Principles and practice of cardiac surgery
Cardiac surgery is a modern surgical specialty. The development of the heart-lung machine in 1953 provided total circulatory support and oxygenation while intracardiac procedures were performed on the empty, and preferably still (asystolic), heart. Other milestones were the successful introduction of cardiac valve replacement in 1960, and coronary artery bypass surgery in 1968.
Cardiopulmonary bypass: heart-lung machine
Cardiopulmonary bypass (CPB) had revolutionised cardiac surgery, allowing precise intracardiac repair while vital-organ perfusion, oxygenation and function were maintained. The essential components of the CPB circuit are described in .
The duration of CPB for most operations is between 1 and 2 hours. Complex operations may require 3–4 hours of CPB and occasionally several days or weeks (see ‘Circulatory Support’). Major shortcomings are blood cell destruction (roller pump) leading to haemoglobinuria and thrombocytopenia, coagulation factor consumption and systemic inflammatory response (due to contact with silastic tubing), as well as neurologic, renal, and hepatic dysfunction. All these problems are time-related, becoming noticeable after 2 hours of CPB.
Hypothermia (30–34°C) is used to help protect vital organ function against brief periods of possible hypotension. Haemodilution (haematocrit 25–30%) is used to help reduce blood product use, reduce red cell loss during surgery, and improve small vessel blood flow in hypothermic conditions. For complex thoracic aortic arch aneurysm surgery, CPB is used to cool the patient to 18°C (profound hypothermia), blood is drained into the CPB reservoir, and the circulation arrested for up to 60 minutes, allowing excellent, rapid, asanguineous access to major vessels, yet maintaining cerebral and renal protection. At the completion of the vascular procedure the patient is rewarmed to 37°C over 30–40 minutes.
In some conditions it is possible to perform an excellent cardiac operation using CPB but with the heart normally perfused and beating (e.g. closure of an atrial septal defect [ASD]). However, precise coronary artery anastomoses and complex valvular procedures are best performed in a still flaccid heart.
Ideally, this state is achieved by clamping the distal ascending thoracic aorta and infusing ‘cardioplegia solution’ (oxygenated blood with additional potassium, magnesium, lignocaine and amino acid substrates) at 10–20°C to arrest the heart, to reduce its metabolic requirements and provide appropriate substrates, thus protecting the heart while being operated upon and being deprived of its normal coronary blood flow. There are many formulae of cardioplegic solutions, and methods of administration, although the principles remain the same. The usual cardiac arrest times are 30–90 minutes, although up to 180 minutes is possible with preservation of cardiac function. Sinus rhythm is usually restored, within 1–2 minutes of re-establishing coronary blood flow.
Closed cardiac surgery
Many procedures do not require CPB. The early operations were performed with the heart beating. Such operations are possible where they are remote from the heart (e.g. closure of patent ductus arteriosus [PDA]), or where disruption of cardiac function is transient and can be well tolerated (mitral valvotomy). Coronary surgery can also be performed on the beating heart without CPB (see ‘Off-Pump Coronary Surgery’). Operations commonly performed without CPB are listed in Cardiac surgery without CPB The vast majority (>90%) of cardiac operations worldwide are performed using CPB.
Coronary artery surgery
Coronary atherosclerosis is a major disease process in Western countries, and is rapidly increasing in incidence in developing countries. Coronary angiography (by retrograde cannulation of the coronary ostia via the femoral or brachial artery under local anaesthetic) was introduced in 1962. Coronary bypass surgery became established in 1968, and coronary angioplasty in 1977.
Atherosclerotic, stenotic lesions develop proximally at the origins of main coronary branches or at major branching points. The coronary vessels are usually free of disease distally. A stenosis of more than 50% diameter loss is considered significant. Atheromatous plaques may disrupt, occlude, or suffer from intraplaque haemorrhage, causing acute spasm, occlusion and possible thrombosis. Gradual progressive chronic stenosis causes angina. Acute spasm results in ischaemic chest pain at rest, and thrombotic occlusion results in acute myocardial infarction.
Risk factors for coronary artery disease include family history, male gender, diabetes, hypertension, smoking, hypercholesterolaemia and obesity.
Angina pectoris on exertion is the most common symptom. Ischaemic chest pain occurring spontaneously at rest (unstable angina) also occurs and is associated with spasm in the vicinity of the stenotic plaque, and/or transient coronary artery occlusion. Myocardial infarction occurs with prolonged or permanent coronary occlusion resulting in severe chest pain lasting several hours. Diabetic patients may not experience chest pain because of neuropathy.
Chest X-ray may indicate cardiomegaly or left ventricular aneurysm as a result of prior myocardial infarction.
Electrocardiogram may show ST segment elevation or depression with acute chest pain, or ‘Q’ waves due to old myocardial infarction.
