Professor Kolesov performed the first beating-heart left internal mammary artery to left anterior descending coronary artery bypass graft in February 1964 in Leningrad, Russia, whilst Dr Favaloro performed the first saphenous vein coronary artery bypass graft (CABG) surgery in May 1967 at the Cleveland Clinic in the USA. Until then, treating angina using surgery, and the feasibility of operating on the delicate and small coronary arteries had been unimaginable. Fifty years later, several million CABG operations have been performed worldwide and it remains the most common operation performed by cardiac surgeons with excellent outcome and very low mortality.
Isolated CABG operations represent about 50–60% of the cardiac surgery workload in the UK. As percutaneous coronary intervention is now often offered early in the course of ischaemic heart disease, patients presenting for CABG are now older and sicker and this trend is set to continue. In addition, people live longer due to advances in treatment of chronic diseases, including hypertension, elevated lipids, diabetes and others. Despite this, mortality from CABG is at an all-time low of between 1 and 2% due to better perioperative management. A low-risk patient with a competently executed CABG operation should have a smooth and uneventful recovery, an ITU stay shorter than 24 hours and an overall hospital stay of around 5 days. In a high-risk patient, however, with multiple risk factors and comorbidities, or after a suboptimally performed CABG operation, the procedure may be followed by complications and longer postoperative hospitalisation.
The limited functional reserve of elderly patients, the presence of chronic kidney disease, peripheral vascular disease, COPD, diabetes and impaired cardiac function are but a few of the challenges which may be faced in the management of this high-risk population.
In the majority of low-risk patients, there is no need for cardiovascular support and an adequate cardiac output can be obtained just with fluid management and rate control by means of temporary pacing wires.
CO = HR × SV.
The stroke volume, SV, is determined by preload, contractility and afterload.
If contractility and afterload are within the normal range, it is obvious that cardiac output can be optimised with fluids (preload) or by simply increasing the heart rate with temporary cardiac pacing. Determination of the optimal filling pressure is often empirical and can be estimated with the use of a fluid challenge and observing the haemodynamic response (see Chapter 14).
If adequate perfusion pressure cannot be maintained with these simple, first line measures, contractility and afterload may need to be addressed pharmacologically. Before making the diagnosis of impaired contractile cardiac function, it is important to exclude tamponade (see Chapter 3). Impaired contractility can be improved with either pharmacological or mechanical means. Dopamine and catecholamines are often the first choice but phosphodiesterase inhibitors may be beneficial in right ventricular dysfunction and elevated pulmonary vascular resistance (see Chapter 15).
The most commonly used mechanical support device is the intra-aortic balloon pump (IABP) (see Chapter 21) which, by simultaneously decreasing myocardial workload and improving coronary perfusion, can immediately alleviate myocardial ischaemia and improve poor cardiac function. The routine use of IABP in routine CABG is not necessary, but in selected high-risk patients there is a significant advantage in survival provided by this device. This was supported by several randomised trials and a recent meta-analysis.
The use of inotropic drugs, vasoconstrictors and mechanical support in the postoperative management of the CABG patient can be guided by clinical assessment. Features of low cardiac output include hypotension, poor peripheral perfusion, falling urine output despite adequate preload and metabolic evidence of impaired perfusion, such as acidosis. In a CABG patient with low blood pressure and inadequate perfusion, it can sometimes be difficult to differentiate between inadequate filling (preload), poor cardiac function (contractility) or low systemic vascular resistance (afterload). The cause may also be multifactorial. If there is doubt in interpreting clinical and simple haemodynamic findings, more invasive haemodynamic monitoring using transoesophageal echocardiography or a pulmonary artery catheter will directly provide information on the cardiac output and on the state of preload and afterload of both the pulmonary and systemic circulations, thus helping tailor the therapy to the haemodynamic needs of the patient. Routine use of a pulmonary artery catheter is controversial and is not supported by clear evidence. Nevertheless, it may play a role in high-risk patients, but the risk of adverse events and the costs associated with it suggest that its use be restricted to those patients in whom the aetiology of the haemodynamic instability cannot be identified by more simple methods and those who require multiple vasoactive agents and their fine titration.
Myocardial ischaemic event presenting soon after CABG surgery is a rare but troublesome finding that can be difficult to diagnose and to treat. Many factors can contribute to myocardial injury during a CABG operation, including surgical trauma due to manipulation and suturing, less than ideal myocardial protection, incomplete revascularisation, acute graft thrombosis and iatrogenic injury to the native vessels. Because of these confounding factors, the diagnosis of MI following CABG is not straightforward and uncertainties remain around the correct threshold for biomarker elevation and the need for associated criteria. According to the 2012 third universal definition of myocardial infarction after CABG, at least two of the following criteria should be present for diagnosis: cardiac biomarkers (with troponins preferred) rise >10 times 99% upper reference limit from a normal preoperative level; and new pathological Q-waves or new left bundle branch block (LBBB) or imaging or angiographic evidence of new occlusion of native vessels or grafts, new regional wall motion abnormality, or loss of viable myocardium. In daily clinical practice in many centres, cardiac biomarkers are not routinely measured after CABG surgery. Therefore, in the immediate postoperative period, when the patient is fully sedated and intubated, the first sign of possible ongoing myocardial ischaemia or infarction may be unexpected haemodynamic or rhythm instability. This finding should lead to a thorough assessment of the patient, which includes ECG for new abnormalities, echocardiogram for new regional wall motion abnormalities and cardiac biomarkers. If it is then believed that myocardial ischaemia is a genuine possibility, a low threshold for emergency angiography should be adopted. If a technical problem such as acute graft or native vessel occlusion is demonstrated, surgical revision and emergency re-grafting of the affected territory should be considered as it may save both myocardium and life. Additional treatment options include an intra-aortic balloon pump, GTN infusion, antiplatelet agents and beta-blockers.
