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Cardiac Surgery

Cardiac Surgery. Anatomy and Terminology. Ao, aorta; LA, left atrium, LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle; TV, tricuspid valve. Classification. Congenital heart disease: ASD,VSD,PDA,F4 Acquired Heart Disease: Coronary Insufficiency

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Cardiac Surgery

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  1. Cardiac Surgery

  2. Anatomy and Terminology Ao, aorta; LA, left atrium, LV, left ventricle; MV, mitral valve; RA, right atrium; RV, right ventricle; TV, tricuspid valve.

  3. Classification • Congenital heart disease: ASD,VSD,PDA,F4 • Acquired Heart Disease: Coronary Insufficiency • Valvular • Vascular

  4. Diagnosis • A thorough history and physical examination • A wide variety of diagnostic tools:

  5. Diagnostic tools • Plain Radiography • Cardiothoracic ratio indicative of cardiomegaly or pericardial effusion, presence of atrial enlargement, presence or absence of the pulmonary artery shadow, and arch sidedness. • 2.Electrocardiogram • The QRS duration and axis yield important information concerning conduction delay and abnormal ventricular forces. • 3.Echocardiography • Excellent anatomic detail may be obtained.

  6. Diagnostic tools • Magnetic Resonance Imaging • Provide anatomic detail where echocardiographic detail is lacking or unattainable( the extracardiac great vessels and systemic and pulmonary venous connections). • Cardiac Catheterization • Gold standard :obtain precise hemodynamic information.

  7. Classification of CHD • Acyanotic Heart Disease • 1. Increase pulmonary blood flow • 2. Obstruction of blood flow • Cyanotic Heart disease • 1. Decrease pulmonary blood flow • 2. Mixed blood flow

  8. Acyanotic Heart Defect Move blood from arterial to venous system

  9. ASD(Atrial Septal Defect ) The defect develops as the result of incomplete closure of the embryologic patent foramen ovale. Most children are not overtly symptomatic but may exhibit some degree of exercise intolerance or frequent respiratory tract infection. Symptoms typically become more prevalent in adulthood and include dyspnea on exertion, palpitations, and ultimately evidence of right heart failure.

  10. Types of atrial septal defects as viewed through the right atrium: ostium secundum, ostium primum, and sinus venosus.

  11. Treatment Suggestion: ASD closure before school age The standard therapy for ASDs for the past 50 years has been surgical closure using cardiopulmonary bypass support

  12. Figure  Surgical closure for ASD. A, Right atriotomy. B, Direct suture closure. Ao, aorta; CS, coronary sinus; PA, pulmonary artery; SVC, superior vena cava; TV, tricuspid valve. C, Patch closure. D, Deairing the left atrium (LA).  

  13. VSD (Ventricular Septal Defect ) A ventricular septal defect (VSD) is a pathologic communication involving a defect in the interventricular septum

  14. Figure The location of VSDs in the ventricular septum. (This is a view of the ventricular septum from the right side.) 1, Perimembranous VSD. 2, Subarterial VSD. 3, Atrioventricular canal–type VSD. 4, Muscular VSD

  15. Surgical indications • Relate to: • The size of the VSD • The degree of shunting • The associated lesions

  16. Surgical indications • Thus, small babies presenting with large VSDs, refractory heart failure, and large shunts undergo surgical closure of the defects in the newborn period irrespective of age or size. • Other defects are addressed based on the ongoing concerns of left-to-right shunting, aortic valve cusp distortion, and risk for endocarditis. • Asymptomatic patients with evidence of significant shunts and cardiomegaly are put forward for surgical therapy.

  17. Persistent Arterial Duct (or Patent Ductus Arteriosus) PDA closes spontaneously, being completely closed in most people by 2 to 3 weeks of life.

  18. Treatment • Closure is recommended for all PDAs : • pulmonary hypertension(Eisenmenger's syndrome) • pulmonary congestion and left heart volume overloading • endocarditis

  19. Figure   The anatomic relationships of a patent ductus arteriosus, exposed from a left thoracotomy.  

  20. Cyanotic Congenital Heart Disease-F4 Figure Drs. Alfred Blalock, Helen Taussig, and Vivien Thomas.

  21. Figure   Anatomy of tetralogy of Fallot. • A malalignment ventricular septal defect (VSD) • Aortic override, • Right ventricular outflow tract obstruction (RVOTO), • Right ventricular hypertrophy.