Stress test (treadmill or bicycle with electrocardiograph (ECG) monitoring), where positive, will result in chest pain, ST segment depression on the ECG and a fall in blood pressure.
Thallium, sestamibi, and positron emission tomography (PET) scans may indicate areas of hypoperfusion, ischaemia, viability and reversibility of left ventricle (LV) function.
Coronary angiography is the definitive investigation, objectively outlining the number, location and severity of the stenotic lesions, and the size and quality of the vessels beyond.
Low-dose aspirin, nitrates (sublingual, spray or topical), beta-blockers (metoprolol, atenolol), calcium antagonists (nifedipine, amlodipine, felodipine) and cholesterol-lowering agents (simvastatin, privastatin) are used.
Discrete, appropriately located, stenotic plaques in one or two arteries may be treated by percutaneous transluminal coronary angioplasty (PTCA) to dilate the plaque to its normal lumen size (2–2.5 mm), and the plaque held open by placement of a stent. However, re-stenosis rates of between 5% and 10% at 1 year are reported.
Coronary artery bypass graft surgery
Multiple severe coronary artery stenoses associated with chronic uncontrolled angina, or unstable angina, are best treated surgically. Coronary artery bypass graft (CABG) comprises 75% of all adult cardiac operations. There are many variations of surgical techniques but the general principles are as follows.
Sternotomy is performed. The left internal thoracic artery (LITA) is harvested and is usually anastomosed to the left anterior descending artery (LAD), which is considered to be the most important artery. In younger patients (<60 years) the right internal thoracic artery (RITA) is harvested and anastomosed to the second most important affected coronary vessel. Other coronary vessels are grafted using either the saphenous vein or radial artery (Typical coronary artery revascularisation of the anterior, lateral and inferior walls of the heart. LITA, RITA, left and right internal thoracic artery; RA, radial artery; LAD, left anterior descending artery; RCA, right coronary artery; CxOM, circumflex (obtuse) marginal artery.).
Cardiopulmonary bypass is used with the patient at 30–34C. The heart is arrested while performing the distal anastomoses. The proximal graft anastomoses may be performed to the ascending thoracic aorta while the heart is arrested, or using a specially designed clamp. Alternatively the proximal inflow may be from the subclavian artery or the construction of pedicled grafts off the internal thoracic artery (ITA). A typical operation takes 3–4 hours, including cardiac arrest for 30–60 minutes, and bypass times of 60–90 minutes, depending on the number of bypasses performed (average of three to four bypasses). The pericardium is usually closed, drain tubes placed behind the sternum and into the pleural cavities if they have been entered, and the sternum is re-wired so that it is extremely stable.
The patient spends 24–48 hours in the intensive care unit, where blood pressure, right atrial pressure, pulmonary artery pressure, left atrial pressure, and cardiac and urine outputs are measured and interventions performed as appropriate.
The patient is mobilised on the first or second postoperative day, and aspirin and calcium antagonists recommenced. Most patients are discharged 5–7 days post-operatively. Recovery is rapid with most returning to work in 4 weeks, and to full activity within 3 months.
Results of coronary artery bypass graft
The operative mortality is 1% (although higher in reoperations or where LV function is poor). The main morbidity relates to peri-operative stroke (1%), myocardial infarction (2%), sternal and mediastinal infections (1%), and haemorrhage (2%) (see ‘Complications of Cardiac Surgery’).
Graft patency is best for the left ITA and worst for the saphenous vein (Coronary bypass graft patency).
|Left internal thoracic artery||96%||95%|
|Right internal thoracic artery||93%||90%|
Long-term freedom from recurrent angina pectoris is 85% at 5 years and 70% at 10 years (recurrence rate of approximately 3% per annum).
Long-term survival is excellent; 90–95% at 5 years and 80–85% at 10 years. Survival is significantly influenced by age at surgery (current mean age 68 years), presence of diabetes, extent of left ventricular dysfunction, and control of risk factors post-surgery. The presence of one or more internal thoracic artery grafts enhances survival and long-term freedom from angina, and it is hoped that coronary revascularisation using artery grafts only will produce further benefits, although this is not yet proven.
Coronary surgery confers prognostic benefits (over medical management), to patients that have stenosis of the left main coronary artery, those with high-grade proximal left anterior descending stenoses, those with triple vessel coronary disease (left anterior descending [LAD] artery, right and circumflex coronary arteries) and where there is left ventricular dysfunction. These groups account for approximately 85% of patients undergoing coronary surgery.
Surgery for complications of myocardial infarction
Complications of coronary artery disease, especially myocardial infarction, may require treatment in conjunction with the coronary artery bypass grafting. Myocardial infarction involving the left ventricular wall, including papillary muscles of the mitral valve, in combination with left ventricular dilatation may result in severe ischaemic mitral regurgitation (MR). This would need correction by mitral valve repair or replacement (operative mortality approximately 10%). Left ventricular aneurysms, particularly in relation to occlusion of the LAD, may require excision and repair (operative mortality 3%).
