Abstract
The AV is composed of three semilunar cusps left (posterior), right (anterior) and non-coronary cusp, which are related to the three sinuses of Valsalva. The main functions of the AV are to permit unimpeded LV systolic ejection and to prevent regurgitation of the LV stroke volume during diastole. The normal adult AV orifice area is 2-4 cm2.
The AV is composed of three semilunar cusps left (posterior), right (anterior) and non-coronary cusp, which are related to the three sinuses of Valsalva. The main functions of the AV are to permit unimpeded LV systolic ejection and to prevent regurgitation of the LV stroke volume during diastole. The normal adult AV orifice area is 2-4 cm2.
Aortic Stenosis
AS is defined as a fixed obstruction to systolic LV outflow.
Clinical Features
Patients may be asymptomatic for many years, although normally present with one or more of the classic triad of symptoms; angina, syncope or breathlessness. Less fortunate patients may present with sudden death. Fifty per cent survival rates from onset of symptoms are as shown in Table 9.1.
Table 9.1 Survival rates from onset of symptoms in AS
| Presenting symptom | 50% Survival rate |
|---|---|
| Angina | 5 years |
| Syncope | 3 years |
| Breathlessness | 2 years |
Pathology
In most cases, AS is an acquired disease. Degenerative calcification causes thickening and stiffness of the leaflets. It is associated with advanced age (>70 years) and often with MV annular calcification. Chronic rheumatic AV disease causes commissural fusion and AR is more common.
Bicuspid AV, with a prevalence of 2%, is one of the commonest congenital heart lesions. Patients with a bicuspid AV have a shorter latency period to symptom onset due to earlier degeneration and calcification.
More rarely, AS may be at a supra- or subvalvular level. Similar principles of anaesthetic management apply.
Pathophysiology
The fixed obstruction to LV ejection causes chronic LV pressure overload and increased wall tension (wall tension = LV pressure × LV end-diastolic radius/(2 × LV wall thickness) – Laplace’s law). This increase in wall tension is offset by the development of concentric LVH at the price of diastolic dysfunction secondary to impaired relaxation and reduced compliance, manifest as elevated LVEDP (Figure 9.1). LV end-diastolic dimensions are usually preserved in early AS.
Figure 9.1 Pressure waveforms obtained simultaneously from the LV cavity and the aortic root (Ao) in AS. The peak-to-peak gradient is measured in the catheter laboratory and is the difference between the peak systolic pressures in the LV cavity and aortic root. Note that peak aortic root pressure is reached later than peak ventricular pressure. The maximum or instantaneous gradient is usually measured by CWD ultrasound.
Angina Pectoris
An imbalance between myocardial DO2 and VO2 may occur even in the absence of significant coronary artery disease. The combination of LVH and wall tension increases the systolic myocardial VO2, while a reduction in coronary perfusion pressure decreases the myocardial DO2.
Syncope
Syncope typically occurs on exertion. The SV is limited in moderate or severe AS, giving a ‘fixed’ or ‘limited’ CO. An inability to compensate for exercise-induced peripheral arterial vasodilatation is the most common explanation for syncope. Ventricular dysrhythmia is another potential cause.
Dyspnoea
Breathlessness, particularly orthopnoea, is the most sinister of the triad of symptoms and may herald the onset of LV decompensation/dilatation. An increased LVEDP necessitates higher left-sided filling pressures, which leads to pulmonary congestion (Figure 9.2). Decompensation arises when the LV wall tension can no longer be maintained by systolic wall thickening and the LV dilates. LV dilatation is associated with increased wall tension (Laplace’s law).
Investigations
ECG: Increased R- and S-wave amplitude, T-wave inversion (strain pattern) in anterior chest leads.
2D echocardiography: AV anatomy and function, LV function, aortic root size. Typical features are: leaflet thickening, calcification, reduced opening. Planimetric measurement of the AV orifice area (AVA) is unreliable in the presence of calcification.
CFD: Turbulence across valve. Does not permit assessment of severity. May demonstrate associated regurgitation.
CWD: Because alignment of the ultrasound beam with blood flow through the AV is easier, TTE provides a more accurate assessment of the AV gradient than TOE using the deep transgastric view (Chapter 34). Peak AV gradient = 4 × peak velocity2 (modified Bernoulli equation). The AVA can be measured using the continuity equation (Chapter 34).
Coronary angiography: To exclude coronary disease. Mandatory in males >40 years or females >50 years.
Ventriculography: LV function, peak-to-peak AV gradient.
Multidetector row CT (MDCT): To define valvular anatomy and AVA in poor TTE subjects unable to undergo TOE (Figure 9.3).
Figure 9.3 64-slice MDCT axial view of AVs. (A) Normal valve. (B) Bicuspid valve. (C) Measurement of AVA by planimetry in a stenotic calcified valve.
Anaesthetic Goals
Sinus rhythm and the late diastolic ‘atrial kick’ are very important in these poorly compliant hearts. Atrial contraction can account for 30–40% diastolic filling in these patients (cf. 15–20% in normal patients). AF and nodal rhythms result in the failure to maintain preload and are poorly tolerated (Box 9.1).
