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disease, in those with “three -vessel disease” and decreased ventricular function, and in diabetics with three -vessel disease. CABG is highly successful at relieving angina pectoris: More than 90% of patients are free of angina 1 year after surgery.

Prognosis after bypass surgery

The results of coronary artery revascularization depend on multiple factors. Risk is increased in patients with renal failure, urgency of operation, the presence of peripheral vascular disease, etc.

Overall mortality for CABG in North America is between 2% and 3%.

Ten-year patency rates for internal mammary artery (IMA) grafts are more than 90%, whereas vein graft patency is only 50% at 10 years. Therefore, the IMA is the conduit of choice for coronary artery bypass.

Surgical treatment of myocardial infarction complications. Myocardial infarction and many of its complications are treated medically, but some complications warrant surgery. These complications include the following:

Ventricular aneurysms. The scarred myocardium may produce either akinesia or dyskinesia of ventricular wall motion, decreasing the ejection fraction.

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This decrease may result in congestive heart failure, ventricular arrhythmias, or rarely, systemic thromboembolization.

Surgical correction of the aneurysm is undertaken when these problems occur.

Coronary revascularization may also be warranted at the same time.

Ruptured ventricle is rare, and the mortality rate is approximately 100% without surgery.

Rupture of the interventricular septum (postinfarct ventricular septal defect) carries a high mortality rate. Again, early operative repair is important.

Mitral valve papillary muscle dysfunction or rupture

The posterior papillary muscle is usually involved.

Treatment is by mitral valve replacement or repair.

Long-term survival depends on the extent of myocardial damage.

F Cardiac tumors

Types of tumors

Benign tumors

Myxomas, which account for 75%–80% of benign cardiac tumors, may be either pedunculated or sessile. Most are pedunculated and are found in the left atrium attached to the septum.

Other benign tumors include rhabdomyomas (most common in childhood), fibromas, and lipomas.

Malignant tumors. Overall, primary malignant tumors account for 20%–25% of all primary cardiac tumors. The various types of sarcomas are the most common.

Metastatic tumors occur more frequently than primary cardiac tumors (benign or malignant).

Autopsy studies show cardiac involvement by metastatic disease in about 10% of patients who have died of malignancy.

Melanoma, lymphoma, and leukemia are the tumors that most often metastasize to the heart.

Clinical presentation. Cardiac neoplasms may be manifested by pericardial effusion, which results in cardiac tamponade. The neoplasms may also be manifested by congestive heart failure, arrhythmias, peripheral embolization (especially with myxomas), or other constitutional signs and symptoms.

Treatment is by surgical excision if possible.

G Cardiac trauma

Injuries to the heart may be divided into several categories.

Penetrating injury may involve any area of the heart, although the anterior position of the right ventricle makes it the most commonly involved chamber.

Penetrating wounds may result from gunshots, knives, and other weapons. In addition, penetrating injury may be iatrogenic, as a result of catheters or pacing wires.

Bleeding into the pericardium is common. Pericardial tamponade may result, manifested by:

Distended neck veins

Hypotension

Pulsus paradoxus

Distant heart sounds

Small wounds may spontaneously seal, in which case pericardiocentesis may suffice; however, open thoracotomy may be required.

Blunt trauma may be more extensive than is usually appreciated.

History of a significant blow to the chest, with or without fractured ribs or sternum, should create a high index of suspicion of a cardiac contusion or infarction. A patient with such a history should be observed and monitored in a manner similar to a patient with myocardial infarction because the trauma is likely to cause a similar myocardial injury.

Serial electrocardiograms and cardiac enzyme studies should be obtained.

Echocardiography may be helpful in determining myocardial injury.

The appearance of new murmurs should be investigated and may require cardiac

catheterization.

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Treatment. Blunt trauma may cause rupture of a tricuspid, mitral, or aortic valve, requiring treatment by valve replacement or repair.

H Pericardial disorders

Pericardial effusion

The pericardium responds to noxious stimuli by an increased production of fluid.