Extensive infarction may result in left ventricular free wall rupture into the pericardium (tamponade) or rupture of the interventricular septum (acute cardiogenic shock). These complications are almost universally fatal. Surgical repair using appropriate techniques (patches and biological glues) is essential, although operative mortality is high (25%), relating predominantly to the precarious pre-operative state of the patients.
New concepts in coronary artery bypass graft
Total arterial coronary revascularisation may produce even better long-term results and possibly avoid the need for re-operation.
Endoscopic harvesting techniques for saphenous vein are being developed that minimise incisions, discomfort and infection.
Performance of coronary surgery on the beating heart without use of CPB is also evolving.
Cardiac valve surgery
The initial valve operations were performed on the beating heart (mitral valvotomy). The first successful aortic and mitral valve replacements were performed in 1960. Valve pathology is still a significant factor in clinical cardiac disease. A high incidence of rheumatic valve disease persists in developing countries (India, China, Indonesia, South America). In Western countries the most common valve problems are due to degenerative processes and ageing, which have increased in incidence, while rheumatic pathology has declined.
The two most common valve pathologies in Western countries are calcific aortic stenosis, and degenerative myxomatous mitral regurgitation. Aortic stenosis results from dystrophic calcification of either a bicuspid aortic valve, or as part of the degenerative ageing process, and is more commonly seen in older patients (a result of improved living standards and longevity). There is progressive narrowing of the aortic valve orifice with resultant left ventricular hypertrophy, and left ventricular failure in advanced cases. Aortic valve distortion may also result in aortic regurgitation with additional deleterious effects.
Myxomatous degeneration predominantly affects the mitral valve (collagen and elastin abnormalities, and increased mucopolysaccharide production). It results in varying degrees of annulus dilatation, chordae tendineae elongation, leaflet redundancy and prolapse and, in extreme cases, rupture of chordae tendineae and mitral leaflet flail, resulting in massive mitral regurgitation. Sequelae are left ventricular and left atrial dilatation and eventually left heart failure, atrial fibrillation and pulmonary hypertension. Myxomatous degeneration affecting the aortic valve results in progressive aortic regurgitation.
The chronic affects of rheumatic fever are cardiac valve leaflet thickening and retraction. In the aortic valve this results in a combined lesion of aortic stenosis and regurgitation. In the mitral valve, stenosis is the predominant effect of leaflet thickening, fusion at commissures, and shortening of chordae tendineae. Regurgitation occurs with severe leaflet fibrosis, retraction, and failure of leaflet coaptation.
The key symptom is dyspnoea, although this occurs late in the course of valve disease as each of the valve pathologies is generally well tolerated because of left ventricular reserve, and the initial compliance of the left atrium. Dyspnoea requires immediate investigation and aggressive intervention because it indicates exhaustion of the cardiac compensatory mechanism and a poor prognosis and rapid demise for the patient if left untreated.
Angina and syncope may be additional symptoms in aortic stenosis due to pressure loss across an extremely stenotic aortic valve and resultant poor coronary and cerebral perfusion.
Cerebral emboli or endocarditis may occur if the valve lesions are complicated by valvular or left atrial thrombus, infections or vegetations.
Chest X-ray may show cardiomegally, calcification in the aortic or mitral valves, and pulmonary congestion.
Electrocardiogram may show left ventricular hypertrophy, a wide bifid P wave in severe mitral stenosis, or atrial fibrillation.
Echocardiography is the key investigation in valvular heart disease. Accurate measurements can be made of the cardiac chambers, pulmonary artery pressure and the valvular orifices. Calcification, degree of stenosis or regurgitation, leaflet excursion, flow, valve area, gradient and annular size can be precisely measured and compared to prior or future measurements. Transthoracic echocardiography (TTE) is an excellent screening tool. Transoesophageal echocardiography (TOE) gives greater anatomic detail of valves and their pathologies and is particularly useful in the intraoperative setting (Transoesophageal echocardiogram to evaluate the aortic valve (centre of image). LA, left atrium posteriorly; LV, left ventricle; Ao, ascending thoracic aorta. Dots represent 1-cm markings.).
Coronary angiography is performed in patients older than 40 to screen for coexistent coronary artery disease. Thirty per cent of patients undergoing cardiac valve surgery require concomitant coronary artery bypass surgery.
Where patients are asymptomatic, and echo shows normal function and cardiac chamber size and normal pulmonary artery pressures, conservative management is indicated. Peripheral vasodilating medications such as calcium antagonists (nifedipine, amlodipine), or angiotensin-converting enzyme (ACE) inhibitors (captopril, enalapril, etc.), are useful in aortic regurgitation and mitral regurgitation to reduce the afterload for left ventricular ejection. Diuretics (fruse-mide) are required for pulmonary congestion. Warfarin anticoagulation and digoxin may be required if there is atrial fibrillation.
