Thorax

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CHAPTER 9 Thorax

Heart and great vessels 148
Pleura and lungs 159
Mediastinum 165

Heart and great vessels

Principles of cardiac surgery

Surgery for heart disease has advanced to a point where safe and effective treatment can be offered for most conditions. Assessment of patients has become more refined with the development of special diagnostic techniques, e.g. echocardiography, scintigraphy, cardiac catheterization and cineangiography. Improvements in diagnostic techniques, anaesthesia, surgical techniques and postoperative management have led to better results with lower mortality rates and a reduction in complications.

Indications for surgery

• Failed medical treatment
• Where the mortality and morbidity of a surgical procedure is perceived to be less than that of the condition.

Contraindications for surgery

Correction of a defect alone may be contraindicated in the presence of the following:

• Irreparable myocardial damage
• Irreversible failure of other organs, e.g. kidneys and lungs.

However, it is now possible to correct these problems with multiple organ transplants and the above are only contraindications to repair of the defect alone.

Preoperative preparation

• Accurate diagnosis. This requires not only a full examination but a variety of investigations, including CXR, ECG, echocardiography, Doppler’s, cardiac catheterization, MRI, cardiac CT, radionuclide scanning, pulmonary function tests
• Psychological preparation, especially for intensive care
• Control of cardiac failure with drugs
• Correction and/or investigation of anaemia
• Correction of electrolyte imbalance
• Correction of nutritional deficiencies
• Chest physiotherapy, bronchodilators, antibiotics, cessation of smoking.

Surgery

Most open-heart surgery is carried out via a median sternotomy incision. Closed mitral valvotomy used to be carried out via a left thoracotomy – the operation is rarely performed nowadays. A left posterolateral thoracotomy is used for ligation of a patent ductus arteriosus.

Cardiopulmonary bypass

The heart and lungs are excluded from the circulation, being replaced by a pump and membrane oxygenator. Venous blood returning to the heart is diverted, through tubes inserted into the right atrium, to an oxygenator. A roller pump is used to return oxygenated blood to the patient through a cannula placed in the ascending aorta, which is cross clamped below its point of entry. A small amount of blood returning to the LA from the bronchial arteries via the pulmonary veins is sucked out by additional suckers, defoamed and returned to the oxygenator. When the aorta is occluded, the myocardium becomes ischaemic. Two methods are available to preserve the myocardium:

• Intermittent or continuous coronary perfusion
• Depression of myocardial metabolism (cardioplegia).

The former consists of cannulation of either of the coronary ostia and infusion of blood or intermittent release of the aortic cross clamp. Reduction of myocardial metabolism is accomplished by cooling the heart with a ‘cardioplegic’ solution at 4°C infused into the coronary arteries, which arrests the heart in diastole. Aortic occlusion is well tolerated for 1–2 h using cold blood. After closure of the cardiac incisions, the heart is allowed to fill up with blood, air is removed from the heart, the aorta unclamped, the heart restarted and bypass discontinued.

Postoperative complications

Low cardiac output

This may result from haemorrhage, cardiac failure, tamponade, pulmonary hypertension, or cardiac arrhythmias.

Respiratory failure

This may be due to pulmonary oedema or atelectasis giving rise to hypoxia. Pain from the surgical incision reducing respiratory effort may be contributory.

Renal failure

Due to ATN, resulting from renal hypoperfusion. Haemofiltration/haemodialysis may be required.

Jaundice

Usually a result of transfusions or haemolysis, occurring as a result of cardiopulmonary bypass. Occasionally, liver failure occurs because of low cardiac output.

Cerebral damage

May be due to anoxia, air embolism, thrombus, cerebrovascular disease or fat embolism. Cerebral oedema may occur.

Postoperative treatment

Maintenance of cardiac output

Ensure adequate filling pressure of ventricles (preload). Maintain adequate CVP. Ensure myocardial contractility – inotropes. Maintain heart rate around 90/min. Use isoprenaline or pacing wires inserted at surgery. Reduce peripheral resistance (afterload) with vasodilators, e.g. GTN. Metabolic acidosis may occur and is an indication of poor perfusion. Aortic balloon pumping may be used to reduce cardiac afterload. Haemorrhage and tamponade require urgent re-exploration. Pulmonary hypertension may respond to prostacyclin. Arrhythmias require drugs, cardioversion or pacing.

