Anatomy and Terminology

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

• Congenital heart disease: ASD,VSD,PDA,F4

• Acquired Heart Disease: Coronary Insufficiency Valvular Vascular

Classification

Diagnosis

• A thorough history and physical examination

• A wide variety of 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.EchocardiographyExcellent anatomic detail may be obtained.

Diagnostic tools

•Magnetic Resonance ImagingProvide anatomic detail where echocardiographic detail is lacking or unattainable( the extracardiac great vessels and systemic and pulmonary venous connections).

•Cardiac CatheterizationGold standard :obtain precise hemodynamic information.

Diagnostic tools

• 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

Classification of CHD

Acyanotic

Increased in pulmonary blood flow

1. ASD2. VSD3. PDA

Obstruction of blood flow form ventricle

1.Pulmonary stenosis2.Aortic stenosis

Acyanotic Heart Defect

Move blood from arterial to venous system

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.

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

Suggestion: ASD closure before school age

The standard therapy for ASDs for the past 50 years has been surgical closure using cardiopulmonary bypass support

Treatment

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).  

Figure  Surgical closure for ASD.

VSD (Ventricular Septal Defect )

A ventricular septal defect (VSD) is a pathologic communication involving a defect in the interventricular septum

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

Relate to:

• The size of the VSD• The degree of shunting • The associated lesions

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.

Surgical indications

Persistent Arterial Duct (or Patent Ductus Arteriosus)

PDA closes spontaneously, being completely closed in most people by 2 to 3 weeks of life.

Closure is recommended for all PDAs :

•pulmonary hypertension(Eisenmenger's syndrome)

•pulmonary congestion and left heart volume overloading

•endocarditis

Treatment

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

Cyanotic Congenital Heart Disease-F4

Figure Drs. Alfred Blalock, Helen Taussig, and Vivien Thomas.

•A malalignment ventricular septal defect (VSD) • Aortic override, • Right ventricular outflow tract obstruction (RVOTO), • Right ventricular hypertrophy.

Figure   Anatomy of tetralogy of Fallot.

Pathophysiology

systemic venous blood through the VSD to mix with the systemic cardiac output

Move blood from venous to arterial system

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

Clinical manifestation

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

TOF is a surgical disease

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.

Figure Complete repair of tetralogy of Fallot.

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

Acquired Heart Disease: Coronary Insufficiency

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).

Pathogenesis :atherosclerosis

Figure   Anatomy of the atherosclerotic plaque

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.  

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.

Reductions in luminal diameter

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.

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.  

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.  

STERNOTOMY

fullSternotomy.avi

HEART EXPOSURE

STABLIZATION

IMA HARVESTED

ANASTOMOSIS(DISTAL)

ANASTOMOSIS(PROXIMAL)

SHUNT

BLOWER

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%

Complications

Acquired Heart Disease: Valvular

•Etiology:degeneration

•Rheumatic fever

•Congenital valvular abnormalities (bicuspid aortic valve )

Aortic stenosis

Figure   The natural history of medically treated aortic stenosis.  

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.

Prognostic

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).  

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.

Figure A to E, the specific pathology is a flail posterior leaflet. It is repaired by resection of the flail segment, reapproximation of the leaflet, and reduction of the mitral annulus circumference using an annuloplasty ring.  

Mitral valve repair

MITRAL ANNULOPLASTY

Operative Mortality Rates

Independent Risk Factors for Operative Mortality (Odds Ratios) for Valve Replacements

Cause of valve-related death

There are two principal choices of cardiac valve prostheses: mechanical and bioprosthetic

Anticoagulation (warfarin sodium).

Valves be placed in the aortic position in patients older than 65 years and in the mitral position in patients older than 70 years

Aortic Aneurysm and Dissection

About 20% of aortic aneurysms and dissections are related to hereditary connective tissue disorders. Marfan syndrome is the most common of these disorders, occurring in the worldwide population at a frequency of 1 in 5000.

Classification

Figure Aortic dissection classification based on the site of the intimal tear. Left, Stanford type A, DeBakey types I and II. Right, Stanford type B, DeBakey type III

Figure Normal (left) versus abnormal (right) aortic wall.

Medical Treatment: anti-impulse therapy

Esmolol for IV β-blockade (range, 50-300 μg/kg/min)

•Heart rate (60-80 beats/min)•Systolic blood pressure (<120 mm Hg)•Mean arterial blood pressure (80 mm Hg)

The natural history of acute type A aortic dissection is associated with a significant mortality rate.

•1% per hour in the first 48 hours •50% at 2 days•75% at 2 weeks•90% at 1 year

The natural history

Patients who are diagnosed with aneurysms greater than or equal to 5 cm or with rapid aneurysm enlargement are considered for surgical repair.

Indications for Operation of aneurysms

Natural History and Incidence

Figure Thoracoabdominal aortic aneurysm: comparison of survival rates in untreated.

Figure Components of cardiopulmonary bypass (CPB) system: A indicates the venous reservoir and blood filter; B indicates the membrane oxygenator; and C indicates the heat exchange coil. D shows the following components: (1) CPB control console, (2) roller pump for infusing oxygenated blood, (3) cardioplegia, and (4) controlling suction catheters. E is the cardioplegia reservoir and heat exchanger.  

Establishment of (CPB)

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