Aortic valve surgery
A mean gradient of more than 40 mm Hg in aortic stenosis or a left ventricular end-diastolic diameter of more than 60mmin aortic regurgitation are indications for surgery. The mean age for aortic valve replacement (AVR) is 69 years. Sternotomy and CPB are required. The aorta is opened transversely 2–3 cm above the aortic valve. Rarely the valve can be repaired. The valve is excised, all calcium removed from the annulus, and an aortic valve prosthesis is placed using non-absorbable sutures. The aortotomy is then closed, and air is evacuated from the heart prior to reestablishment of circulation through the heart. Carbon dioxide in the operative field (heavier and more soluble than oxygen and nitrogen) is used to minimise potential air embolism. The ascending aorta is usually occluded for 60 minutes, CPB time 80 minutes, and total operative time approximately 3 hours.
Mitral valve surgery
Rheumatic mitral stenosis may be treated by percutaneous balloon valvuloplasty. The procedure is carried out by catheterisation of the femoral vein, passing superiorly into the right atrium, across the interatrial septum into the left atrium and eventually dilatation of the mitral valve.
Alternatively, closed mitral valvotomy via a left thoracotomy and trans-left atrial or trans-left ventricular dilatation of the mitral valve is performed. These procedures are performed under TOE guidance, and are best when the valve leaflets are pliable and there is no valve calcification, nor thrombus in the left atrium.
Valve leaflet thickening, calcification, fused chordae and left atrial thrombus are all indications for open operation (via sternotomy and CPB), which may include commissurotomy to free the fused commissures between the anterior and posterior mitral leaflets, debridement of calcification, and fenestration or resection of portions of thickened chordae. A severely distorted valve, especially if additionally regurgitant, will require replacement. Myxomatous degenerative mitral valve regurgitation is most commonly due to elongated and ruptured chordae, leading to prolapse and flail, of the central scallop of the posterior mitral valve leaflet, usually in combination with mitral annular dilatation. If the gross changes are localised to a specific part of the valve (e.g. central scallop of the posterior leaflet), mitral valve repair is possible. If the changes are widespread with multiple areas of prolapse, flail and lack of leaflet coaptation, then valve replacement is indicated.
Mitral valve repair is performed via a sternotomy, CPB and direct left atriotomy. Many techniques are used and include quadrangular resection of the flail or prolapsed segment, annulus and leaflet repair, placement of an annuloplasty ring to reinforce the annulus repair, correct annular dilatation and valve geometry. Leaflet prolapse can also be corrected by shortening or replacing elongated or ruptured chordae and relocating the heads of the papillary muscle. Retention of the native mitral valve avoids the need for warfarin anticoagulation in the long term (if the patient is in sinus rhythm), and maintains the geometry and function of the left ventricle.
Mitral valve replacement (MVR) is performed if the valvular pathology is too extensive. However, as much of the subvalvular mechanism (including leaflet tissue, chordae and papillary muscles) is retained to maintain left ventricular geometry and function, hence resulting in a low operative mortality, and improved long-term left ventricular function and patient survival. Lowprofile mechanical valves are used in patients less than 70 years (see below). Warfarin anticoagulation is always required when a mitral valve prosthesis has been placed.
Cardiac valve prosthesis
There are two categories of valve prosthesis available for implantation: mechanical and tissue.
Mechanical valves are made of pyrolytic carbon with a Dacron sewing cuff, are low-profile, inert, and commonly have two semicircular leaflets (St Jude, CarboMedics, ATS). Mechanical valves always require warfarin anticoagulation maintaining International Normalised Ratio (INR) values between 2.5 and 3.5.
Tissue valves (bioprostheses) are derived from humans (allograft-human cadaver aortic valve) pulmonary valve autografts (discussed later) or xenografts (specially treated porcine or bovine valves). Additionally, tissue valves may be mounted on a stent for ease of implantation, or may be stentless to enhance haemodynamics, allowing a larger valve and orifice into any anatomic situation.
Advantages and disadvantages of each type of valve are indicated in Cardiac valve prosthesis.
|Higher bleeding and thromboembolic rates|
|Tissue||No anticoagulation||15-year durability|
|(Ca+++, dehiscence), re-operation|
|Better haemodynamics (stentless valves)|
In the mitral position mechanical valves are used in patients younger than 70 years, or if the patient is to be on long-term warfarin (AF). Xenograft tissue valves may be used in older patients, often with lesser degrees of warfarin anticoagulation. However, xenografts fail rapidly in young patients.
In the aortic position there are a number of choices determined by age and patient lifestyle. In patients older than 70, a xenograft tissue valve is generally used. Only low-dose aspirin is required long-term if the patient is in sinus rhythm.
