodynamic significance and is not considered as ASD
  12. 12.  PATHOPHYSIOLOGY. – left-to-right shunting increased pul. blood flow  At atrial level in Os and SV  Both at atrial and ventricular level in OP – The degree of left-to-right shunting is dependent on:  the size of the defect  the relative compliance of the right and left ventricles  and the relative vascular resistance in the pulmonary and systemic circulations. – The paucity of symptoms in infants with ASDs is related to the structure of the right ventricle in early life when its muscular wall is thick and less compliant, thus limiting the left-to-right shunt.
  13. 13. Clinical manifestations • Usually asymptomatic • Failure to thrive • Varying degree of exercise intolerance • Child tires easily when playing • Infant tires easily when feeding • Fatigue • Sweating • Tachycardia ,tachypnea
  14. 14.  The physical findings.  mild left precordial bulge.  A right ventricular systolic lift is generally palpable at the left sternal border.  A loud 1st heart sound and sometimes a pulmonic ejection click can be heard.  In most patients, the 2nd heart sound is characteristically widely split and fixed.  A systolic ejection murmur is best heard at the left middle and upper sternal border.  A short, rumbling mid-diastolic murmur at the tricuspid valve is often audible at the lower left sternal border.  Holosystolic murmur at the apex in OP(ECD)
  15. 15.  DIAGNOSIS.  Clinical  Chest x-ray  ECG  ECHO  Catheterization  COMPLICATION  Pulmonary hypertension -eisnmenger syndrome  arrhythmia  tricuspid or mitral insufficiency  heart failure • Rx –medical and surgical • Prognosis =excellent
  16. 16. VSD • VSD is the most common cardiac malformation . • Defects may occur in any portion of the ventricular septum. • 3 types – membranous - commonest – Supracristal- less common – Muscular • single or • multiple (Swiss cheese septum).
  17. 17. • PATHOPHYSIOLOGY – Left-to-right shunt increased pul. blood flow. • Restrictive VSDs(usually <0.5 cm2) – right ventricular pressure is normal – the size of the defect limits the magnitude of the shunt • Nonrestrictive VSDs (usually >1.0 cm2) – right and left ventricular pressure is equalized – the direction of shunting and shunt magnitude are determined by the ratio of pulmonary to systemic vascular resistance
  18. 18.  The magnitude of intracardiac shunts is usually described by the Qp : Qs ratio.  If the left-to-right shunt is small (Qp : Qs <1.75 : 1),  the cardiac chambers are not appreciably enlarged and the pulmonary vascular bed is probably normal.  If the shunt is large (Qp : Qs >2 : 1),  left atrial and ventricular volume overload occurs  right ventricular volume overload and pulmonary arterial hypertension.  The main pulmonary artery, left atrium, and left ventricle are enlarged.  When the ratio of pulmonary to systemic resistance approaches 1 : 1,  the shunt becomes bidirectional  the signs of heart failure abate, and the patient becomes cyanotic (Eisenmenger physiology)
  19. 19. • CLINICAL MANIFESTATIONS – The clinical findings of patients with a VSD vary according to the size of the defect and pulmonary blood flow and pressure. • Small VSDs with trivial left-to-right shunts and normal pulmonary arterial pressure are the most common. – These patients are asymptomatic – Characteristically, a loud, harsh, or blowing holosystolic murmur is present and heard best over the lower left sternal border – it is frequently accompanied by a thrill.