Acute kidney injury (AKI) is a common postoperative complication of cardiac surgery and is associated with an increased risk of morbidity, mortality and length of stay
Between 5% and 30% of patients undergoing CABG may suffer this complication in the postoperative period. The use of serum creatinine rather than urine output as main criterion for the diagnosis of postoperative AKI is appropriate in the cardiac surgery population, since manipulation of the urine output with diuretics makes this a less reliable indicator of AKI. A limitation of defining AKI based on serum creatinine measurements is the delay in detecting the onset of injury. Optimisation of renal perfusion, avoidance of hypovolaemia and avoidance of nephrotoxins are the only options to prevent or mitigate the effects of postoperative AKI. Pharmacological interventions have been attempted with inconsistent results, and there are no drugs that have demonstrated a definitive renal protection.
The widely used drug furosemide was found not to be protective and to be potentially harmful, as the incidence of AKI was twice that of the dopamine or placebo group in a double-blind randomised controlled trial. Similar negative results have been seen in other studies.
Arrhythmia: Postoperative arrhythmia is common in cardiac surgical patients. The commonest observed arrhythmia is atrial fibrillation. The precise reasons for developing arrhythmias are not always clear, but overall the prognosis is good as frequently these recover and sinus rhythm is restored. It is important to exclude poor right ventricular perfusion as a cause of malignant ventricular arrhythmias. Occlusion of right coronary graft needs be ruled out in such cases. The treatment of postoperative arrhythmia is no different from the treatment for other patients in the ICU, and is described in Chapter 10.
Postoperative bleeding: Patients undergoing coronary surgery often receive antiplatelet medication, which may have long lasting effects, and hence they are at a higher risk of coagulopathy. Thus postoperative bleeding can be a problem. The management of this problem is discussed in detail in Chapter 36.
Haemothorax: CABG patients are at a higher risk than other cardiac patients of bleeding in the left hemithorax when the left internal mammary artery has been used. The ICU team needs to be vigilant for this complication if haemodynamic instability is a problem or if there is a massive blood loss postoperatively.
Several randomised controlled studies, including a meta-analysis, have shown a clear benefit of early administration of aspirin in the prevention of early and late vein graft occlusion. This beneficial effect of early aspirin declines after 24 hours and disappears after 48 hours. In the appropriate clinical settings, early administration of postoperative aspirin following CABG is not associated with increased blood loss or transfusion requirement. The advantages of early aspirin administration include a reduction in mortality, myocardial infarction, stroke, renal failure and bowel ischaemia. The antithrombotic effect of aspirin is greatly potentiated when used in combination with clopidogrel. The use of dual antiplatelet therapy following CABG is still controversial and a clear benefit in vein graft patency has not been clearly demonstrated. In conclusion, the use of aspirin within 6 hours following CABG is strongly recommended and supported by clinical evidence.
CABG is the most common operation performed by cardiac surgeons, with an overall mortality between 1 and 2%.
The risk profile of the patient population is changing, multiple comorbidities and advanced age are now common features of the patient referred for CABG.
Fluid challenges and different pacing strategies can significantly increase the cardiac output.
Haemodynamic instability in the early postoperative period may represent the first sign of ongoing myocardial ischaemia.
In the appropriate clinical setting, the use of aspirin within 6 hours following CABG is strongly recommended.
1. One hour following a routine CABG operation the mean pressure of your patient is dropping below 60 mmHg. Looking at the monitor you notice a sinus rhythm of 50 bpm and a CVP of 12. The patient is not bleeding, there is no suspicion of tamponade and urine output is adequate. You want to increase the cardiac output in order to prevent obvious complication due to hypoperfusion. What is your strategy?
2. Your patient has just arrived in the unit. Mr Cabbage has just received a total arterial revascularisation by a very experienced surgeon. When the nurses looking after him roll him slightly in order to insert the sliding sheet and reposition him in the bed, you notice a sudden drop of the blood pressure. The monitor shows a BP of 50/30 a heart rate of 100 and a CVP of 4. What is your first action?
3. Mr Bacon is a 66 year old man with diffuse coronary disease. His LIMA was not used since the flow was considered poor, and he received a triple vein graft. The surgeon is not too happy about him since the conduits and the targets were poor. The patient shows some haemodynamic instability with a blood pressure of 80 over 55, CVP of 16 and a heart rate of 100 bpm. The urine output is low and peripheral perfusion is poor. What is your first action?
4. Mr Stone underwent a CABG operation in the morning. Now it is 2 pm and the nurse calls you for poor urine output since his arrival in the unit. Blood pressure is 130/70, heart rate 80, CVP 10. Haemoglobin is 95, base excess is −2 and lactate 2.5. On examination you notice cold peripheries, but Mr Stone is otherwise unremarkable. What is your approach?
5. You are asked to prescribe the standard medication to be administered in the first 24 hours following a routine CABG operation for Mrs Dark. Which of the following should be included in the list?
The post cardiac valve surgical patients follow the same general management principles as any other cardiac surgical patients. Adequate basic requirements such as oxygenation, ventilation management, optimal heart rate and cardiac output, coagulation management and early detection and management of pericardial tamponade, as well as pain management, are not different. However, patients undergoing valve surgery tend to have higher risks of morbidity and mortality. They may require more invasive monitoring, including with a pulmonary artery catheter, and infusion of vasoactive medication. Early re-evaluation of post-intervention valvular function by echocardiography is frequently needed. Electrophysiological interventions and pacing techniques are needed more often than for uncomplicated coronary artery bypass graft surgery patients. Sometimes, patients at a particularly high risk need preoperative ICU admission for preoptimisation. In this chapter we will discuss the salient features and basic principles of preoperative and postoperative heart valve pathology challenges and management in the cardiac surgical ICU.