A pericardial effusion volume as small as 100 mL may produce symptomatic tamponade if the fluid accumulates rapidly, whereas larger amounts may be tolerated if the fluid accumulates slowly.

Pericardial effusion is treated by pericardiocentesis or by tube pericardiostomy via a subxiphoid approach.

Chronic effusions, such as those that occur with malignant involvement of the pericardium, may require pericardiectomy via left thoracotomy or sternotomy.

Pericarditis may be acute or chronic.

Acute pericarditis

Causes of acute pericarditis include:

Bacterial infection, as from staphylococci or streptococci. Acute pyogenic pericarditis is uncommon and is usually associated with a systemic illness.

Viral infection

Uremia

Traumatic hemopericardium

Malignant disease

Connective tissue disorders

Treatment consists of managing the underlying cause. Open pericardial drainage may be required. Most cases of acute pericarditis resolve without serious sequelae.

Chronic pericarditis may represent recurrent episodes of an acute process or undiagnosed longstanding viral pericarditis. The etiology is often impossible to establish. It may go unnoticed until it results in the chronic constrictive form, causing chronic tamponade.

Chronic constrictive pericarditis presents with dyspnea on exertion, easy fatigability, marked jugular venous distention, ascites, hepatomegaly, and peripheral edema.

The pericardium may become calcified, which is evident on a chest x-ray.

Cardiac catheterization may be needed to confirm the diagnosis.

Once the diagnosis has been established in the symptomatic patient, pericardiectomy should be undertaken with or without the use of cardiopulmonary bypass.

II Congenital Heart Disease

A Overview

The incidence of congenital heart disease is approximately 3 in 1000 births.

Etiology. In most cases, the etiology is unknown.

Rubella occurring in the first trimester of pregnancy is known to cause congenital heart disease (e.g., patent ductus arteriosus).

Down's syndrome is associated with endocardial cushion defects.

Types. The most common forms of congenital heart disease are in decreasing order:

Ventricular septal defect

Transposition of the great vessels

Tetralogy of Fallot

Hypoplastic left heart syndrome

Atrial septal defect

Patent ductus arteriosus

Coarctation of the aorta

Endocardial cushion defects

History

The mother should be questioned about difficulties during the pregnancy, especially in the first trimester.

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The mother often states that the child shows the following symptoms, which indicate pulmonary overcirculation and congestive heart failure:

Easy fatigability and decreased exercise tolerance

Poor feeding habits and poor weight gain

Frequent pulmonary infections

A history of cyanosis should be sought, as this indicates a right -to -left shunt.

Physical examination

Abnormalities in growth and development should be identified.

Cyanosis and clubbing of the fingers may be noted.

Examination of the heart should proceed in the same manner as in the adult.

Systolic murmurs are frequently found in infants and small children and may not be clinically significant.

A gallop rhythm is of great clinical importance.

Congestive heart failure in children is frequently manifested by hepatic enlargement.

Diagnosis

History and physical examination suggest the presence of a cardiac abnormality.

Echocardiogram is the mainstay of diagnosis and can define abnormal anatomy and physiology.

Cardiac catheterization may be required.

B Patent ductus arteriosus

Pathophysiology

Hypoxia and prostaglandins E 1 (PGE 1 ) and E 2 (PGE 2 ) act to keep the ductus open in utero.

In the normal infant born at term, circulation of the blood through the pulmonary vascular bed results in elevated oxygen levels and breakdown of the prostaglandins, which results in closure of the ductus within a few days.

The natural history of patent ductus arteriosus is variable.

A few patients experience heart failure within the first year of life.

Many patients remain asymptomatic and are diagnosed on routine examination.

Some patients eventually develop pulmonary vascular obstructive disease, which can lead to elevated pulmonary vascular resistance.

Patent ductus arteriosus may be seen in combination with other defects, such as ventricular septal defect and coarctation of the aorta.

