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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
Valvular
Vascular
Diagnosis
• A thorough history and physical examination
• A wide variety of diagnostic tools:
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.
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.
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
Acyanotic Heart Defect
Acyanotic
Increased in pulmonary
blood flow
1. ASD
2. VSD
3. PDA
Obstruction of blood flow form
ventricle
1.Pulmonary stenosis
2.Aortic stenosis
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.
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
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).
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
Surgical indications
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.
Persistent Arterial Duct (or
Patent Ductus Arteriosus)
PDA closes spontaneously, being completely closed in
most people by 2 to 3 weeks of life.
Treatment
Closure is recommended for all PDAs :
•pulmonary hypertension(Eisenmenger's syndrome)
•pulmonary congestion and left heart volume overloading
•endocarditis
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.
Figure Anatomy of
tetralogy of Fallot.
•A malalignment
ventricular septal
defect (VSD)
• Aortic override,
• Right ventricular
outflow tract
obstruction (RVOTO),
• Right ventricular
hypertrophy.
Pathophysiology
systemic venous blood through the VSD to mix with the
systemic cardiac output
Move blood from venous to arterial system
Clinical manifestation
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Incresed activity .increased cyanosis
Polycythemia
Dyspnea, murmur
Growth retardation
Clubing finger
Hypoxic episodes with crying
Knee/chest position
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.
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.
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.
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.
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
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%
Acquired Heart Disease: Valvular
Aortic stenosis
•Etiology:degeneration
•Rheumatic fever
•Congenital valvular abnormalities (bicuspid aortic valve )
Figure The natural history of medically treated aortic stenosis.
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.
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.
Mitral valve repair
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 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
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
Indications for Operation of aneurysms
Patients who are diagnosed with aneurysms greater than or
equal to 5 cm or with rapid aneurysm enlargement are
considered for surgical repair.
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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