In patients younger than 70, generally a mechanical valve together with warfarin anticoagulation is used. A human cadaver allograft is used if warfarin is to be avoided (e.g. patient lives in a remote area, patient participates in contact sports) or when there is endocarditis affecting the aortic valve annulus. However, allografts are relatively difficult to procure and are in short supply.
Some younger patients (15–50 years) have a pulmonary autograft (Ross) procedure in which the diseased aortic valve is replaced with the patient's own pulmonary valve, which in turn is replaced with a human cadaver pulmonary valve allograft. This is an extensive procedure, but well tolerated in young patients. Anticoagulation is avoided. However, long-term results beyond 5 years are not established.
Unfortunately, all tissue valves are subject to wear and tear and gradual degeneration. Inevitably, if any type of bioprosthesis is used in patients younger than 60, there is a very high probability that re-operation will be required, although this is uncommon within 10 years.
Peri-operative prophylactic antibiotics are given to protect against endocarditis (prior to anaesthesia, and for 48 hours post-operatively) and meticulous care taken to avoid any sepsis. Warfarin anticoagulation (if appropriate) is commenced 24 hours post-operatively, and a therapeutic INR of 2.5–3.5 achieved by day 7. Warfarin is continued indefinitely (except in mitral repair or where aortic tissue valves have been used). Diuretics and ACE inhibitors are usually required for several weeks or months. General post-operative management and progress is similar to that of patients undergoing coronary artery surgery.
Other valve conditions
Severe endocarditis affecting either the aortic or mitral valve is usually caused by Staphylococcus aureus and results in fever, aortic or mitral regurgitation and eventual renal and hepatic dysfunction. It is best managed aggressively with appropriate antibiotic loading and early surgery to eradicate the infection and either replace or repair (uncommon but possible) the affected valve. Tricuspid valve surgery is uncommon. Tricuspid regurgitation may be the end product of chronic aortic or mitral valve disease, left heart failure and pulmonary hypertension. The mechanism is that of right ventricular and tricuspid valve annular dilatation and loss of central leaflet coaptation. The leaflets and chordae are otherwise normal. Tricuspid valve annuloplasty to correct the tricuspid annulus size and shape to normal is performed at the time of aortic or mitral surgery. Organic tricuspid valve stenosis or regurgitation due to rheumatic disease is rare, and is managed following the principles of mitral valve surgery.
Operative mortality varies from 1% (AVR, MVR) to 3% (MVR). Operative mortality for combined CABG and valve surgery is 3–5%, and for re-operation is 10%. Long-term results are excellent. Survival following mitral valve repair, or AVR, is 90% at 5 years, and 80% at 10 years. Survival following MVR is a little less than this due to late referral and excision of the subvalvar apparatus in the previous era.
Morbidity of valve replacement surgery
Unfortunately each valve prosthesis has a group of long-term problems associated with its use:
- anticoagulant-related haemorrhage, which may be extremely serious (cerebral, gastrointestinal) thromboembolism from small thrombi that form around the annulus or within the prosthetic valve
- endocarditis from an infection on the valve prosthesis
- peri-valvular leaks, or structural deterioration of tissue valve which, when severe enough, would require re-operation.
Each of the above complications occur with an annual incidence of approximately 0.5–1.0%, and hence the potential for a patient to be totally free from any one of these complications over the course of 10 years is only of the order of 70%.
Congenital cardiac surgery
Cardiac anomalies occur in 8 per 1000 live births. The range of anomalies is extensive. Only the common ones are discussed below. Congenital cardiac abnormalities are best corrected as early as possible after birth (preferably in the first 3 months). Some, such as a large, persistent PDA, which creates a huge shunt from the aorta to the pulmonary artery, or severe coarctation of the aorta, which places a large afterload on the left ventricle, need urgent correction at birth.
Patent ductus arteriosus
A PDA allows blood flow from the pulmonary artery trunk to the aorta when the lungs and pulmonary circulation are not functioning in utero. The PDA usually closes at birth. A persistent, small PDA is vulnerable to endocarditis. Persistent, large PDAs allow shunting of blood from the aorta back into the pulmonary circulation, overloading it as well as the right heart, eventually leading to pulmonary hypertension and right heart failure. Closure of the PDA is essential and this can be achieved either by percutaneous catheter closure, or by direct suture ligation or division and oversewing by thoracoscopy, or a small left thoracotomy.
Coarctation of the aorta
The most common site is just distal to the left subclavian artery, the lumen of the aorta often narrowed to 1–2 mm. Left untreated, upper body hypertension, left ventricular hypertrophy and left ventricular failure develop. Correction is by either percutaneous retrograde (from the femoral artery) catheter balloon dilatation, or surgical resection and repair via a small left thoracotomy.