Prevention of respiratory problems

Optimize cardiac output. Use positive pressure ventilation, diuretics, pain relief, physiotherapy.

Maintenance of urine output

Optimize cardiac output, diuretics, e.g. furosemide, renal dose of dopamine.

Prevention of cerebral problems

Maintain normal BP. Reduce CO2 by positive pressure ventilation, avoid hyperpyrexia, give dexamethasone.

Congenital heart disease

This occurs with an incidence of 8:1000 live births. Aetiological factors include maternal rubella, Down’s syndrome and maternal drugs, e.g. warfarin and phenytoin.

The following lesions are most commonly encountered (in order of decreasing frequency): VSD, ASD, PDA, pulmonary stenosis, aortic stenosis, tetralogy of Fallot, coarctation of the aorta and transposition of the great vessels. Congenital heart disease may be classified as cyanotic (significant R-to-L shunt) or acyanotic (L-to-R or no shunt). The reader is referred to a textbook of medicine for the symptoms, signs and investigations of these conditions. The treatment and prognosis are indicated below.

Acyanotic

Ventricular septal defect (VSD)

Small defects may close spontaneously but surgery is indicated for large defects, cardiac failure, increased pulmonary vascular resistance and patients with pulmonary blood flow 1.5 times greater than systemic flow. The defect is closed with a prosthetic patch using cardiopulmonary bypass. Mortality and morbidity depend on the preoperative state of the patient and degree of pulmonary vascular resistance. An uncomplicated VSD has an operative mortality of less than 5%.

Atrial septal defect (ASD)

Surgery is indicated if pulmonary flow is 1.5 times systemic. The defect is closed with a patch. Ideally, the operation should be carried out before a child goes to school. Mortality is less than 1% but increases in the presence of pulmonary vascular resistance. Percutaneous device closure is increasingly used.

Patent ductus arteriosus (PDA)

At birth, the pulmonary vascular resistance decreases markedly as the lungs inflate and the ductus arteriosus closes within a few days. Failure of closure may occur in premature babies, hypoxia or maternal rubella. In premature babies a prostaglandin synthetase inhibitor, e.g. indomethacin, may promote closure. All persistent ducts should be closed to prevent infective endocarditis. The ductus is doubly ligated via a left thoracotomy. Endovascular techniques are now in common use. Mortality is less than 0.5%.

Coarctation of the aorta

There are two types: adult and infantile. In the adult form, the aorta is narrow in the region of the ligamentum arteriosum just beyond the origin of the left subclavian artery. Proximal hypertension and LV overload occur. Most adult types can be stented. If surgical correction is required, the ideal age is 7–15 years. Operative procedures include resection with end-to-end anastomosis. If the gap is too large, a woven Dacron graft is inserted. Complications include residual hypertension, spinal cord ischaemia during surgery, recurrent laryngeal nerve palsy, and mesenteric ‘arteritis’ due to increased pulse pressure. Without surgery, the majority of patients are dead before the age of 40. Death occurs from aortic rupture, infective endocarditis, LV failure, cerebral haemorrhage. The operative mortality is about 5%.

The infantile form is rare and usually preductal. It may be associated with other cardiac defects in 60% of infants. Operative mortality is high, reaching 70% for surgery in the first 3 months of life.

Coarctation is commonly now treated by angioplasty in small children.

Congenital valve disease in children

Aortic stenosis or pulmonary stenosis may occur. Treatment is by balloon dilatation during cardiac catheterization or occasionally by open surgery.

Cyanotic

Congenital cyanotic heart disease is uncommon. The two common forms are the tetralogy of Fallot and transposition of the great vessels. Cyanosis may also occur where the L-to-R shunt of a VSD reverses owing to pulmonary hypertension (Eisenmenger complex).

Tetralogy of Fallot

This consists of a VSD, overriding aorta, pulmonary stenosis and RV hypertrophy. Correction involves reconstruction of the RV outflow tract and closure of the VSD. Nearly all children are corrected by a one-stop procedure – early correction in infancy is now the procedure of choice. Very rarely, an aortopulmonary shunt is used for palliative purposes in the first instance. A Blalock–Taussig shunt is the most common. The subclavian artery is divided on one side and anastomosed to the ipsilateral pulmonary artery to improve pulmonary blood flow. The shunt is closed and the defects corrected between the ages of 3 and 5 years. There should be no mortality associated with the shunt operation. However, the quality of cardiopulmonary bypass in children has now improved considerably such that one can expect to get good results with a one-stop procedure.