  22. Pathophysiology systemic venous blood through the VSD to mix with the systemic cardiac output Move blood from venous to arterial system

  23. Clinical manifestation • Incresed activity .increased cyanosis • Polycythemia • Dyspnea, murmur • Growth retardation • Clubing finger • Hypoxic episodes with crying • Knee/chest position

  24. TOF is a surgical disease The natural history of untreated TOF is dismal, with most children succumbing to the ravages of progressive cyanosis before 10 years of age.

  25. Figure Complete repair of tetralogy of Fallot. A, Enlargement of the right ventricle–main pulmonary artery (MPA) connection with a transannular incision if necessary. Ao, aorta. B, Resection of muscle from the outflow tract and identification of edges of the ventricular septal defect (VSD). C, Patch closure of the VSD. D, Placement of a transmural patch if required.

  26. Long-term complications • Severe pulmonary insufficiency and a noncontractile infundibulum • Progressive tricuspid insufficiency and elevated central venous pressure • Hepatomegaly, peripheral edema, and severe exercise intolerance

  27. Acquired Heart Disease: Coronary Insufficiency

  28. Coronary artery anatomy Figure left: Left main coronary artery (A), left anterior descending coronary artery (B), left circumflex coronary artery (C), and obtuse marginal vessels (D).   Figure right: Right coronary artery (A) and posterior descending artery (B).

  29. Pathogenesis :atherosclerosis Figure   Anatomy of the atherosclerotic plaque

  30. Figure   Thrombosis of a disrupted atheroma: weakening of the fibrous cap. Most coronary syndromes are caused by thrombosis of a disrupted atheroma, which can result from weakening of the fibrous cap and enhanced thrombogenicity of the lipid core.  

  31. Reductions in luminal diameter 60%: have minimal impact on flow. 75% or more: coronary blood flow is significantly compromised. Clinically, this often coincides with the onset of exertional angina. 90%: resistance is 256 times greater than a 60% stenosis, and coronary flow may be inadequate at rest.

  32. Figure   Coronary artery bypass procedures are performed through a median sternotomy. The divided sternum is lifted by controlled retraction that provides exposure but must not be so excessive as to fracture the sternum or ribs. Dissection proceeds proximally and distally until adequate length is obtained for the intended graft and usually terminates at the bifurcation of the internal mammary artery. Heparin is then administered systemically before the internal mammary artery is occluded. The internal mammary artery is prepared for grafting after transection.

  33. Figure The technique of anastomosis between the left internal mammary artery and the left anterior descending coronary artery illustrates the general principles used to construct all proximal and distal anastomoses. The graft is opened longitudinally to match or exceed the length of the coronary arteriotomy. This opening prevents kinking at the site of the anastomosis of the internal mammary artery and aorta to the saphenous vein. This opening is not necessary at the distal vein anastomotic site, but a slight bevel cut of the distal vein helps prevent kinking of the saphenous vein to the coronary artery anastomosis.  

  34. Figure The anastomosis begins midway along the side of the graft so that the final knot will not be at the most distal or proximal portion of the anastomosis, thereby decreasing the chances of technical error that would impede graft flow. The polypropylene suture permits a portion of the anastomosis to be completed before the two vessels are joined.  

  35. STERNOTOMY

  36. HEART EXPOSURE

  37. STABLIZATION

  38. IMA HARVESTED

  39. ANASTOMOSIS(DISTAL)

  40. ANASTOMOSIS(PROXIMAL)

  41. SHUNT

  42. BLOWER

  43. Complications • The morbidity estimates in CABG patients from this large database are as follows:    • Stroke—1.63%    • Renal failure requiring dialysis—3.53%    • Prolonged postoperative ventilation—5.96%    • Mediastinitis—0.63%    • Reoperation within 24 hours—7.17%

  44. Acquired Heart Disease: Valvular

  45. Aortic stenosis • Etiology:degeneration • Rheumatic fever • Congenital valvular abnormalities (bicuspid aortic valve )

  46. Figure   The natural history of medically treated aortic stenosis.

  47. Prognostic Patients with aortic stenosis without symptoms, survival is excellent. The risk for sudden death in symptom-free patients with a transvalvular gradient greater than or equal to 50 mmHg or a valve area of less than 0.5 cm2 is about 4% per year.

  48. Figure   Aortic valve replacement. The diseased leaflets are excised (A), and the prosthetic valve is sewn in place with interrupted pledgeted mattress stitches (B and C).

  49. Figure A to C, Mitral valve replacement with preservation of the posterior leaflet. This preserves the annular-apical connection by means of the chordae tendineae.

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