Atrial septal defect
Atrial septal defects occur as a result of failure of development of the interatrial septum and can be high (sinus venosus), mid (ostium secundum) or low (ostium primum) defects. A significant ASD is more than 1 cm in diameter and if left uncorrected results in a persistent left atrium to right atrium shunt, eventually leading to right atrial and ventricular enlargement, atrial fibrillation, and pulmonary hypertension. Life expectancy may be reduced by 10–30 years (depending on the size of the ASD and shunt).
Echocardiography gives excellent depiction of the anatomic location, size of the ASD and the flow through it, as well as the size of the cardiac chambers and pressure in the right ventricle and pulmonary artery.
Atrial septal defect closure is indicated if the pulmonary circulation flow is more than 1.5 times the systemic circulatory flow. Surgical repair is readily performed (using CPB) by either direct suture or a patch of autologous pericardium with an extremely low mortality (1 : 400). Percutaneous ASD closure via the femoral vein with a catheter-mounted baffle-type device has been developed and is applicable where the ASD is well circumscribed with a defined rim circumferentially. Early experience has been promising.
Ventricular septal defect
Ventricular septal defects (VSDs) occur when ventricular septal development is incomplete and may be single or multiple and placed either just below the tricuspid valve and the origin of the great vessels, or more inferiorly in the body of the muscular septum. Most commonly they occur in isolation, but may also be present as part of a more complex cardiac anomaly (e.g. Tetralogy of Fallot). Small VSDs, particularly in the central muscle septum, may close spontaneously with cardiac growth. Larger VSDs associated with pulmonary-tosystemic flow ratios of more than 1.5 : 1 are repaired to avoid endocarditis, and also the sequelae of pulmonary and right heart overload (see above). Surgical closure is by using CPB, and by direct suture or patch. The main specific complication is heart block as the conducting bundle passes near the inferior rim of the VSD, and care is taken not to damage the conducting bundle with sutures at VSD closure.
Other congenital abnormalities
Some other congenital abnormalities that may be surgically corrected with excellent long-term results include pulmonary valve stenosis, Tetralogy of Fallot, transposition of the great vessels and endocardial cushion defects (aortic valve canal). However, there are numerous rarer, more complex conditions (e.g. hypoplastic left heart syndrome, single ventricle, tricuspid atresia) where surgery is also possible, but often multiple procedures are required, with suboptimal results. (The reader is directed to texts of paediatric cardiology and cardiac surgery).
Surgery of the thoracic aorta
Aneurysms of the thoracic aorta, especially the transverse arch, are challenging. The most common pathology is myxomatous degeneration of the aortic wall media, leading to aneurysmal dilatation and eventually rupture or dissection. Marfan's syndrome is one entity that is part of the spectrum of myxomatous degeneration of connective tissues. Hypertension and atherosclerosis are now better controlled in the population and are less common contributing factors to thoracic aneurysms. Dilatation of the thoracic aorta to a diameter of more than 5 cmis associated with a marked increase in the possibility of rupture or dissection and so elective repair/replacement is advised.
The patients are usually asymptomatic. The aneurysm is often noted on routine chest X-ray. Rupture or dissection is associated with severe chest and interscapular pain, possibly collapse, hypotension (due to blood loss into the mediastinum, pleural cavity or pericardium) and unequal pulses (due to dissection around the origins of the large artery). The ECG is usually normal.
Transoesophageal echocardiography is the most important diagnostic test, and should be performed urgently. It will show the size and location of the aneurysm, any dissection flaps, the site of the aortic wall tear, extent of dissection, and the function of the aortic valve, which may partly dehisce from the outer aortic wall and become regurgitant.
Elective repair is indicated when the aneurysm is more than 5 cm in diameter. This may involve replacement of the aneurysm with a Dacron tube graft, but may also require AVR, re-implantation of the coronary artery ostia, or even replacement of the transverse arch with re-implantation of the great vessels. Results of elective surgery are excellent, with operative mortality generally less than 5%.
If rupture or dissection has occurred, emergency surgery is indicated with the TOE as the sole investi investigation (which can be performed in the operating room prior to anaesthesia induction). Similar operative techniques are used preserving the aortic valve if possible. Biological glues are used to glue together and stiffen the fragile myxomatous layers of the aorta at the site of anastomoses and repair. This complex surgery is usually facilitated by use of deep hypothermia (18°C) and total circulatory arrest (see ‘eCardiopulmonary Bypass: Heart–Lung Machine’). Major morbidity may result from these urgent, difficult operations and includes post-operative haemorrhage, stroke and renal dysfunction. The operative mortality is between 10% and 30%.
Vigilant long-term follow-up with control of hypertension, and serial computed tomography (CT) scans or echocardiograms, are required because other parts of the aorta (descending thoracic or abdominal) may dilate over time.
Pacemaker and dysrhythmia surgery
Degenerative fibrosis associated with age can affect the cardiac conducting mechanism to produce heart block. The heart rate may fall to 30 beats per minute (ventricular escape rhythm) and result in dizziness or syncope. This is a common clinical problem in older patients. Occasionally, heart block may result from trauma to the conducting bundle at cardiac surgery, or from some anti-arrhythmic medications (verapamil, sotolol).