  20. 20. • Large VSDs – dyspnea – feeding difficulties – poor growth – profuse perspiration – recurrent pulmonary infections – cardiac failure in early infancy Physical finding – Prominence of the left precordium is common – palpable parasternal lift – laterally displaced apical impulse – apical thrust, and a systolic thrill – The holosystolic murmur of a large VSD is generally less harsh than that of a small VSD and more blowing . – Early systolic murmur at pulmonic area – a mid-diastolic, low-pitched rumble at the apex(shunt ratio >2:1) – The pulmonic component of the 2nd heart sound may be increased
  21. 21. • DIAGNOSIS. – Clinical – Chest x-ray – ECG – ECHO – catheterization • Rx =medical and surgical • Prognosis after surgery=excellent
  22. 22. Con’d • COMPLICATIONS – Pulmonary hypertensions – Infective endocarditis – Heart failure – Recurrent lung infections – PS – AR
  23. 23. Patent Ductus Arteriosus(PDA) • Functional closure of the ductus occurs soon after birth • The aortic end of the ductus is just distal to the origin of the left subclavian artery, and the ductus enters the pulmonary artery at its bifurcation. • Female patients with PDA outnumber males 2 : 1. • PDA is associated with maternal rubella infection during early pregnancy. • It is a common problem in premature infants, where it can cause severe hemodynamic derangements and several major sequelae
  24. 24. Con’d
  25. 25. Con’d • CLINICAL MANIFESTATIONS. – A small patent ductus does not usually have any symptoms. – A large PDA will result in: • heart failure. • Retardation of physical growth may be a major manifestation in infants with large shunts
  26. 26.  physical signs in large PDA – wide pulse pressure( runnoff blood) – bounding peripheral arterial pulses. – The apical impulse is prominent and, with cardiac enlargement, is heaving. – A thrill, maximal in the 2nd left interspace – The classic continuous murmur is localized to the 2nd left intercostal space or radiate down the left sternal border , to the left clavicle or toward the apex – The murmur radiates along the pulmonary arteries and is often well heard over the left back. – When pulmonary vascular resistance is increased, the diastolic component of the murmur may be less prominent or absent. – a low-pitched mitral mid-diastolic murmur may be audible at the apex – Splitting of S2
  27. 27. • DIAGNOSIS. – Clinical – Chest x-ray – ECG – ECHO – catheterization • TREATMENT. – Medical=indomethacin – Surgical • Irrespective of age, patients with PDA require surgical or catheter closure. • preferably before 1 yr of age
  28. 28. • COMPLICATIONS – Heart failure – Pulmonary hypertension (Eisenmenger syndrome) – Infective endarteritis. – Pulmonary or systemic emboli may occur – Rare complications include • aneurysmal dilatation of the pulmonary artery or the ductus • calcification of the ductus • noninfective thrombosis of the ductus with embolization • paradoxical emboli
  29. 29. Obstructive lesions • AS • PS • TS Pressure load • MS
  30. 30. Coarctation of aorta • Occur at any site from the arch of aorta to iliac bifurcation • 98% juxta ductal Pathogenesis • In utero arch hypoplasia Rt heart output passes through the ductus
  31. 31. Clinical Manifestation  Hypertension → mechanical obstruction → renal  Differential cyanosis → pale upper extr. → cyanosed lower extr.  Classic signs - Disparity in pulse & BP - Radio-femoral delay - Systolic M at LMSB & inter-scapular area  Systolic or continuous murmurs may be heard over the left and right sides of the chest laterally and posteriorly  A palpable thrill can occasionally be appreciated in the intercostal spaces on the back.
  32. 32. Diagnosis - Clinical - CXR - cardiomegaly & pulm. congestion - Notching of ribs - ECG - Echocardiography Prognosis – Untreated cases succumb by 20-40 years Complications - CVA(cerebrovascular accident) - I/E - Aneurysms Treatment - Medical - IV PGE1 in neonatal age - Surgery
  33. 33. Pulmonary Vascular Disease (Eisenmenger syndrome) - Occur in shunt lesions VSD - mainly ASD PDA - Reversal of shunt due to pulm. HTN → Cyanosis
  34. 34. 1. Cyanotic lesions with decreased pulmonary blood flow 1.1 Tetra logy of Fallot Consists: 1. Rt ventricular outflow obst. 2. Ventricular septal defect 3. Dextroposition of the aorta 4. Right ventricular hypertrophy
