3. Mitral Valve Disease Flashcards
Why important
risk that anaesthesia and surgery will cause perioperative decompensation.
discussion of physiology and pharmacology applied to a fixed cardiac output state.
Mitral Stenosis
Mitral stenosis is almost always due to untreated rheumatic fever, usually following
streptococcal infection. It is increasingly rare to see this in the UK.
Pathophysiology:
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
LV filling
- 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.
Pulmonary pressures
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).
Anaesthetic Implications of Mitral Stenosis
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:
Contractility
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): + PVR
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
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.
Mitral Incompetence/ MR
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.
Pathophysiology MR
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
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
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.
Infective bacterial endocarditis
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.
Symptoms of MS
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.