Aortic valve replacement is generally indicated in patients with symptomatic severe aortic stenosis and/or regurgitation.
Options for aortic valve replacement include stented and stentless xenograft tissue valves, mechanical valves, homografts and, less commonly, pulmonary autografts.
The commonest cause for aortic stenosis in elderly patients is degenerative calcific disease, while in younger patients the commonest aetiology is congenital bicuspid aortic valve.
Several important structures that are in close proximity to the aortic valve may be damaged at the time of surgery. These include the bundle of His, the anterior leaflet of the mitral valve and the ostial origin of the coronary arteries. The bundle of His runs beneath the commissure between right coronary and non-coronary cusps. A deep suture placed in this region may result in injury with resultant complete heart block. The anterior leaflet of the mitral valve is separated from the aortic annulus by the aortomitral curtain in the region of the non-coronary cusp and left coronary cusps. Iatrogenic damage to the anterior leaflet of the mitral valve may result in mitral regurgitation. Lastly, due to the close proximity of the coronary ostia to the aortic annulus, there is a risk of coronary ostial blockade or compromise and ensuing ischaemia. Accurate suture placement and carefully securing the prosthesis in place should reduce the risks of paravalvular leak.
Intraoperative transoesophageal echocardiogram is essential in all cases of valvular surgery, allowing for early detection and immediate correction of complications.
In aortic stenosis, there is pressure overload of the left ventricle that results in concentric hypertrophy and diastolic dysfunction. The stiff non-compliant ventricle is dependent on adequate preload and atrial contraction – the latter may contribute up to 30% of left ventricular filling.
In chronic aortic regurgitation there is a volume as well as pressure load to the left ventricle, resulting in dilatation and hypertrophy. In the acute setting of aortic regurgitation, such as in cases of aortic regurgitation secondary to infective endocarditis or aortic dissection, the left ventricle may be normal in size. These patients often display marked haemodynamic compromise with a small ventricle that has not adapted to the large regurgitant volume during diastole.
Arrhythmia: Atrial arrhythmia must be immediately treated with antiarrhythmic medications as the atrial contraction contributes up to 30% of the ventricular filling. The threshold for synchronised cardioversion to maintain atrioventricular synchrony should be low, especially in patients with haemodynamic compromise.
Bradycardia: Postoperative bradycardia is treated with atrioventricular sequential pacing in order to maximise the cardiac output. Transient or permanent complete heart block may occur following aortic valve surgery due to oedema, haemorrhage, debridement or damage to the atrioventricular bundle. If complete heart block persists for more than 4–5 days then due consideration should be given to the placement of a permanent pacemaker.
Hypotension: Adequate preload is essential for patients with aortic valve disease due to accompanying diastolic dysfunction. Hypotension and hypovolaemia must be avoided as they could lead to a vicious cycle of coronary hypoperfusion, reduced cardiac output and worsening hypotension.
Hypertension: Hypertension tends to develop a few hours following surgery secondary to the relief of left ventricular outflow tract obstruction, often in the setting of left ventricular hypertrophy. Severe hypertension should be aggressively treated in order to protect the surgical aortic suture lines and reduce myocardial oxygen demand.
Stroke: Stroke may be caused by emboli in the presence of atheromatous aortic disease, particularly in elderly patients and/or those with known history of cerebrovascular disease. Cerebral hypoperfusion may also lead to cerebral ischaemic injury with or without concomittent embolism in light of the high prevalence of large and small vessel cerebral vascular disease.
TAVI Patients in ICU: Novel technology of minimally invasive treatment for aortic valve stenosis by percutaneous valve implantation has allowed for patients with greater comorbidities and hence high surgical risk to be treated. These patients do not normally need ICU post-surgical admission. However, in case of complications intraoperatively and postoperatively, these patients can need intensive care. Common reasons for ICU admissions are haemodynamic instability (bradycardia, arrhythmia, hypotension, hypertension), pulmonary oedema, renal failure and stroke. The support for these patients follows the same principles as for surgical aortic valve patients.
Hypovolaemia: In the setting of diastolic dysfunction that accompanies ventricular hypertrophy, large fluid challenges often result in minimal change in filling pressures. Adequate preload is important in these patients for maintenance of an adequate cardiac output.
Hypotension: Hypotension is not uncommon following aortic valve replacement for regurgitation. The reasons can be multifactorial, and include post cardiopulmonary bypass vasodilatation, low cardiac output due to reduced contractility, pericardial collection or reduced preload. Post cardiopulmonary bypass vasodilatation is not uncommon and is readily treated with vasopressor medication. However, it is important to establish that this is the reason for hypotension, and not reduced cardiac output or pericardial collection. Therefore, use of ultrasound imaging to rule out a pericardial collection and cardiac output measurement is advisable.
Mitral valve surgery is generally indicated in patients with severe mitral stenosis not amenable to percutaneous mitral balloon valvuloplasty and those with severe symptomatic mitral regurgitation.
Mitral valvular pathology may arise due to dysfunction of the mitral annulus, leaflets, subvalvular apparatus as a result of ventricular dysfunction or a combination of some or all of these components.
Rheumatic heart disease is the commonest cause of mitral stenosis, whereas degenerative disease is the commonest cause of mitral regurgitation. Other causes of mitral regurgitation include ischaemic heart disease, rheumatic disease and endocarditis.