Clinical presentation. Common presenting complaints are dyspnea, fatigue, and palpitations, signifying congestive heart failure.

Diagnosis is based primarily on the physical findings.

Physical examination

The classic continuous “machinerylike” murmur is usually heard, but it may be absent until 1 year of age.

Other signs include a widened pulse pressure and bounding peripheral pulses.

Cyanosis may be seen in patent ductus arteriosus, which is associated with other anomalies or in right -to -left shunt from pulmonary vascular disease.

Echocardiography can define a patent ductus arteriosus and other associated anatomic abnormalities.

Treatment

Surgical management consists of ligation of the ductus. This is reserved for:

Premature infants with severe pulmonary dysfunction

Infants who suffer from congestive heart failure within the first year of life

Asymptomatic children with a patent ductus that persists until 2 or 3 years of age

Indomethacin, a prostaglandin inhibitor, has been used with some success to close the ductus in premature infants with symptomatic simple patent ductus arteriosus.

C Coarctation of the aorta

Overview. Coarctation, a severe narrowing, is found twice as often in male children as in female children.

It is commonly located adjacent to the ductus arteriosus.

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Coarctation may be fatal in the first few months of life if not treated.

Associated intracardiac defects, present in up to 60% of patients, include patent ductus arteriosus, ventricular septal defect, and bicuspid aortic valve.

Clinical presentation

Some children are asymptomatic for varying periods of time.

In others, symptoms suggesting congestive heart failure are present shortly after birth.

Headaches, epistaxis, lower extremity weakness, and dizziness may be seen in the child with symptomatic coarctation.

Diagnosis

Physical findings include:

Upper extremity hypertension

Absent or diminished pulses in the lower extremities

A systolic murmur

Chest x-ray may reveal “rib notching” in older children, representing collateral pathways via intercostal arteries.

Echocardiography suggests the degree of flow limitation and other associated anomalies.

Cardiac catheterization is usually recommended to define the location of the coarctation and any associated cardiac defects.

Treatment

Surgical correction of the coarctation is indicated for all patients and may be delayed until 5 or 6 years of age in asymptomatic patients.

Operative procedures include:

Resection and end -to -end anastomosis

Prosthetic patch graft

A subclavian flap procedure

The distal subclavian artery is transected.

A proximal -based subclavian artery flap is used to enlarge the aorta at the level of the coarctation.

Any associated defects must also be corrected.

Complications

Residual hypertension may be a problem postoperatively.

Spinal cord injury due to ischemia during surgery rarely occurs.

Postoperative mesenteric ischemia is seen in a small but significant number of patients and is related to postoperative hypertension.

Postoperative aneurysm may develop at the site of the operative repair.

D Atrial septal defects

Classification. Atrial septal defects occur twice as frequently in female children as in male children. Three types are commonly seen:

Ostium secundum defects , which account for most atrial septal defects, are found in the midportion of the atrial septum.

Sinus venosus defects are located high up on the atrial septum and are often associated with anomalies of pulmonary venous drainage.

Ostium primum defects are components of atrioventricular septal defects and are located on the atrial side of the mitral and tricuspid valves.

A patent foramen ovale is not considered an atrial septal defect.

Pathophysiology

Atrial pressures are equal on both sides of a large atrial septal defect.

Since atrial emptying occurs during ventricular diastole, the direction of shunt at the atrial level is determined by the relative compliances of the right and left ventricles (diastolic phenomena). Because the right ventricle is more compliant than the left ventricle, the flow is left to right across an atrial septal defect.

This results in a modest increase in pulmonary blood flow, which causes mild growth retardation. P.131

If left uncorrected, pulmonary vascular obstructive disease may develop. This condition results in the right ventricle becoming less compliant than the left, with blood flow shunting right to left across the atrial septal defect.

Clinical presentation

Mild dyspnea and easy fatigability are seen in infancy and early childhood.

If left untreated, symptoms may progress to congestive heart failure as an adult.