Treatment is relatively simple and achieved by implantation of a pacing lead into the right ventricle via the cephalic or subclavian vein below the clavicle and implantation of a lithium-powered, low-profile pacemaker generator, all performed under local anaesthesia. The pacing rate is adjusted to 70–80 beats per minute as required. An atrial lead can also be inserted to allow sequential atrial/ventricular pacing, which is more efficient. The pacemaker may be programmed to allow spontaneous increase of pacing rates according to patient activity.
Programmed sequential biventricular pacing may be beneficial in patients with left ventricular dilatation, severe dysfunction and cardiac failure.
Rapid atrial arrhythmias (atrial fibrillation, atrial flutter, junctional tachycardia) that remain uncontrolled on medication (digoxin, sotolol, amiodarone) and are significantly symptomatic, can be treated either surgically or more commonly by percutaneous catheter radiofrequency ablation.
Life-threatening rapid ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation) may also be treated by implantable cardioverter defibrillators (ICD) with minimal operative mortality and morbidity, and excellent long-term results.
Circulatory support may be required to allow time for cardiac recovery after a temporary but reversible insult, or permanently.
Nitroprusside and nitroglycerine infusions allow rapid peripheral, arterial and venous dilatation.
Calcium antagonists (nifedipine, amlodipine) and ACE inhibitors (captopril, enalapril) are oral medications that cause peripheral vasodilatation and reduce cardiac afterload, allowing myocardial contraction and ejection of stroke volume against a lower systemic vascular resistance.
Inotropic agents are usually given as infusions for short-term use (hours or days) and include dopamine, dobutamine, adrenaline, isoprenaline, milrinone and calcium. All have varying properties and effects, but the underlying mechanism is an enhanced inotropic effect on the myocardium.
Intra-aortic balloon pump
Intra-aortic balloon pump (IABP) is indicated when hypotension and poor cardiac output persist despite appropriate inotropic support. A catheter with a 34- or 40-mL balloon is introduced into the descending thoracic aorta usually percutaneously by the femoral artery. The balloon inflates (helium) and deflates in sequence with the ECG. It inflates in diastole, suddenly increasing diastolic pressure, mean blood pressure and organ perfusion, especially coronary blood flow and myocardial perfusion. The balloon rapidly deflates just prior to cardiac systole, dramatically reducing the afterload for the left ventricle. The usual duration of IABP support is between 1 and 5 days, but use up to 21 days has been reported.
Potential problems include leg ischaemia, systemic infection and mechanical blood cell destruction leading to anaemia and thrombocytopenia.
Ventricular assist devices
Ventricular assist devices (VADs) provide additional mechanical support (when inotropes and IABP are insufficient). Typically, cannulae are placed on the inlet side (left atrium) and into the outlet side (aorta) with a mechanical device in between, effectively performing the work of the left ventricle. (A similar circuit can be constructed for the right side of the heart.) Numerous devices are available (Biopump, Thoratec, Novacor, Heartmate, Abio-Med) with varying characteristics relating to size, implantability, portability, ease of use and expense. Ventricular assist devices may be in situ from 3 to more than 100 days.
Extracorporeal membrane oxygenation (ECMO)
Where support of both the circulation and also oxygenation is required (e.g. virulent but reversible pulmonary infection or asthma, where oxygenation cannot be maintained with mechanical ventilation, 100% O2, and maximum positive end-expiratory pressure), extracorporeal membrane oxygenation (ECMO) can be used. Extracorporeal membrane oxygenation is identical to regular CPB but with special cannula and circuit modifications for long-term use. The management is extremely demanding as the patient requires anticoagulation and constant supervision.
The first human cardiac transplant was performed in 1967 by Dr C. Barnard in South Africa. This was preceded by extensive laboratory work by Dr N. Shumway and coworkers at Stanford University, USA. The initial results were suboptimal because of difficulties with rejection and fulminating infections.
Cyclosporine, which was introduced in 1980, dramatically reduced the severity of the rejection and infection episodes to readily manageable levels, promoting renewed interest. Other advances included superior donor heart preservation, better tissue typing, myocardial biopsy surveillance, and more efficient anti-rejection regimens.
Indications for cardiac transplantation include permanent severe heart damage and failure from myocarditis, cardiomyopathy and multiple myocardial infarctions. Donor hearts are usually procured following brain death from motor vehicle trauma or cerebral trauma. Recipients are usually less than 65 years of age with no other significant coexisting medical or psychological problems.
The results or cardiac transplantation are very good with an operative mortality of 2–3%, 1-year survival of 90% and 5-year survival of 80%. Approximately 100 cardiac transplants are performed in Australia each year and almost 3000 are performed annually worldwide; however, numbers are limited by donor shortages. In response to this, much development is centred on implantable ‘artificial hearts’.