The mitral valve is a complex structure that has an important role in the left ventricular geometry and function. The subvalvular apparatus, which includes the chordae tendinea and papillary muscles, plays an important role in maintaining the integrity of the mitral valve as well as the function of the left ventricle. The anterior and posterior leaflets of the mitral valve are arbitrarily divided into A1, A2, A3 and P1, P2, P3 regions, respectively. The circumflex artery runs in the atrioventricular groove near the posteromedial commissure and in close proximity to the medial half of the posterior leaflet of the mitral valve. Injury or compression to the circumflex artery results in inferobasal and lateral wall ischaemia (Figure 38.1).
Figure 38.1 Mitral valve and its relation to various structures.
The coronary sinus is close to the anterolateral commissure and adjoining part of the posterior leaflet, while part of the anterior leaflet is close to the non-coronary cusp of the aortic valve. Care must be taken when annular sutures are placed in these regions.
Mitral annular calcification causes difficulties and challenges during mitral valve surgery. Overenthusiastic decalcification of the mitral annulus may result in atrioventricular disruption, which is associated with high mortality and morbidity. Excessive removal of the subvalvular apparatus may result in left ventricular rupture.
Mitral stenosis is generally associated with a small left ventricular cavity size. Advanced cases may be complicated by pulmonary hypertension (which may be reversible or irreversible) and occasionally right heart dysfunction. Affected patients are prone to low cardiac output postoperatively as a result of low end-diastolic and end-systolic volumes. The onset of congestive heart failure may coincide with the development of atrial fibrillation. Postoperatively, stroke volume is largely dependent on the maintenance of adequate ventricular preload. The pathology of degenerative disease of the mitral valve causing mitral regurgitation ranges from fibroelastic deficiency to Barlow’s disease. Barlow’s disease is characterised by pronounced annular dilatation, bileaflet prolapse and the presence of thick, spongy leaflets due to excessive myxomatous tissue proliferation. It may also be associated with annular calcification. Fibroelastic deficiency is found in older patients whereas Barlow valve with congenitally excessive valve tissue is seen in younger patients.
There may be prolongation or rupture of the chordae giving rise to a flail or prolapsing leaflet. Chronic mitral regurgitation causes volume overload of the left ventricle that leads to ventricular and atrial dilatation. Mitral regurgitation leads to increased ventricular preload as the regurgitate volume generated during systole returns to the ventricle during diastole. There is also reduced ventricular stress along with reduced afterload due to offloading of the ventricle. As the ventricle accommodates to the excess volume by dilatation, there is minimal elevation of the pulmonary vascular resistance initially. Increased pulmonary vascular resistance occurs due to chronic volume overload, ultimately leading to left ventricular failure.
Acute ischaemic mitral regurgitation is most often due to annular dilation and malfunction of coaptation due to ventricular remodelling. However, it can also be due to ruptured chordae or head of the papillary muscle following myocardial infarction. The posteromedial papillary muscle is most commonly involved as it is only supplied by the posterior descending branch of the right coronary artery (or the circumflex artery in the case of a left dominant coronary circulation). The heart has little time to adapt to the regurgitant mitral valve, which results in rapid rise of pulmonary pressure, pulmonary oedema and development of cardiogenic shock. This is associated with high mortality.
Chronic ischaemic mitral regurgitation is generally a disease of the ventricle. Features include annular dilatation and tethering of the papillary muscle and posterior leaflet due to ventricular remodelling following ischaemia.
Ventilatory failure: This can occur in patients with long standing mitral stenosis who have pulmonary hypertension. It is important to avoid hypoxia and hypercarbia in the early postoperative period. Therefore management of pulmonary congestion by reducing preload (diuresis, haemofiltration, vasodilatation), pulmonary vasodilatation and mechanical ventilator support is important. Where prolonged mechanical ventilation of the lungs is needed, the team need to judge the risks of ventilator associated pneumonia and other complications of mechanical ventilation versus earlier extubation.
Right ventricular dysfunction: Following surgery for mitral stenosis, right ventricular dysfunction normally improves over time. However, right ventricular dysfunction can be problematic. A pathophysiological approach to treatment is advisable. Optimising preload, and maintaining adequate contractility, along with reduction in right ventricular afterload where possible, are the usual strategies. Medical treatment with phosphodiesterase inhibitors, intra-aortic balloon counterpulsation and right ventricular extracorporeal support (temporary right ventricular assist device, Impella) may be needed.
Atrial fibrillation: Many patients undergoing mitral valve surgery have pre-existing paroxysmal or chronic atrial fibrillation. The Maze procedure or pulmonary vein isolation may be used as an adjunct to mitral valve surgery in these patients. A left atrial diameter of less than 5 cm and duration of atrial fibrillation of less than 5 years is associated with greater success of the Maze procedure. The left atrial appendage may also be excised or obliterated in these patients to reduce the risk of stroke due to chronic atrial fibrillation and embolisation of thrombus from the appendage. In addition, around 30–40% of patients develop new onset of atrial fibrillation following mitral valve surgery needing electrical or chemical cardioversion with amiodarone therapy.
Tricuspid valve surgery is commonly indicated for moderate–severe functional tricuspid regurgitation due to left sided valvular heart disease or less commonly pulmonary vascular disease. Tricuspid valve surgery is also indicated for right heart failure refractory to medical therapy or progressive dilatation of the right ventricle. Severe tricuspid regurgitation is not a benign process because of its effects on systemic venous congestion, atrial rhythm and right ventricular function.
The anterior leaflet is the largest of all the leaflets. The tricuspid valve has papillary muscle and chordal attachments to the ventricular septum, unlike the mitral valve. The atrioventricular node lies just posterior to the commissure between the anterior and septal leaflets. Deeply placed sutures in the medial half of the septal leaflet may result in atrioventricular block. The right coronary artery lies in close proximity to the posterior leaflet. A deep suture placed in this region may result in injury to the coronary artery or kinking of the artery.
