3. Aortic Valve Disease. Flashcards
Causes + prevelance
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.
Severity + Mortality
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
Sx
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.
Pathophysiology
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
Anaesthetic Implications of Aortic Stenosis
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
Contractility:
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) + DBP +Preload
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) + DBP +Preload
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:
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.
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.
Aortic Incompetence
incidence + causes
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.
Pathophysiology
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
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.
Anaesthetic Implications of Aortic Incompetence
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.
