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.