Most cases of tricuspid valve dysfunction are caused by failure of the coaptation of the leaflets due to annular dilatation. Tricuspid valve replacement is only rarely indicated, as an annuloplasty ring is adequate to correct functional tricuspid insufficiency in most cases.
Choice of Prosthesis
According to the American Heart Association Guidelines 2014, bioprostheses are recommended for patients over the age of 70 years while mechanical prostheses are recommended below 60 years of age provided there are no contraindications to anticoagulation. Between 60 and 70 years either prosthesis is reasonable. Patient choice is essential in the decision making process.
Prosthetic heart valves are susceptible to thrombosis. For patients with mechanical mitral valves and those with associated risk factors (i.e. atrial fibrillation, previous thromboembolism and hypercoagulable condition) receiving mechanical aortic valves, aspirin (75—100 mg once daily) as well as warfarin (with a target INR of 3) should be commenced in the early postoperative period and continued in the long term. Bridging anticoagulation with unfractionated heparin should be considered if warfarin therapy is interrupted for any future cardiac or non-cardiac procedures.
For mechanical aortic valves without risk factors, warfarin therapy with a lower target INR (2.5) and long-term aspirin (75—100 mg once daily) should be used.
Aspirin (75—100 mg once daily) and warfarin therapy (target INR 2.5) is recommended for the first 3 months following mitral valve repair or replacement with bioprostheses.
Repair of the mitral valve is preferable to replacement. If replacement is carried out, the subvalvular apparatus (papillary muscle and chordae) should be preserved in order to maintain left ventricular function. Mitral repair is associated with better short-term and long-term survival and less incidence of thromboembolism when compared to replacement.
Systolic anterior motion
Mitral valve repair is occasionally complicated by systolic anterior motion (SAM). SAM has long been recognised as a risk factor for left ventricular outflow tract obstruction and residual mitral regurgitation following mitral valve surgery. SAM results from the ‘Venturi effect’ pulling the mitral valve leaflets into the left ventricular outflow tract (LVOT). This may result in obstruction of the LVOT along with severe mitral regurgitation due to displacement of the anterior leaflet.
Intraoperative echocardiogram is essential to identify the risk of SAM and detection should this occur.
1. Narrow aortomitral angle (<120° pre repair).
2. Distance of the ventricular septum to coaptation point of the mitral leaflet <2.5 cm.
3. Posterior leaflet height >1.5 cm.
4. Basal septal diameter >1.5 cm.
When identified intraoperatively, initial measures include maintenance of adequate preload and reduction of tachycardia. If these conservative measures fail then insertion of a larger annuloplasty ring or a sliding annuloplasty should be performed in order to reduce the height of the posterior leaflet.
Postoperative management for prevention of systolic anterior motion includes the following:
1. Maintenance of adequate preload.
2. Increase afterload by using alpha agonists.
3. Reduce tachycardia by using beta adrenoreceptor blockers.
4. Avoidance of inotropic agents.
Combined valvular pathologies
Different valvular pathologies can occur in combination. The combination of aortic regurgitation along with mitral regurgitation carries high perioperative morbidity and carries the worst prognosis if left untreated. The combination of these two pathologies causes left ventricular enlargement, increasing volume overload and ultimately ventricular failure.
Following valve procedures, maintenance of sinus rhythm is beneficial in order to optimise cardiac output, as is careful optimisation of ventricular filling pressures.
Valve procedures can be complicated by heart block due to haemorrhage, oedema, suturing or aggressive debridement near the conductive tissue.
Degenerative disease is the commonest cause of mitral regurgitation. Localised ventricular infarct along with asymmetric ventricular remodelling affecting the posterolateral ventricular wall causes ischaemic mitral regurgitation. Functional mitral regurgitation is caused by a severely impaired and dilated left ventricle.
Although mitral and aortic valve diseases are the commonest indications for heart valve surgery, the tricuspid valve can be a potential source of considerable morbidity and mortality. Tricuspid valve disease commonly occurs secondary to left heart disease or pulmonary vascular disease.
The type of valve prosthesis used is dependent on the patient age, valve preference, comorbidities, valvular pathology and the contraindications to the use of anticoagulants.
1. A 28 year old female needs an aortic valve replacement for severe symptomatic aortic stenosis. She wants to complete her family within the next few years. What are the options for management?
2. An 80 year old female underwent mitral valve repair for severe mitral regurgitation. After coming off bypass her parameters were as follows: mean arterial pressure 45 mmHg, heart rate 95 beats/minute, central venous pressure 10 mmHg. TOE revealed systolic anterior motion of the mitral valve. What should be the next appropriate step?
3. After coming off bypass following aortic valve replacement for severe aortic stenosis, the patient has a mean arterial pressure of 50 mmHg, heart rate of 45 beats/minute and a central venous pressure of 12 mmHg. Atrial and ventricular wires had been inserted before coming off bypass. In order to increase the heart rate what is the best pacemaker mode that should be selected in order to optimise cardiac output?
4. What is the commonest cause of mitral stenosis?
5. After coming off bypass following mitral valve replacement there are ST depressions in leads I, II, V5, V6 and regional wall motion abnormalities in the lateral wall on TOE. What is the possible cause of the wall motion abnormalities?
Injury to the right coronary artery
Injury to the circumflex coronary artery
Injury to the left anterior descending artery
Air embolism of the coronary arteries
Chronic thromboembolic pulmonary hypertension (CTEPH) arises from total or partial occlusion of the pulmonary vascular bed from non-resolving thromboemboli. Although pulmonary embolism (PE) is one of the more common cardiovascular diseases, CTEPH remains an under-diagnosed condition. CTEPH is defined as precapillary pulmonary hypertension with mean pulmonary artery pressure (mPAP) of more than 25 mmHg, pulmonary capillary wedge pressure (PCWP) of less than 15 mmHg and pulmonary vascular resistance (PVR) of more than 2 Wood units.