  35. 35. Pathophysiology - Outflow obstruction to right ventricle - Hypertrophy of subpulmonic muscle - Normal or small pulmonary valve annulus - Rarely pulmonary atresia - VSD - Non-restrictive, located just below aortic valve - Aortic arch is right side in 20% - Right ventricular output shunts to the aorta When obstruction to right ventricular outflow A)mild to moderate=pink B)severe=cyanosis
  36. 36. Clinical Manifestation - Rarely pink TOF - in the absence of obstruction - Cyanosis - Clubbing - Squatting position in walking children - Paroxysmal hypercyanotic attacks  occur during 1st 2 years - Systolic ejection M at pulmonic area - Delayed growth & development - Single 2nd heart sound
  37. 37. Diagnosis CXR - Narrow base & uplifted apex - A boot or wooden shoe - decreased pulm. vascularity - Right side aortic arch in 20% ECG Echocardiography Complication - Cerebral thrombosis - in < 2 years - Brain abscess - Infective endocarditis - Polycythemia - CHF in pink TOF
  38. 38. Treatment Severe outflow obstruction - Medical Px - PGE1 infusion - Prevent dehydration - Partial exchange transfusion -iron supplementation - Oral propranolol for tet spells - Surgery - Blalock Taussig - Total correction
  39. 39. 1.2Pulmonary Atresia - With VSD - Extreme form of TOF - Without VSD - No egress of blood from Rt vent. - Shunt through foramen ovale to Lt atrium Leftventricle systemic circulation Aorta pulmonic circulation(PDA)
  40. 40. Clinical Manifestation - Cyanosis at birth - Respiratory distress - Single 2nd heart sound - No murmur Diagnosis - CXR - ECG - Echocardiography Treatment - PGE1 - Surgery
  41. 41. 1.3 Tricuspid atresia - No outlet from Right atrium to right vent. - Systemic venous return Rt atrium Lt atrium Left ventricle systemic Pulmonic (VSD, PDA)
  42. 42. Clinical Manifestation - Cyanosis at birth - Polycythemia - Easily fatiquability - Exertional dyspnea Diagnosis - EXR -Pulm. Under circulation - ECG -Lt axis deviation & Lt vent. hpertrophy - Echocardiography Treatment Medical=PGE1 Surgery
  43. 43. 1.4 Ebstein Anomaly of the tricuspid valve - Down ward displacement of the tricuspid valve - Right ventricle with two parts - atrialized - normal ventricular myocardium - Abnormal tricuspid valve - Huge Rt atrium - Tricuspid regurgitation - Compromised Rt ventricular function
  44. 44. Clinical Manifestations - Easily fatigability - Cyanosis - Dysrhythmia - Rt to Lt shunt through foramen ovale - Holosystolic M at tricuspid area - Heart failure Diagnosis - CXR - box shaped heart - ECG - Right BBB - Superior axis deviation Treatment - PGE1 - Surgery
  45. 45. 2.Cyanotic CHD With increased pulmonary blood flow 2.1 Transposition of GA a. D -TGA (uncorrected) - Systemic venous return to Rt atrium Normal - Pulmonary venous return to Lt atrium - Aorta arises from Right ventricle patholology - Pulm. artery arises from Lt vent.
  46. 46. *Systemic & Pulmonary Circulations Consists of two parallel circuits *Survival is with associated - patent foramen ovale or - VSD or - PDA Clinical Manifestations - Tachypnea & cyanosis at birth - Rarely congestive heart failure
  47. 47. b. L. TGA (corrected transposition)  Systemic VR to normally positioned Rt atrium  Through bicuspid (Mitral) valve  Right sided left ventricle  Pulmo. artery  pulm. venous return  Normally positioned Lt atrium  Through tricuspid valve  Left sided Right ventricle  Aorta
  48. 48.  Discordant atrio-ventricular relation (ventricular inversion)  Transposition of great arteries Clinical Manifestation Depends on associated malformation
  49. 49. Diagnosis - Clinical - CXR - Cardiomegaly - Narrow mediastinum (egg on string) - Increased pulmonary blood flow - ECG - Echocardiography Treatment - PGE1 - emergency - Surgery
  50. 50. 2.2 Truncus arteriosus - Single arterial trunk for both pulm. & systemic circulation - 4 types depending the origin of pulmonary artery Clinical Manifestation _ Cyanosis _CHF at 2-3rd month _Systolic ejection m . Treatment - surgery
  51. 51. 2.3Total anomalous pulmonary venous re turn
  52. 52. 2.4 Single Ventricle No interventricular septum
  53. 53. 2.5 Hypoplastic Left Heart Syndrome - Under development of Lt Side of the heart - Atretic aortic or mitral orifice - Non functional Lt ventricle - Hypoplasia of ascending aorta  Right ventricle supplies both pulm. & systemic circulation
  54. 54. 2.6Persistent fetal circulation
  55. 55. 2.7 Dextroposition of the heart 2.8 Dextrocardia

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