Complications of cardiac surgery
Most cardiac operations have an operative mortality of approximately 1% (including the first 30 days post-operation). Mortality rates are increased in reoperations (5%), multiple procedures (5%) and with increasing age (>80 years, 10%), age being a marker for multiple associated co-morbidities.
The incidence of major neurologic events in the perioperative period is 1–2%. Causes include primary cerebrovascular disease in older patients, atheroembolism from the ascending thoracic aorta, hypoperfusion during CPB, and air or particulate embolism during valve surgery. Fortunately there is usually a significant recovery. In addition, subtle neuropsychologic dysfunction can occur, with abnormalities lasting up to 6 months.
Sternal and mediastinal infection
Sternal and mediastinal infection is a devastating complication, with an incidence of 1–2%. Risk factors include diabetes, obesity, bilateral ITA grafting, prolonged pre-operative hospitalisation and multiple instrumentations. Prophylactic antibiotics are used in all cardiac surgery. Protection against mediastinitis is afforded by closure of the thymus and pericardium behind the sternum. Common bacteria are S. aureus (including methicillin-resistant S. aureus).
Clinical features are fever, increased sternal discomfort, redness and movement of a previously stable sternum. Early diagnosis is essential, as established mediastinitis has a mortality of 30%.
Treatment depends on the extent of pathology, from intravenous antibiotics, to local debridement and sternal rewiring, to extensive debridement and use of omental and myocutaneous flaps.
Post-operative haemorrhage occurs with an incidence of 2–5%. Specific causes include bleeding from sutures lines, branches of grafts, and the ITA bed. However, in the majority no specific bleeding point is found but reoperation is useful to remove retained blood and clots from the pericardium, mediastinum and pleurae, and establish haemostasis from the oozing areas. Aspirin and other anti-platelet drugs within 7 days of cardiac surgery may be contributing factors.
Numerous other complications may also develop and include atrial fibrillation, pulmonary atelectasis, pneumothorax, and fluid retention. These are all readily treatable and reversible.
Minimally invasive cardiac surgery
Over the past 5 years there has been much interest in less invasive surgery, in minimising trauma, improving cosmesis and, where possible, avoiding the deleterious effects of CPB.
Shorter upper sternal and right parasternal incisions have been used for aortic valve surgery. Right submammary and short lower sternal incisions have been used for ASD repair and for mitral valve surgery (especially in young females). Left submammary incisions are used for isolated coronary bypass to the LAD. Occasionally, groin cannulation of the femoral artery and vein are used in conjunction with small thoracic incisions.
The value of these approaches is not established. Limited exposure may compromise safety and lengthen the duration of the procedure. Additionally, femoral vessel cannulation has been complicated by aortic dissection, leg ischaemia and venous thrombosis. These incisions are of great value when cosmesis is important.
Off-pump coronary surgery
Devices and techniques have been developed that allow excellent stabilisation of the coronary arteries, making it possible to perform precise coronary anastomoses, especially to the LAD and diagonal arteries (anterolateral aspects of the heart), while the heart is beating and maintaining circulation. Similarly, but to a lesser extent, the circumflex and right coronary arteries may be grafted.
Potential advantages are avoidance of CPB and manipulation of the aorta (by cannulae and clamps), which may be an important factor in older patients or where the aorta is atheromatous or calcified, thereby reducing the possibility of bleeding or stroke.
There are potential economic gains through avoidance of CPB: consumables, personnel and potential to reduce intensive care and hospital stays; however, these have not been proved thus far.
There are also potential disadvantages, with greater operative difficulty, possible coronary artery damage, and episodes of hypotension with excessive displacement and manipulation of the heart. The role of offpump coronary surgery (OPCAB), beating heart coronary surgery is still being evaluated.
The future of cardiac surgery
The number of cardiac operations performed worldwide per annum continues to increase. Interventional cardiology techniques such as angioplasty have changed the spectrum of cardiac surgery to more complex and re-do operations, and the mean age of patients is older. Robotics, in relation to cardiac surgery, are being developed, which promises to assist minimally invasive techniques. Substantial endeavour continues in improving prosthetic cardiac valve and artificial heart technology.
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Cohn LM, Edmunds LH Jr. Cardiac Surgery in the Adult. 2nd ed. New York: McGraw Hill; 2003. Also at www.ctsnet.org
Topol EJ, Califf RM, Isner J et al. Textbook of Cardiovascular Medicine. 2nd ed. Philadelphia: Lippincott Williams & Wilkins;2002.Townsend CM, Beauchamp RD, Evers BM, Mattox KL. Sabiston Textbook of Surgery. The Biological Basis of Modern Surgical Practice. 16th ed. Philadelphia: WB Saunders; 2001.