CTEPH is a relatively rare but important sequela of deep venous thrombosis (DVT) and PE, where in up to 4% of patients, the acute embolic material fails to resolve. Given that DVT and PE is as common as 1/1000 population per year, the annual incidence of CTEPH may be of the order of 8–40 cases/million population. However, because some patients diagnosed with chronic thromboembolic disease have no preceding history of acute embolism, the true incidence of this disorder could be much higher.
The majority of DVT and acute PE are managed medically with anticoagulation. Cardiothoracic surgeons rarely become involved in management of acute PE, unless it is in a hospitalised patient who survives a massive embolism that causes life-threatening acute right heart failure and shock. Conversely, the majority of CTEPH cases are amenable to surgical treatment by pulmonary endarterectomy (PEA). PEA is the definitive, and in most cases the curative, treatment for CTEPH. The objective of the surgery is the normalisation of pulmonary artery pressure with resultant significant symptomatic and prognostic benefit. Medical management is only palliative, and lung transplantation has an inferior outcome compared with PEA and is only relevant for very selected patients with distal disease and extreme pulmonary hypertension (PH).
It is uncertain why some patients have unresolved emboli, but a variety of factors play a role, alone or in combination. Initially, thrombus resolution probably results from a combination of thrombus fragmentation and endogenous fibrinolysis. In the majority of patients this leads to complete clot resolution. Further resolution relies on clot organisation and neovascularisation, during which the obstructed vessel becomes recanalised and vessel patency is partially restored.
After the clot becomes wedged in the pulmonary artery, one of two processes occurs:
1. The organisation of the clot proceeds to canalisation, producing multiple small endothelialised channels separated by fibrous septa (i.e. bands and webs).
2. Complete fibrous organisation of the fibrin clot without canalisation may result, leading to a solid mass of dense fibrous connective tissue totally obstructing the arterial lumen.
The generation of PH in CTEPH is not just the result of simple obstruction of the pulmonary arterial bed; indeed, there is little rise in pulmonary artery pressure following a pneumonectomy. The increased pressure as a result of redirected pulmonary blood flow in the unobstructed pulmonary vascular bed can create an arteriopathy in the small precapillary blood vessels similar to that seen in idiopathic pulmonary arterial hypertension. Hence, the pathogenesis of chronic thromboembolic occlusion in CTEPH with resultant raised PVR is thought to be secondary to obstruction by thromboemboli and remodelling of the previously normal pulmonary vascular bed.
Clinical Presentation and Diagnosis
There are no symptoms specific for chronic thromboembolism. The most common symptom associated with thromboembolic pulmonary hypertension, as with all other causes of pulmonary hypertension, is exertional dyspnoea. This dyspnoea is out of proportion to any abnormalities found on clinical examination. Syncope, or presyncope, is another common symptom in severe pulmonary hypertension.
The physical signs of pulmonary hypertension are the same no matter what the underlying pathophysiology. Initially the jugular venous pulse is characterised by a large ‘A’ wave. As the right heart fails, the ‘V’ wave becomes predominant. The right ventricle is usually palpable near the lower left sternal border. The second heart sound is often narrowly split and varies normally with respiration. In the later stages of the disease, signs of right heart failure predominate with oedema and ascites. Tricuspid regurgitation can be severe, with a pansystolic murmur and an enlarged pulsatile liver.
High index of suspicion and awareness of the disease is crucial. The chest radiograph may be entirely normal. Pulmonary function tests reveal minimal changes in lung volume and ventilation. Diffusion capacity is often reduced and may be the only abnormality on pulmonary function testing. Most patients are hypoxic. Dead space ventilation is increased.
The ventilation-perfusion lung scan is the essential test for establishing the diagnosis. An entirely normal lung scan excludes the diagnosis of both acute and chronic thromboembolism.
Transthoracic echocardiogram (TTE) is usually the test that gives the first indication of the presence of PH. Systolic pulmonary artery pressure is significantly raised. Features that may be seen on TTE depend on the chronicity and degree of right ventricular failure; raised right ventricular dimension, impaired right ventricular function and right ventricular hypertrophy.
Currently, pulmonary angiography is said to be the gold standard imaging test for evaluation of operability in CTEPH, but experience is essential for the proper interpretation of pulmonary angiograms. Organised thrombi appear as filling defects, webs or bands, or as completely thrombosed vessels ‘missing’ (Figure 39.1). Distal vessels demonstrate the rapid tapering and pruning characteristic of pulmonary hypertension. Other modalities of imaging, including multislice CT pulmonary angiogram and magnetic resonance angiography, are gaining acceptance and are now favoured over conventional angiography in some centres.
Figure 39.1 Right pulmonary angiography of a patient with CTEPH demonstrating a web in the trifurcation of the lower lobe vessels with complete occlusion of two segments of the lower lobe and both segments of the middle lobe.
Right heart catheterisation is crucial for the diagnosis of pulmonary hypertension, defined as a mPAP >25 mmHg at rest. Right atrial pressure, right ventricular end-diastolic pressure, pulmonary artery pressure and mixed venous O2 saturation are measured directly. Cardiac output and PVR can then be calculated. Coronary angiography and other cardiac investigations are recommended for patients over 40–45 years being considered for surgery.
The main treatment of CTEPH is surgical and all patients with suspected CTEPH should be referred to an experienced unit able to perform PEA. Untreated, the prognosis of CTEPH is very poor with severe debilitation and premature death from right heart failure. In historical case series, the mean survival is 6.8 years, and when the mPAP of patients with thromboembolic disease reaches 50mmHg or more, the 3-year mortality is about 90%.