Initially, patients may present with neurologic symptoms, including cerebrovascular accident or transient ischemic attack.

Diagnosis

Physical examination reveals a systolic murmur in the left second or third intercostal space and a fixed, split, second heart sound.

Chest x-ray reveals moderate enlargement of the right ventricle and prominence of the pulmonary vasculature.

Electrocardiogram reveals right ventricular hypertrophy.

Echocardiography can define the atrial septal defect and note the direction of shunting.

Cardiac catheterization can make the diagnosis from the “step-up” in oxygen saturation in the right atrium. The amount of left -to -right shunt may be calculated.

Treatment is based on the size of the left -to -right shunt.

Some atrial septal defects may close spontaneously.

Closure of the defect is indicated if the pulmonary blood flow is 1-1/2 to 2 times greater than the systemic blood flow. In addition, patients with documented neurologic events should undergo atrial septal defect closure.

Closure may be attempted via a percutaneous approach in the catheterization laboratory.

Surgery carries a mortality risk of less than 1%.

Ideal time for closure is age 4 or 5, before the child goes to school.

E Ventricular septal defects

Classification. Ventricular septal defects are the most common congenital heart defects. Associated anomalies, such as coarctation of the aorta, are common. They may be classified according to their location in the ventricular septum (Fig. 6-1).

Conoventricular defect is the most common ventricular septal defect and occurs in 70%–80% of cases.

Muscular defects may be single or multiple (occurring in 10%–15%).

Inlet septal defect (atrioventricular canal type) occurs in 5% of isolated defects.

Conoseptal defects (outlet defect) constitute 5%–10% of defects (also called supracristal or infundibular defects).

Pathophysiology

Ventricular pressures are equal on either side of a large ventricular septal defect.

Because ventricular emptying occurs during systole, the direction of the shunt at the ventricular level is determined by the relative resistances of the pulmonary and systemic circuits (systolic phenomena).

Because the pulmonary vascular resistance is much less than the systemic vascular resistance, flow is left to right across a ventricular septal defect.

This causes greatly increased pulmonary blood flow, which imposes a volume load on the left ventricle and may lead to early congestive heart failure.

Other adverse effects of pulmonary overcirculation include:

Poor feeding

Failure to thrive

Frequent respiratory tract infections

Increased pulmonary vascular resistance

Development of irreversible pulmonary vascular obstructive disease

This condition results in a higher pulmonary vascular resistance than systemic resistance and leads to reversal of flow across the ventricular septal defect (Eisenmenger's syndrome).

At this point, the patient cannot be operated on.

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Clinical presentation

Small ventricular septal defects rarely cause significant symptoms in infancy or early childhood, and these defects may close spontaneously before they are recognized.

Symptoms are usually seen with ventricular septal defects, which are approximately the diameter of the aortic root.

Children with large defects usually have dyspnea on exertion, easy fatigability, and an increased incidence of pulmonary infections.

Severe cardiac failure may be seen in infants but is less common in children.

Diagnosis

Physical examination reveals a harsh pansystolic murmur.

Chest x-ray and electrocardiogram, especially in large ventricular septal defects, show evidence of biventricular hypertrophy.

Cardiac catheterization is essential for delineating the severity of the left -to -right shunt, pulmonary vascular resistance, and the location of the defects.

Treatment

Surgical closure of the defect should be performed in:

Infants with significant cardiac failure or increased pulmonary vascular resistance

Asymptomatic children with significant shunts who have not had spontaneous closure by 2 years of age

Patients with pulmonary blood flow 1-1/2 to 2 times greater than systemic blood flow

Operative mortality risk (<5%) is related to the degree of preoperative pulmonary vascular disease.

F Tetralogy of Fallot

Pathophysiology

Tetralogy of Fallot, one of the most common cyanotic congenital heart disorders, consists of:

Obstruction to right ventricular outflow

A ventricular septal defect

Hypertrophy of the right ventricle

An overriding aorta