Transposition of the great vessels

The aorta arises from the RV and the pulmonary artery from the LV. Survival is dependent on co-existing defects, e.g. PDA, VSD, ASD, which permit mixing of the two circulations. Definitive surgical correction involves an ‘arterial switch’ where the aorta and PA are transected and reanastomosed, aorta to LV and PA to RV. This operation has to be done in the first 2 weeks of life before the LV decreases in size. Alternatively interatrial repair can be undertaken at 6 months. A ‘baffle’ made of pericardium is created in the atrium to direct caval blood behind the baffle to the mitral valve and LV and PA, with the pulmonary venous return channelled in front of the baffle to the tricuspid valve, RV and aorta. Operative mortality is about 10%.

Acquired valvular heart disease

This is limited to the aortic, mitral and occasionally tricuspid valves. The pulmonary valve is rarely affected. The valve may be narrowed (stenosis) or rendered incompetent (regurgitation), or both may occur. Except for mitral stenosis and tricuspid incompetence, surgical treatment of acquired valvular disease requires valve replacement. Some types of mitral stenosis may be treated by closed mitral valvotomy while tricuspid incompetence may be treated by valvoplasty.

Types of valve

Mechanical valves

These include: Ball valve – The Starr–Edwards is a metal cage with a silastic ball. It is durable for long periods (up to 25 years). Not used nowadays.

Disc valve. In the past Bjork–Shiley tilting disc valves have been used but these are no longer made.

Bileaflet valve, e.g. St Jude (most commonly implanted in USA), Sulzer-CarboMedics.

All three types require(d) lifelong anticoagulation with its attendant risks. There remains a small risk of thrombosis and embolism. Failure is sudden.

Tissue valves

These are usually porcine xenografts or bovine pericardium. They are mounted on a frame with a sewing ring. The embolic rate is very low and therefore anticoagulants are not required. They lack long-term durability, with up to 75% failure rate at 15 years. They fail gradually.

Free aortic homograft is still a major choice.

Antibiotic-preserved fresh homografts may also be used.

Human cryopreserved allograft valves

Usually aortic valve inserted without a frame. Anticoagulants are not required.

Complications of artificial valves

• Thromboses with valve dysfunction or embolism
• Failure – calcification and rupture with tissue valves; mechanical breakage with prosthetic valves
• Bacterial endocarditis
• Obstruction – tissue growth onto valve ring
• Paravalvular leakage
• Haemolysis.

Ischaemic heart disease

This is the commonest cause of death in the UK. Coronary artery disease is four times more common in men than in women although the incidence in women is increasing. It accounts for one-third of all male deaths and one-quarter of all female deaths.

Aetiology

Male sex, smoking, family history, hypertension, hyperlipidaemia, diabetes, obesity, myxoedema.

Symptoms and signs

Angina, MI, CCF. Sudden death. Often nothing to find on examination. Occasionally xanthelasma. Cholesterol nodules. Arcus senilis. Stigmata of diabetes. Peripheral vascular disease.

Investigations

• Hb
• FBC
• Lipid profile
• CXR – occasionally cardiomegaly
• ECG: may be normal at rest in up to 75% of patients; S-T depression with angina – exercise ECG usually confirms diagnosis
• Echocardiogram: LV hypertrophy, ejection fraction, areas of infarction
• Cardiac catheterization and coronary angiography – contrast medium is injected into each coronary artery and views recorded by cinephotography; the site and severity of disease is assessed
• LV function is assessed by ventriculography and intracardiac pressures.

Treatment

Conservative

Stop smoking. Dietary restrictions. Exercise, correct hyperlipidaemia, control anaemia, control diabetes. Avoid stress. Vasodilators, e.g. nitroglycerine spray; β-blockers, e.g. propranolol. Calcium antagonists, e.g. nifedipine, diltiazem. Aspirin. Graduated exercise programme.

Percutaneous transluminal coronary angioplasty (PTCA)

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