Chronic anticoagulation represents the mainstay of the medical regimen. Anticoagulation is primarily used to prevent future embolic episodes, but it also serves to limit the development of thrombus in regions of low flow within the pulmonary vasculature. Historically, inferior vena caval filters were used routinely to prevent recurrent embolisation but this is now not recommended, as there are few data to support this indication.
Data from clinical drug trials in CTEPH are limited. Specific disease targeted drug therapy is therefore not licensed for CTEPH patients, but drugs used for the treatment of idiopathic pulmonary arterial hypertension such as Bosentan and Sildenafil are sometimes used and may provide symptomatic improvement in some patients.
The basis of the operation is the removal of the obstruction of the pulmonary vascular bed by endarterectomy within the superficial media of the arterial wall. Therefore, the reduction in the PVR after pulmonary endarterectomy is dependent on the burden of ‘clearable’ disease as defined on preoperative imaging. The correlation between the degree of ‘clearable’ disease in imaging studies and PVR is the main determinant of operability. The absolute preoperative and resultant postoperative PVR are also the main factors that determine outcome after endarterectomy. Mortality following endarterectomy may be five- to ten-fold higher in patients with a preoperative PVR > 1200 dyne s/cm5. Similarly, a postoperative residual PVR of > 500 dyne s/cm5 is a risk factor for in-hospital mortality.
Although preoperative imaging helps to determine operability, the true extent of the disease can only be determined intraoperatively and has been classified in four types:
Type 1: Central disease where major vessel clots (fresh and/or mature) are present.
Type 2: Lobar and segmental disease where thickened intima is present with webs in the lobar and segmental branches.
Type 3: Subsegmental disease where the disease begins distally at the subsegmental branches.
Type 4: Distal disease where small vessel disease is present and represents inoperable disease.
Surgery is more successful in patients with types 1 and 2 disease, with a greater reduction in PVR and lowest mortality. Surgery in patients with the more distal type 3 disease is more challenging with a smaller reduction in PVR and higher risk. Patients with predominant type 4 disease are considered ‘non-operable’ or to have ‘non-surgical’ disease.
This must be weighed against the amount of ‘clearable’ disease based on imaging and correlated to the pulmonary vascular resistance measured preoperatively.
Other patient comorbidities that will be significant in a prolonged cardiopulmonary bypass time such as age, known cerebrovascular condition, renal impairment and intrinsic lung parenchymal disease should also be considered.
The approach is via a median sternotomy with cardiopulmonary bypass (CPB). The patient is cooled systemically to 20oC and right and left pulmonary arteriotomies are performed within the pericardium. Adequate visualisation for distal dissection necessitates reduction in bronchial arterial collateral return to the pulmonary arteries. This is achieved by periods of complete deep hypothermic circulatory arrest for up to 20 minutes at a time with an intervening period of 10 minutes of re-perfusion on CPB. A cast of the inner layer of the pulmonary arterial tree is then dissected free (Figure 39.2).
Figure 39.2 Endarterectomy casts from both pulmonary arteries of the same patient in Figure 39.1, demonstrating long tapering ‘tails’ which is a hallmark of good clearance.
After completion of the endarterectomies, the patient is rewarmed slowly on full CPB. The procedure time is long because of the time necessary to cool and warm on bypass.
The aim is to achieve an immediate fall in mean PA pressure by approximately 50%, and reduction in PVR to approximately one third of the preoperative level in the majority of patients.
Most of the general principles of postoperative cardiac surgical care apply, but these principles centre around the management of the left ventricle. The management of patients following PEA involves these two principles:
Careful management of the right ventricle;
Minimising the pulmonary vascular resistance.
Most patients with CTEPH have a normal functioning left ventricle in the absence of coronary atherosclerosis and ‘left-sided’ heart valvular disease. Therefore left ventricular cardiac output and ultimately end-organ perfusion is usually dependent on the contractile reserve of the right ventricle and pulmonary vascular resistance in the post-PEA patients.
The contractile reserve of the right ventricle in the post-PEA patients depends on the following:
The varying degree of right ventricular impairment secondary to CTEPH in the preoperative period;
The post-PEA pulmonary vascular resistance that is dependent on the amount of disease cleared during PEA with resultant fall in pulmonary artery pressure. High PVR in the postoperative period can be due to technical failure to clear ‘surgical’ disease and/or presence of type 4 distal disease (inoperable):
Prolonged cardiopulmonary bypass, prolonged myocardial ischaemic time and inadequate right ventricular myocardial protection during PEA which impacts on right ventricular performance upon weaning from cardiopulmonary bypass.
Pulmonary vascular resistance in the post-PEA patient can be affected by the following:
Right ventricular function, hence inexplicably linked;
Hypoxia secondary to poor perfusion matching, intrinsic lung parenchymal disease, fluid overload, lung sepsis and mechanical complications such as pneumothorax;
Vasoconstrictor agents such as noradrenaline;
High peak airway pressures.
Considering the above factors when receiving a patient onto the Critical Care Area (CCA) following PEA surgery will help plan for potential problems that may be encountered during the postoperative period.
Patients returning from the operating room following PEA surgery should have the following monitoring:
3 lead ECG monitoring;
Invasive radial and femoral arterial pressure;
Invasive central venous pressure;
Invasive pulmonary artery pressure;
Peripheral oxygen saturation and respiratory rate;
Blood temperature and end-tidal CO2 measurement.
The femoral arterial line, which is placed after induction, is used in preference to the radial line due to damping associated with cooling and rewarming during surgery. It is used for the first 12 hours in CCA before being removed and arterial monitoring reverts back to the radial line.
