3. Mitral Valve Disease

risk that anaesthesia and surgery will cause perioperative decompensation. discussion of physiology and pharmacology applied to a fixed cardiac output state.

Mitral stenosis is almost always due to untreated rheumatic fever, usually following streptococcal infection. It is increasingly rare to see this in the UK.

The pressure gradient across the narrowed valve is less reliable than estimations of valvular area, which is the key factor determining flow. The cross-sectional area of a normal mitral valve area is 4–6 cm2. Stenosis may be graded as mild (1.6–2.5 cm2), moderate (1.1–1.5 cm2) severe (<1 cm2). Between 2.5 and 4.0 cm2 the narrowing is not clinically significant • LV filling • LAH • Pulmonary pressures

• As the stenosis worsens, the left atrium dilates and hypertrophies, and the contribution of atrial contraction to left ventricular filling becomes progressively more important, increasing from 15% up to 40%. • Compensatory bradycardia allows sufficient time for diastolic flow across the stenosis. • These factors explain why the onset of atrial fibrillation (AF) with the loss of this crucial contribution to left ventricular filling can be calamitous. • In time, the increased left atrial pressure (LAP) is reflected in pulmonary hypertension and right ventricular overload.

As pulmonary venous pressure increases, symptoms will include dyspnoea on exertion, orthopnoea and paroxysmal nocturnal dyspnoea. Impaired exercise tolerance is a good guide to disease severity. Pulmonary sequelae of mitral stenosis may encompass reduced lung compliance and a rise in airway resistance, both of which increase the work of breathing. Gas exchange worsens with a widening of the alveolar–arterial oxygen difference (A–aDO2).

Mitral stenosis can lead to a fixed output state. Anaesthesia must minimize interference with compensatory mechanisms, because attempts to manipulate the cardiac output by the use of fluids or vasoactive drugs may prove fruitless • Heart rate and rhythm: bradycardia may allow increased stroke volume but at the expense of cardiac output; tachycardia will reduce stroke volume and also reduce cardiac output Maintenance of cardiac rhythm: sudden onset of AF must be treated aggressively, with DC cardioversion if necessary, otherwise pulmonary oedema may develop. If AF is already present, the ventricular response rate must be controlled. • Circulating volume: • Contractility • SVR • PVR

Circulating volume: normovolaemia is important. If LAP drops because of reduced venous return, then cardiac output will fall as flow across the stenotic valve decreases. Patients may also be very sensitive to increases in venous return; in severe stenosis cardiac output cannot change, and pulmonary oedema may supervene Contractility: effective myocardial contraction is important and depression must be minimized.

Systemic vascular resistance (SVR): normal SVR ensures adequate coronary perfusion during diastole.
Pulmonary vascular resistance (PVR): hypercapnia, hypoxia and acidosis will all increase PVR. Nitrous oxide further increases PVR in the presence of pre-existing pulmonary hypertension and so should be avoided.

Anticoagulation: patients may be taking oral anticoagulants which may need to be changed to parenteral heparin during the perioperative period, depending on the surgery to be undertaken.

commoner than stenosis. It is rheumatic in origin in around 50% of cases. Other causes include disruption of the chordae tendinea and papillary muscle supporting structures (this can follow myocardial infarction), and dilatation of the valve ring itself.

During systolic left ventricular contraction there is regurgitant flow back into the left atrium in addition to forward flow through the aorta. This can be quantified by measuring the regurgitant fraction: up to 0.3 is classified as mild; a fraction of 0.6 or greater is severe. This regurgitant flow leads to volume overload of left atrium and left ventricle. Although left ventricular end-diastolic volume (LVEDV) may increase fourfold, the function of the ventricle is usually well preserved because the larger volume of blood can be unloaded both through the aorta and the mitral valve, and so systolic ventricular wall tension is not high. In time, however, this process leads to an irreversible decline in contractile function.

The left atrium dilates, and AF may supervene, but this does not cause the critical decompensation in cardiac function that may be seen in mitral stenosis. Mitral incompetence does not in general impose large costs in terms of myocardial oxygen demand (owing to ventricular wall tension, contractility and heart rate). This allows some compensation by a relatively rapid heart rate, which reduces the time for further ventricular overload. The prolonged filling time associated with a bradycardia increases ventricular volume, may cause further functional dilatation of the annulus and with it a rise in the regurgitant fraction. The left ventricle also dilates, with an increase in LVEDV and pressure. Forward flow of blood into the systemic circulation depends on the relative impedances of the two parallel paths, and so is enhanced by low PVR.

Anaesthetic Implications of Mitral Incompetence
Heart rate: relative tachycardia is preferable to bradycardia because it reduces left ventricular overload. Bradycardia may increase ventricular filling and further dilate the valve ring.
Circulating volume: patients may be sensitive to large rises in preload, because this will further distend the left atrium and predispose to pulmonary oedema. Contractility: myocardial depression should be avoided.
SVR: the forward flow of blood is dependent on low peripheral resistance. Vasoconstrictors should be used with caution.

Their most recent guidelines (2015 and 2016) reiterate that although patients with acquired valvular disease should be considered to be at increased risk of developing infective endocarditis, they should not be given routine prophylactic antibiotics. In essence this conclusion was drawn from the lack of any supporting evidence, together with more mundane examples to suggest that prophylaxis is redundant when it is known, for example, that the fact of simple tooth brushing is associated with a transient bacteraemia comparable to that produced by surgical trauma.

Recurrent bronchitis, dyspnoea, cough with bloodstained, frothy sputum (pulmonary oedema) and palpitations (secondary to atrial fibrillation). Eventually, there is fatigue and peripheral oedema with the onset of right heart failure. There may also be symptoms related to systemic emboli and, rarely, a hoarse voice secondary to compression of the left recurrent laryngeal nerve by the enlarged left atrium.

Signs Malar flush Irregularly irregular pulse Tapping, undisplaced apex beat ( ≡ palpable first heart sound) Left parasternal heave On auscultation there is an opening snap (mitral valve) followed by a mid-diastolic, rumbling murmur localized to the apex. There may also be signs of left and right heart failure and tricuspid regurgitation secondary to the back pressure from the left side.

If in sinus rhythm, there will be biphasic P waves and signs of right heart strain. Atrial fibrillation

This is a PA chest X-ray of a female patient. The film is not rotated and is adequately penetrated. There is a double heart border on the right and straightening of the upper left heart border suggesting an enlarged left atrium. The carina is splayed greater than 60◦ and there is upper lobe blood diversion These features suggest mitral stenosis. In addition, there is cardiomegaly (CT ratio>0.5) which only occurs in the presence of co-existing mitral regurgitation. The diagnosis is therefore mixed mitral valve disease.

These are the features of pulmonary hypertension and pulmonary oedema. In addition, the mitral valve annulus may be a calcified

• Pulmonary arteries prominent in perihilar regions but ‘pruned’ peripherally. • Upper lobe blood diversion (mild venous hypertension). • Interstitial oedema (moderate) – fluid in fissures, pleural effusions and Kerley B lines. • Alveolar oedema (severe) – pleural effusions, areas of consolidation and mottling of the lung fields.