3. Aortic Valve Disease.

Aortic stenosis may be caused by rheumatic heart disease, degeneration and calcification of the valve, either as a result of ageing, or in a congenitally abnormal (usually bicuspid) valve. The distinction between a ‘stenotic’ and a ‘sclerotic’ valve is artificial. Sclerosis does stenose the valve but rarely to a critical degree. Severe aortic stenosis is said to affect 2% of those aged greater than 65 years in the developed world, with that figure doubling to 4% in the over-85-year-old group.

Determination of the peak pressure gradient across the valve is less reliable than estimations of valvular area, but the quoted values for grading severity are: Normal <10 (mmHg); Mild <40; Moderate 40–65; Severe >65. The cross sectional area of a normal aortic valve is 2.5–3.5 cm2. An area <1.0 cm2 is usually an indication for urgent surgical valve replacement. At areas of <0.7 cm2 (‘critical’ stenosis), any demand for increased cardiac output, such as occurs during advancing pregnancy or during exercise, is likely to be associated with angina pectoris, syncope and sudden death Asymptomatic but severe aortic stenosis carries a risk of sudden death of around 1%. Once symptoms supervene, then life expectancy shrinks to 2 years with a 50% probability of sudden death

Clinical signs of the disease include narrowed pulse pressure (a value of <30 mmHg suggests severe disease), and a coarse systolic murmur in the aortic area. Systolic blood pressure may be lower than expected because of the reduced cardiac output. The gradient may be misleadingly low in a patient whose failing left ventricle is unable to generate high systolic intraventricular pressures.

As narrowing progresses there is increased pressure loading on the left ventricle, which undergoes concentric hypertrophy. The hypertrophic left ventricle is less compliant, thus myocardial oxygen demand increases while supply falls. Systole through the stenosed valve is prolonged, and so diastolic time during the cardiac cycle is proportionately reduced. The high intraventricular pressures almost completely abolish systolic coronary flow. Diastolic subendocardial perfusion also decreases unless perfusion pressures remain high. The decrease in ventricular compliance and the loss of ventricular filling by passive elastic recoil means that the atrial contribution to filling becomes more important. It may in some cases be responsible for up to 50% of LVEDV. Atrial fibrillation may lead to cardiac decompensation

Aortic stenosis leads to a fixed output state, which is maintained by compensatory mechanisms that may be disrupted by anaesthesia. Decompensated mitral stenosis manifests as heart failure; decompensated aortic stenosis may manifest as death. It is particularly important to maintain coronary perfusion during diastole. • Contractility • SVR • Rate + Rhythym

effective contraction maintains cardiac output in aortic stenosis (as in all valvular lesions), and undue myocardial depression should be avoided. Increasing myocardial drive, however, does increase myocardial work and oxygen demand, and may precipitate subendocardial ischaemia.

Maintenance of systemic vascular resistance (SVR) and diastolic blood pressure: if SVR falls, then coronary diastolic perfusion may fail, with potentially disastrous consequences. Vasodilatation must be avoided and preload maintained to ensure flow across the stenotic valve. This has obvious implications for the use of the many anaesthetic agents which decrease SVR, including local anaesthetics used in neuraxial block. Cardiopulmonary resuscitation in the presence of aortic stenosis and left ventricular hypertrophy is rarely successful.

Maintenance of systemic vascular resistance (SVR) and diastolic blood pressure: if SVR falls, then coronary diastolic perfusion may fail, with potentially disastrous consequences. Vasodilatation must be avoided and preload maintained to ensure flow across the stenotic valve. This has obvious implications for the use of the many anaesthetic agents which decrease SVR, including local anaesthetics used in neuraxial block. Cardiopulmonary resuscitation in the presence of aortic stenosis and left ventricular hypertrophy is rarely successful.

Heart rate and rhythm: bradycardia will decrease cardiac output, but tachycardia is more detrimental because it limits the time for diastolic coronary perfusion. The optimal heart rate in sinus rhythm is 60–80 beats per minute. Arrhythmias, including AF, require urgent treatment, but myocardial depressants such as β-adrenoceptor blockers are better avoided.

Patients with severe aortic stenosis can be difficult to manage. Cases presenting for non-emergency surgery should be referred to a specialist centre for consideration of aortic valve replacement. Otherwise anaesthesia should include invasive monitoring of intra-arterial and central venous pressure, and it may be necessary to run a continuous infusion of vasopressor (such as noradrenaline) to ensure that SVR is maintained.

rare. The overall prevalence in the general population is quoted as around 1%. There are infectious causes (bacterial endocarditis, syphilis, rheumatic fever), congenital abnormalities (bicuspid valve), degenerative and connective tissue disorders (Marfan’s syndrome, Ehlers–Danlos) and inflammatory conditions (rheumatoid arthritis, systemic lupus erythematosus). Abnormal dilatation of the ascending aorta itself may cause regurgitation in the absence of pathology affecting the valve itself.

The condition is usually chronic, although acute aortic regurgitation can occur with dissection or as the result of destruction of the valve by bacterial endocarditis. The regurgitation during diastole of part of the left ventricular stroke volume decreases forward blood flow through the aorta. This results in continuous volume overload of the left ventricle, which initially dilates to accommodate this extra volume. On the ascending part of the Frank–Starling pressure–volume curve, the increase in myofibril length improves the efficiency of contraction. With increasing dilatation, the heart moves on to the descending part of the curve, at which point acute cardiac failure may supervene. In acute aortic incompetence, the left ventricle is unable to dilate, and there is an increase in left ventricular diastolic pressure and pulmonary venous pressure with the potential for pulmonary oedema.

Compensatory mechanisms act to reduce the volume of regurgitant blood. As with mitral incompetence, a regurgitant fraction of 0.6 or greater denotes severe disease. There is an increase in left ventricular size with eccentric hypertrophy. There is also an increase in ventricular compliance, which allows an increase in volume at the same pressure. This means that end-diastolic pressure is reduced, and with it ventricular wall tension which is an important determinant of myocardial oxygen demand. The left ventricular ejection fraction is maintained, since the stroke volume and LVEDV increase together. A rapid heart rate is advantageous, because it reduces the time for diastolic filling. LVEDV is decreased, and so there is less ventricular over distension. — Lower SVR offloads the myocardium and ensures forward flow.

Preload: normovolaemia should be maintained to ensure that the dilated ventricle remains well filled.
SVR: this should be kept low so as not to increase the impedance to outflow with an increase in the regurgitant fraction. Heart rate: bradycardia increases the time for ventricular over distension. A relative tachycardia will reduce the regurgitant fraction.
Contractility: it is obvious that undue myocardial depression should be avoided.