The balloon at the tip of the pulmonary artery catheter is disabled and never inflated. Pulmonary artery wedge pressure is taken as a default at 10 mmHg to allow comparison of pulmonary vascular resistance over time. Cardiac output and other haemodynamic measurements are taken at 4 hourly intervals during the first 24 hours. The pulmonary arterial catheter is usually removed 24 hours after the patient is extubated, and providing there are no concerns regarding residual pulmonary hypertension.
Patients are connected to the ventilator in the operating room before weaning of cardiopulmonary bypass. The patient is then transferred to the CCA with the same ventilator to ensure a continuous level of positive end-expiratory pressure (PEEP).
A chest radiograph is usually obtained within an hour of arrival in the CCA, to exclude the presence of pneumothorax and early signs of reperfusion lung injury (see below).
The patient is nursed in a slight upright position of at least 30° to reduce the preload on the right ventricle.
Recommended ventilator settings on arrival to the CCA are as follows:
SIMV or SIMV PRVC mode;
Fraction inspired oxygen percentage (FiO2) of 80%;
Tidal volume set at 10 ml/kg;
Respiratory rate at 16/minute;
PEEP of 6 cmH2O;
Pressure support of 12 cmH2O above PEEP level.
An aggressive ventilator weaning protocol is adopted with the aim of facilitating extubation by the first postoperative day. The FiO2 is decreased by 10% every second hour, as long as the PaO2 is above 12 kPa (or every hour if PaO2 is above 25 kPa). Once FiO2 of 40% is reached, the PEEP is decreased at a rate of 1 cmH2O every hour down to a minimum of 2 cmH2O. Peak airway pressure should be less than 30 cmH2O.
Most patients who have had a good surgical clearance during PEA surgery with resultant mPAP of less than 25 mmHg and a low PVR, who are haemodynamically stable with satisfactory acid–base balance, should achieve these ventilator targets by the first postoperative day. The sedation is then turned off and the patient is allowed to wake up and is extubated.
In some cases, it may be necessary to extubate the patient onto a continuous positive airway pressure (CPAP) mask, especially when the PaO2 is borderline low or the patient is cerebrally agitated or obtunded, to avoid hypoxia and maintain normocapnoea.
The specific aim is to achieve a negative daily fluid balance and support the right ventricle. Mannitol (12.5 g, 6 hourly for 6 doses) and furosemide (40 mg, 6 hourly for 6 doses then decrease to 8 hourly on day 2 and 12 hourly on day 3) are used to keep these patients ‘dry’. At Papworth Hospital NHS Foundation Trust, the standard inotropic support following PEA surgery is dopamine at 3–5 µg/kg/min until the patients are discharged to the ward.
Rarely, the patients develop systemic hypertension during the first 24 hours due to a systemic vascular resistance that remains high and this is associated with low or borderline low cardiac indices. Most patients can tolerate this and do not require intervention unless the low cardiac output impacts on end-organ perfusion such as renal function. Phosphodiesterase inhibitor such as Enoximone is sometimes used in this situation.
In situations where residual pulmonary hypertension remains post PEA surgery, preoperative drugs such as Bosentan and Sildenafil may be continued in the postoperative period. In cases where residual pulmonary hypertension is significant post PEA with concomitant right ventricular impairment or failure, ilioprost (nebulised) is frequently used as an adjunct (see residual PH and right ventricular failure below).
The prophylactic antibiotic of choice is Tazocin, which is a combination antibiotic containing extended-spectrum penicillin antibiotic piperacillin and β-lactamase inhibitor tazobactam. The combination has activity against many Gram-positive and Gram-negative pathogens and Pseudomonas aeruginosa. This covers both the sternotomy wound and the potential pathogens that the lung may be exposed to. In patients who have penicillin allergy, vancomycin and aztreonam are used instead.
Fluid Balance and Renal Support
In patients who develop acute or acute-on-chronic kidney injury secondary to the effects of prolonged cardiopulmonary bypass and surgery, maintaining aggressive diuresis can be challenging. Furosemide may be switched to an infusion. Haemofiltration is often used to maintain acid–base balance and maintain negative balance, especially when the kidney injury impacts on ventilatory weaning and haemodynamic stability.
Dilutional and consumptive coagulopathy is not uncommon after a prolonged cardiopulmonary bypass with low platelet counts and clotting factors. Unless there is significant bleeding, transfusion of blood products such as pooled platelets, fresh frozen plasma and cryoprecipitate are to be avoided in the first 24–48 hours. Infusion of these products into a pulmonary vasculature that is denuded of its intimal layer can result in release of cytokines and formation of microemboli, which result in a rise of the mPAP and PVR.
Enoxaparin 40 mg once daily is usually started on the evening of the first postoperative day. If the patient is extubated, warfarin is commenced on the second postoperative day. If warfarin cannot be instituted, heparin infusion is commenced. This is an important part of PEA management as anticoagulation with warfarin or another novel direct Xa inhibitor like Rivaroxaban is the mainstay of CTEPH prevention post PEA surgery.
Prolonged cardiopulmonary bypass and periods of deep hypothermic circulatory arrest may impact on the neurological function especially in the elderly. In addition, elderly patients on long term warfarin have a very small but significant prevalence of chronic subdural haematomas. Combined with a coagulopathy in the immediate postoperative period, all these can contribute to cerebral agitation or obtunded neurological state when sedation is switched off. In addition, tranexamic acid infusion (started during surgery to prevent fibrinolysis) may give rise to small incidences of epileptic fits.
Therefore, the threshold to perform CT brain scans in these patients who do not wake up appropriately should be low to avoid missing treatable causes of an altered neurological state. Otherwise, if the CT scans are inconclusive, the treatment is largely supportive and patients usually recover with conservative management.